Second Edition

DIAGNOSIS AND

TREATMENT OF

PAIN OF

VERTEBRALORIGIN

Second Edition

Robert MaigneEdited byWalter L. Nieves

DIAGNOSIS AND

TREATMENT OF

PAIN OF

VERTEBRALORIGIN

Boca Raton London New York

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Library of Congress Cataloging-in-Publication Data

Maigne, Robert.Diagnosis and treatment of pain of vertebral origin / by Robert Maigne and Walter L. Nieves.--2nd ed.

p. cm. -- (Pain management ; 1)Includes bibliographical references and index.ISBN 0-8493-3121-81. Spine--Disease--Treatment. 2. Manipulation (Therapeutics). 3. Spinal adjustment. 4. Bachache--Treatment. 5. Pain--Treatment.I. Nieves, Walter L. II. Title. III. Series.[DNLM: 1. Spine--anatomy & histology. 2. Spine--physiopathology. 3. Manipulation, Orthopedic. 4. Pain--therapy. 5. Spinal

Diseases. WE 725 M218d 2005]RD768.M28813 2005 616.7'306--dc22 2005041836

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FOREWORD

At a time in medicine when pain assumes a great pro-portion of disability, and much is related to the neuromus-culoskeletal system, all approaches merit exposition.

Dr. Maigne has been a strong proponent of diagnosticmanual medicine and has offered a scientific basis forrelief by manipulative techniques. He has written exten-sively in French, and his methods have been studied byphysicians from many countries. Physicians and studentsthe world over have been privileged to study his methodsand techniques. His books have literally become tomes ofvaluable information, and his concepts have becomeaccepted in medical orthopedics.

Manipulative technique, however, is only a small, albeitprominent, aspect of this text. Dr. Maigne has scientif-ically verified and explained many peripheral impairmentsas being related to their origin at the vertebral level fromthe posterior radicular branches and minor articular ordiscal abnormalities. His neuroanatomical explanationsare brilliantly illustrated and documented with a profoundreview of the literature. In today’s epidemic disabilitiesresulting from neuromuscular etiologies, Maigne’s con-cepts and clinical evaluations are welcomed.

The modality of vertebral manipulation has enjoyedadvocacy for centuries, but the precise indications and thespecific techniques indicated for the pathologies ascer-tained remain inaccurate. Dr. Maigne has developed diag-nostic procedures that accurately ascertain the exactpathology and its vertebral site. Such accuracy has beendeficient in most osteopathic and chiropractic specialtiesthat advocate manipulation.

The concept of regaining lost joint range of motion,which is considered the basis of osteopathic and chiro-practic techniques, by forcing that particular segment fur-

ther is disputed by Maigne. He advocates manipulating inthe direction that is free and contralateral to the directionthat provokes pain. The direction, the precise vertebralsegment, and its pathological significance are the bases ofthe Maigne techniques.

Manipulative technique also begs clarification anddemands personal hands-on learning. This has been Dr.Maigne’s success in personally training physicians fromall over the world. The benefit he has given patients whohave come from all over the world for his services affirmsthe benefit of his method.

In this text, his techniques are clearly and preciselydemonstrated and allow the trainee to learn from reading.The illustrations for appropriate diagnosis and ultimatetreatment are extremely well presented. To reiterate, how-ever, the value of this text is to acquire the technique ofmanual evaluation of the mechanism of common pain ofspinal origin that justifies manipulative intervention.

Many practitioners of medicine were denied this textbecause it was in French. Fortunately, it is now availablefor English-reading physicians and therapists and willbecome a mandatory text in all medical libraries andoffices.

Rend Cailliet, M.D.Professor Emeritus, School of Medicine,

University of Southern CaliforniaEditor, Neuromusculoskeletal Pain Series,

F.A. Davis Company, Philadelphia

This foreword appeared originally in the first edition of Diagnosis and Treatment of Pain of Vertebral Origin published by Williams & Wilkins.

v

PREFACE

The purpose of this book is to invite the reader to takea new look at common pains of spinal origin. My firstbook, Les manipulations vertebrales, published in 1960,aimed at recognition of this therapeutic method by themedical profession. At that time, manipulation was widelycriticized, rejected, and even considered a kind of charla-tanism. It is true that manipulation was used as the onlyform of treatment by certain nonmedical schools that con-sidered hypothetic vertebral microdisplacements thesources of all disease. However, experience convinced meof their potential. Therefore, I attempted to present theirindications and contraindications precisely, to select thereliable techniques, describe them in an objective way,and assign clear rules of application. I proposed the “ruleof pain-free and opposite motion.” That is to say that themanipulation must be performed in a direction in whichthe range of motion is free and opposite to the directionin which the motion is painful, rather than simply attempt-ing to restore a real or supposed limitation of the mobilityof a vertebral segment.

This rationale for manipulation achieved recognitionby the Faculty of Medicine, and in 1969, a diploma ofOrthopaedic Medicine and Manual Therapeutics was cre-ated at the University of Paris VI (Broussals Faculty, HôtelDieu). I was offered the directorship of the program — aprogram that extended far beyond the simple teaching ofthese techniques and covered broadly common vertebralpathology. During the following 20 years, teachingfounded on the same model was organized in other med-ical schools in France; Marseille was the first in 1975.

My second book, Douleurs d’origine vertebrale ettraitements par manipulations, had the subtitle, Lesderangements intervertebraux mineurs. The sometimessurprising results of these treatments compelled one toreflect. Often, in a very spectacular way, vertebral manip-ulation relieved a certain pain, whose spinal origin wasevident (although the mechanism of action was not clear),and other pains, apparently unrelated to the spine, woulddisappear. However, when inappropriately executed, thesetechniques could provoke both types of pain.

Traditional practitioners of manipulation, coming forthe most part from osteopathy, maintained that the loss ofmobility of specific vertebral segments, which according

to them was detectable by palpation, could explain andjustify their maneuvers. In fact, I noticed that the segmentsat the origin of a local or referred pain were themselvestender when certain maneuvers of direct pressure (seg-mental examination) were carried out. After a successfulmanipulation, these same segments became pain-free onsegmental examination. The key point, then, was the seg-mental tenderness and not the hypothetic loss of mobility;this finding corresponded perfectly with the applicationof manipulation according to the rule of pain-free andopposite motion.

I therefore proposed the term painful minor interver-tebral dysfunction (PMID [English]; DIM [French]) forthis painful, benign, self-sustained dysfunction of the spi-nal segment. Frequently resulting from trauma, exertion,false movement, or secondary to static or postural prob-lems, these painful minor intervertebral dysfunctions areusually reversible and have no radiologic findings. Theycan affect radiologically normal segments as well as seg-ments with signs of degeneration.

While PMID originally served merely as a hypothesisabout the indications and actions of manipulation, it hasnow become an uncontested clinical reality extending farbeyond the frame of manipulation, even though the under-lying pathophysiology has not yet been clearly estab-lished. The frequent appearance of PMID shows us thatit is at the origin of most common intervertebral painsyndromes.

Another element became apparent, both confirmingand clarifying the role played by manipulation. With sys-tematic palpation of the skin folds, muscles, and tendons,I realized that a PMID was associated frequently withabnormal tissue reflexes in the homologous spinal seg-ment. These changes became apparent through modifica-tions in tissue consistency and sensitivity: painful thick-ening of the skin folds to pince-roule (pinch-roll)throughout all or part of the dermatome, areas of focalmuscular hypertonus among certain muscles of the myo-tome, and hypersensitivity to palpation of the tenoperi-osteal insertion. Moreover, I also found these neurotrophicdisturbances in the same distribution in other spinal seg-mental pain syndromes, for example, disc herniation, facetjoint capsulitis, and synovitis. These manifestations,

vii

which I group under the term segmental celluloperioste-omyalgic syndrome, can be the origins of certain mislead-ing pains such as pseudoradicular, pseudoarticular, andpseudovisceral syndromes.

Furthermore, their topography is rather consistent fora given spinal segment, particularly in the case of cellu-lalgia, which allows one to demonstrate objectively therole played by the posterior rami in a number of painfulsyndromes of the back, such as cervicogenic dorsalgia andlow back pain with an origin in the upper lumbar spine,and to describe some frequent but misunderstood condi-tions such as thoracolumbar or other junctional syn-dromes.

Radiographic imaging has made marked progress inrecent years. It provides a nearly perfect means of detect-ing many of the serious spinal lesions — inflammatory,infectious, neoplastic, traumatic, or otherwise. However,it is not as useful in the domain of common pain syn-dromes. While this imaging technique provides a sophis-ticated means of delineating degenerative lesions andother structural anomalies, the relationship between theseimages and a patient’s pain complaint is often difficult toestablish. While it has been known for quite some timethat significant vertebral spondylosis and disk degenera-tion can be entirely painless, it is now readily apparentthat there are also some cases of frank disk herniation,

clearly visible on CT or MRI, that produce no discomfortwhatsoever. Conversely, many patients who present withsignificant degrees of painful symptoms have normalimaging studies or studies that disclose lesions so benignthat it is difficult to identify them as causative agents.

It is especially in these cases that the guidelines devel-oped for PMID and segmental celluloperiosteomyalgicsyndrome are of great value. These guidelines provide uswith an understanding of many pains that are not welldefined and, therefore, are not well treated. They furnishus with a kind of “Ariadne’s thread” to help us find ourway through the maze of all these pains with which aphysician is confronted daily. The guidelines also broadenthe semiology and restore to the clinical examination allits superiority.

Nevertheless, we shall neglect neither the traditionalrepertoire of the well established semiologic, classic, andpathogenic notions nor the recent advances that facilitatediagnosis and treatment of common painful syndromes ofthe spine. Indeed, it is not sufficient merely to diagnosis;one must treat as well. For this reason, a significant seg-ment of this book deals with treatment, particularly by useof manual therapies that when well executed are so ofteneffective.

Robert Maigne

viii

EDITOR’S INTRODUCTION

Dr. Robert Maigne was born in 1923 in one of thecentral regions of France. He graduated from the Facultyof Medicine, Sorbonne, Paris. At the very beginning ofhis medical career, he specialized in rheumatology andwas interested in physical treatments of patients witharthritis as well as in their rehabilitation. He was particu-larly intrigued by the problems offered by minor derange-ments of the spine as he was the physician for a teampracticing Judo (at which he is an expert). In 1947, hestarted to develop his therapeutic system. He went toEngland (1950–1951) and studied relevant techniquesthere, including those of osteopaths. This is how he pro-gressively arrived at developing the strictly medical meth-odology presented in this book.

Dr. Maigne is one of the founders of the FrenchNational Society of Physical Medicine and Rehabilitation(1952). He has been secretary of this organization for anumber of years. He also is one of the founders of theFrench Society of Manual Medicine and served as itspresident from 1964 to 1966. He has also been presidentof the International Federation of Manual Medicine. Heis a physician of the Hotel Dieu Hospital affiliated withthe University of Paris School of Medicine, where hedirects a physical medicine and rehabilitation serviceand, assisted by a team of specialized physicians, con-tributes the training of students and physicians interested

in physical medicine in general and manual medicine inparticular.

Dr. Maigne has also contributed to training physicianson the American side of the Atlantic. On numerous lecturetours, he has given a great number of demonstrations ofhis methodology in Canada and in the United States. Hiscourses in the United States have always been wellattended. He has made a significant impact on the thoughtgoverning rational approaches to painful disorders ema-nating from the vertebral spine. His students are foundworldwide.

This new edition of Pain of Vertebral Origin containsDr. Maigne’s classic thinking on the subject and his ther-apeutic approaches. It also includes new thoughts of Dr.Maigne that address the problem of manual medicine inthe fragile cervical or lumbar spine and takes a closer lookat issues of particular importance including failed backsyndrome.

A section on the physiology of nociception has beenadded to reflect recent advances in the understanding ofmechanisms underlying nociception and contributes to abetter understanding of the physiologic foundations ofmanual, medical, surgical, and infiltrative techniques inthe management of pain.

Walter L. Nieves, M.D.Director, Headache Center, Hudson Valley, New York

ix

CONTENTS

S E C T I O N I

A N AT O M Y

1. Curvatures ........................................................ 3Types .................................................................... 3Embryology............................................................ 3Spinal Curves and Resistance to Loading.................... 3

2. Typical Vertebra................................................ 7Different Groups of Vertebrae.................................... 7Structure of the Vertebral Body .................................. 7

Vertebral Endplate .............................................. 7Bony Framework ................................................ 7

Architecture of Posterior Arch .................................... 8Cartilaginous Endplates............................................ 8Zygapophyseal Joints............................................... 8

Joint Capsule ..................................................... 9Meniscoids........................................................ 9

3. Intervertebral Disk ......................................... 11Hydrophilic Properties ....................................... 12

4. Ligamentous System..................................... 15Anterior Longitudinal Ligament ................................. 15Posterior Longitudinal Ligament ................................ 15Interspinous Ligament ............................................. 15Ligamentum Flavum ............................................... 16

5. Spinal Characteristics by Region................. 17Cervical Spine ..................................................... 17

Facet Joints ...................................................... 17Spinous Processes............................................. 17Supraspinous Ligament ...................................... 18Uncinate Processes ........................................... 18Transverse Processes and Vertebral Artery ............. 19Anomalies of Occipitocervical Junction................. 19

Cranial Settling............................................ 20Other Anomalies.......................................... 21

Thoracic Spine ..................................................... 21Lumbar Spine ....................................................... 21

Spinous Processes............................................. 22Transverse Processes ......................................... 23

Sacroiliac Joint ..................................................... 23

6. The Muscles.................................................... 27

Paraspinal Muscles ............................................... 27Muscles Located Anterior to the Plane of the Transverse Process ................................... 27Muscles Located between the Transverse Processes........................................................ 28Muscles Located Posterior to the Plane of the Transverse Processes ................................ 29

Small Deep Muscles of the Neck Situated at the Craniocervical Junction ........................ 29

Erector Spinae Muscles within the Vertebral Sulcus ............................................................ 29

Abdominal Muscles............................................... 29Muscles of the Neck and Back............................... 30Muscles of the Lumbar Region ................................ 30

7. Vascular Supply of Spine ..............................31Arterial Supply ..................................................... 31Venous Supply ..................................................... 31

Intraspinal Venous Plexus ................................... 31Perispinal Venous Plexus .................................... 31

8. Innervation of Vertebral Structures ..............33Posterior Primary Rami ........................................... 33Sinovertebral Nerve .............................................. 35Innervation of Disk ................................................ 36Innervation of Facet Joints ...................................... 37Innervation of Ligaments......................................... 38Innervation of Vertebral Periosteum........................... 38Innervation of Spinal Musculature ............................ 38Muscle and Tendon Receptors ................................ 38

Neuromuscular Spindles .................................... 38Efferent Fibers ............................................. 39Afferent Fibers............................................. 39Gamma Loop ............................................. 40Renshaw Loop ............................................ 40

Golgi Tendon Organs....................................... 40Free Nerve Endings.......................................... 40

Articular Receptors ................................................ 40

9. Autonomic Nervous System..........................43Sympathetic System............................................... 43Parasympathetic System ......................................... 44

xi

xii

CONTENTS

S E C T I O N I I

B I O M E C H A N I C S

10. Spinal Kinematics .......................................... 49Mobile Segment ................................................... 49

Automaticity of Spinal Function ........................... 49Regional Spinal Motion.......................................... 50

Cervical Motion ............................................... 51Superior Cervical Segments ........................... 52Inferior Cervical Segments ............................. 53Global Cervical Motion................................ 54

Thoracic Motion............................................... 55Lumbar Motion................................................. 56

11. Biomechanics of Sacroiliac Joint ................ 59Types of Articulations ............................................. 59Joint Motion ......................................................... 59

Interpretations of Axis of Movement ..................... 59Weisl’s Concept .......................................... 59Axial Sacroiliac Articulation ........................... 62

Motion Evaluation............................................. 62Displacements of Sacrum According to Positions ................................................. 62

Asymmetry of Movement............................... 62Studies of Living Anatomical Relationships........ 63

Conclusion .......................................................... 63

12. Forces Acting on Vertebral Column .............65The Disk: Shock Absorber and Pressure Diffuser......... 65Pressure .............................................................. 65Role of Abdominal Wall ........................................ 66Role of Vertebral Body as a Shock Absorber............. 66Role of Sacroiliac Joints ......................................... 67

13. The Aging Spine .............................................69Effects on Vertebral Body ....................................... 69Effects on Intervertebral Disk ................................... 69

Nucleus Pulposus ............................................. 69Formation of Osteophytes .................................. 69

Effects on Facet Joints ............................................ 70Trophostatic Syndrome of Menopause ................. 70Intervertebral Foramen....................................... 71

S E C T I O N I I I

PA I N O F S P I N A L O R I G I N

14. Experimentally Provoked Pain...................... 75Spinal Nerve Root ................................................ 76

Sensory Root ................................................... 76Motor Root ...................................................... 76

Disk .................................................................... 76Facet Joints .......................................................... 77Interspinous Ligaments ............................................ 78Posterior and Anterior Longitudinal Ligaments ............. 79Ligamentum Flavum ............................................... 80Vertebral Body...................................................... 80Muscles............................................................... 80Dermatomes ......................................................... 82

15. Vertebral Lesions and Common Pain Syndromes...................................................... 83Intervertebral Disk Lesions ....................................... 83

Herniated Disks................................................ 83At Lumbar Level ........................................... 84At Thoracic Level ......................................... 84At Cervical Level ......................................... 84

Lesions of Facet Joints ............................................ 86Anomalies ....................................................... 86

Congenital Anomalies................................... 86Acquired Anomalies ..................................... 86

Degenerative Lesions......................................... 86Facet Arthrosis ............................................. 86Facet Joint Periarthritis ................................... 87Other Lesions .............................................. 87Meniscoid Formations ................................... 87

Objective Muscular Lesions..................................... 87

16. Postural Disorders and Pain .........................89Scoliosis.............................................................. 89

Minor Scoliosis ................................................ 89Thoracic Hyperkyphosis ......................................... 89

Kyphotic Posture in Adolescents .......................... 89Hyperkyphosis Due to Dystrophic Spinal Growth ... 90

Transitional Zone Abnormalities ............................... 90Spondylolisthesis................................................... 90Asymmetry of Lumbar Transverse Process Orientation and Facet Joint Development .................................. 92Short Leg Syndrome .............................................. 92

Evidence ........................................................ 92Clinical Evaluation ....................................... 92Radiologic Evaluation ................................... 92

False and True Short Leg ................................... 93False Short Leg ........................................... 93True Short Leg ............................................. 93

Procedural Considerations ................................. 93

17. Painful Minor Intervertebral Dysfunctions...95Definition............................................................. 95Diagnosis ............................................................ 95Differential Diagnosis............................................. 96

Acute Synovitis ................................................ 96PMID and Herniated Disks................................. 97

Different Types of PMIDs ........................................ 97Acute PMIDs ................................................... 97Chronic PMIDs ................................................ 97Active PMIDs................................................... 97Latent PMIDs ................................................... 97

CONTENTS

xiii

Localization and Number ....................................... 97Association of PMID at Different Levels ..................... 98PMID and Pain Threshold ....................................... 98Treatment ............................................................. 98

Acute Cases .................................................... 98Chronic Cases ................................................. 98Recurrent PMID ................................................ 98Should Latent PMIDs Be Treated? ........................ 99

Do Painful Minor Intervertebral Dysfunctions Have Visceral Repercussions? .......................................... 99Hypotheses on Mechanism of PMID......................... 99

Possible Role of Discal or Facet Joint Pathology ..... 99Discal Pathology .......................................... 99Facet Joint Pathology .................................... 99

Reflex Mechanism........................................... 100PMID and Facet Syndrome ................................... 101PMID and “Osteopathic Lesion” ............................ 102Conclusion......................................................... 102

18. Segmental Vertebral Cellulotenoperiosteomyalgic Syndrome.... 103Clinical Manifestations of Segmental Vertebral Syndrome .......................................................... 105

Cellulalgia .................................................... 106Examination: “Pinch-Roll” Test ....................... 106Topography .............................................. 107

Myalgic Indurated Cords (Taut Bands with or without Trigger Points) ................................. 108

Target Muscles .......................................... 108Trigger Points and Referred Pain................... 108

Tenoperiosteal Hypersensitivity .......................... 110Cellulotenoperiosteomyalgic Manifestations: Active and Latent ........................................... 110Hypotheses on Pathophysiology of These Manifestations ............................................... 110

Cellulalgia................................................ 112Trigger Points ............................................ 112

19. Myofascial Pain of Nonvertebral Origin (Panniculalgia, Myogelosis, Tendomyosis, Trigger Points) ......................113Cellulalgia or Panniculalgia.................................. 113

Remarks ................................................... 113Tendomyosis ...................................................... 113Muscular Trigger Points ........................................ 114Fibromyalgia...................................................... 115

S E C T I O N I V

E X A M I N AT I O N O F T H E S P I N E

20. General Principles........................................ 119Clinical History................................................... 119Physical Examination ........................................... 120

General Inspection: Static ................................ 120Frontal Plane Anomalies .............................. 120Sagittal Plane Anomalies ............................. 121

General Inspection: Dynamic............................ 123Assessment of Forward Flexion..................... 123Assessment of Side Bending ........................ 123Assessment of Extension .............................. 124Assessment of Rotation ................................ 124Assessment of Regional Mobility ................... 124

Segmental Examination.................................... 127Basic Maneuvers ....................................... 127Remarks ................................................... 128Contralateral Pressure (Maigne) .................... 128Precautions and Sources of Error in Segmental Examination ............................... 129

Radiographic and Advanced Studies ..................... 132

21. Regional Applications ................................. 133Examination of Cervical Spine .............................. 133

Range of Motion Assessment ............................ 133Patient Seated ........................................... 133Patient Supine ........................................... 134Axial Traction and Compression ................... 136

Segmental Examination.................................... 136Examination of Facet Joint Irritability .............. 136PA Pressure on Spinous Process .................... 137Transverse Pressure against Spinous Process ... 137Pressure against Interspinous Ligament ........... 137

Anterior Cervical “Door Bell” Sign (Maigne)......137Examination of Cervical Spinal Nerve Roots....... 138

Anterior Rami ............................................ 138Posterior Rami ........................................... 139

Examination for Manifestations of Segmental Vertebral Neurotrophic Syndrome of Maigne ...... 140

Cellulalgia................................................ 141Trigger Points ............................................ 142Tenoperiosteal Tenderness ........................... 144

Examination of Thoracic Spine.............................. 144Examination of Mobility................................... 144

Flexion..................................................... 145Extension.................................................. 146Lateroflexion ............................................. 146Rotation ................................................... 147

Segmental Examination ................................... 147Tenderness to PA Pressure on Spinous Process .................................................... 147Transverse Pressure against Spinous Process ... 148Pressure against Interspinous Ligament ........... 148Examination for Presence of Facet Joint Tenderness................................................ 148Sources of Errors ....................................... 149

Examination of Thoracic Spinal Nerves ............. 150Anterior Rami ............................................ 150Posterior Rami ........................................... 150

Examination for Manifestations of Segmental Vertebral Neurotrophic Syndrome of Maigne ...... 150

Cellulalgia................................................ 150Trigger Points ............................................ 150Tenoperiosteal Tenderness ........................... 150

Examination of Lumbar Spine................................ 152

xiv

CONTENTS

Examination of Mobility ................................... 152Active Motion Testing ................................. 152Passive Motion Testing ................................ 153

Segmental Examination.................................... 154PA Pressure on Spinous Process .................... 155Transverse Pressure against Spinous Process ... 155Contralateral Pressure ................................. 155

Longitudinal Friction Overlying Facet Joints ..... 155Pressure against Interspinous Ligament ........... 156

Examination of Lumbar Spinal Nerves ............... 156Anterior Rami ............................................ 156

Examination for Manifestations of Segmental Vertebral Neurotrophic Syndrome of Maigne ...... 157

S E C T I O N V

T R E AT M E N T

22. Spinal Manipulation ..................................... 165General Concepts............................................... 166

Basic Principles .............................................. 166Remarks ................................................... 167

Definitions ..................................................... 167Manipulation............................................. 167Mobilization.............................................. 167“Cracking”................................................ 168Mechanism ............................................... 168

Different Types of Manipulation ............................. 168Direct Manipulation ........................................ 168Indirect Manipulation ...................................... 169Semi-Indirect Manipulation ............................... 170

Assisted Semi-Indirect Manipulation ............... 170Resisted Semi-Indirect Manipulation ............... 171

Localization of Manipulation ................................. 172Remarks ................................................... 173

Indications for Manipulation.................................. 173Components of Manipulative Movement............. 173Description of Manipulation ............................. 174

Level at Which Manipulation Is Performed ..... 174Direction Given to Maneuver ....................... 174Examples.................................................. 175

Rule of No Pain and Opposite Movement (Maigne) ........................................................... 176

Practical Application of Rule of No Pain and Opposite Movement ....................................... 178Technical Contraindications to Manipulation ....... 179Particular Cases ............................................. 179Rule of No Pain and Opposite Movement in Direct Manipulation..................................... 181

Remarks ................................................... 181Protocol of Manipulative Session ........................... 181

When Is Manipulative Treatment Justified? .......... 182First: Establish Diagnosis ............................. 182Then Take Necessary Precautions ................. 183

When Is Manipulative Treatment Possible?.......... 183How Is Treatment Managed? ........................... 183Manipulation Session ...................................... 183

Maneuvers of General and Local Relaxation .. 183Maneuvers of Oriented Mobilization ............. 183Maneuvers of Manipulation (Thrust Techniques)...................................... 183

Evaluation of Response to Treatment .................. 184Reactions following Manipulative Treatment......... 184

Stiffness .................................................... 184Transient Exacerbations ............................... 184

False Reactions or Premature Recurrences ...... 185Sympathetic Reactions ................................ 185

Evolution of Pain after Manipulation Session ....... 185Number and Frequency of Sessions .................. 186Age Considerations with Respect to Manipulation ................................................. 186Quality of Results ........................................... 186

General Indications for Spinal Manipulation............ 187Cervical Region ............................................. 187Thoracic Region............................................. 188Lumbar Region............................................... 188Coccyx ........................................................ 188Visceral and Functional Disorders...................... 188

Contraindications to Manipulation ......................... 189Clinical Contraindications................................ 189Technical Contraindications.............................. 189

Errors of Manipulation ......................................... 190Errors in Diagnosis..................................... 190Errors in Rheumatology ............................... 190Errors in Neurology ................................... 190

Vertebrobasilar Insufficiency ............................. 191Thromboembolic Vertebrobasilar Insufficiency .............................................. 192Hemodynamic Vertebrobasilar Insufficiency .... 192Vertebrobasilar Insufficiency Due to Osteophytes Compressing Spinal Artery ........ 193

Accidents and Incidents of Spinal Manipulation ....... 193Dramatic Accidents ........................................ 194Serious Accidents ........................................... 195Incidents ....................................................... 195Prevention of Accidents: Postural and Rancurel’s Tests .............................................. 196

Postural Testing.......................................... 196Rancurel’s Test ........................................... 196

Medical Responsibility .................................... 196Mechanism of Action of Manipulation.................... 196

Effects of Manipulation on Normal Spine........... 197Possible Mechanical Factors ............................ 197

Disk Lesions .............................................. 197Facet Joint Lesions...................................... 197

Reflex Factor ................................................. 198Articular Cracking and Gapping.................. 199

23. Spinal Traction ..............................................201Mode of Application........................................... 201

Traction Table ................................................ 201Cervical Traction ................................................ 202

CONTENTS

xv

Application.................................................... 202Traction on Inclined Plane ................................ 202Traction on Special Table................................. 202Traction in Sitting............................................ 202

Lumbar Traction .................................................. 202Fastening Thorax ............................................ 202Fastening Pelvis .............................................. 203Application of Traction .................................... 203Traction in Bed............................................... 203

Mode of Action of Traction................................... 204Mechanical Action ......................................... 204Reflex Action ................................................. 204

Indications for Traction ......................................... 204Cervical Spine ............................................... 204Lumbar Spine................................................. 205

24. Massage ........................................................ 207Massage for Paraspinal Muscle Relaxation.............. 207

Acute Muscle Spasm....................................... 207Chronic Muscle Spasm ................................... 207

Massage and Cellulotenoperiosteomyalgic Manifestations .................................................... 207

Cellulalgia..................................................... 208Trigger Points ................................................. 208Tenoperiosteal Pain, Tenalgias, and Tendinitis...... 210

Deep Transverse Massage (DTM)........................... 210

25. Stretching...................................................... 213Longitudinal Stretching ......................................... 213

Manual Stretching .......................................... 213Global Stretching of Extensor Muscles................ 213Postural Stretching........................................... 214Stretching Exercises......................................... 214

Vapocoolant Spray and Stretch ............................. 214Transverse Stretching............................................ 214

26. Therapeutic Injections................................. 217Spinal Injections.................................................. 217

Epidural Injection............................................ 217Sacrococcygeal Hiatus ............................... 217Translumbar Route ...................................... 218First Sacral Foramen ................................... 219Remarks ................................................... 219

Intrathecal Injection ......................................... 219Adverse Effects .......................................... 220Accidents ................................................. 220

Facet Joint Injections........................................ 220Lumbar Region .......................................... 221Remarks ................................................... 221Thoracolumbar Junction ............................... 221Thoracic Region......................................... 221Cervical Region......................................... 221

Ligamentous Injections ..................................... 222Interspinous Ligaments ................................. 222Iliolumbar Ligament .................................... 223

Selective Neural Blockade.................................... 223Injection of Anterior Primary Rami of Spinal Nerves ....................................... 223Injection of Posterior Primary Rami of Spinal Nerves ....................................... 223

Trigger Point Injections ......................................... 224Injection of Scars ................................................ 225

Accidents Associated with Injection of Local Anesthetic.............................................. 225

Allergic Reactions........................................... 225Toxic Accidents.............................................. 225Diffusion of Local Anesthetic toward Neuraxis ..... 225

Complications of Steroid Injection ......................... 225Therapeutic Injections .......................................... 226

Botulinum Toxin (Botox) Injections ...................... 226Medications and Complications of Medication Use . 226

27. Hydrotherapy, Thermal Therapy, Cryotherapy, Radiofrequency Denervation, Rhizotomy, and Implantable Devices .....................................227Hydrotherapy and Thermotherapy.......................... 227

Hotel Dieu Method......................................... 227Results .......................................................... 227Contraindications ........................................... 228

Cryotherapy ...................................................... 228Ice Application .............................................. 228Ice Massage ................................................. 228Cold Pulverization .......................................... 228

Radiofrequency Denervation ................................. 228Rhizotomy.......................................................... 228Implantable Devices ............................................ 229

28. Electrotherapy in Pain of Spinal Origin .....231Spine ............................................................... 231Manifestations of Neurotrophic Spinal Segmental Syndrome.......................................................... 231

Cellulalgia .................................................... 231Tendinous Pain............................................... 231Trigger Points................................................. 231Periosteal Pain ............................................... 231

29. Lumbar Orthoses..........................................233Indications ......................................................... 233

Acute Low Back Pain...................................... 233Sciatica........................................................ 233Chronic Low Back Pain................................... 233

Fabrication of Rigid Lumbar Orthosis...................... 233Plaster Orthosis Syndrome ............................... 234

Mode of Action ................................................. 234

30. Lumbosacral Corsets ...................................235Indications ......................................................... 235Types................................................................ 235Mode of Action ................................................. 237Contraindications................................................ 237

31. Cervical Collars.............................................239Types of Collars ................................................. 239

Flexible Collars .............................................. 239Collars with Rigid Reinforcement ....................... 239Mini Minerva Collars...................................... 239

Indications ......................................................... 239Cervical Trauma ............................................ 239Acute Cervical Pain........................................ 239Cervicobrachial Neuralgia .............................. 239Chronic Cervical Pain..................................... 239

xvi

CONTENTS

32. Therapeutic Exercise ................................... 241Cervical Pain ..................................................... 241Thoracic Pain ..................................................... 241Low Back Pain ................................................... 241

Low Back Pain of Lumbosacral Origin ............... 241Low Back Pain of Thoracolumbar Origin ............ 242Rehabilitation of Lower Limbs ........................... 242

S E C T I O N V I

C L I N I C A L A S P E C T S O F PA I N O F S P I N A L O R I G I N

33. Chronic Neck Pain ....................................... 245Diagnostic Errors to Be Avoided ....................... 245

Clinical Signs of Neck Pain Syndromes .................. 245History.......................................................... 246Range of Motion Assessment ............................ 246Segmental Examination.................................... 246Evaluation of Cellulotenoperiosteomyalgic Manifestations of Segmental Vertebral Syndrome...................................................... 246Radiographic Examination................................ 247

Different Origins of Neck Pain and Treatment .......... 248Cervical Spondylosis....................................... 248

Inflammatory Attacks................................... 248Arthrotic Stiffening ...................................... 248Spondylosis and PMID................................ 249

Painful Minor Intervertebral Dysfunctions ............. 249Localization............................................... 249A Particular Case: Post-Traumatic Cervical Pain......................................................... 249

Cervical Pain of Muscular, Subcutaneous, or Ligamentous Origin ......................................... 250

Muscular Origin ........................................ 250Subcutaneous Origin .................................. 250Ligamentous Origin .................................... 250

Cervical Pain and Psychologic Disorders ............ 250

34. Torticollis (Wryneck) and Acute Cervical Pain................................................. 251Benign Acute Torticollis ........................................ 251

Torticollis Due to PMID .................................... 251Treatment .................................................. 251

Torticollis of Muscular Origin ............................ 251Treatment .................................................. 252

Torticollis of Mixed Origin................................ 252Acute Cervical Pain............................................. 252

Due to Acute Synovitis..................................... 252Treatment .................................................. 252

As Result of Herniated Disk .............................. 252Treatment .................................................. 252

35. Cervicobrachial Neuralgia........................... 253Pain.................................................................. 253Examination of Neck ........................................... 253

Examination of Affected Level ........................... 253Test of Manual Traction ................................... 253

Interscapular Pain................................................ 253Clinical Examples by Segmental Level .................... 254

C5 Syndrome ................................................ 254C6 Syndrome ................................................ 254

C7 Syndrome................................................ 254C8 Syndrome................................................ 254

Etiologies .......................................................... 254Cervicobrachial Neuralgia Due to Cervical Spondylosis................................................... 254CBN Due to Disk Herniation............................ 255CBN Due to PMID ......................................... 255

Differential Diagnosis........................................... 255Entrapment Syndromes .................................... 255Referred Pain Syndromes ................................. 255

Intramedullary Tumors ................................. 255Infectious Discitis........................................ 256Spinal Metastases...................................... 256Pancoast Tumors ........................................ 256

Treatment........................................................... 256Manipulation ................................................. 256Spinal Traction............................................... 257Manipulation and Traction ............................... 257Manipulation under Traction............................. 257

Residual Pain and Cellulotenoperiosteomyalgic Manifestations of Spinal Origin.................... 257

36. Chronic Thoracic Pain..................................259Interscapular Thoracic Pain of Low Cervical Origin (Maigne) ........................................................... 259

Clinical Picture............................................... 259Clinical Examination ....................................... 259

Examination of Back .................................. 259Examination of Neck ................................. 261Cervical Spine and Thoracic Pain ................ 262Pathogenic Mechanism: A Personal Hypothesis ............................................... 263

Posterior Primary Rami of the Second Thoracic Nerve Root ................................................... 263

A Few Particular Cases .............................. 264Treatment ...................................................... 266

Psychologic Factors.................................... 266Physical Modalities .................................... 267Prevention ................................................ 267

Thoracic Pain of Thoracic Origin........................... 267Thoracic Pain Due to Thoracic PMID ................. 267

Treatment ................................................. 267Thoracic Pain of Discogenic Origin................... 267Thoracic Pain Due to Thoracic Arthrosis ............. 268

Treatment ................................................. 268Thoracic Pain and Scheuermann’s Disease ......... 268Thoracic Pain and Osteoporosis ....................... 268Thoracic Pain and Interspinous Ligaments ........... 268

Chronic Thoracic Pain of Muscular Origin .............. 268Treatment ...................................................... 268

CONTENTS

xvii

37. Acute Thoracic Pain..................................... 269Acute Interscapular Thoracic Pain of Cervical Origin............................................................... 269

Treatment ...................................................... 269Acute Thoracic Pain of Thoracic Origin .................. 269

Treatment ...................................................... 269Acute Thoracic Pain Due to Disk Calcification ......... 269Acute Thoracic Pain of Muscular Origin.................. 269

38. Costal Sprains.............................................. 271Clinical Presentation ............................................ 271

Faulty Movement or Forceful Effort ..................... 271Direct Trauma ................................................ 271

Clinical Picture ................................................... 271Diagnosis .......................................................... 271

Posterior Costal Sprains ................................... 271Anterior Costal Sprains.................................... 272

Is It Really a Sprain? ........................................... 272Treatment ........................................................... 272“Hooked Rib”..................................................... 272

39 Chronic Low Back Pain ............................... 275Examination of Patient with Low Back Pain.............. 275

Clinical History .............................................. 275Physical Examination ....................................... 275Active Range of Motion Assessment................... 275

Forward Flexion......................................... 276Extension .................................................. 277Lateroflexion.............................................. 277Rotation.................................................... 277Functional Assessment ................................. 277

Segmental Examination.................................... 277Palpation of Lower Ribs in Cases of Low Back Pain....................................... 278

Examination of Subcutaneous Tissues ................. 278Examination of Muscles ................................... 278

Paraspinal Muscles..................................... 278Muscles of Lumbar Fossa ............................ 279Muscles of External Iliac Fossa ..................... 279

Lasegue’s Sign ............................................... 279Neurologic Examination .................................. 279Radiographic Examination................................ 279

Conclusions of Clinical Examination ....................... 279

40. Low Back Pain of Lumbosacral Origin...... 281Low Back Pain Due to Disk Lesions ........................ 281

Discogenic Low Back Pain ............................... 281Low Back Pain Due to Segmental Instabilityfollowing Disk Degeneration............................. 282

Role of Facet Joint in Low Back Pain ...................... 282Low Back Pain of Ligamentous Origin .................... 283Low Back Pain Syndromes of Lumbosacral Origin and Painful Minor Intervertebral Dysfunction............. 283Low Back Pain of Lumbosacral Origin and Cellulotenoperiosteomyalgic Segmental Vertebral Syndrome .......................................................... 284

Treatment ...................................................... 284Spinal Treatment ........................................ 284Cryotherapy, Thermotherapy, and Hydrotherapy ............................................ 285

Treatment of Manifestations of Segmental Vertebral Syndrome.................................... 285Postural Re-education and Corrective Actions.. 286Lumbosacral Corsets and Rigid Lumbar Orthoses .................................................. 286Therapeutic Exercise................................... 286

Low Back Pain of Extraspinal Origin ...................... 287Low Back Pain of Myofascial Origin ................. 287Low Back Pain of Cellulalgic Sheeting............... 287

Treatment ................................................. 287Low Back Pain and Iliolumbar Ligament ............. 287

41. Low Back Pain of Thoracolumbar Origin (T11–T12–L1) (Maigne).................................289Anatomic Review................................................ 290

Facet Joints ................................................... 290Transitional Vertebra........................................ 290Posterior Rami of Thoracolumbar Spinal Nerve Roots ........................................................... 291

Innervation of Subcutaneous Tissues.............. 291Iliac Crest Crossing Point ............................ 293

Clinical Signs..................................................... 293Clinical Examination ....................................... 293

Examination of Lumbogluteal Region at Iliac Crest............................................. 293Examination of Thoracolumbar Region........... 293

Confirmation of Thoracolumbar Origin of Low Back Pain ..................................................... 294

Radiologic Examination ....................................... 295Incidence .......................................................... 295Atypical Forms ................................................... 296

Ectopic Referral Patterns .................................. 296Treatment........................................................... 297

Manipulation ................................................. 297Facet Joint Injection ........................................ 297Electrotherapy................................................ 297Treatment of Cellulalgic Lumbogluteal Region ...... 297Surgical Capsulectomy.................................... 297Percutaneous Rhizotomy .................................. 298Corrective Actions .......................................... 298Therapeutic Exercise ....................................... 298

42. Acute Low Back Pain ...................................299Acute Low Back Pain of Lumbosacral Origin ........... 299

Clinical Picture............................................... 299Mechanism ................................................... 299Treatment ...................................................... 299

Manipulation ............................................ 299Relaxation Techniques in Acute Low Back Pain Syndromes......................................... 301Injection ................................................... 302Rigid Lumbar Orthosis ................................ 303Medication............................................... 303Prevention (Prehabilitation) and Rehabilitation . 303

Acute Low Back Pain of Thoracolumbar Origin........ 303Clinical Signs ................................................ 303

At Inferior Lumbar Level............................... 303At Thoracolumbar Junction........................... 303

Treatment ...................................................... 303Manipulation ............................................ 303

Acute Low Back Pain of Calcifying Discopathy ........ 304Acute Low Back Pain of Myofascial Origin ............. 304

xviii

CONTENTS

43. Sciatica.......................................................... 305Onset and Topography ........................................ 305Clinical Examination ............................................ 305

Examination for Cellulotenoperiosteomyalgic Manifestations................................................ 305

Imaging............................................................. 308Radiography.................................................. 308Computed Tomography ................................... 308Myelography ................................................. 308Discography .................................................. 308Magnetic Resonance Imaging .......................... 308

Clinical Forms of Sciatica..................................... 308Hyperalgic Sciatica ........................................ 308Paralytic Sciatica............................................ 308Sciatica in the Young ...................................... 309Sciatica in the Elderly ..................................... 309Sciatica and Spinal Stenosis ............................ 309Central Spinal Stenosis .................................... 309Lateral Recess Stenosis .................................... 309Foraminal Stenosis .......................................... 310

Differential Diagnosis ........................................... 310Pseudosciatic Syndromes ................................. 310

Treatment ........................................................... 310Treatment of Attack ......................................... 310

Medication ............................................... 310Surgery: Chemonucleolysis .......................... 310

Treatment by Manipulation ............................... 310Treatment of Sequelae ..................................... 311Rehabilitation ................................................. 311Paralytic Sciatica............................................ 311

Sciatica in the Young Patient........................ 311Sciatica in the Elderly ................................. 311

44. Femoral Neuralgia........................................ 313Initial Symptoms and Topography .......................... 313Clinical Examination ............................................ 313

CelIulotenoperiosteomyalgic Manifestations ......... 313Differential Diagnosis ........................................... 314Treatment ........................................................... 314

45. Meralgia Paresthetica .................................. 315Canalicular Origin .............................................. 316Spinal Origin ..................................................... 316Mixed Origin ..................................................... 316

46. Coccygodynia............................................... 317Diagnosis .......................................................... 317Treatment ........................................................... 317

Massage of Levatores ..................................... 317Osteopathic Technique .................................... 317Authors’ Technique.......................................... 317

47. Perforating Branch Syndrome of T12 and L1................................................ 319Anatomy............................................................ 319

Classic Studies............................................... 319Maigne Study................................................ 319

Clinical Examination ............................................ 320Clinical Presentation ............................................ 320

Pseudoperiarthritis of Hip ................................. 320

Pseudomeralgia Paresthetica ............................ 322Pseudosciatica ............................................... 322

Treatment........................................................... 323

48. Headache of Cervical Origin .......................325Common Characteristics of Cervical Headaches ..... 325

Cervical Semiology ........................................ 325Different Aspects of Headache of Cervical Origin .............................................................. 325

Occipital Headache....................................... 326Friction Sign of the Scalp (Maigne) .............. 326

Occipitotemporomaxillary Headache................. 327Supraorbital Headache ................................... 328

Eyebrow Sign (Maigne) .............................. 328Cheek Sign (Maigne) ................................. 328Different Aspects of Supraorbital Headache of Cervical Origin ..................................... 329

Triggering Factors ............................................... 329Frequency of Cervical Headaches......................... 329

Frequencies of Different Forms .......................... 330Remarks ................................................... 330

Pathophysiologic Mechanisms............................... 330C2–3 Facet Joint Tenderness............................ 330Craniofacial Signs.......................................... 330Hypotheses about Mechanisms ........................ 330

Treatment of Headache of Cervical Origin ............. 331Manipulation ................................................. 331Facet Joint Injection (C2–3).............................. 331Other Treatments ............................................ 331

Cervical Muscles and Headaches ......................... 331

49. Cervical Migraine..........................................333True Migraine .................................................... 333Cervical Migraine .............................................. 333Migraine and Superior Cervical Spine ................... 333

50. Cervical Syndrome .......................................335Elements of Cervical Syndrome............................. 335

Headaches ................................................... 335Vestibular Symptoms ....................................... 335Auditory Symptoms......................................... 335Visual Symptoms ............................................ 335Pharyngolaryngeal Symptoms........................... 335Vasomotor and Secretory Symptoms .................. 335Psychologic Symptoms .................................... 335

Diagnosis .......................................................... 336Examination of Cervical Spine.............................. 336Mechanism........................................................ 336Treatment........................................................... 336

Physical Modalities......................................... 337Remarks ................................................... 337

51. Levator Scapulae Syndrome .......................339Clinical Picture ................................................... 339

Different Aspects of Pain ................................. 339Mechanism ................................................... 339

Local Cause ............................................. 340Cervical Cause ......................................... 340Mixed Causes .......................................... 340

Treatment........................................................... 340

CONTENTS

xix

52. Acroparesthesias of Upper Limbs and Cervical Spine .............................................. 341Acroparesthesias with Radicular Topography ........... 341Nocturnal Global Acroparesthesias ........................ 341Acroparesthesias with Entrapment .......................... 342

Carpal Tunnel Syndrome.................................. 342Treatment .................................................. 343

Guyon’s Canal Syndrome ................................ 343Cervical Spine and Acroparesthesia ...................... 343

Arm Elevation Test .......................................... 343Double Crush Syndrome....................................... 344

53. Shoulder Pain and the Cervical Spine ...... 345Generalities on Tendinous and Capsular Lesions ...... 345

Subacromial Impingement (Neer) ...................... 345Asymptomatic Lesions ...................................... 346Subcoracoid Impingement Syndrome ................. 346

Examination of Shoulder....................................... 346Assessment of Active Range of Motion............... 346Assessment of Passive Range of Motion ............. 346

Muscles of Shoulder Girdle ......................... 346Assessment of Resisted Range of Motion ............ 346

Supraspinatus (Abduction)............................ 346Infraspinatus (External Rotation) ..................... 347Subscapularis (Internal Rotation) .................... 347Biceps...................................................... 347Pectoralis Major, Latissimus Dorsi, and Teres Major .............................................. 347

Painful Arc .................................................... 347Palpation ...................................................... 347

Subcutaneous Tissues.................................. 347Muscles.................................................... 347Tendons.................................................... 347

Assessment of Clavicular Joints.......................... 348Acromioclavicular Joint ................................ 348Particular Cases......................................... 349Sternoclavicular Joint................................... 349

Assessment of Scapular Mobility (Scapulothoracic Joint) ..................................... 349Glenohumeral Mobility and Assessment of Glenoid Fossa............................................ 349

Testing Joint Play ........................................ 349Glenoid Fossa........................................... 349

Examination of Cervical Spine.......................... 351Cervical Shoulder ............................................... 351

Diagnosis of Cervical Shoulder......................... 352Mixed Shoulder Pain Syndromes ........................... 352

Taut Bands, Trigger Points, and Atypical Shoulder Pain ................................................ 352

Manual Therapy for Painful Shoulder ...................... 353Mobilization of Glenohumeral Joint.................... 353Mobilization of Scapulothoracic Joint ................. 353Manipulation of Acromioclavicular Joint .............. 353Manipulation of Sternoclavicular Joint................. 354

54. Lateral Epicondylar Pain ............................. 357Clinical Examination ............................................ 357

Elbow........................................................... 357Palpation .................................................. 357Manual Muscle Testing against Resistance ..... 357Examination of Active and Passive Range of Motion ................................................. 357

Lateral Joint Play of Elbow........................... 358Joint Play of Distal Radioulnar Joint ............... 358Radiography............................................. 358

Cervical Spine .............................................. 358Evaluation of Lateral Epicondylar Pain .................... 358

Classification................................................. 359Lateral Epicondylar Pain of Local Origin ........ 360Remark .................................................... 363

Distal Radioulnar Dysfunction ................................ 363Lateral Epicondylar Pain and Cervical Spine ........... 364

Treatment ...................................................... 366

55. Medial Epicondylar Pain ..............................367

56. Pubic Pain and Spinal Factors....................369Theories ............................................................ 369

Nesovic’s Theory ........................................... 369Spinal Factor (Maigne) ................................... 369

Clinical Stages of Pubic Pain with Spinal Facilitation......................................................... 370

Stage I ......................................................... 370Stage II ........................................................ 371Stage III ....................................................... 371Stage IV ....................................................... 371

Treatment........................................................... 371Stage I ......................................................... 371Stage II ........................................................ 371Stage III ....................................................... 371Stage IV ....................................................... 371

57. False Hip Pain of Spinal Origin ..................373Trochanteric Pain and L5 Segmental Vertebral Syndrome.......................................................... 373False Hip Pain and T12–L7 Segmental Vertebral Syndrome.......................................................... 373Entrapment Syndromes of Perforating Cutaneous Branches of T12 and L1...................................... 374Total Hip Arthroplasty and False Hip Pain............... 374

58. Knee Pain of Spinal Origin..........................375Examination ....................................................... 375Clinical Picture ................................................... 376

Cellulalgia of L3 or L4 .................................... 376Tenoperiosteal Tenderness (L4) .......................... 376Trigger Points of Vastus Medialis and Pseudoblockage of Knee................................. 376Entrapment Syndrome of Saphenous Nerve ........ 376

Knee Pain and Proximal Tibiofibular Joint ................ 377Proximal Tibiofibular (PTF) Blockages ................. 377Proximal Tibiofibular Arthritis and Sciatica .......... 378

Treatment ................................................. 378

59. Pseudovisceral Pain of Spinal Origin ........379Origin of Pain.................................................... 379

Role of Cellulalgia ......................................... 379Trigger Points................................................. 379

Thoracic Pain..................................................... 379Pseudocardiac Pain ........................................ 379False Breast Pain ........................................... 379Pseudopleuropulmonary Pain............................ 379

xx

CONTENTS

Abdominal Pain .................................................. 379Pseudogastrointestinal Pain ............................... 380Acute Pain .................................................... 381Pseudogynecologic Pain .................................. 381Pseudourologic Pain........................................ 382

Case Example.................................................... 382Abdominal Pain and Lumbar Herniated Disks ...... 382

Treatment ........................................................... 382

60. Thoracolumbar Junction Syndrome .......... 383TL J Anatomy and Physiology ................................ 384Physical Signs .................................................... 384

Examination of Thoracolumbar Junction .............. 384Cellulotenoperiosteomyalgic Manifestations ......... 384

Cellulalgia ................................................ 385Trigger Points ............................................ 386Tenoperiosteal Tenderness............................ 386

Crestal Points ................................................. 386Clinical Symptoms............................................... 386

Low Back Pain ............................................... 386

Pseudovisceral Pains ....................................... 386False Hip Pain............................................... 387Pubic Tenderness............................................ 387Functional Disorders........................................ 387

Treatment........................................................... 388

61. Transitional Zone Syndrome .......................389Characteristics of Transitional Zone Syndrome ......... 390

Semiologic Characteristics ............................... 390Clinical Characteristics.................................... 390Treatment ...................................................... 390

Perpetuating and Precipitating Factors .................... 390Compensatory Postures ................................... 390

Clinical Picture ................................................... 391Typical Clinical Picture .................................... 391Other Clinical Features ................................... 391

62. Failed Back Syndrome .................................393Failure-to-Improve Syndrome.................................. 393

S E C T I O N V I I

M A N U A L T E C H N I Q U E S

63. Introduction to Manipulative Techniques.................................................... 397Equipment.......................................................... 397Basic Manipulative Techniques .............................. 398

Seven Basic Techniques................................... 398Cervical Spine: Techniques 1 and 2............. 398Thoracic Spine: Techniques 3 and 4............. 398Thoracolumbar Junction: Technique 5 ............ 399Lumbar Spine: Techniques 6 and 7 .............. 399

Seven Accessory Techniques ............................ 399Cervical Spine: Technique I ......................... 399Cervicothoracic Junction: Techniques II and III.................................... 401Thoracic Spine: Technique IV ....................... 401False Ribs: Technique V .............................. 401Lower Thoracic and Lumbar Levels: Techniques VI and VII ................................. 401

64. Cervical Techniques..................................... 403Massage ........................................................... 403Relaxational Maneuvers ....................................... 403Mobilization and Manual Traction ......................... 405

Mobilization .................................................. 405In Rotation ................................................ 405In Lateroflexion .......................................... 406In Flexion.................................................. 406

Manual Traction ............................................. 407Suboccipital Traction .................................. 408Traction with Towel..................................... 408Traction with Belt ....................................... 408

Manipulation...................................................... 409Basic Technique: Chin Free .............................. 409

Example ................................................... 409Remarks ................................................... 411

Pure Rotation (with or without Flexion or Extension) ................................................. 412

Accessory Technique (Chin Grasp) .................... 415Manipulation with Combined Rotation and Lateroflexion ............................................. 415

Chin Grasp Technique .................................... 416Manipulation in Rotation with or without Flexion/Extension............................ 417Manipulation in Rotation and Lateroflexion..... 418

Anterior Hand Technique ................................. 419Manipulation in Left Rotation ....................... 419

Posterior Hand Technique ................................ 421

65. Cervicothoracic Junction Techniques........423Massage of Subcutaneous Tissues ......................... 423Relaxational Maneuvers ....................................... 423

Patient Seated ............................................... 423Mobilization ...................................................... 425

In Extension................................................... 425Patient Seated........................................... 425

In Flexion...................................................... 426Patient Supine ........................................... 426

In Rotation .................................................... 426Patient Supine ........................................... 426

Manipulation: Basic Techniques ............................ 427Cervicothoracic Technique in Lateral Decubitus Position ........................................................ 427

In Pure Lateroflexion (without Rotation) ........... 427In Lateroflexion Associated with Rotation........ 429

Chin Pivot (Accessory Technique) ...................... 430Patient in Prone ......................................... 430

Lateral Pressure against Spinous Process (Accessory Technique) ..................................... 432

Patient Seated........................................... 432

CONTENTS xxi

66. Thoracic Techniques.................................... 435Massage ........................................................... 435Relaxational Maneuvers ....................................... 435

Scapular Muscle Stretching .............................. 436Mobilization....................................................... 437

In Extension ................................................... 437In Lateroflexion ............................................... 439In Rotation..................................................... 439

Manipulation...................................................... 440(Basic) Epigastric Technique.............................. 440

Hands-on-Neck Position .............................. 440Hands-Front Position ................................... 441

Localizing Manipulation to Specific Spinal Segment ....................................................... 442

Hands-Front Position ................................... 442Hands-on-Neck Position .............................. 443

(Basic) Sitting Astride Technique ........................ 444In Pure Rotation ........................................ .445Variations of Patient’s Arm Position ................ 446Positions of Examiner’s Arms and Feet ........... 446

(Accessory) Knee Technique ............................. 450Localizing Manipulation to Specific Spinal Segment ................................................... 451

(Basic) Supine Technique ................................. 452Hands-on-Neck Position .............................. 452Crossed Arms Position ................................ 453Direct Technique ........................................ 454

67. Lumbar Techniques...................................... 455Massage ........................................................... 455Relaxational Maneuvers and Muscle Stretching ........ 455

Relaxational Maneuvers ................................... 455Buttock and Lower Limb Muscles .................. 455Paraspinal Muscles..................................... 456

Stretching ...................................................... 457Gluteus Medius and Tensor Fascia Lata ......... 457External Rotators of Hip .............................. 458Internal Rotators of Hip ............................... 458Extensors of Hip and Spine ......................... 458Axial Traction of Leg................................... 459

Mobilization....................................................... 460In Flexion ...................................................... 460

Contact on Both Knees ............................... 460Contact on One Knee ................................ 460

In Lateroflexion ............................................... 461In Extension ................................................... 462In Rotation..................................................... 462

Manipulation...................................................... 463(Basic) Lateral Decubitus Technique in Flexion ...................................................... 463

Variation of Manipulation in Flexion .............. 465(Basic) Lateral Decubitus Technique in Extension... 466

Variation................................................... 467Lateral Decubitus Technique in Neutral Position (without Extension or Flexion) ............................ 468

First Technique .......................................... 468Second Technique ..................................... 468

(Basic) Astride Technique ................................. 470Manipulation in Pure Rotation ...................... 470Manipulation in Rotation Combined with Lateroflexion, Flexion, or Extension................ 472

(Accessory) Double Knee Technique .................. 473(Accessory) Belt Technique ............................... 474

In Pure Rotation ......................................... 474In Rotation with Ipsilateral Lateroflexion.......... 475In Rotation plus Contralateral Lateroflexion ..... 475

68. Rib Techniques..............................................477(Accessory) First Technique (for Inferior Ribs) ............ 477Second Technique (for Inferior Ribs) ....................... 477

Manipulation for Last Ribs: Second Technique..... 477Variation: Patient Standing .......................... 478

Third Technique (for Middle and Inferior Ribs) .......... 479Technique for First Rib.......................................... 480Technique for Anterior Costal Sprain ...................... 480

69. So-Called Sacroiliac Joint Techniques.......481Generalities ....................................................... 481

Semiology of SI Joint Disorders in Traditional Medicine...................................................... 481Semiology Proposed by Supporters of SI Joint Blockage ...................................................... 481J.B. Mennell’s Signs ........................................ 482Osteopathic Signs .......................................... 483Blockage in Nutation...................................... 483Blockage in Counter-Nutation........................... 483Signs Based on Alterations in Bony Landmarks.... 483

Piédallu’s Test ............................................ 483Other Tests ............................................... 484Tests of Sell and Neumann ......................... 484

Personal Opinion ........................................... 485So-Called SI Joint Manipulative Techniques ............. 485

First Technique ............................................... 485Second Technique .......................................... 485Third Technique.............................................. 486Fourth Technique ............................................ 486Fifth Technique............................................... 486Sixth Technique.............................................. 486

Traction on Leg ......................................... 486

70. Techniques Not Requiring Vertebral Manipulation..................................................489Techniques Applicable to Gluteal Region Pain ......... 489Techniques Applicable to Thoracic Region .............. 490Techniques for Perispinal and Interspinal Region Pain ................................................................. 490Cervical Region Techniques.................................. 490Patient Recumbent............................................... 491

xxii CONTENTS

S E C T I O N V I I I

T H E P H Y S I O L O G Y O F PA I N

71. The Neurophysiology of Pain ..................... 495Overview .......................................................... 495Physiologic Systems ............................................. 495Nociception ....................................................... 495Physiologic Plasticity of Pain.................................. 496

The Genome ................................................. 496Epigenetic Inheritance ..................................... 496

Genomic Activation and Repression ....................... 496Cellular Plasticity ............................................ 497Cellular Communication and Synaptic Plasticity ... 497

The Neuron ....................................................... 497Glia.................................................................. 498The Synapse ...................................................... 499

Neurotransmitters ............................................ 499Neuromodulators ............................................ 500Synaptic Field Plasticity.................................... 502

Nociceptive Sensitization ..................................... 502Referred Hyperalgesia ......................................... 502Nociceptive Desensitization .................................. 503Phasic Determinants of Nociception ....................... 504

Taut Bands .................................................... 505Anatomic Determinants of Nociception ................... 506Hormonal Determinants of Nociceptive Plasticity ...... 506Suprasegmental Determinants of Plasticity ................ 506Immunologic Determinants of Nociception ............... 507

Suprasegmental Determinants of Nociception .......... 508Nociceptive Rationalization .................................. 508Nociceptive Localization ...................................... 509

Bibliography ...........................................................511

Author’s Principal Bibliographic References .............. 529Textbooks...................................................... 529Painful Minor Intervertebral Dysfunction .............. 529Segmental Vertebral Syndrome ......................... 529Zygapophyseal Joints and Posterior Primary Rami ................................................. 529Interscapular Pain of Cervical Origin................. 529Low Back Pain of Thoracolumbar Origin ............ 529Thoracolumbar Junction Syndrome..................... 530Shoulder Pain and Cervical Spine .................... 530Headache of Cervical Origin .......................... 530Epicondylar Pain ............................................ 530Pubalgia....................................................... 530Manipulation ................................................. 530Perforating Branch Syndrome of T12 and L1 ...... 530Miscellaneous................................................ 530

Index........................................................................531

I

ANATOMY

3

1

CURVATURES

The vertebral column, or spine, is the axis of the humanbody. Its functions are to protect the spinal cord and thenerve roots that emerge from it, to sustain the viscera thatare fastened to it, and to provide support to the head andthe shoulder girdle.

The spine is a flexible axis composed of articulatedvertebrae that allow the column to readily deform its shapewhile still maintaining its rigidity. The vertebral columnhas been compared to a mast placed on a ship’s hull (thepelvis), supporting a large transverse yard (the shouldergirdle). At all levels, there is a musculoligamentous frame-work that braces the column. All of these structures, whichare controlled by extrapyramidal pathways, readily adaptinstantaneously and automatically to changes in posture,position, or physical exertion by a permanent adjustmentin muscular tone.

The spinal column is composed of 24 articulated ver-tebrae (Fig. 1.1): 7 cervical, 12 thoracic, 5 lumbar, 5 sacral(fused into one), and 3 coccygeal (often fused into one).Fibrocartilaginous disks that act as shock absorbers arelocated between all articulated vertebrae with the excep-tion of Cl–C2.

TYPES

The spinal column is composed of three curves:

• A cervical lordosis• A thoracic kyphosis• A lumbar lordosis

These curves may vary in their degree of accentuation(Fig. 1.2). The degree of curvature in the sagittal planecan be measured using the “Delmas index” that comparesthe surface length of the entire column to its verticalheight. The mean index is 95 (Fig. 1.3). A spine with anindex lower than 94 is a spine with marked curvature,referred to as the “dynamic spine” of Delmas. A verticalaxis passing through the body’s center of gravity passesthrough the two extremities of the spine (Fig. 1.4):

• Superiorly, the craniocervical junction• Inferiorly, the lumbosacral junction

This axis passes just posterior to the body of L3.

EMBRYOLOGY

At birth, the spinal column assumes the form of a C-shaped curve concave anteriorly; as the child progressivelyattains the ability to extend the neck, the

cervical lordosisis

formed. The

lumbar lordosis,

which develops as a resultof the human’s upright posture, begins at age 3 andbecomes fully developed around age 10 (Fig. 1.5).

The “keystone” vertebrae of these curves are the onesthat are situated at the apex:

• C6 for the cervical curve• T7 for the thoracic curve• L3 for the lumbar curve

SPINAL CURVES AND RESISTANCE TO LOADING

The spinal curves increase the shock-absorbing capac-ity of the vertebral column and facilitate its stability andequilibrium. The vertebral column acts like an elastic col-umn with alternating curves. Because it has 3 curves, thespine is 10 times more resistant to loading than if therewere no curves.

The law of physics that governs elastic columns withalternating curves is expressed as follows: if n is the num-ber of curvatures and 1 is the resistance of a straightcolumn system, the resistance of the system with alternat-ing curves is equal to n

2

+ 1, in this case 3

2

+ 1 = 10.Although this law cannot be strictly applied to the spine,it nevertheless gives us an appreciation of the effect ofspinal curves on stability.

4

SECTION I ANATOMY

Figure 1.1

Vertebral column and sacrum.

a.

Posterior view.

b.

Anterior view.

c.

Lateral view.

CHAPTER 1 CURVATURES

5

Figure 1.2

Vertebral curves.

a.

Normal curve.

b.

Accentuated curvature.

c.

Attenuated or diminished curvature. There is arelationship between the degree of curvature and the inclination of the sacral promontory.

Figure 1.3

Delmas index: H x 100/L, where L is the lengthof the entire vertebral column and H is the height of thevertebral column.

Figure 1.4

The plumb line passes through the foramen mag-num on a line tangent to the posterior aspect of L3 andthrough the middle of the sacral promontory.

6

SECTION I ANATOMY

Figure 1.5

Evolution of the vertebral curves (according to Tittel).

7

2

TYPICAL VERTEBRA

DIFFERENT GROUPS OF VERTEBRAE

Each vertebra is unique and differs, sometimes veryslightly, from its neighbor. There are three groups:

• Cervical vertebrae• Thoracic vertebrae• Lumbar vertebrae

The vertebrae in each group possess common characteris-tics, and each is a variant of the “typical vertebra” (Fig. 2.1)that serves as a prototype for description. The “typicalvertebra” is composed of a posterior neural arch of ahorseshoe shape that is attached to the posterior aspect of

the vertebral body, thus forming the spinal canal. This archgives rise to the zygapophyseal joints on either side, whichare anchored to the vertebral body via the pedicles. Twolaminae form the posterior aspect of the spinal canal andunite in the midline to form the spinous process. Twotransverse processes are formed, one on each side of thebody, at the posterior aspect of the arch near the articularpillars.

STRUCTURE OF THE VERTEBRAL BODY

Vertebral Endplate

The vertebral body is cylindrical. Its superior and infe-rior margins are referred to as endplates. These endplatesare slightly concave in all directions. They are composedof two parts:

• A central part layered with cartilage and riddledwith small apertures that play an essential role inthe nutrition of the disk

• A peripheral part, white in color, that forms an annu-lar pad into which the annulus fibrosus of the diskis inserted.

This peripheral part is the ring epiphysis, which acts asthe ossification center for the body; it fuses at about age 14.

Bony Framework

The vertebral body is composed of a trabecular systemthat projects in three directions: vertical, oblique, and hor-izontal. The function of the

vertical trabeculae

is

to sup-port the vertebral column. The oblique trabeculae aremade up of two bundles (Fig. 2.2 and Fig. 2.3). One arisesfrom the inferior aspect of the endplate and passes throughthe pedicles to form the superior articular facet andspinous process. The other arises from the superior end-plate and passes through the pedicles to form the inferiorarticular process and spinous process. This creates a region

Figure 2.1

Typical vertebra.

8

SECTION I ANATOMY

of enhanced posterior resistance, the posterior column(described by G. Rieunau and P. Decoulx), which is com-posed of the posterior aspect of the vertebral body and thepedicles. Rieunau and Decoulx have therefore classifiedvertebral fractures as stable if they spare the posteriorcolumn and as unstable if they do not. The anterior surfaceof the vertebra, containing only vertical trabeculae, is a

zone of least resistance and hence a frequent site of com-pression fracture. This region is triangular with a posteriorapex and corresponds to the vascular equatorial zone. The

horizontal and radial trabeculae

join the lateral corticaltrabeculae.

ARCHITECTURE OF POSTERIOR ARCH

The posterior arch is formed by (a) an intertransversetrabecular system that extends from one transverse processto the other and passes through the laminae and (b) a U-shaped trabecular system bordering the superior part ofthe laminae between the two superior articular processes(Paturet). It is independent of the superior and inferioroblique trabeculae that open like a fan in the thicknessesof the superior and inferior articular processes.

CARTILAGINOUS ENDPLATES

Cartilaginous endplates are the reproductive zones thatprovide growth in height. They are thin in the adult andthick in the child in accordance with their respectivedegree of function.

Some pathologic processes can damage the endplatesand impair bony growth, resulting in vertebral body mal-formations. The cartilaginous endplates detach more eas-ily from the vertebral body than from the disk; in fact,they are considered part of the disk by H. Junghanns.

ZYGAPOPHYSEAL JOINTS

While the disk allows for vertebral mobility, the zyg-apophyseal joints (or facet joints) provide a restraint forvertebral motion.

Their orientation varies with the different vertebral lev-els. In the cervical spine, the superior articular processesface posteriorly and slightly laterally. In the thoracic spine,they face posteriorly; in the lumbar spine, they face medi-ally. The angles of inclination of the facet joints in thehorizontal plane are 45° for the cervical spine, 60° for thethoracic spine, and 90° for the lumbar spine (Fig. 2.4 andFig. 2.5).

The superior articular process of the T12 vertebra isthoracic, while the inferior articular process is morpho-logically lumbar.

The articular surfaces of the facets are covered withcartilage. The facet joints are enveloped by a baggy cap-sule, which covers them like a hood and imparts to thejoint a degree of elasticity. The degree of freedom ofmovement at each vertebral level is largely governed bythe orientation of the facets.

Figure 2.2

Trabecular system: 1, oblique superior trabecularbundle; 2 and 4, supporting trabeculae of the facet joints; 3,interior oblique bundle. Not shown are the vertical system(vertical trabeculae that aid in the essential function of weightbearing) and the horizontal radicular system of trabeculae(that radiate out from the axial line to the periphery).

Figure 2.3

Osseous vertebral trabeculae: 1, sheaf bundles;2, transverse bundles.

CHAPTER 2 TYPICAL VERTEBRA

9

Joint Capsule

The facet joint capsule is the most richly innervatedpart of the spine with respect to nociception as well asproprioception. This degree of innervation allows theproximal and distal supporting structures to adjust thenumerous combinations of tension and pressure imposedby various different postures or physical exertion. Theelastic properties of the joint capsule provide for solidsupport at their superior and inferior poles and tend tomaintain the articular surfaces in close contact with eachother. Each movement must overcome the surface tensionof the capsule, and as soon as the mobilizing force ceases,the articular processes recoil to their original positions.These elastic forces impart a stabilizing effect on the spinewithout augmentation of joint tension as is the case with

the action of the musculoligamentous apparatus duringexercise. The lateral aspects of the joint capsule are muchmore lax and contain fewer elastic fibers according toTöndury.

Meniscoids

Meniscoids were described by Schmincke and Santoand then later by Emminger and Zuckschwerdt and werestudied in depth by Töndury and by Kos. They have incor-rectly been referred to as “menisci.” (Due to their potentialrole in certain vertebral pain syndromes, meniscoids arediscussed in greater detail in Chapter 17.) They are com-posed of simple synovial folds, sometimes extremely thin,like cigarette paper.

According to Kos (1972), a “typical meniscoids forma-tion” is made up of three parts: the capsular part, composed

Figure 2.4

Orientation of the facet joints as seen from thefrontal plane: C, cervical vertebrae; T, thoracic vertebrae; L,lumbar vertebrae.

Figure 2.5

Orientation of the facets in the sagittal plane: C,cervical vertebrae; T, thoracic vertebrae; L, lumbar vertebrae.

10

SECTION I ANATOMY

of loose connective tissue; the highly vascularized syn-ovium; and a free terminal part, which is avascular andoften contains chondrocytes (Fig. 2.6).

According to Töndury:

If the joint capsules are carefully removed from the nearbyintervertebral foramina, careful dissection reveals small,shiny, semilunar-shaped wedges of a soft gelatinous con-sistency visible at the edge of the articular facet. In a freshspecimen, numerous small blood vessels are evident.According to their morphology, they are folds of synovialmembrane connected to the periarticular filling andthrough to the intervertebral filling.

These inclusions exist in 84% of facet joints (Emminger).They form part of the usual structure of these joints andare maximally developed in the midlumbar region.

“Embryologically,” according to Töndury, “their devel-opment is completely separate from that of a meniscus,even though in the adult, there is a certain structural sim-ilarity between these vertebral meniscoids and, for exam-ple, the meniscus of the knee.”

When ossification of the vertebral arches begins in anembryo of 70-mm length, one can distinguish a cleararticular split in the fold of synovial membrane at the

medial aspect of the joint. These folds can either be com-posed of mesenchymal tissue (lumbar region) or resultfrom a secondary invagination at the level of the interver-tebral foramina (cervical region).

The regions of the capsule adjacent to the intervertebralforamina are well vascularized. They invaginate second-arily into the joint, forming small folds that, at their wid-ened base, are connected to the tissue of the intervertebralforamina.

The definitive structure is formed at birth. In the adult,they are of varying size, form, and thickness and aresometimes very thin. According to Engel and Bogduk,there are three types of intra-articular structures, eachdistinctive in its location within the joint and in its micro-scopic structure. The three types of structures are a con-nective tissue rim, an adipose tissue pad, and a fibro-adipose meniscoid. At least one type of structure wasrepresented in every one of the joints examined, and 47of 82 joints contained more than one type.

Giles and Taylor (1982) describe two types of forma-tion located in the cervical spine and within the lumbosa-cral junction (L5–S1), in addition to adipose formations:(a) a thick inclusion projecting from the ligamentum fla-vum into the superior medial part of the joint, and (b) awide synovial inclusion, well vascularized, projecting intothe medial part of the joint.

Töndury suggests that these formations, unlike thedisks and articular cartilage, do not degenerate with agedue to their rich blood supply. When the cartilage degen-erates, however, the meniscoid inclusions are exposed toabnormal biomechanical forces that may result in their“wearing out.” It was his impression that the function ofthese meniscoids was to adapt to the incongruity of thearticular surfaces. The meniscoids are readily able to adaptwith the configuration of the joint surface, and their posi-tion within the joint varies dynamically with movement.Decreases in intra-articular pressure allow the meniscoidto penetrate more deeply into the joint; with increases inpressure, they are wedged toward the outside. Therefore,there is never any dead space within the joint (Töndury).*

Figure 2.6

Typical meniscoid formation (taken from a facetarticulation) according to Kos: 1, capsule; 2, cartilage; 3,base of the meniscoid formation; 4, medial aspect; 5, terminalaspect.

* The zygapophyseal joint was the theme of the Third Congress of theInternational Federation of Manual Medicine (1971), organized and pre-sided over by the author. The principal papers (H. Junghanns, G.Lazorthes, G. Töndury, J. Kos and J. Wolf, E. Emminger, A. Wacken-heim, C. Gillot, R. Maigne) were published in the

Annales de MedecinePhysique

(1972), which has since become

Annales de Readaptation etde Medecine Physique

(see the remark in the bibliography under “MinorIntervertebral Dysfunction”).

11

3

INTERVERTEBRAL DISK

The intervertebral disk is a fibrocartilaginous structure,biconcave in configuration, and situated between contig-uous vertebral bodies. Although there are 24 vertebrae (26if the sacrum and coccyx are included) and thus 25 inter-vertebral spaces, there are only 23 intervertebral disks.This discrepancy is due to the fact that there are no inter-vertebral disks between the occiput (CO) and the atlas(C1) or between the atlas (C1) and the axis (C2). The firstdisk is therefore located between C2 and C3.

The ratio ofthe disk to vertebral body

height

determines the amplitudeof segmental motion.

• In the cervical spine, the disks measure between 5and 6 mm in height, with a disk to vertebral bodyheight ratio of 1:3 (atlas and axis not included).

• In the thoracic spine, the disk height varies. Thethoracic disks are smallest (3 to 4 mm) between T2and T6, where the vertebral spinal index shows afunctional reduction. Above T2, and especiallybelow T6, the disk height becomes larger. On aver-age, the disk to vertebral body height ratio is approx-imately 1:5 to 1:6 in the thoracic spine.

• The lumbar spine contains the largest disks in thespine (10 mm on average). However, the disk tovertebral body height ratio is only 1:3, as the verte-

bral bodies of the lumbar spine are also high andmassive.

Of all the spinal segments, the least mobile are thosein the thoracic spine because of the relatively smaller sizesof the intervertebral disks (i.e., one-sixth vertebral height)compared with the cervical (one-third vertebral height)and the lumbar (one-third vertebral height) disks(Fig. 3.1). The larger intervertebral disks in the cervicaland lumbar spines allow for more segmental motion.

The shape of the disk

determines the curvature of thevertebral column. When the anterior disk height is notice-ably greater than the posterior height, the vertebral bodieswithin that segment will be slightly extended. Theopposite is true for intervertebral disks with a higher pos-terior border. Both the cervical and lumbar disks arethicker anteriorly than posteriorly (especially at the lum-bosacral junction). The thoracic disks, on the other hand,are thicker posteriorly than anteriorly.

The disk is composed

of a central part, the nucleuspulposus, and a peripheral part, the annulus fibrosus(Fig. 3.2 and Fig. 3.3). The nucleus pulposus, or centralcore, is gelatinous in substance and situated slightly poste-rior to the center of the disk. It has characteristic non-compressibility and plasticity that one associates with fluids

Figure 3.1

Relative heights of the intervertebraldisks and the bodies of the spinal vertebrae.

a.

Atcervical level, approximately one-third.

b.

At tho-racic level, approximately one-sixth.

c.

At lumbarlevel, approximately one third.

12

SECTION I ANATOMY

and is basically a ground substance in which collagenfibers and isolated chondrocytes are embedded. It isencapsulated in a kind of “box” between the vertebralendplates by the annulus fibrosus. If there is a distinctdifference between the annulus and nucleus macroscopi-cally, the passage from one to the other is actually gradual;microscopically, no sudden transition actually exists(Fig. 3.3).

The image of the nucleus as a “round marble within afibrous ring” must be abandoned. The nucleus acts as ahydraulic chamber without clear boundaries (Rabischonget al.).

The annulus fibrosus, or “fibrous ring,” is composed ofthin layers of fibrocartilage in which are embedded flat-tened chondrocytes, creating a very firm consistency andthick texture. The fibers in each layer are orientedobliquely, with each layer running in the direction oppo-site to the adjacent layer (Fig. 3.4). The degree of obliquityincreases from the periphery of the disk to the center.Thus, the central layer of fibers is directed more in the

horizontal plane. These fibers blend into the cartilaginoussurface of the vertebral endplate. The annulus fibrosus isthus firmly adherent to the margin of the endplate, pro-viding the disk with a structure that is highly resistant totensile loads. The anterior border of the annulus fibrosusis the most resilient, since these fibers blend and penetratedeeply into the anterior vertebral rim via Sharpey’s fibers:the posterior portion of the annulus fibrous is its weakestpoint

The water content of the annulus fibrosus varies withage, but to a lesser degree than at the nucleus. At birth,the annulus is 79% water, and this decreases to approxi-mately 70% by age 70. The annulus is able to absorbpressure generated by the nucleus pulposus in an elasticmanner; this is done, however, with the relatively littlereal elasticity of 15%. This unique characteristic, in addi-tion to the alternating obliquity of the annular fibers,helps a healthy disk to maintain its shape under normalpressures.

HYDROPHILIC PROPERTIES

The intervertebral disk is well suited to absorb pressureby both dissipating it and redirecting it. This is achievedby means of its structure. The central aspect of the inter-vertebral disk or the nucleus pulposus is composed of ahydrophilic center that is high in water content and istherefore essentially noncompressible but deformable inshape. Pressure on this fluid center is dissipated radiallyto the annulus fibrosus, which, due to its toughness andrelative elasticity, is able to absorb the pressure without asignificant alteration in size or shape.

If the disk is sectioned in the transverse or sagittalplane, the gelatinous material inside spurts out as if it werejelly. The ability of the disk to dissipate pressure and

Figure 3.2

Sagittal section of an intervertebral disk: 1. Ante-rior longitudinal ligament seen in the front. 2. Posterior longi-tudinal ligament seen in the rear.

Figure 3.3

Transverse section of an intervertebral disk. Thenucleus is at the center; the annulus fibrosus is at the periphery.

Figure 3.4

Lateral external view of an intervertebral disk.Note the oblique orientation and the crisscrossing of thefibers of the annulus.

CHAPTER 3 INTERVERTEBRAL DISK

13

tension is directly linked to its hydrophilic properties andhigh water content. It is noteworthy that the water contentis not constant for all ages, being approximately 88% ina newborn and showing progressive dehydration with timeso that by age 14 it is 80% and by age 70 it is approxi-mately 70% (Keyes and Compere).

The disk is avascular

in the adult. It relies on osmosisto meet its nutritional needs. Numerous microscopic poresallow nutrients to flow from the nucleus to the vertebralbody via the cartilaginous endplate. When the disk isexposed to prolonged pressure (such as in the standingposition), some of its water content diffuses into the ver-tebral body. As a result, disks are thinner in the eveningand a person is actually somewhat shorter. This decreasein height can reach up to 2 cm in some people, withrestoration after resting. With age, the hydrophilic prop-erties of the disk are less pronounced, with a correspond-ing decrease in the shock-absorbing capacity of the disk.In conjunction with the increased incidence of vertebralbody compression fractures and accentuation of the spinalcurves that occur with aging, the loss in hydrophilic prop-erties contributes to the gradual decrease in height seenamong older people.

The mechanism of this hydration

is not yet fully under-stood. The contents of the nucleus are governed by the

laws of osmosis. The nucleus behaves like a solutionbound by a semipermeable membrane (the cartilaginousendplate). Depolymerization of the polysaccharides aug-ments the osmotic pressure and thus the force drawingwater from the vertebral bodies through the multiple poresof the endplate. With age, the passage of water becomesincreasingly difficult, and the nucleus loses its hydrationcapacity; this is called the “imbibition factor.” The forceone must apply to a colloidal jelly to separate the dispersedphase from the dispersing phase is called the “imbibitionpressure.” Within the disk, these two phases refer to theproteoglycan matrix and the interstitial fluid, respectively.The imbibition pressure is significant in young people,reaching approximately 250 mm Hg (Charnley). Thispressure varies both with age and from day to day, alongwith the pressure transmitted the nucleus.

In an attempt to study the hydrational characteristicsof the intervertebral disk, Nachemson, Lewis, Maroudas,and Freeman (1970) utilized radiographic contrast mate-rials and radioisotopes to study the permeability of liquidsthrough the cartilaginous endplate to the disk and thelacunae of the subchondral bone. They concluded that onlythe central part of the disk was permeable.

15

4

LIGAMENTOUS SYSTEM

ANTERIOR LONGITUDINAL LIGAMENT

The anterior longitudinal ligament forms a long fibrousnetwork from the anterior tubercle of the atlas to thesacrum. It is essentially attached to the anterior and anter-olateral parts of each vertebral body. It is not attached tothe margin of the vertebral body and adheres only slightlyto the disk, from which it can be easily detached. It has ahigh degree of tensile strength and, in general, maintainsits integrity in vertebral compression fractures (Fig. 4.1and Fig. 4.2).

POSTERIOR LONGITUDINAL LIGAMENT

Unlike the anterior longitudinal ligament, the posteriorlongitudinal ligament is firmly adherent to the disk. It iswidest at its point of attachment to the disk and narrowsas it borders the vertebral body (Fig. 4.3). The paraspinalvenous plexus is situated posterior to the vertebral bodies,thus separating the ligament from attaching to the verte-brae. Pathophysiologically, the posterior longitudinal lig-ament plays an important role, since it reinforces the diskposteriorly where the annulus is at its weakest point, andthus provides a barrier to disk extrusion.

The posterior longitudinal ligament is composed of (a)long, superficial, ribbon-like, median fibers that extendover four or five contiguous vertebrae, and (b) a deep layerof short arciform fibers that skip alternate vertebrae andattach on the side opposite to their origin. This ligamentis strongest in the thoracic spine and weakest at the lumbarlevels.

INTERSPINOUS LIGAMENT

The interspinous ligament connects the contiguousspinous processes and is reinforced by the supraspinousligament. It plays a major role in limiting spinal flexion.

Figure 4.1

Sagittal section (

top

) and transverse section(

bottom

) showing the different ligaments of the spinal verte-brae

:

1, anterior longitudinal ligament; 2, posterior longitudi-nal ligament; 3, ligamentum flavum; 4, interspinous ligament;5, supraspinous ligament; 6, nucleus pulposus.

16

SECTION I ANATOMY

LIGAMENTUM FLAVUM

The ligamentum flavum is composed of two halves thatmeet in the midline, adjoining the vertebral laminae andthus closing the vertebral canal. This ligament’s high con-tent of elastin affords it a high degree of resilience andalso accounts for the yellow color

(flavos

is the Greekword for yellow). The ligamentum flavum is also attachedto the medial aspects of the facet joints and thus restrictstheir range of motion.

Figure 4.2

Vertebral sections at the level of the pedicles to demonstrate the superior dorsal aspectof the vertebrae.

Left

, Anterior view.

Right

, Posterior view. 1, Ligamentum flavum; 2, anterior longi-tudinal ligament.

Figure 4.3

Posterior longitudinal ligament.

17

5

SPINAL CHARACTERISTICS BY REGION

CERVICAL SPINE

The cervical spine is composed of seven vertebrae,forming a curve that is convex anteriorly. The apex of thecurve is situated at C4, and its convexity continues distallyuntil T2 (Fig. 5.1 and Fig. 5.2).

The two most proximal cervical vertebrae, the atlas andthe axis, are distinguished from the other typical cervicalvertebrae as there is no intervertebral disk between them(Fig. 5.3). The first intervertebral disk is located betweenC2 and C3. There are several characteristics that distin-guish the cervical spine from other regions of the vertebralcolumn that are necessary to note here.

Facet Joints

The cervical facet joints are obliquely oriented, with agradual increase in obliquity from the horizontal as one

descends from top to bottom. Beginning with the facetsof the axis, which are quasi-horizontal, there is a progres-sive increase in inclination, reaching a maximum ofapproximately 45° in the distal-most cervical vertebrae.In the sagittal plane, the articular surfaces of the facetsface dorsally and slightly medially. This alignment facili-tates gliding of contiguous surfaces in all directions, espe-cially in flexion and extension (Fig. 2.4 and Fig. 2.5).

Spinous Processes

The atlas has no spinous process. The size of thespinous process increases gradually from C3 to C7. Theorientation of the spinous processes is nearly horizontal,and, in hyperextension, they come into contact with eachother. On palpation, C7 is the first spinous process thatdiffers from the other cervical segments; it is the only onethat is not bifid, and it is the most prominent of the neck(Fig. 5.1 and Fig. 5.2).

Figure 5.1

Cervical spine.

a.

Lateral view.

b.

Anterior view.

c.

Oblique view.

18

SECTION I ANATOMY

Supraspinous Ligament

In both the thoracic and the lumbar spines, the supra-spinous ligament is a flattened tissue layer closely adher-ent to the posterior aspect of the interspinous ligament. Inthe cervical spine, it is much more developed and formsthe ligamentum nuchae, attached proximally to the occiputand distally to the spinous processes of all the cervicalvertebrae with the exception of C1 and C7.

In certain animals, such as the horse, this ligament ishighly developed. Its strength and resiliency assist thecervical extensors by passively supporting the weight ofthe head.

Uncinate Processes

The uncinate processes are unique to the cervical ver-tebrae from C3 to C7. These processes are situated later-ally and give a saddle-shaped appearance to the vertebralbody (Fig. 5.4a). The inferior aspect of the vertebral bodyhas a reverse shape with a notch on each side that iscomplementary to the uncinate processes.

The significance of these “articulations” lies chiefly intheir proximity to the vertebral artery and the sympatheticchain in close juxtaposition to it.

These processes can be the source of spondylosis withformation of osteophytes that may extend posteriorlytoward the vertebral canal, encroaching on the nerve rootor the vertebral artery. Luschka was the first to point outthis peculiarity.

Figure 5.2

Cervical vertebrae.

a.

Posterior view.

b.

Anterior view.

c.

Lateral view.

Figure 5.3

There are no intervertebral disks between theocciput and the atlas or between the atlas and the axis. Thefirst intervertebral disk is seen between C2 and C3.

Figure 5.4

a.

Uncus. It causes the superior cervical endplate of the cervical vertebrae to take the form of a stirrup (1 and 2).

b.

The classic interpretation is that there exists an articular cavity (Luschka).

c.

Töndury’s interpretation is that there is nouncovertebral articulation, but after 10 years of age, there is formation of lateral fissures in the annulus. These fissuresprogressively make their

way

to the central disk.

CHAPTER 5 SPINAL CHARACTERISTICS BY REGION

19

Since Luschka, the fissures between the uncovertebraljoints and the disk have been considered true articulationswith joint cavities, articular cartilage, and joint capsules.The anterior part of the joint capsule blends with theannulus fibrosus of the disk (Fig. 5.4b).

In a degenerating disk, the nucleus pulposus canimpinge upon the arthritic uncovertebral joint. Contactmade by nuclear material with osteophytes originatingfrom the uncinate process forms a nodule that may bulgeinto the intervertebral foramina. This nodule was namedthe “disco-osteophytic nodule” by de Séze. Cervicobra-chial neuralgia is often the result of nerve root impinge-ment by this nodule. These nodules are often referred toby a surgeon as “hard herniations,” as opposed to “softherniations” that are formed when the nucleus herniatesthrough an annular tear.

According to Töndury (Fig. 5.4c), there is no formal“uncovertebral joint.” He states that “lateral disk fissures”appear at approximately age 10 and progressively widenmedially with age, eventually communicating with thenucleus pulposus, allowing it to reach the periphery andform the disco-osteophytic nodule.

Töndury bases his opinion on study of the uncus inrelation to age. The uncinate processes belong to the neu-ral arches of the cervical vertebrae. In the fetus, collagenfibers join the processes of contiguous vertebrae, and nofissure is evident. The disks extend only to the epiphysealcartilage. In the newborn, the collagen fibers of the unci-nate processes become adherent to the peripheral laminaeof the disks. Even in children of ages 6 to 7, there is noevidence of a true uncovertebral “articulation.” These fis-sures, still very narrow, first begin to appear in the disksof the inferior cervical spine in children of approximately9 to 10 years of age. Töndury showed, with the aid ofmicroscopic sections, that these fissures are not articularsplits, but ruptures in the collagen fibers that are initiallylimited to the lateral aspects of the disk. Examination of

disks in adults of various ages demonstrates that fissuresextend progressively toward the center of the disk, even-tually communicating with the gelatinous nucleus; inextreme cases, the fissure may extend from one end of thedisk to the other. When this occurs, a lateral disk extrusioncan result, narrowing the intervertebral foramina; thisextrusion is the “disco-osteophytic nodule.”

Transverse Processes and Vertebral Artery

The cervical transverse processes arise from the mid-point of the lateral masses by two roots. These roots formthe transverse foramen (Fig. 5.5).

Foramina are located on all the cervical vertebrae.However, at C7, the opening is much smaller, allowingpassage of the vertebral vein only. The foramina of thefirst six vertebrae form a discontinuous canal throughwhich the vertebral artery (a branch of the subclavianartery), its sympathetic plexus, the vertebral vein, and thespinal nerve pass (Fig. .5.6).

In the superior cervical spine, the artery takes a com-plex route, as the transverse foramina of the atlas aresituated much more laterally than those of the axis; theartery thus has to pass laterally and then medially, thusmaking a double bend before reaching the foramen mag-num (Fig. 5.7). Jung notes that the artery, whose dimen-sions are the same as those of the transverse foramen,often appears cramped in this passage. One can easilyenvision the stretch to which the artery is subjected withextreme movements of the head. Arteriography has shownthat when a subject positions the neck in extension andexternal rotation, the circulation is compromised on theside contralateral to the rotation (Fig. 5.8).

The proximity of the vertebral artery to the cervico-occipital junction explains the possibility of injury to thearterial wall that may occur with inappropriate maneuversof the cervical spine. Serious accidents have beendescribed after certain “manipulations,” or even after someprolonged abnormal postures of the cervical spine that canresult in vertebral artery compression and thus restrictblood flow between the atlas and the occiput. In normalpatients, the transient interruption of the vertebral arterycirculation is normally compensated by the blood supplyof the contralateral vertebral artery. This is not the case ifthe latter is narrowed by atheroma or is hypoplastic. Ana-tomic variations and anomalies are indeed very frequentat this level.

Uncinate spondylosis and, less frequently, facet arthro-sis can create bends or segmental narrowings of the ver-tebral artery.

Anomalies of Occipitocervical Junction

Anomalies of the occipitocervical junction are notuncommon. Many are subclinical and can go on to produce

Figure 5.5

Neural foramen (T).

20

SECTION I ANATOMY

serious neurologic sequelae that are often discovered oraggravated by trauma.

Cranial Settling

The most common anomalies of the cervico-occipitaljunction may result in cranial settling. This is character-ized radiologically as a rise in the odontoid process aboveChamberlain’s line (which, in a lateral radiograph of thecervical spine, connects the posterior edge of the bonypalate and the posterior edge of the foramen magnum).See Fig. 5.9 and Fig. 5.10.

Figure 5.6

Spinal nerve (1) with the anterior primary ramus (2), posterior primary ramus (3), and vertebral artery (4).

Figure 5.7

Intervertebral canal.

Figure 5.8

Rotation with hyperextension of the head impairsblood flow in the vertebral arteries on the side contralateralto the rotation.

Figure 5.9

Chamberlain’s line. This line connects the poste-rior border of the bony palate to the posterior border of theforamen magnum. In normal individuals, the odontoid pro-cess is found below this line. The basal angle is normally130°. It can be greater in persons with conditions such asplatybasia.

CHAPTER 5 SPINAL CHARACTERISTICS BY REGION

21

Another landmark is Fischgold’s line (Fig. 5.11 andFig. 5.12). This line is seen on a standard anteroposteriorradiograph of the cervical spine (forehead and nose onplate) as a line joining the two mastoid processes, whichnormally passes through the atlanto-occipital articulation.With cranial settling, the odontoid process ascends abovethis line.

Other Anomalies

Cranial settling can be accompanied by other anoma-lies such as occipitalization of the atlas, spina bifidaocculta of the atlas, stenosis or deformation of the foramenmagnum, subluxation or dislocation of the atlas on theaxis, cervical block vertebrae, spina bifida, or platybasia.

These bony anomalies are often associated with neu-rovascular anomalies. Often, a patient with such an anom-aly has a short neck, a low hairline, and restricted rangeof neck motion. Sudden maneuvers should be avoided inthese susceptible spines.

THORACIC SPINE

The thoracic spine is composed of 12 vertebrae. Thevertebral bodies are taller than the disks. The articularsurfaces of the facets are oriented in close approximationto the frontal plane and are inclined 60° from the horizon-tal. The superior articular processes face posteriorly,slightly superiorly, and laterally (Rouviere). The spinousprocesses are long and directed obliquely and inferiorly.The ribs articulate with the thoracic vertebrae (Fig. 5.13through Fig. 5.17).

The vertebral body is semicylindrical in shape, hencethe semicircular appearances of the vertebral endplates.The intervertebral foramen is circular. Two costal demi-facets (superior and inferior) are situated on each side ofthe posterolateral aspect of the vertebral body with theexceptions of T1, T11, and T12. Each of the latter threevertebra has a complete articular facet for the homologousrib (Fig. 5.14).

The transverse processes are massive and extend pos-terolaterally. With the exception of T11 and T12, they havearticular facets on their anterior surfaces for the homolo-gous ribs (costotransverse articulation). See Fig. 5.14 andFig. 5.16. The spinous processes are directed obliquely insuch a manner that the tip of the process of T6 lies at thelevel of the superior part of the body of T8 (Fig. 5.15).This degree of obliquity increases progressively down-ward to T8 and then gradually decreases for the final fourthoracic vertebrae, whose spinous processes are somewhatshorter. The spinous processes of the last two vertebraemore closely approximate those of the lumbar spine.

The facets are oriented 60° from the horizontal planeand lie in the frontal plane. This facilitates mobility in alldirections (Fig. 2.4 and Fig. 2.5).

LUMBAR SPINE

The lumbar spine is composed of five vertebraearranged in a lordotic curve that is convex anteriorly(Fig. 5.18). The disks are thick and measure approxi-mately one-third the height of the corresponding vertebralbody. The facets are oriented in such a way as to consid-erably limit lateral flexion (Fig. 5.19 and Fig. 5.20). Rota-tion would thus be impossible were it not for some laxitybetween them. Indeed, the superior articular process isflattened transversely; its medial aspect has an articularsurface in the shape of a vertical sulcus whose concavity

Figure 5.10

Chamberlain’s line in cases of cranial settling.The odontoid process is noted to be above this line.

Figure 5.11

Fischgold’s line (frontal tomography passingthrough the mastoid processes). In the normal individual, thebimastoid line (2) passes through the occiput-atlas articula-tions and is tangential to the upper pole of the odontoidprocess. The digastric line (1) passes above the base of thecranium and 1 cm above the level of the atlanto-occipitalarticulations.

Figure 5.12

In cases of cranial settling, the odontoid pro-cess is seen to be significantly above the bimastoid line (2).This is also noted for the atlanto-occipital articulation.1, digastric line.

22

SECTION I ANATOMY

faces medially and slightly posteriorly. The inferior artic-ular processes, in contrast, have convex articular surfacesshaped like cylindrical segments facing laterally andslightly anteriorly, which permits the disk to glide into theconcavity of the superior articular process of the vertebrabeneath it. Anomalies of the facets are frequent.

T12 is a transitional vertebra with superior articularprocesses that are typically thoracic in morphology andinferior articular processes that are typically lumbar. Onoccasion, T11 plays the role of a transitional vertebra.

Spinous Processes

The spinous processes are massive. They are directedhorizontally and are shaped like knife blades, ending invertically lengthened tuberosities.

Figure 5.13

Thoracic vertebra seen posteriorly (

a

), anteriorly(

b

), and in lateral view (

c

).

Figure 5.14

Articular facets of the thoracic vertebrae asso-ciated with the ribs, consisting of two semifacet articulations,one superior and one inferior at the head of the rib (2 and3), and one articular facet for the tuberosity of the ribs (1).This last facet does not exist for the last two vertebrae, whicharticulate with a facet between T11 and T12.

CHAPTER 5 SPINAL CHARACTERISTICS BY REGION

23

Transverse Processes

In the lumbar spine, these processes are called “costi-form.” They are long and serve as the insertion sites ofpowerful muscles.

SACROILIAC JOINT

The pelvic girdle represents the junction between thespine, which rests on top, and the lower limbs below. Itis formed by two symmetric iliac bones, the right and theleft, and by the sacrum, a median triangular segment com-posed of five fused vertebrae. Thus, the sacrum articulateson each side with an iliac bone (Fig. 5.21).

The symphysis pubis joins the iliac bones anteriorly.The pelvic girdle is in the shape of a funnel with theopening facing superiorly: the pelvic inlet. The pelvis iswider, broader, and shorter in women than in men.

Figure 5.15

Tip of the T6 spinous process is found to reach approximately one third of the way down the vertebral body of T8.

Figure 5.16

Costotransverse articulation (1) and costoverte-bral articulation (2). At T11 and T12, the ribs are noted notto be true ribs, as they do not have costotransverse articu-lations.

24

SECTION I ANATOMY

The sacrum is triangular, with its apex inferior and itsbase superior; thus it acts like a keystone between the twoiliac bones. The sacrum articulates with the two ilia viathe sacroiliac joints:

• The lateral aspect of the sacrum is shaped like acircular arc (articular surface). The center of thatcircle is situated at the level of the tubercle of S1,which represents the point of insertion of the pow-erful supporting ligaments.

• The coccyx, located at the posteroinferior aspect ofthe sacrum, has an articular surface identical in con-tour to that of the sacrum. Its shape is also like anarc of a circle or a crescent. The midpoint of thecircle corresponds to the level of the iliac tuberosity,on which supportive ligaments are inserted.

These surfaces have highly irregular contours; they areneither flat nor symmetrically curved. The coccygeal sur-face has been compared to a rail (Farabeuf), because itslongitudinal axis has a bulge separating two depressions.The inferior sacral surface is rather convex, while thesuperior and middle portions are rather flat.

Delmas has described two types of sacroiliac joints:

• The first, which he refers to as “dynamic” (Fig. 5.21),is typical among those who must stand for pro-longed periods and whose spinal curvatures are thusaccentuated.

• The second, which he refers to as “static” (Fig. 5.21),is common among individuals whose spinal curvesare attenuated.

Figure 5.17

Rib cage.

Figure 5.18

Lumbar vertebrae and sacrum seenposteriorly (

a

) and in lateral view (

b

).

CHAPTER 5 SPINAL CHARACTERISTICS BY REGION

25

Figure 5.19

Lumbar vertebrae seen posteriorly (

a

), anteriorly (

b

), and in oblique view (

c

).

Figure 5.20

Facet joint orientation at the lumbar level. This orientation does not allow for rotation.

Figure 5.21

a.

Sacroiliac articulation.

b.

Dynamic-type sacroiliac articulation according to Delmas.

c.

Static-type sacroiliacarticulation according to Delmas.

26

SECTION I ANATOMY

The “dynamic” type of sacrum, which is seen in 25%of the population, tends to be oriented horizontally, andthe concavity of the articular facets is more pronounced.This type of sacroiliac joint is capable of greater mobilityand is more prevalent in females.

The “static” type, which can be found in 25% of thepopulation, tends to be oriented vertically with the artic-ular facets very elongated, vertical, and almost flat. Thistype is most characteristic of primates. It is an articulationthat has more limited mobility and a greater capacity for

weight bearing and effort and is a characteristically mas-culine feature.

Between these two schematic types, there are interme-diary forms (50%). The articular surfaces are lined withcartilage.

The sacroiliac joint and its ligaments are innervatedby the dorsal rami of L5 and S1, as well as by branchesoriginating from a posterior plexus formed by the dorsalrami of the inferior lumbar roots and the roots of S1 toS3.

27

6

THE MUSCLES

The muscles are the power sources of the spine. Theycan be categorized as intrinsic, such as the paravertebralmuscles, which are made up of short bundles that actdirectly on individual spinal segments with short leverarms, and extrinsic, which act via long lever arms and playa role in stabilizing spinal movement.

Figures 6.1 to 6.4 depict the superficial and deep musclesof the back.

PARASPINAL MUSCLES

The paraspinal muscles have been categorized byC. Gillot according to their positions relative to the planesof the transverse processes. He describes them as follows:

Muscles Located Anterior to the Plane of the Transverse Process

Muscles located anterior to the plane of the transverseprocess are situated along the lateral surface of the verte-bral body and the anterior surface of the transverse pro-cesses. They are well developed in the lumbar and cervicallevels and are absent from T4 to T11.

• At the cervicothoracic level are the longus colli andthe rectus capitis anterior muscles. These musclesare flexors and accessory rotators. They are com-pleted by the rectus capitis lateralis, a flexor andlateral flexor of the occiput.

• In the lumbar spine, the psoas muscle acts as a flexorof the hip (or of the trunk, depending on whether itacts in an open or closed kinetic chain) as well asan external rotator of the hip.

Figure 6.1

Superficial muscles of the trunk: 1, trapezius; 2,deltoid; 3, latissimus dorsi.

Figure 6.2

Deep muscles of the trunk: 1, serratus posteriorsuperior; 2, iliocostalis; 3, serratus posterior inferior; 4,sacrospinalis.

28

SECTION I ANATOMY

Muscles Located between the Transverse Processes

These muscles are situated in the frontal plane as follows:

• In the cervical spine, the scalenus anterior, medius,and posterior. These muscles are ipsilateral latero-flexors and assist in contralateral rotation.

• In the lumbar spine, the quadratus lumborum is alateral flexor of the trunk, or, when the spine is fixed,

it elevates the ipsilateral hemipelvis toward thespine.

• At both the lumbar and cervical spines are smallintertransverse (intertransversaria) muscles that arereplaced by ligaments in the thoracic spine. Thesemuscles assist in lateral flexion (Gillot).

• In the thorax, Delmas and Gillot consider the inter-costal muscles as paravertebral muscles.

Figure 6.3

Deep muscles of the trunk: 1, levator scapulae;2, rhomboideus; 3, serratus anterior; 4, quadratus lumborum.

Figure 6.4

Deep muscles of the trunk: 1, iliocostalis; 2, long-issimus thoracis; 3, multifidus.

Figure 6.5

Muscles of the abdominal wall (seen in section): 1, rectus abdominis; 2, obliquus externus.

CHAPTER 6 THE MUSCLES

29

All of the above muscles, with the exception of theintertransverse muscles, are innervated by branches of theanterior primary rami.

Muscles Located Posterior to the Plane of the Transverse Processes

These are the muscles of the paravertebral sulcus.According to Gillot, they can be categorized as:

• The small deep muscles situated at the craniocervi-cal junction

• The erector spinae muscles within the vertebral sulcus

Small Deep Muscles of the Neck Situated at the Craniocervical Junction

There are four small deep muscles situated at the cran-iocervical junction (Fig. 6.7):

• Rectus capitis posterior• Rectus capitis anterior• Obliquus capitis superior• Obliquus capitis inferior

These are the “vernier muscles” of Kapandji that offerfine tuning to the movements of the upper cervical spine.The obliquus capitis superior is a rotator; the rectus capitisposterior is an extensor and assists in rotation; the rectuscapitis major acts as a rotator; the obliquus capitis inferioracts as an extensor and an accessory rotator. These muscles

are innervated by the posterior ramus of Cl. The obliquussuperior also receives some fibers from C2.

Erector Spinae Muscles within the Vertebral Sulcus

These muscles extend from C3 to the sacrum, and theirdescriptions are very complex. They are:

• Multifidus, the deepest layer• Iliocostalis, located most laterally

Along with the longissimus thoraces, they form a groupof spinal muscles whose inferior insertion on the sacrumconstitutes a common mass.

In the cervical spine are the splenius and semispinalismuscles. The semispinalis capitis maintains the cervicallordosis and is essential in maintaining the head in theupright position. The splenius, which lies more superficial,is a rotator and acts as an antagonist to the sterno-cleidomastoid.

The right sternocleidomastoid rotates the head to theleft, whereas the right splenius rotates it to the right. Bothmuscles, however, are synergists in lateral flexion to theipsilateral side. All these muscles are innervated bybranches of the dorsal primary rami.

ABDOMINAL MUSCLES

The abdominal muscles play a very important role asflexors of the thoracic and lumbar spine, in maintainingvertebral balance and in reducing strain on the lumbosac-ral spine. They are, laterally, the obliquus externus abdom-inis, the obliquus internus abdominis, and transversusabdominis, all located on both sides of the midline.

The rectus abdominis is located on either side of thelinea alba. Unilateral contraction of the abdominal muscles

Figure 6.6

Posterior muscles of the neck: 1, splenius; 2,semispinalis capitis; 3, levator scapulae.

Figure 6.7

Muscles of the occipital region. 1, Obliquus capi-tis superior; 2, rectus capitis posterior minor; 3, rectus capitisposterior major; 4, obliquus capitis inferior; 5, interspinal lig-ament; 6, supraspinal ligament.

30

SECTION I ANATOMY

results in rotation and lateral flexion of the trunk; rotationis contralateral for the external oblique and ipsilateral forthe internal oblique.

MUSCLES OF THE NECK AND BACK

The trapezius muscle acts as an extensor of the head(Fig. 6.1).

The sternocleidomastoid muscle, when contracted uni-laterally, acts as a powerful lateral flexor of the cervicalspine with contralateral rotation. When both sternocleido-mastoid muscles contract simultaneously, they act as flex-ors of the inferior cervical spine.

During cervical rotation, the sternocleidomastoid actssynergistically with the contralateral splenius capitis muscle.In the upper cervical spine, the obliquus is the principalrotator.

MUSCLES OF THE LUMBAR REGION

The lumbar spine is supported by powerful muscles. Itlooks like a central column surrounded by four thick mus-cular pillars: the two psoas muscles anteriorly and theerector spinae masses posteriorly, form a “compositebeam” composed of bone and muscle (Rabischong,Dolto). See Fig. 6.5.

31

7

VASCULAR SUPPLY OF SPINE

ARTERIAL SUPPLY

Each radicular artery gives rise to an intercostal or alumbar artery. Prior to entering the intervertebral foramen,each artery subdivides into three tributaries:

• One supplying the spinal nerve accompanied by theradicular artery.

• One that courses along the midline of the posterioraspect of the vertebral body and subdivides into twobranches: one that penetrates the corresponding ver-tebral body and a second that descends one leveland penetrates the vertebral body below.

• One that courses along the inferior aspect of thepedicle and gives rise to a few branches that supplythe posterior arch and the most medial paravertebralmuscles. The most lateral muscles are supplied bya posterior collateral branch of the intercostal orlumbar artery.

VENOUS SUPPLY

The venous system is composed of two parts, theintraspinal venous plexus and the extraspinal venousplexus (Fig. 7.1).

Intraspinal Venous Plexus

The veins of the intraspinal venous plexus are locatedwithin the epidural space, and on each side they consistof two ascending plexiform cords (plexus venosi verte-brales externi and interni). They course away from thedisk and converge in the interpedicular space. They areunited by a transverse anastomotic vein (plexus transver-sale) that receives the basivertebral vein, which also drainsthe vertebral body. This vein also forms an anastomosiswith the paraspinal plexus.

Perispinal Venous Plexus

The veins of the perispinal venous plexus are locatedalong the anterior and lateral aspect of the vertebral body(anterior vertebral plexus) and on the posterior aspect ofthe posterior neural arch (posterior vertebral plexus). Theycommunicate with the intraspinal plexus via the veins ofthe intervertebral foramina.

Depending on the level, the vertebral blood supply maydrain via any of the ascending lumbar veins (lumbalisascendens), the azygos veins, the hemiazygos veins, or theposterior intercostal veins (venae intercostales posteriores).

Venous pressure is very low in the spinal veins. There-fore, even the slightest degree of venous compressionanywhere along their course in the intervertebral foramencan result in venous congestion in the territory drained bythese vessels.

Figure 7.1

Vertebral basilar veins: 1, azygos; 2, interverte-bral venous plexus; 3 and 5, perispinal venous plexus; 4,vertebral draining veins.

33

8

INNERVATION OF VERTEBRAL STRUCTURES

The vertebral structures are innervated by the posteriorprimary rami as well as the sinovertebral nerves.

POSTERIOR PRIMARY RAMI

The spinal nerve is formed by the union of the ventralmotor root and the dorsal sensory root. As it exits theintervertebral canal, it subdivides into a large anteriorprimary ramus and a much smaller posterior primaryramus. C1 and C2 represent exceptions to this rule. Theposterior ramus courses around the facet joints, giving riseto branches supplying the joints, ligaments, and all thesegmental spinal muscles as well as providing for thecutaneous supply over the back from the vertex to thecoccyx. In their anatomic studies, Lazorthes and Gaubert(1956) demonstrated the intimate relationship betweenthese nerves and the zygapophyseal articulations they sur-round and innervate (Fig. 8.1 to Fig. 8.3).

Each posterior ramus divides into a lateral branch anda medial branch. The first is a muscular branch, and thesecond has both muscular and cutaneous supplies. Distalto T8, the first is muscular and cutaneous, while the secondis muscular.

In the lumbar spine, the medial branch passes within1 cm of its origin, through a 6-mm long fibro-osseous tunnel,where it is flattened against the root of the transverse process(Bradley). It then passes between the intermamillary andmamillostyloid fascicles of the intertransverse muscle andtravels inferiorly and medially, skipping one or two ver-tebrae (Fig. 8.4).

The medial branch innervates the structures that liebetween the two facet joints: the interspinal muscles(interspinalis), the transverse spinal muscles (multifidus),the innermost portion of the erector spinae (sacrospinalis),the joint capsule, the ligamentum flavum, and the supra-spinous and interspinous ligaments.

The lateral branch innervates the intertransverse (inter-transversarii) muscles, the iliocostalis and longissimusmuscles, and the dorsal lumbar fascia.

Not all posterior rami have a cutaneous branch. Forexample, C1, L4, and L5 are exclusively motor nerves.While most authors agree on these exceptions, there issome disagreement as to whether a cutaneous branchexists for C6–C7 and C8. Certain authors (such as Grant,Lazorthes, and Töndury) deny the existence of cutaneousbranches for these lower cervical segments. Our clinicalfindings support those of the above authors and suggestthat the cutaneous branches of C5 and T1 are also incon-sistent.

The cutaneous territory of the posterior rami is alwayslocated distal to the level of the corresponding vertebra,with the exception of C2 and C3. The displacementincreases progressively from superior to inferior. Forexample, the skin overlying the posterior aspect of thebuttocks is innervated by the posterior rami of the thora-columbar junction.

Most dermatome charts do not appear to correspondwith these clinical findings, especially the depiction of thecutaneous supply of the upper and midthoracic regions.Keegan and Garett’s chart, probably the most well known,shows the dermatomes of C5, C6, C7, and T1 as smallstrips distributed in a fishbone-like manner overlying thesuperior thoracic region. In fact, we have noticed in a

Figure 8.1

The spinal nerve root (1) on exiting the interver-tebral canal branches into an anterior primary ramus (2) anda posterior primary ramus (3). The latter further divides intolateral (4) and medial (5) branches.

34

SECTION I ANATOMY

series of dissections that the cutaneous branch of T2 isoften much larger than its neighbors and supplies a muchlarger cutaneous territory. The cutaneous branch of T2becomes superficial at the T5 level before ascendingtoward the acromion. The neighboring territory of cuta-neous supply is that of C4 superiorly and T3 inferiorly(Fig. 8.5; see Chapter 36).

We have also studied the innervation of the skin over-lying the upper buttocks. This region is supplied by the

cutaneous branches of the posterior rami of T12, L1, andL2. Occasionally, there is a contribution from L3 to thisregion, but this branch is inconsistent (J.Y. Maigne).Again, the classic dermatome charts do not appear tocorrespond with these clinical findings (see Chapter 41).

A Chinese team at Ninghsia College studied the lumbarregion and noted the frequency of anastomoses betweenthe medial and lateral branches at the various levels neartheir origin. At the sacral level, the branch of S2 is the

Figure 8.2

a.

Posterior primary rami of the spinal nerve and facet joint (according to G. Lazorthes).

b.

Posterior primary ramiof the spinal nerves innervate the intrinsic muscles of the spinal column and the skin overlying the trunk (according toG. Lazorthes). C, at cervical level; T, at thoracic level; L, at lumbar level.

CHAPTER 8 INNERVATION OF VERTEBRAL STRUCTURES

35

largest. In conjunction with branches from S1, S3, and S4,it forms a true plexus innervating the lumbosacral musclesand the periosteal and periligamentous surfaces. The ter-minal branch in this plexus is the

posterior gluteal nerve

(Trolard), which in fact does not have a cutaneous branch.This nerve, approximately 10 cm in length, courses alongthe inferior aspect of the sacrum, giving rise to a fewbranches to the sacrococcygeal articulation before termi-nating in two branches. The first ascends to the secondsacral foramen and innervates the overlying skin; the sec-ond terminates in the coccygeal region (Lazorthes).

SINOVERTEBRAL NERVE

The sinovertebral nerve (Fig. 8.6), which is the size ofa thick thread (Hovelacque), is formed by the junction ofa spinal nerve with a sympathetic nerve root. The branchfrom the spinal nerve originates immediately after its exitfrom the intervertebral foramen. Occasionally, it arises

from either the posterior or the anterior primary ramus.The branch from the sympathetic chain arises from theadjacent white communicating ramus; most often subja-cent. Once formed, the sinovertebral nerve courses poste-riorly and enters the intervertebral foramen following a

recurrent

course anterior to the spinal nerve. Lazorthes,Poulhis, and Espagno (1948) described the distribution ofits terminal branch as purely segmental. The branches aredistributed to the vertebral body, the laminae, the posteriorlongitudinal ligament, the epidural tissues, the dura mater(G. Lazorthes), the anterior longitudinal ligament, theannulus fibrosus (Jung and Brunschwig), and the diskabove the corresponding vertebral body via numerousfibers and occasionally to a disk below. Hovelacque writes,“We have never seen the nerve divide into two terminalbranches: one ascends and one descends with reciprocalanastomosis between the branches of the nerves above andbelow.” Lazorthes confirms Hovelacque’s opinion con-cerning the lumbar region. Luschka, however, hasdescribed such anastomoses.

Figure 8.3

At lumbar level, the branches of the posteriorprimary rami of the spinal nerve follow the contours of thefacet joints and pass through a fibro-osseous tunnel (Brad-ley). Then they enter the intermamillary fascia and mamillo-styloid and transverse spinal muscle. 1, Interspinous muscle;2, intertransverse process muscle; 3, intermamilIary fasci-cles; 4, mamillary styloid fascicles; 5, interstyloid fascicles;6, spinal nerve root; 7, anterior primary ramus of the spinalnerve root; 8, posterior primary ramus of the spinal nerve root;9, external branches of the posterior primary ramus; 10, inter-nal branches of the posterior primary ramus and the osteofi-brous canal.

Figure 8.4

Cutaneous branches of the posterior primaryramus. Individual variations are frequent. The cutaneousbranches of C5 are not constant. This diagram is a summaryof clinical investigations performed by the author.

36

SECTION I ANATOMY

INNERVATION OF DISK

The disk is not innervated except at the superficiallayers of the posterior and posterolateral regions of theannulus. Hirsch et al. discovered some free nerve endingsof small-caliber myelinated fibers in the superficial layer ofthe annulus adjacent to the posterior longitudinal ligament.

Cloward noted that the superficial anterior layers arealso innervated, at least in the cervical region. This inner-vation depends on the sinovertebral nerve, but this isdebatable.

Rabischong and Serrano-Vella have noticed numerousnerve fibers in the anterior and posterior longitudinal lig-aments, in the region separating them from the annulus,and even 1 to 2 mm inside the annulus. They add that this

Figure 8.5

a.

Dermatomes according to Keegan and Garrett. This is the most frequently reproduced diagram of the der-matomes. We do not believe this diagram is consistent with clinical findings, particularly with regard to the dermatomes of theposterior half of the body, including the trunk.

b.

Dermatomes consistent with results of our research. This diagram representsgenerally accepted territories that involve the upper and lower limbs, including the anterior part of the trunk. It is consistentwith our findings, particularly with regard to the dermatomes of the posterior half of the limbs and trunk. (

Figure continues

.)

CHAPTER 8 INNERVATION OF VERTEBRAL STRUCTURES

37

innervation does not come exclusively from the sinover-tebral nerve, but also from some “nerve fibers that aremost likely unmyelinated.”

INNERVATION OF FACET JOINTS

The facet joints are innervated by the posterior primaryrami, with the exception of the occipito-atlanto-axial artic-ulations that are innervated by branches of the anteriorramus. The joints are supplied by a branch from thehomologous level as well as one from the subjacent level.Moreover, Paris et al. (1980), in their study of the lumbarspine, were able to show the existence of an ascending

branch arising from the medial division of the posteriorramus. This branch courses laterally through the spacebounded by the intertransverse ligament and ascends tothe facet joint above it. The facet capsules are richly inner-vated, as are the joint surfaces themselves. Hirsch et al.noted:

• Free endings of myelinated fibers of small diameter(3 µm)

• Nonencapsulated endings of medium diameter (5-12 µm) typical of Golgi tendon organs or Ruffini’scorpuscles

• Encapsulated endings typical of Golgi-Mazzoni andpacchionian corpuscles

The articular cartilage is not innervated.

Figure 8.5

(

continued

)

38

SECTION I ANATOMY

INNERVATION OF LIGAMENTS

The supraspinous and interspinous ligaments are inner-vated by the posterior primary ramus.

The anterior longitudinal ligament, the posterior longitu-dinal ligament, and the ligamentum flavum are innervatedby the sinovertebral nerve. Both free and encapsulatedendings can be found in these ligaments. The posteriorlongitudinal ligament is richly innervated. Hirsch et al.discovered some free nerve endings in the superficial andposterior layers of the ligamentum flavum. However, Jack-son et al. have found none.

INNERVATION OF VERTEBRAL PERIOSTEUM

The vertebral periosteum is innervated by the sinover-tebral nerve. Hirsch et al. discovered free nerve endingsas well as nonencapsulated endings of medium-diametermyelinated fibers.

INNERVATION OF SPINAL MUSCULATURE

The spinal muscles are innervated by motor branchesarising from the posterior primary rami. Electromyo-graphic studies performed by Gough et al. on subjectswith paraplegia or quadriplegia demonstrated that motorinnervation of muscles supplied by the posterior primaryrami originate below the level of the nerve of origin,sometimes as far away as six vertebral segments for nervesthat originate in the inferior cervical spine. This is muchlower, according to these authors, than is cutaneous inner-vation.

Walts, Koepe, and Sweet, in a similar study, demon-strated the existence of anastomoses among branches ofthe cervical posterior rami in monkeys.

MUSCLE AND TENDON RECEPTORS

According to Sherrington, 40% of the nerve fibersassigned to muscle are sensory. They are fibers that endon neuromuscular spindles, Golgi tendon organs, and freenerve endings.

Motor outputs originate in the medulla and descend viathe corticospinal tract, terminating on the anterior horncells. The axial musculature is controlled by the medialpart of the anterior horn, while the limbs are controlledby the lateral part.

Neuromuscular Spindles

Neuromuscular spindles (Fig. 8.7 and Fig. 8.8) are longformations distributed within the muscle according to thedegree of complexity of that muscle’s function. They mea-sure only a few millimeters (3 mm on average). A spindleis composed of two components in parallel alignment with

Figure 8.6

Spinal nerve in the intervertebral foramen: 1, spi-nal nerve root; 2, anterior primary ramus; 3, posterior primaryramus; 4, sinovertebral nerve formed by a single nerve rootcoming from the spinal nerve and a sympathetic root fromthe gray ramus communicantes (5); 6, artery.

Figure 8.7

Muscle of the neuromuscular muscle spindlecomplex: M, intrafusal fibers; E, midregion of the fiber bundle;

γ

, gamma fibers; la, sensory fibers carrying afferent inputfrom the terminations of the spiral center situated in the mus-cle bed; II, sensory fibers carrying afferent information fromthe terminal ends of the muscle spindle.

CHAPTER 8 INNERVATION OF VERTEBRAL STRUCTURES

39

the extrafusal muscle fibers. The two ends of the spindleare formed by very fine intrafusal muscle fibers that con-tain numerous motor endplates. The central part (equa-torial zone) has no muscle fibers and is purely sensory.

Efferent Fibers

The intrafusal fibers are innervated by small-diametergamma motor neurons originating from the gamma cellsof the anterior horn. The extrafusal fibers are innervatedby alpha motor neurons. Gamma motor neurons, althoughvery fine individually, constitute a relatively importantmass, since their volume represents approximately onethird of the total mass of the efferent nerves located in theanterior root.

Afferent Fibers

The afferent fibers innervate the equatorial region ofthe spindle. The annulospiral, or type IA fibers, surroundthe equatorial zone of the spindle in a

spiral fashion.

Theyare of large diameter and conduct rapidly. They are partic-ularly sensitive to the rate of change in length. A fewscattered type II fibers are also found in the primary end-ings. These fibers are of smaller diameter and are moresensitive to the absolute change in length. Any type ofstretching action, whether passive (caused by the muscleitself) or active (caused by contraction of the intrafusalfibers under gamma control), will cause these fibers toincrease their firing rate. The intrafusal fibers are main-tained under some degree of tension (gamma tone) in a

Figure 8.8

Spinal reflexes.

a.

General scheme.

b.

Detailedscheme;

α

, motor neuron to the muscle;

γ

, motor neuron tothe muscle spindle; R, inhibitory Renshaw cell; li, inhibitoryinterneurons; SNC, corticospinal tract; la, primary afferentfiber; ll, secondary afferent fiber; lb, afferents from the organof Golgi. The myotactic (monosynaptic) reflex circuit can bedescribed as

γ

Ia

α

. The inverse myotactic reflex (bisynaptic)can be described as lb Ii

α

. The Renshaw inhibitory circuitcan be described as R

α

. The cortical spinal modulation ofthe system is performed by two means: (a) directly, throughmodulation of the activities of the alpha motor neurons, and(b) indirectly through activities of the gamma motor neurons.

40

SECTION I ANATOMY

muscle at rest, thus allowing for the maintenance of restingmuscle tone. This gamma tone is capable of modifyingthe muscle’s reaction to stretching.

When a muscle is lengthened, the spindle is stimulated,resulting in reflex extrafusal contraction. Conversely, ifthe muscle is shortened, the activity of the spindledecreases. This characteristic of the muscle spindle causesthe muscle to resist changes in length. This role is essentialfor the maintenance of posture.

Gamma Loop

The gamma loop is the name given to a reflex circuit.It consists of the gamma motor neuron of the anteriorhorn, whose axon ends on intrafusal muscle fibers and inthe afferent IA and II fibers that leave the equatorial zoneof the spindle and enter the spine through the dorsal root.It is this circuit that produces the myotatic reflex, whichis most often monosynaptic.

Myotatic Reflex —

Liddell and Sherrington haveshown that passive stretching of a muscle provokes a reflexcontraction of this muscle that is often accompanied byrelaxation of the antagonist muscle (law of reciprocalinnervation). It is the myotatic reflex that occurs when aneuromuscular spindle is activated by muscle stretch. Thisreflex helps maintain a constant tone in the antigravitymuscles. Clinically, this reflex is applied when one tapsthe tenoperiosteal junction with a reflex hammer.

Inverse Myotatic Reflex —

This reflex causes relax-ation of the agonist that occurs suddenly in a muscleinitially subjected to a strong and prolonged stretch. Thisreflex is activated by the Golgi tendon organ.

Renshaw Loop

Renshaw demonstrated the existence of a small celllocated in the anterior horn of the spinal cord near theanterior horn cell. The alpha motor neuron, prior to exitingthe anterior horn, gives rise to a collateral branch with arecurrent course that terminates on the Renshaw cell.From there an interneuron arises, terminating on the motorneuron from which the original collateral branch origi-nated.

This Renshaw loop has an inhibitory effect, in contrastto the excitatory gamma loop. Its purpose is to facilitatefine movement control.

The gamma cell is under the control of the centralnervous system, which may exert an inhibitory or excita-tory action. The degree of sensitivity of the gamma systemcan be modulated by descending tracts from the centralnervous system that allow fine adjustments in the gammasensitivity to movement. Emotional states also have animportant influence on the gamma system and, in certaincases, can adversely affect muscle coordination, whichcan produce excessive strain on a joint that is under toomuch tension.

Golgi Tendon Organs

Golgi tendon organs are located within a tendon at themusculotendinous junction, as well as in the intramuscularaponeurotic wall. They are sensitive to tension placed onthe tendon, either through muscular contraction or passivestretching of the muscle. Because these receptors arealigned in series with the muscle, rather than in parallelas is the case with the neuromuscular spindle, these recep-tors are sensitive to stretching at the musculotendinousjunction rather than to stretching of the entire musculo-tendinous unit. These receptors have a quasi-permanentbaseline activity whose firing rate is increased with signifi-cant increases in muscle tension that stretch the musculo-tendinous junction. Thus, there is a threshold that must beexceeded by a sufficient increase in tension to increase thefiring rate proportional to the amount of tension produced.

Afferent impulses are transmitted via type IB sensoryfibers that enter the dorsal root and terminate on inhibitoryinterneurons (Renshaw cells). Their activity thus resultsin inhibition of the agonist muscle, resulting in a decreasein muscle tension if the firing threshold is exceeded. Theythus facilitate the action of the antagonist muscle.

Free Nerve Endings

Free nerve endings are found in muscles and tendonsin the vicinity of blood vessels. They relay nociceptiveimpulses that may be produced when the muscles or ten-dons are pinched.

ARTICULAR RECEPTORS

The articular and periarticular structures have receptorsthat relay messages to the central nervous system aboutposition, tension applied to them by the tendons, andmuscle length.

The facet joints are innervated by the posterior primaryramus. They receive the majority of their innervation froma branch of the posterior ramus from the homologousvertebral level, which courses close to the joint surface.However, each facet joint also receives input frombranches from the posterior ramus above as well as fromthe one below. Several types of different nerve endingshave been described.

Because of certain similarities, these nerve endingswere given the name of Ruffini or Pacchioni by analogy.This terminology is now avoided (Brodal), and a neutralterminology has been proposed (Freeman, Wyke). Theseauthors identify four categories, each having distinct char-acteristics but all having sensitivity to tension in common.

In articular and periarticular structures are located typeI, type II, type III, and type IV receptors. Types I, II, andIII are mechanoreceptors. Type IV receptors are noci-ceptors.

CHAPTER 8 INNERVATION OF VERTEBRAL STRUCTURES

41

Type I receptors

are found mainly in the joint capsulesand are analogous to the Ruffini corpuscles. They aresensitive to changes in joint position as well as to thevelocity of their movement. They have a baseline firingrate and are sensitive to stimuli that exceed this threshold.They are innervated by thin myelinated fibers of 5 to 8µm in length.

Type II receptors

are approximately twice as large asthe type I receptors. Their axons are composed of thickermyelinated fibers of approximately 8 to 12 µm. Thesereceptors resemble the pacchionian corpuscles and reactrapidly to changes in joint position. These receptors arelocated within the capsule.

Type III receptors

are the largest of this group. Theiraxons are composed of thick, myelinated fibers. They areextracapsular and are located within the ligaments resem-bling Golgi tendon organs. They react slowly and have ahigh excitation threshold. The function of these receptorshas not yet been well defined.

Type IV receptors

are composed of a plexus of fineunmyelinated nerve fibers located within the joint capsule,ligaments, and fat pads. They have never been found inthe synovial membrane (Wyke). These receptors are noci-ceptors. A stimulus of sufficient strength to activate thetype IV receptors results in contraction of the periarticularmuscles, resulting in immobilization of the joint.

43

9

AUTONOMIC NERVOUS SYSTEM

The autonomic nervous system regulates the functionsof the various organ systems. It not only involves visceralinnervation but also acts on vasomotoricity, glandularsecretion, smooth muscles, joint capsules, connective tis-sues, and the central nervous system (CNS) itself. Sym-pathetic efferent fibers have been found among numerousnociceptors and mechanoreceptors.

Although the autonomic nervous system is not undervoluntary control, it is integrated into the function of theCNS. That is, it is not a separate system, but rather asubsystem that can be thought of as having particularcharacteristics.

The autonomic nervous system is made up of CNSnuclei that extend down and into the spinal cord. Theoutflow information of this system is provided via hor-monal and neural outputs. The neural output or efferentactivity is conducted by two types of fibers in the auto-nomic system: the sympathetic and parasympathetic.Although there is no histologic difference between thesetwo fiber types, each is an anatomically discrete systemwith separate functions and neurotransmitters.

SYMPATHETIC SYSTEM

The sympathetic system (Fig. 9.1 and Fig. 9.2) is com-posed of two types of neurons:

• Preganglionic fibers situated in the lateral columnof the spinal cord (located between T1 and L2 only)

• Postganglionic fibers situated in the ganglionicchain

The axons of the sympathetic preganglionic fibers aremyelinated. They exit via the ventral root and then, as thewhite rami communicantes, enter the ganglionic sympa-thetic paravertebral chain.

The sympathetic paravertebral chain is segmented. Atcertain stages, the ganglia may fuse, however, and thus inthe cervical spine, we find three cervical ganglia knownas the superior, the medial, and the inferior ganglion.

(Occasionally, the medial ganglion is absent.) Otherwise,these are named the stellate ganglia, which are traversedby the vertebral artery. Approximately 12 thoracic ganglia,3 to 5 lumbar ganglia, and 3 to 5 sacral ganglia exist. Thus,there are approximately 22 ganglia for 30 spinal nerves.

Some fibers synapse in the paravertebral ganglion. Theunmyelinated postganglionic fibers reenter the spinalnerve (forming the gray rami communicantes) to form thesympathetic component of the peripheral nerves. The dis-tribution of these fibers does not strictly correspond totheir radicular level, since the lateral column does notextend throughout the entire spinal cord.

The superior preganglionic thoracic fibers ascend to thecervical ganglia. The lower thoracic and lumbar fibers can,in a similar fashion, descend to the lumbosacral ganglia.These fibers are destined to reach the muscles, organs, andcutaneous tissues; the efferent effect of the sympatheticsystems affects numerous receptors of various types,including nociceptors and mechanoreceptors. The organsare predominantly innervated by the sympathetic system(G. Lazorthes).

Figure 9.1

Organization of the sympathetic nervous system:1, spinal center (spinal cord gray matter); 2, sympathetictrunk ganglion; 3, preganglionic fibers; 4, postganglionicfibers; 5, spinal nerve.

44

SECTION I ANATOMY

Other fibers traverse the ganglia without synapsingthere, but rather in the perivisceral (prevertebral) ganglia.These form the prevertebral plexus, cardiac plexus, solarplexus, and hypogastric plexus. These plexuses are alsoinvolved in the innervation of glandular secretions andvarious other organ functions.

The existence of afferent sympathetic fibers is contro-versial. English and American authors do not believe thatthe few afferent fibers that accompany this system areactually part of the sympathetic system. French authors,however, accept their existence (Delmas, Lazorthes).

PARASYMPATHETIC SYSTEM

The parasympathetic system is also composed of twofiber types:

• Preganglionic fibers• Postganglionic fibers

Preganglionic fibers have myelinated axons that arisefrom cell bodies in the gray matter of the brainstem andthe middle three segments of the sacral cord. In the brain-stem, these fibers are incorporated as part of cranial nervesIII, VII, IX, and X.

The postganglionic fibers have unmyelinated axons andare found in association with ganglia, annexed to the cra-nial nerves (ophthalmic, sphenopalatine, optic, and sub-maxillary ganglia) and in prevertebral and perivisceralganglia for the pneumogastric and erectile nerves(Lazorthes).

In contrast to the sympathetic postganglionic fibers, thepostganglionic fibers are quite short. Similar to the sym-pathetic fibers, however, they probably have an afferentcomponent.

The sympathetic system functions through the use ofintermediary neurotransmitters:

• Acetylcholine is the neurotransmitter for both sym-pathetic and parasympathetic preganglionic fibers,as well as for parasympathetic postganglionic fibers.These fibers are referred to as cholinergic.

• Adrenalin (epinephrine) is the neurotransmitter forsympathetic postganglionic fibers (adrenergic), withthe exception of the sympathetic postganglionicfibers that innervate the sweat glands. These latterfibers exert their effect through acetylcholine(sympathetic cholinergic).

Most organs are under the dual influence of both sym-pathetic and parasympathetic systems. In most cases, thesetwo systems have antagonistic effects on their end organs,including increasing or decreasing the heart rate and dilat-ing or constricting the bronchial airways.

The autonomic nervous system (ANS) is under reflexcontrol at the level of the spinal cord (e.g., micturition).In addition, modulation occurs through relays in the brain-stem that are under supranuclear influence. The extent ofall the anastomoses between the CNS and the ANS is notfully known.

The sympathetic system is also involved in the modu-lation of pain pathways. This is frequently manifested inreferred pain phenomena, such as the arm referral thatoccurs with cardiac ischemia. This may occur as nociceptive

Figure 9.2

Generalized distribution of the sympa-thetic system (according to G. Lazorthes): 1, pregang-lionic fiber; 2, postganglionic fibers (2a, sympatheticcollateral to the spinal nerve; 2b, periarterial visceralplexus; 2c, periarterial somatic plexus) 3, perivisceralganglion; 4, artery; 5, visceral organ; 6, skin.

CHAPTER 9 AUTONOMIC NERVOUS SYSTEM

45

afferent input is relayed to the stellate ganglion via sym-pathetic afferents. From there, sympathetic afferents enterthe spinal cord to synapse on neuronal grey matter sup-plied by somatic afferent fibers from the upper limb. Asa result, the cortex interprets the origin of the pain to bein the arm. There is concordance between the spinal(radicular) level of the viscera and the dermatomal levelwhere pain is referred. Pain, however, can be referred ina more diffuse fashion, as is the case with referral to thejaw with cardiac ischemia. Bourreau noted that sometimesthe zone to which pain is referred is a function of apatient’s prior painful experiences. He also noted thatacute pain might be referred to a previously injured scarzone or chronic lesion.

The sympathetic system is also implicated in reflexsympathetic dystrophies (causalgia), as well as in any painsyndrome characterized by cutaneous hypersensitivity.These conditions cannot be explained simply on the basisof nociceptive relays (as in referred pain). Instead, thereseems to exist a dysregulation of the system — moreprecisely, a hyperactivity — that appears to be the sourceof the pain. Because of this, sympathetic neural blockadeis often beneficial in the treatment of certain pain syn-dromes.

It is important to keep in mind that the hypothalamusis under the control of higher cortical centers, and thusboth consciousness and autonomic functions are highlycoordinated (Gouaze).

II

BIOMECHANICS

49

10

SPINAL KINEMATICS

The vertebral column is a flexible structure that readilyadapts to a variety of different positions while still main-taining the ability to withstand compressive loads at eachsegmental level. The delicate precision by which it con-tinuously adapts to changes in posture ensures the protec-tion and mobility of the fragile neurovascular structurescontained within the bony framework.

With the exception of the first two cervical segments(that lack intervertebral disks), segmental motion is a func-tion of the disk. Posteriorly, the facet joints limit and directsegmental motion.

During flexion, the nucleus pulposus migrates posteri-orly, and the articular processes diverge slightly (Fig. 10.1).

During extension, the nucleus migrates anteriorly whilethe articular processes converge toward each other(Fig. 10.2).

Lateroflexion results in nuclear migration toward thecontralateral side, with ipsilateral convergence and con-tralateral divergence of the articular processes (Fig. 10.2).Rotation results in displacement of the ipsilateral trans-verse process posteriorly and the contralateral transverseprocess anteriorly (Fig. 10.3).

MOBILE SEGMENT

H. Junghanns, known for his work on the spine incollaboration with Schmorl, considered all the elementsthat adjoin or separate two adjacent vertebrae as a func-tional unit. He coined the term “mobile segment” referringto the intervertebral disk, facet joints, and adjoining liga-mentous system that form the unit (Fig. 10.4 to Fig. 10.6).

The vertebral column consists of 23 mobile segments,with each one representing a unit of spinal mobility. Thereis a very close relationship among the elements of the mobilesegment and the intervertebral foramina (Fig. 10.7).

The mobile segment, or intervertebral joint, is an inte-grated unit. Any mechanical perturbation affecting anyone of its elements affects the others; just as any move-ment of a large segment of the column, even if only to

maintain balance, affects all the other segments. The spinalcurves are also interdependent: a lumbar lordosis resultsin a thoracic kyphosis and a cervical lordosis.

Automaticity of Spinal Function

The concept of the mobile segment as a mechanicalunit of the spinal column helps to explain the mechanicalrelationships among the different elements of the spineduring movement and the consequences of lesions to theseelements.

This concept is not enough, however, to explain theautomatic functions of the vertebral column. Propriocep-tive input, indispensable to maintenance of posture andmotion, is received from all elements of the motion seg-ment, including the facet joints, muscles, and tendons.

Through the action of proprioceptors, any change in posi-tion, whatever its origin, alters the distribution of force onthe elements of the motion segment, resulting in a redistri-bution of muscular contraction. In addition, the mobile seg-ment also receives input from Golgi tendon organs (type IBafferents) and muscle spindles (types IA and II afferents).All of these inputs are ultimately under kinesthetic monitor-ing performed at the cortical level. Thus, the complexity ofthe auto-regulation of the mobile segment results from theconstant interplay of afferent and efferent activity associatedwith vertebral segment activity (most often) and is reflectedin its highly precise control over a wide range of conditions.

Therefore, it would be an oversimplification to considervertebral lesions only in regard to mechanical implica-tions, especially since the spine is subject to neural regu-lation, allowing it to function with a high degree of auto-maticity. Any richly innervated element, if affected, willproduce a “wrong note” in the harmonious function of thespine by stimulating protective muscle guarding (spasm)as a local protective measure. The role of spasm is essen-tial, therefore, to the concept of “painful minorintervertebral dysfunction.” Since muscles are not uniseg-mental in innervation, however, a mechanical displace-ment that affects only one vertebral segment (most often)

50

SECTION II BIOMECHANICS

may result in a multisegmental biomechanical structure ofextraordinary complexity, and segmental motion is farfrom simple.

REGIONAL SPINAL MOTION

At each spinal region, global movement is a productof motion at each of its mobile segments. At each spinalsegment, the segmental physiodynamics change, resulting

in marked regional differences. For example, the kine-matics of cervical segments differ significantly from thoseof lumbar segments. The disk to vertebral body heightratio, the vertebra’s width to height ratio, and the orientationof the articular processes determine the motion available toeach spinal segment and, to a large extent, the mechanicaldisplacements that can occur. The functional features of themobile segments also help to determine and explain whichtypes of therapeutic modalities are efficacious. We shall

Figure 10.1

Spinal segmental motion:

N, neutral position; F, flexion; E, extension.

Figure 10.2

Spinal segmental motion:

a.

Lateroflexion to the right, posterior view.

b.

Lateroflexion seen in section through thenucleus pulposus.

CHAPTER 10 SPINAL KINEMATICS

51

study spinal motion, which varies with age, at the cervical,thoracic, and lumbar levels.

Cervical Motion

The cervical spine is extremely mobile, and yet remark-ably resistant to loading. It supports the head, whichweighs 4 to 5 kg, in a variety of different positions and isable to withstand great stress.

Cervical segments are the most mobile of all the spinalmotion segments. This is due to the:

• Disk to vertebral body height ratio (1:3 for the cer-vical spine, 1:6 for the thoracic spine, and 1:3 forthe lumbar spine)

• Relatively small anteroposterior and transverse diam-eters in relation to the body height

• Presence of the uncinate processes• Anatomy of the first two cervical segments, the atlas

and the axis, which form the cervico-occipital junc-tion

The cervical spine can be divided into two functionalunits (Fig. 10.8):

• Superior cervical spine, formed by the first two ver-tebrae

• Inferior cervical spine, formed by the remaining five

These two units complement each other functionallyand allow precisely coordinated movement in every plane.The inferior cervical spine is capable of two degrees offreedom: flexion/extension and coupled side bending with

Figure 10.3

Segmental rotation.

Figure 10.4

Mobile segment of Junghanns, lateral view.

Figure 10.5

Mobile segment of Junghanns, anterior view.

Figure 10.6

Elements of the mobile segment: 1, vertebralbody; 2, cartilaginous endplates; 3, annulus fibrosus of thedisk; 4, Sharpey’s fibers; 5, nucleus pulposus; 6, facet joints.

Figure 10.7

Intervertebral foramen.

52

SECTION II BIOMECHANICS

rotation. The superior cervical spine, on the other hand,has three degrees of freedom, allowing precise adjust-ments in positioning the head in space.

Superior Cervical Segments

The superior cervical spine is composed of the atlanto-axial articulation and the atlanto-occipital articulation.The movements at these two joints can be analyzed sep-arately. In reality, however, these two articulations form afunctional unit that must be considered as a whole.

Atlanto-Occipital Articulation

Flexion/extension

is the primary articular motion. Itrepresents the “yes” movement that is accomplished byanteroposterior translation of the occipital condyles on thefacets of the atlas for flexion, and posteroanterior forextension. The amplitude of this movement varies withthe individual. Figures given for normal range of motionat this articulation vary according to the method of exam-ination and the population examined; an average of 30 to60° for the complete range of motion has been established;Fielding assigns 25° for extension and 10° for flexion(Fig. 10.9).

Lateroflexion

is possible in the range of 5 to 8°.

Rotation

is not possible at this articulation.

Atlanto-axial articulation

, which is the most mobilesegment of the spine, allows mostly rotational movement,although small degrees of flexion/extension and latero-flexion are possible.

Flexion/extension

is possible because of the relativelaxity of the transverse alar ligament in the atlanto-odontoid articulations as well as a certain degree of trans-lation in the atlanto-axial articulation. This movement is inthe range of 2° in extension and 9° in flexion (Kottke andMundale) to 10° in extension and 5° in flexion (Fielding).

Lateral inclination

is in the range of 5°.

Rotation

is the “no” movement. This movement, whichis not a pure rotation, is important, since it represents arange of motion of 30 to 35° in each direction (approxi-mately half of available cervical rotation). Rotation aboutthe longitudinal axis results in translation of the two lateralmasses of the atlas in an anteroposterior plane, but inopposite directions on the lower adjacent facets. Rotationof the head results in anteroposterior translation of theipsilateral lateral mass and posteroanterior translation forthe contralateral lateral mass. The marked convexity of

Figure 10.8

Cervical spine.

Physiologically, one should dis-tinguish between the upper cervical spine and the rest of thecervical spine (see text).

Figure 10.9

Movement of atlanto-occipital articulation: N, neutral position; F, flexion; E, extension.

CHAPTER 10 SPINAL KINEMATICS

53

the facets in the anteroposterior direction makes thismotion like that of a screw, with the atlas descending 2 to3 mm during rotation. This simultaneous axial depressionthat occurs with rotation compensates for the twistingaction on the spinal nerve roots and the vertebral artery(G. and C. Oliver).

Inferior Cervical Segments

The inferior cervical spine is composed of the inferiorfive cervical vertebrae. Notwithstanding some slight vari-ations from one vertebra to another, the movements arethe same at each segmental level. The inferior cervicalspine functions as a distinct biomechanical unit.

Possible movements are flexion/extension, lateral flexion,and rotation. Physiologically, the latter two are coupledand therefore inseparable.

Flexion/Extension.

During flexion/extension (Fig. 10.10),there is a true migratory movement on the ball bearingformed by the nucleus pulposus on the subjacent vertebra(Fig. 10.11). During flexion, the nucleus is compressedtoward the rear of the disk, placing pressure on the pos-terior annular fibers and gapping the articular processesof the facet joints; the superior articular process glidesanteriorly on the inferior process.

The absence of nuclear migration and a marked anteriorpinching during flexion are the first signs of disk degen-eration; this has been documented on 50 slow-motioncineradiographic examinations (Fig. 10.12 and Fig. 10.13).Flexion is limited by ligamentous tension in the posteriorlongitudinal ligament, the ligamentum flavum, the inter-

spinous and supraspinous ligaments, and the facet jointcapsule. For this reason, anterior subluxations can occurin sudden flexion injuries such as “whiplash,” in whichthe constraints of these ligamentous structures are over-come. An example of this occurs with “jumped” cervicalfacets where the inferior articular process slips out fromunderneath the superior process. This condition is oftenassociated with spinal cord injury, and the reduction ofthe facet dislocation is very difficult. This is the onlyexample of a dislocation without fracture at this level ofthe spine.

In extension, the nucleus is compressed toward thefront, while the articular processes converge on each other;nuclear migration, however, prevents the articular pro-cesses from closing completely, and there is a slight gapanteriorly that remains at end range. Extension is limited

Figure 10.10

Movement at mid or lower cervical spine level: N, neutral position; F, flexion; E, extension.

Figure 10.11

Flexion produces a “translation” of the loweradjacent vertebra, as though it were sliding on ball-bearingdisks.

54

SECTION II BIOMECHANICS

by abutment of the neural arches, by contact madebetween the superior articular process of the subjacentvertebra and the transverse process of the upper adjacentvertebra, as well as by tension in the anterior longitudinalligament. Several authors have studied extension. Raoustudied movement in cadavers, while de Séze, Djian, andAbdelmoula studied radiographs of live subjects. Theirresults are presented in Table 10.1. Kottke and Mundale’sresults, obtained from subjects 15 to 30 years of age, areshown in Table 10.2. By analyzing lateral flexion/extensionviews, Kapandji determined a total amplitude of 100 to110° for flexion/extension of the inferior cervical spine.

Rotation and Lateral Flexion.

These

are large-amplitude movements in the inferior cervical spine. Fickand Lovett demonstrated these two movements to be cou-pled at this level; during rotation, the vertebra undergoessimultaneous ipsilateral side flexion (Fig. 10.14).

The amplitude of these movements is difficult to eval-uate. Kapandji estimated lateral flexion to be 37° androtation to be 66 to 76° in the inferior cervical spine.

Global Cervical Motion

Global cervical motion is a synthesis of the motions ofthe two functional units: the inferior and superior cervicalspine. The base is formed by the inferior unit, while thesuperior segments adapt to perform precise movements.

Thus, in complete right lateral flexion or right rotationof the cervical spine, the movement of the inferior cervicalsegments is similar; it is the superior cervical spine thatdetermines the final outcome of this triplanar motion bypositioning the head in the desired position. In lateralflexion, the superior cervical segments rotate contralateralto the inferior segments to maintain the face in the frontalplane, while in rotation, the superior segments are ipsilateral

Figure 10.12

Normal cervical spine in flexion. Note thateach vertebra slides on top of the subjacent vertebra in agliding movement.

Figure 10.13

In this example, the C5–C6 disk has degener-ated and translation of C5 is not possible. In flexion, therefore,an anterior impingement is produced between C5 and C6.

Table 10.1

Flexion Extension Total

C2–C3C3–C4C4–C5C5–C6C6–C7

Total

5°5.5°7°9°6.5°

33°

8°10°12°18.5°11°

59.5°

13°15.5°19°27.5°17.5°

92.5°

Table 10.2

Flexion Extension Total

C2–C3C3–C4C4–C5C5–C6C6–C7

Total

8°7°

10°10°15°

50°

3°9°8°

11°5°

36°

11°16°18°21°18°

84°

CHAPTER 10 SPINAL KINEMATICS

55

to the inferior segments. Numerous combinations are thuspossible. The small, phasic muscles that govern superiorcervical segmental motion are:

• Rectus capitis major• Rectus capitis minor• Obliquus capitis superior• Obliquus capitis inferior

Range of Motion.

The variability of the values assignedby different authors to motion that

a priori

seems rela-tively simple is noteworthy. The results are dependent onthe author and on the method employed: whether studyinglive or cadaveric subjects, and whether performing radio-graphic studies or goniometric measurements.

Total cervical flexion/extension

—

Using goniometryon young students, Buck et al. obtained the followingaverage results:

Complete cervical lateral rotation

—

Raou measuredthe maximum range of motion on cadavers and obtained30 to 50° for the entire cervical spine bilaterally. Kottkeassigned 45 ± 10°.

Complete cervical rotation

—

Buck et al. assigned146° for young men and 147° for young women. Kottkenoted 75 ± 10° for rotation to either side.

Thoracic Motion

In the thoracic spine, the disk to vertebral body heightratio does not allow much mobility. On the other hand,the orientation of the facet joints would otherwise allowrotation and lateroflexion were it not for the ribs restrictingtheir mobility (Fig. 10.15).

The plane of the facets faces posteriorly and slightlysuperolaterally. Moreover, the articulations form concentric

circles with the center of the corresponding vertebral body(Fig. 10.16). The movement of rotation of the upper thoracicspine would theoretically be great were it not for the rib

Figure 10.14

Intervertebral movement is complex. The motions of lateral flexion and rotation are coupled. Thus, a right lateralflexion of vertebra A on B is accompanied by a posterior right rotation on B.

a.

Posterior view.

b.

Anterior view.

FunctionYoung Men

Young Women

Total Flexion 66° 69°

Total Extension 73° 81°

Figure 10.15

Thoracic rotation.

Figure 10.16

Rotation is facilitated by the fact that the facetjoints and the axis of the thoracic vertebral body show acommon point from which one can inscribe concentric circles.

56

SECTION II BIOMECHANICS

cage. At this level also, rotation is coupled with lateralflexion and is similarly restricted. In the lower thoracicspine, these movements can be produced with greater ease,as there are only a few false ribs to restrict movement.

When the thorax is flexible, as in young people, tho-racic rotation is easy. It becomes more difficult with age,when the thorax becomes a semirigid cylinder.

Flexion is limited by the tension in the interspinous lig-aments, the ligamentum flavum, the posterior longitudinalligament, and the facet joint capsule. Thoracic extension islimited by the abutment of the articular and spinal processes.

Range of Movement

Rotation

—

In cadaveric studies, Raou found a rangeof 35° available bilaterally for each thoracic vertebra, withthe T8–T9 zone being (without ribs) the most mobile.Kapandji, citing the works of Gregersen and Lucas, mea-sured 35° bilaterally at each thoracic level.

Lateroflexion

—

This movement was measured up to3 to 5° for each vertebra. When it is slight, it produces anipsilateral rotation (Rouviere, Lovett). Gonon et al. have

shown the range to be greater at the inferior thoracicvertebrae: 6° for T10–T11, 10° for T11–T12, and 8° forT12-L1. Kapandji cites 20° of total thoracic lateroflexionbilaterally.

Flexion/extension

—

There are about 5° for flexionand 5° for extension at each level (Raou). Kapandji assigns45° totally for flexion and 25° for extension, but he empha-sizes the great variability with age and the individual.Gonon et al. note 6° for T10–T11, 9° for T11–T12, and10° for T12–L1.

Lumbar Motion

Flexion/extension is the cardinal movement of the lum-bar spine. All elements of the vertebrae at this level con-tribute to this type of movement (Fig. 10.17): the disk tovertebral body height (one-third) and the orientation ofthe articular facet joints. The alignment of the articularprocesses limits rotation at L1 and L2, and it is only theelasticity of the disks and the ligaments that permits rota-tion below L1 and L2 (Fig. 10.18 and Fig. 10.19).

Figure 10.17

Lumbar vertebrae:

a.

Flexion.

b.

Extension.

Figure 10.18

Orientation of the facet joint blocks lumbar rotation.

CHAPTER 10 SPINAL KINEMATICS

57

On the other hand, lateral flexion is facilitated by con-tralateral divergence and by ipsilateral convergence of thearticular processes.

Flexion/extension

—

Extension is limited by thespinous processes that are large at this level, while flexionis limited by the tension in the interspinous and supra-spinous ligaments, the posterior longitudinal ligament,and the ligamentum flavum.

Raou, in cadaveric studies, found 20 to 36° of totalflexion and 16 to 21° of total extension. In radiographicstudy, Kapandji measured 60° for total flexion and 35° fortotal extension. Chopin determined an average range ofextension to be 70 to 80°, while flexion was found to be40° with respect to neutral.

Farfan cited flexion/extension as representing 80 to 90°for the entire vertebral column. Allbrook found an average

of 62° in young men and a much greater mobility in youngwomen.

Farfan also found 7.5

°

(flexion plus extension) forL1–L2 and L2–L3, 18° for L3–L4, 22° for L4–L5 (thesefigures represent half for extension and half for flexion),and 18° for L5–S1 (6° for extension and 12° for flexion).

Gonon et al. noted the following for each segment:

L5–S 120°L4–L5 15° L3–L4 12° L2–L3 12°L1–L2 10° T12–L1 10°

Lateroflexion

—

According to Raou, lateral flexionwas found to be in the range of 20 to 30°. Kapandji foundit was 10° for each side. According to Chopin, it was inthe 20 to 30° range. The iliolumbar ligament limits move-ment at the level of L5–S1.

Rotation

—

Rotation is very limited at this level and,in general, is considered to be 1° per level, except forsome authors who believe it to be in the range of 5 to 6°at L5–S1. This rotation is not pure, and there is an asso-ciated coupling with ipsilateral lateroflexion. In cadavericstudies, Raou noted 7 to 14° on each side. With freshcadavers, we observed that this rotation increased whenthe spine was slightly flexed and became virtually impos-sible with the spine in hyperextension. Gonon et al. citedthe following for each segment:

L5–S 14

°

L4–L5 7

°

L3–L4 10

°

L2–L3 8

°

Ll–L2 6° T12–L1 18°

Figure 10.19

A slight amount of rotation is possible at thelumbar level and is primarily performed by a lateral translationof the body of the vertebrae aided by the elasticity of theintervertebral disk.

59

11

BIOMECHANICS OF SACROILIAC JOINT

Since Hippocrates, who was the first to note it, it hasbeen universally accepted that the sacroiliac joint plays animportant role in childbirth. In contradistinction to priorauthors (Vésale included), Ambroise Paré confirmed thata certain mobility also existed outside the state of preg-nancy and also in men. The works of Delmas and Weisluncovered facts that led to an understanding of the anat-omy and physiology of this articulation that differedgreatly from the classic concept of Farabeuf.

TYPES OF ARTICULATIONS

Delmas studied the anatomy of the sacroiliac joint inbipedal primates (gorilla, chimpanzee, orangutan, and gib-bon, proceeding from the lesser to the more highly evolvedspecies). Indeed, the gorilla is quadrupedal, the orangutanis exceptionally bipedal, and the gibbon is bipedal on theground. The changes that occurred in the articular surfaceswere significant and directly paralleled the stages of evo-lution leading to the erect position and walking. In thegorilla, the articular surfaces are interlocked, in the gibbonthey are flattened (planes), and in the human they areconcave on the sacral side.

In humans, the final stage of the evolution, Delmasfinds three types of articulations he refers to as dynamic,static, and intermediary.

•

Dynamic type

. The dynamic articulation occurs in25% of humans. It is freely mobile, highly evolved,and

“

overadapted,

”

corresponding to optimal adap-tation for bipedal locomotion. The sacral auricle isconcave, and the areas of ligamentous attachmentare taut. These subjects have accentuation of theirspinal curvatures (Fig. 11.1).

•

Static type

. The static articulation occurs in 25% ofhumans. In this type of articulation, the articularsurfaces are flat and the areas of ligamentous attach-ments are more lax. These subjects have moderate

spinal curvatures and resemble the primates moreclosely (Fig. 11.2).

•

Intermediary type

. The intermediary is the mostwidespread type and occurs in 50% of humans. Thesacroiliac articulations are firmly maintained byvery strong ligaments. Weisl describes the ligamen-tous system in a very original and schematic manner.He divides the fibers of the posterior ligaments intotwo groups: caudal with cranial direction and cranialwith lateral direction, which is distended in the nuta-tion movement, i.e., the act of nodding, especiallyinvoluntary nodding. These two ligamentous sys-tems balance the weight of the trunk.

JOINT MOTION

Nutation results in rotation of the sacrum on an imag-inary “axis of nutation” formed by the iliac bones. Move-ments about this axis are classically described as follows:forward inclination of the anterior surface of the sacrumis termed nutation, while backward inclination is calledcounternutation (Fig. 11.3 and Fig. 11.4).

Interpretations of Axis of Movement

Numerous studies and discussions, especially amongobstetricians, have focused on determining the exact loca-tion of the axis. Bonnaire defended the theory of an axispassing through a point of the articular surface (auricularaxis) (Fig. 11.5 and Fig. 11.7). Others, especially Fara-beuf, maintained that the axis passes to the rear of theauricle through the axial ligament (retroauricular axis)(Fig. 11.5 and Fig. 11.8). This concept was highly criti-cized, and modifications of it were offered, especially byDelmas and Weisl.

Weisl’s Concept

Weisl, after conducting extensive radiographic studies,formulated a new concept:

60

SECTION II BIOMECHANICS

• There is no rotational movement at the sacroiliacarticulations (Fig. 11.4 and Fig. 11.10, Fig. 11.5 andFig. 11.9).

• Movements of the sacroiliac articulation are posterior-anterior movements, but the rostral segment of thearticular surface is submitted to a more severe dis-placement than is the caudal segment (Fig. 11.9).

• This displacement, which is almost a transference,is around a virtual axis located about 5 to 10 cmbelow the promontory (preauricular axis). The seatof that axis varies from one individual to anotherand in the same individual by the movement per-formed (the displacement of that axis could then

Figure 11.1

Dynamic spine of Delmas in a subject with pro-nounced vertebral curves. The sacral auricle is indented.

Figure 11.2

Static type of curvature of Delmas in which thereis a reduction in the vertebral curvature. The auricle is flat.

Figure 11.3

Nutation. The base of the sacrum is antetilted,and the coccyx moves posteriorly.

Figure 11.4

Conternutation. The base of the sacrum is ret-rotilted, and the coccyx is displaced anteriorly.

CHAPTER 11 BIOMECHANICS OF SACROILIAC JOINT

61

exceed 5 cm). In 12 to 14% of subjects, this is asimple movement of transference from front toback; therefore, there is no axis of nutation in theseindividuals.

Wilder et al. have studied sacroiliac joint motion andhave made the following remarks:

• Given the prominence of the articular surfaces (inthe sagittal and frontal planes), rotation could notbe accomplished about the proposed axes.

• If rotation occurred according to the described axes,a notable separation of the auricular surfaces wouldbe necessary, but this is impossible because of theligamentous restraint.

• A certain transference can be performed, providedthere exists a sufficient amount of spacing for thearticular surfaces. This spacing is necessary becausethe surfaces are not planes. The most favorable axisfor this translation is called by the authors the

“

rough axis.

”

Figure 11.5

Different axes of movement of the sacroiliacarticulations according to Bonnaire (1), Farabeuf (2), Weisl(3), J. B. Mennell and, later, Bakland and Hansen (4).

Figure 11.6

According to Bakland and Hansen, there existsan axial articulation.

Figure 11.7

Movement according to Bonnaire.

Figure 11.8

Movement according to Farabeuf.

Figure 11.9

First type of movement according to Weisl (86to 88% of individuals).

62

SECTION II BIOMECHANICS

Axial Sacroiliac Articulation

Accessory sacroiliac articulations have been describedthat are inconstant and located in the rear of the principalarticulation (Fig. 11.6). Hadley describes a superficialarticulation at the level of the second sacral foramen aswell as a deep one at the level of the first sacral foramen.What is curious is that the incidence of these articulationsincreases with age, which may be explained by themechanical work of these formations.

Bakland and Hansen, restudying sacroiliac articula-tions, described an axial sacroiliac articulation located 15mm in the rear of the sacroiliac articulation (very muchat the level of the deep accessory articulation of Hadley).It is, according to these authors, constant in the adult. Itis formed by an iliac protuberance and a sacral cavityopposing each other very narrowly. These surfaces areslightly incongruous, but this incongruity is decreased bythe juxtaposition of a loose conjunctive tissue rich in adi-pocytes. The iliac protuberance is often lined with articularcartilage. These authors think that the axis of rotation ofthe sacroiliac articulation goes through this axial sacroiliacarticulation. It is noteworthy that this corresponds to theopinion of J. B. Mennell, who described an axis of rotationgoing through an “iliac protuberance and a deep sacraldepression,” which corresponds perfectly with the axialarticulation as described by Bakland and Hansen.

Motion Evaluation

A certain degree of sacroiliac joint motion is available.Proof of this is the existence of a layer of articular cartilagecovering the articular surfaces; but its appearance, grayishred with shaggy extensions, shows that it is very mobile(Olivier).

Pregnancy accentuates the normal mobility of thisarticulation but does not create any particular movementat that level (Sureau).

Displacements of Sacrum According to Positions

These displacements have been studied, especially byobstetricians. They are caused by movements of the trunkand lower limbs. Crouzat in 1881 and Walcher in 1889tried to use this concept to widen the superior apertureduring delivery (Sureau). Weisl showed these relationsradiographically:

• The promontory is displaced posteriorly duringtrunk or hip extension. Forward displacement occurswith flexion.

• Moving from supine to standing, which correspondsto the maximum range of motion of the sacroiliacarticulation, results in an anterior displacement ofthe promontory in 90% of the cases.

In standing, the sacrum is close to the anterior limit ofits course. In the supine position, it is close to the posteriorlimit of its course.

Sureau remarked that in a subject in the upright positionwhere the sacrum is already in maximum anterior tilt,trunk or hip flexion cannot add to the existing nutation.Trunk extension in standing more or less displaces thepromontory posteriorly. In the supine position, however,flexion of the thighs can displace the promontory anteri-orly, but further extension does not lead to furtherdisplacement of the promontory posteriorly.

According to Testut, displacing the base of the sacrumby 2 mm results in a movement of 5 to 6 mm at the topof the coccyx. This motion is, of course, accentuated dur-ing delivery.

Nutation is maximal when one is standing and carryinga heavy load on the shoulders. The movement of counter-nutation is maximal in acrobats doing the “bridge.”

Asymmetry of Movement

Stracha et al. (cited by Piédallu) investigated the pelvisand vertebral column in a cadaveric study. They immobi-lized one of the iliac bones in a vise, leaving the pubicsymphysis free to move. The displacements were recordedby the movements of rods and sliders fixed to the sacrumand to the free iliac bone. The lumbar spine was thenflexed, extended, rotated, laterally flexed, distracted, andcompressed axially. The authors concluded that the move-ments of the sacroiliac articulation are complex, combin-ing translation with rotation. This is similar to Weisl’sconcept and shows the asymmetry of function of the twosacroiliac articulations. In 1949, Ingelrans and Oberthurnoted that outside of pregnancy the movements werereduced, but they drew attention to the movements oftorsion and lateroflexion that occur simultaneously and inopposite directions in each sacroiliac joint: “during ambu-lation, i.e., during the stance phase, the ipsilateral iliacwing tilts posteriorly, while the sacrum antetilts slightly.”

Figure 11.10

Second type of movement according to Weisl(12 to 14% of individuals). It represents a translation.

CHAPTER 11 BIOMECHANICS OF SACROILIAC JOINT

63

This is what is described as the position of “anteriorsacrum” by osteopaths. In France, it is referred to as theposition of the forward step (Piédallu).

Studies of Living Anatomical Relationships

Colachis et al. studied the problem of sacroiliac mobil-ity

in vivo

. To study the live anatomic relationships, theydrove Kirschner’s wires into the posterior superior iliacspines of 12 medical student volunteers. Two pins wereplaced in one side of the spine and one in the other side.This was done to avoid any error that could occur if therewas only one pin on each side; i.e., rotation of the sacro-iliac joint could occur without any modification of thedistance between the two pins, while with two pins on oneside, there was a fixed plane of reference.

The authors avoided subjects who were obese, and theyinserted the pins at the most superficial part of the bone,so that the traction of the soft tissues on the pin duringmovements would not be a source of error. Movementsexecuted by the volunteers included sitting, standing, for-ward trunk flexion, and maximal flexion of a thigh on thetrunk with the contralateral thigh in maximal extension.The authors came to the following conclusions:

• Sacroiliac joint motion did in fact occur in the exam-ined subjects (young men).

• This motion was very small and varied very muchfrom subject to subject.

• The greatest motion was seen during anterior trunkflexion, when a 5-mm separation of the iliac spineswas noted in the most marked case.

This study was not an attempt to measure the articula-tion between the iliac and sacrum but was an attempt tomeasure the relative movements between the two iliacbones.

Using the photogrammetric technique of Suh, Lavi-gnolle et al. (1983) studied the displacement of the iliacbones on the body in relation to the sacrum and the ampli-tudes of these displacements in precise movements. There

were only five cases in this study, but the findings areinteresting:

• The position of the axes was variable from subjectto subject; nevertheless, the axes were in a ratherconsistent position in front of and below the sacro-iliac articulations.

• The types of displacements of the iliac bones wereidentical in all subjects, uniting rotation and trans-lation on these axes with a phenomenon of anterior“unlocking” of the articulations.

• Joint range of motion was reduced and variable,depending on the individual, but was on average 10to 12° of rotation and at 6 mm of translation (sub-jects were young, below 25 years of age).

The range of motion was greater here than in the move-ments measured by Egund et al. (1977), who used a ste-reophotogrammetric method and noted a range of motionof about 2°.

CONCLUSION

Wilder considered the functional role of the sacroiliacjoint to remain an enigma. Given the results of most stud-ies, however, he believed it would be safe to say that thejoint plays a role as a shock absorber, absorbing the energyimparted by its powerful ligamentous system.

We are in agreement with this broad conclusion. Thesearticulations have a very variable morphology, dependingon the individual. But it is evident that regardless of theirdifferences of mobility, they all still have, with more orless efficiency, the same functions:

• In women, the sacroiliac joint plays a role in laborand delivery.

• In all individuals, this articulation is like a shockabsorber, absorbing the enormous pressures trans-mitted by the spine through ligamentous tension andjoint microdisplacements.

65

12

FORCES ACTING ON VERTEBRAL COLUMN

THE DISK: SHOCK ABSORBER AND PRESSURE DIFFUSER

The disk absorbs shock and diffuses pressure on thespine. The farther down the spinal column toward thelumbar region one goes, the more the pressure loading ofthe column increases.

The superior cervical spine is nevertheless capable ofsupporting the head and performing precise movementswithout the aid of intervertebral disks. Thus, in spite ofits apparent fragility and thin articular surface, it is sub-jected to considerable loads.

In the normal vertebral spine, the healthy disk is per-fectly homogeneous and very hydrophilic. When it isloaded axially, its height decreases (Fig. 12.1) and theannulus bulges at the periphery like a tire under an exces-sive load. The decrease in the height of the disk space canbe 1.5 mm for the lumbar disk of an individual carrying100 kg on the shoulders. In fact, one must first add to this100-kg weight, the weight of the trunk, and of the head,which is about 40 kg for a man weighing 80 kg, and thenthe intrinsic compressive force produced by muscular con-traction that increases compression on the disk. Thismeans that the disk will have to support a load of morethan 150 kg when the individual is upright and the diskis in normal position. If the individual bends forward, thepressure on the nucleus pulposus will be transmitted mostforcefully to the posterior annular fibers — the weakestof the fibers that make up the annulus fibrosus.

PRESSURE

Some authors have calculated the approximate com-pressive and distractive forces on the mobile segment indifferent anatomic positions, both with and without extrin-sic loads. Here are a few examples taken from the studiesof Herbert:

•

Subject standing, without overload:

the lumbar diskis submitted to a pressure of 15 kg/cm

2

in thenucleus, taken in tension by the annulus, and to astrain of shearing of 13 kg in the corresponding facetjoints.

•

Subject in forward flexion:

the disk is submitted toa pressure of 58 kg/cm

2

in the nucleus, taken intension by the annulus, and to a shearing of 47 kgin a plane perpendicular to the axis of the column,absorbed in compression of the facet joints.

•

Subject in full flexion, lifting up a bar of 100 kg:

thedisk is submitted to a compression of 144 kg/cm

2

in the nucleus, taken in tension by the annulus, andto a shearing of 126 kg supported by the facet joints,absorbed in compression.

In this case, theoretically, there is a total pressure of1000 kg on the nucleus. This demonstrates the enormouspressures exerted on the intervertebral segments.

By measuring intradiscal pressure, Nachemson intro-duced some new notions: (a) load on the nucleus is greaterwhen sitting than when standing (measured on the L3disk); (b) pressure is maximal during sitting, with thesubject bent forward and lifting a load, arms hanging; (c)the lowest pressure is measured with the subject supine;and (d) intradiscal pressure increases 45% with coughingand 45% with trunk rotation. For a 70-kg man in theupright position (Fig. 12.2), for example, the pressure onthe L3 disk is 70 kg. It is about 120 kg if he bends forward20°, and it is 340 kg if he lifts a load of 20 kg with hislegs extended.

In a preliminary study, Drevet, using a material capableof taking both static and dynamic measures (a miniatur-ized piezo-resistive capacitor), noted:

• Important variations in the basal pressures in sub-jects of the same age and of identical morphotype

• Extremely rapid variations according to exogenousfactors (suspension, carrying loads, etc.)

• Piezo-resistive measurements ranging from 1 to 3,depending on contraction of the muscles

66

SECTION II BIOMECHANICS

The lumbar spine is not alone in being subjected tosuch stresses. There is, for example, the cervico-occipitaljunction, with its narrow bony structures and slender artic-ular surfaces that support and allow for the mobility ofthe head — a large 5-kg ball that rests in equilibrium ontwo small facets the size of nails and can be mobilized inall directions. Some persons carry on their heads loads ofover 50 kg that are transmitted in their entirety to thearticulations of the first two vertebrae, since at that levelthere is no disk to dissipate compressive loads (Fig. 12.3).

ROLE OF ABDOMINAL WALL

Intra-abdominal pressure generated by the contractionof the abdominal musculature has to be taken into account(Bartelink) when evaluating the effective load that thelumbar spine must support. Any lumbar effort in effect“leans” on contracted abdominal muscles. The intra-abdominal pressure absorbs part of the load: 30%, accord-ing to Morris et al. The contraction of the abdominalmuscles can be replaced or supplemented by the resistance

that a corset or belt provides (as with a weight lifter’sbelt). A corset or belt helps by providing an inelasticresistance against which an elastic, contracted, or laxabdominal wall cannot expand, thus increasing the intra-abdominal pressure. Thus, good abdominal muscle toneand a strong diaphragm and pelvic floor aid in reducingthe load on the lumbar spine by reducing the pressuresthat it must support. Furthermore, because of their attach-ment to the thoracolumbar fascia, the abdominal musclescreate an extensor moment upon the spine when theycontract, imparting further stability.

ROLE OF VERTEBRAL BODY AS A SHOCK ABSORBER

The disk may not be the only shock-absorbing elementof the spine. In light of the studies of Lamy and Farfan,it appears that the vertebral body itself functions as a shockabsorber with variable resistance. First, the authorsexpressed the liquid contained in a vertebral body, approx-imately 0.8 to 1 mL for each vertebral body. Then they

Figure 12.1

a, b.

The axial pressure dissipated by the disk is transmitted to the annulus fibrosus and to the vertebral endplates.

c.

During anterior flexion, the nucleus pulposus moves posteriorly.

CHAPTER 12 FORCES ACTING ON VERTEBRAL COLUMN

67

studied 60 cadavers. From 30 of them, they squeezed outhalf of the vertebral liquid, using pipettes placed in thevascular holes (0.5 mL/vertebra). The other 30 cadaversremained untouched and formed the second group. Toeach of the columns, the researchers applied increasedaxial loads. Under weak loading, the two groups behavedsimilarly. When the load was increased gradually, the nor-mal vertebrae of the second group demonstrated increasedresistance in contrast to the vertebrae of the first group.The authors concluded that the vertebral body has anautomatic hydraulic system that modifies its resistanceaccording to the load received. They also believed thatwhen the lumbar spine is in a flexed position, the posteriorligaments act like a valve, blocking venous circulation onits return course, while intra-abdominal pressure is suffi-cient to block the external venous system. These twomechanisms that block intervertebral venous circulationact synergistically to increase the elastic resistance of thevertebral body during effort.

ROLE OF SACROILIAC JOINTS

It seems clear that the essential role of the sacroiliacjoints is serving as very powerful shock absorbers (seeChapter 11).

Figure 12.2

For a 70-kg standing man, the pressure on theL3 disk is on the order of 70 kg. It changes during forwardflexion, when the angle reaches 20° from the vertical, to apressure on the order of 120 kg. When a weight of 20 kg islifted with the legs extended, the pressure reaches 340 kg(numbers according to Nachemson). Intradiscal pressure,however, depends not only on the weight lifted, but also onthe intensity of the contraction of the muscles involved.

Figure 12.3

The subject is holding on his head a weight of 30 kg. This mass and weight are transmitted to the atlanto-occipitaland the atlanto-axial articulations. The first disk to encounter this pressure is between C2 and C3.

69

13

THE AGING SPINE

EFFECTS ON VERTEBRAL BODY

Aging results in progressive bone loss, which beginsat 30 to 40 years of age and continues for the remainderof a person’s life. This process accelerates considerablyin women for 8 to 10 years following menopause. Itmainly affects trabecular bones, especially the vertebralbodies. Bone loss is 1 to 2% per year and can reach 12%2 years following oophorectomy (Genant, Riggs). Thisloss of bone mass, or osteopenia, results in compressionfractures, often spontaneous or following trivial trauma.

EFFECTS ON INTERVERTEBRAL DISK

With age, the intervertebral disk dehydrates and thephysicochemical state of the ground substance is altered.The result is that the collagen fibers, which are few andslender at the beginning of life, become tight, thicken, andtend to group together with age, in almost parallel direc-tion, and form fibrous bundles. This can be seen on mac-roscopic sections of the aged disk. The process is calledthe “maturation of collagen,” and it increases notably inthe second part of life, after about age 40. The rate ofmucopolysaccharide production increases briefly, andthen progressively diminishes for the duration of life.

Nucleus Pulposus

Little by little, the nucleus pulposus loses its gelatinoushomogeneous character, the very quality that makes it aremarkable shock absorber. While this is occurring, thebiaxial alignment of the fibers of the annulus fibrosuschanges; they become unidirectional bundles, resulting ina significant loss of elasticity. They become less hydro-philic as the years go by, with water occupying a smallerproportion of the disk (79% in young children to 70% at70 years of age). As we previously remarked, this processof aging also affects the cartilaginous endplates, reducing

possible sources of nutrition for the nucleus, which getsits nutrition from the apertures of the endplates. The morethis osmotic exchange decreases, the more rapidly a diskdeteriorates. Fortunately, this process occurs without clini-cal manifestations. At the same time that a disk ages, theligaments stiffen and progressively limit spinal motion.As humans age, however, they progressively reduce theiractivities, and therefore an equilibrium can often be estab-lished between a fragile disk and reduced disk mobility(de Séze) (Fig. 13.1).

For various reasons (e.g., trauma), some disks degen-erate earlier than others. A disk can become old in a youngsubject. When a disk becomes vulnerable, it is generallythe posterior annulus fibrosus that is most affected. Thisis the part that is subject to most of the compressiveloading and thus fails; it is either compressed, forced back,or torn, resulting in a posterior or posterolateral disk her-niation.

Formation of Osteophytes

De Séze states, “In other cases, under the isolated orcombined influence of aging, professional activities, andconstitutional weakness, while the central nucleus pulpo-sus degenerates, the annulus fibrosus is progressivelydriven anteriorly toward the periphery, where it comes incontact with the anterior longitudinal ligament. At thispoint a process of subligamentous ossification will occur,resulting in the formation of an osteophytic ring aroundthe degenerated disk” (Fig. 13.2 and Fig. 13.3).

This osteophyte originates at the vertebral body in thesubligamentous zone found between the anterior longitu-dinal ligament (which, as we noted previously, adheresloosely to the disk but firmly to the vertebral body on theside of the endplate) and the attachment of the annulusfibrosus. It is molded on that ligament, which, due to diskdegeneration, will bulge more and more. This explains thetendency for osteophytes to form horizontally when a verydeteriorated disk is flattened; their orientation is morevertical when a disk is less flattened (Fig. 13.3).

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EFFECTS ON FACET JOINTS

Prior to stiffening of the ligamentous system, loss ofdisk height creates instability of the intervertebral jointand, in some cases, joint hypermobility (Junghanns). Thedegenerating disk will also affect other elements of amobile segment: facet joints (Fig. 13.4 and Fig. 13.5) thatbecome arthrotic and interspinous ligaments. In hyperlor-dosis, two spinal segments can come into contact in thelumbar region. This is known as the “kissing spine” or, ifit has progressed by one more degree, becomes a truearthrosis with molding of the spine at contact (syndromeof Baastrup; see L2, L3, and L4 on Fig. 13.6).

In 30 postmortem examinations of subjects 30 to 70years of age, Rissanen showed that there were an equalpercentage and parallelism between the degeneration ofthe disk and the degeneration of the interspinous ligament.

Trophostatic Syndrome of Menopause

All the consequences of intervertebral disk degenera-tion of maximum intensity can be seen in what de Sézeand Caroit have called the “trophostatic syndrome of themenopausal woman.” Heaviness and loosening of theabdomen, together with postural collapse and compressionof the vertebral column produce the following deforma-tions. Hyperlordosis occurs, which results in increasedstress on the lower lumbar facet joints. This increasedstress results in increased shearing and a tendency towardanterolisthesis. As a consequence of the same stress,

Figure 13.1

a.

Normal intervertebral disk.

b.

Degenerative disk including deterioration of the annulus fibrosus and nucleus pulposus.

Figure 13.2

Formation of an anterior osteophyte (in section).

Figure 13.3

Lateral view. The osteophyte has formed a ring.

CHAPTER 13 THE AGING SPINE

71

retrolisthesis of the vertebrae of the superior lumbar regioncan occur, which results in the vertebrae resting in a pos-terior position on the subjacent vertebra, producing shear-ing of the facet joints. As a result of the deformation, thespinous processes come into contact with each other toproduce an arthrosis.

Intervertebral Foramen

The intervertebral foramen also undergoes changes asa result of the proliferation of osteophytes and disk degen-eration. This occurs particularly at the level of the cervicalspine because of the existence of the uncinate process andthe formation of disco-osteophytic nodules (Fig. 13.7) andbecause of the frequency of spondylosis of the facet joints.The latter causes a narrowing of the posterior neurofo-ramina and is most commonly seen at its superior aspect.

The inferior aspect is affected only in the advanced stageof the spondylosis. At the cervical level, posterior spondy-losis can exist without a concomitant discal lesion (Hirsch,Payne et al., Friedenberg et al.).

The evolutionary formation of the disco-osteophyticnodule is debated. For some, there is an uncovertebralarticulation with an articular cavity and a synovial mem-brane. This articulation could become arthrotic. When afragment of the nucleus of the degenerated disk bulgesinto the articulations, it creates a “hard herniated disk”called a disco-osteophytic nodule (Fig. 13.8).

Figure 13.4

With further disk deterioration, there is increasedstress on the facet joints, resulting in posterior element arthrosis.

Figure 13.5

Lateral view of a segment with complete diskdegeneration and arthrosis of the facet joint.

Figure 13.6

Postmenopausal syndrome of de Séze andCaroit.

Figure 13.7

Osteophytic nodule (N) at cervical level.

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According to Töndury, there is no uncovertebral artic-ulation (Fig. 13.9). He believed that after age 10, fibrousfissures form in the annulus at the periphery, graduallyextending toward the center. When they reach the annulus,the discal jelly reaches the periphery, forming a hard her-niated disk (Fig. 13.8 and Fig. 5.4).

At the level of the cervical spine, these formationsaffect not only the elements going through the foramen

intervertebrale, but also the vertebral artery that extendsinto the transverse openings. This was demonstrated onarteriograms, but it could not be definitely affirmed thatthese formations, like those seen in spondylosis, play adirect pathologic role because images of sinus arteries areseen in asymptomatic patients. In spite of this, the successof uncinate processectomies has been demonstrated insome cases (Jung).

Figure 13.8

Formation of the osteophytic nodule: classictheory.

a.

There is an uncovertebral articulation with an artic-ular cavity and synovial tissue. This articulation can thusundergo arthritic degeneration.

b.

The disk degeneration pro-duces fissures in the annulus in the region of the nucleuspulposus. This can cause enlargement and reach the periph-ery. As a result, a fragment of the nucleus pulposus can thenslip out into the arthrotic articulation and create a hard discalherniation known as a discal osteophyte.

Figure 13.9

Formation of the osteophytic nodules: Töndurytheory.

a.

There is no uncovertebral articulation.

b.

After theage of 10, there is fissuring of the annulus fibrosus, whichallows a progressive movement of the nucleus pulposus out-ward. As this happens, the material of the nucleus pulposushardens in the fissures and, on gaining entry into the periph-ery, forms the osteophytic nodules.

III

PAIN OF SPINAL ORIGIN

75

14

EXPERIMENTALLY PROVOKED PAIN

Pain is one of the most frequent presenting complaintsamong patients with vertebral pathology leading to med-ical consultation. It may be felt and described in manydiverse ways, varying from patient to patient. It is themajor symptom in those conditions where the prognosisis rarely in question and where the functional prognosisis only rarely so.

It results from a complex process combining centralsensory phenomena with affective and emotional pro-cesses. Its repercussion depends on the personality of thesubject. Acute pain is an alarm symptom, while chronicpain can become an illness by itself, without any relationto the initial lesion. A modern understanding of the ana-tomic structures and the neuromediators involved in thetransmission of nociceptive impulses has led to a betterunderstanding of some pain phenomena.

The nociceptive impulses coming from the peripheralreceptors reach the central nervous system via severalroutes, with synaptic relays in the posterior horn of thespinal cord gray matter, the nuclei of the thalamus, andthe cerebral cortex.

These impulses are regulated by a negative feedbackloop. One theory of how inhibitory controls work is calledthe gate control theory (Melzack and Wall). According tothis theory, nociceptive impulses are modulated at thesegmental level in the spinal cord; stimulation of large-diameter proprioceptive fibers can inhibit the activity ofthe smaller-diameter nociceptive fibers.

Another inhibitory mechanism at work is the systemof suprasegmental verification that, via a descending sero-tonergic pathway, is capable of blocking the transmissionof nociceptive impulses at the spinal cord level. It has beenshown that electrical stimulation of certain cerebralregions, notably the periaqueductal gray matter, can bringon analgesia (Reynolds). This control can be inactivated,however, by the morphine antagonists, naloxone andnalorphine. The endorphins (

β

-endorphins andenkephalins) intervene at several levels in this verification,playing a role in the modulation of pain.

On a practical level and in the framework of commonvertebral pain syndromes, it is important to try to under-stand what creates pain at the vertebral level in order tobe able to determine the involved segments (to know therelays and referral patterns in relation to its origin). Weknow clinically that pain can be local, regional, or radic-ular in distribution, but it can also be referred at a distanceand be difficult to diagnose.

In this section, we look at experimentally provokedpains arising from different spinal structures and theirresemblance to those seen clinically. We then consider thedifferent vertebral lesions, whether degenerative,mechanical, or static, seen in current pathology. We thenconsider that the lesions in the classical repertoire do notcorrespond to or explain the nature of these painful dis-orders or the often rapid and favorable responses thatcarefully performed spinal manipulation can provide.

In most pathology, the lesions detected radiographicallyare in many cases irrelevant and not responsible for thepain complaint; in many cases, even the most sophisticatedexaminations leave us without diagnostic answers. Often,however, an attentive clinical examination including seg-mental palpation techniques that are normally painlessreveals a specific painful vertebral segment. The “lesion”detected is an example of a “painful minor intervertebraldysfunction” (PMID) (Maigne), consisting of painful seg-mental vertebral dysfunctions often associated with skinhypersensitivity and altered tissue texture in a metamericdistribution: cellulalgic, myalgic, and tenoperiosteal. Theyconstitute the “segmental vertebral celluloperiosteomyalgicsyndrome” of the author, of which the PMID is often thesource.

Pain can only arise from the irritation of an innervatedstructure or from a nerve. The anatomy shows us, forexample, that the nucleus pulposus is not innervated. Itcannot, therefore, be a source of pain. However, it canprecipitate pain if it irritates an innervated element or anerve root. This occurs when the nucleus bulges andimparts tension to the superficial and posterior annular

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fibers, the posterior longitudinal ligament, or the nerveroot.

Experiments confirm these facts. They have delineatedthe sensitivities of different spinal structures and revealedthe local and referred pain patterns of experimentally pro-voked pains. The comparisons that can be made betweenexperimentally provoked pains and the ones seen daily atclinic are highly useful in telling us something about theorigins of these pains.

In this chapter, we look first at pain resulting from theirritation of the spinal nerve roots, then at pains provokedby the irritation of each of the components of the mobilesegments (annulus fibrosus, facet joints, anterior andposterior longitudinal ligaments, interspinous ligament),and finally at pains that originate in muscles and tendons.

SPINAL NERVE ROOT

Sensory Root

Experimental stimulation of the sensory root provokessharp pain in the area of the corresponding dermatome. Itis demonstrated easily by irritative infiltrations of thenerve. Pricking the nerve provokes a sharp and suddenflash of pain all along its pathway. During interventionson the cervical spine, Cloward directly excited the sensoryroot and obtained the same result.

If a nerve root is subjected to sustained pressure, how-ever, pain is not elicited; numbness occurs instead (Inmanand Saunders, Burke). According to Inman and Saunders,“the usual concept that sciatic pain is only due to pressureon the nerve root is not supported by experimental evidence.”

Neither does nerve root traction appear to be the causeof root pain. Falconer performed animal experiments inwhich small pieces of wax were placed under the nerveroots at the level of the lumbar intervertebral disks. Whenthe animals awoke, a paralysis in the corresponding areawas seen. The animals returned to their normal behaviorin 48 hours without paralysis. A reintervention showedthat the wax did not move; the nerve had adjusted. Sucha stretching, therefore, is not sufficient to cause pain.Admittedly, in cases of radicular pain of mechanical originsuch as sciatica, reactive inflammation of the nerve rootis often implicated in pain production, making the nervousfibers hyperexcitable.

Another notion, held by Frykholm, is of great interestin understanding the radicular pains of mechanical verte-bral origin. Frykholm noticed that compression of a cervi-cal root by a hard hernia (disco-osteophyte nodule) canbe tolerated a long time. To cause pain, another mechan-ical element must intervene, suddenly provoking a force-ful or strenuous variation of pressure; or a fibrosis of thecul-de-sac of the dura mater must occur; or a reactiveinflammation must start.

This notion that a forceful or strenuous variation ofpressure is necessary to cause pain is interesting. It helpsexplain why a patient with a herniated disk can haveviolent pain after a sudden movement, and why pain can,in many cases, with or without treatment, decrease ordisappear while the herniated disk remains unchanged.

Motor Root

It is not usual to consider that irritation of a motor rootcan provoke pain. However, Frykholm and then Clowardexcited the motor roots of the cervical nerves and pro-voked pains in patients that reproduced typical pains theyexperienced during cervical radicular irritation as a resultof herniated disks. This provoked pain was described as“deep, exasperating,” very different from the one resultingfrom excitation of the sensory root.

For these two authors, common radicular pain consistsof two pains: one is due to the irritation of the sensoryroot, while the other is myalgic, i.e., due to the irritationof the motor root. This is consistent with the sensationsfelt by patients with sciatica or cervicobrachial neuralgia.Remember that cramps are frequent sequelae in patientswith sciatica; they are very painful and often associatedwith fasciculations. Electromyographic examinationsoften reveal fibrillation potentials that are spontaneoussingle muscular fiber discharges seen in association withnerve root pathology. In some cases of sciatica or femoralneuralgia, this myalgic element is characteristic (see Chap-ter 43, “Sciatica,” and Chapter 44, “Femoral Neuralgia”).

DISK

All authors agree that the nucleus pulposus is not inner-vated although the superficial annular fibers are. Wibergstudied the sensitivities of different vertebral structures atthe lumbar and cervical levels in patients under localanesthesia. He concluded that pressure on the posteriorsurface of the disk and posterior longitudinal ligament inthe lumbar spine resulted in lumbosacral pain in everycase. It is a deep pain ipsilateral to the side of excitation.Anesthesia of the corresponding spinal nerve does notmodify the result.

At the lumbar level, Cloward arrived at the same con-clusions as Wiberg. By irritation of the superficial fibersof the lumbar hemidisk, Cloward provoked pains radiatingto the sacroiliac region, the hip, and the buttock of thesame side. He concluded that these pains are related to anirritation of the sinovertebral nerve that innervates theperipheral fibers of the disk and the ligaments that sur-round it. He drew a distinction between this “discogenic”pain and the “neurogenic” pain arising from irritation ofthe spinal root:

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77

An intradiscal injection of 0.2–0.3 mL of opaque radio-logic liquid does not cause any pain if the disc is normal.However, if the fibers of the annulus are torn and if thesolution injected under pressure reaches the periphery ofthe disc, pain is felt. Its localization, its character and itsintensity will depend on the site and the extent of thediscal tear.

This point is debatable. Holt made 148 discograms on50 young volunteers without any vertebral pains. He notedthat the intradiscal injection of the contrast liquid can bepainful without the presence of a tear in the annulus.However, in patients with discal pathology, it is the exactreproduction of their typical pain during discography thatis felt to be significant in addition to the morphologicfeatures seen radiographically.

The results obtained by these authors are very muchthe same at the cervical level as at the lumbar level whereirritation of the posterior surface of the annulus and pos-terior longitudinal ligament is concerned. When the infe-rior cervical spine is involved, pain is referred to theshoulder and the upper arm (Falconer et al., Wiberg, Clo-ward). Cloward also noted the possibility of provokingreferred pain by pinching or pressing the anterolateralparts of the last cervical disks. He thus produced a dorsalperiscapular pain often associated with cervical herniateddisks. There, too, he found that the sinuvertebral nerve ofLuschka played an important role.

Cloward’s observation is consistent with our own stud-ies of periscapular pain of low cervical origin. But webelieve that the source of this pain referral can arise fromcertain cervical spinal structures other than the disk. Ourclinical observations do not allow us to share Cloward’sopinion on this point or on the mechanism of that referredpain (see Chapter 36, “Chronic Thoracic Pain”).

Rabischong and Serrano-Vella have found many smallnerve endings in the anterior longitudinal ligament, in thefeltwork separating this ligament from the disk, and in thesuperficial laminae of the annulus. They do not believethat this innervation is exclusive of the sinuvertebral nerve.

Recent studies utilizing the adolescent porcine modelhave demonstrated that stimulation of the nerves of theposterolateral annulus fibrosis of the disc at L3–L4 elicitedmuscle activation in the paraspinal muscles, namely thelumbar multifidus and longissimus. Introduction of phys-iologic saline into the zygapophyseal joint was demon-strated to result in a reduction in the motor unit actionpotential amplitude. This reduction was manifest as animmediate and constant reduction, a graded reduction, ora delayed reaction during which the reduction occurredan average of 5 minutes after saline injection. This dem-onstration that physiologic saline injections into the zyg-apophyseal joint are able to reduce the stimulation path-way from the intervertebral disc to the paraspinalmusculature supports the concept that the zygapophyseal

joints appear to have a regulatory function controlling theintricate neuromuscular balance in the lumbar motion seg-ment (Indahl).

FACET JOINTS

By injecting 11% hypertonic saline into the lumbarfacet joints, L4–L5 or L5–S1, Hirsch et al. noticed theappearance of a sharp lumbar pain after a few seconds. Afew moments later, the pain radiated to the sacroiliac andgluteal regions and to the great trochanter, and then in afew minutes disappeared.

Taillard’s findings were a little different. After irritatingthe capsules of the lumbar facet joints under local anes-thesia in patients with spondylolisthesis, he provokedreferred pains producing a sciatic, pseudoradicular referralpattern:

[I]nteresting observations have been made in patientsoperated under local anesthesia. It is easy to obtain a goodNovocaine infiltration in the subcutaneous tissues, thelumbar fascia, the paravertebral muscles, the periosteumof the laminae. But in general this anesthesia is not strongenough to make the capsules of the facet joints insensitive.It is almost always possible to reproduce the patient’stypical pain complaint by pinching or rubbing the capsuleclose to the joint. Not only the lumbar pain, but also thesciatic pain radiating into the thigh, the calf and some-times even the foot, are produced.

Since the publications of Rees (1971) and Shealy(1975), the lumbar facets have been in the forefront ofwork evaluating the patterns of lumbar pain. By variousmeans, such as injection of hypertonic saline solution(Mooney and Robertson, 1976) and electrical stimulation(Bogduk and Don Long, 1980), lumbar pains have beenprovoked and referred to the inferior limbs in a diffuse,vague, and generalized fashion, often suggestivelyreproducing a more or less radicular topography; i.e., thepain is referred in a sclerotomal pattern.

Such pain referral patterns are frequently seen in clinic.They are often relieved by infiltration of the correspondingfacet joint if the latter was found painful on examination(see Segmental Examination in Chapter 20, “General Prin-ciples”). During the injection, it is not rare to momentarilyexacerbate the referred pains. These pains have an appar-ently radicular distribution.

Sometimes, facet injection provokes transitorily referredpains that do not apparently correspond to any diagramof anatomic or embryologic distribution. Thus, we havenoticed that infiltration of the thoracolumbar junction fac-ets occasionally reproduces a transitory pain in the poste-rior aspect of the leg ipsilaterally, a sciatic distribution,although it usually does not extend below the superiorgluteal region.

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INTERSPINOUS LIGAMENTS

Kellgren injected a few drops of 5% hypertonic salinein the interspinous ligaments after anesthesia of the skinand provoked local and distant pain. According toKellgren, the topography of this pain corresponded to thereferral pattern expected for the innervating spinal roots,with some differences at the level of the limbs. This painwas characterized as a profound deep pain. Still accordingto him (1948), the infiltration of the interspinous ligamentsL1–L2 provoked pain in an area that was noticeably inthe area of the LI root. But this pain seemed more likethe pain of renal colic than the pain of a radiculitis, andit was accompanied by retraction of the testicle (Fig. 14.1).

Feinstein (1954) used the method of Kellgren andobtained similar results. Studying five subjects, he pre-pared a map of the pain provoked by injection in each of

the interspinous ligaments from the occiput to S3. Painhad a constant recurrent characteristic topography thatcould be demonstrated in subjects when reexamined afteran interval of several days. It lasted for about 10 minutesafter the injection, but in some cases, persisted for severaldays. It radiated locally and at a distance. The extent ofthe zone of diffusion varied according to the quantity ofthe liquid injected (0.2 to 1 mL); tolerance varied fromone subject to another. Some did not tolerate the maximaldose.

Feinstein insisted that this distribution did not corre-spond to the dermatome; it was, as he says, “segmental.”It corresponded to the whole of the tissues innervated bythe corresponding sensory nerve root (muscle, bone, lig-ament, skin), not only to the cutaneous area (dermatome).

We are concerned here with where the pain was “felt.”Each of the five subjects noted the precise area where itwas felt. The

dark areas

in Fig. 14.2 indicate where allsubjects felt pain and where it was strongest. Feinstein

Figure 14.1

Injection of hypertonic saline into the interspinous ligament of L1–L2 provokes low back pain and a pain in theinferior abdominal region radiating toward the testicle (according to Kellgren).

CHAPTER 14 EXPERIMENTALLY PROVOKED PAIN

79

remarks that when examining the objective sensitivity,there is often a slight hypoesthesia, more rarely a hyper-esthesia, in these areas.

Glover (1960), using a pin, regularly found zones ofhypersensitivity in patients with back pain; he looked forthem in the paravertebral region. To elicit pain, the pinhad to be inclined to 40° and lightly pressed against theskin. The sensations reported by the patients includedremarks such as “you press too much,” “it is scratching,”and “it tickles.” Sometimes, the patients reported an elec-tric feeling. A spot was often found to be particularlysensitive, most often 4 to 5 cm lateral to the midline, inthe middle of a region that was less sensitive.

Glover also remarked that 90% of these spots disap-peared after manipulation, at the same time that the paindisappeared. He did not notice any difference in temper-ature between these zones and the painless symmetriczones. In one of two cases, however, he found that theelectric impedance of the skin was lowered, probably

related to the start of perspiration, which was not observ-able on other objective tests.

The zones of hyperesthesia of the back described byGlover correspond well to the zones described by Kellgren(1939) and by Inman and Saunders (1944). As is shownlater, these zones coincide, for the most part, with thezones where we find cellulalgic hypersensitivity duringthe “pinch–roll” test — hypersensitivity that was notlooked for by the preceding authors (see Chapter 18, “Seg-mental Vertebral Celluloperiosteomyalgic Syndrome”).

POSTERIOR AND ANTERIOR LONGITUDINAL LIGAMENTS

It is difficult to experimentally differentiate the irrita-tion of the superficial fibers of the disk from the irritationof the posterior longitudinal ligament closely joined to it.

All authors recognize that the posterior longitudinalligament has a very rich innervation.

Figure 14.2

Pain produced after injection of different interspinal ligaments of different intervertebral segments with hypertonicsaline (according to Feinstein).

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According to Hirsch, it was the irritation of this liga-ment that was believed to give rise to the particular typeof pain associated with the herniated lumbar disk. Its rolein painful vertebral pathology is very important, especiallyat the lumbar level.

Remember the experiments of Smyth and Wright dur-ing interventions for sciatica. They attached fine nylonthreads to the sacrolumbar fascia and to the facet joints,to the ligamentum flavum and to the posterior part of theannulus fibrosus, to the posterior longitudinal ligament,and to the nerve root. Three to 4 weeks later, when thethreads were pulled, these formations were irritated. Thepatients re-experienced their former pain, which had beenlumbosciatic in nature, when a traction was performed onthe threads of the annulus fibrosus, the posterior longitu-dinal ligament, and the nerve itself. Rabischong andSerrano-Vella found nerve endings in the anterior longi-tudinal ligament. They thought that pressure on this liga-ment could be responsible for some pains.

LIGAMENTUM FLAVUM

Pressure on the ligamentum flavum is not painful(Wiberg). Stretching of this ligament, as in the experimentof Smyth and Wright, is not painful either.

VERTEBRAL BODY

Pressure on the posterior side of the vertebral bodiesprovokes no pain (Wiberg).

MUSCLES

It has often been observed that the intramuscular injec-tion of an irritating liquid in the gluteal region causes apseudosciatic pain along the thigh, even if this injectionis performed at the external iliac fossa, which is distantfrom the sciatic trunk (Fig. 14.3).

Kellgren and Lewis studied these pain referral patterns.After anesthesia of the skin, they injected a solution of5% hypertonic saline in different muscles and tendons.While the pain provoked in the tendons remained local,the one provoked by the injection in the muscle was dis-tant. An injection in the distal triceps resulted, for exam-ple, in a pain extending from the medial side of the fore-arm to the fifth finger. An injection in the trapezius causedpain that radiated to the occiput. An injection in thescalene muscle caused pain that radiated in a diffuse man-ner to the arm and chest (Fig. 14.4). If performed on theinfraspinatus muscle, it produced pain referred to the ante-rior side of the shoulder, radiating into the arm (Fig. 14.5).

Kellgren established precise diagrams of these referralpatterns and came to the following conclusions:

• The distribution of pain for a given muscle is thesame for all subjects. There might be some intra-subject variations, with some having a dorsal pre-dominance, while others have a ventral one, and thepattern is more or less distal, depending on the partof the muscle that has been injected.

• The referral pattern is related to the nerve root inner-vating the muscle under consideration, so that themuscles innervated by this same root have a com-mon pain diagram.

• The topography of the referral pattern coincideswith the spinal root that innervates the muscle inquestion.

• Pain is independent of the mode of stimulation. Thesame experimental pain can be provoked by theinjection of hypertonic saline or by electric stimu-lation performed during some surgical interven-tions.

According to Travell and Simons, the pain referral ofcertain trigger points by pressure or by pin does not cor-respond to any radicular or segmental distribution. Dailyexperience confirms their remarks. Some muscles (e.g.,glutei medius and minimus), however, have pain referralpatterns starting in the area corresponding to the nerve

Figure 14.3

Injection of an irritating substance into the glu-teus minimus provokes pain that radiates into the lower legin a pseudosciatic distribution.

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81

Figure 14.4

Injection of several drops of hypertonic saline into the scalene muscle provokes pain that radiates diffusely tothe upper arm and the anterior chest.

Figure 14.5

Injection of several drops of hypertonic saline into the infraspinatus muscle provokes pain in the anterior shoulderand radiates into the arm.

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that innervates them. As for the paravertebral muscles,injection in the trigger points of the low thoracic regioncauses pain toward the ischium, while injection in spotsof the high lumbar region causes pain higher in the lumbarfossa, toward the iliac crest.

DERMATOMES

The works of Denny-Brown, Kirk, and Yanagisawahave demonstrated that there is no simple correspondencebetween a given dorsal root and an area of skin; rather,dermatomal sensory loss depends on the anatomical and

physiological characteristics of large regions of nervoustissue, multiple adjacent dorsal ganglia, and the nearbyspinal cord. Perhaps because of the complexity it implies,their work has not had significant clinical effects and hastended to be ignored. However, their view is now sup-ported by subsequent studies. In this vein, the potentialfor the Lissauer tract to modulate gross expansions in thereceptive field of dorsal horn interneurons has recentlybeen demonstrated along with many other plastic aspectsof nocioception that must modify our concept of whatdermatomal areas may be involved with given pathologiesand physiologic states (Greenberg).

83

15

VERTEBRAL LESIONS AND

COMMON PAIN SYNDROMES

Back pain is often attributed to lesions of the interver-tebral disk or facet joints or to static disorders. Many ofthese lesions visible on x-rays are painless, and manypatients with painful backs have normal x-rays.

INTERVERTEBRAL DISK LESIONS

Besides the lesions brought on by normal aging, whichare generally well tolerated, the disk can demonstrateapparently similar degenerative changes at an earlier-than-expected age that, because of their premature characterand location, can be pathologic.

There are strong analogies, but not complete similari-ties, between the aberrations of the aged disk and thoseof a degenerated disk in a young patient. In the agingprocess, the rate of mucopolysaccharide productionincreases for a short time around age 40 and then returnsto a rate equal or slightly inferior to that at its startingpoint. On the other hand, in cases of herniated disks, thedecline in mucopolysaccharide production is rapid,significant, and progressive. In patients 20 years of age,one can already notice slight localized degeneration offibers in the deep layers of the annulus, most often pos-teriorly. Gradually, their number and size increase andform (about at age 40) small fissures in the laminae. Byage 30, these areas become susceptible to injury by tearingor enlarged by pressure on the nucleus. There are twotypes of rupture of the annulus: radial tears and concentricsplits or tears. The latter form cracks in the shape of archesparallel to the laminae, localized usually to the lateral andanterior parts of the disk.

The radial tears start at the contact region between thenucleus pulposus and the annulus fibrosus and extend tothe periphery. They are predominant in the posterior orposterolateral aspect of the disk. They are of variable size,narrow or wide, and generally unique; there may be twoor three (de Séze).

When the tears are wide, segments of the nucleus pul-posus can protrude into them. If a fragment goes towardthe front or the sides, there will be no pain, but it will leadto the formation of osteophytes. On the other hand, frag-ments extending posteriorly will bulge and contact thesuperficial annular fibers. The distention of these fibersand the forceful or strenuous pressure exerted simulta-neously on the posterior longitudinal ligament will causepain of the acute lumbar disk type. Finally, frank ruptureof the superficial annular fibers may occur, resulting inextrusion of the nucleus pulposus. This is known as anoncontained herniated disk (Fig. 15.1).

The substance of the nucleus pulposus can also infil-trate through a tear in the annulus fibrosus. This is themechanism of painful internal disk disruption. Finally, theposterior superficial laminae distended under the influenceof postural forces or exertion effort can be sources ofchronic lumbar disk pain.

The production of pain need not be solely a mechanicalphenomenon. Soft tissue injury can produce many typesof substances with algogenic potential. For example, therupture of a herniated disk has been shown to provoke theliberation of a primary mediator of the inflammatory cas-cade, phospholipase A

2

, which acts as the rate-limitingstep in the production of prostaglandins and leukotrienes(J.S

.

Saal, R.C. Franson, R. Dobrow, J.A. Saal, A.H.White, and N. Goldthwaite).

Herniated Disks

A posteriorly herniated disk can come into contact witha nerve root, compress it, irritate it, and cause inflamma-tion, which is the primary source of pain. This is the usualmechanism of the common femoral neuralgia and sciatica.

At the cervical level, foraminal stenosis due to osteo-phyte formation (de Séze) is most often the cause for thecervicobrachial neuralgia. The protrusion of a fragmentof the nucleus, generally after excessive activities, is veryrarely the cause.

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SECTION III PAIN OF SPINAL ORIGIN

Herniated disks are most frequent at the lumbar level.In statistics cited by the Clinique Universitaire de Neuro-chirurgie de Zurich on 2941 cases, there were:

• 1098 herniations of the L5–S1 disk• 1667 herniations of the L4–L5 disk• 135 herniations of the L3–L4 disk• 14 herniations of the L2–L3 disk• 7 at the level of the inferior dorsal spine• 20 at the level of the last cervical disks

At Lumbar Level

The herniations are most often posterolateral, as theposterior longitudinal ligament reinforces the interverte-bral disk posteriorly. Some herniations remain subliga-mentous, but others break through this ligament (Fig. 15.3).

Posterolateral herniation

—

This is the most frequenttype of herniated disk often leading to compression orirritation of the corresponding spinal root (Fig. 15.1 andFig. 15.2). It can compress the nerve root from either alateral or medial side. It can also compress the root of thesubjacent level superiorly or extend inferiorly via asequestered fragment. It is then said to be in superior orinferior sublaminar position.

Posterior herniation

—

This type of herniation candeform the posterior longitudinal ligament and compressthe dural sac without irritating the nerve roots. It can beresponsible for chronic lumbar pain with acute exacerba-tions or for subacute lumbar pain with lumbar stiffness(Fig. 15.2).

Transligamentous herniation

— Among the hernia-tions (sometimes small) that have broken the posteriorlongitudinal ligament, some remain in continuity with thedisk while others are separated into multiple sequesteredfragments that pose difficulty for surgical dissection.These free fragments can be visualized on magnetic res-onance imaging (MRI) and in certain cases, with sacrora-diculography.

Discography may also be useful in demonstrating theexistence of an anterior or lateral herniation. Classically,these types of herniations are asymptomatic. Schmorl’snodules are also forms of herniation into the vertebralbody. These lesions can contribute to some instability ofthe segment (see Chapter 17, “Painful Minor Interverte-bral Dysfunctions”).

At Thoracic Level

Disk herniations are rare in this region. They producethoracic pain or pain referred to the pelvic region and thelegs. Often, they are accompanied by nocturnal paresthe-sias (hyperesthesia, burning pains, stiffness). The motordeficit can range from a simple impression of weaknessin one leg to total paraplegia. MRI is the imaging studyof choice to detect these herniations.

At Cervical Level

At the cervical spine level, there are hard herniationsformed by the disco-osteophytic nodule, a spondyloticreaction at the level of an uncinate process, and the true

Figure 15.1

Horizontal flexion.

Left.

Posterolateral herniated disk with compression of the nerve root.

Right.

Median diskherniation compromising the dural sac and cauda equina.

a.

Normal disk.

b.

Bulging disk due merely to an outward bulgingof the superficial fibers of the annulus fibrosus that are not broken.

c.

Herniated disk with the superficial fibers of the annulusfibrosus ruptured and the nucleus pulposus able to gain exit and compromise the spinal nerve.

CHAPTER 15 VERTEBRAL LESIONS AND COMMON PAIN SYNDROMES

85

herniated disks called soft herniations that are much rarer.These can be:

• Posterolateral, compromising the spinal nerve(Fig. 15.4, 1)

• Intraforaminal, threatening the spinal nerve also(Fig. 15.4, 3)

• Much more rarely, posterior and median, threaten-ing the dura mater, spinal cord, and anterior spinalartery (Fig. 15.4, 2)

MRI or computed tomography (CT) scanning afterinjection of myelographic contrast can be of help in iden-tifying them.

Figure 15.2

Transverse section showing different modes of compression by a herniated disk.

a.

Normal state.

b.

Simpleprotrusion.

c.

Posterolateral disk herniation.

d.

Posterior disk herniation.

Figure 15.3

Different types of herniated disks (according to Junghanns).

a.

Without rupture of posterior longitudinal ligament.

b.

With rupture of posterior longitudinal ligament.

c.

Disk extrusion beneath posterior longitudinal ligament.

d.

Sequesteredfragment.

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SECTION III PAIN OF SPINAL ORIGIN

Intervertebral discs may also be subject to annular tearswhich in some cases may be painful with or without localnerve compression.

Pain related to annular disc tear may have painful fea-tures related to local segmental sensitization reflected bypresentations typical of segmental cellulotenoperi-osteomyalgic syndrome.

LESIONS OF FACET JOINTS

The facet joints can be associated with acquired orcongenital anomalies, degenerative lesions, and lesionsdue to mechanical pain. Thanks to various scanningdevices and arthrography, they have been studied com-pletely and thoroughly.

Anomalies

Congenital Anomalies

Congenital anomalies have been chiefly noted in thelower lumbar areas. Anomalies involving the positions ofthe facet joints and asymmetries of the articular facetjoints have been well studied.

The facet asymmetries have been verified and evaluatedby using CT scanning. They have not only been seen atthe lumbosacral junction, but have also been found at thelevel of the thoracolumbar junction (Malmivaara et al.,Maigne et al.).

It is possible that such anomalies can induce instabilityat a segment and cause articular spondylosis. When thereis a significant asymmetry in the inclination of the poste-rior articular spaces, a CT scan demonstrates a stronglycondensed aspect of the articular edges or subcortical gapsexpressing the articular hypertension.

Acquired Anomalies

Gillot, working on cadavers, noted the prevalence ofsmall and transverse bony crests on the inferior lumbararticular surfaces in old patients. This was believed to bedue to the reduction of articular play during flexion andextension associated with the aging process. The crestswere thought to be evidence of the successive loss of rangeof motion.

Degenerative Lesions

Facet Arthrosis

Facet joint arthrosis is located at the level of the lordoticregions of the spine, the neck, and lumbar region. It is theresult of excessive pressure caused by hyperlordosis ordiscal deterioration. Arthrosis is, in fact, very rare at thelevels of the articulations without disks, such as at theocciput and atlas and at the atlas axis, which are extremelymobile and sustain significant pressure. Arthrosis can,however, affect the atlas-odontoid articulation.

Arthrosis can also be found on segments with appar-ently intact disks. Most often, however, they are seg-ments adjacent to segments presenting very severe disklesions.

At the cervical level, posterior articular arthrosis isespecially located between C2–C3 and C3–C4, but it canaffect the inferior levels. At the lumbar spine level, arthro-sis is frequently seen in patients over age 50. Most often,it is localized to only one level; it is seen in 45% of casesaccording to Louyot, i.e., 1% at L2–L3, 8% at L3–L4,17%at L4–L5, and 19% at L5–S1. It affects several articula-tions in 17% of the cases and is generalized in 38% ofcases.

The mechanical factors that foster it are found togetherin the “trophostatic syndrome of the postmenopause” thataffects women past 60 years of age who are hyperlor-dosed, often obese, and have slackening of the abdominalwall. The L4–L5 level is most often affected. The L4–L5and L5–S1 levels can be affected simultaneously. Some-times, the lesions extend to L2–L3.

Pathologic Role —

Arthrotic lesions, when significant,can modify the morphology of the vertebral canal and leadinto acquired stenosis that can be superimposed on a con-genital stenosis, resulting in myeloradiculopathy at thecervical level and lumbar stenosis syndrome at the lumbarlevel. At the lumbar level also, facet hypertrophy cannarrow the lateral recess and facilitate radicular pain syn-drome. At the cervical level, osteophytes can compressthe vertebral artery in the transverse canal.

In the above cases, facet arthrosis plays direct andmechanical roles. These represent, however, only a smallpercentage of the cases of vertebral arthrosis usually seen.

Figure 15.4

Different varieties of herniated cervical disks: 1,posterolateral protrusion; 2, posteromedial protrusion; and 3,intraforaminal protrusion (as per Frykholm). In this scheme,the posterior arch is resected for better viewing.

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87

Vertebral arthrosis is painful during inflammatoryattacks. Some people experience them often episodically,and some rarely or never.

The condition can be uncomfortable because of thenumbness it produces; if it is not painful, however, thepatient may not complain. Finally, acting like rust on ahinge, it can promote painful minor intervertebral dys-function, which generally improves after mobilization andsometimes improves after manipulations if the state of thespine allows them.

Facet Joint Periarthritis

CT scans allow the detection of calcification of thecapsules and ligaments of the facet joints. Calcification iscommon at the thoracolumbar junction, localized to thefacet joint capsule and/or the ligamentum flavum (Maigneet al.). Para-articular reactions without any radiologic evi-dence are probably much more frequent at all levels.

Other Lesions

Facet joint arthrography has shown the existence oflesions not revealed by conventional radiography: hydrar-throtic manifestations, diverticular formations, and, morerarely, synovial cysts or communications between adja-cent articulations.

Synovial cysts can compress the root in the neurofora-men. The communication between adjacent articular cav-ities corresponds to the junction of several cystic cavities(Chevrot et al.). Thanks to CT scanning, hypodenseimages of the joint of gaseous type have been shown,revealing an articular void. This void is usually associatedwith a posterior articular arthrosis.

Meniscoid Formations

The lesions of the synovial fold are discussed in Chap-ter 17, “Painful Minor Intervertebral Dysfunctions.”

OBJECTIVE MUSCULAR LESIONS

In popular language, acute lumbar pain occurring afterlifting is most often attributed to a “muscular tear.” Thistype of lesion is not rare in athletes, but it is uncommonin the thoracic or lumbar muscles.

Apart from the usual reflex protective guarding, therole of the muscle in vertebral pain syndromes is rarelyraised. However, a careful examination of the paraverte-bral muscles can help to identify, in some cases, smallfirm cords the size of a match that are very painful topalpation. They can be the sources of severe pain distally.These “trigger points” found on palpation do not corre-spond to any objectively demonstrable lesion. They seemto be due to a functional perturbation that tends to becomepermanent. They can be relieved, sometimes permanently,by injection of local anesthetic.

Nevertheless, Drevet (1983) has shown that some myal-gic points that are localized to the lumbar muscles and areresponsible for unilateral lumbar pain correspond toabnormal zones that are often hypoechogenic on ultra-sonographic examination. His morphologic and structuralstudies of samples have shown an intensive perimysial andendomysial fatty infiltration massively invading the mus-cular bundles. This could explain the building of the hypo-echogenic image and of the pain associated phenomena(see Chapter 39, “Chronic Low Back Pain”).

89

16

POSTURAL DISORDERS AND PAIN

When a patient with vertebral pain presents with apostural disorder, one is tempted to accept the disorder asthe cause of the pain. Such static disorders can consist ofscoliosis, dorsal hyperkyphosis, lumbar hyperlordosis, orflat lumbar curve. They can also take the form of a spon-dylolisthesis that is a malformation and not really a staticdisorder.

SCOLIOSIS

Scoliosis is usually a painless disorder in the adoles-cent. In the adult, however, many vertebral pains are usu-ally attributed to scoliosis, although many patients withscoliosis do not experience pain. According to Stagnara,a scoliotic adolescent has a 50% chance of having spinalpain as an adult, but the percentage of scoliotic patientswith pain is similar to that of patients without scoliosis.Stagnara studied 100 cases of adult scoliosis with spinalpain and concluded that neither the patient’s sex, nor thepatient’s profession, nor the angle of the scoliosis playeda determinant role in who would experience pain. Jacksonet al. arrived at the same conclusion after studying painin 197 scoliotic adults (above 18 years of age) with amedian age of 31 and comparing them to 180 nonscolioticpatients. The frequency of pain was the same in bothgroups (51%).

However, it is clear from the study by Jackson et al.that when pain was present, scoliotics had more severepain than nonscoliotics and the progression of the painwas different. Spontaneous resolution occurred in 64% ofthe scoliotic group and in 83% of the nonscoliotic group.The pain and severity of the scoliosis were noted to worsenwith age; the pain’s origin was essentially related to theconcavity of the spine but could also be of discal, articular,or radicular origin. Nevertheless, there is general agree-ment among those who work with lumbar scoliotics thatthey suffer severe social and professional handicaps as aresult of their condition.

According to Stagnara, physical rehabilitation alonewas able to ameliorate pain in 40%. Orthotic devicesincluding the use of corsets for limited periods of timehelped in 60% of cases. Surgery was reserved for the mostsevere cases and was able to help reduce pain in 65% ofthe cases.

Minor Scoliosis

Physicians not specialized in the treatment of scoliosisrarely see severe cases. Most of the cases they treat areof the minor scoliotic variety, i.e., scoliosis of less than30°. These patients present with thoracic and lumbar spinepain of mild to severe intensity. Almost all of these indi-viduals are diagnosed as having pain due to their scoliosis.Most of the patients have the same clinical picture as canbe noted in nonscoliotics in that they also present withinterscapular thoracic pains of cervical origin (see Chap-ters 36 and 37 on thoracic pain) or lumbar pain of thora-columbar junctional origin. Treatment is similar for thosewith scoliosis as for those without scoliosis, and similarresults are obtained. In the absence of precise statistics, itis difficult to say whether recurrence is more common forscoliotics than for nonscoliotics; this tendency, however,is not evident to us. Mild to moderate scoliosis should not,therefore, be automatically diagnosed as the cause for allpain of vertebral origin.

THORACIC HYPERKYPHOSIS

Exaggeration of the thoracic kyphosis is most often dueto Scheuermann’s disease. It is usually the sequela in theadult with spondylosis. In the adolescent, a kyphotic pos-ture should be distinguished from true kyphosis.

Kyphotic Posture in Adolescents

In the kyphotic posture seen in preadolescents and ado-lescents, shoulders coil forward, and the lumbar region

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appears hollow. It is important to note that there is noradiologic lesion and that the kyphosis is reducible.

Conversely, true kyphosis is not reducible and exhibitsradiologic lesions. In the beginning, however, the diagno-sis is not always easy to make; therefore, regular super-vision is necessary.

Hyperkyphosis Due to Dystrophic Spinal Growth

Scheuermann described a developmental abnormalityof the thoracic spine, which is named after him. It is dueto an impairment of the fibrillar system of the cartilage ofthe vertebral endplates during growth. These impairmentsare benign and precocious. They can be seen in the veryyoung (about age 4) but are generally seen after age 8;they are numerous and extensive in some patients. Theythen form zones of least resistance to pressure, makingthe vertebral body vulnerable to compression, especiallyin its anterior part. Increased anterior loading squeezesthis fragile zone, which increases the kyphosis, furtherincreasing the pressure anteriorly, leading to more dam-age, and a vicious circle is started.

In adolescents, pain is rare and generally moderate(20% of cases). It appears on waking, disappears duringthe day, and reappears in the evening. Severe cases aretreated by rest and, when it is not possible, by immobili-zation in a plaster cast to reduce pain. The midthoracicregion is most often affected.

In adults, dystrophic growth produces spondylosis,which is rarely painful. When these patients have inter-scapular thoracic pain, the origin is very often the inferiorcervical spine (Maigne) (see Chapters 36 and 37 on tho-racic pain).

When the thoracolumbar junction is affected, low lum-bar pain is frequent, especially in the adult. In the adoles-cent, according to Fauchet, 90% of lumbar conditions arepainful, presenting as posturally exacerbated low backpain. This condition can result in the reduction or disap-pearance of the normal lumbar lordosis. In the early stagesof the condition, the kyphosis is evident only in the sittingposition; it appears in the standing position only when thevertebra has become wedge shaped. An early sign is thepigmentation of the skin at the level of the spinous pro-cesses of the affected vertebral segments.

The lumbar pain of youth, if left untreated, can con-tinue and become serious in the adult. If treatment suchas plaster cast, corset, and physical therapy is appliedbefore bony vertebral maturity occurs, the dystrophic ver-tebrae will be able to remodel themselves and reduce oreradicate the development of future lumbar pain.

TRANSITIONAL ZONE ABNORMALITIES

Lumbosacral transitional zone abnormalities are fre-quent. Their frequency is estimated at 20% by all authors,whether lumbarization or hemilumbarization of S1 or thesacralization or hemisacralization of L5. Although theseabnormalities do not play any direct role in lumbar pain,it is often admitted that they can play a fostering role.

In a study by Schiano et al., a comparison was madeof 200 patients with lumbar pain and 200 patients of thesame median age without lumbar pain. In both groups, thefrequencies of transitional zone abnormalities were thesame. Castellini studied 200 cases of herniated disks andfound transitional zone abnormalities in 60 patients. Heclassified these malformations and studied their influenceon the incidence of herniated disks. He was able to classifythem into four groups (Fig. 16.1):

• Group I had one or two big transverse processes ofmore than 19 mm in height. There was no pathologicincidence of a herniated disk noted in this group.

• Group II had incomplete unilateral or bilateral sac-ralization. There was a diarthrodial articulationbetween the transversarium and sacrum. This grouphad the highest incidence of herniated disks at thelevel subjacent to the abnormality and also at thelevel of the transition, contrary to generally acceptedopinion.

• Group III represented a unilateral or bilateral fusionof the transverse process to the sacrum. No patho-logic incidence of herniated disks was noted. Noincrease in the frequency of herniated disks at thesubjacent level in relation to normality was notedeither.

• Group IV represented a unilateral fusion witharthrodial articulation of the transverse process withthe sacrum on the other side. The same conclusionsas for group III were noted in this group, except thatthere was no increase in the frequency of herniateddisks.

SPONDYLOLISTHESIS

Spondylolisthesis is relatively frequent. Most authorsagree that about 5 to 7% of the total population is affected,with some variations according to race. Stewart found thecondition in 27.4% of Eskimos, 6.3% of American Indi-ans, and 2.8% of African Americans.

In European countries, the frequency is 1.5 to 3%,depending on the author. Spondylolisthesis can be classi-fied according to a system of stages that depends on thedegree of displacement between the vertebrae, with stage

CHAPTER 16 POSTURAL DISORDERS AND PAIN

91

Figure 16.1

Different types of abnormal transitional lumbosacral joints according to Castellini.

Group I:

large transverseprocess type, usually larger than 19 mm.

a.

Unilateral.

b.

Bilateral.

Group II:

diarthrodial articulation between the transversespine and the sacrum.

a.

Unilateral.

b.

Bilateral.

Group III:

osseous union between the transverse process and the sacrum.

a.

Unilateral.

b.

Bilateral.

Group IV:

mixed type, with the osseous union on one side and a diarthrodial articulation on the other.

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SECTION III PAIN OF SPINAL ORIGIN

I having a displacement of less than 30% and stage IIhaving a displacement of 30 to 40%. Stage III demon-strates spondylolisthesis with a major displacement orsliding of more than 40%. In stage I, the L5–S1 disk isnormal. In stage II, it is slightly degenerated. In stage III,it is completely destroyed where there is also a majordysplasia of L5 (Roy-Camille).

The evolution of spondylolisthesis over time is mostoften asymptomatic if the displacement is under 40%, asis seen in groups I and II. The prognosis is much worsefor patients in stage III. Nevertheless, spondylolisthesiswith significant displacement can long remain asymptom-atic in people who perform heavy work or other activitiesbut can manifest itself by lumbar pain or benign episodicsciatic pain.

The disk subjacent to the listhetic vertebra is most oftenasymptomatic, whether it is normal or demonstrates abenign degeneration on discography. In cases of severesciatica, it is usually the listhetic disk (and rarely thesubjacent disk) that is responsible (Roy-Camille).

The facet joints of the listhetic vertebra, when submit-ted to excessive pressure, can serve as the origins of sciaticpain (Taillard). Frequently, there is involvement of thethoracolumbar junction (Maigne) that can be responsible forlow lumbar pain falsely attributed to the listhetic segment.

Spondylolisthesis is frequent in athletes who start whenthey are very young and whose sport demands hyperex-tension of the lumbosacral spine or repeated falls (judo,gymnastics). Coned lumbosacral radiographic studies ofyoung athletes with lumbar pain can show a fissure of theinternal edge of the isthmus, which can be strengthened byrest. This constitutes the early stage of a spondylolisthesis.

ASYMMETRY OF LUMBAR TRANSVERSE PROCESS ORIENTATION AND FACET JOINT DEVELOPMENT

Asymmetric development of the lumbar facet jointspaces, pedicles, and transverse processes is frequent, par-ticularly in the lower lumbar vertebrae. In studying 550subjects who were without pain, Southworth and Bersackfound 26% to have asymmetric spaces at the L4–L5 leveland 17.4% to have asymmetric spaces at the L5–S1 level.Putti (1936) thought that this asymmetry was a source offacet pain, lumbar pain, and sciatica.

Asymmetry modifies the distribution of the mechanicalpressure. It seems reasonable to assume that it could havesome pathologic consequences. Farfan noted that of 52patients who had operations for herniated disks, 38showed posterior articular asymmetries at the concernedlevel. The herniated disks in 94.7% of cases were localizedcontralateral to the side of the sacralized facet joint.

The unilateral sacralization of an articular space canprovoke a mechanical overloading of the contralateral pos-terior hemiarch and cause an isthmic lysis (Maldague andMalghem). Then the isthmus and the pedicle on the sag-ittal side endure increased mechanical forces, causing acondensation of the isthmus and of the pedicle (anisoco-ria). The evolution can remain stable or continue towarda bilateral isthmic lysis.

SHORT LEG SYNDROME

“Short leg” syndrome is often held indiscriminatelyresponsible for all types of spinal pain. Here we are notreferring to significant shortening of 3 cm or more, whichis part of the orthopedic domain and deserves to be rec-ognized and treated. Instead, we are concerned with smallinequalities of leg length on the order of 1 cm.

Statistical studies have shown that 2 out of 5 personshave one leg shorter than the other, in the 0.5- to 1.5-cmrange. What is the real influence of these inequalities onthe spine? What is their role in the painful pathology ofthe spine? Should the condition be corrected and, if pos-sible, how? Opinions on these points vary.

Evidence

Clinical Evaluation

An inequality in the length of the inferior limbs issuspected when there is a slight lumbar scoliosis withconvexity on the side of the suspected short leg. To verifythe presence or absence of the short leg, the patient isexamined in the following manner. First, the patient isexamined in the standing position, with the legs in a sym-metric stance; the height of the iliac crests and of theposterior and superior iliac spines is then inspected. Thissame examination is performed with the patient in a sittingposition on a hard and horizontal plane, and verificationis made to see whether the scoliosis persists in this posi-tion. It disappears if it is the result of a short leg. Itdisappears also if the patient is made to stand on aninclined plane that compensates for the difference in thelength of the limbs. Finally, with the patient lying down,a comparison of the medial malleolus is performed. Thisgives an approximation that can be fairly exact with prac-tice but it is not enough. This examination has no valuefor acute lumbar pain with lumbar contracture.

Radiologic Evaluation

Radiologic study is the only way to prove the existenceof a short leg. The technique is properly performed withthe patient in the standing position. The x-rays must passhorizontally at the levels of the femoral heads. Tele-radiography can show the entire spine and allows a better

CHAPTER 16 POSTURAL DISORDERS AND PAIN

93

assessment of the effect of the shorter leg on the vertebralalignment. The important point to evaluate is the horizon-tal plane of the sacral endplate.

False and True Short Leg

Radiologic examination will show (a) either the trueshortening of one leg, with its repercussion on the sacralendplate and the spine, inclination of the sacral endplateon the short side, flexion of the lumbar spine (with convex-ity on the short side), and compensation at the level of thedorsal and/or cervical spine, or (b) equality of the two legswith the horizontal plane of the sacral endplates. Clinicalexamination may demonstrate a difference in length; it isa false short leg.

False Short Leg

Piédallu and classic osteopaths consider the false shortleg to be one of the signs of blocking in malposition ofthe sacroiliac joint in “anterior sacrum,” i.e., in positionof nutation. To correct for this malposition, the iliac alais rotated anteriorly in relation to the sacrum. This tech-nique is described under Lateral Decubitus Techniques inExtension (see Section VII titled “Manual Techniques”).After this maneuver is performed, the clinical examinationmay immediately show a return to equal lengths of thelegs and the disappearance of the other signs. The resultingreturn of symmetric leg length is, for supporters of theconcept of sacroiliac blocking, proof of its existence. Thereturn of symmetric leg length is also used to justify thevalue of the signs of the examinations they perform andof the corrective techniques they use.

This interpretation is controversial and highly debat-able. Given what is known about such cases, it would seemmore reasonable to ascribe false short legs to posturalchanges resulting from pain caused by deep lumbosacralmuscular contractures or painful lumbar dysfunctions.

True Short Leg

The true short leg is confirmed by radiologic examina-tion after short leg is noted by clinical impression. Thesestudies are used to confirm a difference of at least 1 cmin the heights of the femoral heads. The position of thesacral endplate is verified by this technique:

• If it is level, asymmetry of the sacrum or of the iliacala compensates the shortening of the leg; then thereis nothing to correct.

• If it is not level, then the possible use of com-pensatory techniques such as the use of the footpadcan be considered.

Determining what therapeutic route will be takendepends on factors such as spinal flexibility and patientage.

Procedural Considerations

Young subject with a flexible spine —

The conditionshould be corrected, and the sacral endplate should bebrought to a horizontal plane. It is safe to start with halfof the correction; the other half can be performed a monthlater. Periodic controls are to be made during the growthperiod.

Subjects with inflexible or stiff spines —

In oldersubjects, one would think that the spine would adapt andthat the use of a heel lift would perturb the acquiredfunctional balance. Nevertheless, there are cases wheretrying a foot pad is reasonable. This is particularly true inpatients presenting with lumbar or thoracolumbar pain,especially in the standing position, which is temporarilyrelieved by vertebral treatments.

During the first month, a heel pad corrects half of thetrue shortening. If the result is favorable and sufficient,the correction is maintained. If it is insufficient, the cor-rection is set at three-fourths of the measured leg lengthdiscrepancy. In all cases, the patient is seen again 3 monthslater.

It is surprising to note sometimes the positive effect ofa heel lift of 5 to 6 mm on lumbar thoracic or cervicalpain, even in cases where the spine is arthrotic and stiff-ened. One can think of it as a favorable modification ofpressure placed on the concerned vertebral segment. It isnoteworthy that there are some patients who feel veryrelieved by a heel lift they have mistakenly placed on theside of the long leg. Does this mean that there is a favor-able mechanical effect regardless of the logic used todetermine which side should be treated, or is this a signalthat we are dealing here with a placebo or purely psycho-logic effect?

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PAINFUL MINOR

INTERVERTEBRAL DYSFUNCTIONS

Many common pain syndromes of spinal origin do notcorrespond to lesions that are radiographically visible. Ourhypothesis, consistent with clinical reality, is that thesepains often have their origins in the painful dysfunctionsof one or more vertebral segments, which we call painfulminor intervertebral dysfunctions (PMIDs). These PMIDsare often the results of trauma, forced movement, or pos-tural or static disturbance.

Spinal manipulation often relieves these benign seg-mental pains, which have a reversible character. Althoughspinal manipulation may be of help, it is not the onlytechnique available to manage this condition and may beinsufficient by itself or even contraindicated.

DEFINITION

PMID is generally a reversible benign, painful, seg-mental vertebral dysfunction of mechanical and reflex ori-gin (Maigne). This term (1964) is purposely vague, sincewe are not certain about the mechanism that generates thebenign painful dysfunction. These dysfunctions appear tobe the common denominator of common local or regionalvertebral pain and can also act as the origin of referredpain:

• Pain associated with the region served by a spinalnerve, most often of its dorsal ramus

• Referred pain due to irritation of some constituentsof the spinal segment (facet joints, ligaments)

• Pain for which a common denominator is the PMID,including also cellulalgic reactions and tenoperi-osteal or myalgic reflexes (segmental vertebral cel-luloperiosteomyalgic syndrome of Maigne)

DIAGNOSIS

The diagnosis of PMID is based on finding a painfulspinal segment on segmental examination and on theabsence of any clinical or radiologic features revealing asignificant pathologic process. The absence of these fea-tures allows one to conclude that a benign mechanicalprocess is the cause of the pain.

In Chapter 20, in the section titled “Physical Examina-tion,” we discuss the segmental examination in detail. Fornow, in brief, the examination consists of examining eachspinal segment (Fig. 17.1) by selected palpation maneu-vers. These maneuvers do not provoke pain in normalsegments but are painful in the symptomatically involvedsegment. These maneuvers are always painful in cases ofa PMID (Fig. 17.2).

Figure 17.1

Mobile segment of Junghanns.

a.

Lateral view.

b.

Frontal view.

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The segmental examination consists of the following:

• Axial pressure on the spinous process.• Transverse pressure against the spinous process. In

PMID, pain is most often elicited by pressureapplied in one direction (from right to left or fromleft to right), but in some patients, it may be presentin both directions. This maneuver provokes verte-bral rotation about an oblique axis.

• Friction overlying the facet joints. Facet joint painto palpation is a constant sign in PMID. It is usuallypainful on one side only.

• Transverse pressure on the interspinous ligament ofthe concerned segment, performed with the tip ofthe finger or, better yet, with a key ring, is oftenpainful (inconstant sign).

DIFFERENTIAL DIAGNOSIS

Segmental pain uncovered by segmental examinationdoes not necessarily point to or indicate a diagnosis ofPMID (Fig. 17.3). The segmental examination helps tofocus attention on a segment that needs to be explored.Among the common causes of segmental pain other thanPMID are inflammatory conditions, spondylosis, and diskherniations.

Acute Synovitis

It is not necessary for the spondylosis to be radiologi-cally severe to present as an episode of acute synovitis.

Figure 17.2

A segmental examination uses maneuvers that allow studies ofdifferent segmental vertebrae. The examination is usually nonpainful in normalsegments. If pain is provoked, it suggests the existence of underlying pathol-ogy of the segment. This pathology may be benign or malignant. This deter-mination can only be made in the context of further clinical and radiologicevaluations.

a.

Axial pressure.

b.

Transverse pressure on the spinous process.

c.

Friction pressure over the facet joint.

d.

Transverse pressure on the inters-pinous ligament.

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Usually, the cervical spine is involved. It can be difficultto differentiate between mechanical causes of pain andacute synovitis, particularly when the examination revealssevere painful sensitivities of several of the facet jointsand when mobilization is painful in all directions. It iseven more difficult when only one facet is affected. Thetests of repeated mobilization centered on the concernedspinal segment can aid in the diagnosis. The spinal seg-ment is usually painful in one direction, right or left, ifpain is due to a PMID; the spinal segment is always painfulin both directions if pain is due to an acute synovitis.

Confusion in determining the suitability of manipula-tive therapy for this type of condition is rare, although theuse of manipulation in the case of synovitis could aggravatethe condition. The reason that little confusion surrounds thisissue is that when the rule of manipulation only in the pain-less range of motion — the rule of no pain — is used, thelack of any range of movement that is nontender woulddictate that no manipulation be performed.

PMID and Herniated Disks

The situation is somewhat different with regard to her-niated disks. Manipulation can be of utility in some casesof disk degeneration characterized by disk bulge or a truehernia, as can, at times, be seen in sciatica. A herniateddisk is not a minor dysfunction. There is no problem interminology when a herniated disk is irritating a nerveroot.

But some situations are less clear; e.g., on examinationa painful segment demonstrates a discopathy with a diskbulge but without a radicular pain syndrome. Is the disc-opathy directly responsible for the segmental pain, or hasa PMID been fostered by this discopathy?

If manipulation is possible and produces a lastingrelief, does this mean that we are dealing with a case ofPMID? If the clinical findings and the development of thecondition demonstrate that the symptoms are due to thedisk lesion itself, then support for the diagnosis of PMIDwould not be as clear. This situation is seen often in dailypractice. In fact, the issue is more one of semantics, whichhas little bearing on the actual outcome of these cases.

DIFFERENT TYPES OF PMIDS

PMIDs can be acute or chronic, active (responsible forpain) or latent (not responsible for pain).

Acute PMIDs

PMIDs can present acutely. They occur most often asresults of sudden movements or strenuous efforts and areaccompanied by strong muscular spasms.

Chronic PMIDs

Chronic PMIDs are the commonest forms of PMIDs.They usually develop without initial acute phases. Whena PMID is responsible for chronic episodic pain, the find-ings on examination are constant, though attenuated, andpresent even during the nontender phase of the condition.This should be emphasized, as it is very important formaking the diagnosis. The same is true for the cellulalgictenoperiosteomyalgic chronic PMID.

Active PMIDs

Active PMIDs are responsible for pain, either directlyor through celluloperiosteomyalgic and neurotrophic man-ifestations.

Latent PMIDs

Sometimes a segmental vertebral examination demon-strates subclinical PMID not associated with episodes ofspontaneous or ongoing pain. In fact, these segments arerarely totally “inactive” but cause only very slight discom-fort or occasional mild pain that is quickly forgotten andis usually ascribed to other causes such as stiffness orfatigue.

LOCALIZATION AND NUMBER

PMIDs can be found at all levels of the spine. However,it is especially frequent in the segments of the transitionalzones of the spine.

For a given region, there is usually only one segmentinvolved with PMID. Rarely, two adjacent segments maybe involved. Involvement of three segments is very rare.

Figure 17.3

PMID due to a benign painful dysfunction of thespinal segment, which is mechanical in nature and reflex inorigin. The segmental examination (Maigne) allows one todemonstrate the painful dysfunction

of the spinal segment.

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In the same patient, however, it is not rare to find severalnonadjacent segments involved with PMID, some asymp-tomatic, some not, localized to different spinal regions,such as the cervical and thoracic regions.

ASSOCIATION OF PMID AT DIFFERENT LEVELS

Finding PMID at different spinal levels is rather fre-quent in chronic cases. In a patient with chronic lumbarpain coming from L4–L5, the examination will often showsome PMID localized to T12–L1, C6–C7, and C2–C3 ora nearby segment; the PMID may simply be examinationdiscoveries or may be responsible for the production ofpain. PMIDs are almost always present with painful facetjoints on the same side, right or left, at all levels. Theyare generally at the level of the transitional zones of thevertebral column. Thus, a “syndrome of the transitionalzones” can be defined (Maigne) by the association andgrouping of these painful segments (see Chapter 61,“Transitional Zone Syndrome”).

PMID AND PAIN THRESHOLD

Certain PMIDs can remain asymptomatic (inactiveMIDs) or disappear spontaneously without having pro-duced discomfort. Others manifest themselves by episodicpain, while the examination demonstrates findings thatpoint to the involved segment and can persist during non-painful periods.

Thus there is a threshold of tolerance at which thePMID provokes pain and below which it may not provokeany. This threshold varies from one patient to another andcan vary over time in the same individual. Some patientshave low thresholds and others have high thresholds. Psy-chologic factors may play a role, especially in cases ofdepression or anxiety.

Spasmophilia (with all the reservations this term canarouse) is a frequent factor capable of potentiating PMIDby lowering the tolerance threshold and by neuromuscularhyperexcitability, but the threshold of pain can also bealtered by:

• Mechanical factors aggravating PMID, such asstrenuous effort, poor posture or position at work orduring sleep, or forced movements.

• Internal, digestive, gynecologic, or other organiccauses or a state of fatigue due to overwork or lackof sleep that decreases the tolerance of the subject.

• External causes, such as exposure to irritations suchas cold or air drafts that will increase the sensitivitiesof tissues. It seems also that the PMID can be reacti-vated or become symptomatic by irritation of one

of the cellulalgic, tenoperiosteal, or myalgic mani-festations that it provokes, as we shall see in Chapter18, “Segmental Vertebral Cellulotenoperiosteomy-algic Syndrome” (Maigne).

TREATMENT

There is no standard treatment for PMID. The treatmentmust be tailored according to the underlying cause, thegeneral state, the vertebral state, and the state of the areaand associated neurotrophic manifestations.

Acute Cases

Treatment often consists of immobilization, but facetjoint injection or manipulation can be used in many cases.

Chronic Cases

Manipulation is often the treatment of choice. For var-ious reasons, it can be contraindicated in some cases.Articular injection is useful in cases of strong para-articular reaction; injection of the interspinous ligamentis sometimes necessary. When manipulation and infiltra-tion are contraindicated, electrotherapy in association withmodalities such as diathermy, and ultrasound is the besttreatment. Local treatment of the associated cellulotenoperi-osteomyalgic manifestations is often indispensable.

Treating the whole patient is important. Many PMIDsstart only if the tolerance of the patient decreases, as isseen in fatigue, depressive states, spasmophilia decompen-sation, and concurrent illnesses. Postural disorders shouldget attention, and the patient should be re-educated andmade aware of incorrect postural habits.

Recurrent PMID

Patients often present with painful syndromes whoseconnections with PMID are well established. They aretypically relieved by the treatment, but the conditionrecurs 3 or 4 months later. Usually examinations of thesepatients reveal the same PMID, and the same maneuverproduces relief in one or two sessions. Between two pain-ful episodes, the segmental examination often demon-strates a progressive reappearance of the PMID. ThePMID in these cases often remains latent for long periodsof time before again becoming symptomatic.

The causes of these recurrences are multiple. Poor pos-tural habits are most often the cause. The cervical spinecan be affected by sleep positions, especially sleeping onthe abdomen, which results in excessive rotation of theneck, made possible by the increased laxity of the musclesduring sleep. It can also be due to repetitive occupationalmaneuvers such as turning the head to look at somethingbehind or making numerous movements in parking a car.

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Seats or work stations can also be the causes. All theserecurrent factors should be looked for attentively duringthe interview. “Short legs” or postural disorders of the feetcan sometimes be found on examination, but their cor-rection rarely produces the solution.

The syndrome of the transitional zones (Maigne; seeChapter 18) can be a cause of these chronic and recurrentpains and should be investigated. As we have seen, it ischaracterized by the existence of PMIDs on several spinalsegments belonging to transitional vertebral zones. Evenwhen latent, the syndrome of the transition zones can facil-itate the recurrence of the PMID. In these cases, all thepresenting PMIDs should be treated.

Finally, the persistence of neurotrophic manifestationssuch as cellulalgia (see page 103) depending on the PMID,infiltrates; and trigger points, from which arise nociceptiveimpulses and which contribute to the maintenance of avicious circle, should be treated. Physical therapy is essential.

Should Latent PMIDs Be Treated?

Latent PMIDs should be treated if they seem to con-tribute to the maintenance of other PMIDs that are active(see Chapter 18), provided they are isolated and theirtreatment is easy. Otherwise, they should be watched reg-ularly, and the patient should be aware of the positions ormovements to be avoided.

DO PAINFUL MINOR INTERVERTEBRAL DYSFUNCTIONS HAVE VISCERAL REPERCUSSIONS?

The segmental dysfunction that produces somatic neu-rotrophic manifestations probably has repercussions onthe sympathetic visceral system. However, if effects onthe sympathetic visceral systems do exist, as has been thehypothesis of osteopaths, no objective clinical demonstra-tion yet exists.

In the practice of manipulative therapies, clinical obser-vations sometimes suggest that some minor visceral func-tional disorders may be related to PMIDs, especially thosearising from the thoracolumbar region, which can beaccompanied by flatulence or constipation that disappearsafter vertebral treatment. Flatulence can be exaggeratedin the hours following manipulation. But given these fewfacts, we are unable to leap to the conclusion that the spineis at the origin of most functional disorders or organicvisceral disorders.

HYPOTHESES ON MECHANISM OF PMID

The notion of PMID is perfectly consistent with thefindings of a clinical examination, but the mechanismprovoking this dysfunction is not evident.

It is logical to look first for a mechanical element, notvisible on the radiographs, that is capable of explainingthe segmental dysfunction. If such a reversible lesion wereto exist, it would most likely have to involve the disk orfacet joints.

Possible Role of Discal or Facet Joint Pathology

Discal Pathology

Discal pathology modifies the function of the mobilesegment, often resulting in stress on the facet joints. Someauthors (Copeman, Taillard, Brugger, and others ) consider(and rightly so) facet joint dysfunction to be an additionalsource of pain in the herniated disk.

One can imagine that some intradiscal lesions, althoughunrevealing alone, could cause painful dysfunctions of thefacet joints or of the interspinous ligaments. This couldbe a mechanism of PMID that could possibly explain thebeneficial effects of manipulation that would unlock theincarcerated disk fragment.

If there are cases where this mechanism could occur,the PMID is most often localized to segments where thedisk appears normal on radiographs and remains so forsome years. Moreover, some MIDs are seen at superiorcervical levels that lack disks. The role of the disk lesioncannot, therefore, be rejected but does not provide a suf-ficient explanation for the vast majority of cases seen.

Facet Joint Pathology

The common lesions of these articulations capable ofgiving rise to mechanical dysfunction are essentiallyarthrosis and malformations. Some authors have also con-sidered the role of meniscoid formations in the causes ofthese lesions.

Spondylosis —

The segmental examination of a patientwith a facet spondylosis is usually painless. It becomespainful only in the case of an acute synovitis.

Can it favor PMID? It may be possible although mostarthrotic segments are painless on segmental examination.When there is PMID on these arthrotic spines, it is alsofound frequently on the segment that is apparently theleast affected. In some cases, the arthrotic state of thesegment seems to complicate the PMID, make the treat-ment more difficult, and foster recurrences. Most often,the spondylosis seems to foster segmental stiffness, morethan does the PMID.

Articular malformations —

Articular malformationswere previously described. Remember that Putti (1927)gave to the facet joints the usual responsibility for lumbarpain and sciatica. Besides the arthrotic lesions, he gavesome importance to their asymmetry of surface and ori-entation. These lesions can now be uncovered on com-puted tomography sections, but nothing has been found

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that would convincingly prove the causal connectionbetween these facet tropisms and painful states.

Gillot and Freudenberg noticed the frequency of suchabnormalities at the level of the lumbosacral spine. Theother vertebral regions have not been studied as far as weknow. Gillot also emphasized the frequency of transversecrests on the surfaces of the lumbosacral articulations andthought that they could be responsible for “joint block-age.” Farfan noted that these crests are frequent in oldpeople or in people with significantly developed discopa-thy at the same level, but they do not play any role inpossible blockage. While these lesions may explain certaincases of segmental dysfunction, they do not explain allcases.

Meniscoid formations —

Some authors have thoughtthat they could explain the favorable actions of manipu-lations by the release that they would cause to intra-artic-ular blockage of the meniscoid formation (see “SpinalManipulation” in Chapter 22).

Entrapment of a meniscoid formation would result inalteration in tension of the richly innervated facet jointcapsule to which it is attached, resulting in reflex muscleguarding. The latter then further increases capsular tensionand thus propagates a vicious circle.

This fascinating mechanism evoked by Kos (1972) wasrefuted by many. Taking up their anatomic study, Bogduk(1984) noticed that most of these “meniscoid” formationshave a form that could not permit such a blockage, andeven if this blockage could be possible, the laxity of itsbase would preclude any increased tension on the facetjoint capsule.

According to Giles (1986), this is incorrect as far asthe lumbosacral articulations are concerned. He criticizedBogduk’s study, which concerned only the lumbar artic-ulations and not the lumbosacral articulations. At thatlevel, as at the cervical level, Giles noted two types of“synovial inclusions” that were susceptible to entrapmentbetween the articular surfaces during some movementsand thus resulted in increased tension on the facet jointcapsule, with associated reflex muscle guarding. They area large, fatty vascular inclusion localized at the inferome-dial aspect of the joint and a dense and fibrous inclusionarising from the ligamentum flavum and localized to themedial aspect of the joint. This discussion is very inter-esting, but the PMIDs are found not only at the cervicallevel but also at the level of L5–S1.

The problem is to know whether these synovial foldsare innervated. According to Mooney and Robertson(1976), the synovial membrane is richly innervated, butthey did not produce any histologic proof. According toWyke (1981), there are no nerve endings of any kind insynovial joints or in the pseudomeniscus of these articu-lations. Giles and Taylor (1982) showed, by the silverimpregnation method, the existence of nerve endings inthe synovial folds of the inferior lumbar facets that “seem

to be some afferent nerves having probably a nociceptivefunction.” If these studies are confirmed, it will remain tobe shown that these endings exist at all levels of the spine.

Reflex Mechanism

Most of the PMIDs seen in daily practice are localizedat vertebral segments that seem devoid of disk or facetpathology, in the present state of possible investigations.We must remark, however, that in the particular systemthat is the spine, with a strictly automatic functioning, itdoes not seem necessary to think of the existence of apermanent mechanical element to explain a lasting seg-mental dysfunction.

Both a single macrotrauma as well as repetitivemicrotrauma can lead to dysfunction of the facets or inter-spinous ligaments and lead to reflex muscle guarding toprotect the segment. Muscles spanning one or two verte-bral segments having rotary functions appear to play dom-inant roles. This muscle guarding can only partially pro-tect the involved segment, given the enormous lever armsplaying on the sensitive elements during rapid forcefulmovements or during some positions. There are perpetualopportunities to reactivate the vicious circle and maintainit. This characteristic of vertebral functioning can be illus-trated as follows. If one suffers a slight ankle sprain, onelimps, if one walks without thinking (automatic walk),because the painful stimuli coming from the affected lig-ament create a functional blockage that tends to maxi-mally immobilize the joint. But if one does not want tolimp and if the pain can be mastered, it may be possibleto impose normal movement on the muscles and the jointand use the foot normally. This is not possible at thevertebral level. The most courageous person can neithernormally straighten out with acute lumbar pain nor obligethe neck to be flexible with torticollis (wryneck). Anyattempt to overcome the blockage will only exaggeratethe reflex muscle action. Because of the automatic func-tioning of the axial spinal muscles, volitional control overthese muscular groups or on such vertebral segments islost. Spinal motion is a global movement. It brings intoplay a significant number of muscles with complex inser-tions that must function in perfect synergy to perfectlydistribute the loads imparted on the mobile segment duringmovements or efforts. The proprioceptive impulsesrelayed to the spinal cord come from the richly innervatedspinal ligaments, muscles, and facet joints.

If a spinal segment becomes painful, there is an imme-diate response from the muscles that tend (without reallysucceeding because the pressures are powerful) to func-tionally block or splint segmental motion. These pressureswill self-reactivate perpetually unless there is completerest of the region and this parasite circuit. The persistentreflex produces a functional surcharge at the level of theconcerned muscles, which becomes a source of pain,

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while with time, periarticular reactions settle in. The out-of-control mechanism has a progressively reduced ten-dency to spontaneous normalization. Everything tends tomaintain it, at least while the pressure weighing on theconcerned segment from weight persists. Often, tempo-rarily resting the affected segment (bed, collar, etc.) willbreak the self-maintained mechanism.

It is not always easy or possible to rest a reflex alreadyput into action. The dorsal ramus of the spinal nerve isalso concerned; it innervates these joints and muscles. Itis wrapped against the articular pillar, as Lazorthes hasshown, and its medial branch passes through a narrowmuscular passage composed of the mamillomamillary andmamillostyloid bundles (Winckler), both of which areaffected by reflex muscle guarding.

In this mechanism of maintained pain, the role of algo-genic substances, resulting from the irritation of the nerve,is also to be considered.

The reflex that maintains the PMID is probably not justlocal. As seen in Chapter 18, PMID is often accompaniedby reflex modifications of the sensitivities of the tissues(skin, muscles, tendon, periosteum) and even of their tex-tures (cellulalgic thickening, indurated myalgic cords) ina metameric distribution. This is why a thickening of thecutaneous fold, painful under the “pinch–roll” maneuver,is practically constant in the cutaneous area of the dorsalramus of the spinal nerve corresponding to the PMID. Thenociceptive influx coming from these “cellulalgic condi-tions” and from these myalgic cords “maintains thevicious circle which contributes to the maintenance of thesegmental dysfunction.”

The PMID appears as the common denominator of agreat number of common vertebral pains, either directlyor through the reflex manifestations that they determine,which can be responsible for or may misleadingly producepseudoradicular, pseudovisceral, or pseudopara-articularpain syndromes.

PMID AND FACET SYNDROME

The term ‘facet syndrome” is, at present, very much inuse. Ghormley was the first to use it in 1933. This termimplied that facet joint arthrosis was responsible for theorigin of sciatica. He was not the first to suggest a rolefor these joints in sciatic pain. Others pointed it out beforehim: Goldthwait in 1911, Danforth in 1925, Putti in 1927,and Ayers in 1927. Ghormley was the first to give it aname that was going to be used. He was also the first todemonstrate radiographic evidence of the narrowing of theintervertebral foramen. This was considered to be thecause of sciatica and felt to be due to facet joint arthrosisor to an excessive encasing of these articulations. Heemphasized that he could cure sciatica with a facetectomy,but he advised fusing the facet to a lumbosacral and sac-

roiliac graft. At that time, the sacroiliac articulation wasthought to be a common source of lumbosacral pain and,according to Ghormley, was part of the facet syndromesince it was a synovial articulation.

Shortly thereafter, Mixter and Barr, with their publica-tion in 1934, began the period of the disk that overshad-owed “facet syndrome” until the publication by Rees in1971 of “Multiple Bilateral Percutaneous Rhizolysis ofSegmental Nerves in the Treatment of the IntervertebralDisc Syndrome,” with which he had 99.8% success (i.e.,denervation of the posterior articulations of the last threelumbar levels, which he performed with a scalpel, using thepercutaneous approach). His work was taken up by Shealy(1974), who proposed denervation of the facets by “percu-taneous radiofrequency rhizotomy” under fluoroscopic guid-ance — a technique later used by numerous authors.

The term “facet syndrome” was taken up again byMooney and Robertson (1975), who proposed to extendit to the pain referred into the inferior limb from the facetsof the last lumbar segments. They also proposed the useof a “facet block” for diagnosis of this condition, i.e.,anesthetic injection performed under fluoroscopic controlin the three contiguous articulations from which the painwas supposed to come. In case of success, percutaneousrhizotomy was performed on these three articulations, i.e.,the last three lumbar segments. In the English literature,the term “facet syndrome” is usually used to designate thepains coming from articulations that are arthrotic or unstabledue to discal pathology and concerns only the inferiorlumbar articulations.

Facet joint tenderness is a consistent finding in whatwe have defined as a PMID. One could, seeing thingssuperficially, consider this facet tenderness of a PMID a“facet syndrome” since, in some cases, facet joint injectioncan effectively relieve the patient. This does not explainthe usual pain of the other constituents of the mobilesegment. If the facet tenderness is often dominant in thePMID, it is sometimes secondary to the pain of the inter-spinous ligaments or of a muscle directly affecting thesegment in question. Moreover, these MIDs are seen atall levels of the spine, not only at the inferior lumbarregion, and most often, no lesion is seen on radiography.

Since 1960, we have used facet blocks at all levels ofthe spine to determine the role of the facet joint in referredpain when the segmental examination as described in thisbook demonstrates a precise pain of that articulation. Thefacet block has provided us with a means of studying therole played by facet joint dysfunction of the inferior cer-vical spine in the generation of interscapular mediodorsalthoracic pain (1964), in some pain syndromes of the shoul-ders and epicondyles and of the superior cervical spine innumerous headache syndromes, and, a little later (1970),the role played by the thoracolumbar junction in some lowback pain syndromes.

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PMID AND “OSTEOPATHIC LESION”

Osteopaths and chiropractors, convinced of the effica-cies of their manipulations, have tried to justify their usewith concepts such as the “osteopathic lesion” (osteo-paths) and “subluxation” (chiropractors). A subluxationwould show itself by a deviation of the vertebra, revealedby palpation. Radiographs could show it objectively. It istreated by manipulation, which is supposed to “readjust”the subluxation.

The osteopathic lesion (referred to as “somatic dys-function”) is defined as a dysfunction of the vertebralsegment characterized by a modification of its mobility— hypomobility most of the time, hypermobility some-times. Osteopaths state that the aim of mobilization is to“restore the normal joint play” of the concerned segments(Fig. 17.4; see also Chapter 22, “Spinal Manipulation”).Osteopathic medicine makes no reference to pain pro-voked by these maneuvers in the vertebral segment. (Thenotions of hypomobility and hypersegmental mobility arefundamentally different from the concept entertained in“minor intervertebral derangements” of Dr. Maigne,which are defined as painful dysfunctions.) This essentialpoint is found in the osteopathic literature and has been

confirmed to us by some American osteopathic authorities.The concept of segmental dysfunction, founded only onthe loss of segmental mobility, has been adopted by mostschools of manual medicine in the world.

The concept of “painful minor intervertebral dysfunc-tion,” or PMID (Maigne), on the contrary, defines a minordysfunction whose characteristic feature is pain. The con-cerned segment is painful when it is called into play bymaneuvers exaggerating its movements. In our definition,we do not take into account the mobility of the segment,inasmuch as it can be noted. Besides, it is reasonable tosuppose that only a segment whose functioning is painfulcan be at the origin of nociceptive influxes sufficient toresult in or produce local referred pains.

CONCLUSION

The concept of PMID gives a medically acceptable andclinically logical substratum to the use of manipulations.It also widely extends beyond the frame of this therapeuticmeans, since it explains a great number of common ver-tebral pain syndromes for which manipulation is notalways indicated.

Figure 17.4

“Osteopathic lesion” with regard to somatic vertebral dysfunction. This is, above all, defined by osteopaths as amodification of vertebral segment mobility. It is believed to consist most often of hypomobility; sometimes, however, hypermo-bility is cited. The diagnosis of hypomobility or hypermobility is made by palpation of the spinous processes and by movementof the transverse processes.

A.

An osteopathic lesion (in segment GH) indicated by “segmental movement restriction.” Thespinous processes of vertebrae G and H separate poorly during the flexion movement. This is described as a lesion in“extension.” The inverse of this is noted in

B,

where the spinous processes of vertebrae G and H come together poorly in themovement of extension. This is called a lesion in “flexion.” One could create similar schemes for rotation and lateroflexion.

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18

SEGMENTAL VERTEBRALCELLULOTENOPERIOSTEOMYALGIC

SYNDROME*

Under the title of “segmental vertebral cellulotenope-riosteomyalgic syndrome” (SVCPMS), we describe agroup of palpable modifications of the texture and sensi-tivity of the soft tissues — cutaneous (cellulalgia), mus-cular taut bands, with or without trigger points, and teno-periosteal (in relation to a segmental spinal dysfunction).These manifestations are localized to a constant territoryfor a given spinal segment. Clinically, this territory corre-lates well with that of the corresponding nerve root, butat some levels, the cellulalgia extends beyond this area,and a cellulalgic zone can be common to two or threeadjacent spinal segments.

The manifestations

of this syndrome can be active andresponsible for pains that are often misleading: pseudo-radicular, pseudopara-articular, or pseudovisceral. Theycan also be latent — discoveries found only onexamination.

In the framework of common pain syndromes, the mostfrequent cause of segmental dysfunction responsible forthese manifestations is “painful minor intervertebral dys-function” (PMID). Segmental dysfunction can also be dueto a herniated disk or an acute synovitis or spondylosis.

By systematically palpating the muscles and cutaneoustissues in common radicular sciatica and in femoral neu-ralgia, we have noticed the existence of trigger pointswhose mechanism of appearance seemed different to us,since it was tied to the spinal segmental dysfunction.These trigger points were always localized to the samemuscles and often to the same parts of these muscles forthe same roots.

Another remarkable fact is that they were often associ-ated with a localized zone of cellulalgia specific for L5,S1, L3, and L4 and demonstrated similar findings with the

pinch-roll maneuver (Fig. 18.1). These manifestationscould disappear with the termination of the episode orcould persist partially and sometimes be responsible forchronic pain (Maigne, 1961).

Given their distribution, these manifestations seemedto be tied to the irritation of the dorsal primary ramus ofthe spinal nerve, especially since they did not refer to thelower limbs as in the case of pure lumbar pain (withoutsciatica) coming from L4–L5 or L5–S1. Later, we wereable to note the existence of such manifestations in casesof segmental dysfunction without radicular pain syndromein the trunk and upper limbs (Fig. 18.2).

It is from these remarks that the “celluloperiosteo-myalgic syndrome of the segmental vertebral dysfunction”was described (Maigne 1968).

“Vertebrospinal” syndromes fostering some pain withnonradicular topography have been described. They areessentially referred pains provoked by experimental irri-tation of different vertebral structures (Kellgren, Fein-stein), as discussed above (see “Interspinous Ligaments”in Chapter 14). They are pains felt by a patient in a givenarea and not modifications of texture or sensitivity of thetissues found on the palpation examination.

Later in this chapter, we discuss the studies that havepointed out, in the past and under different names (myo-gelosis, hartspann, trigger points), in the centers of somemuscles, the presence of indurated cords responsible forlocal or radiating pains. These cords can be thought of asan explanation for the surcharge of activity due to forcefulmovement, static problems, or fatigue.

Some authors in a few isolated cases have thought ofa possible vertebral origin for a cellulalgia responsible fora pseudovisceral or referred pain (May et al., Judovich

* In this book, we use the terms

segmental vertebral cellulotenoperiosteomyalgic syndrome

(SVCPMS),

segmental vertebral neurotrophic syndrome

(SVNS) and, more briefly,

segmental vertebral syndrome

(SVS) interchangeably to designate this syndrome and its manifestations.

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and Bates). Others have described some modifications oftexture and sensitivity of muscles and of paravertebraltendons (systematic tendinomyositis) in the neighborhoodof the involved segment by vertebral or sacroiliac dys-function

(ecole osteopathique).

Brugger also described“tendinomyose” tied to the distress of the joints of the

limbs and of the facet joints provoked by postural disor-ders. For example, he mentions the reflex tendomyosis ofthe musculature of the cervical or thoracic spine tied to afacet joint dysfunction and the reflex tendomyosis of theparaspinal and gluteal muscles tied to dysfunction of thelumbar facet joints.

Figure 18.1

Cellulalgic, myalgic, and tenoperiosteal manifestations that one can find by palpation of the sciatic nerves L5 (

a

)and S1 (

b

). Dark zones represent trigger points, gray zones represent cellulalgic zones, and circles represent painfultenoperiosteal sites.

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105

As far as we know, however, no one described beforewe did the neurotrophic changes systematically uncoveredby palpation in the presence of segmental spinal dysfunc-tion localized to a constant area for a particular segment,essentially that of the dermatome, which involved simulta-neously the skin and subcutaneous tissues (cellulalgia), themuscles (trigger points), and the tenoperiosteal insertions.

CLINICAL MANIFESTATIONS OF SEGMENTAL VERTEBRAL SYNDROME

Segmental dysfunction usually alters the sensitivity andtexture of the soft tissues detected by careful palpation ofthe cutaneous, muscular, and tenoperiosteal tissues. Thesesoft tissue manifestations are consistently found in thesame locations in the involved tissues in a manner uniqueto each segmental level and in the territory of the corre-sponding spinal nerve root.

These cellulalgic, tenoperiosteal, and myalgic manifes-tations always affect the same muscles, the same cutane-ous zones, and the same tenoperiosteal insertions for agiven spinal segment. This altered soft tissue sensitivityand texture associated with segmental spinal dysfunctionconstitute the SVCPMS (Maigne). For a given spinal seg-ment, this syndrome groups:

• Skin and subcutaneous swelling and induration inall or part of the dermatome

• Indurated myalgic cords (trigger points) localizedin some muscles of the myotome

• Hypersensitivity of the tenoperiosteal insertions(entheses) of the sclerotome on palpation

Embryologically, “sclerotome” refers to that part of thesomite that will develop into the axial skeleton (spine). Inthe English literature, however, this term is currently usedto indicate also the bones of the limbs developing fromthe same somite. This is the meaning we use in this book.

These manifestations are reversible and disappearwhen the segmental spinal dysfunction resolves. Inchronic cases, however, they can become organized andpersist autonomously. They are usually unilateral, and allare localized to the same side, the side of the dysfunctionalfacet joint uncovered by the segmental examination. Theycan be bilateral if the dysfunction is also bilateral, but thisis rare.

All the elements of this syndrome need not necessarilyalways present together. Especially in the trunk, cellulal-gia is generally an isolated manifestation. To find mani-festations, the palpation examination should be thorough,with side-to-side comparisons and include adjacent zones.

Segmental spinal dysfunction can lead to perturbationsthat are more extensive than the ones perceived only byclinical examination. In practice, however, we can relyonly on the clinical examination and note the radiculartopography of their distribution.

Figure 18.2

Cellulalgic, myalgic, and tenoperiosteal manifestations that can be found on palpation in cases of C5–C6segmental dysfunction (see the explanations for the various zones in Fig. 18.1). Areas shown here are only those most commonlyfound.

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Some overflow is possible; there are some areas wherecellulalgia has a topography common to two or three adja-cent spinal segments. This is the case in the cervical spineand, to a lesser degree, at the thoracolumbar junction. Thesame trigger points of a given muscle can also be facilitatedby dysfunction of two adjacent spinal segments, which isnormal, since all muscles (with the exception of the rhom-boids) are innervated by more than one spinal nerve root.

These manifestations, generally improved by spinal treat-ment, can sometimes be responsible for local, regional, orreferred pains that are often misleading. They also constitutea source of nociceptive influx maintaining a vicious circle.

This SVCPMS gives a better understanding of the per-sistence of some pains and explains why some purelyspinal treatments often instantly relieve the tendinous,muscular, or pseudovisceral signs and symptoms thatotherwise do not appear to have a spinal source.

Cellulalgia

Cellulalgia, or skin and subcutaneous tissue irritability,is the most frequently seen manifestation and the only oneeasily detectable in the trunk. It is characterized by

increased texture thickness with acute tenderness to thepinch-roll, the key maneuver of this examination.

Examination: “Pinch-Roll” Test

To perform the pinch-roll examination, a fold of theskin is pinched firmly between the thumb and index finger.Tension is applied to the skin fold as it is rolled betweenthe fingers in one direction and then in the other — as ifrolling a cigarette — maintaining a firm pinch throughout.The pinch should never be released during the maneuver(Fig. 18.3). It is better to use both hands for this maneuver.

The examination should be performed bilaterally andsymmetrically throughout all cutaneous surfaces. Consis-tent pressure is necessary. The examination is generallyperformed over the trunk from inferior to superior andtransversely for the limbs. All the tender cutaneous areascovering a wide zone should be explored. This maneuver,apparently simple, requires a certain practice to be per-formed appropriately. It should be measured by perform-ing the same examination on a nontender or normal cuta-neous zone. In practice, several trials with differentdegrees of pressure should be made, comparing both sides.

Figure 18.3

a.

Pinch-roll maneuver at the lumbar level.

b.

Different phases of the pinch-roll maneuver. Using both hands,grasp the skin between the thumb and index finger, firmly pulling it away from the underlying tissue, continually maintainingtraction as it is rolled upward. In the course of this, a pinch-roll motion is carried out.

CHAPTER 18 SEGMENTAL VERTEBRAL CELLULOTENOPERIOSTEOMYALGIC SYNDROME

107

Of the involved zones, two observations can be made:

• The skinfold is thickened.• The maneuver is very painful.

The thickening of the fold is more or less significant,depending on the region of the body and on the subject.Sometimes, the fold is very thick and firm, giving theimpression of a sausage between the fingers; at othertimes, it is so edematous that it is impossible to graspbetween the thumb and index finger. In some subjects, thethickening is hardly noticeable; only pain is present.Often, these persons have thin skin. Pain on the pinch-rollexamination is constant and sometimes intolerable if thepinch is a little firm in the involved zone. As for thethickening of the fold, comparison should be madebetween the symmetric zone and the adjacent zones whilemaintaining an equal pressure.

In some subjects, especially obese women with signif-icant diffuse global thickening of the soft tissues andregions of subcutaneous fat deposition (nape, shoulders,arms, loins, buttocks, hips, internal side of the knee, etc.),examination may be difficult because of unilateral, cellu-lalgic, and limited zones tied to a segmental vertebralsyndrome (SVS). Nevertheless, in these subjects, it is gen-erally possible to find a true hypersensitivity in a smallzone of involvement in relation to the contiguous zonesin the same nerve root distribution.

The “pinch roll” test when positive should conform toa segmental topography. Random reports of discomfortshould not be taken to be a positive test.

Topography

The affected zone is more or less extensive. It coincideswith all or part of the dermatome and is usually unilateral.In the trunk, especially over the dorsal aspect, its topo-graphy coincides reliably with the cutaneous area of thedorsal primary ramus of the corresponding spinal nerve

.

It gives the only semiologic sign that is convenient(Maigne).

Careful study of the dorsal cellulalgic zones at ourclinic in relation to the involved spinal segments hascaused us to reconsider the cutaneous path and distributionof these posterior rami. We noted that they did not alwayscorrespond to the generally accepted sensory distributions(C4, T2, T12, L1, L2) as depicted in classical dermatomalmaps. Verifications by dissection have confirmed our clin-ical findings.

Over the ventral aspect of the trunk, the cellulalgiczones are found in the areas corresponding to the usuallyaccepted areas of the dermatome. They are less constantthan are those over the dorsal region (Fig. 18.4).

In the lower limbs, the cellulalgic areas of L2, L3, andL4 also correspond to the classical dermatomes, while theareas of L5 and S1 are reduced to a very limited zone.

Figure 18.4

Cellulalgic zone involved in segmental dysfunction of T9–T10 and T12–L1. These zones are situated in the territoryof cutaneous branches of the corresponding posterior primary rami overlying the torso.

a.

Constant findings of the anteriorbranches overlying the abdomen.

b.

Findings not constant.

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What is noticeable for these last two segments is that thecellulalgia exists only when the segmental dysfunction atL4–L5 or L5–S1 is accompanied or was accompanied bysciatica.

In the upper limbs, the topography is less clear. Thecellulalgic zones of spinal origin are seen only in the upperarm and the superolateral forearm.

The presence of a localized cellulalgic zone, especiallyif it is unilateral, requires a careful examination of thecorresponding spinal segments and a search for other neu-rotrophic manifestations (trigger points, tenoperiostealhypersensitivity). It is often the only objective sign foundin cases of neuralgia in which there is no hypoesthesia orhyperesthesia to touch or pinprick. These cellulalgic zonescan be responsible for misleading pains, which can be feltsuperficially or as burning pains but are more usually feltas a deep pain mimicking a visceral pain of abdominal orthoracic origin (Fig. 18.3). In the back, these zones resultin regional pain (thoracic pain, lumbar pain) clearly local-ized below the involved spinal segment, since they notice-ably cover the cutaneous territory of the dorsal rami whoseterritory lies somewhat inferiorly to the correspondingvertebra (Fig. 18.3). Thus, pain arising from the segmentsof the thoracolumbar junction, T11–T12–L1, is often feltby the patient over the buttocks and can simulate a lowabdominal pain or a gynecologic pain anteriorly.

In the limbs, it is possible to have a limited cellulalgiczone, found only after a detailed examination, which canbe responsible for the persistence of regional or pseudo-radicular pain.

Injection of local anesthetic into the cellulalgic zonecan momentarily suppress the refractory pain. These zonesare usually ignored by the patient, who is surprised whenthey are revealed.

These cellulalgic zones disappear when the segmentaldysfunction that precipitated them resolves. In chroniccases, they can persist partially, being less painful and lessthick on pinch-rolling and, moreover, not responsible forpain (Fig. 18.5).

Thermographic imaging studies have demonstrated incutaneous cellulalgic zones differences of

½

to 2°C coolertemperature while associated posterior articulations werenoted to be warmer. Thermographic temperature differ-ences in cephalgias demonstrated persistent perturbationfor up to three weeks after the induction of a pain freestate. (Gatto: Personal communication, 1977)

Myalgic Indurated Cords (Taut Bands with or without Trigger Points)

Myalgic indurated cords present as one or several tautbands that (when found) are very tender to palpation. Thetrigger points vary in diameter (from the size of a needleto the size of a cigar, depending on the involved muscles)and are usually a few centimeters long (Fig. 18.2).

Palpation of the muscle should be performed with thepalm of the hand with fingers slightly flexed, rubbing therelaxed muscle fibers perpendicular to their orientation,as if one were strumming the strings of a guitar (Fig. 18.6).The pressure applied with the pad of the finger on themost sensitive point of the taut band often reproduces thepain felt by the patient and its referral pattern. Injectionof this point with a few drops of local anesthetic oftenreproduces, at the start of the injection, the acute local andreferred pain. This pain disappears rapidly with the effectof the anesthetic. The same injection performed in anadjacent part of the muscle a few millimeters away fromit may not reproduce any reaction. Injection at the mostsensitive point often produces a sudden muscle twitch thatis palpable and visible, and thus is called a “trigger point.”

Target Muscles

Remarkably, these trigger points are most often local-ized to the same part of the same muscles for the samespinal segment. They are “target muscles.” Some seem tobe specific to a segment. The short head of the bicepsfemoris, for example, is practically always involved insciatica (S1) as are the fibers of the lateral head of thegastrocnemius. As mentioned above, however, these mus-cles are innervated by two or more spinal segments; there-fore, the gluteus maximus, medius, and minimus musclesare always involved when there is a segmental dysfunctionof either one of the last two lumbar segments. Piriformismuscle involvement helps distinguish L5 from S1 dys-function, as it is involved only when S1 is affected. Sim-ilarly in the upper limbs, the target muscles are thesupraspinatus, infraspinatus, teres minor (C5, C6), supi-nator (C5, C6), extensor carpi radialis longus and brevis(C6, C7), triceps, common extensor (C7), subscapularis(C6), etc.

Trigger Points and Referred Pain

These trigger points may become chronic sources ofrefractory pain. They can be responsible for the persis-tence of pseudoradicular pains in femoral neuralgia, sci-atica, or cervicobrachial neuralgia. Only one taut band ofthe inferior aspect of the biceps femoris, for example, canproduce a persistent sciatica increased in the sitting posi-tion, since in that position the muscle fibers in questionare compressed against the seat. A trigger point of thegluteus medius or minimus can be a perpetuating factorin an L5 sciatica, while a trigger point in the infraspinatuscan mimic shoulder pain, etc. Although not all taut bandsresult in painful syndromes, they surely play a role whenthe pressure performed on a particular point of the cord(trigger point) reproduces the pain at a distance known bythe patient.

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109

Regional pain or referred pain, for which they areresponsible, is very misleading. The painful projection isthe same as that resulting from injection of a few dropsof hypertonic saline in the same normal muscle.

The painful muscular points attributed to local muscu-lar fatigue by most authors seem often to have a spinalorigin.

If local treatment of the trigger point momentarilyrelieves the local or referred pain, then a spinal treatmentalone may have a long-lasting effect when the trigger pointis affected by a SVS and is due to segmental dysfunction.However, it is not uncommon for some trigger points ofa SVS to be aggravated and be made more sensitive if theinvolved muscle is overworked because of direct activityor poorly maintained posture.

Figure 18.5

SVCPMS (Maigne). Representation of the painful cellulalgic zones on pinch-roll tests, with their usual associatedsegmental dysfunctional level. At the hairline level, the pinch-roll test is replaced by the “friction sign.”

Figure 18.6

Palpation of a taut band involving the tricepssurae.

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Tenoperiosteal Hypersensitivity

Tenoperiosteal hypersensitivity is seen frequently.Sometimes, it presents as a spontaneous pain; most often,however, it simply is local and discovered on examination.The sensitivity of a tendon can be discovered by the con-traction of the muscle against resistance or, better, bycomparative palpation. It can disappear or decrease con-siderably as soon as the segmental spinal dysfunctionresponsible for it resolves or decreases. This is why theeffect of manipulation or facet joint injection on this signcan be quasi-instantaneous. This tendinous sensitivity ofspinal origin is particularly frequent in the shoulder(supraspinatus, infraspinatus, biceps). Many apparentcases of “tendinitis” disappear immediately after spinaltreatment. In these cases, there are always one or moretrigger points in the involved muscle.

Epicondylar palpation will be tender in a patient witha segmental dysfunction of C5–C6 or C6–C7 due to aPMID or synovitis, in 70% of the cases ipsilateral to thefacet joint tenderness. This epicondylar hypersensitivityis usually ignored by the patient. If, however, thesepatients take up activities to which they are not accus-tomed (using a screwdriver, using pruning shears to trima tree, playing tennis excessively, or playing tennis witha different racket, i.e., one that modifies the patient’s mus-culoarticular habits), epicondylar pain often results, whichwill respond quickly, sometimes immediately, to cervicaltreatment. In cases where the irritation is light, local treat-ment of the epicondyle (injection) can be sufficient. If thecervical factor is more pronounced, however, this treat-ment may be ineffective or have only a temporary effect,or the epicondylar pain will recur at the first opportunity(see Chapter 53). It is the same for other tenoperiostealinsertions such as certain types of pubalgia, which areoften of spinal origin or have a spinal component (T12,L1) (Fig. 20.19; see Chapter 56, “Pubic Pain and SpinalFactors”) or of pseudotendinitis of the “crossroads” (L3,L4) or of the trochanter (L5) (Fig. 18.7 and Fig. 20.12)(Maigne).

It appears that tenoperiosteal hypersensitivity of spinalorigin sometimes provokes and often facilitates “enthes-ites” or “pseudotendinitis.” The significance of the roleplayed by local stress and its ability to provoke sponta-neous pain are inversely proportional to the degree ofspinal facilitation. General factors such as an individual’scharacteristics can also play a role.

Cellulotenoperiosteomyalgic Manifestations: Active and Latent

Many cellulotenoperiosteomyalgic (CTPM) manifesta-tions of SVSs that are asymptomatic on systematic exam-ination can be found in the area corresponding to a seg-mental spinal dysfunction. They are “silent” or “latent”;

the ones responsible for spontaneous pain can be called“active.”

When there are several CTPM manifestations tied tosegmental dysfunction, frequently only one of them isfound to be active; it can be a cellulalgic zone, a triggerpoint, or a tenoperiosteal insertion. The others are inactive,but they can, at any moment, become active as a result of(a) accentuation of the segmental spinal dysfunction, (b)a local irritation, or (c) a decrease in the pain tolerancethreshold.

Even when latent, they sometimes seem to be able tomaintain this vicious circle of pain. Thus, in some cases,when they do not yield to spinal treatment, it becomesnecessary to institute a local treatment to make these latentmanifestations disappear, to obtain the complete disap-pearance of the active CTPM manifestations that areaffecting the same segment and are responsible for thecomplaint of pain. These CTPM manifestations, them-selves, are the sources of nociceptive impulses capableof maintaining reflex reactions, periphery–center–periphery,perpetuating, and reactivating the segmental spinal irri-tation.

Hypotheses on Pathophysiology of These Manifestations

Only hypotheses are available to explain the patho-physiologic basis for these manifestations, i.e., cellulalgic,tenoperiosteal, and myalgic pain of spinal origin. Thismechanism is probably related to spinal cord function;however, the topography and the clinical characteristicsof these tissue perturbations suggest a “focusing” factor,probably the irritation of the corresponding spinal nerveor of one of its branches.

If a nociceptive impulse bombards the spinal cordalmost constantly, it can bring about a state of facilitationof a neuron whose cellular body is localized to the samespinal cord segment and provoke motor (anterior horn)and autonomic (intermediolateral horn) responses (Korr,Perel). Sato and Schmidt have shown that sympatheticresponse to nociceptive stimuli, measured on the whiterami communicantes, takes place in a very segmental way.But from there, this modality can be upset, since theefferent impulses are going to reach the periphery in amuch more diffuse way, either because of the distributionof the preganglionic fibers to several ganglions of theparavertebral chain or the ratio of preganglionic fibers topostganglionic fibers that can reach 1:80 (Astegiano). Thisdiffusion effect is restricted to the sympathetic system. Insome regions (lower limbs and trunk), however, the CTPMmanifestations are often clinically very localized (local-ized cellulalgia, “target muscles”) and, as we haveremarked in our earlier publications, are in an area corre-sponding to all or part of the area of the spinal nerve or

CHAPTER 18 SEGMENTAL VERTEBRAL CELLULOTENOPERIOSTEOMYALGIC SYNDROME

111

one of its branches. Here we should suspect the existenceof some superimposed local factors.

Indeed, another element must be taken into consider-ation: we have regularly noticed that discopathy of L4–L5or L5–S1 may not provoke the same manifestations if itis responsible for a pure lumbar pain or a sciatic neuralgia.It is, however, the same segmental dysfunction.

In the case of lumbar pain, there are always some tautbands in the glutei and, often for L5, tenoperiosteal ten-derness of the trochanter.

In the case of sciatic pain, the same elements can befound. In 90% of cases, however, there are also taut bandsin the lateral gastrocnemius and biceps femoris (at itsinferior aspect) with sciatica (S1). In 60% of cases, thereis also a small cellulalgic zone localized to the posteriorsurface of the calf for S1 and at the anterolateral surface

of the leg for L5. These neurotrophic manifestations ofthe lower limb exist only when there is or was a sciaticneuralgia. The irritation of the nerve thus also plays a role.

The irritation of the nerve is probably the case for thedorsal primary ramus of the spinal nerve. If the cellulalgiais more constant in its area than in the area of the anteriorramus, it appears likely that the posterior ramus is victimto a constant irritation in its difficult course after its emer-gence from the spine between muscular bundles that aretight and contractured.

Upton and McComas (1973) have shown that pressuresin series on the course of a nerve facilitate the creation ofa distal pathology: this is what is called the “double crushsyndrome.” For example, in carpal tunnel syndrome, com-pression of the distal part of the nerve can readily provokepain when the axons constituting the median nerve have

Figure 18.7

SVCPMS (Maigne). This diagram represents tenoperiosteal zones that are often hypersensitive to palpation incases of segmental spinal dysfunction. Often, these points are apt to present as tenoperiosteal insertional tenderness insituations in which the attached muscles are overworked.

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been irritated or compressed in their proximal course atthe level of the root or plexus. Both authors evoke thepossibility of a perturbation in the axonal flux, resultingin trophic neural dysfunction. A fundamental part of theirhypothesis is that the nerve fibers normally have a “safetyfactor” that can be reduced by numerous mechanical fac-tors (stretch or chronic pressure on the nerve) or generalfactors. Such a mechanism could then play a role in theformation of the CTPM manifestations of the SVS.

Cellulalgia

It is surprising how quickly the neurotrophic disorderof cellulalgia can disappear when it is recent, especiallywhen it is in a zone of the back corresponding to the areaof a dorsal primary ramus of the spinal nerve. It is suffi-cient to inject a few drops of 0.5% lidocaine into thepainful facet of the segment affected by the PMID, aninjection that also involves the posterior ramus attachedto it, and, in a few minutes, one notices that the fold ofthe skin that was thick, lumpy, and painful to pinch-rollingbecomes supple and painless. The same result can beobtained by manipulation if the maneuver makes the seg-mental pain disappear. When the cellulalgia is morechronic, the effect is less complete, but the skin becomesless thick and less painful.

An axon reflex may be at the origin of cellulalgia. Itcould start the local liberation of algogenic substances,creating a local vasodilation with extravasation and local

edema. These local reactions perpetuate the quantity andintensity of painful impulses reflexively. Pain due to cel-lulalgia while active is felt as a local deep pain —pseudovisceral, pseudovertebral.

Trigger Points

The trigger points that are part of an SVS are found inthe same parts of the same muscles for the same segment.But similar taut bands can also be seen under other cir-cumstances. They have been described by many authorsunder varied names (myogelosis, hartspann, taut bands,muscular trigger points, etc.). They are attributed to afunctional adaptation of the muscle, resulting from staticand postural disorders or muscle fatigue due to overworkor impairment of the articulation they move (e.g., coxar-throsis). Thus, they are theoretically different from the oneswe classify in the SVS. The usual descriptions include allthe taut bands, those of local origin and those we considerpart of an SVS from which they are not differentiated.

This relationship is confirmed by the coexistence of alocalized cellulalgic zone located in the same nerve rootdistribution, by the discovery of the tenderness of thecorresponding spinal segment, and especially by theirlessening or disappearance after spinal treatment. Severalstudies have been done on the mechanism or nature ofthese localized muscular indurations attributed to a localorigin, but none has resulted in a totally satisfactoryexplanation (see Chapter 19).

113

19

MYOFASCIAL PAIN OF NONVERTEBRAL ORIGIN (PANNICULALGIA, MYOGELOSIS,

TENDOMYOSIS, TRIGGER POINTS)

The origin of local or referred soft tissue pain, present-ing as alterations in tissue consistency and sensitivity, haslong been recognized by numerous authors. Various nameshave been used for this condition: “cellulitis” and “pan-niculalgia,” for the skin and subcutaneous edema; “fibrosi-tis,” “myogelosis,” “tendomyosis,” “myofascial pain,”“hartspann,” “trigger points,” etc., for the taut muscularbands. The distribution and mechanism for soft tissue painreproduction are different from those of the segmentalvertebral celluloperiosteomyalgic syndrome of Maignethat is described in the preceding chapter. But there is nodoubt that much of the pain of myalgic cords resulting inthis syndrome and disappears with vertebral treatment hasbeen attributed by other authors to different causes.

CELLULALGIA OR PANNICULALGIA

Cellulalgia or panniculalgia was first described by Bal-four in 1816 and has been studied by numerous authors,especially Wetterwald, since then. It is a painful sensitivityof the subcutaneous adipose tissue localized preferentiallyand symmetrically in some regions, most often in the napeof the neck, the supraspinous fossa, the lateral shoulder,the peripheries of the hips, and the medial fat pads of theknees. It affects women primarily. It can be responsiblefor diffuse, generalized, or localized pains and is aggra-vated by heat. The skin is thickened and adheres to thedeeper tissue planes; pinching a fold of skin demonstratesthe phenomenon of “orange peeling,” revealing the dila-tion of the pores. Pinching and kneading the skin are verypainful and feared by the patient.

There seems to be a genetic factor. Cellulalgia is oftenfamilial, tied to general and neurohormonal factors. Painis attributed to compression of free nerve endings by internalpressure. It is increased by external pressure. Numerouspainful symptoms have been attributed to it. In France,Laroche and Meurs-Blatter and May et al., among others,

have published observations of misleading abdominal paindue to the cellulalgia. In the English literature, the term“fibromyalgia” includes altered sensitivity of the skin andsubcutaneous tissues — muscles and tenoperiosteal inser-tions — that include the cellulalgia as just described andthe musculotendinous pain described below.

Remarks

The localized cellulalgic edema that we describe in theframework of the segmental spinal cellulotenoperios-teomyalgic syndrome is different. It can be seen in anysubject and can be located in any region of the body. It isgenerally unilateral and occupies only a small surface. Itcan be more marked in some patients than in others. Itcan be superimposed upon a regional cellulalgic condition,making the diagnosis more difficult to establish. Thetopography is, of course, directly linked to the correspond-ing spinal segment.

TENDOMYOSIS

As “tendomyosis” and under other names (“myogelo-sis” and “hartspann”) are pain syndromes of muscles andtendons that are not normally included in the category ofclassic pathology (tendinitis, tenosynovitis, bursitis).

The English word “fibrositis” includes in a rather vagueway all pains of the soft tissues. Some authors havedivided the condition into muscular fibrositis, subcutane-ous fibrositis, tendinous fibrositis, enthesitis, etc. Theword “tendomyosis” underlines the usual concomitantsensitivity of muscles and tendons. According to Brugger,“tendomyosis is a painful functional disorder, acute orchronic, without a humoral or anatomic pathologic sub-stratum that is known at present. It is a syndromecharacterized by precise muscular characteristics, provokedby different pathogenic factors.” Tendomyosis links painwith movement — making it and limiting it. The affected

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muscle is indurated or nodular. In these painful reflexstates, Brugger sees four groups of etiologic factors:

1. Muscular strain due to excess activity or poorposture.

2. Painful projection in some muscles. Forexample, after a severe attack of migraine, thereare often pains in the musculi cutanei of theface, especially the frontalis muscle; and in apatient with angina pectoris, tendomyosis of thedeltoid and the supraspinatus can exist, sincecardiac pains are referred to these zones.

3. Local trauma. Muscular pain can persist aftertrauma. There can be pain not only at the levelof the contusion but also at the level of thecorresponding tendon.

4. Reflex of articular origin. This is the case forthe painful tendinous and muscular statesfound, for example, in osteoarthritis of the hipand knee. The clinical aspect is sometimes lessclear. This is the case for tendomyosis of theshoulder girdle, provoked by the dysfunction ofthe acromioclavicular joint; musculotendinouspain here is most significant. The articular dys-function is not always clear and should belooked for. Injection of the joint immediatelysuppresses the spontaneous pain and the reflextendomyosis. These types of tendomyosis canthen be responsible for local pain that occasion-ally has a periarticular or pseudoradicular com-ponent. The role of the facet joints is the sameas that of the other synovial articulations, i.e.,a possible source of a tendomyosis of theparaspinal muscles.

The pathogenic mechanisms of these types of tendomy-osis are not clear. According to Brugger, the mechanismis an “alteration in muscle function, mediated by neuralreflex mechanisms and presenting with symptoms thatinhibit function.” This “starts by pain with contraction andleads to alterations in motor unit recruitment (fascicula-tion) until the appearance of muscular blocking (fascicularmuscle spasm, rigidity).” Tendomyosis is, therefore “theexpression of an effect of neuroautonomic blocking” andis among the most important autonomic reflexes. Thesetypes of tendomyosis or myogelosis can precipitate andperpetuate regional pain, especially a pain with a pseudo-radicular component.

MUSCULAR TRIGGER POINTS

The term

trigger points

is used to convey the fact thatthey can “release” regional or referred pain. They arelocated in taut bands of muscle whose centers are partic-

ularly painful; palpation performed on such a point orcontact with a needle often reproduces the pain referralpattern for which it is responsible. Anesthetic injectionreduces the pain immediately.

Travell made these “trigger points” known and, alongwith Simons, studied them and mapped out their painreferral patterns. Their topography is rather constant fora given part of a muscle, as the same muscle can presentseveral trigger points whose referral patterns are different.These authors attribute the

taut bands to a fatigue of theconcerned muscle due to overuse or static or posturalproblems (e.g., short leg). Thus, they are manifestationsanalogous to the ones described under the name of myo-gelosis or tendomyosis in the Germanic countries. But theresearch there to find the smallest taut band capable ofpresenting a trigger point whose treatment would relievea given referred pain seems finer and has been done morecarefully.

In our experience, although some of these taut bandsmay have local sources, many belong with their triggerpoints to a “segmental vertebral syndrome” and respondto spinal treatment. When they have become chronic orwhen a local factor (of mixed origin) increases them,however, local treatment is also necessary. Several studieshave been done on these trigger points.

Electromyographic examinations do not reveal any-thing in particular when a needle penetrates an induratedbundle, but if a needle is put into a trigger point of thecord, it provokes a brief visible twitch of the muscularbundle. At that moment, some repetitive high-frequencybrief-duration discharges have been recorded, while therest of the muscle behaves normally (Travell and Simons).A thermoelectric couple introduced into a muscular triggerpoint demonstrated first a temperature higher than that ofthe surrounding tissues, then a rapid (15 to 60 seconds)temperature fall to the level of the nearby tissues.

Numerous explanations have been proposed for thecharacteristically firm consistency of these taut bands —fibrous conjunctive tissue, local edema, myogelosis (mod-ification of the colloids of the muscle) — but these expla-nations have never been confirmed. Palpation of the musclegives the impression of a localized contraction of thismuscle. However, the electromyograph may not reveal anymotor unit activity; besides, how can the nervous systemorder the isolated contraction of some muscle bundleswhile others are left relaxed?

This is why Simons thinks that there is a localizedmuscle contracture (contraction without action potentials).As a result of effort that exceeds the capacity of the con-tractile elements, this muscle contracture could lead tomicrolesions responsible for local metabolic disturbancesfrom repetitive muscle pressure, resulting in an identicalprocess on a vulnerable part of the muscle. The injuredregion would then become incapable of getting rid of theexcess of liberated calcium ions that would provoke this

CHAPTER 19 MYOFASCIAL PAIN OF NONVERTEBRAL ORIGIN

115

permanent local muscle spasm with strong vasoconstric-tion. The circulatory disturbance seems well establishedwith the study of the temperature, and many authors haveadmitted that trigger points are a region of local ischemia.The common characteristic of all these trigger points oflocal or vertebral origin is their hyperirritability, as if theafferent neurons of the muscle were sensitized.

The role of agents such as serotonin, histamine, brady-kinin, or prostaglandin is often raised. The biopsies byAwad, which at the electron microscopic level shownumerous plaques (that free the serotonin) and mast cells(that free histamine), are not contrary to that hypothesis.The hypersensitivity of the cords and particularly of theircentral points could be due to mechanoreceptors or sensi-tized nociceptors. As in the case of cellulalgia, there seemsto be both a peripheral factor and a spinal reflex thatfacilitates this state. We should think here also of thestudies of Drevet (see “Objective Muscular Lesions” inChapter 15).

FIBROMYALGIA

Since the beginning of the 20th century, the word“fibrositis” has been used in some English-speaking coun-tries for some imprecise cervical, thoracic, or lumbar painsyndromes or limb pain, when palpation detected soft

tissue pain in the region. This idea was taken up by Yunus(1981) who used “fibromyalgia syndrome” to describepain involving muscle, joint, and tenoperiosteal insertions.

This fibromyalgic syndrome is usually found in womenabout 50 years of age who are fatigued and complain ofdiffuse pain, early morning stiffness, emotional hypersen-sitivity, and excessive reactivity to physical stress, head-aches, irritable bowel symptoms, etc. On examination,they exhibit an essential sign: multiple “tender points.”Smythe could find 12 or 14 sites of such pain. The numberof points and sites has varied according to the authors.These sites are generally symmetric (trochanters, supras-pinous fossae, epicondyles, etc.).

Nonrestorative sleep is frequent in these patients, andthere is a significant amount of interrupted deep sleep thatneeds to be explained (Moldofsky). Personality and psy-chologic disorders are frequent. Generally, the tricyclicantidepressants (Herisson et al.) are very useful in themanagement of this condition.

The bilaterality of the pain and the multiple painfulzones make this “polyenthesopathy,” also called “diffuseidiopathic polyalgic syndrome,” a condition still vague butvery different from the cellulotenoperiosteomyalgic syn-drome which is described here and is always unilateraland occupies a territory strictly metameric (dermatomes,myotomes, sclerotomes).

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119

20

GENERAL PRINCIPLES

The spinal examination should always be preceded bya clinical history in order for a practitioner to becomebetter acquainted with the patient’s presenting complaintand past medical history. It is essential to know the preciselocation of the pain, its character, its evolution, and itspossible impact on the patient’s activities of daily livingand daily work, while trying at the same time to developan appreciation of the patient’s psychologic behavior.

In many cases of so-called typical back pain, the phys-ical examination alone can uncover the source of thepatient’s complaint and identify the responsible spinalsegment. It is important to inspect for any posturalasymmetries, assess the range of motion for limitation,and examine the soft tissues for any signs of increasedmuscle tone or contracture. The spinal examination shouldbe performed scrupulously according to the techniquesindicated below, including a segmental examination toelicit the signs of the cellulotenoperiosteomyalgic syn-drome that correspond to the painful spinal segment.

The neurologic examination follows the spinal exami-nation. Its purpose is to find all objective signs of nerveinvolvement as manifested by motor, sensory, or reflexdysfunction. Sometimes, signs of upper motor neuroninvolvement can be detected, indicating a possible spinalcord or cortical lesion.

Certain isolated trigger points or segmental spinal dys-functions may be the source of pain referred distally, occa-sionally of a nonradicular pattern. Depending on theresults of the clinical examination, ancillary testing,including imaging and electrodiagnostic assessments, maybe performed. In most cases, the benign nature of thespinal disorder is confirmed, but occasionally a more omi-nous diagnosis of a spinal disorder is uncovered includinginflammatory, metabolic, metastatic, or infectious condi-tions.

The psychologic component of painful spinal disordersshould not be overlooked. Furthermore, referred pain ofvisceral origin can occasionally be mistaken for spinalpain, especially when the clinical features are nonspecific.Finally, in the presence of subclinical spinal pain, one

must consider the possibility of an intraspinal disorder, assome evolve very slowly and can be clinically misleadingfor a long time.

CLINICAL HISTORY

The clinical history should elicit the following infor-mation:

• The precise location of the pain, its referral pattern,aggravating and relieving factors, consistency ofreferral pattern, changes in pain with respect to rest,exertion, and work, and the extent to which thepatient has modified behavior in response to thepain.

• The mode of onset, whether acute (as in trauma,overexertion, or a sudden movement) or insidious,without any apparent cause.

• A history of any previous episodes and their simi-larity to the current presentation.

• The evolution: whether static, progressively wors-ening, or with a consistent baseline but with acuteflares (whose frequency and duration should benoted precisely). Certain patients may complain ofisolated attacks occurring during overexertion orsudden movement or occasionally, spontaneously.Therefore, the effects of various positions should benoted precisely: standing (stamping, walking), lyingdown (hard, firm, or soft bed), sitting (firm, soft,high, or low seat), stooping, positions of effort (car-rying, lifting), and times when the pain appears.

These latter points may help distinguish pain of inflam-matory origin, which is usually associated with morningstiffness and improves with activity. Conversely, pain ofmechanical origin is usually improved by rest, while thepain of neoplastic conditions is frequently worse at nightand subsides in the morning.

In addition, one should keep in mind that a soft bedthat offers poor support can be an underlying cause of

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severe nocturnal pain, as is the case with ordinary lumbarpain; cervical pain is usually aggravated in the recumbentposition when the neck is unsupported and cannot find acomfortable position.

It is essential to know:

• The nature of the patient’s work, including degreeof effort, workplace ergonomics, and whether thereis a need to drive a long distance to and from theworkplace.

• The patient’s leisure activities: tinkering, gardening,sports, etc.

• Past medical history, including an inquiry into thepatient’s review of systems and any ongoing treat-ments. A previous history of a peptic ulcer, diabetes,or hypertension will help clarify which treatmentstrategies may or may not be used.

• The manner in which a patient describes the prob-lem and responds to questions often helps in inter-preting whether any psychologic component ismodifying the patient’s pain complaint. The detec-tion of significant inorganic features, including painbehavior, can play an essential role in the diagnosisand management of the patient. An organic causefor the patient’s pain complaint should be ruled outprior to attributing the patient’s presentation to psy-chologic factors.

PHYSICAL EXAMINATION

Physical examination of the spine includes:

• A general inspection, static and dynamic, in thestanding position

• Range of motion assessment in flexion, extension,rotation, and side bending of the cervical, thoracic,and lumbar regions

• The segmental examination (Maigne) to assess forany specific painful segments

General Inspection: Static

The patient should be standing comfortably with thelegs extended. Curvature abnormalities in both the frontaland sagittal planes should be looked for. The patient isexamined:

• From the rear: both shoulders, the top of the scap-ulae, and the iliac crest should be on the same hor-izontal plane with respect to the sagittal bisectorformed by the spinous processes (Fig. 20.1).

• From the front: the anterior superior iliac spinesshould both be on the same horizontal plane(Fig. 20.1).

• From the side: the sagittal curvatures are examinedwith a plumb line held tangentially at the top of the

thoracic kyphosis to determine the sizes of the cur-vatures. The static examination is completed with astudy of the lower limbs, including thighs, legs, andfeet.

This examination can reveal abnormalities of the cur-vatures in the frontal or sagittal plane.

Frontal Plane Anomalies

Frontal plane anomalies are due to (a) scoliosis orpseudoscoliosis and (b) antalgic posturing.

Antalgic posturing —

During an acute episode of lowback pain, with or without sciatica, the patient may man-ifest a lateral lumbar shift either ipsilateral or contralateralto the painful side. Often, there is a loss of lumbar lordosisand, occasionally, a lumbar kyphosis. This posturing isinvoluntary and nonreducible, either actively or passively,and can be distinguished from true scoliosis by the lackof a rotatory component to the involved vertebrae. Thelumbar shift is thought to arise from positioning the spinein a manner that decreases the pain, and it is maintainedby involuntary muscle guarding. These findings resolvespontaneously with resolution of the factors that led to theacute attack (Fig. 20.2).

Scoliosis and pseudoscoliosis —

In pseudoscoliosis,there is no rotoscoliosis. The curve asymmetry correctswhen the patient bends forward at the waist while keepingthe knees extended (Fig. 20.3). A leg length discrepancycan produce static postural asymmetry resulting in obliq-uity of the sacral base and a convexity in the frontal plane.A wedge placed under the short limb levels the pelvis andthe pseudoscoliosis resolves (Fig. 20.4 and Fig. 20.5).

In true scoliosis, there is a rotatory component to theinvolved segments that produce the characteristic gibbousdeformity. Furthermore, the scoliotic curve does notresolve in forward bending (Fig. 20.6). Radiographs per-formed in the prone or supine position can distinguishbetween scoliosis and pseudoscoliosis, as the latter con-dition corrects in nonweight-bearing positions, while theformer does not. The major curve and the minor (com-pensatory) curve are clearly delineated radiographically.

The scoliotic deformity may be either balanced orunbalanced. In a balanced scoliosis, a plumb line droppedfrom the spinous process of C7 falls in the midlinebetween the two gluteal folds; in an unbalanced scoliosis,the same plumb line falls to one side of the midline(Fig. 20.7).

The degree of scoliosis may be assessed clinically interms of the gibbous deformity that manifests in forwardflexion. This can best be appreciated when the examinerstands behind the patient and inspects tangent to thespinous processes (Fig. 20.6). This angle can be measuredradiologically by the Cobb method in which lines areextended tangentially to the superior or inferior endplateof the most inclined superior and inferior vertebrae,

CHAPTER 20 GENERAL PRINCIPLES

121

respectively. The angle formed by the intersection of per-pendiculars dropped from each of these two lines is theCobb angle, which represents the angle of curvature ofthe scoliosis (Fig 20.8).

Most cases of scoliosis may be classified as idiopathic(80%). The curve may be thoracic, lumbar, thoracolumbar,or appear in two of the above regions.

Sagittal Plane Anomalies

The sagittal plane curves may be:

• Exaggerated, resulting in lumbar hyperlordosis orthoracic hyperkyphosis

• Attenuated, producing a “flat back”• Reversed, resulting in lumbar kyphosis and thoracic

lordosis

A thoracic kyphosis is considered to be excessive whenthe angle of curvature exceeds 50°. The measurement is

made from a lateral upright radiograph of the thoracicspine. Kyphotic curves can be separated into those curveswith a smooth gradual angular deformity as well as thosewith acute angulation (Stagnara).

The apex of the thoracic kyphosis usually is situatedat T7–8 where the plumb line rests tangential to the spine(Fig. 20.9). The perpendicular distances from the plumbline to the C7 and L3 spinous processes can be measuredreadily, and in the adult, usually equal 60 and 90 mm,respectively. The angle of curvature of the kyphosis canbe derived radiographically at the intersection of tangen-tial lines extending from the superior and inferior end-plates of the upper- and lowermost vertebrae of the curve,respectively. Photographic techniques are also used toassess the degree of kyphosis. The subject is upright andphotographed in side view against a background grid of5-cm squares.

Kyphosis is of clinical significance in the adolescentpopulation, with the most common presentation being

Figure 20.1

a.

Posterior view of a patient standing with legs spread slightly shows that the right and left shoulders, the angleof the scapula (right and left), the iliac crest (right and left), and the iliac spine (right and left) are all level.

b.

Anterior viewshowing the biclavicular line of the shoulders and the horizontal line of the iliac spine anteriorly and superiorly.

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SECTION IV EXAMINATION OF THE SPINE

Figure 20.2

Antalgic posture or painful scoliosis. A laterallumbar shift can be due to protective muscle guarding as isseen in sciatica resulting from disk disease or acute low backpain.

Figure 20.3

a.

Scoliotic posture.

b.

It disappears with for-ward flexion. There is no rotation of the vertebrae.

Figure 20.4

Short leg can be responsible for scoliotic posture.

Figure 20.5

A wedge under the foot can re-equilibrate thevertebral spine.

CHAPTER 20 GENERAL PRINCIPLES

123

Scheuermann’s apophysitis. The thoracic spine is mostfrequently involved, but occasionally the lumbar region isaffected. The latter case is most evident with the patientin the seated position, as the lumbar lordosis is replacedby a kyphotic curve.

General Inspection: Dynamic

Assessment of Forward Flexion

The patient is asked to bend forward at the waist fromthe upright position while keeping the legs adducted andthe knees extended (Fig. 20.11). One should note:

• A normal lumbopelvic rhythm with smooth reversalof the lumbar lordosis.

• The persistence (as in scoliosis) or the reversal (asin pseudoscoliosis) of any frontal plane anomalies.

• Pain limiting flexion (measured as the distance fromfingertips to floor; Fig. 20.12).

• The presence of paraspinal muscle fullness (spasm)or a lumbar shift that may only be present during asmall arc of flexion, then resolve with further flex-ion.

• Whether the limitation in flexion (fingertips to floor)is due to painless stiffness of the spinal extensors or

hamstring muscles, this is frequently the case inthose subjects with otherwise normal lumbopelvicrhythms. This lack of resiliency can increase thestress on the lumbosacral junction. Conversely,some patients can occasionally touch their fingersto the floor, despite a stiff spine, if the hamstringsare loose enough (Fig. 20.13 and Fig. 20.14).Schober’s test measures the degree of lumbar excur-sion (see “Examination of Lumbar Spine” in Chap-ter 21). Badelon’s

rachimeter

can precisely measurethe excursion of the spine and the hamstrings (supra-and infrapelvic excursion).

Assessment of Side Bending

In the upright position, with the legs slightly abductedand knees extended, the patient is asked to bend laterallyto the right and then to the left, sliding the hand down theleg.

One should note whether the spinal curves are smoothand symmetric from side to side or if any segmental stiff-ness appears that may be more pronounced in one direc-tion, and whether or not this is associated with pain. Thefingertip-to-floor measurement may be used to quantifythe amount of lateroflexion (Fig. 20.15). Alternatively, the

Figure 20.6

a.

True scoliosis is due to a rotation of the ver-tebrae.

b.

In true scoliosis, forward flexion results in a gibbousdeformity that can be measured as the difference betweenthe high and the low points of the back.

Figure 20.7

a.

Scoliosis is said to be in equilibrium when aplumb line is able to pass through the middle of the occiputand the natal cleft (intergluteal groove).

b.

Scoliosis is saidto be in disequilibrium when a plumb line does not passthrough the middle of the occiput and the natal cleft.

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SECTION IV EXAMINATION OF THE SPINE

position where the fingertip overlies the thigh can be com-pared on both sides.

Assessment of Extension

This aspect of the examination is more specificallyaddressed in the regional spinal assessment. However, aglobal sense of the degree of extension, the presence orabsence of pain or stiffness can be inferred by asking thepatient to bend backward with the hips and neck in exten-sion and the shoulders retracted.

Assessment of Rotation

This examination is performed as part of the regionalassessment.

Assessment of Regional Mobility

This portion of the examination assesses the compo-nents of triplanar motion made up of flexion and exten-sion, right and left rotation, and right and left lateroflexion.Each spinal region — cervical, thoracic and lumbar — isassessed.

First, the subject is requested to perform the activerange of motion, followed by passive range assessment bythe examiner. Attention is given to whether there is any

specific segmental stiffness and which degrees of freedomare restricted or painful.

The degree of discomfort is noted as well as where inthe arc of motion it is produced. A “star diagram” (Maigneand Lesage), in which each of the six primary movementsis represented by an arrow, is a convenient way to recordthis information (Fig. 20.16).

Previously, the degree of pain or motion restriction wasindicated by hatches (from 1 to 3, according to degree)assigned to the branch of the involved plane of motion.This diagram can be improved upon by distinguishingpainless restriction (–) from painful restriction (

×

). Thepositions of the markings on the branch (i.e., the distancefrom the center) indicate where in the arc of motion therestriction occurs. The intensity of the pain or limitationis indicated by the number of

×

’s or strokes, respectively.A painful but unlimited arc is marked with a circle (Fig.20.17), Thus, all possible combinations can be readilyvisualized, and a markedly restricted but painless arc ofmotion can be distinguished from a marked restriction thatis mildly painful (Fig. 20.18 through Fig. 20.20).

Figure 20.8

Measurement of the angles of the scolioticcurves: 1, vertebral upper limit; 2, vertebral lower limit; and3, vertebral apex. Tangential lines are extended through theendplates of the vertebrae at the superior and inferior limitsof the scoliotic curve, which are usually the vertebrae mostinclined from the horizontal plane. The angle formed by thesetwo tangential lines is described as the angle of scoliosis (

α

).It is easy to obtain this angle by dropping perpendicularsfrom these tangents, as demonstrated in the drawing.

Figure 20.9

Posture in the sagittal plane is measured bydropping a plumb line tangent to the most posterior part ofthe spinal column. This apex is usually at approximatelyT7–T8. From this line, one can then measure the distancebetween C7 and that line, which in the normal individual isin the range of 30 mm and demonstrates a similar distanceat the L3 level.

CHAPTER 20 GENERAL PRINCIPLES

125

Figure 20.10

Subjects with abnormal curves.

a.

Accentuated curves.

b.

Attenuated curves.

c.

Lumbar hyperlordosis.

d.

Thoracic hyperkyphosis. (The arrow does not measure the lordosis. One must deduct the sacral distance to obtain themeasure of lordosis. In case c, for example, the L4 arrow measures 80 mm, and the S2 arrow measures 20 mm; 80 mm –20 mm = 60 mm. Thus,. the subject is said to have a measured lordosis of 60 mm.)

Figure 20.11

Forward flexion with legs extended. Thismotion requires a flexible spine or flexible hamstrings.

Figure 20.12

If the spine is rigid, the lumbar lordosis doesnot reverse on forward flexion.

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SECTION IV EXAMINATION OF THE SPINE

Figure 20.13

Patients who lack hamstring flexibility mayhave limited forward flexion, as measured by the distancebetween the fingers and the floor, despite normal vertebralflexibility.

Figure 20.14

Conversely, an individual who has a stiff lowback but can stretch the hamstring may be able to easilytouch the floor.

Figure 20.15

a.

Trunk side-bending produces a smooth C curve of the spinal vertebrae.

c.

Loss of lumbar mobility translatesto an abnormality called the sign of Cassure.

CHAPTER 20 GENERAL PRINCIPLES

127

Segmental Examination

The segmental examination assesses each spinal seg-ment individually. Its purpose is to elicit tenderness in aspinal segment by one or more specific maneuvers. Seg-mental tenderness may be indicative of many differentpathologies: mild, severe, benign, or malignant.

The examination should be performed slowly andfirmly maintaining at all times an active dialogue with thepatient in order to determine the presence or absence ofpain associated with palpation.

Often the patient prior to examination may be unawareof painful areas and may insist that their pain is elsewhere.The examiner should nonetheless perform the full exam-ination in order to determine the exact location and originof segmental symptoms.

Basic Maneuvers (Fig. 20.21)

The four basic maneuvers of the segmental examina-tion are as follows:

1. Posteroanterior (PA) pressure over the spinousprocess

2. Transverse pressure against the lateral aspect ofthe spinous process

3. Longitudinal friction overlying the facet joints4. Pressure against the interspinous ligament

Figure 20.16

Star diagram of Drs. Maigne and Lesage: E,extension; F, flexion; LLF, left lateral flexion; RLF, right lateralflexion; LR, left rotation; and RR, right rotation.

Figure 20.17

A bar placed on one of the branches of thestar is used to mark a limited but nonpainful range of motion.Depending on the severity of this limitation, one can note one,two, or three bars.

×

indicates a painful limitation in range ofmotion. One can note one, two, or three

×

’s, indicatingincreasing severity. A circle indicates a normal range ofmotion with a painful arc.

Figure 20.18

If one wishes to be more precise in terms ofdocumenting the results of the examination, one can placethe bars or

×

’s closer or farther from the center according tothe level of severity obtained or the movement limitation. Inthis case, one would place the

×

’s closer to the center if theyappear early in the movement or farther out along the branchif they occur late in the movement. One would translate thisdiagram as follows: severe pain on extension at the onset ofmovement, severe pain on right rotation, and mild pain at theend of right lateral flexion.

Figure 20.19

A region of the spine where the flexion/exten-sion is free, with pain on flexion; right and left lateral flexionand right and left rotation are very limited but not painful.

Figure 20.20

Pain without any free movement.

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SECTION IV EXAMINATION OF THE SPINE

PA pressure over spinous process (Fig. 20.22)

—

This is best performed with the pad of the thumb. Firm,gradual anteriorly directed pressure should be applied tothe spinous process and held for a few seconds. It may bepreferable to interpose the other thumb between thespinous process and examining thumb.

Transverse pressure against spinous process(Fig. 20.23) —

This maneuver can be used for all spinalsegments except the cervical segments above C7 and insome cases C2. Slow gradual pressure is applied to bothsides of the spinous process, right and left alternately, inthe plane of the skin. This maneuver imparts rotation aboutan oblique axis on the involved vertebral segment. Theexample in Figure 20.23 depicts vertebra B, which istender with transverse pressure from right to left or rightrotation. Contralateral pressure to either vertebra A above

or C below helps distinguish which of the two motionsegments, AB or BC,

is involved.

Remarks

It is essential that pressure truly be applied transverselyto the spinous process rather than obliquely to the junctionof the spinous and transverse processes. The latter maneu-ver can produce false-positive results through irritation ofthe underlying branches of the posterior rami.

Contralateral Pressure (Maigne)

While applying transverse pressure to a vertebra in thepainful direction, the opposite thumb may apply a contralat-eral transverse pressure to the spinous process of the vertebraabove or below. Usually, one of these two maneuvers will

Figure 20.21

The four maneuvers of the segmental examination of Maigne.

a.

PA pressure over the spinous process.

b.

Transverse pressure against the spinous process.

c.

Longitudinal friction overlying the facet joints.

d.

Pressure against theinterspinous ligament.

CHAPTER 20 GENERAL PRINCIPLES

129

increase the tenderness provoked with unilateral trans-verse pressure, allowing for precise localization of thesegmental dysfunction. In the example in Figure 20.24,vertebra B is painful to transverse pressure applied fromright to left. This pressure on B is maintained while asimultaneous contralateral transverse pressure is appliedfrom left to right. When this counterpressure is applied tovertebra A, the pain is not modified. However, when thesame counterpressure is applied to vertebra C, the pain isnotably increased. One can conclude that the origin of theprovoked pain is segment BC. The most effective positionfor the thumbs is shown in Figure 20.25.

Longitudinal friction overlying facet joints(Fig. 20.26) —

Facet joint tenderness is elicited by lon-gitudinal friction. This maneuver does not provoke painin the absence of dysfunction involving one (rarely, both)of the facet joints. The friction is applied to the sub-cutaneous tissues and paraspinal musculature that is super-ficial to the facets. In the cervical assessment, the parac-ervical muscles readily relax in the supine position. Thisfacilitates this maneuver, allowing nearly direct palpationof the articular pillars. This direct palpation is not presentin the thoracic or lumbar regions. Nevertheless, whenlongitudinal friction is applied and produces tendernessone fingerbreadth lateral to the midline, the location ofthe tender point practically always corresponds (except inthe midthoracic segments, T4–7) to the facet joint, as hasbeen verified fluoroscopically. This is seen in the contextof other signs of segmental dysfunction.

Pressure against interspinous ligament (Fig. 20.27) —

Interspinous ligament sensitivity is often seen in spinalsegmental dysfunctions. Ligamentous tenderness is elic-ited by transverse friction over the ligament, applied bythe pad of the index finger or, preferably, with a key ring.

Precautions and Sources of Error in Segmental Examination

All the maneuvers of the segmental examination shouldbe applied gradually, progressively, and firmly. The exam-ination should be unhurried, repeated, and compared withthat of adjacent spinal segments. The pressure applied toeach side should be equivalent. Proficiency in these tech-niques requires a degree of practice. Practitioners skilledin these methods consistently concur on the level of seg-mental findings in a given patient.

Faulty examination technique can lead to spurious con-clusions. Excessive and improperly applied pressure canprovoke tenderness in normal segments, leading to falsepositives. More importantly, false negatives occur wheninsufficient pressure is applied to involved spinal seg-ments.

Errors to avoid:

• Pain with PA pressure on the spinous process may,in some cases, be due to periosteal sensitivity (apo-physitis) rather than to painful segmental motion.Pain with friction over the spinous process that isof the same intensity as pain with PA pressure ismost suggestive of apophysitis. A few milliliters oflocal anesthetic applied subcutaneously over thespinous process usually eliminate this apparent seg-mental tenderness (Fig. 20.28).

• Entrapment of a skinfold against the spinous processwith PA or transverse pressure (Fig. 20.29) is oftena source of false positives. This is most commonlyseen in the midthoracic level (see Chapter 36). It istherefore important to be certain that the portion ofskin receiving the pressure with these maneuvers isnot overly sensitive to pinch-rolling (Fig. 20.30).

Figure 20.22

PA pressure over the spinous process. Thisprocedure is performed with the thumb or both thumbs super-imposed over the top of the spinous process. This imparts aposteroanterior motion to the spinal vertebrae.

Figure 20.23

Transverse pressure against the spinous pro-cess. This is performed from right to left and then from leftto right on each vertebra. It imparts a movement of rotationabout an oblique axis to the vertebrae.

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SECTION IV EXAMINATION OF THE SPINE

Figure 20.24

Restricted transverse pressure. To make the prior exami-nation more sensitive, one can use lateral counterpressure simulta-neously (Maigne).

a.

For example, one can produce tenderness topressure from right to left on B, indicated by

××××

. One would like to knowwhether this pain is due to involvement of segment AB or segment BC.

b.

While maintaining pressure on B from right to left, one simultaneouslyapplies a counterpressure on A. This maneuver did not increase theprovoked pain.

c.

By contrast, the same maneuver executed on C notablyincreased the pain provoked by the isolated pressure on B (indicatedby

××××××××××××

). Thus, segment BC is identified as the cause of the pain.

Figure 20.25

Lateral counterpressure method applied to the spinous process.

CHAPTER 20 GENERAL PRINCIPLES

131

• In the midthoracic spine, particularly at the levelof T5–6, sensitivity one-finger breadth from themidline can result from an irritable facet joint orirritation of the cutaneous branch of the dorsalramus of T2 as it runs superficially at this level(see Chapter 36). This is the only site where thesuperficial emergence of the cutaneous branch ofthe dorsal ramus overlies a facet joint. Below T6,the emergence of this branch is more lateral. When

this tender point is detected, the adjacent skinfoldsshould be examined by pinch-rolling. Sensitivityto pinch-rolling indicates irritation of the dorsalramus of T2 and the tender point corresponds tothe site of its superficial emergence. Confusionwith a T5–6 segmental dysfunction can be elimi-nated by finding tenderness to pinch-rolling in theterritory of the dorsal ramus of T5, which corre-sponds to the level of T9 (Fig. 20.31).

Figure 20.26

Longitudinal friction maneuver over the facet. Facet joint tenderness is consistently found in many commonvertebral pain disorders. In this case, there is thoracolumbar pain (left) and cervical spine pain (right).

Figure 20.27

Pressure can be applied against the inter-spinous ligament with the fingertips or, more easily, with thehead of a key.

Figure 20.28

Source of error in the segmental examination:pain is produced by friction over a tender spinous process.This type of pain tends to be superficial and usually disap-pears after injection of local anesthetic.

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RADIOGRAPHIC AND ADVANCED STUDIES

As part of a general examination, studies including x-rays, bone scans, MRI scans, and CAT scans will generallybe available. In addition, routine radiologic studies mayalso be available.

The value of SPECT (Single Photon Emission Com-puterized Tomography) scans is also under consideration.Recent studies performed to evaluate the value of SPECTscans and the identification of facet joint pathology sug-gest that SPECT can enhance the identification of backpain sufferers likely to obtain short-term benefits fromfacet joint injection. However, these findings, like otherstudies that preceded them and involved only small num-bers of patients demonstrated that the informationobtained by this imaging technique does not supersede theinformation obtained with a proper physical examination(Dolan et al.).

Figure 20.29

Another source of error in the segmental exam-ination: if one pinches the soft tissues against the spinousprocess, a region of skin that is unusually sensitive or cellu-lalgic may falsely reproduce tenderness. The same error mayoccur when looking for painful facets or ligaments.

Figure 20.30

To avoid error when performing the segmentalexamination, one should always start by examining the skinwith the pinch-roll technique.

Figure 20.31

Most errors in the segmental examination aremade in the interscapular region, since these areas are oftencellulalgic.

133

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REGIONAL APPLICATIONS

EXAMINATION OF CERVICAL SPINE

Range of Motion Assessment

Patient Seated

With the patient seated, the global range of flex-ion/extension, rotation, and side bending can be assessed.The active range of motion is assessed first by asking thepatient to initiate the movements. This is followed bypassive range of motion performed by the examiner withthe patient maximally relaxed. The movements that arepainful or restricted are carefully noted.

When assessing

flexion and extension,

the examinergrasps the patient’s chin with one hand, while stabilizingthe base of the neck with the other. A normal range ofmotion allows the patient to flex the chin to the chest andextend so that the eyes are oriented vertically. In practice,it is difficult to measure this range goniometrically; it can,however, be measured radiographically with flexion/extension lateral views depicting a normal range in flexionas 80° and extension as 70° (Fig. 21.1 and Fig. 21.2).

Rotation

is assessed by grasping the patient’s chin andguiding the head to the right and then the left while theopposite hand stabilizes the shoulder girdle (Fig. 21.3).

Lateroflexion

is

assessed by guiding the head to theright and then the left, using one hand as a guide and the

Figure 21.1

Flexion.

Figure 21.2

Extension.

Figure 21.3

Left rotation.

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other as a stabilizing counterforce on the contralateral side(Fig. 21.4).

Finally, the

compound triplanar movements

such asrotation with flexion or extension are assessed (Fig. 21.5and Fig. 21.6).

It is evident that the ranges of all of these movementsdiminish with age.

Patient Supine

The examination of cervical segmental mobility isfacilitated by patient relaxation. This is best achieved withthe patient supine and the head supported by the examiner.The passive range of cervical rotation and lateroflexionincreases in supine. First the global range is assessed,followed by a more precise localization of the site ofrestriction, whether at the upper, mid, or lower cervicallevel (Fig. 21.7 through Fig. 21.15).

In cases of mild restrictions, each vertebral segmentis examined using the techniques of mobilization and

Figure 21.4

Left lateral flexion.

Figure 21.5

Right rotation with associated extension.

Figure 21.6

Left rotation in full flexion.

Figure 21.7

Total flexion of neck.

Figure 21.8

Flexion limited to upper cervical spine.

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135

Figure 21.9

Flexion of midcervical spine and lower cervicalspine. The upper cervical spine is maintained in a neutralposition.

Figure 21.10

Total extension.

Figure 21.11

Extension limited to upper cervical spine.

Figure 21.12

Extension limited to midcervical and lower cer-vical spine. The upper cervical spine is maintained in flexion.

Figure 21.13

Total left lateral flexion.

Figure 21.14

Left lateral flexion of upper cervical spine.

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manipulation described below. These are performed bilat-erally at each segmental level, taking up the slack pas-sively and without excessive force. The maneuver isapplied with the fingertips and repeated by oscillating thesegment at end range. This is most important in assessingrotation and lateroflexion.

Axial Traction and Compression

Axial pressure may be applied to the vertex with thepatient seated or supine. This maneuver may temporarilyexacerbate pain of cervical origin (Fig. 21.16). Of greaterimportance is the test of manual traction (Fig. 21.17), whichis indispensable in relaxing the patient prior to treatment,when it results in pain relief. Occasionally, traction can exac-erbate the pain and should therefore be avoided.

Segmental Examination

After assessing the active and passive cervical range ofmotion in sitting and supine positions, the cervical spinecan be examined segmentally.

It is not unusual in cases of pain syndromes associatedwith chronic segmental dysfunctions to have the globalactive or passive range of motion be full and painless,while the segmental examination reveals abnormal hyper-sensitivity of the involved segment. This segmental dys-function can be due to a painful minor intervertebral dys-function (PMID), an inflamed facet or uncovertebral joint,or occasionally a more ominous pathology. The diagnosisis reached in the context of the clinical and radiologicexaminations.

In the cervical spine, segmental dysfunction is essen-tially detected by finding tenderness to palpation over thearticular pillars (sometimes two) with the patient insupine. In the sitting position, the involved segment maybe painful to PA pressure over the spinous process. Trans-verse pressure to the spinous process can be applied at C7only. The segmental examination is completed by lookingfor signs of cellulotenoperiosteomyalgic syndrome in thedistribution of the anterior or posterior.

Examination of Facet Joint Irritability

This step is the most important part of the segmentalassessment of the neck (Fig. 21.18). With the patient inthe supine position, the examiner, seated at the patient’shead, cradles the occiput with the palms of the hands,extending the fingers over the cervical paraspinals. Themiddle or index fingers, placed symmetrically on each sideof the neck, are utilized for palpation.

To best achieve the desired muscular relaxation, it maybe necessary to gently rotate the head from right to leftseveral times. Once relaxed, the paraspinal muscles areeasily displaced for deep palpation, allowing the pad ofthe examiner’s finger to contact the posterior aspects ofthe articular pillars at each segmental level. It is mostefficacious to begin palpation at the cervicothoracic leveland proceed superiorly to the suboccipital region to C2–3,which is the most rostral level palpable.

Figure 21.15

Full rotation.

Figure 21.16

Axial compression.

Figure 21.17

Axial traction.

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137

The palpation technique involves slow longitudinalstrokes with the fingerpad creating friction against thearticular pillar. With a consistent pressure, palpationprogresses centimeter by centimeter to adjacent segmentallevels, allowing comparisons between ipsilateral and con-tralateral vertebrae. In cases of zygapophyseal spondylo-sis, a bony prominence can often be discerned beneath thepalpating finger. Often, this is painless and without a doubtnot the cause of the painful symptoms; on other occasions,this palpation can be very painful.

Occasionally, the articular pillar may feel boggy andtender as can be seen in traumatic sprains or inflammatorysynovitis. Most often, only the involved segment is tenderto palpation, while adjacent and contralateral levels, exam-ined in a similar fashion, are asymptomatic. With practice,one can detect focal muscular hypertonus restricted to theinvolved level. In these instances, a minor intervertebraldysfunction (MID) may be present and must be distin-guished from more ominous pathology.

PA Pressure on Spinous Process

After having established that superficial tenderness ofthe spinous process is not present upon light superficialrubbing, a firm posteroanteriorly directed pressure isapplied (Fig. 21.19). This maneuver should be repeatedwith the spine in neutral position, flexion, and extension.

Transverse Pressure against Spinous Process

This maneuver can be performed only at C7. The rightthumb applies pressure from right to left, followed byopposite pressure directed by the left thumb (Fig. 21.20).

Pressure against Interspinous Ligament

Interspinous ligamentous tenderness can be elicitedwith pressure applied by a key ring. This sensitivity isoccasionally the only source of refractory post-traumaticcervical pain (Fig. 21.21).

Anterior Cervical “Door Bell” Sign (Maigne)

This maneuver is sometimes quite useful in assessingsegmental dysfunctions of the cervical region. With thepad of the thumb (the right for the patient’s left side andvice versa), the examiner applies firm transverse pressureto the anterolateral aspect of the cervical vertebrae onesegment at a time. This pressure should be held for a fewseconds (Fig. 21.22). It is evident that pressure applied inthis fashion is distributed over many anatomic structures.Nevertheless, the soft tissues are readily retracted, allow-ing the thumb to contact the vertebra’s transverse process.

A positive sign consists of the reproduction of arm painor, in some instances, periscapular pain, confirming thecervical origin. Used systematically, this maneuver hasallowed us to show a cervical origin for dorsal or

Figure 21.18

Examination for facet joint tenderness.

Figure 21.19

Pressure applied to spinous process.

Figure 21.20

Lateral pressure against spinous process (thisexamination is variable only for C7 at cervical level).

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periscapular pain. It is also useful in the assessment ofacroparasthesiae, when one considers the possibility of acervical source. Finally, it is important to assess resistedmotion of the cervical spine in flexion (Fig. 21.23), exten-sion (Fig. 21.24), and rotation (Fig. 21.25).

Examination of Cervical Spinal Nerve Roots

Cervical spinal nerve root examination is performed byassessing the integrity of sensation, motor power, andstretch reflexes within their distribution. Following thisevaluation, the patient should be examined for celluloten-operiosteomyalgic manifestations of the “segmental ver-tebral syndrome.”

Anterior Rami

Cutaneous Topography.

The cutaneous territory ofthe anterior rami is shown in Fig. 21.26. Depending onthe author, there are a few variations. The dermatomalmaps commonly depicted are those of the anterior rami,which usually do not take into consideration the territorialdifferences for the dermatomes of the posterior rami.

Figure 21.21

Evaluation of interspinous ligament for pain.

Figure 21.22

Doorbell point. Horizontal pressure is appliedwith the pad of the thumb to the involved segment, whichcan reproduce pain of cervical origin in the arms andperiscapular region.

Figure 21.23

Testing neck flexors.

Figure 21.24

Testing neck extensors.

Figure 21.25

Testing rotator muscles with patient seated.

CHAPTER 21 REGIONAL APPLICATIONS

139

Muscles.

Table 21.1, as adapted from Grossiord,depicts the myotomal distribution of the anterior rami.Schematically, the C5 root governs abduction of the arm;C6, flexion at the elbow; C7, extension at the elbow, wrist,and fingers; and C8–T1, the intrinsic muscles of the hand,especially those innervated by the median for C8 and bythe ulnar for T1. Muscular strength is evaluated by clas-sical manual muscle testing.

Reflexes.

Testing of reflexes of the anterior rami isperformed as follows.

C5: Biceps reflex — Tapping the biceps tendon at theelbow crease produces flexion of the forearm upon thearm.

C5–6: Brachioradialis reflex — The brachioradialistendon is tapped at the radial styloid, resulting in flexionand supination of the forearm.

C7: Triceps reflex — The triceps tendon is tapped justproximal to the olecranon, producing extension of theforearm.

C6–7: Pronator reflex — The ventral surface of theradial styloid is tapped with the forearm in supination,resulting in pronation of the wrist.

C8: Finger flexor reflex — The long flexors are tappedover the carpal tunnel or the pads of the fingers, resultingin finger flexion.

Posterior Rami

The posterior ramus of C4 innervates the entire supe-rior surfaces of the shoulders and back. The dermatomeimmediately adjacent to C4 is T2, as the cutaneousbranches of the posterior rami of C5, C6, C7, C8, and T1

Figure 21.26

a.

Anterior dermatomes.

b.

Posterior dermatomes.

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are either vestigial or nonexistent due to their embryogen-esis. The inferior cervical dermatomes are distributedthroughout the upper limb. Clinically, however, the cuta-neous branch of the T2 dorsal ramus, which is physicallyquite large and covers a vast cutaneous territory, encom-passes the cutaneous contributions of the dorsal rami ofC5, C6, C7, and C8 (Maigne) that are nonexistent (C6,C7, C8) (Lazorthes, Töndury) or inconsistent (C5). TheT2 posterior ramus becomes superficial at the level of T5and supplies an area extending superiorly toward the acro-mion (Hovelacque; Fig. 21.26; see Chapter 36, “ChronicThoracic Pain”). The ramus of T3 sometimes seemsaffected. The only way to explore the dysfunction of thesenerves is examination of the skinfolds by the pinch-roll

test as we have proposed (see “Examination: The ‘Pinch-Roll’ Test” in Chapter 18).

Muscles.

The posterior rami innervate the axial spi-nal muscles. This area of innervation extends down verylow, as it has been noted in some tetraplegics and para-plegics. Cough revealed some muscle innervations extend-ing down five to six levels below their anatomic levels oforigin. There is no easy exploration of these muscles.

Examination for Manifestations of Segmental Vertebral Neurotrophic Syndrome of Maigne

The search for the cellulalgic tenoperiosteomyalgicmanifestations resulting from painful dysfunction of aspinal segment should be an integral part of the spinalexamination. Below, we give their most usual topography.

Table 21.1Muscular Innervation of C4–T1

C4 C5 C6 C7 C8 T1

Rhomboids

Deltoid

s

Biceps

Brachialis

Coracobrachialis

Supinator

Extensor carpi radialis longus and brevis

Triceps

Extensor indicis proprius

Extensor

digitorum longus

Flexor carpi ulnaris

Anconeus

Pronator teres

Palmaris longus

Flexor digitorum sublimis

Flexor digitorum profundus

Flexor policis longus

Extensor carpi ulnaris

Intrinsic muscles of hand

Infraspinatus

Supraspinatus

Teres minor

Teres major

Pectoralis major

Latissimus dorsi

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141

Cellulalgia

Posteriorly —

A disorder of the inferior segments(C5–T1) presents as a cellulalgia affecting a large dorsaland common zone extending from T5 to the acromion.This large cellulalgic area is present in all inferior cervicalspinal (C5–T1) irritations and is common to all thesesegments. It depends, in fact, on the posterior ramus ofT2. The cutaneous branch of T2 seems to represent theentire posterior cutaneous contingent of the last cervical

segments (Maigne; Fig. 21.27 and Fig. 21.28: see Chapter36, “Chronic Thoracic Pain”).

Just above the T2 dermatomal territory lies a zonecorresponding to the C4 segment, which includes the skinoverlying the supraspinous fossa. The C3 segment corre-sponds to the nape of the neck (with C2 for the superiorpart and C4 for the inferior part). See Fig. 21.32.

The pinch-roll maneuver is not used for examinationof the scalp. It is replaced by the friction maneuver(Maigne). Firm pressure is applied to the scalp against theskull as if shampooing. This maneuver, usually painless,becomes painful if the nerve root innervating the con-cerned zone is irritated (see Chapter 48, “Headache ofCervical Origin” and Fig. 21.38). If one considers the areaof scalp situated posterior to a line passing through thevertex and joining the two ears, one finds

• Near the midline, the zone corresponding to theposterior branch of C3

• More laterally, the middle zone corresponding to theposterior branch of C2

• Supra-auricular and retro-auricular regions inner-vated by branches arising from the anterior rami ofC2 and C3

Anteriorly —

The clavicular region corresponds to C4.The anterolateral surface of the neck corresponds to C3(Fig. 21.32 through Fig. 21.35). For Cl and C2 (and some-times C3) we have described an astonishing sign situatedin the area of the ophthalmic division of the trigeminal

Figure 21.27

Segmental vertebral syndrome of C6.

Cellulalgia:

lateral aspect of arm and superior lateral forearm. Cellulalgiais noted in the interscapular region and is common with inferior cervical segment involvement.

Trigger points:

the musclesmost often involved are the infraspinatus, biceps, supinator, and pectoralis.

Tenoperiosteal insertion:

the lateral epicondyleand the radial styloid.

Figure 21.28

Pinch-roll test in interscapular region (segmen-tal vertebral syndrome of C5, C6 or C7, C8).

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nerve, the “eyebrow sign” (Maigne; Fig. 21.37 andFig. 21.39). It consists of a thickening of the skin of thesuperciliary region, with pain on the pinch-roll test. It cansometimes be associated with the “cheek sign” on thesame side (Maigne); i.e., pinch-roll testing of the skin ofthe submandibular region produces pain. These signs aredescribed in detail and their mechanisms are discussed inChapter 48, “Headache of Cervical Origin.” Cellulalgic

edema of the region of the angle of the jaw correspondsto C2 (Fig. 21.39).

The zone corresponding to C5 is at the lateral aspectof the shoulder. The zone corresponding to C6 is at themiddle portion of the lateral aspect of the arm and thesuperior lateral forearm.

Trigger Points

Cl trigger points are located in the suboccipital muscles.The trigger points of C3–4 involve the scapular rotators(levator scapulae). For C2, they also sometimes involvethe sternocleidomastoid muscle, and for C3, they involvethe trapezius muscle. For C5, C6, and C7, they involvethe muscles of the shoulder girdle and upper limb,including some “target muscles”: supraspinatus, deltoid,infraspinatus (C5, C6), teres major and teres minor, bra-chialis anterior, and supinator (C6). For C7, they involvethe triceps, brachioradialis, and extensor carpi radialismuscles (Fig. 21.29 through Fig. 21.31).

They may also involve other muscles. In the upperlimb, trigger points of local origin that are not associatedwith a segmental vertebral syndrome are relatively fre-quent, and at all levels, they are frequent in the paraspinalmuscles.

Trigger point palpation is not always easy. A triggerpoint can be the direct result of a segmental dysfunctionor be part of a segmental vertebral syndrome, in whichcase, the points are located caudad to the responsiblesegment. They can also be the direct result of a localsegmental dysfunction. In this case, they are locatednoticeably at the level of the responsible segment.

Figure 21.29

Trigger point palpation of infraspinatus muscle(segmental vertebral syndrome of C5 or C6).

Figure 21.30

Palpation of biceps tendon (segmental ver-tebral syndrome of C5 or C6).

Figure 21.31

Palpation of lateral epicondyle (segmentalvertebral syndrome of C6 or C7).

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143

Figure 21.32

Segmental vertebral syndrome of C4.

Cellulalgia:

supraclavicular fossa, infraclavicular region.

Myalgic cords:

levator scapulae.

Tenoperiosteal insertion:

levator scapulae (which may also be related to involvement of C3 and, rarely, C5).

Figure 21.33

Top left:

examination of cellulalgia in supras-capular region (segmental vertebral syndrome of C4).

Topright:

palpation of insertion of levator scapulae (segmentalvertebral syndrome of C3 or C4).

Bottom left:

examinationfor cellulalgia in infraclavicular region.

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Tenoperiosteal Tenderness

Tenoperiosteal tenderness affects the scapular insertionof the levator scapulae for C3 and C4; the rotator cufftendons (infraspinatus, supraspinatus, biceps, etc.) for C5and C6; the lateral epicondyle for C6 and C7; the radialstyloid for C6; and the medial epicondyle for C7 and C8.

EXAMINATION OF THORACIC SPINE

Examination of Mobility

To test thoracic mobility in all directions, it is mostconvenient to have the patient seated astride the end of

Figure 21.34

Segmental vertebral syndrome of C3.

Cellulalgia:

posterior inferior region of the neck, anterolateral neck, andat the level of the scalp. Cellulalgia is replaced by scalp tenderness that can be elicited on frictional palpation. The regionwhere C3 is involved is the occipital paramedian region. Sometimes this is also associated with a cellulalgic zone over theeyebrow area.

Trigger points:

levator scapulae, sternocleidomastoid, and trapezius.

Tenoperiosteal insertion:

levator scap-ulae.

Figure 21.35

Left:

examination for cellulalgia at the level of the neck.

Right:

examination for cellulalgia of the anterolateralneck (segmental vertebral syndrome of C3).

CHAPTER 21 REGIONAL APPLICATIONS

145

the examining table, if possible, as though sitting in asaddle (Fig. 21.40 through Fig. 21.43). Otherwise, thepatient can sit with legs over the side of the examiningtable. A chair or stool is not stable enough.

The examination can be more precise if the examinerexplores the upper, middle, and lower regions with thetechniques described below as techniques of mobilization(see Chapter 66, “Thoracic Techniques”). Passive-assistedrange of motion is applied until resistance is felt and thenrepeated with mobilization at end range. This allows betterjudgment of the mobility and flexibility of each level.Flexion, extension, lateroflexion, and rotation are studied.

Flexion

As seen in Figure 21.40, the patient is asked tostraighten the back. Is this movement painful? Is the curve

Figure 21.36

Segmental vertebral syndrome of C2, characterized by:

Scalp sensitivity to the friction maneuver.

At this level, this finding is equivalent to findings on the pinch-roll test. Theparamedian region of the scalp corresponds to the posterior branch of C2. The retroauricular and infra-auricular regionscorrespond to a territory supplied by cutaneous branches of the anterior primary ramus of C2 and, to a lesser degree, C3.

Cellulalgia of the angle of the jaw

(innervated by the cutaneous branches of the anterior primary ramus of C2 and C3).

Cellulalgia of the eyebrow region

or “eyebrow sign” of Maigne, associated usually with pain on the pinch-roll test, oftenassociated with pain and submandibular tenderness (see Chapter 48, “Headache of Cervical Origin”). This sign is commonto the first three cervical segments.

Trigger points of the sternocleidomastoid muscle

(rarer for C3).

Figure 21.37

Segmental vertebral syndrome of C1.

Cellulalgia:

region of the eyebrow and, occasionally, of the submandibularcheek.

Trigger points:

suboccipital muscles.

Figure 21.38

Frictional maneuver (Maigne).

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SECTION IV EXAMINATION OF THE SPINE

of the spinous processes smooth? Is there any segmentalstiffness? Then, while grasping the base of the neck andupper thoracic spine with the left hand, the examinerapplies pressure, resulting in slight flexion alternating witha return to the neutral, while the right hand palpates thespinout processes, which should open like a fan, in flexion.The examiner should look for regions of hypomobility andshould also check to see whether repetitive mobilizationagainst resistance is painful.

Extension

As seen in Figure 21.41, the patient’s arms are crossedon top of the head. The examiner’s left hand and forearmsupport the patient. While applying counterpressure withthe right hand at different levels of the spine, the examinerrhythmically mobilizes, with the left hand producinghyperextension of the segment on which the hand appliesthe counterpressure. These maneuvers are painless to anormal spine. During the maneuvers, the examiner’s handshould feel an elastic resistance.

Lateroflexion

With the patient in the same position as for the exten-sion examination (Fig. 21.42), the examiner applies slowand repeated movements of lateroflexion to the back. Withthe other hand, a counterpressure is applied to localize themovement and also to prevent the maneuver from involv-ing the lumbar segment. This movement is difficult withthick and stocky persons. Caution:

The examiner shouldnot displace the shoulders of the patient laterally; other-wise, the movement of lateral inclination is at the level ofthe lumbar spine.

Figure 21.39

Left:

eyebrow sign (Maigne).

Right:

sign of the angle of the jaw (Maigne).

Figure 21.40

Flexion. The examiner applies a gradual pres-sure at the upper thoracic spine, which causes a forwardflexion of the thoracic spine.

Figure 21.41

Extension. The patient sits with arms crossedover the head. With the left hand, the examiner grasps thepatient’s arm in front and from the left. With the right hand,the examiner then places pressure on the back and appliescounterpressure with several slow movements that cause thethoracic spine to arch forward to the maximum of its extension.

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147

Rotation

The patient sits in the same position as for examinationof extension (Fig. 21.43) but the arms can be kept crossedon the chest, especially for examination of the inferiorthoracic spine. The examination maneuver is the same asfor extension. To examine left rotation, for example, theexaminer stands behind the patient, with the left arm infront of the patient’s thorax, holding the patient’s rightarm, and assists the patient’s spine into left rotation. Thisrotation is done at the same time in the thoracic and lumbarspine, although it is minimal in the latter. The examinernotes whether the movement is limited globally andwhether it produces or exaggerates pain as it is performedfirst from one side and then from the other.

Then the examiner tests the mobility of each region ofthe thoracic spine — upper, middle, and lower — applyinglocalized pressure with the other hand. Alternating rota-tion with a return to the neutral position, the examinerpresses with the right hand on the right paraspinal regionto assist rotation to the left and presses with the left handon the left paraspinal region to assist rotation to the right.The hand pressing the spine should recognize the normalsensation of elastic resistance; this movement should notprovoke any pain. The examiner should carefully note anylocalized stiffness or pain.

Segmental Examination

Segmental examination includes assessment for facetjoint tenderness, tenderness to PA pressure on the spinousprocess, transverse pressure against the spinous process,and pressure against the interspinous ligament.

Tenderness to PA Pressure on Spinous Process

Pressure is applied, preferably with the thumb. Thispressure should be dissociated from the superficial sensi-tivity of the spinous process as a result of apophysitis,frequently seen at this level. Examination for superficialtenderness due to apophysitis can be performed with gen-tle friction with the pad of the finger on the spinous pro-cess (Fig. 21.44). This tenderness disappears with super-ficial anesthesia.

Figure 21.42 Lateroflexion. The patient sits as for the exten-sion examination shown in Figure 21.41. The examiner, stand-ing to the left of the patient with a hand on the patient’s rightelbow, pulls the patient toward him. While this is performed,the examiner uses the right hand to put counterpressure onthe lateral side below the axilla against the thorax.

Figure 21.43 Rotation. The patient sits as for the extensionexamination shown in Figure 21.41. To test left rotation, theexaminer takes the patient’s left shoulder and pulls, bringingthe back into a rotation, while the examiner’s right handassists in controlling the movement. To test right rotation, theexaminer reverses the placement of the hands and the move-ment.

Figure 21.44 PA pressure on spinous process.

148 SECTION IV EXAMINATION OF THE SPINE

Transverse Pressure against Spinous Process

The patient should be in the prone position, face downacross the table, although it is possible to examine theupper thoracic spine with the patient seated (Fig. 21.45).Pressure is applied in a slow and progressive manner toeach spinous process from the left and then the right.The same precautions for applying PA pressure to thespinous process should be taken to eliminate pain ofapophysitis.

Pressure against Interspinous Ligament

This examination is performed with the aid of the roundend of a key (Fig. 21.47).

Examination for Presence of Facet Joint Tenderness

The upper thoracic spine can be examined with thepatient seated, back slightly flexed, shoulders rounded,and elbows resting on the knees (Fig. 21.46). For exami-nation of the middle and lower thoracic spine, however,the patient should be in the prone position, lying face downacross the table.

It is better to use the pad of the finger for this exami-nation. The middle finger is placed 1 cm lateral to themidline and slid slowly, parallel to the line of the spinousprocesses, stopping every centimeter to execute a to-and-fro movement vertically, in deep pressure friction. Theindex finger can reinforce the middle finger by pressingon its dorsal face (Fig. 21.46).

Figure 21.45 Transverse pressure against spinous process. Left: this maneuver is effective for patients who are seated forexamination of the upper thoracic spine. Right: it can also be performed on a patient lying down across the table to betterexamine the inferior thoracic spine.

Figure 21.46 Left: examination for facet joint tenderness in upper thoracic spine. Patient is seated. Right: examination forfacet joint tenderness in the inferior thoracic and midthoracic region. The patient is lying across the table.

CHAPTER 21 REGIONAL APPLICATIONS 149

Sources of Errors

As we have seen in Chapter 20, some errors of inter-pretation are possible in the thoracic spine, particularly atthe midportion.

Hypersensitivity of subcutaneous tissues — The sub-cutaneous tissues of the thoracic spine, particularly of themidthoracic segments, are often very sensitive to palpation(see Chapter 36, “Chronic Thoracic Pain”). Pain resultingfrom pressure on the spinous process or facet joints canbe due to compression of skin and subcutaneous tissuesthat are abnormally sensitive. This hypersensitivity isdetected by the pinch-roll test, which should be performed

before any segmental examination at the mid-thoraciclevel (see “Precautions and Sources of Error in SegmentalExamination” in Chapter 20).

Points of emergence of cutaneous branches of pos-terior rami — The cutaneous branches of the posteriorrami of T2, T3, and T4 become superficial very close tothe midline, emerging between T5 and T8, noticeably onthe line of the facet joints. The subjacent branches clearlyemerge more laterally.

Thus, tenderness to longitudinal friction applied withthe pulp of the finger at the level of T5, T6, and T7 doesnot necessarily mean that there is a particular sensitivityof the corresponding facet joints but that there is, moreoften at that level, tenderness over one of the points ofemergence of the posterior ramus of a spinal nerve fromabove. This is particularly frequent at T2 (see Chapter 36,“Chronic Thoracic Pain”). The zone adjacent to the tenderpoint corresponding to the cutaneous territory of the nerveis in that case painful to pinch-roll (Fig. 21.48).

If, on the contrary, there is true facet joint tendernessat T5–6 or T6–7, the adjacent subcutaneous tissues arenot tender to pinch-roll. On the other hand, three to foursegments lower, the cutaneous territory corresponding tothe dermatome of that nerve may be sensitive to pinch-roll (Fig. 21.48).

Figure 21.47 Examination for interspinous ligament tender-ness.

Figure 21.48 Sources of error in segmental examination of the thoracic spine. Left: at the midthoracic level, the examinermust avoid placing pressure on painful skinfolds, thus provoking pain. The examiner should always perform the pinch-roll testbefore going on to the segmental examination. Right: another source of error peculiar to the midthoracic region results fromthe superficial emergence of the cutaneous branches of the posterior primary rami of T2 and T3, perpendicular to the segment.At the T4–5 and T6–7 region, these branches become superficial far below those segments. In other segments, the emergencepoint is more lateral.

Finding a painful point or palpating the median line with the fingers can, on the right, be due to a compression of theemerging branch of the posterior primary ramus of T2 or T3 (see Chapter 36, “Chronic Thoracic Pain”) or pain on the facetjoints of T4–5 or T5–6. In the first case, one will find a cellulalgic zone that corresponds to the dermatome of the branch ofthe posterior primary ramus. In the second case, the cellulalgic band is situated several segments below this territory andcorresponds to a posterior primary ramus of T5 or T6, i.e., at T9 or T10 level.

150 SECTION IV EXAMINATION OF THE SPINE

Detection of facet joint tenderness in the lower thoracicspine does not present the same risks. The cutaneousbranches arising from the lower thoracic levels innervatethe subcutaneous tissues overlying the flanks and upperbuttocks; their point of emergence is clearly more lateraland cannot be compressed against a hard surface.

Examination of Thoracic Spinal Nerves

The neurologic examination follows the same courseas that of the cervical level.

Anterior Rami

Cutaneous territory — Anterior rami are known andunanimously accepted. The cutaneous territory of T4 cor-responds to the nipple line; T6, to the xiphoid; T10, to theumbilicus; and T12, to the inguinal ligament.

The muscles are difficult to examine. The monoradic-ular intercostal muscles cannot be tested, and the flat mus-cles of the abdomen (rectus, obliquus, transversus) arepluriradicular (from T6 to T12).

The reflexes corresponding to thoracic roots are theabdominal cutaneous and abdominal muscular reflexes.

Abdominal cutaneous reflexes — These reflexes aresought with a blunt point and produce a contraction of theipsilateral abdominal muscles to the region that has beenexcited.

• Superior: excitation of the cutaneous supraumbilicalregion, corresponding to T6–7

• Middle: excitation of the paraumbilical region, cor-responding to T8–9

• Inferior: excitation of the hypogastric region, corre-sponding to T10–11

Abdominal muscular reflexes — Tapping over thesymphysis pubis produces contraction of the abdominalmuscles corresponding to T8–12.

Posterior Rami

We have already pointed out the particular importanceof the posterior ramus of T2, which seems to be respon-sible for the entire cutaneous territory of the posterior ramifrom C5 to T1 (Maigne). Caudally, the dermatomes courseobliquely and laterally. As a general rule, T11 is abovethe iliac crest, while T12 is below it.

Examination for Manifestations of Segmental Vertebral Neurotrophic Syndrome of Maigne

Cellulalgia

Superior thoracic spine — Cellulalgia of the supra-spinous fossa corresponds to the C4 segment. The zone

relating to the supraspinous fossa and the mediodorsalregion corresponds to the inferior cervical segments(Maigne) and, as we have seen above (see “PosteriorRami” in Chapter 21, p. 139), coincides with the verylarge cutaneous territory covered by the cutaneous ramusof the posterior ramus of T2 and sometimes of T3 (seeChapter 36, “Chronic Thoracic Pain”). This large territoryof T2 does not appear on the maps of dermatomes that areusually published. Below T2, the thoracic dermatomes fol-low each other from top to bottom (Fig. 21.49).

Middle and inferior thoracic spine — As shown inFigure 21.49, the topography of the cellulalgic zones cor-responds to that of the cutaneous territory of the posteriorrami for the back and of the anterior rami for the chestand abdomen. The posterior cellulalgia is practically con-stant in thoracic segmental dysfunction, whereas the ante-rior cellulalgia is less so.

Thoracolumbar junction — For T11, T12, and L1(Fig. 21.50), the cellulalgic zones are more or less com-mon to the three segmental levels and correspond to thecutaneous territory innervated by the respective spinal seg-ment:

• Posterior zone, to the upper buttocks and low back• Anterior zone, i.e., inferior part of the abdomen,

with a small triangular zone overlying the supero-medial thigh

• Lateral zone, at the level of the trochanter

According to a Chinese study done by the School ofNinghsia, very common anastomoses exist between thenearby posterior rami at the inferior dorsal and superiorlumbar levels. Most of the nerves contain fibers comingfrom two to three vertebral segments. The anastomosesoccur either between the lateral branches or between alateral and medial branch. This would explain why thecellulalgia of the upper buttocks belongs to T12 and Llbut is sometimes identical when T1 and even T10 areaffected.

Trigger Points

Trigger points are found in the paraspinal muscles butare relatively rare. When the thoracolumbar junction isinvolved, they can be localized to the level of the inferiorpart of the rectus abdominis and quadratus lumborum.

Tenoperiosteal Tenderness

Tenoperiosteal tenderness is present only when the tho-racolumbar junction is affected and involves the ipsilateralhemipubis, which is often painful to palpation only, with-out giving the patient any pain spontaneously (Fig. 21.50;see Chapter 60, “Thoracolumbar Junction Syndrome”).

CHAPTER 21 REGIONAL APPLICATIONS 151

Figure 21.49 Cellulalgia of the midthoracic and subscapular regions corresponds to segmental dysfunction of the inferiorcervical spine. Anatomically, the large territory is innervated by the posterior ramus of T2 and of T3 (see Chapter 36, “ChronicThoracic Pain”). The T4 level corresponds to the territory of approximately the T8 level and, anteriorly, approximately the levelof the mammary glands. The T7 level corresponds to the territory posterior to the T11–12 level and anterior to the level of thelast ribs. The T11 level corresponds to the territory just above the iliac crest and anteriorly (seen less frequently) in the lowerquadrant of the abdomen.

Figure 21.50 The segmental vertebral syndrome of T12 and L1 is characterized by common cellulotenoperiosteomyalgicfindings. Cellulalgia: upper buttock; anteriorly, the inferior aspect of the abdomen and superior thigh region; laterally, thetrochanteric region. Trigger points: noted less frequently and usually of minor significance; can be found in the inferior rectusabdominis region. Periosteal sensitivity: noted to involve the hemipubis and be homologous to the level of the insertions ofthe abdominal muscles.

152 SECTION IV EXAMINATION OF THE SPINE

EXAMINATION OF LUMBAR SPINE

Examination of Mobility

Mobility is first assessed with the patient at rest. Thepatient stands with legs apart, in double support. Theexaminer looks to see whether the patient’s lumbar lordo-sis is normal, accentuated (hyperlordosis), or decreased(flat loins) or is replaced by a kyphosis. The examiner alsolooks for scoliosis or lumbar shift and a possible unbal-anced pelvis because of a leg length discrepancy.

• The degree of lumbar lordosis is generally tied tothe angle of inclination of the sacral endplate withrespect to the horizontal.

• Abdominal muscle weakness results in accentuationof the lumbar curvature with antetilting of thesacrum. It is a frequent cause of hyperlordosis andis one of the elements of the “trophostatic syndromeof the postmenopause” (de Séze et al., 1961).

• In some patients, there is no accentuation of thelumbar curvature, but there is a break tied to thehorizontal line of the sacrum.

• In cases of spondylolisthesis, such a break can exist,but palpation especially is used to feel the depres-sion of the spinous process, which gives the impres-sion of the step of a stairway. An antalgic list, oftenseen in cases of disk problems, is characterized bythe presence of a lumbar shift and by protectivelumbar muscle guarding, causing deviation of thespine.

Active Motion Testing

Flexion — As shown in Figure 21.51, the upright sub-ject is asked to bend forward at the waist with the legsextended. The examiner should note the presence of asmooth curvature in kyphosis, of stiffness, and of a fixedincomplete reversal of the lumbar lordosis when flexionis exaggerated by a few degrees. The degree of flexioncan be determined by measuring the distance between thefingertips and the ground on forward flexion, although thisdistance depends on several factors, especially the flexi-bility of the hamstrings and the mobility of the hip joints.Some subjects, even if they have stiff spines, can touchthe ground with their fingers (Fig. 20.11 throughFig. 20.14) if their hamstrings are sufficiently flexible,provided that their hips have enough mobility to allow thismotion. Nevertheless, with all its obvious limitations, thisconvenient maneuver provides some very useful screeningcomparison from one examination to another with respectto the global flexibility and degree of pain with motion.

Schober’s test, a very good test of spinal flexibility, isdescribed below:

• A mark is traced at the level of the spinous processof S1, and another is traced 10 cm higher(Fig. 21.52).

• At the end of flexion, the two marks should havediverged an additional 4 to 5 cm if the inferiorlumbar spine has normal flexibility. In case of stiff-ness, these figures are lower (Fig. 21.52).

Lateroflexion — The patient, standing with arms atthe sides, is asked to bend laterally to the right, then tothe left, allowing the hand to slide along the thigh. Thecurvature should be smooth and symmetric. Is there abreak in the lateroflexion on one side or a global stiffness?The examiner should note (a) the distance from the endsof the fingers to the ground or the level of the inferiorlimb reached by the hand stretched on the bent side and(b) whether that movement provokes pain (Fig. 21.53). Incases of acute lumbar pain most often due to a disk lesion(acute sciatica due to a herniated disk), the patient presentswith an antalgic list with marked unilateral protectiveparaspinal muscle guarding. This attitude is called antalgicbecause it tends to decrease the problem responsible forthe pain by splinting the involved spinal segment andprotecting against painful motion. The pseudoscoliosisthus provoked can be convex to the side of the pain; i.e.,the patient can bend freely away from the pain but cannotbend on the other side. This is known as the “crossedantalgic attitude” of de Séze. Conversely, the pseudoscoli-osis can be concave to the side of the pain, and the patientcan bend freely toward the painful side but not away fromit. This is known as the “direct antalgic attitude” of deSéze (see Chapter 42, “Acute Low Back Pain”).

Rotation — The patient is seated astride the end of thetable and is asked to rotate to the right and then to theleft. Notice is taken of any range of motion restriction,especially when pain is produced with motion in one

Figure 21.51 Distance between the floor and fingers on for-ward flexion depends largely on hamstring flexibility.

CHAPTER 21 REGIONAL APPLICATIONS 153

direction or in both. [Note: If the patient cannot assumethe astride position, the patient can sit normally on thetable, and the examiner can stabilize the patient’s pelviswith both hands.]

Extension — The patient, standing or sitting, is askedto lean backward and throw out the chest. The examinernotes whether that movement is possible, limited, or pain-ful.

“Hollow round” maneuver — This interestingmaneuver (Fig. 21.54) tests both the lumbar mobility inflexion/extension and the muscular control of the patientwho can perform this simple movement more or less eas-ily. The patient, standing, partially flexed, with arms out-stretched and hands placed on the edge of the table, isasked to alternately arch and hunch the back (i.e., into“kyphosis”), forming a hollow round shape. Any antero-posterior stiffness can thus be observed. Many patientswith lumbar pain are unable to sustain this posture, as if

this part of the body was not under their control. Regainingconscious control of these movements and restoring theproprioceptive capability of the region can be some of theaims of physical therapy.

With the patient in this position, the examiner can alsotest lateroflexion of the pelvis by asking the patient tounilaterally contract the quadratus lumborum muscle. Thisis the “happy dog” movement of Peillon.

Passive Motion Testing

To test passive motion, the patient sits astride the endof the table or, if the hip joints do not allow the patient toassume the astride position, sits on the table, with legsdangling. The examiner moves the patient’s spine to detectrestricted or painful motion that may not have been appar-ent with active motion testing. It is not easy to test flexionin this position, but it is excellent for examination ofextension, rotation, and lateroflexion.

Figure 21.52 Schober’s test. Top left: with patient standing,the examiner marks the S1 spine (A, bottom left) and thenmeasures 10 cm above it (B, bottom left). Top right: with thepatient forward flexed, if the lumbar spine has normal mobility,the spinous marks are noted to diverge, and the distancebetween A and B (bottom left) is noted to elongate by about4–5 cm (B′′′′). If the spine is rigid, this distance will not bemodified. Bottom left: results of test seen in profile.

154 SECTION IV EXAMINATION OF THE SPINE

Fig. 21.55 through Fig. 21.57 show those maneuverswhose results can be reported on a star diagram. Theexaminer first moves the patient’s spine in all the rangesthat are possible. Then, at the end of the movement range,the examiner performs some repetitive movements of ten-sion to better test flexibility and elicit tenderness.

Extension — The patient sits with arms crossed on thechest. The examiner’s left forearm passes in front of the

superior part of the thorax and grasps the patient’s rightshoulder (Fig. 21.55). With the right hand, the examinerapplies counterpressure successively at the level of thesuperior, middle, and inferior lumbar regions while mov-ing the spine in extension.

Lateroflexion — While stabilizing the patient’s pelviswith one hand, as shown in Fig. 21.56, the examiner usesthe other hand to induce lateral inclination by graspingthe front of the patient’s opposite upper arm and depress-ing the shoulder.

Rotation — For testing left rotation as is shown, forexample, in Fig. 21.57, the examiner’s left hand movesthe patient’s right arm (crossed on the chest) forward,while the examiner’s right hand presses on the patient’sright paraspinal region. The trunk is brought into left rota-tion with the examiner’s left hand, while maintaining thepatient in a vertical position. The right hand assists themovement by amplifying it on the zone where it receivessupport.

The thoracolumbar, midlumbar, and lower lumbarregions are tested this way to look for some loss of normalflexibility and for any tenderness. The maneuvers arerepeated on the opposite side.

Segmental Examination

For the segmental examination, the patient lies prone,across the table, with a cushion under the abdomen ifnecessary (Fig. 21.58). Each spinal segment is examinedindividually from bottom to top or from top to bottom,from T10 to L5. The examiner should remember thecauses of error in regard to the spinal process or thepinching of a painful skin fold between the thumb andspinous process.

Figure 21.53 Lateroflexion. The examiner can note the curveformed by the spinous processes and visualize the presenceor absence of a smooth curve. The examiner can also notethe sign of Cassure and whether the movement provokeslumbar or rib pain.

Figure 21.54 Patient, standing, flexes forward slightly, placing both hands on the table. a. Patient is then asked to round theback. b. Patient is asked to arch the back. Aside from any stiffness, many patients are unable to perform this maneuver. Thisimplies a lack of control and coordination and an underlying lumbar problem.

CHAPTER 21 REGIONAL APPLICATIONS 155

PA Pressure on Spinous Process

Slow, firm pressure is applied with both thumbs placedover each other (Fig. 21.59).

Transverse Pressure against Spinous Process

This is performed with the thumb, or better, with boththumbs placed over each other, moving from bottom totop, then from top to bottom of the spine (Fig. 21.60).

Contralateral Pressure

This is performed as described for examination of thethoracic spine.

Longitudinal Friction Overlying Facet Joints

These articulations are deep at the lumbar level(Fig. 21.61). Nevertheless, they can be irritated by firmpressure applied with the thumbs placed over each other,with one reinforcing the other and executing small move-ments of deep friction. Above L2, the examiner can use(as for the thoracic spine) the pad of the middle finger,with the index finger pressing on its dorsal side and rein-forcing it.

Figure 21.55 Extension.

Figure 21.56 Lateral flexion.

Figure 21.57 Rotation.

Figure 21.58 Position for lumbar and lower thoracic seg-mental examination (Maigne). This position is comfortable forboth patient (even one with acute lumbar pain) and examiner,since it exposes the thoracolumbar region well and opensup the spinous processes. A variation of this position consistsof having the patient assume a similar position at the foot ofthe examining table; with this position, the curve of the backis less pronounced.

156 SECTION IV EXAMINATION OF THE SPINE

Pressure against Interspinous Ligament

This is performed with the round end of a key(Fig. 21.62).

Examination of Lumbar Spinal Nerves

Anterior Rami

Cutaneous territory — There are rather pronounceddifferences in the cutaneous territory, depending on theauthors. We do not discuss the description of Keegan andGarrett, which has been reproduced often, but discussanother that is closer to the present concept (Fig. 21.63)and takes into account our own clinical and anatomicfindings.

Muscular innervation — Table 21.2 demonstrates themuscles innervated by roots T12–S2. In practice, muscularinnervation can be tested as follows:

Hip flexors (psoas iliac) L1, L2, L3Knee extensors L3, L4Dorsiflexors and toe extensors L4, L5Tibialis anterior L4 and, to a lesser degree, L5Extensor hallucis longus L5Triceps surae S1

During the examination, the patient should be standingon one foot on the tips of the toes. This maneuver can besensitized if the examiner presses simultaneously on theshoulders of the patient to make the movement more dif-ficult.

Reflexes — Testing of the anterior rami reflexes isperformed in the following manner.

L4: Patellar reflex — Tapping the patellar tendonproduces knee extension.

L5: Medial hamstring reflex — The examiner graspsthe medial hamstring of the patient’s flexed knee firmly withthe index finger and then taps the index finger, producingadduction of the thigh, and occasionally, knee flexion.

Figure 21.59 PA pressure on spinous process.

Figure 21.60 Transverse pressure against spinous process.At this level, it is good to use two thumbs superimposed.

Figure 21.61 Longitudinal friction overlying facet joint.

Figure 21.62 Pressure against interspinous ligament.

CHAPTER 21 REGIONAL APPLICATIONS 157

S1: Achilles reflex — Tapping the Achilles tendonproduces plantar flexion of the foot.

Examination for Manifestations of Segmental Vertebral Neurotrophic Syndrome of Maigne

A segment-by-segment description provides a simplerand more logical examination for manifestations of thesegmental vertebral neurotrophic syndrome of Maigne.

L1 has been looked at with the thoracolumbar junction(T12, L1). See “Examination of the Dorsal Spine” aboveand Fig. 21.51.

For L2, the cellulalgic zone involves the anterolateralaspect of the mid and lower thigh. It corresponds to theterritory of meralgia paresthetica, seen with entrapmentof the lateral femoral cutaneous nerve. A small cellulalgia

zone overlying the medial iliac crest can exist simulta-neously.

L3 and L4 (Fig. 21.64). The cellulalgic zones corre-sponding to L3 and L4 overlap one another, but the medialaspect of the knee and the superomedial aspect of the legbelong to L4. Trigger points are located in the rectusfemoris and the vastus medialis. Periosteal tenderness overthe medial knee is rather frequent in disorders of L4.

L5 (Fig. 21.65). Trigger points are located in the glu-teus medius and minimus and the tensor of the fascia lata(Fig. 21.67). A tenoperiosteal pain of the greater tro-chanter is frequently noted in dysfunction of the L4 andL5 segments (Fig. 21.68). In the lower limb, the mani-festations exist only when there is or was an irritation ofthe root. For L5, this is a small cellulalgic zone of the

Table 21.2Muscular Innervation of T2–S2

T12 L1 L2 L3 L4 L5 S1 S2

Quadratus lumborum

Serratus posterior

Iliopsoas

Adductor longus

Adductor magnus

Quadriceps femoris

Rectus femoris

Tibialis anticus

Gluteus medius

Gluteus minimus

Tensor fasciae latae

Semitendinosus

Semimembranosus

Extensor digitorum longus

Extensor hallucis longus

Peroneus brevis and longus

Tibialis posterior

Popliteus

Gluteus maximus

Pyriformis

Biceps femoris

Gastrocnemius and soleus

Flexor digitorum longus

Flexor hallucis longus

Intrinsic muscles of foot

158 SECTION IV EXAMINATION OF THE SPINE

superior anterolateral aspect of the leg, seen also in halfthe cases of sciatica of L5 (Fig. 21.66). Trigger points ofthe toe extensors and tibialis anterior are rare.

S1 (Fig. 21.69 and Fig. 21.70). S1 trigger points involv-ing the gluteal muscles are consistently found in all casesinvolving L5–S1 segmental dysfunction. Pyriformis trig-ger points are inconstant but can be associated with S1

segmental dysfunction. Trigger points of the biceps fem-oris and those of the lateral gastrocnemius and soleus arefound only in cases in which L5–S1 dysfunction is asso-ciated with S1 sciatica; then, it is a constant finding(Fig. 21.72). Similarly, the cellulalgic zone of the poste-rior calf is not found unless there is S1 sciatica; then, itis seen in 50% of cases (Fig. 21.71).

Figure 21.63 Lumbosacral dermatomes.

Figure 21.64 Segmental vertebral syndrome of L3 and L4. Cellulalgia: seen on the anterior thigh at a higher level for L3 andat a lower level for L4. Trigger points: noted in the rectus femoris, vastus medialis, tensor fascia lata, and gluteus medius.Periosteal hypersensitivity: pes anserinus.

CHAPTER 21 REGIONAL APPLICATIONS 159

Figure 21.65 Segmental vertebral syndrome of L5. Cellulalgia: anterolateral calf. Trigger points: the gluteus medius, gluteusminimus, tensor fascia lata, and gluteus maximus, particularly involving the upper muscle bundles throughout. Periostealhypersensitivity: greater trochanter.

Figure 21.66 Test for cellulalgia in segmental vertebral syn-drome of L5. This is found only in cases of sciatica or thesequelae of sciatica involving more than 60% of cases.

Figure 21.67 Palpation of trigger points of gluteal musclesin the segmental vertebral syndrome of L5. They are alwayspresent.

160 SECTION IV EXAMINATION OF THE SPINE

Figure 21.68 Palpation of trochanter. It is often painful in thesegmental vertebral syndrome of L5.

Figure 21.70 Examination of subcutaneous tissues in thesegmental vertebral syndrome of S1. As in the segmentalvertebral syndrome of L5, it is generally seen that casessimultaneously involve sciatica (found in 60% of cases).

Figure 21.69 Segmental vertebral syndrome of S1. Cellulalgia: posterior calf. Trigger points: primarily the muscles of thegluteus maximus, piriformis, gluteus minimus, and gluteus medius; also the inferior biceps femoris and the lateral soleus.

CHAPTER 21 REGIONAL APPLICATIONS 161

Figure 21.71 Trigger point palpation of the inferior bicepsfemoris. Trigger points are present in almost all cases of S1sciatica and in cases involving sequelae of this condition.They are not found in cases of segmental distress involvingL5–S1 without sciatica.

Figure 21.72 Palpation of trigger points in gastrocnemiusand soleus. The same procedure can be performed for thebiceps femoris (Fig. 21.71).

V

TREATMENT

165

22

SPINAL MANIPULATION

When applied in sensibly chosen cases and well exe-cuted, spinal manipulation provides excellent treatmentfor numerous disorders of the spine. However, it has oftenacquired a bad reputation as a result of fanciful pathogenicinterpretations, accidents, and incidents produced by non-medical hands and abuses by some who wanted to use thesemanual techniques to treat the most varied of diseases.

Spinal manipulation has been hypothesized to be effec-tive by acting upon “spinal subluxations,” “sacroiliac sub-luxations,” “dysfunctions of bones of the skull,” “jointfixations,” etc. Each maneuver was justified in the contextof a specific paradigm by the existence of a particularlesion diagnosed empirically by means of palpation tech-niques whose subtlety often defied common sense. Otherusers of manipulative techniques limited their practice totwo or three routine maneuvers that were used to treat allcases.

The use of manipulation was largely justified by sometheoretical frameworks in which some perturbations of theinterspinal movement, such as “hypomobility,” “jointblockage,” and ”subluxation,” were represented as inter-fering with the normal function of the organ, facilitatingor leading to illness. These spinal perturbations, known asosteopathic lesions (or somatic dysfunctions) by osteo-paths and subluxations by chiropractors are detected byparticular techniques of palpation by the former and byradiography by the latter. For these schools, manipulationpracticed according to varied modalities constitutes anessential means of restoring normal function to the spineand thus to the entire organism. This leads to the use ofmanual techniques, either alone (chiropractic) or in asso-ciation with methods of traditional medicine (osteopathy)to treat a diverse list of conditions. The ambition wasalways to treat the entire organism. Specifically relievingsciatica or low back pain was not the aim; the aim was torestore some “general equilibrium.”

J.B. Mennell was the first to use certain manipulativetechniques, most of them borrowed from osteopathy, withthe exclusive aim of treating musculoskeletal disorders.

He adhered to the osteopathic concept and its diagnosticuse of palpation and included an interest in blockage ofthe sacroiliac joints. His successor at St. Thomas Hospitalof London, James Cyriax, used only a few simple manip-ulative techniques that were applied routinely in somerestricted indications, essentially with regard to disks.

The method proposed in this book is based on differentprinciples, although many of the techniques used are thesame. This method aims only to treat certain common painsyndromes resulting from painful mechanical dysfunctionsof the spine and related to the locomotor apparatus.

These pains can be local or regional; can be cervical,thoracic, or lumbar; and occasionally are associated withneural dysfunction of radicular, sciatic, femoral, or cervi-cobrachial neuralgic origin. They can also be referreddistally in the corresponding nerve root territory: pseudo-tendinous, pseudovisceral, etc., as discussed in Chapter18, “Segmental Vertebral CellulotenoperiosteomyalgicSyndrome” (Maigne).

Segmental dysfunction is sometimes due to degenera-tive disk disease. Most often, however, it is due to painfulminor intervertebral dysfunction defined as a benign andpainful dysfunction of the spinal segment and not as a lossof segmental motion appreciated by palpation. The clinicaldiagnosis is simple; it is based on pain elicited during thesegmental examination. In this method, the choice ofmanipulative technique is determined by the pain pro-voked during the segmental examination. Manipulation isthus executed according to “the rule of no pain and ofopposite movement” (Maigne).

In this system, therapeutic manipulation derives fromclear clinical diagnosis and is within the capability of anyphysician. Its application is controlled by strict rules. Exe-cution of the maneuvers requires long and regular training.

In France, this system of manipulations has beenapproved in a 1-year program of special training at theuniversity. This program was begun in 1969 at the Facultyof Medicine of Broussais Hotel Dieu by the author(University of Paris VI). It was the first of its kind in the

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SECTION V TREATMENT

world to be implemented in a traditional medical curric-ulum. It was followed by a program at Marseilles (taughtby Prof. Bardot and Dr. Guillemet) in 1976 and, in thefollowing years, at other faculties of medicine scatteredthroughout France: Lyon, Renne, Toulouse, Grenoble,Strasbourg, Tours, Montpellier. Depending on the deci-sions made by the council of each university, this coursewas reserved for physician specialists qualified in physicalmedicine or rheumatology or for physician generalistswith a year more of postgraduate study. Since its incep-tion, the course in Paris has been widely attended byforeign physicians, often funded by scholarships fromtheir countries.

These manipulative techniques not only are efficienttherapies when used properly, but also provide exceptionalmeans of studying the common pain syndromes of spinalorigin. Their effectiveness provides evidence of spinalsources of numerous pain syndromes that would neverhave been attributed to the spine were it not for theirresolution with manipulation. Performed correctly on theinvolved segment, the techniques can relieve pain. Whenperformed incorrectly or in the wrong direction, they canaggravate or produce the pain caused by these segments.In many cases, their favorable action has led us to questionour fundamental understanding of common pain mecha-nisms. Manipulation for us has been a key — an Ariadne’sthread in the analysis and understanding of many commonpain syndromes. It has caused us to reconsider many wellestablished ideas.

GENERAL CONCEPTS

Basic Principles

There are three steps in manipulation:

• Position the patient and physician properly.• Place the segment under tension.• Perform the manipulative thrust itself.

Let us imagine a patient lying supine. The physiciangrasps the patient’s head with two hands (Fig. 22.1). Thisis known as the

position set.

The physician then rotatesthe patient’s neck toward the left as far as possible. Therotation is increased slightly until end range is reached.This is known as

taking up the slack.

If the physician then returns to the starting point andrepeats the movement several times, it is called a seriesof mobilizations in left rotation. If, after having taken upthe slack, the physician suddenly applies an additionalslight rotation with a rapid, low-amplitude thrust of theright wrist, the resistance to motion yields, and the avail-able segmental motion increases by a few more degrees.The manipulative thrust just described is accompanied bya characteristic “cracking” noise. This forced, brief,unique movement, performed only after the slack has beentaken up, is characteristic of manipulation (Fig. 22.2).

The manipulative thrust should always be executed aftertaking up the slack as a low-amplitude movement. A large-amplitude forceful movement is violent, immeasurable,

Figure 22.1

If the patient voluntarily turns his head all the way to the left, this is noted to be an active movement and isdesignated by line A. If the examiner turns the patient’s head in rotation to the left, this is considered a passive movementand is designated by line P. At this point, the examiner and the patient have the same impression that further movement isnot possible. This is referred to as the “taking-up-the-slack” point (T). If, after the taking-up-the-slack phase is complete, theexaminer uses a forceful brief thrust and exaggerates the movement, resistance is noted to “melt away,” and a cracking soundis produced. This brief force and very limited movement, going beyond the point of tension, constitutes what is termed themanipulation or the manipulative thrust (M). If the thrust goes beyond the anatomic limit (AL), it is possible to produce asubluxation (L). By not going beyond this point, the examiner has exercised perfect control of movement.

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painful, and dangerous. This movement should be per-fectly controlled by the operator and, to be well executed,requires experience. The manipulation should be perfectlypainless. It can be executed by a trained physician at alllevels of the spine of a normal patient without being pain-ful or uncomfortable. It should not be rough, and theoperator does not have to use great force if the techniqueis perfect and the patient is positioned properly.

Remarks

The correct technical execution of a manipulation demandsabsolute attention to the three steps:

1. Correct positioning of both patient and examineris necessary for proper execution of the maneu-ver. The examiner should focus completely onperforming the positioning perfectly. It should

be controlled from start to finish, and the exam-iner should always remain perfectly balanced.

2. The examiner should start the maneuver in thechosen direction slowly, until a resistance indi-cates end-range to examiner and patient. Thetension is then increased slightly without com-ing back, thus creating a torsional pressure.

3. With the slack taken up and firmly maintained,the manipulative thrust is executed in the cho-sen direction after a brief pause (Fig. 22.3 andFig. 22.4).

Definitions

Manipulation

Manipulation is a very specific movement that we shalldefine as follows.

Manipulation is

a forced passive movement that tendsto bring the elements of a joint or a group of joints beyondtheir usual physiologic range of motion. Thus, in the spineit consists of rotation, lateroflexion, flexion, or extension,isolated or combined, on the chosen spinal segment.

Thus understood, manipulation is a medical act. It is aprecise movement whose coordinates are determined aftera preliminary examination, and it is used for very definiteindications. In the English literature, the word

manipula-tion

often implies the entire spectrum of manual therapy(with the possible exception of massage). Here, we dis-tinguish manipulation as thrust techniques or “low-ampli-tude, high-velocity techniques” and mobilizations as artic-ular techniques.

Mobilization

If, after having taken up the slack as described above,the examiner returns to the starting point and repeats thesame maneuver several times in a rhythmic and elasticway, we say that the examiner has executed a series ofmobilizations in left rotation (Fig. 22.3). Mobilization isa passive movement, performed repetitively, which doesnot include any forceful or strenuous or movement.

Figure 22.2

Amplitude of movements discussed in Fig. 22.1.From a neutral position, a movement can be performed intwo opposite directions: rotation to the right or left, lateroflex-ion to the right or left, and flexion and extension. On thisdiagram, one can note the range of active (voluntary) move-ment, passive (induced) movement, and the manipulatedrange of movement. T

marks the taking-up-the-slack point.Beyond this normal anatomic range of motion, there is asubluxation.

Figure 22.3

a.

Mobilization is a movement only up to the point of taking up the slack (T), with return to the neutral position(N), and is repeated many times. It can be performed in both directions (in rotation to the right (R) and left (L), in flexion andextension, and in lateroflexion to the right or left). AL = anatomic limit.

b.

The manipulative thrust (MT) is always performed ina manner that provides fine movement beyond the point of tension (T). The movement is brief, rapid, and not repeated. Themovement must never go beyond the anatomic limit.

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“Cracking”

Cracking accompanies the manipulative thrust. Itpleases the novice manipulator and satisfies the patient,who thinks (wrongly) that it is proof that “something hasbeen put back in its place.” In reality, it only means thatthe degree of movement has been sufficient to overcomethe tonic and periarticular resistances and allow a suddenseparation of the articular surfaces. This noise is proof ofthe manipulation, nothing else. There are cases when themanipulator should not go beyond the cracking, and caseswhen the examiner must go beyond that point. Crackingis the usual companion of the manipulation. It is not heardduring supple passive mobilizations. Such cracking canbe produced by the spine as well as the limbs. Even thefingers and feet can undergo cracking whenever certainmechanical conditions make the sudden separation of twoarticular surfaces possible.

Mechanism

In the spine, the facet joints, not the disks, are thesources of the cracking sound. Increasing the gap betweenthe articular surfaces decreases the intra-articular pressure,which is already negative. In some regions, because of thedegree of surface congruity and the angle of stretching,there is a thin lamina of synovial fluid between the twoarticular surfaces. At a certain degree of separation, thephenomenon of cavitation is produced at the level of thisthin layer. In a way, a void (empty bulb) is created. Thegases dissolved in the synovial fluid rush in, producingthe cracking noise and forming a bubble of gas (Unsworthet al.). When the joint returns to its normal position, thesegases are resorbed in the synovial fluid. This takes approx-imately a quarter of an hour, which is why the manipulator,

having produced such a cracking in a joint, should waitsome time before doing it again. This

time of recharging

varies from one person to another.Cracking does not mean that the manipulation is a

success. Any manipulation — correct, incorrect, approx-imate, or useless — can produce a crack. Cracking is ofinterest only if the manipulation was justified and wasperformed on the right segment and in the right direction.Cracking is neither necessary nor sufficient and is a normaloccurrence.

A good manipulator should be able to crack the spine ofa normal person completely, vertebra by vertebra, withouthurting the person at all, and this according to any of theorientations of the movement. Nevertheless, a joint thatcracks does not have quite the same behavior as the one thatdoes not crack, as is indicated in the section titled “Mecha-nism of Action of Manipulation” at the end of this chapter.

DIFFERENT TYPES OF MANIPULATION

To classify, we divide the manipulative techniques intothree groups: (a)

direct, because they consist of directpressures performed on the spine itself; (b) indirect,because natural lever arms such as the head, shoulders,pelvis, and legs are used to move the spine; and (c) semi-indirect, since the examiner provides direct support to thespine during these maneuvers.

Direct Manipulation

Direct manipulations are maneuvers executed with theheel of the hand. Generally, the pisiform is the point ofpressure. The thrust employed is sudden, brief, and flat;it is applied to either the transverse or the spinous process.

Figure 22.4

a

and

b.

Example of a cervical manipulation in left lateral flexion. The thin arrow (2) demonstrates a position thatis being set in tension (T). The thicker arrow (3) demonstrates the direction of the manipulative thrust, which is brief and limited.

CHAPTER 22 SPINAL MANIPULATION

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For example, as shown in Fig. 22.5, pressure on the lefttransverse process of B will produce rotation toward theright; if, using the other hand, a counterpressure is appliedsimultaneously on the right transverse process of C as indi-cated in Fig. 22.6, this movement will act electively on seg-ment BC.

The pressure should be followed by a very quickrelease. These maneuvers are more difficult to execute thanthey may seem; the pressure is difficult to measure, andtherefore, the maneuver is sometimes dangerous. In practice,however, these maneuvers offer unlimited possibilities.

Indirect Manipulation

In contrast to direct manipulation, indirect manipula-tions are of an infinite variety. With them, all of the spinalsegments can be manipulated in all directions, always witha measurable strength; repeated and progressive mobili-zation can be executed, allowing excellent analysis of thesegmental mobility. Indirect manipulation has an evidentsuperiority over direct maneuvers. Briefly, the followingis an example of indirect manipulation that should beexecuted according to the three steps described above.

Figure 22.5

a

and

b.

Direct manipulation applied to the left transverse process of B with the palm of the hand. This resultsin a forced rotation to the right in vertebra B.

Figure 22.6

a

and

b.

Direct manipulation with counterpressure applied in the same maneuver as in Fig. 22.5. In this case,however, the other hand is used to apply counterpressure to the transverse process to the right of C and helps to localize themovement to segment BC.

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SECTION V TREATMENT

1. Positioning the patient: As shown in Fig. 22.7,the patient has been placed in the right lateraldecubitus position. The examiner stands in frontof him, puts his left forearm under the patient’sleft axilla, and rests his right forearm on thepatient’s left ischium.

2. Taking up the slack: The examiner fixates thepatient’s left shoulder at 45° relative to theplane of the table and maintains it in this posi-tion while with his right arm, he pushes in theopposite direction on the patient’s left hemipel-vis, rotating the lumbar spine until there is afeeling of resistance. Manipulation is useful atthis point because it is the best time to takeadvantage of taking up the slack to obtain amore efficacious terminal thrust.

3. Manipulative thrust: Finally, while maintainingthe tension (taking up the slack), the examinerexaggerates his pressure on the ischium with asudden and brief thrust, resulting in a manipu-lation.

By changing the amount of inclination of the shouldersand pelvis, by placing the lumbar spine in lordosis orkyphosis, by using other points of support, and by modi-fying the direction of the manipulative thrust, the examinerhas within his or her grasp various maneuvers meeting thedifferent needs of the patients to be treated.

Semi-Indirect Manipulation

To obtain greater precision for some regions, semi-indirect manipulation techniques are used. In this type ofmaneuver, taking up the slack is always done by supportat distance, but the examiner also provides direct supportin the segment to be manipulated, with the hand, knee, or

chest. On the spine set in tension, the manipulative thrustcan be performed in two ways: either by the sudden exag-geration of the movement at a distance, with the knee orthe hand applying counterpressure to localize the manip-ulation —resisting it — or by exaggerating the local pres-sure that assists and locally accentuates the movementstarted by taking up the slack at a distance. Thus, we candescribe manipulations that are “assisted semi-indirect”or “resisted semi-indirect.”

Assisted Semi-Indirect Manipulation

At the start, this type of manipulation is indirect. Theexaminer applies to the spinal region to be manipulated amovement in the desired direction by an action at a dis-tance. At the same time, with the other hand, the examinerlocalizes its action on the precise segment where themaneuver should act. Thus, the examiner accentuates theglobal movement by acting in the same direction.

Consider, for example, a manipulation of the thoracicspine in which a left forced rotation of T9 on T10 isdesired. The patient is sitting astride the end of the table,with his hands behind his neck (Fig. 22.8). The examiner,standing behind him, passes his left arm under the patient’sleft axilla and grasps the patient’s right shoulder. Pullinghis left hand toward the left and backward, the examinerimparts a rotatory moment to the patient’s trunk while theheel of his right hand is placed over the right transverseprocess of T9. Taking up the slack occurs in two steps:first, by the left hand for the global movement, and thenby a slow and progressive pressure of the right hand onthe transverse process of T9. In practice, these two move-ments are simultaneous. The manipulative thrust is pro-vided by the right hand, which increases the rotationlocally by assisting the movement. This is why we call

Figure 22.7

Indirect manipulation.

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171

this technique

assisted manipulation.

In this case, it is anassisted manipulation in left rotation.

Resisted Semi-Indirect Manipulation

The converse to the procedure described above, resistedsemi-indirect manipulation allows the examiner to localizethe actions of some maneuvers to a precise point on thespine. Consider again the manipulation of the same seg-ment, T9–10. To impart a manipulation that produces max-imal segmental flexion, we employ the technique ofmanipulation that makes use of the examiner’s knee,described below and illustrated in Fig. 22.9.

The patient is seated on a stool, with hands crossedbehind the neck. The examiner passes his forearms underthe patient’s axilla and grasps the patient’s wrists. By theposition in which the patient’s body is placed and theactions of the examiner’s forearms, the patient’s spine isbrought to a position of global flexion; i.e., the disks are“gapping” backward. To localize the maneuver, the exam-iner performs it in such a way that the global curvatureimposed to the spine has its apex at T9–10 and then appliescounterpressure with the right knee against the spine, pro-tected by a small pad or towel over the spinous processof T10. Taking up the slack is performed by raising thepatient’s axillae. Then, while firmly maintaining counter-pressure with the knee, the examiner delivers the thrustvertically and slightly toward himself, which produces amanipulation with the usual cracking.

Let us now analyze what happened. Figure 22.10 showsthe vertebrae in maximal flexion, and the

arrow

at G isthe point of counterpressure of the knee at T10. Suddenly,flexion is exaggerated, while at the same time the physi-cian pulls the patient’s whole spine toward himself; thepoint of counterpressure provided by the knee preventsvertebra A from following the movement. When raisingthe axillae, the physician brings the spine into flexion, andthe maximum force of distraction is imparted to the jointbetween A and B. When the physician suddenly exagger-ates the raising of the shoulders and brings them slightlytoward himself, he has exerted a force F opposing forceG of the motionless knee maintaining the spinous process,pressing on it to the front and bottom. The knee is a fixedpoint of resistance toward the imposed global movement,and this is thus a “resisted” maneuver. Thus, to obtainforced flexion of a spinal segment, the examiner needs tosupport the spinous process of the inferior vertebra of the

Figure 22.8

Semi-indirect assisted manipulation.

Figure 22.9

Semi-indirect resisted manipulation.

Figure 22.10

See text.

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SECTION V TREATMENT

segment while maintaining the supra-adjacent region inforced flexion. Conversely, to produce extension on thissame segment, the region is brought into extension, thencounterpressure is applied to the spinous process of T9(superior vertebra of the concerned segment). This is con-sidered an assisted semidirect manipulation, since thelocal support increases simply the imposed global move-ment.

Figure 22.11 demonstrates a resisted semi-indirectmaneuver used currently for lateroflexion on the inferiorcervical spine or on the cervicothoracic junction. Thepatient is lying on his right side. With one hand (here theleft one) the physician holds the patient’s head and pullsthe neck into left lateroflexion while applying counter-pressure with the pad of his thumb to the left side of theC7 process to apply the essential manipulative impact tothe supra-adjacent segment C6–7.

LOCALIZATION OF MANIPULATION

The semi-indirect assisted or resisted manipulationallows precise localization of the manipulation on a givensegment of the spine. This localization is also a functionof the technique used. Because of their particularcharacteristics, such maneuvers exert their effects pri-marily on a particular spinal region.

If the case allows, the examiner can also use the par-ticularities of spinal physiology. For example, if a rotationof the trunk to the right or left is applied to a seated subjectwith the thorax in neutral position, the pivot point of therotation is at T10–11, but if the trunk is flexed prior toimparting rotation, the pivot point ascends a few levels.Conversely, if the trunk is extended prior to rotation, thepivot point rests at a lower point in the spinal column. If

a thoracic manipulation is indicated in rotation, the pre-cision of its localization is facilitated by the use of thisparticularity.

Another characteristic feature of spinal mechanics canalso be used. In the thoracic and cervical spine, latero-flexion and rotation are coupled movements. If a rotationalmanipulation is desired at a given segment in a givendirection, the spinal region is placed into ipsilateral later-oflexion first, so that the segment to be manipulated issituated at the apex of the lateral curvature so formed. Ifa right rotation is desired, a right lateroflexion is per-formed first. If a left rotation is desired, a left lateroflexionis performed first.

This particularity can be illustrated by a metallic tapemeasure. Imagine a segment of that tape measure. It ismaintained vertically by the examiner holding each endbetween the thumb and index finger of each hand. If it isthen rotated, this rotation is distributed along the entireheight of the tape, with maximal rotation at the midpoint.But if it is side-bent slightly while maintaining the rota-tion, the examiner can, at will, modify these two coordi-nates and vary the position of the pivot point of the cur-vature, from top to bottom in a very precise manner. Thisposition is the point of least resistance. A slight degree oflateroflexion results in a high pivot point, while a greaterdegree results in a lower pivot point. The more markedthe lateroflexion, the lower the rotation (Fig. 22.12).

When possible, it is convenient to take advantage ofthese particularities, although this cannot always be done.The examiner can, for example, be led to perform amaneuver combining lateroflexion and rotation of oppo-site direction on the same segment, thoracic or cervical,or to perform a midthoracic manipulation (T7–8) in rota-tion and in extension.

Figure 22.11

a

and

b.

Semi-indirect resisted manipulation in lateral flexion. The counterpressure is applied with the thumb tothe left spinous process (here C7) subjacent to the segment being manipulated (C6–7).

CHAPTER 22 SPINAL MANIPULATION

173

Remarks

The exact correlation of the manipulative movement andits therapeutic aim with a purely physiologic movementis not possible. When there is a meniscal blockage in aknee, for example, the maneuver necessary for a possibleunblocking of the affected knee cannot be chosen on thebasis of the normal physiology of the knee. The necessarymovement must be based on the results of the clinicalexamination of the affected knee. The same principleapplies at the spinal level and in the system that we pro-pose. In all cases, the rule of “no pain and of the oppositemovement” described below should be the guide.

INDICATIONS FOR MANIPULATION

It is absolutely necessary to be able to identify theindications for manipulation. Here, we propose a classifi-cation of manipulation according to the movement as char-acterized by an observer.

Usually, the manipulative techniques are describedaccording to the “lesions” they are supposed to correct ona given vertebra. For example, the manipulation for a rightL5 posterior means that the fifth lumbar vertebra is rotatedto the right relative to the sacrum; “subluxed” or “fixated”in this malposition for some instances or having lost itsfreedom of movement in left rotation for others. Themaneuver will have as its aim restoring a vertebra to itsproper alignment in some cases or restoring a movementthat has been judged limited in others.

Such nomenclature is, of course, extremely convenient.It explains the corrective movement and visualizes it. Thediagnosis and direction of the maneuver to be used areincluded in these few words, “right L5 posterior.” Twoexaminers can thus communicate easily. What remains tobe known is the validity of diagnoses based on the pal-pation and the reality of such subluxations or hypomobil-ities. To describe a maneuver intended to correct a leftatlas posterior or a right sacrum anterior means that oneis able to assert that the atlas has lost partial or totalpossibility of right rotation (it is fixated in left rotation)

or that the right sacroiliac joint is blocked “in position ofnutation.”

Even if this was true, it would remain to be proven thata loss in mobility in right rotation is treated by forcingthe right rotation or that a loss of extension is treated byforcing the extension. Is a blocking of the knee, whoseextension is limited by a meniscal lesion, treated by asudden extension? If posterior disk blocking produces anacute low back pain and extension of the concerned seg-ment is made impossible (bringing together the spinousprocesses), is it logical to play “nutcracker” in forcing thisextension? We shall come back to this essential point, butfor now, let us stress that if we describe the maneuvers asthey are seen from the outside, it is because we shouldnot judge too early what a manipulation can correct. Pres-ently, it is the only way to proceed objectively, even if itis schematic, and it is the one we have always used(Maigne, 1959).

Manipulation is a global gesture that can be brokendown in all cases to its elementary components withrespect to the three cardinal planes; i.e., any manipulativemovement can be defined perfectly by its coordinates, aslong as the examiner takes into consideration that an ele-ment of segmental traction is practically always involved.Consequently, it can now be concluded that there is a verygreat variety of possible maneuvers.

Components of Manipulative Movement

The degrees of freedom available for spinal segmentalmotion are flexion, extension, lateroflexion (both to theright and left), and right and left rotation. Manipulationcan, therefore, be performed in all these orientations, iso-lated or combined (Fig. 22.13 through Fig. 22.16).

During extension, the posterior edges of the vertebralendplates converge, the nucleus pulposus migrates anteri-orly slightly, the anterior edges of the spinal endplatediverge, and the facet joints converge.

Figure 22.12

Tape measure (see text).

Figure 22.13

Flexion.

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SECTION V TREATMENT

With flexion, the opposite occurs; i.e., the anterioredges of the vertebral endplates converge, the posterioredges diverge, the nucleus migrates posteriorly, and thefacet joints diverge.

In right lateroflexion, the vertebral endplates and facetsconverge on the right side and diverge on the left.

In right rotation, the right transverse process of theconcerned vertebra tends to move backward in relation tothe subjacent vertebra.

By convention, spinal segmental motion is alwaysdescribed with respect to the subjacent segment. Imaginea male patient standing, with pelvis fixed. He rotates thetrunk toward the right; i.e., his right shoulder becomesposterior in relation to the plane of the pelvis. It is athoracolumbar rotation toward the right. Now consider thesame person in the same position but this time with hisshoulders fixed while his pelvis turns. His pelvis rotatesto the left, and the left hip becomes posterior while theright hip becomes anterior. This is also considered a tho-racolumbar rotation toward the right because the rotationof the trunk is judged in relation to the pelvis (subjacentsegment) considered fixed. This is true even for the rota-tion of only one spinal segment or a flexion, extension, orlateroflexion movement. Thus, its relation to the subjacentsegment considered fixed is the defining element.

Description of Manipulation

To accurately and precisely describe a given manipu-lation so that it can be rapidly and easily conveyed toothers, exactly reproduced, or recorded in the chart, theexaminer should do the following.

• Designate the segmental level at which the manip-ulation is performed.

• Specify the exact direction given to the maneuver.• Indicate the technique used.

Level at Which Manipulation Is Performed

Most often, this level is the precise level (C5–6, T3–4,L5–S1) where a segmental dysfunction (painful minorintervertebral dysfunction or PMID) has been discovered.In other cases, we cannot be as selective, and then themaneuver must be designated as a cervical (C), cervico-thoracic (CT), thoracic (T), thoracolumbar (TL), or lum-bar (L) manipulation on the superior (s), middle (m), orinferior (I) part of the region that has been considered;e.g., superior cervical spine (Sc), midthoracic spine (Mt),inferior lumbar spine (Il).

Direction Given to Maneuver

The manipulation should be perfectly defined in thethree planes: frontal, sagittal, and horizontal. Any move-ment, passive or active, of the spine is a combination ofthe elementary movements: flexion or extension, right orleft rotation, and lateroflexion, right or left. The directionscan be written as follows.

Flexion (forward flexion) FExtension (backward flexion) ERight rotation RRLeft rotation LRRight lateroflexion RLFLeft lateroflexion LLF

Figure 22.14

Extension.

Figure 22.15

Rotation.

Figure 22.16

Lateroflexion.

CHAPTER 22 SPINAL MANIPULATION

175

Direction of Manipulative Thrust.

When an exam-iner writes “manipulation in right rotation,” the directionof the thrust is clear. When an examiner writes “manipu-lation in right rotation, right lateroflexion, extension,” theposition of the segment during the manipulation is definedvery well, but the direction of the manipulative thrust isnot precisely described. The latter can be performed some-times in a direction resulting from the three orientations,although generally it favors one of them.

This example allows three possibilities. Based on theposition, the thrust can be made either in extension, inright lateroflexion, or in right rotation. Daily practicedemonstrates that the therapeutic effectiveness of each ofthese maneuvers is different. Note that rotation and later-oflexion are, as already seen, similar movements com-bined at the cervical and thoracic levels; this is true insome physiologic conditions for a normal segment. It isprobably not the same in the case of the imposed, forcedmovement that the manipulation induces on a segment thatis no longer functional. Furthermore, these differentmaneuvers are going to exert powerful stretching actionson different muscles, depending on the direction of thethrust. This point is essential in understanding the actionof the manipulation. Nevertheless, it is convenient to limitourselves here to mechanical notions only.

To define a manipulation and give it identity, the exam-iner should describe exactly the direction of the terminalthrust. For example, in the case of a manipulation in rightrotation (RR) performed on a spinal segment positionedin right lateroflexion (RLF) and in extension (E), themovement can be written by underlining the direction ofthe thrust: RR + RLF + E.

Technique Used.

As for the technique used, one cancreate a personal terminology. In later chapters, we givea few names to certain techniques:

chin-free

(Chapter 64),

epigastric

(Chapter 66),

single-knee

(Chapter 66), or

dou-ble knee

(Chapter 67) techniques. A technique can also beidentified by describing exactly the position of the patientduring the manipulation.

Recumbent

• On the back or in supine (S) position (Fig. 22.17)• On the abdomen or in prone (P) position (Fig. 22.18)• On the side or in lateral decubitus (LD) position

(Fig. 22.19)

Sitting

• Normally, with both legs hanging over one side oftable (Fig. 22.20)

• Seated astride table (SA; Fig. 22.21)

Standing

• Note as (S)

Examples

Manipulation of lower cervical spine (C6–7) —

Thepatient is lying on his right side (RLD; Fig. 22.22). Themanipulation is performed on C6–7 in left lateroflexion(LLF); the examiner would write “C6–7 (RLD) (LLF).”

Manipulation of superior cervical spine (C2–3) —

The patient is lying supine (S). The segment is in neutralextension, and flexion and is brought in left rotation(Fig. 22.23); the examiner would write “C2–3 (S) (LR).”

Manipulation on T12–L1 in left rotation —

Thepatient is sitting astride (SA) the table (Fig. 22.24); theexaminer would write “T12–L1 (SA) LR.

Low lumbar manipulation on L4–L5 —

The patientis lying on his right side (RLD; Fig. 22.25); the segmentis in left rotation (LR), and the spine is positioned inflexion; the examiner would write “L4–5 (RLD) F + LR.”(LR is underlined here because it is the direction of theterminal thrust.)

Figure 22.17

Dorsal decubitus (DD) or supine position.

Figure 22.18

Ventral decubitus (VD) or prone position.

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RULE OF NO PAIN AND OPPOSITE MOVEMENT (MAIGNE)

For any case necessitating a manipulative treatment,there are useful maneuvers, harmful and dangerousmaneuvers, and indifferent maneuvers, i.e., maneuversthat are neither helpful nor harmful. The examiner shouldfind the former and avoid the latter, determining the direc-tion of the maneuver that gives the best results. This direc-tion does not depend on the side where the patient feelsthe pain. If we look at several cases of common right

sciatica, we notice that a maneuver where the left rotationis dominant relieves the condition in some cases, whilethe same maneuver is difficult and aggravating in othercases, which, conversely, can be relieved by a maneuverin right rotation.

This basic problem in manipulation has been consid-ered by very diverse authors and schools. Some ignore itdeliberately, and from the moment that a manipulativetreatment is decided according to their criteria, they applythe same global, stereotyped, and symmetric maneuvers,almost ritually, to all patients, which reduces notablythe possibilities and indications. Such is the case withJ. Cyriax, who insists especially on the associated use oftraction.

Figure 22.19

Lateral decubitus (LD) position.

Figure 22.20

Patient in seated (S) position.

Figure 22.21

Patient sitting astride (SA) table.

CHAPTER 22 SPINAL MANIPULATION

177

Others think, with some small differences, that manip-ulation corrects “malpositioned joint blockage” or “lossof segmental joint play” and use palpation or sometimesradiographic means to diagnose the “malposition” or“hypomobility.” Thus, they justify their manipulation anddetermine the adequate maneuver or maneuvers (they areoften numerous) to use.

According to Mennell, restoration of “joint play” isessential. With some notable exceptions, this is the doc-trine of the American school of osteopathy, as well as thedoctrine of the German and Czech schools of manualmedicine. For these schools, the aim of manipulation is torestore the mobility of a vertebra supposed to have lost itsplay of normal movement. This loss of play is appreciatedby palpation of segmental motion: degree of separation andorientation of the spinous processes in flexion/extension.

Figure 22.22

Patient in right lateral decubitus position (RLD).

Figure 22.23

Patient in supine (S).

Figure 22.24

Patient seated astride (SA) table.

Figure 22.25

Patient in right lateral decubitus position (RLD).

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SECTION V TREATMENT

Thus, in these schools, it is assumed that if such avertebra has a normal play in extension (its spinous pro-cess comes close to the subjacent one) but has a decreasedplay in flexion (its spinous process does not separate wellfrom the subjacent one), then the manipulative movementthat can be applied will tend to force that vertebra inflexion. Similarly, if it is assumed that such a vertebraturns well toward the left but not well toward the right, amaneuver forcing a rotation to the right should be per-formed.

The system of application of manipulation that we pro-pose is different. It is not based on the notion of spinalmobility, in which hypomobility becomes an indicationfor manipulation, and hypermobility is treated as acontraindication for manipulation. Rather, it is based onthe notion that one can locate the responsible segment byfinding in which segment pain can be produced by passivemovement.

It is not the loss of segmental joint play that seems tous to be the fundamental element, insofar as it can beappreciated by palpation. What seems characteristic to usis the segmental pain; i.e., when a spinal segment isresponsible for a local or referred pain (whether a PMIDor a disk problem), it is painful when it is directly solicitedby forced maneuvers that exaggerate its movement in cer-tain directions, while it is painless in the opposite direc-tion. The painless directions are precisely the ones thatwe chose for the manipulation.

Indeed, experience has shown us that the direction ofthe useful manipulation is always opposite to the oneproducing the pain or the symptoms of the patient, pro-vided that this direction is also free and painless. Notethat we mean here the pain produced by the movementthat has been applied passively on the concerned segment,not the pain produced by an active movement performedby the patient. Generally, there is a concordance betweenthe two, but not always. The manipulation performed inthis nontender direction we call the “rule of no pain andopposite movement” (Maigne).

The rule of no pain and opposite movement consistsof forcing the passive, free, and painless movement (nopain) rather than the passive and painful movement (oppo-site movement). For clarity, let us take the example of apatient presenting with a cervical pain resulting from aforced movement. The C5–6 level is painful. Taking upthe slack in right rotation is free, while taking up the slackin left rotation is painful and blocked. Thus, by impartingright rotation to the involved segment, left rotation can befreed and the pain of the patient can be eliminated.

In practice, things are a little more complicated becauseeach spinal segment can be moved in six directions: flex-ion, extension, right lateroflexion, left lateroflexion, rightrotation, and left rotation. The necessary maneuver can bea triplanar thrust, combining all of the available pain-freeand unblocked motions; or a series of unidirectional

maneuvers can be performed according to each of the freedirections. Thus, it is on a pragmatic basis, constantlytested by experience, that we have proposed this rule ofapplication of manipulation (1959). But it also has a phys-iologic justification. Forcing at the end of its course, witha brief and sharp thrust, the free passive movement in thedirection opposed to the one producing the pain producesan inhibitory reflex. This reflex eliminates or diminishesthe mechanisms perpetuating the painful segmental spinaldysfunction and its radicular consequences (cellulalgia,trigger points).

This rule of no pain and opposite movement impliesthe necessity of describing exactly the techniques and theirdirections that are adapted to each case. This means thatwe have to proscribe the standard techniques and the rou-tine of manipulating systematically to the right and thento the left. It is fortunate that the lack of precision of mostof the standard techniques, which decreases their effi-ciency, also decreases their possible harmfulness.

Practical Application of Rule of No Pain and Opposite Movement

The result of the clinical examination is reported on aschema in the form of a six-branched star (Fig. 22.26),showing the directions of the spinal movement. The coor-dinates of the necessary manipulative movement appearclearly; the schema shown in Fig. 22.26b demonstrates acase in which the passive examination has disclosed thatright rotation, right lateroflexion, and extension are pain-ful, while left rotation, left lateroflexion, and flexion arefree and painless. The necessary manipulation in this case(if the clinical context favors this type of treatment) willthus be maneuvers that utilize these free directions ratherthan the painful or blocked directions and that are eitherunidirectional or combined.

It is not the side of the patient’s pain complaint thatdetermines the direction of the manipulation, but the direc-tion of the pain produced by the passive movement. InFig. 22.27, two examples of right sciatica are presented.The clinical context and the previous examination seemedto indicate that these patients would be good subjects forthe use of manipulation. In both, the sciatica was locatedon the right side; one presented with an antalgic scoliosisconvex on the right side, while the other presented withan antalgic scoliosis concave on the right side. Results ofpassive lumbar movements on the patients in sitting posi-tion until the segments were set in tension showed thatthe free and painful movements were different in thesecases; they were completely opposite. The manipulativemovements required by the rule of no pain and oppositemovement were also opposite. The star diagrams(Fig. 22.27) reveal this difference clearly.

As shown in Fig. 22.27, the following maneuvers wereperformed: for patient A sitting astride the table, latero-

CHAPTER 22 SPINAL MANIPULATION

179

flexion performed in left rotation (plus left lateroflexionplus flexion); for patient B sitting astride the table, later-oflexion performed in right rotation (plus right lateroflex-ion plus extension); for patient A lying on his right side,left lateroflexion plus left rotation; for patient B lying onhis left side, right lateroflexion plus right rotation; forpatient A lying on his right side, a combined maneuver ofleft rotation plus flexion; and for patient

B

lying on hisleft side, a combined maneuver of right rotation plusextension.

Technical Contraindications to Manipulation

If all directions are painful, all branches of the stardiagram are crossed out and no manipulation is possible(Fig. 22.26c). This is common in infectious, inflammatory,or tumoral lesions, etc. and can also happen in commonmechanical disorders.

In this case, the nature of the disorder would normallylead to a manipulative treatment, but because of the ruleof no pain and opposite movement, manipulative treatmentis not possible. We say that the disorder is a “technicalcontraindication” to manipulation.

In practice, the manipulative treatment will have a goodchance of success when at least three degrees of freedomare available. If there are only one or two free directions,repetitive mobilization can be applied in these directions,and its effect can be estimated before manipulation isperformed.

Particular Cases

Application of the rule of no pain and opposite move-ment is evident and simple when the examination demon-strates clearly painful and clearly free passive movements.It can, however, be a little less evident and simple whenthese movements are less clear. For example, a PMID canexist in a segment that was painful on segmental exami-nation, while the active and passive movements imposedon the region were painless in all directions. These find-ings are not rare. The examiner must then face severalpossibilities.

• The findings of the segmental examination clearlyshow that the rule can be applied. If pressure onspinous process C in Fig. 22.28 is painful from rightto left, and pressure in the opposite direction (left

Figure 22.26

Rule of no pain and opposite movement.

a.

Star diagram with normal movement, without pain.

b.

Right rotation(RR), right lateroflexion (RLF), and extension (E) are painful and limited. The manipulation should be performed with rotationto the left (LR), lateroflexion to the left (LLF), and flexion (F), utilizing maneuvers that combine these diverse orientations.

c.

Movement in all directions is painful. The rule of no pain and opposite movement cannot be applied; thus, this represents acontraindication to manipulation.

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SECTION V TREATMENT

to right) is painless, manipulation can be performedin the painless direction, i.e., in left rotation.Remember that pressure on the spinous processfrom right to left produces right rotation, while pres-sure on the spinous process from left to right pro-duces left rotation. If lateral pressure is painful inboth directions, a rotational manipulation should notbe performed.

• Occasionally, one can repeatedly mobilize the seg-ment to end-range in each direction. Performed inunfavorable directions, however, the action can pro-duce a disagreeable feeling for the patient andaccentuate the facet joint tenderness to palpation andthe local paraspinal protective muscle guarding. Per-formed in pain-free directions, the action decreasesthe facet joint tenderness and other signs.

Figure 22.27

Application of rule of no pain and opposite movement in two cases of right sciatica.

A.

Patient with right sciaticafor whom rotation to the right (RR), lateroflexion to the right (RLF), and extension (E) are painful movements.

B.

Patient withright sciatica for whom rotation to the left (LF), lateroflexion to the left (LLF), and flexion (F) are blocked and painful movements.As a result, therapeutic maneuvers are performed in the opposite directions in these two cases. The examiner will performthree maneuvers on each patient: first, rotation to the left for

A

and rotation to the right for

B

; then, lateroflexion to the left androtation to the left for

A

and lateroflexion to the right and rotation to the right for

B; followed by flexion and rotation to the leftfor A and extension and rotation to the right for B.

CHAPTER 22 SPINAL MANIPULATION 181

This way of proceeding is especially useful at the cer-vical level where facet joint palpation is easy and wherethere is often some PMID responsible for chronic prob-lems (e.g., headache) without the existence of any limita-tion or pain produced by the movement.

Rule of No Pain and Opposite Movement in Direct Manipulation

With direct manipulation, pressure is applied directlyto the concerned vertebra. Thus, the segmental examina-tion determines the direction of the maneuver to be per-formed. In Fig. 22.29, for example, the spinal segment BCpresents a PMID. The pressure toward the left on processB is painful (Fig. 22.29a). While maintaining that pressureon B, a counterpressure in the opposite direction is per-formed simultaneously on the process of C, exaggeratingthe produced pain (Fig. 22.29c). The converse maneuver,pressure toward the right on B and toward the left on C,is painless. The manipulation chosen consists of exagger-ating this last movement, which can be performed bypressure on the right transverse process of B and counter-pressure on the left transverse process of C (Fig. 22.29d).

RemarksWhen manipulation is painful but nevertheless producesrelief, most often it is because one of the secondary coor-dinates has not been well chosen, while the principal coor-dinate was correct. This could also be due to joint orperiarticular irritation or even an awkward or poorly per-formed maneuver. When spinal motion is limited by sim-ple stiffness without the presence of a precise PMID andwhen the limited movements are not painful during thephase of taking up the slack, it is possible to act according

to the limited directions with progressive mobilizationsand continue these up to the manipulation if the latter iseasy to do.

In conclusion, we can say that the rule of no pain andopposite movement (a) provides a set of indications orcontraindications for the manipulative treatment, (b)determines the maneuver to be executed, and (c) setsconditions for the execution of a maneuver. This rule is avaluable guide from which the examiner should not depart,but it is not sufficient to guarantee good manipulativetreatment. The indication should be clearly established,and the technique should be perfectly applied, well mea-sured, and well centered on the responsible segment.

PROTOCOL OF MANIPULATIVE SESSION

Manipulation is a treatment just like any other treat-ment. It may be evident, but we should evaluate it as wewould any other proposed treatment. Its correct usedepends first on a proper diagnosis. The disorder shouldbe mechanical, although not all mechanical disordersrespond to manipulation. There are also many contraindi-cations to manipulation: the patient’s general state ofhealth, state of the spine, vascular state, etc. In addition,manipulation should be technically possible; the rule ofno pain and opposite movement should be applicable, andthe spine should not be too stiff.

The selected maneuvers should be perfectly executed,and the applied force should be exactly measured. If theapplied force is insufficient, it can be inefficient, too exag-gerated, and traumatic. The selected maneuvers should be

Figure 22.28 Rule of no pain and opposite movement with lateral pressure on the spinous process. a. Movement from rightto left produces a painful right rotation of the vertebra (× = pain). b. The opposite movement (left rotation) is nonpainful.c. Manipulation is performed with a forced rotation to the left, which is free and nontender.

182 SECTION V TREATMENT

applied judiciously. Sometimes, one or two maneuvers aresufficient during one session; sometimes, several will benecessary. The frequency of the sessions also plays a role.What has to be performed depends on the results and onthe reaction of the tissues, which can be appreciated bycareful palpation. Sometimes, priority should be given tomobilization or stretching and sometimes to a brief butmeasured maneuver. The possible association with otherlocal or general treatment is also part of the management.

When Is Manipulative Treatment Justified?

First: Establish Diagnosis

Any spinal pain requires clinical and radiologic assess-ment, with support by laboratory and electrodiagnosticdata where appropriate. Remember:

• Any inflammatory, tumoral, or infectious lesion ofthe spine may become symptomatic during an effortor a forced movement. Therefore, it is serious tomiss the correct diagnosis.

• Appropriate radiographic studies of high quality thatclearly reveal all the elements of the concernedregion are necessary and are to be completed bydynamic studies if necessary. Sometimes radio-graphic abnormalities become apparent only after adisease process is well established, as is the casewith many serious disorders of the spine. If there isthe slightest doubt, it is better to abstain from manip-ulation and try to arrive at the diagnosis by othermeans, such as laboratory testing, including analysisof blood and urine, electrodiagnostic evaluationwith nerve conduction studies and electromyogra-phy, bone scan, computed tomography scanning,and magnetic resonance imaging.

• Finally, remember that manipulative treatment israrely an irreplaceable therapeutic modality. It is, ofcourse, attractive because of its rapid action and itselegance, but it is valuable only if well executed. Itis better to do something else than to manipulatewrongly; “Primum non nocere.” Then take all nec-essary precautions.

Figure 22.29 Rule of no pain and opposite movement with lateral andopposed movements. a. Lateral pressure from right to left on segment Bproduces pain. One would like to know if the cause of this pain is due tosegments AB or segments BC. b. While maintaining pressure on B fromright to left, one may simultaneously execute a counterpressure in theopposite direction on segment A. This does not increase the pain alreadyproduced. c. In contrast, the same maneuver executed on segment Cnotably increases the pain (××××××××××××) that could be produced purely by pres-sure on segment B alone. Thus, we are able to demonstrate that segmentsBC are the cause of the pain. d. As a consequence, the manipulativemaneuver, directed and applied according to the rule of no pain or of theopposite movement, will consist of a movement opposite in direction tothat noted in c. A counterpressure (××××) is applied to the left transverseprocess of C, while pressure is applied to the right transverse process of B.

CHAPTER 22 SPINAL MANIPULATION 183

Then Take Necessary Precautions

Once the manipulative treatment has been decided, besure that the manipulation can be performed on the spinein question. The state of the spine must be evaluatedradiographically. The presence of a significant osteopo-rosis is, of course, a contraindication to manipulation, evenif a real mechanical problem is present.

Cervical manipulation should be avoided in patientswith abnormalities of the cervico-occipital junction. Pos-tural testing (see below) should also be performed touncover the possible presence of vertebrobasilar insuffi-ciency that has not been recognized and is an absolutecontraindication to cervical manipulation. The neck of apatient whose general and vascular state is not soundshould not be manipulated (see “Contraindications toManipulation” below).

When Is Manipulative Treatment Possible?

Although a manipulative treatment may be justified onthe basis of the diagnosis (mechanical problem), this doesnot mean that it can be performed even if the conditionsdiscussed above are favorable.

• The rule of no pain and opposite movement is appli-cable.

• Manipulation is easily feasible. In cases of stiffspines in which the maneuvers bump against pain-less and global resistances, manipulation should beavoided, and progressive mobilization treatmentsused instead.

• Manipulative treatment, if performed, should showrapid proof of its effectiveness. Therefore, a startingschedule should be prepared.

How Is Treatment Managed?

A complete starting schedule is necessary to determinethe results of each treatment. All measurable or apprecia-ble elements of the clinical examination as describedabove are first noted and, if possible, reported on a stardiagram.

Manipulation Session

Once the premanipulative diagnosis has been estab-lished, the treatment session will consist of three phases:

• Maneuvers of general and local relaxation• Maneuvers of oriented mobilization• Maneuvers of manipulation (thrust techniques)

Maneuvers of General and Local Relaxation

With the patient in an adequate position, the examinerstarts by executing slow, rhythmic maneuvers of relax-ation. This allows the examiner to appreciate the quality

of the patient’s muscle tone and find deep contracturesthat were not apparent at the beginning of the examination.These maneuvers, performed slowly, have a real relaxingeffect and can result in significant improvement. It is notuncommon to see a resistant (chronic) sciatica relieved bymassage of the muscles of the external iliac fossa. Relax-ation of the muscles of the supraspinous and infraspinousfossae often has a favorable effect on the sequelae ofcervicobrachial neuralgias.

Maneuvers of Oriented Mobilization

After the maneuvers of relaxation, just as after eachsequence of treatment, a quick examination can be per-formed to evaluate the improvement in the limited andpainful movements. The second step of the treatment isthe execution of mobilizations and stretchings that areoriented in the pain-free directions. The spinal segmentshould be brought slowly to end-range. Then a pause ishelpful, followed by relaxation of the pressure andresumption of the mobilization. These movements shouldbe slow and elastic, with pressure well linked and wellexecuted rhythmically. Each maneuver is repeated severaltimes according to each of the orientations and in combi-nation with them.

These oriented mobilizations should first be global,affecting the whole region; then they can be more specific,with manipulation techniques that will not go beyond tak-ing up the slack, localizing the effects on the concernedspinal segment. Often, it is necessary to stop the treatmenthere during the first session, especially in difficult casesthat are acute or very well established. It is wise also tolimit these maneuvers in the treatment of frail spines.Otherwise, the session will continue until the so-calledmanipulative time is reached.

Maneuvers of Manipulation (Thrust Techniques)

The patient is now accustomed to the movements exe-cuted on the spine and does not feel any more uneasinesswhen the spine is pulled a little or put under slight tensionbecause painful movements are theoretically avoided. Inmost cases, the first manipulation can be performed in thedirection opposed to the one that is the most blocked andpainful. It can be monodirectional or combined withanother free orientation. The result of this first maneuveris judged according to the elements noted below. Depend-ing on the result of the first maneuver, a second maneuveris executed with another free orientation as principal coor-dinate. After a new examination, a third maneuver can beapplied, possibly using some orientations that the preced-ing maneuvers have freed. The examiner should not domore than three consecutive manipulations on a spinalsegment in one session. Sometimes, it is necessary to limitit to one maneuver.

184 SECTION V TREATMENT

Experience is irreplaceable. The examiner will adjustand vary maneuvers according to the patient’s responsesand especially the results of the palpation examination.The maneuvers can be varied in terms of the degree ofpressure — light when done with the tips of the fingersor more forceful — and the time maintained. Sometimes,they can be a little sharper to obtain a more marked reflexeffect.

Evaluation of Response to Treatment

The effect of each therapeutic gesture, such as massage,mobilization, injection, and especially manipulation,should be immediately assessed before the next therapyis begun. This assessment can be based on the following.

• A simple objective sign: Lasegue’s sign, distancefrom the fingers to the ground, range of motion,modification in pain produced by an exactlydescribed spinal movement, etc.

• An ordinary gesture that has been impossible ordifficult before manipulation and that has becomeeasier or possible later (e.g., putting on a sock).

• Manifestations of the segmental vertebral cellulo-tenoperiosteomyalgic syndrome: decrease in thesensitivity or disappearance of a cellulalgic zone,especially in the territory of the posterior ramus ofthe spinal nerve; decrease in the tenoperiosteal sen-sitivity (shoulder tests, epicondylar pain tests, pal-pation); decrease in the sensitivity of a trigger point,as many elements expressing the favorable action ofthe gesture that is executed.

• Decrease in the number of the local signs of thePMID; disappearance of these signs is not alwaysimmediate; decrease or disappearance of the facetjoint tenderness is a very accurate test.

• Subjective impression of the patient who feels betteror not, with the clear limitations of such a subjectiveaccount taken into consideration.

At the end of this manual treatment, some attenuatedsigns of PMID may persist, even if the patient is perfectlyrelieved. The active PMID has become a latent PMID. Inthis case, should the treatment be continued? The answervaries. Sometimes, all the treatments that can be givenwill not make a perturbed segment become totally painlesson examination. It is often sufficient to have a later sessionto stop the pain (two or three times per year). Otherwise,complementary treatments, manual or other, the correctionof other zones of dysfunction (see Chapter 61, “Transi-tional Zone Syndrome”), and a well organized course ofphysical therapy will generally overcome a refractoryPMID and make all the signs disappear.

Reactions following Manipulative Treatment

In about one third of cases, the patient can experiencesome reactions after the first session. After the secondsession, these reactions are less common and always lesspronounced; they are benign and most often mild. Theyare characterized by stiffness or a temporary increase inthe pain that has been treated, usually occurring after aninterval of a few hours. They can exist even if the manip-ulation has been soft, done with the tips of the fingers.The reactions would be more pronounced, however, if themaneuvers were more numerous and more forceful. As arule, they do not interfere with the good result this treat-ment can bring unless the patient, who has been told orwarned, stops treatment before undergoing the one or twosupplementary sessions (without reactions) that wouldhave relieved the problem.

Stiffness

Post-treatment stiffness is usually moderate and readilyresponds to anti-inflammatories and application of heat.It tends to last 6 to 48 hr. Cases of stiffness can be moresevere. Stiffness is generally less of a problem in latersessions, or it is very much reduced in intensity and dura-tion, similar to postexercise soreness.

Transient Exacerbations

Transient exacerbations of the treated pain can occurimmediately after the first session of manipulation in casesin which the patient will eventually experience significantimprovement. In 20 to 25% of cases, however, a patientmay experience a momentary reaction characterized by arecurrence or an increase of the pain 6 to 12 hr after thetreatment. It may last for a few hours and sometimes for1 or 2 days. These reactions are rarely very severe but areseen, as in the following example.

Case History — Mr. C., a 26-year old judo champion,fell on his head, which resulted in acute headache withvertigo. Radiologic, ENT (ear, nose, and throat), andneurologic examinations were normal. The manifesta-tions persisted for 3 wk after the incident. A segmentalexamination revealed a PMID of C2–3. Only one mildand painless manipulation was executed in rotation.There was an immediate improvement in cervical rangeof motion with relief of pain. The following night, theheadache recurred, radiating toward the ear with suchintensity that in the morning the patient consulted withan ENT physician, thinking he had an acute otitis (hesuffered one 2 years earlier). The ENT examination wasunremarkable. In the evening, the symptoms seemed todecrease. By the next morning, all manifestations —vertigo, headache, cervical discomfort — had disap-peared and did not recur.

CHAPTER 22 SPINAL MANIPULATION 185

This patient was an athlete accustomed to shocks andblows, and the manipulation had been performed with thetips of the fingers. Nevertheless, reactions occurred. Asecond manipulative session thus should not be performeduntil the reactions of the first session, whether postmanip-ulative stiffness or temporary increases of pain, are gone.Reactions usually occur only after the first session, theyare very much attenuated after the second, and they arerare after the third. Their recurrence at each session with-out improvement in the treated state means that the treat-ment should be discontinued and the diagnosis reevalu-ated.

These reactions are always preceded by a free time of6 to 12 hours after treatment. Their presence or absenceis not prognostic of the result of the treatment. A “reac-tion” occurring 48 hours after the treatment is usually nota reaction; it is usually a recurrence whose cause is oftenrelated to the patient’s behavior.

False Reactions or Premature Recurrences

Besides these normal reactions, many postmanipulativepseudoreactions are due to patient behavior. Since patientsfeel very relieved after the treatment or want to test theresult, they may try to do what was difficult or impossibleto do a day earlier or take risks, including forceful physicalefforts, postural stressful positions, or exposure to climaticirritants. Often, notwithstanding explanation, the patientdoes not understand the nature of the ailment very well.For example, a farmer suffering from a chronic effort-related low back pain that was relieved immediately aftermanipulation rushed, as soon as he returned home, to theheavy object that caused his ailment. “Then I put myselfexactly in the position I was when I felt pain, and thistime I lifted it without pain! Doctor, one can say that yourrepair was good.” For this patient, the vertebra either wasin place or was not in place. If it was in place, he believedthat he had been mechanically returned to his full func-tional capacity.

For a few days after manipulation, a patient remainsvery vulnerable to recurrence, especially if the treatmentresulted in substantial relief. If the patient performs anactivity such as the one that caused the problem initially,there may be not only a temporary irritation but also asevere recurrence. A patient should understand that a ses-sion of manipulation, even if it results in noticeable relief,leaves him or her “fragile” for a while, and therefore, thepatient should compensate by modifying some activitiesof daily living.

The session should be followed by relative rest for 48hours. This does not mean the patient should remain inbed. Although there are some exceptions, the patientshould avoid the efforts, movements, and positions thatbrought on the usual pain. These precautions should befollowed much longer in old or difficult cases.

Sympathetic Reactions

In addition to painful reactions, there are sometimesfunctional sympathetic reactions that can be immediate.After even minimal manipulation of the cervicothoracicregion, it is not unusual for patients to experience axillaryperspiration. It happens at every session, whether sessionsare a few days or a few months apart. This demonstratesthe action of the maneuvers on the sympathetic system,and it has no effect on management of the treatment.

There is another type of reaction, which is rather rarebut about which we should be aware. In the hours follow-ing a high lumbar or low thoracic manipulation, a patientcan experience an attack of abdominal discomfort anddiarrheal episodes. Modifications of menstruation can beseen exceptionally; manipulation can either start menstru-ation, hasten it, or make it more profuse. One of our femalepatients who underwent manipulation of the neck fourtimes per month for shoulder pain also experienced men-strual blood flow starting the evening of the day of treat-ment and lasting 4 days, absolutely the same as her normalmenstruation. Seen again 3 years later, three times permonth for cervicobrachial neuralgia, she experiencedmenstrual blood flow lasting 4 days after each treatment.Rarely, 24 hours after a manipulation session, somepatients (especially those who complain more or less fre-quently of analogous symptoms) experience painful epi-gastric attacks or pelvic or abdominal pains, sometimessharp, lasting a few hours. This reaction generally indi-cates the disappearance, perhaps definitively, of thesesymptoms.

Evolution of Pain after Manipulation Session

After the first session, followed by lessening of possiblereactions, a patient may have several possible outcomes.

One is complete and immediate disappearance of pain,which can be permanent or transient, with pain reappear-ing, attenuated, the following day. This is the most fre-quent occurrence and is a good prognosis for the rest ofthe treatment. The intensity of the pain may not change.The signs remain the same. After two or three sessions,the treatment can be discontinued.

Sometimes, immediately after manipulation, a patientmay not note a significant improvement, and 1 or 2 dayslater, notice a distinct improvement of the painful state.In some very chronic cases, the improvement is seen onlya few days after manipulation, after a moderate reactionmixed with stiffness and exacerbation of the usual pain orof the dysfunction being treated.

An increase in pain is a rare outcome if the indicationsare appropriate and the treatment well executed. The diag-nosis should be reviewed but only after determining whatthe patient did after the treatment. Most often, we learnthat a patient, feeling “miraculously” cured of low backpain, drove several hundred miles, stood for an extended

186 SECTION V TREATMENT

period, carried heavy packages, or was exposed to cold.The pain could also be due to an acute synovitis thatappears coincidentally and is unrelated to the treatment.

Number and Frequency of Sessions

Sometimes, a single session is sufficient; other times,several sessions are necessary. Three sessions are the aver-age, and in some chronic cases, five or six sessions arenecessary. It all depends on the case treated and on thepartial results obtained at each session. In general, if noimprovement in the spontaneous pain and especially inthe signs of the examination occurs after three sessions,it is useless to continue.

These sessions represent an “acute” intervention. Amaintenance treatment (i.e., a session every 3 or 6 mo)that, with some simple maneuvers, reduces pain in theneck or flank is perfectly justified in some chronic lowback pain syndromes or cervical pain syndromes.

There is no problem when a patient experiences com-plete relief immediately. Nevertheless, in a chronic case,the patient should be reexamined 3 or 4 wk later to besure the signs have disappeared.

When several sessions are necessary, their frequencywill vary depending on the case and the findings on sub-sequent examinations. One or two sessions each week isa reasonable average. Some patients will react better toshort intervals between sessions; others will react betterto longer intervals between sessions. In cases of acute lowback pain or torticollis (wryneck), for example, whichusually can be cured spontaneously in 3 to 7 days, it iscertainly not necessary to do four manipulations in 7 days;one or two manipulations can be performed at 2- or 3-dayintervals.

With a subacute disorder such as refractory sciatica,the first manipulation can be performed, and its resultassessed 4 days later. Depending on that result — a sharpor mild reaction — the manipulation can be performedthree or four times at intervals of 3 to 4 days, with a pauseas soon as relief is obtained. The patient is seen again 1mo later.

In the case of a chronic disorder such as low back painor cervical headache, one manipulation a week for 3 weekswill allow better evaluation of the results of different tech-niques. If a result is not obtained, two or three additionalsessions can be tried at 2- or 3-day intervals. When thespine is very stiff but tolerates the manipulation, sessionsperformed at very short intervals will lead to a result thatsessions performed with long intervals would never pro-duce.

The dosage of maneuvers (i.e., the frequency of thesessions) is very important in manipulation. Patients donot all tolerate these treatments in the same way. The stiffbrachymorphic type of patient generally tolerates strongertreatments at short intervals. The hyper-relaxed lanky type

of patient does not tolerate this type of treatment verywell. With those types of patients, it should be sufficientto perform the minimum of manipulation with long inter-vals between sessions. Otherwise, they may develop truepainful spinal syndromes with some misleading improve-ments after the sessions, which may eventually contributeto worsening of their conditions.

Should we simply content ourselves with treating thesegment responsible for the pain that brought the patientto consultation? Yes, as a first step. If the result is easilyobtained, maybe a certain balance has been reached in thespine whose regional mobility is perturbed. But this is notthe case if there is a recurrence. Then it is necessary torelax the stiffened zones of the spine and to treat the latentPMIDs that could exist at other levels, especially if theyare located in the junction zones (see Chapter 61, “Tran-sitional Zone Syndrome”).

Age Considerations with Respect to Manipulation

It has often been written that manipulation should bereserved for young patients, with the indication of choicebeing acute low back pain. This is incorrect. The acutelow back pain of the young is less regularly relieved thanis the pains of patients in their 40s and 50s. If this disorderis often a good indication for manipulation, it is neitherthe only one nor the best.

Manipulation can be used for most individuals, withthe execution of the maneuvers varied according to age.Many maneuvers should be performed very gently. If theindications of manipulation are limited to the sensibleones, it is rare to have to treat children, but it can be donewith positive results. With children, only the necessarymovement is to be performed very gently; there is noconcern other than the difficulty of precision.

Quite often, however, it is necessary to treat the elderly.They often receive a great deal of relief from gentle mobi-lization. It gives them greater ease of movement and canalso help relieve the small minor nuisances brought byparaspinal protective muscle guarding perpetuated by seg-mental stiffness. No forceful, strenuous, or sharp maneu-ver should be used. It is remarkable how some aged spinescan be helped considerably by a few gentle movements,where according to clinical and radiologic studies, thesepatients could be considered beyond all possible help.

Quality of Results

Among the criticisms of manipulative treatment, acommon complaint is that the results do not last. Some-times this is true, although many good results are longlasting despite the apparently bad conditions of patientswith poor static, poorly conditioned, or weak muscles,with severe multilevel disk degeneration, etc. In the caseof manipulation relieving reversible dysfunctions, it would

CHAPTER 22 SPINAL MANIPULATION 187

seem logical that such a dysfunction could recur easily,or it would not recur with frequency. The result of themanipulation, however, depends on the accuracy of thediagnosis and largely on the quality of the execution (i.e.,the examiner). This is evident and should be emphasizedbecause many think that from the moment a region has“cracked” and a certain relief occurs, all has been done.A world of difference exists, however, between an electivemanipulation or mobilization that is forced and approxi-mate, with sessions of cracking that are repeated system-atically every 2 or 8 days (even if, to the unskilledobserver, all the maneuvers seem the same) and a wellorganized treatment protocol with appropriately dosed,progressive sessions conducted with appropriate fre-quency. If the maneuver has not been sufficiently precise(i.e., sufficiently “pushed”), the relief it produces mayhave little chance of lasting.

The result is the same if one neglects to relax the stiffspinal segments that are supra-adjacent and subjacent tothe painful zone. This “reharmonization of the segmentalmovements” (Lescure) is a very important part of treat-ment by manipulation, which should not be limited to thepainful segment. When good reharmonization is obtained,the quality of the result is generally such that certainmanipulators neglect completely the physical therapy thatis often indispensable. Indeed, muscular insufficiency andpoor muscular synergy or, even more, the lack of muscularcontrol are greatly responsible for spinal fragility. Recog-nizing these factors and designing an effective therapeuticexercise program to correct them is essential for totalrehabilitation. Finally, let us repeat the need for mainte-nance sessions 1 to 3 times per year for disorders such ascervical spondylosis that include a normal tendency toreblocking. In these cases, manipulation as part of acomprehensive rehabilitation strategy, although not cura-tive, can provide temporary relief, sometimes of longduration, that no other therapeutics can produce as well.

Good training in palpation of tissues enables the exam-iner to appreciate the persistence or disappearance of localchanges generally accompanying PMIDs. If these changespersist after manipulative treatment, it means that theproblem is not completely solved, even if the patient isrelieved and the other symptoms have disappeared. Oneshould not forget that manipulation does not change theanatomic state of the treated segment. It makes the PMIDstolerable and painless, but does not always make themdisappear completely. Of course, in these conditions, thestate of the organism plays an essential role. Certain sub-jects with very low pain tolerance thresholds are signifi-cantly incapacitated by slight dysfunctions that others can-not discern.

GENERAL INDICATIONS FOR SPINAL MANIPULATION

Used judiciously, manipulation is a useful and rapidlyefficacious therapeutic modality. It is the principal treat-ment for PMIDs as we have defined “benign and painfuldysfunctions of the spinal segment” that represent thecommon denominators of most spinal pain syndromes thatare called “common.” Spinal manipulation acts also onthe cellulalgic, myalgic, tendinous, and periosteal mani-festations that result from PMIDs. This explains the oftenfavorable action of manipulation on certain referred painsyndromes that seem to have no ties with the spine.

Thus, the indications for spinal manipulation are painsyndromes tied to PMIDs. These may involve local (cer-vical, thoracic, lumbar), radicular, or referred pain. Manip-ulation can also be useful in some cases of herniated diskor stiffness commonly associated with spondylosis. In thiscase, progressive mobilization is often preferable. AllPMIDs are not systematically amenable to manipulation,however. There are instances in which manipulation canbe inefficient and even contraindicated. Often it is bene-ficial to use manipulation in combination with other ther-apeutic modalities, physical or pharmacologic, in the con-text of a multidimensional rehabilitation program aimingat the local irritation resulting from the PMID or at themanifestations of the segmental spinal syndrome whosepersistence can create a secondary vicious cycle thatimpedes rehabilitation.

There is no irreplaceable therapeutic modality in thetreatment of common vertebral pain syndromes. Cases thatonly manipulation can cure or relieve are infrequent. Othertherapeutic approaches can often lead to good results —maybe less brilliant, but satisfying — if applied properlywhere necessary. It is always better not to manipulate thanto manipulate poorly. The remedy should not be worsethan the disorder treated.

Factors unique to treatment by manipulation are theelegance and the rapidity of the result that is sometimesinstantaneous, in general needing two or three sessions,but occasionally needing more than six. We now surveythe principal indications for manipulative therapy. Thechapters on the principal common disorders of spinal ori-gin detail its place in their treatment.

Cervical Region

Chronic post-traumatic, postural, or static cervical painand pain in which spondylosis fosters stiffness and inter-vertebral dysfunctions are the usual indications.

In acute cervical pain, manipulation can only beapplied if it is of micromechanical origin. Very rarely isthat origin seen, however, even if a forced movementseems to have been the cause.

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Cervicobrachial radiculitis is a frequent indicationwhen it is mild or chronic and mechanical. In addition, awhole pathology whose cervical origins are usually unrec-ognized will benefit from manipulative treatment. As faras the superior cervical spine is concerned, headache isthe problem. Headache of cervical origin is much morefrequent than noted in the classical literature. Its ownsemiology has been described (Maigne), and the conditionis considered in detail in Chapter 48, “Headaches of Cer-vical Origin.”

Some cases of vertigo, nausea, and minor cognitiveproblems seen as sequelae of cervical trauma can alsorespond favorably to a cervical treatment.

Many cases of pseudotendinitis of the shoulder withpain and limitation of movement have cervical compo-nents and are the manifestations of segmental spinalneurotrophic syndromes due to C4–5 or C5–6 PMID. Spi-nal treatment is then very useful. It is often the same forthe pain syndromes of the lateral epicondyle (C5–6,C6–7). The cervical factor is less frequent in the painsyndromes of the medial epicondyle (C7–8).

Thoracic Region

In cases of common thoracic pain of the adult, theinferior cervical spine must be examined with great atten-tion. Eight of 10 times, the condition is an “interscapularpain of cervical origin” (Maigne), with an interscapularparaT5, very specific tender point. Another less frequentform of cervicothoracic pain is due to the dysfunction ofthe levator scapulae. It can be associated with a PMID ofC3–4 or C4–5. Common thoracic pain of thoracic originis less frequent. Some pain syndromes are indications formanipulative treatment. Costal sprains, especially of thefalse ribs, exhibit misleading pain syndromes; their diag-nosis requires adequate manipulative treatment.

Lumbar Region

Manipulation is an excellent treatment for numerousacute and chronic low back pain syndromes referred to as“common.” Half of the acute low back pain syndromesare relieved after the first manipulation. The chronic lowback pain syndromes do not all originate from the inferiorlumbar spine. In chronic low back pain of low lumbarorigin, manipulation is often a useful treatment, even ifthe radiologic findings show significant discopathy, osteo-phytosis, etc. The effect can be long lasting, but it isalways better to complete the treatment with an appropri-ate therapeutic exercise prescription to stabilize the result.

A number of low back pain syndromes have their ori-gins in the thoracolumbar junction (T11–12 or T12–L1)(Maigne). They can be acute or chronic. An adequatemanipulative treatment can most often be applied to thesetypes of low back pain of thoracolumbar origin with excel-lent results. Physical modalities seem to be less effective

in this condition. Sciatica resulting from disk involvementis a good indication when it is of moderate or averageintensity. Manipulation does not seem to have a noticeableeffect on the results obtained in sciatica of recent onset orin recurrent cases; however, the latter seems to react betterand more quickly than the former. It has often been writtenthat manipulation should be reserved for sciatica of recentonset in the young patient. Based on our experience, how-ever, the results of manipulation are less effective inpatients 20 to 30 years of age than in patients 40 to 50years of age.

The femoral neuralgias react noticeably like sciatica.Meralgia paraesthetica is often well relieved because, incontrast to generally accepted opinion, it most often con-tains a spinal factor.

Coccyx

Coccydynia of traumatic origin resulting, for example,from a fall or from delivery is relieved regularly in one tothree sessions with the technique that we propose. This isnot the case with the coccydynia of nontraumatic originresulting from local pathology (see Chapter 46).

Visceral and Functional Disorders

We do not consider visceral disorders to be an indica-tion for spinal manipulation, even if manipulation some-times influences certain functional problems. The use ofmanipulation for prevention or treatment of visceral disor-ders is a major concern for most of those who (with somevariations) use manual techniques aimed at “restoring anormal joint play,” correcting “spinal subluxations,” orcuring “mechanical dysfunctions” of the spine. This isevident with the chiropractic school and, to some extent,the osteopathic school and some medical authors.

According to Korr, one of the best known neurophys-iologists of the American osteopathic school, any func-tional perturbation — muscular, spinal, articular, myofas-cial, or other somatic dysfunction — facilitates thecorresponding spinal cord segment, which can produce aperturbation of any of the neural elements arising fromthat segment. This interrelation of all the physiologic sys-tems is the basis of the osteopathic concept.

Thus, the osteopathic lesion, now called “somatic dys-function,” whose definition includes any dysfunction ofthe musculoskeletal apparatus, is capable of creatingadverse somatovisceral reflexes. This concept is based onsome real findings. It is known that such reflexes exist.Such a mechanism can be responsible for some functionalvisceral pain syndromes that the spinal treatment cansometimes suppress or attenuate.

Indeed, it is not unusual to have some patients whohave been manipulated for low back pain notice that theirhabitual constipation has resolved or that their gastrointes-tinal discomfort has abated after a thoracic manipulation.

CHAPTER 22 SPINAL MANIPULATION 189

But to affirm that these viscerosomatic reflexes play animportant role in organic pathology is a leap of faith.Conversely, visceral disorders can present with certaincutaneous or myofascial manifestations (Mackenzie).There are instances in which anesthetizing these zonesbrings relief or decreases the visceral pain; this is wellknown. For some, however, this could mean that there isoccasionally a facilitative reflex arc acting favorably onthe disorder, although this has not been proved.

The spectrum of manipulation is sufficiently broad andwell established in the domain of musculoskeletal painwithout trying to apply it blindly to pathologic phenomenain which the role of the spine, if it exists, is uncertain. Itis also true that those who tend to use manipulation as ageneral therapeutic modality are those whose medical edu-cation is the weakest.

CONTRAINDICATIONS TO MANIPULATION

A distinction must be made between clinical and tech-nical contraindications. The former are disorders of a non-mechanical nature for which manipulation should not beused and, moreover, could be dangerous, as in cases inwhich osseous or vascular conditions prelude its use. Thelatter are cases in which manipulation appears to be afeasible means of rational treatment in problems of amechanical nature, but is contraindicated because the ruleof no pain and opposite movement cannot be applied.

Clinical Contraindications

Clinical contraindications depend on the nature of thedisorder. Some contraindications are positive. Spinal frac-tures and pain due to infectious, tumoral, or inflammatorydisorders are, of course, absolute contraindications.

Some of these conditions have occult presentations andare only discovered when the patient presents with whatseems initially to be a mechanical problem that beganduring a physical effort or a traumatic episode. Thus,treatment by manipulation is desirable only after an exactdiagnosis has been made on the basis of clinical andradiologic examinations, confirmed if necessary by com-plementary examinations as mentioned previously. It isnecessary to have high quality radiographs, for it is moredangerous to have bad ones than to have none. A badradiographic study of the neck in a patient with a headtrauma can lead to misinterpretation of a fracture of theodontoid or atlas. Anomalies of the cervico-occipitaljunction present contraindications as does significantosteopenia.

The most frequent and serious accidents of manipula-tion are vascular accidents, occurring most often inpatients with a vertebrobasilar insufficiency. If there is the

least doubt, this diagnosis should be eliminated and neu-rologic advice obtained. We discuss below the signs thatcan point to this vertebrobasilar insufficiency, which is themajor trap of the spinal manipulation (see “Errors ofManipulation” below).

Technical Contraindications

Even when the mechanical nature of a spinal problemis clearly established, manipulation can be used only ifthe rule of no pain and opposite movement is respected.As indicated above, manipulation is contraindicated whenall directions of movement are painful. In practice, how-ever, this is also true when only one direction is free. Whentwo directions are free, a few mobilizations can be triedin the free directions, and then the result is assessed. Threedegrees of freedom should be available to maximize thechance of success with manipulation.

Even when there are three free directions, manipulationis contraindicated when a painless resistance is encoun-tered in taking up the slack. For instance, when flexion,left rotation, and left lateroflexion are painful, while rightrotation, right lateroflexion, and extension are painless, amanipulation is still contraindicated if the examiner feelsa painless resistance while taking up the slack.

Another contraindication to manipulation exists in thecase of a patient who has a stiff spine or demonstratesmarked tonic resistance to passive motion. Even if thepatient is well relaxed and the examiner is well trained,only mobilization and stretching should be performed. Theincrease in soft tissue resistance may be temporary anddisappear by the next session.

Patient fear of the manipulation is a contraindicationto manipulation. The patient might, for instance, suddenlycontract during the thrust, and the maneuver could bedangerous. If the examiner has complete control of his orher own maneuvers, however, with progressively insistentand painless mobilization (which might be found to besufficient), the patient may gain enough confidence toallow the examiner to go beyond taking up the slack andperform a manipulative thrust if indicated. This should bedone only with the patient’s consent.

Manipulation is contraindicated if the examiner has notperfectly mastered the techniques of manipulation. Acqui-sition of the manual skills necessary to competently per-form manipulation takes a long time. In a whole year ofdaily work, only the basic techniques and how to applythem in basic cases can be assimilated. From this indis-pensable beginning, the examiner must have daily prac-tice, and just as in sports such as tennis or golf, severalyears are necessary to really master a sufficient numberof techniques. Even then, there will always be importantdifferences between the average practitioner and thosespecialists who take care of a small proportion of difficultcases. It is a matter of skillfulness. A maneuver that is

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forced or held too long or a slight difference in the pointsof support or in the orientation of the movement cantransform a failure into success.

Improperly performed manipulation is contraindicated.It is better not to manipulate than to manipulate incor-rectly. This is also true for a trained examiner when thenecessary equipment (table, stool at right height) is notavailable. A manipulation executed on a bed or a sofa isa dangerous acrobatic maneuver for the patient and some-times for the examiner.

ERRORS OF MANIPULATION

The relief of acute low back pain in a few seconds orimprovement by application of a simple maneuver of apainful neck that has been limited for months is notunusual with manipulation. Because it works rapidly, theexperienced examiner is tempted to apply manipulationwhen faced with a pain whose origin seems benign andmechanical in a patient who has had a previous goodoutcome with manipulation and insists on its use uponexperiencing a similar pain. Some patients do not hesitateto alter their stories slightly just to persuade the examineror themselves that the pain for which they sought consul-tation has certainly started after a forced movement or aneffort. The errors in the use of manipulation are numerous.A patient with a history of several spinal incidents of amechanical nature can have a new disorder of quiteanother nature that manifests itself by spinal pain, remind-ing him or her of a previous incident. An infectious ortumoral disorder can become painful for the first timefollowing a strain or trauma. Sometimes, the symptoma-tology is so similar to the one met every day that theexaminer can be tempted to use the remedy that seemsmost useful: manipulation. Some of these errors are morefrequent than others. Let us examine them successively.

Errors in Diagnosis

Errors in diagnosis are essentially due to the absenceor poor quality of radiographic studies or to views thatare insufficient for evaluating the region in question.

Case History — Mr. B. is 69 years old. His son, aphysician, sent him to us for a possible manipulativetreatment. Mr. B. has had occipital pain syndromes. Twoweeks earlier, he had been hit on the head by a heavyboard. The radiographic studies were of rather goodquality (except for the open mouth view, which couldbarely be interpreted) and showed no spinal lesion, butbecause of the continuous discomfort, the symmetry ofthe blockage, and the suboccipital protective muscleguarding, tomographic studies were requested, whichuncovered a fracture of the atlas.

One can imagine what result a blind manipulationwould have yielded in the following case.

Case History — Mr. C. is 30 years old. A few weeksbefore his visit, he had a trivial cervical trauma whilestopping suddenly at a red light. The force of deceler-ation resulted in cervical pain that was not improved byanalgesic medication and was irritated by massage.The cervical radiographic studies he brought with himseemed normal. Dynamic views were requested andshowed a subluxation of C5 on C6; in flexion, C5translated almost completely on C6.

Errors in Rheumatology

Errors in rheumatology result most often when there isa delay in the radiologic evaluation in relation to theclinical evolution. The physician-manipulator should fallinto this type of trap less frequently than do others. Withrare exceptions, inflammatory arthritides are detected bythe premanipulative assessment that shows that movementapplied to the involved segment is painful or limited in alldirections, making the manipulation technically impossi-ble if the rule of no pain and opposite movement isrespected.

Errors in Neurology

Errors in the neurologic domain certainly provide mostof the errors of manipulation. Many neurologic disorderscan, at their inception, mimic a benign spinal pain.Mechanical treatments in these cases can aggravate theproblems dramatically, even the simple spinal examinationdescribed in the following case history reported by Held.

Case History — A young boy 12 years of age was hiton the neck while playing. Torticollis (wryneck) andcervical discomfort developed during the next severalweeks. A physician performed a physical examination,testing simply the cervical mobility. Suddenly, a tetraple-gia occurred, diagnosed as a spinal cord vascularaccident. If the patient had been manipulated, it wouldhave sparked a formidable medicolegal dilemma! Butwhat if the physician-examiner had been known to prac-tice manipulation? Would anyone be convinced that itwas only an examination?

This case is similar to the next one, the case of a patientwhose cervicobrachial neuralgia was severely and suddenlyaggravated during an examination that was absolutely nor-mal and performed by her rheumatologist. Subsequentexaminations uncovered a cervical tumor. Conversely,manipulation can oddly improve some symptoms whoseorigin is certainly tumoral. Meningiomas and neurinomasare very misleading. They often present as local pain (neckpain in the case of cervical meningioma, most often seen

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in women) or radicular pain syndromes with very slowevolutions and with remissions. The interval between theappearance of the pain and the appearance of the motorproblems can be months, even years. The following casehistory reported by Held is particularly demonstrative.

Case History — A 40-year old woman with cervico-brachial pain radiating to the interscapular region wasseen by her physician, who prescribed traction andmanipulation, which brought about improvements. Sev-eral months later, a more intense relapse occurred, withanorexia, weight loss, and depression. Her general stateof health and gastrointestinal tract were normal. Shewas subsequently admitted to the hospital, where sheunderwent electroconvulsive therapy (ECT), followed bya sleep laboratory assessment that was prematurelydiscontinued by the patient. Another series of manipula-tions followed; the patient improved, gained weight,and had no more pain. Two years later, there was arelapse; the same manipulation had no effect. Progres-sively, new problems appeared: leg spasms and sensoryproblems in the left hand (she burned herself withoutfeeling it). The neurologic examination demonstrated asubtle deficit of the right lower limb, a right Babinski’ssign, hyperreflexia of the right upper limb, and hypoes-thesia to touch, with analgesia in a C4 distribution onthe left. A diagnosis of an ependymoma of the spinalcord was made. Following a surgical intervention, shewas left with impaired neural function in all four limbsincluding spasticity and a sensory deficit.

This case history underlines the difficulty in diagnosingthese tumors. The peculiar improvement, obtained twiceby manipulation and retained for long periods, delayedthe diagnosis. Some patients with syringomyelia canpresent with cervicobrachial neuralgia or acroparesthesia.This diagnosis is easier to make when the pain syndromeshave a lancinating quality, like pain produced by burns orintense cold. The most formidable error is the one set upby the vertebrobasilar circulatory dysfunction, whichcauses the most frequent severe accidents and is some-times the most difficult to foresee in manipulation (dis-cussed below). Cervical manifestations rather similar tothose of the vertebrobasilar dysfunctions are frequentlyseen in neuropathies such as pseudovertigo, headache,visual fatigability, and fainting tendency.

It is, of course, much less dangerous to use manipula-tive therapy on a patient whose manifestations are theexpression of a neurosis rather than a vertebrobasilar dys-function. But it is not harmless to condition such patientsuntil they become “obsessed with the idea of the blockedvertebra” or a “displaced vertebra.” The particularities ofmanipulative therapy, especially when it is performed ina context of illegality, have been described very well byGrossiord:

Manipulation is a very particular therapy whose apparentease of administration has something magic in it to whichpatients are extremely sensitive. The myth of the “spinaldisplacement,” the revealing of “microdisplacements” byviews of the whole spine, the prestige of a foreigndiploma, the external apparatus of the maneuver, the spiritof its execution, the authority of the examiner, its theat-rical elements, all create a climate that does not corre-spond very well with the slow, cautious and unrewardingapproaches that mainstream medicine and therapy imposeon us in general. In these patients, the illegitimately per-formed manipulation creates the “consciousness of block-ings” or of spinal displacements [that] repeat and thatshould be put back in place. Thus the multiple experiencesof manipulative treatments can create a supplementarypoint of attention and of anxiety.

It is what Lescure has called “the obsessional neurosisof the spinal displacement” maintained unconsciously bysome persons under the cover of infantile or mythicalconception of the illness.

The physician who is conscious of these problems mustmake every effort to dissuade patients who are conditionedby a vocabulary now commonly used by the public or bydubious theories presented in books that seem quite seri-ous to the layman and which the media like to promote.Even after lengthy explanations that the physician has not“put back a displaced vertebra” and that “vertebrae do notdisplace themselves,” but that the physician simply“unwedged a disk fragment” or “relaxed the spine,” thepatient will ultimately remind the physician that he or she,for instance, “put back to its place the fifth lumbar thatwas displaced.” It is not very serious when this is limitedto terminology, but it is much more serious when patientsbecome truly obsessed by this myth of displacement and,to be manipulated, go constantly to practitioners who aremore or less qualified or manipulate themselves. The resultis that their neurotic fixations continue to increase, withthe unavoidable risk that one day an amateur may manip-ulate vertebrae and produce a spinal sprain or a disk lesion.

The fashion of spinal displacement seems for now tobe in full regression. But it is being replaced by otherterminologies well received by the public with the help ofthe media. For example, how many problems are due to“dysfunction of the cranial sutures”? Some practitionerspretend even to treat cerebral palsy and Down’s syndromeby normalizing the positions of the sphenoid and the tem-poral bones, while others, with the help of various maneu-vers, will put back into balance the “vital circuits.”

Vertebrobasilar Insufficiency

Vertebrobasilar insufficiency (VBI) is a formidablesource of error. Although rare, it is the most frequent causeof the dramatic accidents associated with manipulation. Itis all the more misleading because the manipulative acci-dents can happen in a patient who never complained

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before and who comes complaining of headache or ver-tigo, symptoms that are frequently tied to PMIDs and areoften relieved by manipulation. In the case of VBI, how-ever, cervical manipulation can have disastrous conse-quences, especially if the maneuvers are forced, repeated,or maintained. But accidents have also followed maneu-vers that seemed to be mild. In fact, two types of VBI canbe distinguished: thromboembolic VBI and hemodynamicVBI described by Rancurel.

Thromboembolic Vertebrobasilar Insufficiency

The existence of thromboembolic vertebrobasilarinsufficiency has been admitted by all. From the physio-pathologic point of view, it is analogous to carotid vascularaccidents.

There can be (a) thrombosis affecting the spinal sub-clavian trunk, resulting sometimes in permanent and tran-sient neurologic deficits, or (b) platelet emboli or thrombicoming from the neck or from an ulcerated atheromatousplaque, producing transient or permanent vascular acci-dents. Depending on the affected artery, it will produce alateral homonymous hemianopia, the Wallenberg syn-drome, or complex attacks of the brainstem, characterizedby a unilateral or bilateral pyramidal syndrome, sensoryproblems, cerebellar syndromes, peripheral paralysis ofone or more cranial nerves, and possibly dysphasia ordysarthria. A well developed collateral circulation canavoid or limit these infarcts, but the two principal anasto-motic systems are often insufficient. The posterior com-municating arteries (which unite the carotid and verte-brobasilar systems) can be nonfunctional, and the basilartrunk is sometimes supplied by only one spinal artery,with the other ending in the inferior cerebellar artery. Inview of their brainstem involvement and potential for pro-ducing tetraplegia, these infarcts with posterior circulatorytopography are the most serious neurologic accidents andthe most typical (but rare) accidents seen with cervicalmanipulation. The treatment is anticoagulation, after rul-ing out the possibility of hemorrhage. The systematicpractice of postural testing, the execution of gentle andprecise maneuvers, and their contraindication in those sus-pect of harboring atheromata constitute the best and mosteffective means of preventing these types of accidents.

Hemodynamic Vertebrobasilar Insufficiency

Rancurel describes a second type of vertebrobasilarinsufficiency, the hemodynamic VBI. It has some specialcharacteristics because of the very particular anatomy ofthe vertebrobasilar system. The spinal arteries behave likeperipheral arteries, with systolic–diastolic pulsation and alow diastolic pressure. The inferior part of the basilararterial trunk is hemodynamically fragile because it is azone where the vertebrobasilar and carotid pressures are

about equal. From that zone emerges a symmetric andpaired artery that is particularly vulnerable because it islong and thin and supplied by a weak pressure; it is themiddle cerebellar artery that supplies the internal ear.

Hemodynamic VBI will manifest clinically if there isa decrease in the blood volume in the spinal artery, ingeneral resulting from a spinal or subclavicular atheroma-tous stenosis. Its neurologic manifestations are brief,always the same in the same patient, and also “postur-osensitive,” happening only in the standing position whenthe diastolic pressure is lower than in the supine positionas well as with abnormal neck posture (hyperextension,rotation). When these abnormal postures are performedpassively, as is the case during postural testing performedprior to any cervical manipulation, certain symptoms indi-cating relative ischemia in the territory of the middlecerebellar artery may be produced, even if the patient islying down (Fig. 22.30):

• Central vestibular dysfunction, especially vertigo,whose pathologic characteristic is recognized if it isassociated with other disorders

• Visual problems, diplopia, or blurred vision• Brief loss of consciousness or poorly defined dis-

comfort; signs that may not be recognized as a VBIunless there are other associated symptoms

• Hypoacusis with tinnitus and buzzing, which shouldbe unilateral

• Amnesia• “Drop attacks” (rarely)

These attacks are usually brief (a few seconds to 5minutes maximum). They are always stereotyped and dis-appear in the supine position. In 105 cases reported byRancurel’s group (Vitte et al.), with patients of an averageage of 62 years, the following problems were noted: acutedysequilibrium (98%), visual problems such as amaurosisand amblyopia (23%), diplopia or blurred vision (36%),problems of vigilance or of consciousness (40%), drop

Figure 22.30 Postural testing. This test is performed with thepatient supine, but it should also be performed with thepatient seated (see text).

CHAPTER 22 SPINAL MANIPULATION 193

attacks (19%), dysphasia followed by dysarthria (18%),and attacks of hypotonia or hypokinesia (15%) along theway that are exceptionally isolated.

Spontaneous reproduction of these signs by posturaltesting (see below) presents an absolute contraindicationfor any manipulative treatment and requires an evaluationfor the existence of a hemodynamic VBI. Four clinicalelements are particularly suggestive:

• Posturosensitive character of the symptomatology• Occurrence in brief and repeated attacks• Presence of a supraclavicular bruit• Reproduction of the syndrome by the compression

of the spinal artery (Rancurel)

This compression at the triangle of Tillaux in the sub-occipital region is performed with the thumbs, movingfrom right to left, and then, if necessary, to both sides for20 seconds maximum, with the patient standing. The testis positive when the symptoms of the patient are repro-duced (Fig. 22.31). The validity of this test has been aidedby the use of Doppler ultrasonography.

Compression should be stopped immediately oncesymptoms are reported. The test can then be performedsafely.

Electronystagmography is of diagnostic interest whenit is performed with spinal compression. The typicalabnormalities are (a) appearance or increase of saccadicmovements on visual pursuit, (b) hypermetria of the sac-cadic movements (two thirds of cases), or (c) hypometria.

This examination supports the diagnosis of VBI andallows the selection of patients having to undergo anangiographic exploration. Doppler ultrasonography is auseful screening tool for the detection of spinal athero-mata, carotid stenosis, or subclavian steal syndrome, butonly angiography can show the exact location and theseverity of that stenosis. Such lesions are, in some cases,amenable to surgical cure by bypass or endarterectomy.

Published postoperative results are very satisfactory.Mixed forms can exist, as in thromboembolic VBI withhemodynamic VBI.

Vertebrobasilar Insufficiency Due to Osteophytes Compressing Spinal Artery

Even if vertebrobasilar insufficiency due to osteophytescompressing the spinal artery is relatively rare, the mid orlower cervical spine can be directly responsible for circu-latory compromise of the spinal artery caused by articularor uncinate process osteophytes compressing it. Duringsome neck movements, paroxysmal attacks can be pro-duced if compensation is not supplied by the rest of thevascular system. Arteriography will show the possibleobstacle, and in some cases, surgical intervention (Jung)can free the artery and reestablish normal blood flow.Table 22.1 lists signs of VBI.

ACCIDENTS AND INCIDENTS OF SPINAL MANIPULATION

Reading the medical literature and the long chapterson errors and accidents in this book could lead one tobelieve that manipulative accidents happen frequently. Infact, manipulation practiced in a medical setting is a treat-ment with very few risks. In 25 years, with about 200,000manipulations performed in our hospital, we have neverhad any significant or serious accident. For many years,manipulation was mentioned in the medical literature onlyas responsible for dramatic accidents. The literature some-times emphasized the nonmedical status of a practitioner butalways emphasized the association between manipulationand the accident.

Fortunately, things have changed, at least in France,thanks to the development of this therapeutic system in

Figure 22.31 Rancurel’s test: compression of the spinal artery in the triangle of Tillaux (see “Hemodynamic VertebrobasilarInsufficiency” above). This test is performed with the patient standing. First, one side is examined, then the other side isexamined (left). Finally, both sides are examined at the same time (right).

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hospitals and to university teaching. There is no usefultherapeutic measure without risk, and in some cases,movements that are usually harmless can have dramaticconsequences. Manipulation, when applied to old and frailspines, is not inoffensive if the examiner does not haveperfect technique or cannot measure the maneuvers properly.

Dramatic Accidents

In the French experience, dramatic accidents are mostlythe results of maneuvers executed by nonphysicians. Com-mon to most dramatic accidents, some of them fatal, is amistake in the diagnosis or an absence of diagnosis. Thebrutal manipulation of a cervical spine with Pott’s disease,with metastases, or with a fracture will lead to suddendeath or quadriplegia. The forced manipulation of a tho-racic or lumbar spine with spondyloarthropathy or of aspine that has become frail due to disease will result inparaplegia. Such are the most frequent, although rare,dramatic accidents.

Besides the accidents in which the error of diagnosisis flagrant, however, we are aware of the possibility ofpostmanipulative vascular accidents happening even in theabsence of any predisposing factors that could be clinicallyor radiologically discovered (Cambier). In general, theseare due to thrombosis of the trunk of the spinal artery or

of the posteroinferior cerebellar artery (Wallenberg syn-drome), whose evolution can be fatal or result in signifi-cant sequelae. These vascular accidents happen in patientswith VBIs whose signs can be very subtle initially. Theinitial lesions affect the spinal artery: intimal tears, sub-intimal hematomas, pseudoaneurysms. It is possible thatthe manipulation produces a transitory protective muscleguarding that is the initial occurrence; then, either bymigration of an embolus, resulting from intimal lesions,by parietal edema, or by a process of an aneurysm dissec-tion, the occlusion of arteries downstream occurs.

The consequences of these dramatic accidents are seri-ous: death in 25% of cases and severe neurologic sequelaein 50% of cases, with only mild sequelae or completecures in 25% of cases (Ali Cherif). The victims are oftenwomen under 40 years of age, which means that athero-sclerosis plays a less prominent role than had beenthought. The contributory role of the birth control pill hasbeen emphasized; 70% of vascular accidents due to thepill happen in the first year of its use. In these patients, aprogressive headache can be the warning sign of a throm-bosis. Most of the observations that have been reportedtake the following course. During the manipulation, mal-aise or nausea occurs followed by a free interval; then thepicture is formed rapidly and progressively, revealing anextensive thrombosis, with spinal cord, brainstem, orcerebellar symptomatology. The Wallenberg syndrome isthe typical picture of these accidents and is characterizedby the following.

• Ipsilateral to the lesion: cranial nerves IX and X areaffected, resulting in ipsilateral paralysis of the mus-cles of the palate, pharynx, and vocal cords; thedescending root of V and the sympathetic fibers areaffected, producing a hemianesthesia of the face andHorner’s syndrome; and a cerebellar disorder pro-ducing hemiataxia and vertigo.

• Contralateral to the lesion: the spinothalamic tractis affected, producing a decrease in the pain andtemperature sensation of the trunk and limbs.

At higher levels, the “locked-in syndrome” (i.e., motordeafferentation) may occur, usually corresponding to alesion of the brainstem, due to infarction or basilar throm-bosis. In this syndrome, there is association of quadriple-gia and paralysis of the last cranial nerve with con-servation of ocular movement in the vertical direction.Consciousness is also preserved. The prognosis for suchpatients is very poor. A typical observation (Ali Cherif) isreported in the following case history.

Case History — A 51-year-old male presented withbrief episodes of vertigo and a temporary diplopia.Cervical manipulation was followed by nausea. Overthe next 24 hours, his condition worsened, progressingfrom right hemiplegia to quadriplegia and then coma.

Table 22.1Signs of Vertebrobasilar Insufficiency

Vertebrobasilar insufficiency is an absolute contraindication to theuse of cervical manipulation. Its signs (listed below according toRancurel and Vitte) should be very well known.

Headache (benign, often occipital)

Vestibular problems Positional rotary vertigoEpisodic vertigo of central origin

Visual problems (often temporary)Blurred vision Diplopia Amaurosis

Concentration and loss-of-consciousness problems Syncopal episodes Temporary periods of coma

Motor problems Drop attacks Transient hemiparesis

Auditory problemsDeafnessHypoacusis

CHAPTER 22 SPINAL MANIPULATION 195

He was hospitalized, and the examination revealed alesion of the brainstem. Death followed. The postmortemexamination demonstrated an old occlusion of a spinalartery and a recent thrombosis of the other spinal artery.

But here is the often-cited observation by Ford andClark.

Case History — A 37-year old bacteriologist, cominghome one evening, found that his wife was twisting herhead from side to side with her hands, which wereplaced on either side of her head. She claimed that herneck was stiff and that this made it feel better. He askedher to do the same for him. She twisted it strongly toone side. He then said, “That feels better. Do it again.”She did so, and he staggered and fell. Vertigo occurred,with vomiting, ocular and auditory problems on the rightside, stiffening of the left arm, and sphincter dysfunction.The next day, he was admitted to Johns Hopkins Hospitalwhere examination revealed an obtunded level of con-sciousness with dysphasia and dysphagia, no weaknessbut a tendency to fall to the left, an ataxia of a cerebellartype, an inequality of the pupils with a ptosis of the lefteyelid, and horizontal nystagmus. His condition deterio-rated rapidly and he died 60 hours after the accident.The autopsy revealed thrombosis of the basilar artery,of the left posterior cerebral artery, and of the left pos-teroinferior cerebellar artery.

Treatment consists of anticoagulation started as soonas possible. Such particularly serious accidents haveoccurred most often in patients who were treated for abenign disorder having nothing to do with the spine. Asa rule, these accidents are due to powerful maneuvers,usually repeated. But softer maneuvers, especially if theyare repeated and maintained, can have similar conse-quences. Besides, in some people, activities performed ina prolonged and awkward head position (e.g., a plumberworking under a sink or an automobile mechanic workingunder a dashboard) can produce vascular accidents of thecerebral trunk (Alajouanine et al.). When ipsilateral neckhyperextension and rotation are performed simulta-neously, there is an interruption to flow in the contralateralspinal artery (Kleyn and Nieuwenhuyse). This has beenconfirmed by angiography. Tatlow and Bammer were ableto be more precise, noting that the interruption occurredat the atlanto-occipital joint. This did not occur in normalsubjects, as the regional circulation is, fortunately, easilysupplied. But in the case where there is only one spinalartery and it is thrombosed, the blood supply is compro-mised, and the accident occurs. This is a very seriousaccident, and even when there is recovery, usually it isslow and incomplete. The accident can be fatal.

Other neurologic complications have been reported; forexample, thrombosis of the carotid (Boldrey, Maas,and Miller) or compression of the spinal cord, producing

quadriplegia or paraplegia. Manipulation can also unmaskor aggravate preexisting occult lesions (neoplastic, Pott’sdisease, unrecognized fracture, etc.)

Serious Accidents

Serious accidents are not rare in the hands of ignorantor awkward examiners. They are due to a lack of diagnosisand often a technical mistake (e.g., a lever arm that iswrongly applied, a forced maneuver performed blindly, ormanipulation in the wrong direction). They can also bedue to aggravation of the treated disorder: torticollis orlow back pain sciatica becoming hyperalgic or refractory.They can also transform torticollis into cervicobrachialneuralgias, or low back pain syndromes into severe sciat-ica, or benign sciatica into paralysis during the same ses-sion. Rib fractures without displacement are often due toawkward examiners, but they can also be seen in the workof good practitioners, as the 11th and 12th ribs are veryfragile under some angles of pressure. Costal sprains,produced by some maladapted maneuvers, are more fre-quent and often foster refractory pain syndromes. Morerarely, there is the possibility of purpura after manipula-tion (Tomlinson). We have seen such a case — a veryextended purpura on the legs the day following a lumbarmanipulation for a benign traumatic low back pain thathad otherwise been very well relieved.

Incidents

Incidents are extremely frequent if the examiner is notwell trained. We should emphasize the inconvenience theycause some patients as a result of their durability, duration,and refractory character. Wrongly performed manipula-tion can create all the symptoms that examiners are ableto treat.

Maneuvers performed on the cervical spine can resultin a refractory headache absolutely identical with the onethat is an indication for manipulative therapy. Patients arefrequently seen who complain of cervical pain, low backpain, and thoracic pain that occurred during a session ofmanipulation and from which they did not suffer beforethe session. Such pain can be due to a benign incident thatis easy to correct at the next session or can be due to amaneuver that was a little too forceful. Most often, how-ever, these incidents are due to spinal sprains, costospinalsprains, or disk injuries that are refractory and resultedfrom maneuvers performed with use of the wrong supportsand in the wrong direction. These incidents, producedbecause of forced maneuvers, are difficult to treat. Theexaminer needs a great deal of patience and the use ofvery soft and progressive movements, as the patients,already alerted, fear any passive movement.

196 SECTION V TREATMENT

Prevention of Accidents: Postural and Rancurel’s Tests

Almost all accidents due to manipulation can beavoided if the diagnosis is correct, the indication is wellchosen, the correct direction of the manipulation isrespected, and the execution of that manipulation is tech-nically perfect.

Obviously, only an examiner who is totally educatedin spinal pathology and in manipulative techniques andtheir use can practice this therapeutic system without riskand with regular results for the patients. As far as thedelicate problem of vascular accidents of the ver-tebrobasilar trunk is concerned (whose diagnosis is notalways easy to make), these accidents should be avoidedif the history and physical examination have not uncoveredthe suspect signs that we have described, by using posturaland Rancurel’s tests as we propose, and most importantly,by abstaining from any manipulative treatment when indoubt.

Postural Testing

The postural test consists of maintaining the superiorcervical spine of the patient in a position of hyperexten-sion, with first right then left rotation for a few seconds,interrupted immediately at the least feeling of vertigo ornystagmus (Fig. 22.30), whose occurrence calls for thegreatest caution. This test is performed with the patient inthe supine and the sitting positions.

Rancurel’s Test

As discussed above, Rancurel’s test (Fig. 22.31) con-sists of compressing the spinal arteries in Tillaux’s trian-gle, with the patient standing.

Medical Responsibility

The physician’s responsibility in the matter of manip-ulation has been very well analyzed by Roussat from thepoint of view of French law. It is no different from theother acts a physician is called upon to practice in thisdomain, but some experts have totally hostile attitudes tothis form of treatment. However, a physician who pre-scribes spinal manipulation to be performed by a nonphy-sician or who covers the activity of a nonphysician couldbe charged with “illegal exercise of medicine” (Cass.Crim. 10 April 1964, Bull. Crim. n. 105, p. 236). In caseof accident, the physician is responsible. Manipulation isa delicate and often difficult therapy to perform; it is atypical medical act in which the physician, in decidingand then in performing the act, engages all of his or herknowledge and takes all of the responsibility. It is notsimply an act of prescribing; besides, prescribing is impos-sible, qualitatively and quantitatively.

MECHANISM OF ACTION OF MANIPULATION

If there is still some mystery about the way manipula-tions work, it is because we still do not know enoughabout most of the disorders that they relieve. What do weknow about the exact pathogenesis of acute torticollis,postural thoracic pain, benign low back pain, and coccy-godynia, to cite only a few of the current indications ofmanipulation?

The responsibility for this ignorance is not to beascribed to the therapeutics or to those who use it. Theother treatment modalities used in these disorders oftenresult in less effective results and are no better justified.The classical concepts in spinal pathology do not help oneto understand the action of manipulation that relievessome pain syndromes quickly and well.

That is why it is necessary to appeal to the hypothesisof a reversible disorder; i.e., a wrong movement createsit, and a right movement corrects it. It is from this per-spective that the “displaced vertebra” of the bone setter (afolk manipulator often found in rural areas), the “sublux-ation” of the chiropractor, and the somatic dysfunction ofthe osteopath have been cited. Most schools of manualmedicine, such as the school of osteopathy, consider thatthis reversible mechanical disorder is due to hypomobilityof the concerned vertebra, restored by manipulation. Thereis nothing more apparently logical.

Unfortunately, this perturbation cannot, except in rarecases, be demonstrated by radiographic or dynamic cine-radiographic examinations. It is detected and analyzedby a refined system of palpations whose validity isunproven, not because of the reality of the modificationof the tissues palpated, but because of the interpretationof the examiner.

It is the critical analysis of these facts that brought usto the concept of painful minor intervertebral dysfunction(PMID), in which only the pain of the segment is consid-ered when it is produced by exactly described palpationalmaneuvers, with these maneuvers being painless on theother segments. When the manipulation results in a satis-fying effect, the segment returns to its painless state and,simultaneously, the patient is relieved of the local orreferred pain that was the cause for the required treatment.

Therefore, to discuss the modes of action of the maneu-vers for most of their indications requires an understand-ing of the mechanism of segmental dysfunction, aboutwhich we can only hypothesize (see Chapter 17, “PainfulMinor Intervertebral Dysfunctions”). Not only is manip-ulation a treatment for PMIDs, it also produces relief indisorders such as common sciatica, where the role of disklesions has been described. One can, in that case, askwhether the mechanism of action is then different and, if

CHAPTER 22 SPINAL MANIPULATION 197

it is, wonder when the manipulation relieves a coccygo-dynia or a costal sprain. Disk pathology has been widelystudied and its lesions are perfectly well known, but themechanism of pain relief by manipulation in sciatica isunclear. Let us first look at the effects of manipulation ona spine that is considered normal.

Effects of Manipulation on Normal Spine

By normal spine, we mean a spine in which no move-ment is limited or painful and no vertebra or paraspinalregion is experiencing any spontaneous pain, with theradiographic studies also being normal. If, for example,cervical maneuvers are executed on such a spine, therecan be no action and no reaction; sometimes, however,axillary perspiration can be seen immediately.

Thus on a normal spine, a well performed manipulation(the risk of a wrongly performed manipulation is not tobe neglected) does not cause any particular phenomenon,any more than a manipulation performed to unlock ablocked meniscus would have any effect on a normal knee.

The localized perspiration suggests action of manipu-lation on the sympathetic system. There are also otheractions such as abdominal disturbances and alterations ofmenstrual periods. Manipulation can have mechanical andreflex effects. Its mechanical effects are:

• To restore normal mobility in a stiffened joint as isperformed, although less efficiently, by classicalmobilization, when the joint has lost a part of itsjoint play.

• To treat a reversible mechanical dysfunction, artic-ular or periarticular, as, for example, release of ameniscal blocking of the knee. Its reflex effect is toproduce a reflex or vasomotor action by the forcefulor strenuous stretching of the muscles, tendons,articular capsules, and ligaments.

Possible Mechanical Factors

Disk Lesions

In the case of disk protrusions and the related acutelow back pain syndrome, one can imagine that manipula-tion tends to reinstate the center of the disk to the displaceddisk fragment. On the other hand, in the case of a herniateddisk that causes a sciatica, it is less likely that the manipu-lation can “put back” the hernia. Chrisman et al. studied 39patients with sciatica who were relieved by manipulation.They found no change in radiologic images performedbefore and after the treatment, even when the latter showeda marked compression, and relief was maintained for 3years or longer. Farfan thinks that 30 to 40% of patientsrelieved of sciatica by manipulation show the same radio-logic findings before and after the manipulative treatment.We have made the same observation. One might imaginein these cases that manipulation slightly alters the relation

of the herniation and the nerve root in a favorable way,without leading to even partial resorption of the herniation.The truth is that it is difficult to put the toothpaste backinto the toothpaste tube.

But even admitting that attenuation or suppression ofthe impingement of the disk upon the nerve root or pos-terior longitudinal ligament could be possible, one wouldthink that it could not last and that the painful phenomenawould come back very quickly. However, the relief is oftenlasting.

The logical hypothesis is that manipulation, by sepa-rating even very temporarily the antagonists, makes itpossible during that short period to obtain a decrease ora disappearance of the inflammatory phenomena respon-sible for pain.

Is the mechanism that results in pain as quickly revers-ible? The manipulative practice offers, in a little differentdomain, the demonstration that it is possible to have arapid change in some physiopathologic phenomena. Whena manipulation is performed in the treatment of a thoracicPMID with cellulalgia in the dermatome of the corre-sponding posterior ramus, one can notice (sometimes inless than a minute) the clear decrease and even the dis-appearance of the pain on the pinch-roll maneuver and ofthe thickening of the fold. This fold, which was thick andedematous, rapidly becomes supple and painless.

Although the inflammatory reaction of discoradicularimpingement differs from reflex cellulalgia, although therole of the inflammatory mediators is credible in bothcases, this example demonstrates the rapidity with whichsome phenomena can regress. There was also the hypoth-esis that manipulation acted on some intradiscal block-ings, releasing a painful dysfunction of the segment, oron some facet joint “blockings” or “rubbings.”

Some authors believe that there may be some incarcer-ated nuclear fragments in annular fissures, which wouldnot compress any sensitive element and would not produceany direct symptom. But by leading to dysfunction of themobile segment, these intradiscal blockings could makeit less mobile and cause acute or chronic dysfunction ofanother part of that segment, especially at the facet joint.

By modifying the position of the fragment that wasdisplaced, the spinal segment would again have a normalplay. This mechanism, if it exists, can involve only afraction of the cases that are treated and can be consideredonly at the inferior lumbar level or at the inferior cervicallevel, the most common locations of disk herniations.

Facet Joint Lesions

With the facet joints, we are in a domain that is muchmore hypothetical than that of the disk lesions, even if itseems that the perturbations start especially at their level—perturbations that manipulation treats very efficiently.

198 SECTION V TREATMENT

A certain number of authors have tried to explain theaction of the manipulation in a “facet joint blockage.”

The intra-articular blocking of a meniscoid formationhas been considered by some; Zuckschwerdt et al. werethe first (1955) to express this hypothesis. The “theory ofincarceration” had some supporters (Keller, Hadley, Kos,and Lewit), but others were against this explanation (Ter-rier, Dorr, Penning, Töndury, and others).

Kos showed that the cartilage lining the facet joints caneasily be deformed. He experimentally made imprints onits surface by pressing steel marbles, other materials, andhairs on the cartilage. The prints he obtained were clearbut temporary (5 min for the hairs). On the other hand,he noticed that the tops of the meniscoid formations werethicker and harder than the rest (chondroid zone; Fig. 2.6).He then suggested that during an excessive movement, themeniscoid formation could be entrapped in the joint. Thefree and hard extremity compressing the cartilage wouldcreate a socket in which it could be retained. There wouldthen be excessive traction on the joint capsule where thebase of the meniscoid formation is inserted. Irritation ofthe capsular mechanoreceptors would produce a reflexmuscular contraction that would increase the pressurewhile maintaining the blocking. Only a manipulationaimed at separating the two articular surfaces could freethe included fragment.

Bogduk, who later studied the anatomy of the menis-coid formation, thought that only a few of them had formsthat would allow such a mechanism. He also thought thatsuch a wedging could not be produced because the baseof the formation is loose and that sufficient pulling on thecapsule would be necessary to produce pain.

Can the role of the meniscoid formations be consideredin chronic cases? For Emminger, these meniscoid forma-tions could show all the “possible effects of wear, be theseat of spondylosis, be the victim of trauma, etc. Some ofthem could remain wedged.” Manipulation could freethem “if there was not already some fixed chronic prob-lems.” Töndury could not find convincing evidence prov-ing the evolution because of age, but “during the wear ofthe cartilaginous covering, the meniscoid formationsundergo stress from a mechanical point of view, and thuswear considerably. Small fragments can even slip into thejoint.” But because of their usual thinness, it does not seemto cause blockage.

Other mechanisms could predispose to a facet jointblockage. Gillot noted the frequency of the irregularitiesof the cartilaginous surface of these joints. He noted, asdid Freudenberg, the frequent presence of transverse crestsin the inferior lumbar spine. Farfan thought they were theconsequences of a progressive dysfunction of the mobilesegment and were linked to disk deterioration, but he doesnot believe that they have a role in blockage (see “PossibleRole of Discal or Facet Joint Pathology” in Chapter 17).

Reflex Factor

The purely mechanical action of manipulation is a con-venient hypothesis for now. But even in the cases whereit seems probable, one should also consider a reflex effectto understand all of the observed phenomena. The sup-porters of the theory of facet joint blockage due to a lesionof the meniscoid formations also give an essential role tothe reflex contraction in maintaining the vicious cycle.

But is the presence of a permanent mechanical lesionin the facet joints a necessary condition for its pain andthe starting point of the excitation of the neural receptors?A benign sprain of the fingers remains painful for a longtime to the least pressure and the least torsion, whileflexion/extension is free and often painless, and there isno detectable mechanical lesion. This can also be the casein the facet joints.

Any dysfunction of the innervated elements of the spi-nal segment, particularly the posterior longitudinal liga-ments, facet joints, interspinous ligaments, and musclesproduces a reflex action that tends to immobilize or, better,limit segmental motion. In this reaction, one would thinkthat protective muscle guarding plays an essential role. Aswe have seen in Chapter 17 on PMID, a temporary dys-function of a spinal segment can, in some conditions,become chronic because of the very particular and strictlyautomatic character of the functioning of the spine.

The facet joint can be the starting point of that dys-function; and if the facet joint itself is not the initial cause,it is the victim. Moreover, this maintained protective muscleguarding strains the intrinsic segmental muscles, whichthen become sources of nociceptive influx. We have pre-viously emphasized the particular relationships betweenthe muscular bundles of the intertransverse muscle andthe internal and external branches of the posterior ramusof the spinal nerve. These branches penetrate the bundlesof that muscle and course around the transverse process.They innervate them after giving off some articularbranches. A mechanism of discomfort in the neuralforamina as a result of muscles permanently in protectivemuscle guarding is possible, as the medial branch passesthrough an osseofibrous tunnel (see Chapter 8, “Innerva-tion of Vertebral Structures”).

This explains the fact that the cutaneous area of theposterior ramus is almost always the source of modifica-tions in texture and sensitivity when there is a segmentaldysfunction, by PMID in particular. This cellulalgia local-ized in the area of the posterior dermatome is, indeed, themanifestation, the most frequent, and the earliest “seg-mental spinal neurotrophic syndrome.”

Whatever the mechanical support considered to explaina reversible blockage of the mobile segment is, the reflexmuscular dysfunction plays an important role. Besides, insome cases, relaxing a tense muscle by using manualtechniques or local anesthetic injection relieves an acute

CHAPTER 22 SPINAL MANIPULATION 199

or chronic spinal pain. Manipulation or stretching the mus-cle can also achieve the same goal, but it also produces asharp traction on tissues that are rich in proprioceptors:tendons, ligaments, articular capsules. When performed inthe correct direction, it produces a powerful inhibitoryreflex at the spinal cord level. It is thought that it is apresynaptic inhibition of nociceptive impulses in the pos-terior horn of the spinal gray matter. But, to us, this inhib-itory reflex seems possible only if the directed traction isperformed in the direction of no pain, opposite the painfuldirection, producing an intense stimulation of the corre-sponding mechanoreceptors.

Articular Cracking and Gapping

Manipulation is, indeed, a very particular movement.Unsworth et al. (see “Cracking” above) studied the mech-anism of articular cracking and concluded that it was theresult of the phenomenon of cavitation. But some otherconclusions can be drawn from their studies. They showedthat the manner in which joint gapping was produceddetermined a difference between cracking joints and those

that do not crack when they are submitted to identicalforces of traction.

The noncracking joints have a progressive gapping pro-portional to the power of the traction. The cracking ones,on the other hand, do not separate during the traction untila point at which, nearly instantaneously and suddenly, thisseparation becomes maximal, which is equal to thatobtained by a progressive gapping. The sudden separationcorresponds to the noise of the cracking.

In both cases, when the traction stops, the return to thenormal position follows the same progressive curve. Theterminal articular gapping in both cases is slightly greaterthan it was at the start. This experiment, although it didnot have that aim, demonstrated clearly that the ultra-rapid, explosive stretching obtained when a joint cracks— the manipulation — thus has an effect on the periar-ticular and muscular structures that is different from theprogressive stretching produced by mobilization. Withoutdoubt, this particular reflex effect gives manipulation theessential aspects of its effectiveness.

201

23

SPINAL TRACTION

Spinal traction is a therapeutic modality that is appliedvia an apparatus that exerts a distractive force in line withthe axis of the spinal column. The use of spinal tractiondates back to the time of Hippocrates, Galen, and Aescu-lapius, with very exact descriptions of the technique intheir writings. Some illustrations show patients who arefirmly attached to the apparatus while axial traction isapplied by the use of ropes, winches, and levers. In mostof these drawings, one of the operators also applies simul-taneous pressure to what appears to be a hump.

Traction is a treatment modality used in the treatmentof mechanical pain of spinal origin. Although traction andmanipulation have some common indications, the indica-tions for traction are more restrictive. However, tractionis less frequently useful and its action is clearly slower.

The operator who can master manipulations finds thattraction has very limited application, which is unfortunatebecause traction is much less difficult and tiring for theoperator.

MODE OF APPLICATION

Lumbar traction is usually performed on a specificallydesigned traction table. Under specific conditions, it canbe performed with the patient in bed. Cervical traction canbe performed with the patient on a table, on an inclinedplane, in bed, or seated.

Traction can be continuous; with the patient in bed, itis performed for periods of several hours per day. Mostoften, it is intermittent. A typical session lasts 10 to 30min, with a frequency varying from twice a day to twicea week. Traction can be maintained continuously duringa whole session or applied intermittently, with the maxi-mal traction maintained for only a brief period. Tractionis thus applied in a cycle, gradually increasing the distrac-tive load and gradually releasing it until no tension isapplied. The choice of method is case dependent.

Traction Table

A typical traction table is depicted in Fig. 23.1. It iscomposed of a stationary surface (to which the thorax hasbeen fastened by straps) as well as a lumbar surface thatis mobile. Movement of the inferior surface will createtraction of the lumbar spine. This traction can be appliedin different ways: with weights or by rolling up a rope ona windlass. One inconvenience accompanies these proce-dures: the traction and especially the detraction areirregular.

It is preferable to have the surfaces spaced by a crank-shaft, or better, by a hydraulic system or motor. The resultsare independent of the system’s mechanics. An automatedsystem is more regular than a manual one, maybe a littleless measurable, but easier for the operator. The tractionspeed should be variable; it should be weak, especially atthe end of the traction (an average of 3 mm/min for thelumbar spine and 2 mm/min for the cervical spine).

Figure 23.1

Traction table.

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SECTION V TREATMENT

CERVICAL TRACTION

Application

The patient’s head is held by a collar with occipito-mental support, such as Sayre’s collar (Fig. 23.2) orMaigne’s cervitractor (Fig. 23.2), which has the advantageof applying pressure neither to the chin nor to thetemporomandibular joints, but which does not adjust topatients who are too brachycephalic or whose occipitalprominences are too flat. Under these conditions it tendsto slip during traction. In spite of this inconvenience (notfrequent in practice), it is more comfortable because itallows the patient to talk and does not require removal ofdental apparatus.

Traction on Inclined Plane

On an inclined plane, the weight of the body suppliesthe force of traction. Since the force of traction is limitedby the friction of the body against the table, the tableshould be as smooth as possible. Varying the inclinationof the plane varies the force of traction. This simple systemis convenient, the patient is generally relaxed, and thetraction is rather easily measured (Fig. 23.3).

Traction on Special Table

The patient lies supine with the shoulders maintainedby straps. Traction is performed either by weights or bya crankshaft or hydraulic system. Here the tractionbecomes efficacious quickly; therefore, it should be veryslow, very progressive, and very well controlled (Fig. 23.1).

Traction in Sitting

The patient is seated on a special table, fastened eitherat the pelvis or the shoulders. The collar is fixed on a polejust above the patient’s head. This is a very comfortableposition.

LUMBAR TRACTION

In lumbar traction, the thorax and the pelvis should befastened.

Fastening Thorax

There is no perfect way to fasten the thorax, and gen-erally, a corset is used to help. The problem is complexbecause the thorax is elastic and compressible and a strongcompression is uncomfortable. Strong pressure is applied

Figure 23.2

a.

Sayre’s collar.

b.

Maigne’s collar.

Figure 23.3

Cervical traction on an inclined plane.

CHAPTER 23 SPINAL TRACTION

203

to the epigastrium, which can be uncomfortable. Tractionshould not be performed immediately after a meal. At thestart of traction, there is always a certain slippage that isdifficult to avoid and which should be limited.

Fastening Pelvis

There are fewer difficulties with fastening the pelvis.Several systems of corsets are used, but obese patientscreate some problems that are difficult to overcome. The

table we have designed (1959) has a very convenient sys-tem that readily fixates the iliac crests and increases thisgrasp in proportion to the traction (Fig. 23.4 andFig. 23.5). The attachment should be comfortable and notable to slip. It should be easy to put on and remove.

Application of Traction

Traction should be applied slowly, progressively, andif necessary, gradually. The patient should feel relievedunder traction. In no case should pain increase; if it does,the treatment should be halted. The maximum amount oftraction applied is determined by the tolerance of thepatient and the resulting relief. The rate of release oftraction (detraction) should be gradual, slower than thetraction. If pain recurs during detraction, the rate of detrac-tion should be slowed and sometimes followed by enoughmild traction to suppress the pain.

Traction in Bed

Bed rest is often prescribed for treatment of acute lum-bar pain and sciatica. It is tempting to increase the effectof the rest by continuous traction to suppress or decreasepain. Continuous traction in bed is tolerated poorly, andpatient compliance is low. Chantraine et al. devised asimple apparatus called the “automotor frame” that is easyto carry. The patient, lying in bed, performs autotractionby pushing the legs, which are flexed on a roller. Thisallows autotraction to be performed in bed comfortablyfor 15 to 30 min, repeated during the day (Fig. 23.6).

Figure 23.4

Dr. Maigne’s examining table.

Figure 23.5

System for lumbar traction (Dr. Maigne’s table).

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MODE OF ACTION OF TRACTION

Most authors seem to think that the aim of traction isto increase the intervertebral spacing. It is true that withsufficient traction, the vertebral endplates can be separatedmeasurably. However, it would be simplistic to believethat the relief is due to the induction of intervertebral diskseparation. Furthermore, traction can occasionallyincrease the pain. It is more sensible to consider twopossible complementary modes of action: a mechanicalaction and a reflex action.

Mechanical Action

The traction separates the involved spinal segments.

Reflex Action

The stretching that is performed reflexively, if it is notpainful, relieves the protective muscle guarding by stim-ulating segmental mechanoreceptors.

Thus, the goal of traction is not to stretch to the max-imum, but rather, in a manner that causes the pain todisappear. Maintenance of painless traction may decreasethe degree of inflammation and vasocongestion, and insome favorable cases, they do not completely return whenthe traction is loosened. Conversely, if traction is painful,it should be discontinued immediately; if it does not bringrelief during a session, it is useless to continue.

We thought that orientation of the traction (1959) thatcould maintain the minimal optimal traction on a givenspinal segment might have a better effect and wouldrelieve a greater number of patients. With this in mind,we designed a suitable table. The thoracic surface can beraised or lowered; the pelvic surface is mobile laterallyand in rotation. One finds the position of lateroflexion andflexion in which the patient is best relieved using minimal

traction. This traction is then progressively increased andis maintained for about 10 min; then the pelvic surface isslowly put back into its normal position. The axial tractionis increased for 3 to 4 min, and the detraction is performedvery slowly. This has produced good results in cases inwhich axial traction was inefficient. This table brings bet-ter relief to the patient, especially because of the systemof pelvic positioning (Fig. 23.5) and the ability to slightlyincline the thoracic surface of some acute lumbar patientswho cannot sustain the strict lying position.

INDICATIONS FOR TRACTION

The usual indication for traction is radicular pain ofspinal origin. We have had the best results with cervico-brachial neuralgia, femoral neuralgia, sciatica (to a lesserdegree), cervical pain, and lumbar pain.

Cervical Spine

Before prescribing traction, a manual test must be usedto determine whether traction on the neck relieves thepatient or increases the pain. Manual traction is performedaccording to the technique shown in Fig. 23.7. If themaneuver increases pain, no traction is performed; if itclearly relieves the pain, then traction is a valuable treat-ment.

A certain number of cases of cervicobrachial neuralgiacannot be treated by manipulation because the rule of nopain and of the opposite movement cannot be applied.They are relieved by manual traction and can thus benefitfrom that treatment.

Figure 23.6

Chantraine’s apparatus for applying lumbartraction.

Figure 23.7

Manual traction test. It is important to performthis test before prescribing cervical traction. Traction is indi-cated if it helps reduce pain, and it is contraindicated if itexacerbates pain.

CHAPTER 23 SPINAL TRACTION

205

On the other hand, one can use both manipulation andtraction. These treatments can be performed separately,for example, traction daily and a manipulation once ortwice a week for 2 weeks. They can also be performedtogether in the same session, but then it is better to min-imize the manipulative maneuvers. In the upper cervicalspine, traction is rarely useful.

Lumbar Spine

Continuous traction in bed has been used historicallyfor severe sciatica treated in hospital. Intermittent tractioncan be used when manipulation cannot be performedbecause of contraindication or because of a lack of anexperienced manipulator.

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24

MASSAGE

Massage is a very effective modality for treating painof spinal origin, when used appropriately. Lately, however,it has been much maligned. First, the orthopedists thoughtit necessary to use an active physical modality for osteoar-thritic and traumatic conditions, and they did not considermassage a useful treatment. Then there was a lack ofscientific evidence to validate its efficacy. This gap appearsdifficult to fill because massage is performed by manydifferent techniques for various indications, and the choiceand the execution of these techniques is highly operator-dependent. But the main reason for a lack of interest inmassage is that most masseurs, physiotherapists, and espe-cially their teachers are no longer attracted to this form oftreatment. Too many of them do not consider it useful, butsimply tiring and of little value.

A good massage, it is true, is difficult to perform. It isuseful only if it is well tailored to the patient, whichrequires some knowledge and experience. A massage isonly as good as the masseur who performs it, which doesnot make it amenable to scientific study according topresent criteria. In any event, a well-executed massageapplied to appropriate indications is an extremely valuabletherapeutic modality that is far too often neglected. Forpain of spinal origin, massage relaxes the paraspinal musclesand relieves the cellulomyalgic manifestations of local orspinal origin.

MASSAGE FOR PARASPINAL MUSCLE RELAXATION

Acute Muscle Spasm

In torticollis (acute wryneck) and low back pain syn-dromes, massage can noticeably decrease the musclespasm or protective muscle guarding. In some cases, itcan even make it disappear completely and halt the viciouspain–spasm cycle.

Executing the maneuver is a matter of experience. Itproduces a kind of “dialogue” between the hand of the

masseur and the muscle of the patient (Dolto). The handshould sense the reactions of the muscle and thus find themaneuver that is most useful. Relaxing maneuvers arealways slow and progressive and are usually associatedwith stretching muscular fibers that are hypertonic, witha slight mobilization in the pain-free direction.

Chronic Muscle Spasm

Any chronic spinal pain always involves protectiveguarding of the paraspinal muscles. Palpation is facilitatedif the skin has been lubricated beforehand. Two techniquesare used: maneuvers that employ deep gliding parallel tothe line of the spinous processes and maneuvers thatemploy transverse stretching. These maneuvers are per-formed in a measured way, slowly, rhythmically, and pro-gressively, and adjusted to the reaction of the muscles.They are useful before manipulative therapy but can alsobe used alone. They are especially useful in cases of per-sistent deep muscle spasm after a treatment by manipula-tion or injection (Fig. 24.1 through Fig. 24.4).

The most useful techniques are described for eachregion along with the techniques of manipulation as“maneuvers of relaxation” (see Section VII, “ManualTechniques”).

MASSAGE AND CELLULOTENOPERIOSTEOMYALGIC MANIFESTATIONS

Massage is a useful treatment of cellulalgic edema andtrigger points. It can also be indicated in some ligamentousand tenoperiosteal pain syndromes.

When these manifestations are part of a spinal cellulo-tenoperiosteomyalgic syndrome, their local treatment isindicated only after the spinal treatment has been per-formed; the latter often suffices to resolve these manifes-tations.

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SECTION V TREATMENT

Cellulalgia

First the cellulalgic zone is mobilized gently in alldirections, as if it had to be detached. Then, very progres-sively, the operator executes some gentle superficial“kneading” maneuvers, without using too much force on

the most painful zones and nodules. Finally, the maneu-vers become more forceful and the nodules can be pro-gressively kneaded.

The most used maneuvers are the ones derived fromWetterwald’s techniques: rolled, stretched, broken, andcompressed skin folds, which are very well known thanksto Dolto (Fig. 24.5 and Fig. 24.6). These alternate withsuperficial and relaxational maneuvers. For instance, pro-longed and progressive subcutaneous tissue massage canbe performed, paying particular attention to the peripheralzones and alternating with muscular maneuvers aiming atthe bulk of the muscle and the tenoperiosteal insertions.

Trigger Points

In the limbs, the most useful and most adequate maneu-vers are the ones that use deep gliding. Often it is bene-ficial to alternate stretching with these maneuvers(Fig. 24.7).

The most sensitive indurated zone should not beapproached directly, but progressively. The maneuversshould be progressive, with very little pressure in thebeginning; they should not provoke acute pain.

Figure 24.1

Massage to relax paraspinal muscles. Thismaneuver is performed in a gliding fashion, with pressurecontinuously applied from the upper back to the lower lumbarregion.

Figure 24.2

Petrissage and stretching of paravertebralmuscles, with the patient lying on her side.

Figure 24.3

Petrissage and stretching of paraspinal muscles. Note the position of the thumb that “kneads” the muscles.

Left:

starting position.

Right:

terminal position. The maneuver should be performed slowly and rhythmically with resting periods.

Figure 24.4

A maneuver closely related to the prior point ofcontact in applying the massage maneuver. Here the thenareminences are used as the contact points.

CHAPTER 24 MASSAGE

209

These trigger points are found most often in the mus-cles of the external iliac fossae. They usually result fromdysfunction of the lower lumbar spine. Here the best tech-nique is deep kneading (Fig. 24.8); the maneuvers shouldbe slow, with progressive pressure. They can occasionallybe painful, but the pain subsides when the operator stops.During the session, pain should decrease progressively;besides, it is a particular pain that the patients like to call“a pain that feels good.” If pain increases despite adjust-ment of the technique, that maneuver should be stopped.

Rhythm and pressure are measured by the muscleresponse. If favorable, the taut bands relax under the fin-ger. Postural stretching is performed with the massage.Subsequent sessions reveal that the taut muscle fibers aresmaller and have less tonicity, indicating that they willdisappear with a few treatments.

If no improvement is noted with these maneuvers, it isuseless to continue; their cause persists.

Pressure maintained for up to 90 sec on a trigger pointcan be useful. It is an interesting technique in some acute

Figure 24.5

Pinch-roll.

Figure 24.6

Skin folding.

Figure 24.7

Petrissage and stretching of muscles of theshoulder girdle in different directions.

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SECTION V TREATMENT

cases, and it can also be used in chronic cases. Caution isrequired, as the risk of aggravation exists.

Firm pressure is applied on the tender point, progres-sively increased with the thumb, and reinforced if necessarywith the other thumb, without ever reducing the pressure.Thumb pressure can be replaced by elbow pressure inlarge muscles (glutei; Fig. 24.9).

The muscle under pressure should be perfectly relaxed.This may not be easy because the pressure should reachthe maximal pain that is bearable. By palpation, onechecks whether the tender point has resolved. If it persists,the same pressure technique can be repeated again, onceor twice, with each sequence interspersed with a few activemovements of the muscle or the application of heat. Briefpressure can also be used, for 5 to 10 sec, and repeatedseveral times a day; this can be performed by the patient.In most cases, the result is clearly not as good as it is withthe preceding technique.

Shiatzu is a technique that replaces the needle implan-tation of traditional acupuncture with pressure applied onthe acupuncture points with the pad of the finger. Its effi-ciency seems to us, with some exceptions, to be veryrelative.

Tenoperiosteal Pain, Tenalgias, and Tendinitis

Spinal treatment usually decreases or relieves the ten-dinous or tenoperiosteal tenderness caused reflexively bya segmental vertebral syndrome, so that it will not besymptomatic. When spinal treatment is impossible or inef-ficient, local treatment can be started. Injection is veryconvenient, but if corticosteroids are contraindicated, mas-sage becomes the best treatment. The deep transverse mas-sage proposed by Cyriax is then the most efficient tech-nique.

DEEP TRANSVERSE MASSAGE (DTM)

Cyriax used DTM in the treatment of tendinitis. Hebelieved that the technique freed adhesions formedbetween sheath and tendon. It should be performed on atendon placed under tension.

Whatever its mode of action, DTM is a disagreeabletechnique but a useful one. Troisier recommends its usefor rotator cuff tendinitis, forearm extensor tenosynovitis,lateral epicondylitis (the epicondyle should not berubbed), medial epicondylitis (the epicondyle can berubbed), and patellar tendinitis, as well as tendonitis ofthe tibialis anterior, tibialis posterior, peronei, and exten-sor digitorum longus muscles.

Massage is performed with the fingertips, the thumb,or the middle finger, with reinforcement provided by theindex finger pressing on the dorsal side of its phalanx(Fig. 24.10). To be useful, it should be performed accord-ing to the following principles (Troisier):

• The finger should be at the precise site of the lesion,perpendicular to the soft tissues.

Figure 24.8

Petrissage of gluteal muscles.

Figure 24.9

Ischemic compression of calf trigger point.

Figure 24.10

Transverse massage of common extensor ten-dons.

CHAPTER 24 MASSAGE

211

• Movements should be back and forth, of short ampli-tude, perpendicular to the fibers of the ligament or thetendon, with a pressure that is sufficient and constant.

• The finger should move the skin as it moves itself;it should not slide on the skin. The treated elementthus receives firm pressure and transverse friction.

The start of the treatment is painful, but the pain generallydecreases during the session. A session lasts 5 to 15 min. Itsfrequency varies from once daily (recommended by Troisier

in forearm tenosynovitis) to twice weekly, usually, as too-frequent massages are not well tolerated. The number ofsessions varies from 6 to 12. After the first session,improvement should occur in spontaneous pain, in thetests against resistance, and in range of motion. If painincreases in proportion to the treatment, the treatmentshould obviously be reconsidered. If no improvement isnoted despite good massage technique, the diagnosisshould be reevaluated.

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25

STRETCHING

Stretching techniques are of great interest in painfulmusculotendinous conditions. They can be performed lon-gitudinally, parallel to the muscle or tendon fibers, ortransversely, with one or more fingers that stretch themuscle or the tendon perpendicularly.

LONGITUDINAL STRETCHING

As the name indicates, a longitudinal stretching tech-nique tries to lengthen a muscle or a tendon. This maneu-ver can be performed manually, posturally, or by activeexercises. It is performed slowly and progressively.

Manual Stretching

As an example, let us take a patient with trigger pointsin the triceps surae and biceps. The patient is positionedin supine with legs extended. The examiner slowly raisesthe leg in question as if to elicit Lasegue’s sign, lockingthe knee in extension and the foot in dorsiflexion(Fig. 25.1). At a certain degree of inclination, 60° forexample, the patient may feel pain with stretching of theinvolved muscles. By palpation, the examiner shoulddetermine whether the provoked pain is from the muscle,the stretching, or irritation of the sciatic nerve with duraltension. Elevation is stopped if the pain becomes toosevere, and the level is maintained. After a while, thediscomfort disappears, allowing an increased stretchrange. In a few minutes, a level is reached that cannot besurpassed, but the elevation of the leg that was painful andimpossible beyond 60° becomes easy and painless at 80°.At the same time, the trigger points become less sensitiveand less hypertonic. The maneuver is repeated severaltimes, depending on the result. This treatment can beperformed every day or every other day. During thesemaneuvers, the patient should be instructed not to resist,to remain well relaxed, and to breathe calmly (Fig. 25.1).

Global Stretching of Extensor Muscles

The same maneuver can be performed on both legstogether. The result is a stretching of the extensor muscles(extensors of the spine and hips). The patient’s shouldersshould be on the examining surface, with the arms pulledcaudad and the head in flexion (chin in), resting on theexamining surface on the inferior part of the occiput(Fig. 25.2). Performed gradually with good respiratorycontrol and good patient relaxation, this posture canrelieve irritable protective muscle guarding of the paraspi-nal muscles and stretch the hamstring and triceps suraemuscles, which are often shortened in patients with lowback pain and sources of trigger points. This stretchingtechnique can be performed on all muscles or musclegroups; the technique to be used depends on the triggerpoints to be treated.

Stretching of the gluteus medius and tensor fascia latais often useful. The technique is shown in Fig. 25.3. The

Figure 25.1

Stretching of triceps surae and hamstrings.

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SECTION V TREATMENT

many techniques described in this book can be used at thevertebral level as stretching techniques for specific regionsof the spinal column by placing the tissues under tensionand maintaining it for 10 to 30 sec or more.

Postural Stretching

In some cases, stretching can be obtained posturally(e.g., by use of a system of pulleys and gradual steps), butthese procedures neither give the same control nor allowas fine an adjustment as do the manual procedures.

Stretching Exercises

Patients can perform their own stretching, using exer-cises or even some postures inspired by yoga.

VAPOCOOLANT SPRAY AND STRETCH

Travell, Mennell, and Simons developed this techniquefor the treatment of trigger points that produced local orreferred pains. As we have seen, these trigger points oftencorrespond to a segmental vertebral syndrome and thushave a spinal origin. In these cases, spinal treatment shouldbe given first. Those that persist can have the treatmentdescribed below, just as the ones whose origin is local.

The patient’s position depends on the region to betreated. After applying vapocoolant spray to the skin over-lying the region to be stretched, the physician passivelystretches the muscle to its end range, gradually and slowly.

During the stretching, the patient is asked to relax andtake deep breaths. With each expiration, the slack is takenup, and further range can be gained with subsequentstretching.

The vapocoolant currently in use is flurimethane, whichreplaces the previously used ethyl chloride. The stream ofvapocoolant is directed on the skin at an angle of 30° anda distance of 45 cm. Several passes of spray are appliedin the direction of the muscle fibers in question. The wholemuscle is sprayed as well as the zone of pain referral.

The authors call this technique “spray and stretch”because they consider the stretching essential. Sprayingfacilitates the stretching; the cooling of the subcutaneoustissues results in an inhibitory reflex of muscle tone (Trav-ell, Mennell). This light cooling likely acts as a counter-irritant that allows the muscle to relax reflexively.

TRANSVERSE STRETCHING

Transverse stretching is one of the basic maneuvers ofthe traditional bonesetter (a folk manipulator usuallyfound in the French countryside). The principle is simple,as is the correct execution and involves brief stretchingmaneuvers. For example, consider a patient with a hard,strained, taut band of muscle. This can be a trigger pointdue to a segmental spinal dysfunction or due to a reflexcontraction of some muscle fibers. The taut bands areoriented in the direction of the muscle fibers in question.The maneuver consists of grasping the taut muscle fiberswith the pad of the thumb and stretching it perpendicularlyto its fibers. The thumb places the fibers under maximumtension and then suddenly releases them, as if pluckingthe strings of a musical instrument. After the maneuver,the taut muscle fibers are less sensitive to palpation, some-times they are insensitive, but in any case, they are lesshypertonic than at the start (Fig. 25.4).

Figure 25.2

Global stretching of extensor muscles.

Figure 25.3

Stretching of gluteus medius and tensor fascialata.

CHAPTER 25 STRETCHING

215

This maneuver is really not as simple to execute as itseems. One must know exactly where the bundle to betreated is. The thumb should probe normal muscle beforecontacting the concerned muscle. The speed of executionshould be slow, and the constant pressure of the thumb isindispensable in the success of the maneuver — how muchpressure is a question of experience. Bellon has demon-strated this very well.

This technique can be applied to the muscles of thelimbs, trunk, and neck. Application of this technique tothe paraspinal muscles is sometimes very effective, but itis difficult. The maneuver is easier if the trigger point canbe stretched over a bony prominence where the grasp iseasier to obtain (e.g., iliac crest or the spine of the scap-ula). If performed with improper technique, this maneuvercan often exacerbate painful tissues.

Figure 25.4

Transverse stretching of biceps femoris.

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26

THERAPEUTIC INJECTIONS

Therapeutic injections are convenient and an effica-cious means of precisely introducing a medicinal sub-stance, usually a local anesthetic or a cortisone derivativeor both into a specific tissue site. They are used to act onneural elements, joints, periarticular structures, tendinoussheaths, muscles, subcutaneous tissues, etc. Thus, anextreme variety of possibilities is offered by this techniquewhose efficiency will depend on the choice of indications,choosing the appropriate tissue to be injected, the sub-stance injected, and the technical expertise of the exam-iner.

SPINAL INJECTIONS

The techniques used are epidural, intrathecal (or intothe subarachnoid space) or facet joint, and ligamentousand selective neural blockade. Asepsis of the skin shouldbe strict, and the hands of the examiner should be disin-fected or gloved. Syringes and needles should be dispos-able; one needle should be used to aspirate the liquid (ifthis is done through a rubber cork that has been carefullydisinfected) and another one used for the injection.

In a patient on anticoagulants, certain injections arerelatively contraindicated. The articular and epiduralinjections should not be performed if the prothrombin rateis greater than 25.

Epidural Injection

Epidural injection is useful in the treatment of lumbarpain and radicular pain due to a disk disorder at L3–4,L4–5, or L5–S1. The substance injected in the epiduralspace penetrates the dura, including the dura mater of thelast lumbar and sacral roots, the superficial layers of thelumbosacral disks, and the posterior longitudinal liga-ment. Three routes of administration are possible:

• Via the sacrococcygeal hiatus• Via the translumbar route• Via the first sacral foramen

Sacrococcygeal Hiatus

This technique was described in 1901 by Sicard. Atpresent, it is used infrequently, with the translumbar routethe method of choice. A 20-ml syringe is filled with 15mL of 0.5% lidocaine and 2 mL of a corticosteroid solu-tion (e.g., 80 to 120 mg methylprednisolone acetate). A2- to 3-in. 20- to 22-gauge needle is appropriate.

The patient is positioned in prone (Fig. 26.1) or inlateral decubitus. The two sacral cornua bordering thehiatus are carefully identified. Local anesthetic is injectedsubcutaneously, followed by insertion of the needle intothe hiatus. The needle is initially angled at 45° to the skin,and once inserted, is redirected tangentially (Fig. 26.2).Once in place, it is essential to be certain that no cere-brospinal fluid appears at the hub of the needle, as canoccur with an inadvertent subarachnoid puncture. Fortu-nately, this is an extremely rare occurrence with thismethod.

If not already in place, a syringe is then connected tothe needle, and a second check is performed by aspiration.There is almost never a problem with needles of 40 to 50mm, but problems can arise with longer needles. In theevent of accidental cerebrospinal fluid (CSF) puncture, theneedle should be removed and the injection aborted. In

Figure 26.1

Patient position for epidural injection.

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SECTION V TREATMENT

most cases, the dural sac descends to S2, but it can some-times be located lower. During the injection, a hand isplaced over the posterior aspect of the sacrum to palpatefor any subcutaneous fluid or air as a result of mal-positioning of the needle behind, rather than in, the sacralcanal. Even with appropriate needle placement, this occa-sionally occurs when a developmental malformation ofthe sacrum (partial spina bifida) is present (Fig. 26.3). Ifabnormal permeability of an anterior sacral foramen ispresent, the liquid can escape anteriorly.

During epidural injection, the patient may experiencea spontaneous recurrence of pain brought on by duralstretch. This pain resolves spontaneously after a fewmoments, once the injection is halted. Following the pro-cedure, the patient is reexamined after lying on his or herback for a few minutes to evaluate the effectiveness of theinjection. The postprocedural assessment should try to elicitsigns of root tension that existed prior to the injection. It is

also useful to ask the patient about general feelings, thenattempt some functional tasks that were impossible ordifficult to execute before the injection, such as puttingon socks. In some cases, O. Troisier used much largerquantities of liquid (at least 50 mL). He used a solutionof 0.5% betoxycaine chlorohydrate. He was convinced ofthe favorable mechanical effect of a larger volume ofinjectate that acted to lavage the epidural space and tem-porarily separate any adhesions between the dural sheathand the bulging disk. The level of the anesthetic block isat a higher level with this increased volume.

Translumbar Route

The translumbar route is most commonly used at present.The patient is seated and slumped forward to open the inter-spinous space. If the supine position is preferred, place apillow underneath the abdomen. The spinous processes of

Figure 26.2

Injection via sacrococcygeal hiatus.

a.

Frontal view.

b.

Lateral view.

Figure 26.3

Sacral anomalies make injection via this route difficult or impossible.

a.

Normal sacrum.

b.

Anomaly of the hiatus.

CHAPTER 26 THERAPEUTIC INJECTIONS

219

L4 and L5 are located. A 20- to 22-gauge spinal needlewith a short bevel is inserted between the two processes.At a depth of 4 to 5 cm, the resistance of the ligamentumflavum is felt, preventing the injection. Then the needle isadvanced 1 or 2 mm more, and injection into the epiduralspace is easily performed. Before the injection, theabsence of CSF is verified by aspiration. Then 3 mL ofthe corticosteroid solution is injected, pure or mixed witha solution of 0.5% lidocaine (3 to 5 mL). See Fig. 26.4.If the dura has been perforated because of an adhesion ofthe dural sac to the ligamentum flavum or because of amistaken maneuver, the needle must be pulled backslightly, checked by aspiration for CSF, and if there isnone, then the corticosteroid solution is injected withoutanesthetic.

First Sacral Foramen

This technique was proposed by Lievre in 1955. Thepatient is seated or prone with a pillow under the abdomen.The spinous process of L4 is located at the level of theiliac crests. From there, the spinous processes of L5 andS1 are located, as well as the posterior superior iliacspines. From the latter, a triangle is outlined whose apexis S1. The line joining the two iliac spines forms the base.

The injection is performed at the middle of the lineconnecting the process of S1 to the posterior superior iliacspine, at right or left (Fig. 26.5). This point is opposite thefirst sacral foramen.

A 20- to 22-gauge 2- to 3-in. needle is directed per-pendicularly until it comes into contact with periosteum;it is slightly advanced until it penetrates the sacral foramenfrom outside. It is preferable not to inject any anestheticsolution because the presence of any anomaly of the durawhich is lengthened around the root, the practitioner facesthe risk of performing a subarachnoid injection resultingin spinal anesthesia. After verification by aspiration, 2 to3 mL of corticosteroid is injected.

Remarks

Other locations can be used. A vertical line is traced onefinger’s breadth lateral to the spinous process of L5. Thena horizontal line is traced a thumb’s breadth below theinferior edge of that process. The injection is performedat the intersection of the two lines (Fig. 26.5).

Intrathecal Injection

This technique was described by Luccherini. It consistsof the intradural injection of a solution of 1 to 2 mL of a

Figure 26.4

Epidural injection via translumbar approach.

a.

The needle encounters resistance produced by the ligamen-tum flavum.

b.

The needle penetrates the ligamentum flavumand makes its way to the epidural space. It is in this areathat one should infiltrate, after aspiration, for an epiduralinjection.

c.

The needle has entered the dural sac. Aspirationresults in the ability to draw back cerebral spinal fluid. Theinjection should not be performed in that space.

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SECTION V TREATMENT

corticosteroid derivative. The technique is the same as forlumbar puncture, and the same precautions must be taken(Fig. 26.4).

Here it is better to use a smaller gauge needle so thata CSF leak is minimized through the puncture site. Afterinjection, the patient remains prone for 1 hr, with largepillows under the abdomen if necessary. The patientremains recumbent for 24 hr.

This technique is indicated in selected lumbar painsyndromes with sciatica. It also provides an opportunityto draw some CSF prior to injection. CSF examination,which has been too long neglected, can help avoid manydiagnostic errors.

It is inadvisable to repeat this type of injection morethan two or three times, especially if the result of the firstinjection is equivocal.

It is essential that the substance injected is suitable forintrathecal usage; corticosteroid derivatives should beused in solution, avoiding whenever possible dexametha-sone, whose solvent is irritating.

Adverse Effects

A very painful spinal headache can follow intrathecalinjection of corticosteroids. It may be due to leakage ofCSF related to the puncture site; hence the need for asmaller gauge needle and the recumbent position for 24hr. Occasionally, an inflammatory reaction is noticed afew days after intrathecal injection of corticosteroids,associated with an increase in CSF proteins. The besttreatment then seems to be the administration of 30 mgof hydrocortisone orally for 3 to 4 days.

Accidents

Meningitis can occur when sterile technique is poorduring performance of spinal puncture and even more sowith injection of corticosteroid derivatives. The adminis-tration of single-use preservative-free materials con-siderably lowers these risks.

Facet Joint Injections

In this book, we have emphasized the role of the facetjoints. Facet joint dysfunction is a constant in PMIDs.Injection is often useful, especially for the treatment of aPMID that has been insufficiently improved by manipu-lation, when manipulation is contraindicated, or duringacute synovitis.

A good segmental examination should be performedalong with a careful search for the facet joint point. Theinjection is justifiable only if the articulation is found tobe tender on examination.

It is performed with 0.5 mL of corticosteroid derivative;an anesthetic should not be used at the cervical level. Ashort-bevel needle is inserted perpendicularly to the skinuntil contact is made with periosteum. The substance isinjected after the needle has been withdrawn 1 mm with-out changing its direction and after aspirating to be surethere is neither blood nor CSF.

When first starting to perform these injections, it is bestto do them under fluoroscopic guidance; experienced phy-sicians often find this unnecessary. However, if the injec-tion performed in this fashion is inefficient and if theclinical examinations continue to point toward the involve-ment of the facet joint, it is then advisable to perform

Figure 26.5

Injection via first sacral foramen. Two methods are recommended: by way of the spinous process of S1 (

a

) andby way of the spinous process of L5 (

b

).

CHAPTER 26 THERAPEUTIC INJECTIONS

221

another injection under fluoroscopic guidance. The pointof injection is marked in case other injections are neces-sary; they will then be performed with the patient in thesame position as when the mark was made.

Lumbar Region

The patient is flexed forward across the table, with acushion placed under the abdomen. Even when a thicklayer of overlying subcutaneous tissue is present, it isusually possible to locate the facet joint point by pressurefriction of the pad of the middle finger. The finger slidesin short movements back and forth, parallel to the spinousprocesses (see “Segmental Examination” in Chapter 21).The injection is performed exactly over the tender pointthat has been located and perpendicular to the skin, witha 2.5- to 3-in. 20- to 22-gauge needle. The point of injec-tion is slightly more lateral to the midline for L5–S1, L4–5than for L1–2, L2-3, and L3–4 (Fig. 26.6). The injectionis performed after aspiration, always keeping contact withperiosteum and aiming toward the lateral aspect of thecapsule where it is more lax.

Remarks

Skin markings can also be used:

• For L5–S1, a horizontal line is drawn tangent to thesuperior edge of the spinous process of Sl. The pointof injection is on this line, about 2.5 cm lateral tothe midline.

• For L4–5, the same tracing is done with the processof L5. The point of injection is 2 cm lateral to themidline.

It is understood that these tracings vary with the morphol-ogy of the subject. They should always be correlated withthe provoked tender paraspinal point. When in doubt,the injection should be performed under fluoroscopicguidance.

Thoracolumbar Junction

Except in particular cases, T12 is a transitional verte-bra; its superior articular processes are thoracic, and itsinferior articulations are lumbar (this role is given some-times to T11).

The location for the facet joints is the same as for L2–3.It is much easier to locate T11–12 and T10–11 with pre-cision using palpation friction performed with the pad ofthe middle finger over the sensitive facet joints. The injec-tion can be performed at the level of this point, perpen-dicular to the skin, until contact is made with the bone.But at that level, it is better to push the needle 1 cm lateralof the midline, then go on until in contact with periosteum,and from there inject while maintaining contact with thebone, going from medial to lateral until the needle losescontact with the bone. In this way, the target is the externalpart of the articular mass (Fig. 26.7).

Thoracic Region

Use same technique as above. See Fig. 26.8.

Cervical Region

As with the thoracolumbar region, cervical dysfunctionis frequently an indication for facet joint injection. Tolocate the tender facet joints, the patient lies supine — thebest position for palpating these joints. The injection canbe performed with the patient sitting on a stool, with theneck in flexion and the head resting on a table. Carefulpalpation is necessary, performed by pressure friction withthe pad of the middle or index finger. A median verticalline is drawn corresponding to the line of the spinousprocesses. The site of needle insertion is located 2 cmlateral to the midline. The needle is inserted perpendicu-larly to the skin until in contact with periosteum.

This contact should be clear. Then the needle is movedslightly laterally and medially to verify the contact. The

Figure 26.6

Lumbar facet injection.

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injection should be performed with a corticosteroid deriv-ative without anesthetic (Fig. 26.9 and Fig. 26.10).

As always, injection is performed strictly on contactwith periosteum, after making sure the aspiration is clearof blood and CSF. It is advisable to use corticosteroidderivatives that are suitable for the CSF, as this lessensthe risk to the patient in case of error. In fact, there is norisk if one carefully follows the rule to inject only oncontact with periosteum at the posterior aspect of the jointand to aspirate and withdraw a little just before injecting.

The effect of the injection occurs rather quickly. In caseof success, movement that was limited and painfulmoments earlier becomes less painful and freer, eventotally painless.

Ligamentous Injections

Interspinous Ligaments

The interspinous and supraspinous ligaments are oftensensitive to pressure in a minor interspinous disorder (keysign). Most often, this sensitivity is discovered during a

systematic examination; it does not produce any discom-fort or spontaneous pain. However, there are cases inwhich the ligament is responsible for a painful spinalsyndrome. It can be demonstrated by a simple test: anes-thetic injection that makes the discomfort and pain disap-pear. However, if the sensitivity of the ligament does notdisappear after a manipulation, then it must be treated

Figure 26.7

Thoracolumbar facet injection. It isgood to verify the disappearance of pain noted onthe pinch-roll test in the territory of the posteriorprimary rami to which that territory corresponds.This test helps to verify the efficacy of the injection.

Figure 26.8

Thoracic facet injection. The patient is posi-tioned lying across the table for the low thoracic region. Forthe upper thoracic region, the patient can be seated, bentforward, with the arms folded in front. The head is laid on topof the crossed arms on the table during the procedure.

Figure 26.9

Low cervical facet injection. The same positionis used as for upper thoracic vertebrae.

Figure 26.10

Upper cervical facet injection.

CHAPTER 26 THERAPEUTIC INJECTIONS

223

locally. In cases with only ligamentous pain without anysign of a PMID, injection is the treatment of choice, andit is performed with a mixture of anesthetic and corticos-teroids.

For resistant cases, the solution recommended byHackett is the best. This author attributes almost all spinalor articular pains to “ligamentous laxity” or tendinousorigin and treats them with sclerosing injections. Thisconcept is questionable, but the treatment is sometimeseffective. Barbor uses the same procedure on more limitedindications and proposes the following mixture, favoredalso by Troisier:

Phenol 0.50 gGlycerin 5 g Glucose 5 gDistilled water To a total volume of 20 mL

This solution is mixed with an equal volume oflidocaine 1%. A few drops are injected onto the perio-steum, trying to contact the superior and inferior inser-tional points of the ligament, at multiple points (1/3 mLusually for each space; Fig. 26.11). There is sometimes avery painful reaction lasting 1 to 3 days. Injection is per-formed again, three or four times at weekly intervals,depending on the degree of improvement. One can admin-ister up to six injections if necessary.

Iliolumbar Ligament

Several authors have noted the frequent existence incommon lumbar pain of a sensitive point at the junctionof the middle and medial thirds of the iliac crest, 7 to 8cm lateral of the midline, and also the fact that anestheticinjection at this point relieves some patients. It has beenthought that this point represents the insertion of the ili-olumbar ligament, but that is not certain. The point that

is usually painful is localized on the posterior surface ofthe iliac crest; however, the ligament is inserted largelyon the anterior surface and is not accessible to palpation.In fact, this point, as we have shown, usually correspondsto the cutaneous branch of the posterior ramus of L1,sometimes L2. This is the “crestal point” of the “low backpain of thoracolumbar origin” described by R. Maigne. Itdisappears with injection of the facet joint causing theirritation (T12–L1 or L1–2) and the cellulalgic zone fre-quently adjacent corresponding to the dermatome of thenerve (see Chapter 42, “Acute Low Back Pain”).

The presence of ligamentous calcification at the iliacinsertion and osteophytes at the level of the spinal inser-tion, visible on radiographs, does not confirm that theiliolumbar ligament is the cause of a lumbar pain.

SELECTIVE NEURAL BLOCKADE

Injection of Anterior Primary Rami of Spinal Nerves

These injections are rarely useful. One must be carefulwhen the sheath of the nerve extends beyond the interspi-nal foramen, as an injection there can result in CSF punc-ture and produce dramatic risks. For the cervical nerves,the needle is advanced a finger breadth lateral to thespinous process. For C5, it is advanced until it contactsthe tubercle of Chassaignac, which is easily found bypalpation; it fills the external extremity of the transverseprocess of C6. The point of the needle is moved slightlyupward. For C6, the needle abuts against the transverseprocess of C7, one then passes under and injects. For C7,the same technique is used; one goes under the transverseprocess to reach the anterior branch of the seventh cervicalnerve root.

Injection of the fifth lumbar root can be useful whenmedical treatment or epidural injections have been inef-fective in relieving pain. The patient lies across the table,and the needle is advanced at a point 4 cm lateral to themidline at the level of the inferior pole of the fifth lumbarvertebra. Advanced perpendicularly, it meets the trans-verse processes of L5, then it is withdrawn slightly andpassed below to reach the L5 root.

Injection of Posterior Primary Rami of Spinal Nerves

A facet injection need not be performed intra-articularlyas it almost automatically involves the posterior branch ofthe spinal nerve that courses around it. If one wants toexamine the role of the posterior ramus in a pain syn-drome, the painful zone should be carefully located, usingthe pinch-roll test in the area of its dermatome.

After having located precisely the facet joint that waspainful on examination, a few drops of a local anesthetic

Figure 26.11

Injection of interspinous ligament.

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are injected at the articular contact, at the thoracic andlumbar regions. The result obtained on the painful cellu-lalgic zone is then rechecked with the pinch-roll test. If itis successful, this zone quickly becomes painless and evensometimes supple. Then the corticosteroid derivative isinjected with the needle still in place. Otherwise, the posi-tion of the needle should be slightly modified and a fewmore drops of anesthetic solution injected. This procedureis repeated two or three times until the expected result isobtained. In case of failure, one checks in the same waywhether the supra-adjacent or subjacent joint is responsi-ble for the irritation. Recall that injection of anestheticshould be avoided at the cervical level.

TRIGGER POINT INJECTIONS

Trigger points can be the sources of both local orreferred pain and tenderness. Some are manifestations ofa segmental spinal cellulotenoperiosteomyalgic syn-drome, while some are isolated and have local causes. Inboth cases, anesthetic injection of a trigger point is avaluable test to determine whether it is responsible for thepainful syndrome. The injection often momentarily exac-erbates the pain, which disappears afterward. If the triggerpoint is part of a segmental spinal syndrome, it is betteras always to first treat the responsible spinal segment.Local treatment is indicated if no result or a poor resultis obtained.

The injection of trigger points should be thorough. Itis sometimes difficult. A few milliliters of 1% lidocaineare injected into the most painful point of the muscle.Thus, the trigger point should be very well localized andisolated; then it is grasped between the index and themiddle finger of the left hand (Fig. 26.12 throughFig. 26.14), or in some cases, pinched between thumb andindex finger. Several successive examinations are neces-sary to localize the most painful point. While introducingthe needle, the needle is aimed at an acute angle, and onedrop is injected as soon as the skin is penetrated. Whilemaintaining the needle underneath the skin, the muscle isrepeatedly probed in a circumferential manner. Contactwith the trigger point produces a brief contraction, a char-acteristic feature of a trigger point known as a local twitchresponse (LTR). This indicates to the examiner that thetarget has been reached. The LTR is sometimes quite sharpand often reproduces the original pain referral pattern. Ateach occurrence of an LTR, a few milliliters of lidocaineare injected. Often one injection is sufficient; sometimestwo or three more may be necessary with intervals of afew days.

When the trigger point is of local origin, and especiallyif it has a tendency to recur, the postural or static problemthat may be a perpetuating factor should be sought. Onecan also use the dry needle (acupuncture) technique,

advanced in the most sensitive point and left until it canbe easily removed, as in the beginning the needle seemsto be held firmly by the tissues. The results are interestingbut not as reliable as tests with lidocaine.

Figure 26.12

Injection of infraspinatus muscle trigger point.

Figure 26.13

Injection of gluteus medius trigger point.

Figure 26.14

Injection of sternocleidomastoid muscle trig-ger point.

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225

INJECTION OF SCARS

It is not rare to see that a scar or part of one is respon-sible for unrecognized pain referral, rarely attributed tothat cause. Referred pain is not always local and can bedistantly referred, generally in the homologous spinal seg-ment. In these cases, the scar can be demonstrated to bepainful by pinching it between the thumb and the indexfinger or by rubbing it with the pad of the index finger.

The painful part is injected with a few drops of a localanesthetic. This is both diagnostic and therapeutic. Thetest is positive if the spontaneous pain disappears after theinjection, and it is a treatment if the relief persists afterthe injection, which can occur immediately or after threeto four injections performed at intervals of a few days.The relief generally persists, but sometimes it is useful toadd scar massages. Of course, some scars may simply besensitive to palpation without being a source of spontane-ous pain for the patient.

ACCIDENTS ASSOCIATED WITH INJECTION OF LOCAL ANESTHETIC

Serious accidents are rare in the use of local anestheticin spinal pathology.

Allergic Reactions

Severe allergic reactions are rare. A reaction is usuallya rash or respiratory in nature, such as asthma. Reactionsare chiefly due to the actions of the esters in lidocaine.

Toxic Accidents

These are especially due to lidocaine. The injectionshould be stopped as soon as the patient demonstratessigns of general malaise, anxiety, paresthesia around themouth and of the tongue, sensations of vertigo, or dizzi-ness. Accidents occur very rarely at the concentrationsused to treat spinal or articular pathology; the quantitiesand the concentrations are usually not strong. Neverthe-less, anaphylactic shock or convulsion can occur. That iswhy it is absolutely necessary to have resuscitation equip-ment on hand, including an appropriate intravenous solu-tion to facilitate the administration of adrenalin, or Valiumin the case of convulsions (Favarel-Garrigues).

Diffusion of Local Anesthetic toward Neuraxis

Several delayed reactions have been reported after aninjection of triamcinolone or dexamethasone withlidocaine at the level of a cervical joint. In these cases, itseems that the lidocaine was injected in the subarachnoid

space; so it is absolutely necessary to always check byaspiration before injecting and to inject only at the bonylevel.

Sanchez reports that according to some literature, alocal anesthetic introduced by paraspinal injection is capa-ble of reaching the spinal cord by simple diffusion andwithout any penetration of the needle into the spinal canalor the intervertebral foramen for the following reasons.

• The meningeal coverings can brim over the inter-vertebral foramen for several centimeters.

• Some arachnoid villi occasionally herniate throughthe dural sheath and perforate it. They particularlypermit the anesthetic to reach the subarachnoidspace.

• It has been experimentally demonstrated (radioactiveisotope dyes) that a substance injected into a nervecan undergo retrograde diffusion into the spinalcenters.

COMPLICATIONS OF STEROID INJECTION

Steroid injections can produce local reactions thatoccur most often immediately after the injection andsometimes after a delay of several hours. These reactionslast 24 to 48 hr, and they can be relieved by the applicationof ice.

With an articular injection, the greatest complication isseptic arthritis. G. Ziegler et al. reported 19 cases of septicarthritis seen in their hospital service, of which 7 wereiatrogenic. This complication is rare when aseptic precau-tions have been taken (1 of 25,000 injections for Poulettyand Besson). But an acute infection can result from aninjection performed in an already-infected joint. The prog-nosis of septic arthritis depends on the rapidity of thediagnosis and treatment. Most resolve without anysequelae, unless the treatment is started late and the causeof the infection remains undetermined.

Corticosteroid injections, periarticular or articular,should not be performed if there is a hemarthrosis orcardiac prosthesis. Repeated corticosteroid injections inthe same joint are responsible for the degradation of dif-ferent articular and periarticular structures.

Intratendinous injections in the Achilles tendon, aspracticed in the past, have been associated with tendinousrupture. With superficial injections, some depigmentationof the skin or local atrophy of subcutaneous tissue canoccur, which produces a dimple that disappears over time.We have used facet joint injections for more than 25 years,and we have never had any accidents.

Meyer et al. reported a case of delayed paraplegia aftersome epidural injections performed too soon after oneanother, using corticosteroid derivatives in microcrystalline

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suspension. Remember that injection of a corticosteroid,even locally, is still an injection of corticosteroid. Oneshould keep in mind the well known contraindications ofthis therapy.

THERAPEUTIC INJECTIONS

Botulinum Toxin (Botox) Injections

Botulinum toxins are potent nerve toxins that bind totransport proteins in nerve cells and hence block therelease of nerve transmitters from nerve endings. Theyhave recently been used in the management of pain andmuscle spasm.

The mode of activity is not entirely clear. In additionto inhibiting the release of acetylcholine, the toxin alsoinhibits the release of glutamate, inflammatory mediatorssuch as arachidonic acid, vasoactive intestinal peptide, andneuropeptide Y. It also inhibits the release of tumor necro-sis factor alpha from immune cells.

Injections to date have varied in terms of location andresults.

Foster reported the efficacy of paravertebral adminis-tration of botulinum toxin A in patients with chronic lowback pain which was noted to improve function at 3 and8 weeks of treatment.

Recently, a study performed by Dr. Jabbari on 28patients noted that botulinum toxin injected into five sitesin the paravertebral muscles from L1–5 unilaterally on theside of maximum discomfort demonstrated pain relief. Noside effects were noted. The relief effects tended to wearoff.

Jabbari also reported an improvement in burning painand allodynia in two patients with spinal cord pathologyfollowing subcutaneous application of botulinum toxin A.The mechanism that accounts for this effect is at this timenot known.

Injection of the temporalis muscle with botox has alsobeen tried in various headache disorders with some degreeof success, depending on the type of headache. Resultshave tended to be temporary and required periodic rein-jection.

Other injection procedures proposed for the manage-ment of pain include epidural steroids and lumbar epiduralblockades. In some cases, particularly of severe pain, asis found in reflex sympathetic dystrophy, stellate ganglionblock and/or celiac plexus block have been noted to be ofsome utility along with lumbar sympathetic blockade andsuperior hypogastric plexus blockade.

These procedures can be associated with significantcomplications secondary to surgery, anesthesia, and aller-gic reactions. Results have been demonstrated to be vari-able even in the best hands.

MEDICATIONS AND COMPLICATIONS OF MEDICATION USE

In addition to the various therapeutic approaches usedto manage pain of vertebral origin already discussed, theuse of medications can be complementary, or they can beused as sole therapies. The use of medications alone or ascomplementary therapies is not without risk to the patient.

Classic attempts to control pain include the use of oralsteroids, nonsteroidal anti-inflammatory agents, opioids,and semisynthetic narcotics. These medications, althougheasy to use, are associated with significant complicationrates. In the case of nonsteroidal anti-inflammatory agents,gastritis, and associated gastric bleeding pose significantproblems. Steroids can be associated with psychiatric dis-orders, osteoporosis, pathologic fractures, and adrenalsuppression to name but a few effects. Opioids and semi-synthetic narcotics, while relatively safe, pose problemswith dependence that are not uncommon.

Medications that have muscle relaxation propertiesincluding medications such as diazepam, cyclobenzaprine,metaxalone, tizanidine, and others are useful in the man-agement of pain. Issues involving sedation are commonto this group. Another particular problem is the occasionaldevelopment of diazepam dependence. These medicationscan and do produce effects beyond muscle relaxation thatmay contribute to their analgesic effects.

Over the past several years, agents originally intendedfor use as antiepileptics have found their place in certainforms of neuropathic pain control. Most of these agentsoperate at the level of affecting ion channel activity.Agents such as divalproex sodium and gabapentin are nowin widespread use.

In addition, medications addressing anxiety and/ordepression have also become commonly used in the man-agement of pain disorders of a chronic type. Many of thesemedications are associated with some side effects includ-ing hair loss and ovarian dysfunction in the case of dival-proex sodium and other effects including dizziness andgastroenterologic dysfunction.

Another drawback currently associated with these med-ications is that few controlled studies have determinedwhat dosage ranges and serum levels should be utilizedas reasonable targets for pain management and empiricuse is currently the rule rather than the exception.

Certain other agents including medications such asbaclofen that are felt to be associated with GABA (gammaaminobutyric acid) agonist activity have also been utilized,again with the drawback that few controlled studies pro-vide guidance as to the exact dosage ranges that are opti-mal for pain management.

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27

HYDROTHERAPY, THERMAL THERAPY, CRYOTHERAPY, RADIOFREQUENCY

DENERVATION, RHIZOTOMY, AND

IMPLANTABLE DEVICES

HYDROTHERAPY AND THERMOTHERAPY

Hydrotherapy has been used a great deal in many coun-tries. In France, it was very popular and fashionable duringthe last century, but later it was mostly used in thermalspas. Although physicians and patients who used it werevery enthusiastic about it, its efficacy and utility werealways questioned by the medical profession. The use ofthese modalities was reawakened by the development ofphysical therapy, and the vogue of thalassotherapy helpedto better elucidate its potential.

Hydrotherapy with all its modalities is certainly a greatasset in the treatment of spinal disorders. Unfortunately,its use is limited by the need for significant investment inthe equipment needed to perform this type of therapy. Wewill describe the technique we use in performing hydro-therapy and thermotherapy in our department of orthope-dic medicine at Hotel Dieu, which we consider most usefulin the management of some cases.

Hotel Dieu Method

We inherited a very old tradition of hydrotherapy inour department, and the technique that we use most oftenin spinal pain and radicular pain disorders originated fromit. The treatment consists of a heat bath, followed by restin the supine position, then followed by a general shower,which can be focused on the affected region, performedthree times a week. The traditional name of these heatbaths is “baths of light.”

The therapy is performed with the patient sitting on awooden stool and enclosed entirely in a hexagonal box.

Only the head, which is covered with a cold wet towel,and part of the neck are outside the box. On the walls ofthe box, there are tubular infrared lights that expose thebody to radiant heat. The disposition of the lights is suchthat there is no danger of burns by contact. The insidetemperature reaches 60°C.

Each session lasts 10 min, but this can vary dependingon the subject. Most find this treatment agreeable. Someadverse effects can occur, such as lipothymia, tachycardia,and pallor, but the side effects are rare. With experiencesuch patients (neurotic, “spasmophilic”) who tend torespond in this manner can be identified and referred toother treatments. During the session, the blood pressureremains stable while the pulse increases slightly, on theorder of about 10 pulses/min.

Afterward, the subject remains recumbent for 8 to 10min, protected by blankets to prolong the perspirationprovoked by the stay in the heat box.

The third part of the treatment is a 38°C jet shower at5-m distance. The temperature can be changed slightlyaccording to the reaction of the subject. The shower shouldnot last more than 5 min. From experience, the operatorchooses a full jet or a “pulsating jet.” In general, for a leanpatient, the broken jet is preferred. For a stocky individual,a more powerful full jet may be selected. A “Scotch”shower is good in sciatica, and it is performed as follows:full jet at 39°C for 6 to 8 min, followed by a cold showerat 11°C in broken jet for 30 sec. The feet are always keptwarm.

Results

To evaluate this treatment, we followed 56 patients withsevere discopathy associated with sciatica of at least 2-mo

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duration who were unresponsive to the usual treatmentsor bed rest, and for whom surgery was contemplated. Ofthese 56 patients, 16 were completely relieved in 9 ses-sions (20 days), and the results were maintained as fol-lows: 12 patients were very much improved and could berelieved by procedures that had previously been ineffec-tive; 28 showed little or no improvement, and amongthose, 15 went on to have surgery; the remaining 13 werelost to follow-up after the last treatment test.

Results were much better in mild cases. The best indi-cations were persistent acute lumbar pain syndromes withsymptoms of sciatica, including chronic vertebrospinalpain with stiffness and diffuse muscle spasms prior to amore specific treatment pain due to acute attacks of syn-ovitis.

Usually nine sessions are given, at a frequency of threetimes a week, and the improvement is noticed in the sixthor seventh session. In some cases, the treatment can beextended by three additional sessions. The safety and effi-cacy of this treatment should be emphasized.

Contraindications

This treatment is certainly contraindicated in patientswho are fragile, those who have venous insufficiencies,those with heat intolerance, and those with hypertension.

CRYOTHERAPY

In France, cold is not often used in the treatment ofspinal or articular pain, although it is efficacious in someacute cases.

Ice Application

The application of ice often produces rapid relief ofacute shoulder pain, periarthritis of the hip, acute torticol-lis (wryneck), or low back pain. In all cases, the skinshould be protected by wool or flannel placed between theskin and the ice bag. Icing is also indicated in the acutetreatment of muscle strains and joint trauma related toathletic activities.

Ice Massage

A good therapeutic approach for many mus-culotendinous disorders, ice massage should be tried incases that are refractory to other treatments. An ice cubethe size of a mustard jar (about 5 cm in diameter) is heldby a hand protected with a cloth and slowly massaged intothe affected muscle, from one end to the other. If thetendinous insertion is affected, it should be included also.

Initially the patient feels the cold, followed by briefacute pain, after which generally there is a feeling ofanesthesia lasting 3 to 5 min after the massage. At that

point, the treatment is stopped. Then some slow stretchingmovements are applied progressively to the muscle, orpostural exercises are performed.

This treatment can also be used in chronic periosteomy-algic pain syndromes, which have their origins in refrac-tory spinal articular disorders.

Cold Pulverization

In the past, cold pulverization was a popular treatmentfor sciatica. It was usually performed with ethyl chlorideor fluorimethane, which was sprayed on the painful area.It is used by J. Travell and J. Mennell in the treatment of”myalgic points” or trigger points to facilitate stretching(see “Vapocoolant Spray and Stretch” in Chapter 25).

RADIOFREQUENCY DENERVATION

The efficacy of clinical percutaneous radiofrequencydenervation of lumbar zygapophyseal joints has been stud-ied in an attempt to reduce pain and improve functionaldisability and physical impairment in patients with backpain originating from the lumbar zygapophyseal joints.Results have been generally positive and demonstratedsignificant alleviations of pain and functional disability inselected groups of patients with chronic low back pain onboth short- and long-term bases (Van Kleff).

As with other ablative procedures, insufficiently per-formed ablations as a result of underestimating the numberof roots involved can limit the utility of this procedure.

RHIZOTOMY

Rhizotomy, the sectioning of nerve roots, is a procedurethat has a long history. Conceptually, rhizotomy aims atnerve destruction. Generally performed at the posteriorroot, this procedure is complicated by the anatomy of thedorsal and anterior roots. Recent studies show that not allpain nerve fibers course through the dorsal roots. As aresult of individual variations, up to 20% of pain nervefibers reach the medulla through the anterior root. Musclenerves also pass through this root and cannot be destroyedsince doing so would cause paralysis of denervated mus-cles.

Therefore, it has been recommended that anestheticinfiltration be performed as a test prior to the performanceof rhizotomy in order to obtain a better understanding ofwhat benefits the procedure may provide. A significantdrawback of the procedure is that it is permanent and, ifnot carried out involving a sufficient number of dorsalroots, may meet with failure as a result of sensitizationand spread.

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229

IMPLANTABLE DEVICES

Various other modalities have recently been tried inattempts to control pain of vertebral origin. They includeimplantable spinal cord stimulators and intrathecal infu-sion pumps utilizing baclofen and, in some cases, mor-phine drips. Such procedures, in particular implantablespinal cord stimulators, depend on electrical stimulationof the spinal cord which has been demonstrated to producean analgesic affect. Generally, the complication rates withprocedures such as this are variable and include infectionand structural damage secondary to scarring.

Other implantable devices utilizing baclofen and mor-phine drips have also been attempted and have similardrawbacks, including infection and the complications aris-ing from instrumentation procedures.

Recently, procedures using artificial discs in an attemptto mimic the spacing of natural discs have been examined.The efficacy of such procedures continues to be underevaluation as are other forms of surgery such as laminec-tomy and other orthopedic procedures that are also asso-ciated with complications, including infection and failuremarked by persistent or worsened pain states.

Other therapeutic approaches, including neurolyticblocks, are essentially similar to nerve blocks induced byanesthetic agents with the drawback that such procedurescan be permanent and, in some cases, associated withcomplications, including infection and inflammation.Nerve blocks utilizing reversible agents demonstrate sig-nificant efficacy when properly applied. The only draw-back is the need for repeated blocks in certain cases.

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ELECTROTHERAPY IN PAIN

OF SPINAL ORIGIN

Electrotherapy is used in different ways and is certainlybeneficial in the treatment of pain of spinal origin. It isused in cases where other forms of medical or manualtreatments are contraindicated and also in cellulotenoperi-osteomyalgic manifestations.

SPINE

During inflammatory arthritic episodes, low frequency(10 to 25 Hz) short wave diathermy is often effective.Higher frequency (200 Hz) short waves, continuous, withthermic effect, can be used for persistent facet joint painor stiffness. However, continuous short waves should beavoided at the cervical level. Continuous thermogenicshort waves are applied to the region of pain referral incases of sciatica, femoral pain, or cervicobrachial neu-ralgia. Afterward, short waves at low frequency areapplied at the spinal level.

Ultrasound can be used in pain of the interspinousligaments. Two to three sessions lasting 3 to 5 min eachgenerally suffice. Microwaves are useful in refractory cer-vicoscapular pain after trauma or in some lumboglutealpains. Midfrequency currents also produce an analgesicaction.

It is sometimes useful to use longitudinal iontophoresiswith calcium or anti-inflammatories. One pole is placedat the root of the limb, the other at the extremity, on thepath of the pain.

MANIFESTATIONS OF NEUROTROPHIC SPINAL SEGMENTAL SYNDROME

Cellulalgia

Iontophoresis (galvanic current) can be performed withnoninjectable products such as chymotrypsin or with anes-thetic products before localized kneading sessions.

Tendinous Pain

Ultrasound is often prescribed, although in our experi-ence good results are infrequent. Iontophoresis with sali-cylates, ketoprofen, or corticosteroids often leads to goodresults (Teyssandier). Pulsed short wave diathermy alsohas a beneficial action (eight to ten sessions).

Trigger Points

Trigger points are the best indications for ultrasound.Pulsed short waves at 200 Hz can be associated with thediadynamic currents of Bernard. Iontophoresis of musclerelaxants seems to have little efficacy.

Periosteal Pain

Pulsed athermic magnetic short waves are useful in thetreatment of periosteal pain.

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LUMBAR ORTHOSES

The use of a rigid lumbar orthosis to immobilize orgive support to the spine is useful in managing some formsof low back pain. It can offer valuable relief and canprevent or shorten the need for bed rest (Fig. 29.1). It isalso useful in the treatment of certain chronic low backpain disorders.

INDICATIONS

Acute Low Back Pain

A lumbar corset can be indicated as a first measure inpatients with acute lumbar disk pain who must remainmobile because of external demands that do not allow theirlevel of activity to be interrupted, when anti-inflammatorytreatments are contraindicated, and when manipulationdoes not help. It can also be prescribed for a patient whois relieved by medical treatment but still feels vulnerableand wants to return quickly to work. The support is usuallyworn for 8 to 15 days, depending on the case.

In acute low back pain of thoracolumbar origin(Maigne), the corset is less efficacious. However, in severecases, when injection and manipulation are contraindi-cated or ineffective, it can be of use. In such cases, oneuses a thoracolumbosacral (TLSO) orthosis of sufficientheight to limit trunk rotation and lateroflexion. Thisorthosis can be difficult to tolerate because it can compressan irritable posterior ramus against the iliac crest andexacerbate a zone of gluteal cellulalgia. The means usedto avoid these complications are not always effective.

Sciatica

A lumbosacral orthosis (LSO) can be used in condi-tions that cause

low

back pain while standing. It can beworn 15 to 30 days.

Chronic Low Back Pain

In some refractory and severe chronic low back painsyndromes, a custom-molded rigid lumbosacral orthosis

gives temporary relief to the painful region. When LSOsare used, it is frequently noted that after a variable time(1 to 4 mo) other treatments that were previously ineffec-tive become efficacious. Sometimes the patient is relievedonly while wearing the LSO, and the pain recurs when itis removed. If wearing an LSO does not produce reliefand the benign nature of the low back pain and its lum-bosacral origin are certain, a spinal fusion should be con-sidered as it may have a good chance of success.

FABRICATION OF RIGID LUMBAR ORTHOSIS

To facilitate fabrication, the subject should be able tostand for 15 min. The fasting patient stands and holds ahigh bar or leans against a wall. The antalgic attitude

Figure 29.1

Plaster lumbosacral orthosis.

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should always be respected and should not be corrected.The patient is naked during the casting process. The skinis sprinkled with talc, then the patient puts on a jersey (orbetter, two). The iliac spines and any other vulnerablebony prominences are protected by felt padding.

Five to six rolls of plaster of 20-cm width are used.With the first two rolls, the cast is applied circumferen-tially from inferior to superior, starting at the pubis, thenup around the abdomen to the xiphoid process. The lateraland posterior parts of the orthosis are reinforced with thenext two rolls. During the entire process, the patient isasked to pull in the abdomen.

The final rolls are applied circumferentially, overlyingthe first four rolls. After each application, the plaster iswell smoothed. Using a paring knife, one makes an inden-tation in front to avoid having the plaster compress thegroin in the sitting position. The edges are folded back toreinforce them.

Finally, the jersey is cut 5 to 6 cm above and belowthe plaster, and is folded back on the superior and inferioredges. A small roll of plaster or adhesive tape often suf-fices. The patient should feel at ease in the cast; sometimesthere is relief. If the orthosis does not lead to improvedsymptoms in the days immediately following its fabrica-tion, it should be modified or refabricated. When the antal-gic posture is severe, it is better to make a new orthosisevery few days; as the antalgic list diminishes, the oldorthosis is no longer comfortable.

In the case of low back pain of thoracolumbar origin(T11–12), the orthosis should sit higher in the back andon the sides, often to the level of the inferior scapularborder, while the anterior part rests below the xiphoid.

In most cases, the orthosis is left closed and is wornnight and day for 2 to 8 days. Then a vertical paramedianincision is performed, which allows its removal. To put itback on, the two sides are fixed with large sticking plaster,or better, with Velcro, so the patient can take it off duringthe night, take a bath, and shower. Usually, it is worn 2to 4 wk in cases of acute low back pain or sciatica and upto 2 to 4 mo for severe chronic low back pain.

Fabrication of an LSO with plaster is quick, easy, andvery economical. The thermoplastic materials now on themarket can be used to fabricate lighter orthoses that aremore convenient for the patient and should be used if thepatient will be wearing the orthosis for long periods or foresthetic reasons because they are less bulky. The plasterLSO increases the waistline a great deal, forcing thepatient to wear loose-fitting clothing.

Plaster Orthosis Syndrome

Plaster orthosis syndrome occurs infrequently, but itcan lead to a fatal outcome (Boegli et al.). It has beenespecially observed after spinal surgery or spinal traumaand in cases in which a cast was made for the treatmentof scoliosis or kyphosis. It has also been noted with casesof femoral fracture.

It starts with a sensation of gastric fullness and nausea,progressing to acute gastric dilation with painful abdom-inal distention and painful flatulence. Gastric decompres-sion by nasogastric suction usually suffices to relievesymptoms, although some patients go on to require sur-gical intervention. This syndrome is due to high duodenalobstruction, with acute secondary gastric distention. Mostauthors believe that “mesenteric artery compression syn-drome” is the primary cause. It is felt that the anatomicdisposition facilitates partial or complete obstruction ofthe duodenum, which may narrow the space between theduodenum and the superior mesenteric artery.

MODE OF ACTION

Numerous authors have studied the mode of action ofspinal orthoses. It seems logical to look at the effects ofthe spinal immobilization they produce, but radiologicstudies have shown that this immobilization is only rela-tive, which is what made some conclude that LSOs pro-duce no real effects. These considerations can beexpressed in the form of a well-known syllogism.

• Spinal orthoses are designed for immobilization.• However, it has been proven that they do not com-

pletely immobilize the spine.• Therefore, their effect is that of a placebo and is of

no therapeutic interest.

However, daily experience demonstrates very well theirutility and efficacy on pain. It is unnecessary to completelyimmobilize the spine to achieve beneficial results, and themode of action of a spinal orthosis is much more complexthan one thinks. One should give consideration to thepossibility that:

• It restricts all movements and suppresses extrememovements.

• It provides a passive support to enable the patientto maintain postures that are comfortable with min-imal effort and avoid postures that habitually pro-duce pain.

• It decreases the pressure on the involved spinal seg-ment and therefore lessens the degree of irritationimposed upon its elements.

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LUMBOSACRAL CORSETS

Lumbosacral corsets are considered poor substitutesfor the natural support of the lumbar spine, which isderived principally from the supporting musculature. Inspite of this, many competent practitioners think otherwiseand often prescribe this form of therapy.

INDICATIONS

The use of the lumbosacral corsets is indicated in thetreatment of low back pain but does not replace a thera-peutic exercise prescription because they are complemen-tary treatment modalities.

Before prescribing the use of a lumbar corset, the indi-cation should be considered carefully. It is unnecessary toprescribe a corset for a patient who suffers from a lowback pain that is present only in the morning and getsbetter as the day goes on. Corsets should be prescribedonly for those who suffer continuously and whose painsincrease with fatigue. A corset is indicated in the followingcircumstances.

• In a patient with an acute attack who is recuperatingslowly. In this case, the corset serves as a temporaryadjunct while physical therapy is performed andproviding results.

• In elderly patients or in patients for whom a thera-peutic exercise program is contraindicated. In thesecases, it is prescribed as a permanent measure.

• In patients with osteopenic lumbar spines or weakmuscles. In such cases, the corset is worn only occa-sionally, when the patient feels vulnerable or whenthe lumbar region is going to be stressed (e.g., dur-ing a long trip).

TYPES

The many types of lumbosacral corsets include:

• A belt for lumbar support with two or three steelribs, thoracic, vertical (Fig. 30.1).

• The lumbar corset with a more or less reinforcedarmature that can be a “closed cage” or an “opencage.” The lateral supports on the iliac crests of aclosed cage are connected to the thoracic supportby steel blades. The lateral supports of an open cageare not connected to the thoracic support (Fig. 30.2).

Depending on the case, one can decide between a veryrigid lumbar corset with a closed cage or a belt withlumbar support. Particular attention should be given to theabdominal bearing (Fig. 30.3), especially in older womenwith large, soft, protuberant abdomens (belt of atlas type;Fig. 30.4).

Figure 30.1

Lumbosacral corset with different types of rein-forcement.

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SECTION V TREATMENT

Figure 30.2

Lumbosacral corset with caged reinforcement.

Figure 30.3

Abdominal corset. This device is indispensable for the patient with obesity and low back pain, par ticularly if theabdomen is pendulous.

Figure 30.4

Dr. Leven’s support belt. This flexible support belt called an “atlas” helps to support the abdomen remarkablywell and supports the lumbar region,

CHAPTER 30 LUMBOSACRAL CORSETS

237

MODE OF ACTION

A patient should feel comfortable in a lumbar corset.Norton and Brow, Million et al., and Revel and Armorhave proved that the lumbar corset does not really limitthe movements of the spine; it is simply a reminder to apatient. It modifies the usual movements; the patientbecomes used to being supported by the corset and somodifies the normal muscular support and zones of ver-tebral stress, and produces warming on the lumbar regions.In fact, for many subjects, simple and supple belts canaccomplish the same ends and are very satisfactory.

Lumbosacral corsets can be prescribed at three levels:T12, T9, and T6. The case of low back pain of thoracolum-bar origin (Maigne) is very particular (see Chapter 41,“Low Back Pain of Thoracolumbar Origin.” Here, fre-quently, the lumbar corset is not well tolerated by thepatient, and it can increase the pain as the superior trans-verse bar pushes on the responsible segment while theinferior bar compresses the region of the iliac crest. Ittherefore presses on the cellulalgic zone and on the cuta-neous branch of the posterior ramus of the irritated spinalnerve. Sometimes there is a problem in the choice oflumbar corset when a low back pain of lumbosacral originis associated with a low back pain of thoracolumbar origin,especially in the elderly. In this situation, the corset shouldbe high (T9) and should not have any rigid element sup-ported on the iliac crest (Fig. 30.5).

CONTRAINDICATIONS

There are no absolute contraindications, but there areinstances in which a lumbar corset is not well toleratedfor extraspinal causes, for example, patients who areunable to tolerate abdominal pressure because of colitis,cholecystitis, gynecologic problems, vesical or genitalprolapses, etc. A lumbosacral corset should not be pre-scribed after an attack if an antalgic attitude persists. This

situation will change over time; however, a lumbar corsetshould not be used during the time when an antalgicposture is present. During this phase, a rigid lumbosacralorthosis may be indicated and of greater utility. The patientshould feel absolute relief and not simply tolerate a lumbarcorset. If the corset bothers the patient or low back painfails to decrease, a prescription for this type of therapyshould be reconsidered.

It is sometimes difficult to convince a patient to weara lumbosacral corset; but sometimes it is more difficult toconvince a patient who feels comfortable with one to takeit off.

The exercise prescription should start early. As soon asit becomes effective, the patient should remove the corsetfrom time to time, then remove it completely and wear itonly for the occasional painful exacerbation, in instancesof prolonged standing, or if he or she fears a painful attack.

Figure 30.5

In cases of low back pain of thoracolumbarorigin, the lumbosacral corset is often poorly toleratedbecause the superior reinforcement of the lumbar corset canpress on the painful spinal segment. Pressure on the iliaccrest can induce pain by compression of the posterior ramus,which is irritated by the compression in the cellulalgic zone.

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31

CERVICAL COLLARS

Cervical collars are a harmless and useful means of treat-ment of acute cervical pain and cervicobrachial neuralgia.

TYPES OF COLLARS

The different types of cervical collars include flexible(soft) or semirigid, both of which provide limited immo-bilization, rigid, and minerva, a type of neck brace of rigiddesignation (Fig. 31.1).

Flexible Collars

Flexible collars are made of felt or polyethylene, envel-oped in fabric. They come in different heights and lengths.

Collars with Rigid Reinforcement

These collars are reinforced by varying amounts ofrigid materials, usually made from polyethylene. Theirheight can be adjusted by different procedures, and theyare fixed by Velcro attachments.

Mini Minerva Collars

This type of collar has a chin support (Fig. 31.2). Somehave only occipital and chin supports; others also havesternal supports for improved immobilization.

INDICATIONS

Cervical Trauma

In acute cervical trauma, a cervical collar is put onimmediately both for patient relief and for safety. Radio-graphic and tomographic examinations such as CT or MRIare then used to assess the cervical spine for evidence ofbony or soft tissue trauma. After the full evaluation, the

decision can be made whether the collar will be worn fora few days or be replaced by a Minerva collar for moreprolonged immobilization. A plaster Minerva is used formaximum immobilization in orthopedic services.

Acute Cervical Pain

Acute torticollis (wryneck) can be relieved by immo-bilization, and the soft collar is usually the most effectivemeasure. An emergency collar can be made in a few min-utes (Fig. 31.3).

With a terry towel

—

For satisfactory immobilization,the towel should support the chin. A long towel is foldedto make a band about 20 cm high and put around the neckincluding the chin; it is then fixed with an adhesive band.The back part can be reinforced with a small piece ofcardboard placed in the towel.

With a newspaper —

The paper is folded in a band,placed in a thin towel, and attached with an adhesive band.Some cotton can be inserted at the level of the maxillaryand clavicular regions for the comfort of the patient.

Cervicobrachial Neuralgia

Cervicobrachial neuralgia is a good indication for treat-ment with a cervical collar, even though the acute phasemay last only a few days. In cases associated with severepain, complete immobilization is desirable. A Minervamade of rigid plastic material with occipital and chin restsshould be used.

Chronic Cervical Pain

Some patients have their cervical pain increased orprecipitated by travel (e.g., long trips by car). In suchcases, it is useful to wear a cervical collar. A collar is alsohelpful during acute attacks of cervical arthritis.

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Figure 31.1

Different types of cervical collars.

a.

Soft foam.

b.

Plastic construction with variable height.

Figure 31.2

Collars with chin support.

a.

Chin and occipital support.

b.

Chin, occipital, and sternal support.

Figure 31.3

A cervical collar can be easily made using a towel and a piece of cardboard.

Left,

supporting the chin.

Right,

without chin support.

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32

THERAPEUTIC EXERCISE

Complete coverage of therapeutic exercise for spinalpain would require a whole book; we present here whatwe think are the most important indications relating to thetherapeutic system proposed in this book.

Physical modalities such as massage are often consid-ered in the systematic treatment of patients having benignmechanical spinal pain. Massage is essential in mostcases, which emphasizes the important role of thephysiotherapist, but it is not always indicated and can attimes be contraindicated. In some cases, it can perpetuatethe pain.

Most subjects with spinal pain need postural reeduca-tion. The physician and therapist will usually evaluate andcorrect the mechanical aspects of typical daily activitiessuch as getting in and out of bed, standing, sitting, andother postures that may be associated with activities ofdaily living and daily work. That is what back schools tryto do.

CERVICAL PAIN

If the techniques of massage, mobilization, and pos-tural advice are indispensable in treating cervical cases ofPMID, the same cannot be said for reconditioning exer-cises, except in the case of fracture, where they are indis-pensable.

However, in some cases, therapeutic exercise can bevery useful, particularly in young women with long necksand slim musculatures who have developed pain becauseof static postures at work over long periods of time andin certain benign traumatic cervical discopathies. Isomet-ric contraction against manual resistance is often veryuseful. The contraction is maintained for 5 to 10 sec,followed by complete relaxation.

Sometimes some micromovements performed in thesame conditions give better results, but excessive activeexercise should be avoided. In all cases, the contractionor the micromovement should be strictly painless. Later,certain exercises can be performed by the patient to retain

permanent dynamic and static cervical muscular protec-tion.

THORACIC PAIN

Thoracic pain of low cervical origin is not oftenimproved by an exercise prescription. One should insiston the importance of physical exercises in two cases: forscoliotic patients, young or old, where it is necessary tomaintain and develop the abdominal and paraspinal mus-culature, and in cases of juvenile- and adult-onset kypho-ses, where contraction of spinal muscles against an iso-metric resistance can be prescribed along with activestretching and autostraightening exercises to fight againstthe tendency toward accentuation of the physiologic cur-vatures.

LOW BACK PAIN

Low Back Pain of Lumbosacral Origin

Low back pain of lumbosacral origin due to disk orfacet joint disorder is the best indication for a comprehen-sive reconditioning and stabilization program. However,it should be tailored to the patient’s needs.

One should not try to correct a lordosis or a kyphosisor excessively develop the paraspinal or abdominal musclesbecause they maintain the spine. The aim of a therapeuticexercise program is to help a patient with low back painlead as normal a life as possible with a minimum ofinconvenience.

Such patients should be advised and helped to regainconscious control of the lumbopelvic mechanism andlearn to control it; the simplest exercise for this is learninghow to tilt the pelvis. On the other hand, it is equallyimportant to learn what types of activities to avoid andhow to reduce stress on the lumbosacral junction duringthose activities. To do this, the patient should learn howto lock the spine in a neutral position while maximizing

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use of the legs for the performance of physical activity.Maintenance of a neutral spine position is the basis of thedynamic stabilization program that is often the corner-stone of physiotherapeutic intervention in low back pain.

These two elements may be supplemented to thepatient’s advantage by other techniques such as muscleconditioning by isometric or isotonic exercises (in casesof progressive degenerative disk disease), “posturaladjustments,” and proprioceptive adjustments in patientswith exertional low back pains (e.g., resulting from ath-letic activities). In these cases, the aim is to provide pro-tection for the affected segment and relative loosening ofthe region with a program that teaches how to avoidextreme or stressful movements.

Therapeutic exercises for low back pain have tradition-ally been categorized as either extension or flexion pro-grams. The rule of no pain and opposite movement shoulddictate which of these exercises is to be used.

Low Back Pain of Thoracolumbar Origin

Low back pain of thoracolumbar origin is generally nota good indication for therapeutic reconditioning exercises.In these cases, priority should be given to postural advice,sometimes with the use of a proprioceptive retraining ofthat region.

Nevertheless, there are two instances in which recon-ditioning is necessary: in subjects who have frequentrecurrence of pain and in athletes. The syndrome of thethoracolumbar junction of Maigne (see Chapter 60) isfrequently found in athletes and can present as low backor pubic pain. Rehabilitation is directed toward protectingthe thoracolumbar transitional zone by exercises (Ledouxand Halmagrand) that will:

• Improve the segmental spinal mobility of the super-adjacent (thoracic) regions.

• Release the paraspinal soft tissues and thoracolum-bar fascia (lumbar region and hamstring muscles).

• Improve the dynamic action of the quadratus lum-borum and the abdominal obliquus muscles.

• Develop proprioceptive function.

Rehabilitation of Lower Limbs

It is fundamental in all cases of low back pain thatreconditioning exercises for the quadriceps are essential.The patient should learn to squat easily (instead of bendingforward at the waist) and use the buttocks instead of thespine. The patient should be taught to perform daily flex-ion and extension exercises of the knees, squatting, andgetting up while keeping the torso straight.

VI

CLINICAL ASPECTS OF PAIN OF

SPINAL ORIGIN

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33

CHRONIC NECK PAIN

Certain pains in their usual forms are always recog-nized as being of spinal origin, such as cervical pain,thoracic pain, low back pain, and radicular, cervicobra-chial, and femoral neuralgia or sciatica. For some painsuch as a headache, a spinal origin is rarely considered.In certain cases such as limb joint pain or pseudovisceralpain, a spinal origin is never considered, as in limb jointpain or pseudovisceral pain.

Before accepting a spinal origin, according to the clas-sical concept, the diagnosis should be supported by diag-nostic imaging, including radiographs or other forms ofradioimaging searching for pathology of the segment orsegments that may be responsible. However, it is wellknown that significant pathology can be painless, andareas with pain may show unrelated pathology or nopathology at all.

The concepts of painful minor intervertebral dysfunc-tion (PMID) that we proposed and the concept of segmen-tal cellulotenoperiosteomyalgic syndrome (CTPM) thatwe described complete the classical semiology and allowobjective examination of the role of the spine in manycommon pain disorders, either as an originator or as anaggravating factor. A combination of clinical examinationtechniques and radiographic examinations permits diag-noses of conditions that previously eluded both properdiagnosis and management; for example, the frequent cer-vical origin of common thoracic pain, the thoracolumbarorigin of some low back pain syndromes, cervical originheadache, epicondylar pain syndrome due to segmental spi-nal dysfunction, pubic pain syndrome, and hip and knee painsyndrome similarly due to segmental spinal dysfunction.

In addition, certain pain syndromes appear as theresults of interacting factors, usually one local (oftenrelated to a local compression) and the other more distant,involving a spinal mechanism.

Finally, unexpected associations of diverse pain result-ing from the same PMID are considered; a typical exampleof this is the “thoracolumbar junction syndrome.” MultiplePMIDs can produce typical clinical pain syndromes ofwhich the “syndrome of transitional zones” is a good

example. Neck pain can be found in many contexts andcan have variable characteristics. The pain may be mildyet be associated with serious pathology.

Diagnostic Errors to Be Avoided

The diagnostic mistakes that should be avoided includeintramedullary tumors (meningiomas, neurofibromas,ependymomas) that can produce symptoms of chroniccervical pain for a long time. The pain can be localizedor associated with occipital or brachial referral patterns.Tumors of the posterior fossa may, for a period of time,produce only local cervico-occipital pain.

Congenital anomalies of the cervico-occipital junctioncan become painful after a trauma, even a trivial one,because of the development of arthritic lesions. Some-times metastatic lesions, primary spinal cord tumors, bothmalignant and benign, a syrinx, or a cyst of the spinal cordcan initially present with findings suggesting benign neckpain. When the cervical spine is affected by inflammatoryconditions, the diagnosis is rarely difficult to makebecause the patient has had similar episodes in the past.The anterior subluxation of the atlas is a known entityrelated to the destruction of the alar ligament. Nontuber-culous infectious discitis is not very common in the cer-vical spine, but it is not difficult to diagnose because itusually presents with pain, inflammation, and, in somecases, evidence of spinal cord compression. Pott’s diseaseis more discrete and can be confused with degenerativediscopathy on radiographic studies. In elderly patients, afracture of the odontoid may not be recognized whenassociated benign cervical pain appears after minortrauma.

CLINICAL SIGNS OF NECK PAIN SYNDROMES

The level of the cervical spine that is affected deter-mines the symptomatology and the possible referral pat-terns of the pain. When the superior cervical spine is

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

affected, pain radiates toward the mastoid or the occiput.Usually, headache is also present, and more rarely, somemanifestations of the “cervical syndrome” (see Chapter 50).

When the midcervical spine is affected, pain radiatestoward the supraspinous fossa, and if the inferior cervicalsegments are affected, it radiates toward the interscapularregion. All these pain syndromes are usually also associ-ated with a variable degree of painful limitation of move-ment. It is usually this limitation of movement that causesthe patient to seek medical consultation (e.g., a patientwho has difficulty backing up a car because of a problemmaintaining the head in a turned position).

History

A good history should document the precipitatingcauses of the pain, its date of onset, progression, condi-tions that ameliorate or aggravate it, its location and pat-tern of radiation, and the effects of movements and dailyactivity patterns on the pain. Associated manifestationssuch as headache, dizziness, thoracic pain, or shoulderpain should also be noted.

Range of Motion Assessment

To test active motion, the patient is seated; for thepassive movements, the patient is examined in supine.Attention is given to range of motion restriction, to move-ments that produce pain, and to where in the arc of motionthey produce it. The result of these examinations can besummarized in a star diagram (see “Assessment ofRegional Mobility” in Chapter 20) that allows one tofollow the progression of the condition graphically in sub-sequent examinations. It also helps in determining whichmanipulative techniques may be useful and in assessing theeffects of these techniques on the underlying condition.

Segmental Examination

The segmental examination allows one to determinewhich spinal segment or segments are responsible for thepain. Three signs should systematically be looked for:

1. Facet joint tenderness, a consistent sign found inall cervical segmental pain syndromes and oftenunilateral. For this examination, the patient isplaced in the supine position (Fig. 33.1).

2. Pain on PA pressure applied to the spinous pro-cesses. The patient is seated for this examination(Fig. 33.2).

3. Interspinous ligament pain that can be found bypressure with the pad of the finger index or witha key ring. Transverse pressure on the spinousprocess is not used at the cervical level, exceptin certain patients in whom it is possible for C2and C7.

Evaluation of Cellulotenoperiosteomyalgic Manifestations of Segmental Vertebral Syndrome

These manifestations are sought systematically. Theyare constant, with or without the presence of referred pain.

The subcutaneous tissues of the interscapular region(between T2 and T6) are carefully studied with the pinch-roll test. A cellulalgic zone, especially if it is unilateraland a painful point by T5 or T7 (the “cervical point of theback” of Maigne), usually proves that there is pain in theinferior cervical spine (C5 to C7; see Chapter 36, “Inter-scapular Thoracic Pain of Low Cervical Origin”). In thesame way, the supraspinous fossae (C4), the posterior andanterior regions of the neck, are examined. In the face andscalp, we also look for the signs of pinch-roll of theeyebrow, the skin overlying the angle of the jaw, andfriction of the scalp (Maigne). The signs are usually theresults of upper cervical involvement (see Chapter 48,“Headache of Cervical Origin”; Fig. 33.3 and Fig. 33.4).

Palpation of the cervical muscles is performed to findtrigger points. Pressure on these points may reproduce the

Figure 33.1

Segmental examination. Evaluation for facetjoint tenderness.

Figure 33.2

Segmental examination. Palpation of spinousprocesses.

CHAPTER 33 CHRONIC NECK PAIN

247

usual pain or symptoms. The most affected muscles arethe shoulder girdle muscles including the levator scapulae,scalene, sternocleidomastoid, trapezius, and the supra- andinfraspinatus (Fig. 33.5). Examination of the shouldermuscles against isometric resistance can reveal tendinouspain, the possible consequence of a CTPM syndromeinvolving C4–5 or C5–6. Palpation of the lateral epi-condyle is often painful ipsilateral to the facet joint ten-derness when segments C5–6 or C6–7 are affected.

Radiographic Examination

Radiographic studies should include an anteroposteriorview of the whole cervical spine (usually C3 and inferi-orly), an open mouth view demonstrating the C0–1–2segments, and a standard lateral view, making certain

(especially in cases of suspected cervical spine trauma)that C7 is easily seen. Occasionally, it is necessary to applytraction to the upper limbs caudally, either with an assis-tant or with Bogy straps, to clear the shoulders fromobstructing the view of the cervicothoracic junction. Occa-sionally, a “swimmer’s view” is necessary in difficultcases. Oblique views can be ordered to better visualizethe neuroforamina.

In post-traumatic cervical pain, “pillar views” shouldbe obtained by inclining the x-ray tube 30° in order tovisualize the articular pillars. Dynamic views in flexionand extension performed later in the trauma work-up arealso necessary. If further studies are needed, CT or MRIof the upper cervical spine can be performed.

Figure 33.3

Throughout the cervical spine, it is important toexamine the subcutaneous tissues of the neck and of thesupraspinous fossa and medial thoracic region by means ofthe pinch-roll test.

Figure 33.5

The search for trigger points should be system-atic, palpating the muscles of the neck and shoulders. Theexamination of the trapezius is depicted.

Figure 33.4

Cellulalgic manifestation of cervical segmental dysfunction. At the level of the scalp, the pinch-roll test is replacedby the friction-sign test.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

DIFFERENT ORIGINS OF NECK PAIN AND TREATMENT

Origins of neck pain include:

• Acute inflammatory arthritic spondylitis• PMID, by far the most frequent cause; the spine is

radiologically normal or arthritic• Muscular caused by myalgic or trigger points• Ligamentous pain• Diffuse cellulalgia of the nape of the neck

Cervical pain with psychologic manifestations is notincluded here, but there is a psychologic element in cer-vical pain, especially when it is accident related.

Cervical Spondylosis

Spondylosis often does not produce pain, so a patientis able to ignore it until he or she has an inflammatoryattack, an accident, a forced movement, or when the painbecomes so inconvenient that they have to see a physician.Radiographs will reveal the spondylosis and from thatmoment, any pain in the neck may be wrongly attributedto it. Therefore, the patient should know what is due tothe spondylosis and what is not.

Inflammatory Attacks

The pain of inflammatory attacks is not due to thespondylosis, but rather to the inflammatory involvementof the facet joints or uncinate processes. The pain can besubacute, acute, episodic, or of variable duration. Motiontesting generally demonstrates pain in all directions ofmovement. Manipulative treatments are contraindicated inthis condition.

Treatment.

If the acute inflammatory arthrosisaffects only one or two facet joints, which is a frequentfinding, then an articular injection with a corticosteroidderivative is an excellent treatment. This treatment is, ofcourse, impossible if the uncinate process is the source ofthe inflammatory reaction, in which case anti-inflammatorymedications should be given and possibly a cervical collarprescribed.

In some patients, inflammatory attacks continue forlong periods, in which case ultrasound therapy may proveuseful. After the acute inflammatory arthrosis, persistingpain and stiffness may be noted because of the stiffnessof the segment, which progressive mobilization and phys-iotherapy can improve.

Arthrotic Stiffening

Spondylosis can cause a progressive stiffening of theneck, which is painless and occurs often without the

knowledge of the patient, except when accompanied bypainful inflammatory attacks. Cervical spondylosis isoften associated with a diffuse cellulitic edema of the napeof the neck and the supraspinous fossae. Spondylosis is amedical term for cervical degenerative changes associatedwith remodeling and loss of mobility of the spine mostoften seen in the cervical spinal region, at times associatedwith episodes of pain.

At the level of the cervicothoracic junction, this cellu-lalgia can produce a “buffalo’s hump,” especially pro-nounced in women, which decreases after a few sessionsof mobilization produce improved joint mobility.

Treatment.

The treatment of the stiff spine shouldconsist of attempts to increase segmental mobility and softtissue flexibility by use of progressively firmer mobiliza-tions without manipulation (Fig. 33.6). Treatment of theparaspinal muscles is very important: relaxing massage,with deep gliding in the longitudinal direction and withtransverse stretching.

The results of this form of therapy are excellent anddo not depend on the degree of radiologic impairment. Avery arthritic spine can be improved rapidly and regainnearly normal articular laxity, while another less affectedspine may prove resistant to therapy. When spondylosisaffects the facet joints, the results of mobilization are lesseffective, and the condition takes longer to improve thandoes degenerative disk disease arthritis or an uncinateprocess spondylosis.

Pulsed magnetic short waves (PMSWs) are useful inthis condition, as we have shown in our department, withG. Van Steenbrugghe, in a double-blind placebo-controlledstudy of 58 patients. In 10 biweekly sessions, PMSWtherapy resulted in 70% good results, versus 28.5% withplacebo. Using placebos is easy with these waves, as theyhave no thermogenic effects that can be felt by a patient.

Figure 33.6

Mobilization with stretching and rotation to theright and right lateral flexion. Mobilization and muscle stretch-ing have special places in the treatment of neck pain.

CHAPTER 33 CHRONIC NECK PAIN

249

Spondylosis and PMID

Arthritic segments can produce PMID more frequentlythan do normal spines.

Painful Minor Intervertebral Dysfunctions

When a cervical pain occurs in a patient with a radio-logically normal or arthritic spine after trauma or withoutapparent cause, it is often due to PMID.

Localization

When the spine is arthritic, PMID is not always local-ized to the level of the radiologically most affected seg-ment, and often it affects only one level, even when thespondylosis affects several segments. PMID of the supe-rior cervical spine can produce occipital pain and cervicalpain, but in most cases, patients do not complain of cer-vical pain, but rather of headaches. The headaches aredescribed as having an occipital topography, but are moreoften described as supraorbital (see Chapter 48, “Head-ache of Cervical Origin,” and Chapter 50, “Cervical Syn-drome”).

PMIDs of the midcervical region (C3–4, C4–5) gener-ally produce cervical pain that radiates toward the supra-spinous fossa or the shoulder, producing a painful discom-fort or a clear limitation of rotation and of lateroflexionof the neck on one side, associated often with triggerpoints of the levator scapulae and tenoperiosteal tender-ness of its scapular insertion.

PMIDs of the lower cervical spine can be responsiblefor low cervical pain, often postural, radiating sometimesto the shoulder, the arm, and between the scapulae. ManyPMIDs are manifested only by an isolated interscapularthoracic pain (see Chapter 36), sometimes by a pseudo-tendinous pain in the shoulder (C4, C5) or by an epicondylarpain (C5, C6). These muscular, tendinous, or tenoperi-osteal hypersensitivities are often revealed by systematicexamination; they are never found clinically.

Treatment.

Manipulation is usually the best treat-ment for PMID, except for some contraindications oftenrelated to the state of the spine (anomalies of the cervico-occipital junction, etc.), the vascular state (postural tests),or technical form (cases for which the rule of no pain andof opposed movement would not apply; Fig. 33.7).

If the response to manipulation is incomplete (i.e., ifthe facet joint remains tender to palpation), one or twoinjections of a corticosteroid derivative usually relieve thepatient completely. When manipulation is contraindicated,injections are the treatments of choice, with or withoutmobilization and electrotherapy (pulsed short waves). Incase of persistent ligamentous pain, a local injection oflidocaine with a corticosteroid is indicated.

The efficacy of the treatment can be judged not onlyby the subjective improvement of the patient and the

amplitude of the movements, but also by the elements ofthe CTPM syndrome discovered at the initial examination.Their disappearance should be sought, if necessary finish-ing the cervical treatment with a local treatment.

Patients should learn to guard the neck, especially inrotation, in positions used at work and with activities ofdaily living. They should also be taught to avoid all fatigu-ing positions, such as reading in bed, watching televisionwhile sitting in a poorly adjusted seat, and sleeping prone.Education is essential to reduce recurrence.

A Particular Case: Post-Traumatic Cervical Pain

The frequency of cervical trauma has increased indirect proportion to the use of the automobile. We do notrefer here to trauma with neurologic or osseous repercus-sions, but to those traumas classified as minor.

The resulting cervical pain is usually attributed to“benign sprains” of the spine. The ligamentous systemremains intact, and the dynamic x-rays are normal or showonly minor static disorders of the spine: segmental stiff-ness, loss of the cervical lordosis, and slight axis alterationof the odontoid processes in relation to the lateral massesof the atlas. Rotation of the atlas on the axis compensatesfor the abnormal mechanics of the subjacent segments tomaintain the horizontal orientation of the eyes. Convexityof the articular surfaces also gives an aspect of false pinch-ing and of false axis alteration. There exists also a func-tional block (Wackenheim) of the superior spine, eitheran atlanto-occipital block or atlanto-axial block. Theformer is characterized by an atlanto-occipital space thatdoes not move at all in flexion or extension, the latter bya constant atlanto-axial or inferior cervical spine pinchingproducing a supra-adjacent hypermobility. The curvatureabnormalities generally persist even if the patient is

Figure 33.7

Manipulation in right rotation on C5–6. The indi-cation for manipulation should be well thought out.

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relieved of pain and the spine has clinically regained itssuppleness.

Treatment.

These cases must be treated with greatcaution during the first weeks because the trauma pro-duces ligamentous microlesions, capsular and muscularmicrolesions that contraindicate manipulative treatment.In the first days, a cervical collar is useful, with analgesic,anti-inflammatories, and some muscle relaxants. The cer-vical collar should not be worn for a long time since thepatient might become dependent on it and refuse to dis-continue its use. However, it can be worn for a whileduring the night if the position of the neck produces pain.

Maneuvers of muscular relaxation without mobiliza-tion can be useful, as can electrotherapy. Manipulationshould not be considered until 1 mo after the accident.Then it should be performed carefully, after a series ofmobilizations to end range; it consists of one or twomaneuvers. Sometimes the result can be spectacular. Asalways, its use depends on negative postural tests.

Sometimes therapeutic exercise is started very early,with isometrics. We prefer to use it when the cervicalmobility has returned and the pain is much decreased. Useof exercise should always, as in manipulation, be deter-mined by the rule of no pain and opposite movement. Theextensor muscles are treated initially, then the flexors,which are often neglected. It consists of multidirectionalisometric contractions to stimulate and readjust the mus-culature whose traumatization has inhibited and perturbedfunction.

This physical therapy should not have the patient focustoo much on the spine, especially when a psychologicelement is involved. It is even better to do without it if itis not indispensable, reassure the patient that the pain isbenign, and explain how to avoid harmful positions.

When the patient is seen late in the course of the dis-order, the usual treatment of PMID and of the CTPMmanifestations can be provided.

Persistent pain on hyperextension or hyperflexion ofthe neck is usually due to the interspinous ligament, whichcan be treated by injection with lidocaine and corticoster-oid derivatives.

Cervical Pain of Muscular, Subcutaneous, or Ligamentous Origin

Muscular Origin

The muscles of the neck can be a source of cervicalpain that can be due to trigger points secondary to articularor disk pain or occur as a result of spinal segmental dys-function. It can also be due to trigger points occurring

after exertion or because of postural problems that resultin excessive fatigue of the muscle, which should bestretched or injected. The trapezius muscle or the levatorscapula is often the one affected.

Subcutaneous Origin

Some patients have cellulalgic zones affecting theentire nape of the neck and the supraspinous fossae. Theseform a “buffalo’s hump” at the level of the cervicothoracicjunction. These regional infiltrates differ from the local-ized infiltrate, are usually unilateral, and belong to theCTPM segmental syndrome. They are often well tolerated,although patients are very sensitive to cold and drafts, butthey are sometimes the only cause of a cervical pain. Thebest treatment is massage, which can be combined withelectrotherapy (iontophoresis).

Ligamentous Origin

In cervical pain syndromes that are tenacious, espe-cially those resulting from cervical trauma, the possibleinvolvement of the supraspinous ligament should be con-sidered and sought. This can be done by palpation withthe tip of the index finger, which can produce an acutepain between two spinous processes. The examination isoften positive between C4–5 or C5–6. This interspinouspain is usually connected to a PMID, but if it persistsdespite treatment and despite the disappearance of thefacet joint pain, it should be treated locally by injectionwith a corticosteroid derivative, lidocaine 0.5%, orprocaine 0.5%. If no results are noted, then careful scle-rosing therapy can be considered (see “Interspinous Lig-aments” in Chapter 26).

Cervical Pain and Psychologic Disorders

The problem of cervical pain, especially when it ispost-traumatic, is that it often has a psychologic elementthat is uncovered under different conditions. The patientsare often anxious and distressed, with a tendency towardhypochondriasis — the kinds of patients who have otherneurotic manifestations, revindications, or compensationneuroses. No treatment can improve them, except ofcourse a satisfactory indemnification. In some cases, thepain may be purely psychogenic; patients project onto thecervical level the conversion symptoms of their neuroticstates, which of course no cervical or antalgic treatmentcan improve, but which can be aggravated by mul-tiplication of paraclinical investigations.

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34

TORTICOLLIS (WRYNECK) AND

ACUTE CERVICAL PAIN

The most frequent cause of acute cervical pain is“benign torticollis (wryneck),” a distressing disorder, usu-ally of short duration. However, it can be chronic if linkedto inflammatory arthritis or to a herniated disk. On rareoccasions it can also be due to severe pathology. Forexample, a progressive or acutely painful torticollis seem-ingly triggered by a mild trauma or sudden movement canactually be due to an underlying benign or malignantspinal tumor.

Patients with acute cervical pain should always beexamined for possible fracture, utilizing radiographicstudies liberally followed by tomographic studies such asCT or MRI if there is the least suspicion.

Episodes of acute cervical pain can be seen in theanomalies of the cervico-occipital junction as transientepisodes of painful blockage of the neck.

Osteomyelitis (due to TB or other infectious agents)can take the form of a torticollis associated with fever andother signs of infection. In children, in the presence offever and acute torticollis, a calcific nucleopathy (och-ronosis) should be considered. Acute stiffness of the neckin a patient with rheumatoid arthritis can be due to anatlanto-axial subluxation, and this possibility should besought.

BENIGN ACUTE TORTICOLLIS

In the medical literature, torticollis is described as aninclination of the head on the neck — an involuntary,irreducible, constant, generally painful inclination ofdeforming appearance. In current language, the word

torti-collis

means the benign torticollis, an acute and painfullocking of the neck in rotation and lateroflexion, generallylasting a few days.

This condition is frequently blamed on cold drafts orsudden forced movements. Pain upon awakening is fre-quently reported. In very severe acute cases, the neck is“frozen” in side bending and any movement, however

small, exacerbates the pain. The neck is only locked onone side. The other side is normal; in some cases, rotationcan be blocked in both directions.

These common forms of torticollis can be due to PMIDor be of muscular origin. It is sometimes difficult to dis-tinguish which is responsible because acute PMID cancause a severe protective muscle guarding.

Torticollis Due to PMID

Torticollis is generally the result of a rapid movementof the neck. Motion is usually free on one side, impairedand painful on the other. A segmental examination canlocalize the responsible level, and the facet joints can befound to be quite tender to palpation (often C2–3).

Treatment

In general, manipulation is possible, but it should bepreceded for a long time by mobilization maneuvers andprogressive stretching in the pain-free directions. Manip-ulation should be mild and well planned and can help toreduce the protective muscle guarding. If manipulation isnot possible (rule of no pain), a cervical collar can helprelieve the patient and shorten the acute phase. Facet injec-tion is also useful.

When torticollis appears after cervical trauma, highquality radiographs are necessary to document PMID andconfirm that no other pathologic explanations exist. In theimmediate post-traumatic phase, the only treatment rec-ommended is the cervical collar; manipulation should notbe performed. After the fourth week, depending on thecondition of the patient, manipulations may be considered.

Torticollis of Muscular Origin

In some cases of acute torticollis, examination does notreveal any particular segmental sensitivity. In these cases,only the muscles seem to be affected, especially thesternocleidomastoid, the splenius, or the levator scapula.Their palpation is very painful. A cold draft is often

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thought to be the cause by the patient; however, a viralorigin is thought possible by some investigators.

Treatment

The basic treatment for this condition is the use of acervical collar, anti-inflammatory medications, analgesics,and muscle relaxants. Injection of the trigger points canbring quick relief. Acupuncture sometimes helps, as doesstretching of the affected muscle.

Torticollis of Mixed Origin

Sometimes the two mechanisms (i.e., articular andmuscular) seem to be associated. In such cases, the mus-cular factor should be treated first, followed by injectionof the affected facets. Mobilization can be performed withgreat caution and only if strictly painless.

ACUTE CERVICAL PAIN

Due to Acute Synovitis

Acute cervical pain due to synovitis can produce mod-erate or acute pain. In the latter case, the neck is not lockedor stiffened by pain but may have a loss of range of motion,with motion being painful even at rest. It is not unusualfor acute cervical pain to be present with radiographicstudies that fail to demonstrate significant pathology whilethe segmental examination demonstrates swollen facetjoints.

Treatment

When only one or two articulations are affected, anarticular injection with a corticosteroid derivative is the

treatment of choice. In other cases, anti-inflammatoriescan be used. The cervical collar can help bring aboutsignificant relief.

As Result of Herniated Disk

A herniated disk can cause acute neck pain and canappear after a violent shock while in hyperflexion. It cansometimes also appear after a simple forced movement inrotation. Initially, the condition presents with acute cer-vical pain, severe protective muscle guarding, and almostalways associated interscapular pain. Typically, the painincreases with coughing or sneezing, and postural posi-tions connected with supine. The patient can assume lesspainful positions such as head flexed forward and on theside. Progressively, the pain will reach the shoulder, thenthe arm.

The cervical herniated disk often evolves into a chronicphase, with the patient having low level continuous pain,with episodic exacerbations lasting a few weeks to a fewmonths at a time.

Treatment

Treatment during acute attacks should consist of immo-bilization with a Minerva cervical collar and the use ofanti-inflammatories. Cervical traction is sometimes effi-cacious, but it is indicated only when the manual tractiontest relieves pain and does not exacerbate it (see Fig. 23.7),as it is not always well tolerated.

Cyriax advocates manipulation that involves both rota-tion and very strong manual traction. We are not convincedof the benefit of this approach.

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35

CERVICOBRACHIAL NEURALGIA

Cervicobrachial neuralgia (CBN) is a pain referred tothe upper limb as a result of an irritation or compressionof a cervical nerve root (C5, C6, C7, or C8). This com-pression is usually the result of osteophytosis, uncarthrosis(disco-osteophytic nodule or “hard hernia”), or, rarely, toa herniated disk. The herniated disk is seen in youngpeople, while the osteophytosis is not seen before the ageof 40. In some cases of common CBN, none of thesecauses may explain the pain.

When there is no clear explanation, PMID or an acutesynovitis of a facet joint spondylosis may be the cause.The pain in these cases is not due to nerve root compres-sion; it is referred pain from any of the segmental spinalelements. In some cases, the cervicobrachial pain is theresult of a serious lesion that can pose significant diag-nostic challenges.

PAIN

In general, the pain of CBN starts progressively andinvolves a painful stiffening of the neck with interscapularor precordial referral. Pain in the arm will occur a fewhours to a few weeks later. For most practical purposes,this pain sums up the clinical picture. The pain can bereplaced by paresthesia in the distribution of the affectedroot down to the hand, ending at one or several fingerswith tingling. It is generally distressing, with nocturnalattacks sometimes triggered by movement of the neck,coughing, or sneezing. The pain can be almost unbearable.The neck may be held in antalgic postures or demonstratesimple stiffness with limitation of movements. Such casesoften demonstrate no objective neurologic findings.Objective findings of other types are seen in only about50% of cases. The reflexes are rarely abnormal, nor aremotor problems usually seen.

EXAMINATION OF NECK

Examination of the neck starts with an evaluation ofthe neck range of motion with the patient seated, followed

by a reassessment in supine with the head slightly pastthe end of the table, in a position of maximum relaxation.

The angle of the neck at which movement triggers painis determined; an increase in this angle usually signals animprovement in the problem.

Examination of Affected Level

The main sign of the segmental examination is pain onpalpation in the corresponding articular pillar. This signis constant in CBNs of mechanical origin. Pressure on thespinous process is also painful. An “anterior doorbellpoint” can reproduce or increase the spontaneous pain.

Axial compression over the vertex, with the patientsitting, can provoke an exaggeration of pain. Conversely,traction on the neck can relieve the patient.

Test of Manual Traction

The patient is in supine position; the physician takeshold of both the chin and occiput and applies progressivetraction on the neck. If this maneuver relieves the pain inthe arm or shoulder, a treatment by mechanical tractionor suspension can be planned (Fig. 35.4). If it exacerbatesthe pain, any manual or mechanical traction should beavoided.

INTERSCAPULAR PAIN

CBNs are often associated with interscapular pain. Itcan precede the attack, come with it, or survive it. Theepicenter of the pain is usually a finger-breadth distancelateral to T5 or T6 and is painful on palpation. This iswhat we describe as the “interscapular point of cervicalorigin” or “cervical point of the back” (Maigne 1968). Itis not specific to CBN; it is our impression that it is thethoracic mirror of the pains of the inferior cervical spine.This cervical point of the back is common to the inferiorcervical segments (see Chapter 36, “InterscapularThoracic Pain of Low Cervical Origin”).

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CLINICAL EXAMPLES BY SEGMENTAL LEVEL

Each cervical root when affected has a unique clinicalsyndrome.

C5 Syndrome

Sensory deficits: varying degrees of paresthesia orhypoesthesia over the anterior shoulder to the lateral bor-der of the elbow.

Motor deficits: deltoid, supraspinatus, teres minor,sometimes biceps, leading to impairment of abductionand external rotation of the shoulder.

C6 Syndrome

Sensory deficits: varying degrees of paresthesia orhypesthesia over the anterolateral shoulder, lateral arm, tothe thumb (Fig. 35.1).

Reflex deficits: decreases or absent biceps, brachiora-dialis, and pronator teres reflexes.

Motor deficits: weakness and atrophy of the biceps,brachioradialis, and thenar muscles, resulting in impair-ment of elbow flexion and pronation.

C7 Syndrome

Sensory deficits: varying degrees of paresthesia orhypesthesia over the cervicothoracic junction, posteriorshoulder, arm, forearm, dorsum of the wrist, index

and middle fingers, and occasionally the ring finger(Fig. 35.2).

Reflex deficits: decreases or absent triceps reflex.Motor deficits: weakness and atrophy of the triceps and

long finger and wrist extensors, resulting in impairmentof extension of the elbow, wrist, and fingers.

C8 Syndrome

Sensory deficits: varying degrees of paresthesia orhypesthesia over the medial arm, forearm, wrist, hand, andfourth and fifth fingers (Fig. 35.3).

Reflex deficits: decreased or absent finger flexor reflex.Motor deficits: weakness and atrophy of the hand, espe-

cially the intrinsics and hypothenar eminence.

ETIOLOGIES

Cervicobrachial Neuralgia Due to Cervical Spondylosis

CBN is considered one of the clinical expressions ofcervical spondylosis. It usually affects people in their 50s,and women more than men.

Cervical radiographs show the degenerative changes,especially of the uncovertebral joints, with osteophytesencroaching on the intervertebral foramen. Inflammationrelated to a disco-osteophytic nodule is felt to be the causeof the CBN.

The pain often decreases, then disappears in 3 to 6 wk,sometimes resulting in persistent paresthesia. There are

Figure 35.1

C6 topography.

Figure 35.2

C7 topography.

CHAPTER 35 CERVICOBRACHIAL NEURALGIA

255

some chronic and refractory forms for which CT/myelo-graphy or MRI may be necessary.

CBN Due to Disk Herniation

In young people, CBN can be the result of a herniateddisk following trauma or a violent effort; the antalgicattitude and the stiffness of the neck are usually pro-nounced. Radiographs of the cervical spine may show arelative gap, laterally or posteriorly. Diagnosis is madewith the aid of MRI or CT studies. Most often, medical

treatment is sufficient. When pain persists or motor deficitor pyramidal signs are found, surgery may be indicated.

CBN Due to PMID

CBN can occur in a patient with no spondylosis (e.g.,after an accident or a forced movement) with less markedsigns than with a herniated disk. The segmental examina-tion in these cases reveals pain at the corresponding ver-tebral level. PMID should be considered as a diagnosticpossibility in cases that have no significant pathologicfindings on cervical x-rays, CT, or MRI. In these cases itis more likely that the pain is referred from an articulardisorder as opposed to pain due to nerve root compression.

DIFFERENTIAL DIAGNOSIS

The diagnosis of cervical spondylosis is usually notdifficult to make. In spite of this, diagnostic errors occuron occasion, as the symptomatology is not always typicaland complete.

Entrapment Syndromes

This radicular syndrome should not be confused withan entrapment syndrome involving the more distal neuralsegments such as the plexus or peripheral nerve; for exam-ple, in the median nerve in the carpal tunnel or the ulnarnerve in the cubital tunnel or Guyon’s tunnel. A cervicalrib can be involved in a thoracic outlet syndrome resultingin a C8–T1 syndrome, characterized by paresthesia andmotor and vasomotor dysfunction of the hand.

Referred Pain Syndromes

Some tendinous pains of the shoulder and elbow canlead one into making a diagnosis of moderate chronicpseudoradicular pain. Many of these tendinous pains arethe result of a cervical PMID. In the acute form of thesyndrome of the levator scapula, there can be a brachialreferral simulating a CBN, the thoracic pain being put inthe background, but there are more serious causes.

Intramedullary Tumors

The glioma is by far the most frequent intramedullarytumor. It results in a refractory CBN, exacerbated by thesupine position. Initially, only local involvement is notedwithout spinal cord signs. Radiographic studies performedin the 3/4 oblique position for visualization of the inter-vertebral foramina may show enlargement of the neuralforamen. Diagnosis is greatly aided and facilitated by theuse of CT or MRI.

Meningioma is less common, as are malignantintramedullary and epidural tumors.

Figure 35.3

C8 topography.

Figure 35.4

Manual traction test. If this maneuver reducescervical brachial pain, then cervical traction will be effective.If it induces pain, it is then in contraindication to the use ofcervical traction.

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Infectious Discitis

As a result of infection by various agents, both tuber-cular and nontubercular, cervical discitis can occur, whichcan induce a CBN. The diagnosis can be made on thebasis of cervical stiffness in association with an infectioussyndrome with abnormal radiographic findings. However,the value of the clinical examination should not be over-looked, nor should the utility of bone and gallium scansbe forgotten.

Spinal Metastases

CBN of metastatic origin can result in extremely severepain that evolves rapidly with progressive neurologicsigns. The monoradicular disorder becomes pluriradicular.The pluriradicular syndrome soon gives way to a spinalcord syndrome with spinal cord pain and findings consis-tent with an extradural compression (metastatic, hemato-logic, etc.).

Pancoast Tumors

An intense cervicobrachial pain is often the first signof a tumor of the pulmonary apex often associated withinterscapular pain. Motor and sensory deficits in a C8–T1or lower plexus distribution are seen, associated with Hor-ner’s syndrome. The diagnosis is confirmed by pulmonaryradiography that shows the opacity of the apex, which inthe beginning is sometimes only a simple decrease intransparency.

TREATMENT

In the acute phase, especially if the pain is intense, abrief (6 days) course of corticosteroid therapy is of use,starting with a high dose then gradually tapering off. Onecan start with smaller doses using the Luccherini tech-nique: an intradural injection of 2 mL of hydrocortisoneacetate, which necessitates a brief hospitalization.

In milder forms, nonsteroidal anti-inflammatory med-ications are sufficient. Analgesics are used but are noteffective unless used concurrently with a medication suchas diazepam.

In the subacute or refractory forms, immobilization ofthe neck with a well adapted Minerva is indispensable. Inmilder forms, the use of a cervical collar decreases painand helps the patient to avoid exacerbating postures, par-ticularly at night. Surgery is rarely needed for this condi-tion. Mechanical treatment such as manipulation and trac-tion can also be used.

Manipulation

In some cases, manipulation can bring quick relief tothe patient. Generally, manipulation is not useful in the

acute phase, where the rule of no pain and opposite move-ment is not applicable. Manipulation is most indicated inthe subacute form and applied only if previous mobiliza-tions resulted in the patient’s having the impression ofrelaxation and relief.

Manipulations are executed in each of the nonpainfuldirections. If the result is good, two or three can be per-formed, one especially on rotation, and on lateroflexion.The third can be in flexion and extension, depending onwhich one of them is free. Between each mobilization andafter each manipulation, the patient is reexamined to deter-mine whether progress has been made and decide whatmaneuvers are to follow. If the final result is going to begood, relief is frequently seen at the first session (Fig. 35.5through Fig. 35.7). In one out of three cases, a patient mayhave a more or less disagreeable reaction the night fol-lowing the first session. He or she should be warned aboutthis possibility. This reaction, however, does not changethe prognosis as far as the final result is concerned. Afterthree sessions without any improvement, the manipulativetreatment should be terminated.

Figure 35.5

Star diagram corresponding to a right C6 cer-vical brachialgia.

Figure 35.6

Technique for rotatory manipulation to the left.

CHAPTER 35 CERVICOBRACHIAL NEURALGIA

257

Spinal Traction

Spinal traction can be very useful. If the manual trac-tion test is favorable (Fig. 35.4), suspensions on aninclined plane or traction on a table can certainly bringsignificant improvement. The head of the patient is main-tained with a Seyre collar (Fig. 23.2a) or with Maigne’sapparatus (Fig. 23.2b).

Manipulation and Traction

It is interesting to try both manipulation and tractionduring the same treatment session; however, in general, itis better to apply them in separate sessions. If they areperformed during the same session, it is better to start withthe manipulation.

Manipulation under Traction

A manipulation is performed in rotation under traction.The physician grasps the chin and occiput of the patientin the cup of the hand and applies progressive traction tothe cervical spine. If this maneuver is painless, it can beexecuted as a manipulation in rotation of the pain-freeside. For herniated disks, Cyriax recommends manipula-tion under very strong traction, with an assistant holdingthe patient’s feet.

Residual Pain and Cellulotenoperiosteomyalgic Manifestations of Spinal Origin

After the acute phase is over, the cellulotenoperiosteo-myalgic manifestations are often responsible for persistentpain, which may appear to be pseudoradicular or tendinous.

A more or less annoying interscapular pain is rather fre-quent.

In such cases, the subcutaneous tissues and musclesthat are most often affected should be carefully examinedby palpation, and trigger points should be sought andevaluated for a possible role in the maintenance of persis-tent pain referral to the shoulder, upper arm, or elbow. Thetarget muscles frequently noted are the infraspinatus, teresmajor, and teres minor (C5–6), triceps (C7), and commonwrist extensors. The trigger point that originates the per-sistent pain is sharply localized and painful on palpation.An injection of xylocaine is necessary to stop the radiatingpain. This injection may be sufficient to treat this condi-tion; otherwise, stretching, massage, or ultrasound therapyshould be used. The tendinous sensitivities especiallyaffect the supraspinatus (C5–6), the biceps (C5–6), andthe lateral epicondyle (C6–7).

Figure 35.7

Manipulation technique in left lateral flexion.

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36

CHRONIC THORACIC PAIN

The “benign” or “common” thoracic pain of the adultis certainly the most neglected aspect of spinal pathology,in spite of its frequency. The literature concerning thisentity is sparse. Most of the literature remarks on thepaucity of clinical findings and tends to relegate this con-dition to the functional area, stressing psychic factors thatcertain authors consider to be the essential causes.

Thanks to the segmental examination set out in thisbook and the study of cellulomyalgic manifestations, wecan demonstrate that most pains in the midthoracic regionpresent with a characteristic clinical picture and have anorigin in the inferior cervical spine (Maigne, 1964). Thepsychic factors and the state of the organism are, of course,not to be neglected, but they only participate in the causeof the pain without explaining it. Other causes of commonthoracic pain exist, such as thoracic vertebral, muscular,or rarely ligamentous origin.

Diagnostic Errors to Avoid —

Visceral disorders, evenwhen they are not yet recognized, can be the cause ofmisleading thoracic pain. Pancreatic lesions, especiallycancers, can produce refractory thoracic pain, as can cer-tain ulcers of the stomach or of the duodenum. Pleuro-pulmonary and cardiac disorders and aortic dissection canproduce, for a certain time, isolated thoracic pain. D.Belaiche observed a paradoxical case of thoracic painlinked to a gastric ulcer that could be relieved only byindomethacin (personal communication). Also spinallesions due to multiple myeloma, metastasis, discitis, orosteoporotic vertebral compression fractures can producea temporary thoracic pain with many aspects in common.

INTERSCAPULAR THORACIC PAIN OF LOW CERVICAL ORIGIN (MAIGNE)

Most common thoracic pains are felt in the midthoracicinterscapular region. Although pain in this region mayoriginate in the thoracic spine, in our experience, the vast

majority of pains in this region originate from the lowerthree cervical spinal segments (1964). In spite of the cer-vical origin of this pain, the patient feels pain in the neckonly exceptionally; instead, it is projected to the thoraciclevel. It disappears with the cervical treatment. Onexamination, this pain at the thoracic level demonstratesconstant and characteristic signs and symptoms.

Clinical Picture

The pain is felt between the shoulder blades; somepatients describe a highly circumscribed point, such as aright or left paraspinal point. Sometimes it is localized toa more diffuse region, which may be unilateral or involvethe midback. The pain may even be described as intratho-racic.

The patient likens the pain to a red hot iron, a cramp,or an intense and localized fatigue. It can appear aftertrauma, a poorly performed manipulation, or an uncor-rected postural stress, etc. The pain usually has an insid-ious onset.

Although the pain is chronic, there are episodes ofworsening, often associated with periods of fatigue, over-work, or postural or psychic stress. Persons in certaintypes of occupations (e.g., typists, keyboard operators,seamstresses) at times suffer from this pain. In general, itis decreased by rest. In some cases, the reverse is noted,with increased pain in the morning upon awakening. Thisis felt to be due to poor postural positioning of the neckduring sleep, especially in people sleeping prone, whichforces the neck into full rotation.

The pain can start out as an acute pain due to a stren-uous effort or sudden movement (see Chapter 37, “AcuteThoracic Pain”).

Clinical Examination

Examination of Back

At the thoracic level, two signs are characteristic ofthoracic pain of cervical origin:

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• A remarkably constant painful point, localized tothe paraspinal levels of T5 or T6, the cervical pointof the back

• A cellulalgic zone adjacent to this point and spread-ing laterally toward the acromion

Cervical Point of the Back (Maigne).

There

isa painful point about 2 cm from the median line at thelevel of T5 or T6. This vertebrointerscapular point is con-stant and seems to reflect the pain of the lower cervicalspine. The pain can have any type of origin: benign, malig-nant, articular, discogenic, or tumoral (Fig. 36.1). Theexamination should thus be as thorough as possible.

The patient is seated with the head flexed, hands onlap, in complete relaxation. The examiner uses the middleor index finger to glide slowly, following a line parallelto the line of the spinous processes, one finger breadthlateral to the midline. The examiner applies firm, contin-uous, and constant pressure with the pad of the fingerwhile at the same time executing small frictional to-and-fro movements repeated every centimeter, just as if theexaminer wanted to mobilize the subcutaneous tissuesover the underlying muscles. This maneuver is performedseveral times. It is exactly the same maneuver performedin the segmental examination during the evaluation offacet joint tenderness.

At T5 or T6, usually 1 to 2 cm lateral of the midline,a very tender point is found. Mild pressure on this pointand on it alone will reproduce the patient’s usual pain,even if it had been reported to be higher, lower, or evenat an intrathoracic point (Fig. 36.2).

Localization of that point is remarkably fixed. We didradiologic localizations in 150 patients and found thispoint opposite T5 or T6 in 138 cases, opposite T4 in 7,and opposite T7 in 5.

N.B.

The cervical point of the back can be confused with facetjoint pain of T5–6 or T6–7 (Fig. 36.5). This occurs much less

frequently in clinical practice, and it is usually quite easy todistinguish the two. If it is really a cervical point of the back,there is a cellulalgic zone adjacent to it overlying the ipsilateralscapula and spreading laterally (Fig. 36.3). If the tenderness isdue to an irritable thoracic facet joint resulting from segmentaldysfunction at T5–6 or T6–7, the corresponding cellulalgic zoneis located lower, toward T9 or T10 in the dermatomal territoryof the posterior ramus of T5 or T6 (Fig. 36.5).

Midthoracic Cellulalgic Band.

The cervical pointof the back usually has a large cellulalgic zone adjacentto it that is demonstrable by means of the pinch-roll test.The zone spreads laterally from the cervical point of theback toward the acromion, a height of 6 to 8 cm. It islarger laterally than medially and is sometimes limited toa smaller surface. The cutaneous and subcutaneous tissuesof that zone are thickened and painful to pinch-rolling.The thickening can be very significant in some chroniccases. Sometimes, the changes are mild and may onlyinvolve a portion of the possible area, while it is painlesson the opposite side or in the subadjacent or supra-adjacentregions (Fig. 36.3 and Fig. 36.4).

One or two taut bands of muscle sometimes occur withthe cellulalgia. They are localized in the paraspinal musclesand sometimes at the level of the lateralmost iliocostalismuscle. Palpation should be performed very thoroughlywith the pads of the fingers, which are held in the mannerof hooks, perpendicular to the direction of the bundles,which are very sensitive and the size of a small pencil ora match.

Radiologic Signs.

The radiologic examination isgenerally normal; however, minor benign abnormalitiesmay be found that are not causally related to the pain,although one is often tempted to blame these lesions, asthough they represented “guilt by association.” Examples

Figure 36.1

The cervical point of the back (Maigne). Incases of thoracic pain of cervical origin, pressure on thispoint reproduces the spontaneous pain of the patient.

Figure 36.2

Method for finding the cervical point of the back.This painful point is found exactly next to T5 or T6, approxi-mately 1 or 2 cm lateral of the median line (see

×

on Fig. 36.1).This is the same maneuver used to find the painful facet jointduring the segmental examination.

CHAPTER 36 CHRONIC THORACIC PAIN

261

of these pathologies noted but not causally related includescoliosis, hyperkyphosis, thoracic arthrosis, and thesequelae of Scheuermann’s apophysitis of adolescence.Sometimes thoracic x-rays may be very misleading. Wehave seen patients with old traumatic compression frac-tures of T5 or T6, to which chronic refractory thoracicpain was wrongly attributed. In these cases, the pain was,in fact, found to be due to a cervical PMID that occurredduring the same accident. The evidence for this was thedisappearance of the pain after cervical treatment.

N.B.

With chronic thoracic pain, the cervical point of the backand the cellulalgia remain on examination, even when the patientdoes not suffer, as in all the cases of chronic PMID.

Examination of Neck

Most often, the patient does not complain about theneck. If the patient feels pain, the cervical pain and theback pain do not seem to be related. Examination some-times demonstrates some impairment in the movementsof the neck. In a few rare cases, forced rotation, forcedhyperextension, or both produce the thoracic pain. In gen-eral, the neck movements are free and painless.

The segmental examination demonstrates that one ofthe last three segments of the inferior cervical spine isaffected. The segmental examination reveals facet jointtenderness (Fig. 36.6), sometimes with pain on palpationof the spinous process and the interspinous ligament. Thecervical point of the back and the cellulalgic zone arealways ipsilateral to the cervical facet joint tenderness.

Among common thoracic pain syndromes, cervicalsegmental dysfunction is often due to a PMID and issometimes the result of synovitis.

Figure 36.3

and

Figure 36.4

Next to the cervical point of the back, the pinch-roll test can detect a cellulalgic zone that extendslaterally.

Figure 36.5

The cervical point of the back (

right

), can beconfused with thoracic facet tenderness due to the T4–5 orT5–6 segment (

left

). In this case, the cellulalgic band thatwould correspond to the posterior ramus of T5 would besituated much lower, nearer the T9–10 level.

Figure 36.6

Segmental examination of the inferior cervicalspine (C5–T1) demonstrating facet tenderness ipsilateral tothe cervical point of the back.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

The “anterior doorbell sign” that we described in ourfirst publications consists of provoking the patient’s usualthoracic pain by applying pressure with the thumb at theresponsible level and at the anterolateral part of the spine(Fig. 36.7). This maneuver demonstrates the link betweenthe cervical spine and the midthoracic pain. This sign isinconstant, and not always easy to demonstrate. There arecases in which this “cervical doorbell point” should belooked for carefully by modifying the point at which pres-sure is applied by a few centimeters. It is found in aboutsix of ten cases of thoracic pain of cervical origin. How-ever, it is not necessary to find it to prove the cervicalorigin of a thoracic pain when other signs are present andare localized to the same side.

Cervical spine radiographs are indispensable to rule outall serious lesions (just as thoracic spine and thorax radio-graphic studies are also needed). The responsibility of thecervical spine cannot be asserted or invalidated by theexistence or absence of signs of spondylosis or of degen-erative discopathy, just as the thoracic spine cannot beheld responsible because there is spondylosis, a sequelaeof Scheuermann’s disease, or scoliosis.

Cervical Spine and Thoracic Pain

The link between thoracic pain, the painful point para-T5, the adjacent cellulalgia, and the cervical spine can bedemonstrated by the following therapeutic test: any treat-ment that makes the painful cervical segment painless onsegmental examination is tried, and the thoracic pain andsigns are then reevaluated for persistence or disappear-ance. The treatment can take the form of manipulation orfacet injection. If this test successfully reduces the pain,the cervical origin of the midthoracic spine pain shouldbe considered confirmed.

Conversely, any treatment that makes the cervical seg-ment more painful on segmental examination increasesthe thoracic pain, the cervical point of the back, and the

cellulalgia. This may be due to performing the manipu-lation for the PMID in the wrong direction.

This type of thoracic pain is currently seen often as aresult of poorly performed manipulations of the inferiorcervical spine. These patients complain little or not at allabout their necks, but a great deal about their backs.

Lack of Simple Anatomic Explanation.

There isapparently no anatomic explanation for this painful pro-jection. The posterior rami of the last spinal cervicalnerves might make it possible, but no anatomist sees theirterritory as so low; most even think they do not have anycutaneous branches.

Thoracic Pain and Cervical Herniated Disk.

Most authors do not view thoracic pain as due to thecervical spine as we do, and the point para-T5 that we callthe cervical point of the back has not been proven to bea sign of cervical dysfunction. Nevertheless, some authors

Figure 36.7

The “doorbell sign” (Maigne). Pressure is applied to the anterolateral aspect of the cervical spine. In most cases,such pressure applied to an involved segment produces a painful referral toward the thoracic spine.

Figure 36.8

Anesthetic block of the posterior primary ramusof T2 at the point where it traverses the T2–3 facet joint canrelieve spontaneous thoracic pain, the cervical point of theback, and pain on the pinch-roll test.

CHAPTER 36 CHRONIC THORACIC PAIN

263

have been intrigued by the sometimes acute interscapularpain preceding and associated with cervical herniateddisks.

Stookey and Michelsen and Mixter on one hand, Elliotand Kramer on the other, report it without giving anyexplanation. Wedell and Feinstein noted the constant “irri-tation” of the paraspinal muscles of the thoracic regionseen on electromyography in patients with cervical herni-ated disks; they concluded that “the protective muscleguarding at that level is not due to the lesion of the spinalnerve compressed by the herniation, but by another sourceof unknown pain.”

Cloward’s Experiments.

During interventions forcervical herniated disks performed under local anesthesia,Cloward electrically or mechanically irritated differentelements of the spinal segmental levels. He noted thatirritation of the superficial anterolateral annular fibers pro-duced acute pain in the ipsilateral periscapular region thatreproduced or exacerbated the usual referral pattern. Heobtained the same effect by irritation of the motor root atthe same level. He reinforced the muscular nature of thatpain with electromyographic evidence and attributed it tothe irritation of the muscles of the shoulder girdle that areinnervated by the lower cervical roots: rhomboideus muscle(roots C4–5), infraspinatus muscle (roots C5–6), and latis-simus dorsi and subscapularis (C6–7). He noted also thatthe patients felt pain at the level of the superiomedial angleof the scapula for C4–5, over the midscapula for C5-6,and the inferior scapula for C6-7.

This experiment deserves comment. It demonstratesdefinitely that a cervical lesion can produce a thoracicpain, which is essential for our thesis. The electromyo-graphic evidence is less convincing in the explanation ofthe pain mechanism. It is normal for muscles that areinnervated by a nerve root that is compressed by a herni-ated disk to show some electromyographic disturbances.It does not prove their responsibility for the pain.

Our observations do not agree with Cloward’s aboutthe level at which the pain is perceived according to thecervical height affected. When patients are asked about it,the various answers obtained do not depend on the respon-sible cervical level.

If the patients are examined, we learn that pressure onthe cervical point of the back and on it alone alwaysreproduces their pain, even if they have the impression offeeling it higher or lower. In numerous cases of cervicalradiculopathy due to C6, C7, or C8 that we have examined,we have always found the cervical point of the back atthe same place, para-T5 or para-T6, whatever the respon-sible level. We have made the same observation in casesof lower cervical PMID without radicular pain syndromes.

Cloward did not note the existence of this point, thereal epicenter of the thoracic pain, nor the existence of theadjacent cellulalgic zone. Therefore, the pathologic expla-nations that he proposed must be reconsidered.

Pathogenic Mechanism: A Personal Hypothesis

To analyze the mechanism of thoracic pain of cervicalorigin, it is first necessary to know to what the cervicalpoint of the back, para-T5 or T6, and the cellulalgic zoneassociated with it correspond. That is what we have firsttried to establish.

Posterior Primary Rami of the Second Thoracic Nerve Root

The anterior primary rami of C5–T1 constitute the bra-chial plexus. Their cutaneous branches innervate the skinof the upper limb. But the posterior primary rami of C6,C7, and C8, like the rami of L4 and L5, have no cutaneousbranches. The posterior ramus of C5 and T1 is inconsistentand small when it exists (in 25% of cases, according toLazorthes).

If, as everything seems to point clinically, the cervicalpoint of the back and the adjacent cellulalgic zone showthe distress of the inferior cervical spine, the questionremains about what link might exist between the cervicaland thoracic spinal regions. The cervical point of the backseems to correspond to the superficial emergence of thecutaneous branch of the posterior primary ramus of thesecond thoracic spinal nerve root (Maigne, 1966). Indeed,if this ramus, when it goes around the facet joints T2–3,is injected with 1 mL of 1% lidocaine, it produces tem-porary disappearance of the:

• Spontaneous pain of the patient, which is marked inthe acute case

• Cervical point of the back• Adjacent cellulalgic zone that becomes flexible and

painless on pinch-rolling

According to Hovelacque, the size and location of theposterior ramus of T2 are important. The branch extends upto the acromion, covering a large surface (Fig. 36.9). Themaps of the posterior dermatomes commonly accepted bymost authors are presented schematically in two ways:

Some, like Keegan and Garret, attribute an equal hor-izontal band to each of the dermatomes from C4 to T3.According to them, this is why C4, C5, and C6 cover thesuprascapular fossa, and T1 and T2 are noticeably at thelevel of the fifth and sixth (Fig. 36.10). Others, like Tön-dury or Brugger, pass directly from the dermatome of C4to the dermatome of T2 — as for the anterior dermatomes.Lazorthes attributes a small paramedian zone betweenthese two territories to C5 and C6 (Fig. 36.10).

No author accords a particularly extended territory to theposterior dermatome of T2. However, according to our clin-ical results, we should consider the existence below C4 ofa large common territory representing C5, C6, C7, C8, T1,and T2. This territory corresponds well to the one of the

264

SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

posterior primary rami of T2 as described by Hovelacqueand as we have found it on a few dissections. The posteriorprimary rami of that level present, in the first part of theirpath, some usual anastomoses with their neighbors (Hovel-acque, Nirayana). It is as if the cutaneous ramus of T2 (andmaybe also of T3) incorporated the complement of inferiorcervical and cutaneous branches that were missing.

This hypothesis provides a satisfactory framework forunderstanding the clinical phenomena and our anatomicobservations. The cervical point of the back and the adja-cent cutaneous zone are the favored sites of pain referralfrom the inferior cervical spine, whatever their nature —benign or malignant, disk or facet joint (Fig. 36.11).

A Few Particular Cases

The interscapular dorsalgia that we have describedaffects women more often than men. Usually, it presentsas a tenacious postural thoracic pain, more or less distress-ing, without any particular radiographic signs, but thereare more disconcerting cases. The three cases below dem-onstrate the variety of conditions in which this cervicalthoracic pain can be seen. The first two teach us that weshould not rush to attribute a thoracic pain to a severescoliosis or a severe epiphysitis. The third demonstratesthe errors to which misdiagnosis of this interscapular tho-racic pain of cervical origin can lead.

Figure 36.9

The cutaneous branches of the posterior primary rami.

Right:

after Hovelacque, note the stress placed on thecutaneous branch of T2, but he acknowledges the presence of cutaneous branches for C5, C6, C7, and T1.

Left:

for mostanatomists, C6 and C7 are not felt to have cutaneous branches. C5 and T1 are noted to have one in four cases (Lazorthes).Our dissections confirm the significant presence of the cutaneous branch of T2. The cutaneous branch of C4 assures theinnervation of the whole region and the supraspinous fossa. This diagram is closer to our clinical experience.

Figure 36.10

Posterior dermatomes.

a.

According to Keegan and Garret.

b.

According to Lazorthes.

c.

According to Töndury.(The arrow was added by Dr. Maigne to demonstrate what has been verified.)

CHAPTER 36 CHRONIC THORACIC PAIN

265

Case History 1

— M.D., a 39-year old secretary seenfor the first time at the age of 22 was referred to us bythe Orthopedic Department because of severe thoracicpain attributed to severe Scheuermann’s disease,affecting particularly the fourth, fifth, sixth, and sevenththoracic vertebrae, the site of the spontaneous pain. Shecould not write or type for more than 1 hr. Numeroustreatments such as massage, therapeutic exercise, andthoracolumbar orthoses tried over many years hadchanged nothing, and the pain had become so over-whelming that the orthopedic surgeon treating herdecided to perform a fusion. A consultation wasrequested at the Rheumatology Department and the con-clusion was the same. Examination revealed a left para-T6 interscapular point showing extreme sensitivity andan adjacent and very thickened cellulalgic zone. Exam-ination of the neck revealed a C7–8 PMID with anipsilateral tender facet joint at that level. There was ananterior cervical doorbell point reproducing the thoracicpain. The cervical radiographs were normal. Four cer-vical manipulations, one per week, improved the patientenough to allow her to resume her work immediately. Amaintenance treatment was performed every 3 mo for1 yr. Since that first treatment, 17 years ago, she hadthree children and never interrupted her work as asecretary. From time to time, she feels a vague point inthe back when she is fatigued or has overworked herself.

Case History 2

— M.C.V., a 27-year old secretary,presented with a severe thoracolumbar scoliosis at 48°and had been seen regularly in a specialized depart-ment since the age of 13. She never had pain. In the2 yr before we saw her, she developed thoracic painsthat became more and more unbearable and had inter-rupted her work for the last 6 mo. The beginning of thepains coincided with a change in her work, which,

interestingly, she preferred to her prior job. She had twoseries of massage and physical therapy treatments thatwere performed without success for 10 mo. The painwas most severe at the apex of the thoracic curvaturenear T7. After several consultations with the Departmentsof Orthopedics and Rheumatology, it was decided totry a fusion. It was then that she was seen in ourdepartment for consultation. She described her pain as“in the two sides,” “throughout her entire back.” Exam-ination uncovered an interscapular point, para-T6 on theright that responded to applied pressure by recreatingall her pains. Also uncovered was a significant adjacentcellulalgic zone. The cervical spine was radiologicallynormal. The segmental examination revealed a typicalC5–6 PMID with right facet joint pain. No anteriordoorbell point was found. After the first cervical manip-ulation, she was very much relieved; after four sessions,she felt well and went back to work. In the new job,she repeatedly performed cervical rotation to the rightand took, for example, some documents behind her, tothe right, which she did by mechanically stretching herarm toward the back. This repeated maneuver resultedin a decompensation of the cervical PMID, which wasperfectly tolerated up to then. She modified her placeof work and now works without any inconvenience. Thepain has not recurred for the past 2 yr.

Most of the patients who present with this interscapularpain feel it moderately and intermittently. That pain issometimes distressing, but it rarely has the hyperalgic anddurable character of the pain seen in the next case.

Case History 3

— M.P., a 57-year old patient, had alobectomy for a massive pulmonary infarct. The day afterthe intervention, he complained about a thoracic painon the side of the intervention. The surgery went withoutcomplication, and the result was excellent. But the tho-racic pain persisted, preventing sleep, and being refrac-tory to any treatment to the point that after 2 yr, arhizotomy at T3–4–5 was performed. The failure wastotal. A few months later, because of the refractory pain,the pulmonologist, neurologist, and neurosurgeonagreed on a chordotomy. At that time, the patient con-sulted us at Hotel Dieu. Thoracic examination uncoveredan acutely painful point, para-T5, on the side of thescar. A slight pressure on it and only on it reproducedthe usual pain. As the patient said, it was the first timein 5 yr that that point was found and his pain wasreproduced. A large band of cellulalgia adjacent to thatpoint extended up to the acromion. The cervical exam-ination demonstrated, besides some limitation in rotationand lateroflexion on the side of the pain, a relativelyacute pain of the ipsilateral C5–6 facet joint. Thoracicand cervical radiographic studies revealed a minordegree of spondylosis. Cervical manipulation wasbegun. At the first session, in a spectacular manner, thethoracic pain disappeared, and the cervical movementsbecame free and painless. The para-T5 point becamehardly sensitive to firm pressure. The cellulalgia wasmore supple and hardly painful. After a second session

Figure 36.11

The cervical point of the back (Maigne). Thisis a reflection of a dysfunction of the inferior cervical spinethat may be due to either disk or facet disorders. It can bebenign or malignant and corresponds to the emergence ofthe posterior primary rami of T2.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

1 wk later, the patient was without pain for a year, untilthe day he lifted a heavy weight and the thoracic painreturned, disappearing again after two cervicalmanipulations.

Treatment

The treatment of interscapular pain of cervical originis essentially cervical. If it is due to PMID, the most frequentcause, cervical manipulation is the treatment of choice whenthe state of the spine allows it and when it is technicallypossible. It is preceded by progressive mobilization.

It should be precise, soft, strictly unilateral, and per-formed according to the rule of no pain and oppositemovement. Generally, the most useful maneuvers are rota-tion with the patient in supine, lateroflexion with thepatient in lateral decubitus, and the chin pivot with thepatient in prone position (Fig. 36.12 through Fig. 36.14).

Manipulation can, if necessary, be replaced or supple-mented by a facet joint injection designed for painfulcervical articulation uncovered by the segmental exami-nation of C5–6, C6–7, or C8–T1. On the side of thethoracic painful point, 0.5 mL of a corticosteroid deriva-tive is injected (Fig. 36.15; see “Facet Joint Injections” inChapter 26); the treatment is repeated two or three times.Cervical electrotherapy (pulsed short waves) can be usefulwhen the two preceding treatments cannot be used. Inacute synovitis, anti-inflammatory medications can beuseful.

In patients who have more pain in the morning, thereason is often postural malpositioning of the neck duringsleep (sleeping on the abdomen). A cervical collar or(sometimes better tolerated) a collar made of a thick towelfolded with a soft cardboard inside worn during the nightfor 3 to 4 wk can often bring relief. In chronic cases, it issometimes necessary to treat the residual cellulalgicmanifestations and more rarely the taut muscle bands.

Massage.

If the cellulalgic zone does not disappearcompletely with cervical treatment, massage using apinch-roll or kneading technique performed superficiallyis often quite useful. This treatment is often quite painful,and it is better to try it after an anesthetic injection eitheron the posterior ramus of T2 or directly on the subcuta-neous tissues. This injection is followed immediately bykneading maneuvers.

Psychologic Factors

Depressive or simply neurotic factors frequently exag-gerate thoracic pain. In these patients, the signs of spas-mophilia (Chvostek’s sign, electromyogram) are oftenpresent. Suitable treatment of these cases starts with anattempt to reduce the muscular hypersensitivity producinga PMID that other subjects would tolerate perfectly or notfeel at all. Relaxation can be a useful adjuvant in thesecases.

Figure 36.12

through

Figure 36.14

Examples of manipula-tive techniques used in the treatment of intrascapular pain ofcervical origin (all performed according to the rule of no painand free movement).

CHAPTER 36 CHRONIC THORACIC PAIN

267

Psychologic Disorders.

In depressed or very anx-ious patients with typical clinical pictures of a thoracicpain of cervical origin, a brief cervical treatment shouldbe performed and its effect judged. If the result is neithergood nor rapid, it is better not to insist. It is imperative totreat the psychologic state.

Physical Modalities

Physical modalities should not ignore the cervical originof thoracic pain because doing so may cause the thoracicpain to persist or aggravate it. Modalities will bring relief tothe patient only if the therapist pays particular attention tomassaging the cellulalgic zone that persists after the acuteepisodes. Used after cervical treatment, it can be a double-edged sword, helping in some cases and causing acute de-compensation of the patient in others through a sudden orforceful movement. All cases must be individualized.

We reserve modalities for recurrent cases. Rememberthat this is a cervicothoracic disorder, not a thoracic one,and often it is associated with postural problems. It isnecessary to have a very competent physical therapist.Swimming for relaxation is often useful (breast strokewith snorkel to allow swimming without raising the heador swimming on the back or side).

Prevention

Prevention is essential in the management of these dis-orders. Patients must be taught to avoid extreme neckrotation (as in backing a car, sleeping in the prone position,etc.), especially on the side of the cervical articular point(placing something behind the back, with retropulsion ofthe arm, especially when seated; closing the back door ofa car while sitting in front; putting or taking somethingfrom the back seat, or taking maps from behind without

getting up; seats that are too low and too soft that inducecervical fatigue resulting in thoracic pain). It is indispens-able to study the postural issues of the work environment.

THORACIC PAIN OF THORACIC ORIGIN

Thoracic pain of thoracic origin is less frequent than ispain of cervical origin. Its principal origins are PMID, acuteinflammatory arthritis, and muscular causes (i.e., myalgiccords, trigger points). At the midthoracic level, there arefrequent causes of error in the segmental examination due to:

• Frequent cellulalgic edema of the subcutaneous tis-sues of the midback region that yields false positivesduring searches for segmental tenderness to trans-verse pressure against the spinous process or forfacet joint tenderness (see Section IV, p. 132).

• The fact that the superficial emergence of the cuta-neous branch of the posterior ramus of T2 occurs 2cm lateral of the median line, and corresponds tothe level of the facet joints of T5–6 (Fig. 36.5; seeSection VI, p. 261).

Thoracic Pain Due to Thoracic PMID

Thoracic pain due to thoracic PMID is the consequenceof forceful activity, forced movement, trauma, or poorposture. The pain produced by PMID is generally felt atthe level of the cellulalgic zone that is induced in thecutaneous territory of the corresponding posterior ramus.It is low thoracic for a T6 or T7 PMID and midthoracicfor a T3 or T4 PMID.

Treatment

Manipulation is the logical treatment, respecting theusual rules. But it often involves stiff spines, so the manip-ulation should be prepared or replaced by flexible mobi-lizations and performed progressively. Massage results inparaspinal muscular relaxation and can treat the cellulalgiczones that do not always disappear completely with treat-ment of the responsible PMID.

Thoracic Pain of Discogenic Origin

Benign thoracic pain has always puzzled clinicians, asmost radiographic evaluations offer no explanation. Thisdoes not surprise us; we consider this pain to be of cervicalorigin in the great majority of cases.

Nevertheless, Bruckner et al. (1989) incriminated diskdeterioration that was detected by MRI. Of ten patients withthat kind of pain, nine had isolated disk deterioration, whilein a control series of 15 patients, Bruckner found such dete-rioration only twice. Only in four cases did the disk lesioncorrespond exactly to the clinically painful spinal segment,and in five cases, there was no coincidence.

Figure 36.15

Injection of a painful cervical facet joint cansometimes replace manipulation or contribute to its effect.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Because of the benign nature of the degenerativelesions at the thoracic level, confirmation of this etiologywill need more demonstrative studies involving morepatients. It seems to us that the segment found to bepathologic on MRI scan must be painful on segmentalexamination.

Thoracic Pain Due to Thoracic Arthrosis

Thoracic arthrosis is very common and is painful onlyoccasionally. Most commonly encountered pain com-plaints involving the thoracic region are of cervical origin.When evaluating someone with what is thought to bethoracic arthrosis, it is best to first make certain that thepain does not have a neurologic or visceral origin or resultfrom other conditions such as malignant illness in an olderpatient, spondyloarthropathy in the young, and discitis inall ages.

Treatment

In painful acute synovitis, anti-inflammatory medicationsare usually useful. If the patient has gastric intolerance tothese medications, electrotherapy can be very useful.

Thoracic Pain and Scheuermann’s Disease

Growth apophysitis is rarely painful at onset duringadolescence. The later episodic painful attacks are oftenrelieved by rest and anti-inflammatory medications. Raresevere forms require wearing a thoracolumbar orthosis.

In the adult, the sequelae of Scheuermann’s disease aresometimes responsible for the thoracic pain, especiallywhen some arthritic lesions fostered by dystrophic alter-ations are present, but they are rarely the cause. Moreoften, pain in these cases is referred pain of cervical origin.

In patients with stiff and round backs, dysfunction ofthe cervicothoracic junction is frequently seen. Becauseit is necessary to keep the head horizontal, the subjectstraightens the neck. The inferior cervical articulations aresubject to increased loading and may cause PMIDs, whichfacilitate a facet joint spondylosis with inflammatoryattacks causing thoracic pain.

Thoracic Pain and Osteoporosis

Osteoporosis after menopause affects one woman infour. It is not painful, but when advanced, it produces suchspinal fragility that even a minor trauma can produce acompression fracture that appears to have no apparentcause, producing thoracic pain that starts abruptly, with athoracolumbar localization. The pain can be severe, con-stant, and increased by coughing, defecation, or move-ment. It can also be moderate to the degree that the patientdoes not recall an acute onset but rather notes a progressivepain that becomes chronic and is relieved by rest andincreased by activity. Diagnosis is made by radiographic

demonstration of the vertebral wedging, which does notalways affect the posterior wall.

Thoracic Pain and Interspinous Ligaments

Examination sometimes reveals an acute pain affectingonly the interspinous ligaments of one or two levels. Oftenthis is post-traumatic. Relief and proof of the origin aregenerally brought by injection of 0.5% lidocaine with acorticosteroid derivative.

CHRONIC THORACIC PAIN OF MUSCULAR ORIGIN

Some muscles can be responsible for thoracic pain,such as the scalenus, trapezius, rhomboideus, iliocostalis,levator scapula, and serratus anterior. The muscle may notseem painful to the patient, but its thorough palpation(Fig. 36.16) reveals a firm taut band with a trigger pointthat under pressure reproduces the usual pain. These trig-ger points can be part of a spinal cellulotenoperiosteomy-algic syndrome or be a direct result of muscle fatiguebecause of excessive use or an incorrect position.

When the levator scapulae is affected, it can causeeither a low cervical or high thoracic pain. When therhomboideus is affected, the pain is in the interscapularregion. If the iliocostal muscle is affected, there is a verydistinct picture of a subacute pain simulating a tenaciouspleuropulmonary or one that recurs. The responsible trig-ger point can be as big as a match, localized most oftenat the level of the seventh, eighth, or ninth, 8 to 10 cmlateral to the midline. Fatigue and muscle cooling are theusual causes of the painful trigger points. In some cases,the pain is acute (see next chapter); the responsible causeis more rarely found in the paraspinal muscles.

Treatment

Treatment consists of injections of the cord with 1%lidocaine. Ultrasound therapy can also be quite useful.

Figure 36.16

Evaluation for trigger points in the examinationof the back.

269

37

ACUTE THORACIC PAIN

Just like chronic thoracic pain, common acute thoracicpain can be of cervical, thoracic, or muscular origin.

ACUTE INTERSCAPULAR THORACIC PAIN OF CERVICAL ORIGIN

Acute thoracic pain most often takes the form of acuteinterscapular pain of cervical origin (Maigne). See “Inter-scapular Pain of Low Cervical Origin (Maigne)” in Chap-ter 36. It has the same signs as chronic thoracic pain. Itcan be the first manifestation of cervicobrachial neuralgia,which will occur a few days later, or can remain isolated.

On examination, at T5 or T6, one finger breadth lateralof the midline, is the cervical point of the back. Exami-nation of the cervical spine will reveal the responsiblesegment: C5–6, C6–7, or C7–Tl. Usually, it is a cervicalmechanical pain (disk herniation or acute spinal disorder)or facet inflammation. Very rarely, pain can be due to aspinal cord tumor, visceral tumor, or other intramedullarylesion.

Treatment

Cervical immobilization with a collar or Minerva is thebest means to relieve the thoracic pain. Cervical manipu-lation is rarely possible. If it is, it can bring spectacularrelief. A facet injection is useful in case of an acute PMIDor facet joint inflammation. Injection of the posteriorramus of T2 at its emergence between T2 and T3 cansometimes decrease the acute pain.

ACUTE THORACIC PAIN OF THORACIC ORIGIN

In the back, there can be an acute painful manifestationsimilar to torticollis (wryneck) or a lumbar pain. It usuallyresults from forceful activity or a wrong movement. deSéze called it a “dorsalgia,” emphasizing the similaritywith low back pain and its discogenic origin. This is evi-

dently possible, but the extreme rarity of thoracic disco-genic disorders is well known. This type of manifestation,which we have encountered rarely, generally concerns thelower or midthoracic segments (T6–9), and it seems to usto be an example of an acute PMID or thoracic sprain.

Treatment

If a manipulation performed according to the principleof no pain and opposite movement is possible, it can bringrelief. Anti-inflammatories, analgesics, and muscle relax-ants are useful.

ACUTE THORACIC PAIN DUE TO DISK CALCIFICATION

Acute lower thoracic pain with associated inflamma-tion and fever has been observed in women over 40 yearsof age and has been attributed to calcification of the annu-lus fibrosis. These patients often have a history of similarepisodes in the recent or remote past. Anti-inflammatorytreatment is useful.

ACUTE THORACIC PAIN OF MUSCULAR ORIGIN

In general, acute thoracic pain of muscular origin isdue to a trigger point of a muscle that has been activatedby cold, fatigue, or wrong movement. The pain is sharp,often poorly localized by the patient. Palpation of the tautbands of the trigger point, often difficult to find, repro-duces the pain and can increase it. Relief can be obtainedwith injection of a few milliliters of 0.5% lidocaine at thatpoint.

The levator scapulae and the iliocostalis muscles aremost often affected. The levator scapula produces the painof a low torticollis with acute referral to the upper limb.However, the pain may remain high thoracic (see Chapter51, “Levator Scapulae Syndrome”). The iliocostalis

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sometimes reveals one or two trigger points in cases ofthoracic pain of cervical origin, but they can exist in anisolated form also (postural fatigue). They can be thesource of very acute pain, either fixed, simulating pleuriticpain and increased by deep respiration, or occurring withsharp and sudden releases produced by deep breathing andsometimes spontaneously.

Although we did not yet know of the muscular origin,we had already described this form in an earlier bookunder the name of

Acute Thoracic Pain and LightningPains.

The observation in the first patient in whom wenoted is reproduced here as it is quite typical of thiscondition:

Case History

— M.C., a 45-year old male, felt a violentpinching in the lower thoracic region 3 days earlier,while slipping his arm in the sleeve of his vest. Thispinching lasted a few minutes, then decreased, as longas he did not move at all, breathing as softly as possiblebecause deep inspiration and expiration caused violentlightning pains. A few minutes later, he felt relieved andagain started his normal movements when suddenly asimilar attack immobilized him. From then on, he noteda succession of calm periods followed by acute attackslasting a few seconds to a few minutes and producedby movements or positions that varied from one momentto the next.

On examination, the spine was flexible and analyticexamination of the movements did not show any limita-tion, pain, or segmental dysfunction. During the exami-nation, an unforeseen gesture produced an attack, butthere was no systematization in the movement that pro-duced it. A movement performed earlier without painwould suddenly, a few minutes later, spark an acuteattack. Often, deep inspiration would trigger it. Radio-graphs obtained the same day as the attack showedno abnormality. There was relief or exacerbation bydifferent maneuvers of mobilization or manipulation thatcould be tried in this case.

An intramuscular injection of 8 mg of thiocolchicosideproduced quick relief (muscle relaxation). This patienthad three similar attacks in 4 yr. No radiologic or clinicalsign had been uncovered during the attacks. Knowingbetter after the first attack, the other two were treatedby intravenous injections of thiocolchicoside as soon aspossible, and relief came quickly, on the first day forone and on the second day for the other.

A few years later, he had a fourth similar attack forwhich he received a different treatment. In the meantime,we had observed similar cases, and a thorough exam-ination of the muscles of the back revealed that thetrigger points of the iliocostalis muscle were responsible.Local anesthetic injection of one or more trigger pointsbrought some relief immediately. He was advised torefrain from exposing his back to the cold.

271

38

COSTAL SPRAINS

Costal sprains often present with features of thoracicor lumbar pain. They may occur after local trauma, force-ful activity, or faulty movement. On examination, no ten-der spinal point is found. The tenderness to palpation islocalized to only one rib, while the adjacent ribs or theribs from the opposite side are painless. Pressure producesor increases the spontaneous pain.

Costal sprains usually resolve in a few days. Occa-sionally, these sprains become chronic, resulting inchronic pain that can lead to diagnostic errors, especiallywhen the false ribs are involved, as is most frequently thecase.

CLINICAL PRESENTATION

Costal sprains can be seen in different conditions.

Faulty Movement or Forceful Effort

In most cases, sprains from faulty movement or force-ful effort result from abnormal rotation, sometimes veryslight, as may occur in making a bed, turning back to closethe back door of a car, at the start of a 100-m dash, etc.In other cases, the condition can be produced by a violentmuscular contraction during heavy lifting or sneezing.

Direct Trauma

A thoracic contusion due to a fall can cause a posteriorsprain or an anterior chondrocostal sprain. It can also beassociated with a vertebral or costal fracture. Occasionalpain persisting after fracture of a rib is due to residualcostal or vertebral sprain, often relieved by manipulation.

CLINICAL PICTURE

Sprains due to a faulty movement most often affect thefalse ribs. During a quick rotation of the trunk, the patientfeels a pain like “a stab with a knife” in the side and bendsforward and lies down immediately.

In a few hours or days, the pain decreases and disap-pears. It can persist longer, with pain on awakening aftera forceful or strenuous movement of the trunk or cough-ing. These episodes become more annoying over time andlose their clear producing cause.

Most of these patients ultimately undergo renal evalu-ations. One of our patients had 5 violent attacks in 4 years.He was hospitalized three times and had five intravenouspyelograms, all negative. He had a sprain of the last riband was relieved after the first treatment. Several otherpatients in our series had various interventions (appendec-tomy, renal surgery). Others were diagnosed and treatedfor lumbar pain and massages. Physical therapy treatmentsprescribed for these patients regularly aggravated theirpain.

DIAGNOSIS

Posterior Costal Sprains

Posterior costal sprains are the most frequent. Pressureor percussion on the affected rib can be painful. The mostsensitive test for this condition is the “rib maneuver”(Maigne). The patient is seated with the physician stand-ing behind. The patient is asked to laterally flex the trunkto the side opposite the pain, with the hand on the painfulside resting on the head. With the pad of the thumb, theexaminer grasps the superior edge of the painful rib andpushes it downward (Fig. 38.1B); then, grasping the infe-rior edge with the pads of the fingers, pushes it upward(Fig. 38.1). In costal sprains, one of these maneuversincreases the pain, while the other is painless. This signis rather characteristic of this disorder; indeed, in costalfractures, both maneuvers are painful. Conversely, they donot modify the pain if it is due to a radicular irritation ofspinal origin or if its origin is muscular or visceral. Insome renal or pleuropulmonary disorders, there are painsin the last ribs, and in some hepatic disorders, pain is feltat the level of the last right rib.

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In certain obese patients, it can be difficult to grasp therib fully. Lateroflexion of the patient’s trunk contralateralto the painful side should be exaggerated to free it. Theintegrity of the rib and the adjacent spine is confirmed byradiography. For the middle ribs, examinations can beperformed on patients lying on their sides.

N.B.

During the examination, the subcutaneous tissues that arepainful and cellulitic should not be pinched between the opera-tor’s finger and the rib; they should be examined first by thepinch-roll test.

Anterior Costal Sprains

There can also exist chondrocostal “sprains” localizedto the chondrocostal junction, resulting from trauma orfaulty movement. They are sometimes confused withTietze’s syndrome.

Manipulation usually provides good results. The prin-ciple of the examination is the same. The patient is supineand the operator, with thumbs opposed end to end, graspsthe upper edge of the rib and pushes it downward(Fig. 38.2 and Fig. 38.3), then grasps the inferior edge ofthe rib and pushes it upward (Fig. 38.4 and Fig. 38.5).

IS IT REALLY A SPRAIN?

The term

sprain

is probably not quite perfect, but itseems difficult to call it a “subluxation,” which is what

the clinical context brings to mind in the absence of anyradiologic proof. Where does this sprain occur? For thefalse ribs, there can be no question. As for the other ribs,we can think of two types of sprains: those at the costo-vertebral joint and those at the costotransverse joint. Ineach case, one joint would act as the fixed point while theother acts as a mobile point. Such mechanisms do notseem likely on anatomic grounds.

TREATMENT

If well performed, manipulation is remarkably helpful,but it is not always easy. The useful maneuver consists inprogressive exaggeration of the movement to be examinedin the pain-free direction, using the respiratory move-ments. The result is often instantaneous. Three to foursessions are sometimes necessary. Injection of the costo-vertebral joint is difficult, even with fluoroscopic guid-ance. Manipulative techniques are described in Chapter68, “Rib Techniques.”

“HOOKED RIB”

When the costal covering of the inferior ribs (from the7th to the 10th) becomes hypermobile occasionally, flex-ion or torsion of the trunk can result in pinching or hook-ing of a rib onto the cartilage of the superior rib, whichcreates a painful and palpable notch or indentation. Ingeneral, this hypermobility is post-traumatic; however, thetrauma can be forgotten or old (E. F. Cyriax). This dys-function can cause tenacious chronic abdominal pains. Asalarming as these pains are, they can be present for manyyears before the diagnosis is made.

One of our patients had such a syndrome for 8 years,with many examinations and hospitalizations. Paininvolved the posterior region on the left abdomen, radiat-ing toward the rear, with occasional nausea. On palpationof the edge of the last ribs, there was a painful point anda small notch.

Passive mobilization of the rib that hooked elicited arecurrence of the usual pain. A local injection of an anes-thetic brought temporary relief. A few injections oflidocaine with a corticosteroid derivative decreased thepain significantly, but not completely. The acute pain wasproduced by certain movements leading to a slight flexionof the trunk forward with rotation. The treatment shouldhave been a resection of the costal end of 6 to 7 cm, butthe patient, reassured about the cause of the pain, refusedthe intervention.

Figure 38.1

Technique for evaluation of the lower rib.

A.

Therib is grasped by the fingertips and pulled upward.

B.

Thenthe rib is pushed downward with the pad of the thumb.

CHAPTER 38 COSTAL SPRAINS

273

Figure 38.2

through

Figure 38.5

Examination of anterior rib sprain. The patient is supine. The examiner applies pressureagainst the superior border of the rib in a caudal direction (Fig. 38.2 and Fig. 38.3). The reverse is then performed. Pressureis applied to the anterior border in a cephalic direction (Fig. 38.4 and Fig. 38.5).

Figure 38.2

Figure 38.3

Figure 38.4

Figure 38.5

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39

CHRONIC LOW BACK PAIN

Chronic low back pain is the most frequent reason forconsultation regarding spinal pathology. In France, lowback pain problems constitute 5% of the total budget ofthe Assurance Maladie (health insurance) and are a leadingcause of absenteeism from the workplace. Different inter-national statistics indicate that low back pain problems areresponsible for a loss of 1% of working days.

Common low back pain has always been thought to beconnected with lesions, usually discogenic, of the inferiorlumbar spine (L4–5, L5–S1). We have shown that somehave their origins higher, at the thoracolumbar junction(T11–12, T12–Ll) (Maigne, 1972). Strangely enough, thepain is never felt at that thoracic level but lower, in thelower lumbar, sacroiliac, or gluteal region, just as in lowback pain of lumbosacral origin (L4–5, L5–S1), withwhich it has always been confused and which only athorough examination can differentiate.

Before describing the different types of low back painof lumbar or lumbosacral origin, we will discuss the prin-cipal causes of low back pain with an origin above thelumbar spine, with which it is sometimes confused. Mis-takes are numerous and need a thorough examination.

The radiologic examination is important for this diag-nosis as are the results of laboratory tests because manycauses of low back pain are not included in the commonpain syndromes (see p. 281). There is also the possibilityof low back pain of visceral origin, usually of ovarian oruterine pathology in young women and of renal, gas-trointestinal, or vascular (aortic aneurysm) origin in eithersex. Furthermore, low back pain syndromes are frequentlyassociated with significant psychogenic components.

EXAMINATION OF PATIENT WITH LOW BACK PAIN

The examination starts as soon as the patient enters theroom. The gait is assessed, as are the static and dynamicpostures, including the ease with which the patient

changes from sitting to lying. The pre-examination inspec-tion can provide a great deal of information.

Clinical History

It is better to listen to the patient initially, and then askquestions. The history should inquire about:

• The location of the pain and its referral pattern• The time course of the current episode• Any precipitating factors related to the patient’s

spine or general health• Whether the pain is improved or worsened with

movement, cough, straining, or sneezing• The effect of posture on the pain (e.g., better or

worse with standing, lying down, sitting, stooping)• Whether the current episode is improving, worsen-

ing, or plateauing• Whether the present pain has had a significant effect

on the activities of daily living including occupa-tional and leisure activities?

• Whether there have been any previous episodes oflow back pain, with or without sciatica, how longthey lasted, the treatments given, and their results

The patient’s spontaneous expression in the beginningand the manner of answering the various questions can beof great help in drawing a psychologic profile.

Physical Examination

The physical examination is performed with the patientnaked or wearing undergarments. Note is made of thepatient’s physique — obese, slim, muscular, etc. The pres-ence of an antalgic attitude or asymmetry of the spine,pelvis, or lower limbs is also noted.

Active Range of Motion Assessment

The patient is standing with legs extended and feet 20cm apart. The legs should remain extended at the kneeduring the entire examination.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Forward Flexion

The patient is asked to bend forward at the waste,maintaining the knees in extension. The lumbar lordosisshould reverse completely by end flexion; its persistenceindicates lumbar segmental stiffness. Following reversalof the lordosis, flexion continues at the hips, consistentwith a normal lumbopelvic rhythm. The degree of lumbarsegmental flexibility is readily assessed by Schober’s test(Fig. 21.52), which may remain unchanged even after atreatment that has relieved the patient completely. In addi-tion to both the quality and quantity of motion, it is impor-tant to observe the point in the arc of motion at whichpain is reported (distance from fingers to floor; Fig. 39.1).

Hamstring Muscle Tightness.

Stiffness on forwardflexion can be due to spinal stiffness or hamstring inflex-ibility, frequently seen in patients with low back pain. Itcan be measured in a simple way: with the patient stand-ing, then in forward flexion, the distance between theposterosuperior iliac spine and the popliteal line is mea-sured. A change of less than 5 cm between the twoextremes is evidence of subpelvic stiffness.

Using an intriguing device called a rachiometer (spi-nometer), Badelon showed that in a normal subject, during

Figure 39.1

Examination performed with the subject stand-ing and in forward flexion. One should note the stiffness, thelimitation of movement, and the point at which low back painappears. An approximate measure of this can be obtainedby measuring the distance between the fingertips and thefloor, with the individual flexed as much as possible.

Figure 39.2

Examination in standing and lateral flexed positions. In the standing position, one notes the presence or absenceof antalgic posture, any spinal stiffness, and the distance between the fingers and the floor on each side. One also examinesmovements that can produce the pain and when the pain appears.

CHAPTER 39 CHRONIC LOW BACK PAIN

277

anterior flexion of the trunk with the legs extended, thespine accounted for 47% of the range of motion, whilethe hips and pelvis accounted for 43%. He also noticedthat in 40% of children (12 years old), there was a signif-icant decrease in the amount of motion at the hips, whichhe attributed to the greater degree of hamstring inflexibil-ity in this population. He followed these youngsters for afew years and noted a much higher proportion of low backpain problems in those with poor hamstring flexibility thanin those with good flexibility. This has important obviousimplications in the prevention of low back pain in suscep-tible subjects.

Primary and Secondary Stiffness.

Is the lack ofhamstring flexibility primary, linked to static problems ofthe lower limb, or is it of reflex spinal origin, due to spinalproblems that are still painless? The “muscle spasm” ofthe hamstrings may be its first manifestation. In youngsubjects with stiff hamstring muscles, we have noted tho-racolumbar PMIDs (T12 to L1) and lumbosacral PMIDsproducing no low back pain yet; and often, by manipula-tion of the affected region, we could briefly eliminate thestiffness of the hamstrings.

Extension

The patient is asked to lean backward. The examinernotes whether this is possible as well as whether the lum-bar lordosis increases smoothly and normally and whetherthe movement is painful or not.

Lateroflexion

The patient is asked to bend to either side, alternately,with the legs extended at the knee and slightly apart, andslide the hand along the lateral thigh to the knee. The spineshould form a smooth C curve, with an ipsilateral concav-ity. Note is made of any signs of a “break” in the C curve

or a “bent stick deformity,” whether this break elicits pain,and where the hand stops in relation to the knee or thefloor (lateral distance, fingers to floor) (Fig. 39.2).

Rotation

With the patient standing, the pelvis is fixed by theoperator’s hands, and the patient is asked to rotate thetrunk to either side to test the range of motion. This tech-nique is very approximate. The study of rotation by pas-sive movements should be made with the patient sitting,or better, astride the end of a table, so that the pelvis isimmobilized (Fig. 39.3, left)

.

This is also an excellent posi-tion for testing extension (Fig. 39.3, right).

Functional Assessment

The patient is asked to perform some functional activitythat is difficult, such as putting on socks, turning over onthe table, or sitting on the table with the legs together.These maneuvers are sometimes more valid than the clas-sical tests for measuring the progress obtained with acertain treatment, particularly after injection or manipula-tion. They also provide the opportunity, by varying thetests in some cases, to find out whether a patient is malin-gering or (as accident victims do at times) exaggeratinghis or her condition.

Segmental Examination

The patient is in prone position across the table, witha cushion under the abdomen. Each vertebral level fromT9–L5 as well as the coccyx is thoroughly examined. First,a slow and insistent PA pressure is applied to the spinousprocess. Then facet joint tenderness is sought, as well aspain produced by transverse pressure against the spinousprocess. If the latter is positive, contralateral pressure is

Figure 39.3

One can best test rotation (

left

), lateral flexion, extension (

right

), and flexion for evaluation of stiffness with thepatient in the seated position, preferably astride the end of the examining table. The table should be narrow enough andcomfortable enough to accommodate this position. One should note any limitation or position in which pain is produced.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

applied to the supra- and subadjacent vertebral levels.Finally, interspinous ligament sensitivity is assessed tolocalize the painful levels (Fig. 39.4). The transverse pres-sure maneuver is usually positive in one direction only. Itis used to determine the rotational direction of manip-ulation, if this treatment is to be performed.

Palpation of Lower Ribs in Cases of Low Back Pain

The lower ribs should always be examined becauselower costal sprains can present with chronic unilaterallow back pain.

Examination of Subcutaneous Tissues

The subcutaneous tissues should be examined system-atically and meticulously with the pinch-roll method. Thewhole lumbar and superior gluteal region is explored. Ifthere is a zone of cellulalgia (thickened and painful skinfolds), the subcutaneous tissues of the corresponding ipsi-lateral inferior abdominal and trochanteric regions shouldbe examined (Fig. 39.5).

A diffuse regional cellulalgic infiltrate is usually oflittle interest. However, a localized zone of cellulalgia ina band-like distribution, especially when unilateral at the

inferior lumbar or superior gluteal level, most often sug-gests that a segment of the thoracolumbar junction is aprobable source and will require more investigation. Thisfinding is often noted in low back pain of thoracolumbarorigin (TL).

Occasionally, the thickening of the cutaneous and sub-cutaneous tissues is such that it looks like a screen overthe medial aspect of the thighs and so thickened that it isimpossible to grasp a skin fold between the thumb andindex finger. This special form of low back pain is dis-cussed below.

Examination of Muscles

Paraspinal Muscles

The paraspinal muscles are often tight and usually verytender to palpation (Fig. 39.6). They can also be the sites

Figure 39.4

Two maneuvers performed in the course of thesegmental examination, which should be performed from T8to L5. This examination evaluates the facet joint (

top

) andtransverse pressure against the spinous process (

bottom

).Note that the patient is lying on the chest across a table.

Figure 39.5

Examination of the subcutaneous tissues by thepinch-roll test should explore the entire back, from the lowerribs to the upper gluteal region.

Figure 39.6

The paraspinal, quadratus lumborum, and ilio-costal muscles should be attentively palpated when search-ing for trigger points that may eventually play a role in lowback pain.

CHAPTER 39 CHRONIC LOW BACK PAIN

279

of taut bands with or without trigger points that only asystematic and thorough palpation would find. If pressureon these trigger points (usually without the patient’sknowledge) reproduces the usual low back pain, then itprobably is of muscular origin.

These trigger points usually result from segmental dys-function at the level of their motor innervation, generallyat a level superior to their location, but they can also havea local origin (fatigue, physical efforts).

Muscles of Lumbar Fossa

The quadratus lumborum is sometimes the source ofone or two very painful trigger points (L1–2).

Muscles of External Iliac Fossa

The muscles of the external iliac fossa always havetrigger points (Maigne) in low back pain of low lumbaror lumbosacral (L4–5 or L5–S1) origin. They are oftenunilateral, even if the low back pain is more diffuse(Fig. 39.7 and Fig. 39.8).

Lasegue’s Sign

Lasegue’s sign is the classic sign of sciatica: radicularpain is produced or increased when the straightened legis elevated. It is normally negative in low back pain with-out dural irritation, but its presence can reveal the onsetof a moderate sciatica not noted by the patient.

This maneuver can also reveal stiffness of the ham-strings and produce or increase an isolated low back pain.Lasegue’s sign can be used to follow the evolution of thesciatica as well as the response to treatment. Mobility ofthe hips and knees should also be tested.

Neurologic Examination

The neurologic examination of the lower limbs willreveal whether there is a motor deficit, a disorder of sen-sitivity, or a change in the Achilles, medial hamstring, orpatellar tendon reflexes. This examination and the problemof low back pain itself must be analyzed in the context ofthe general clinical examination of the patient.

Radiographic Examination

Radiographs of the lumbosacral spine that include thepelvis and the thoracolumbar junction are necessary to ruleout serious pathology and to appreciate the state of the spine.CT imaging may be useful if spinal stenosis is suspected.

Discography, either as an isolated procedure or fol-lowed by CT, can reveal a disk lesion in refractory lowback pain. In general, CT and plain radiography are notvery helpful in benign low back pain because manypatients with disk and facet degeneration are asymptom-atic, while others with normal examinations can have anorganic low back pain. If there are radiologic lesions, theymust be correlated with the clinical and segmentalexaminations.

CONCLUSIONS OF CLINICAL EXAMINATION

At the end of the examination, which is complementedif necessary by laboratory and electrodiagnostic examina-tions, and after having ruled out the possibility of

low backpain of visceral origin

(uteroadnexitis, renal, gastrointes-tinal, vascular, as aorta aneurysm, etc.) or of psychiatricorigin, there can be either:

Figure 39.7

Muscles of the lateral iliac fossa are systemati-cally examined by deep palpation, which is performed per-pendicular to their fibers from the most lateral aspect to thesacrum.

Figure 39.8

Two main categories of low back pain can bedifferentiated: (

A

) low back pain of lumbosacral origin, asso-ciated with trigger points of the gluteal muscles, and (

B

) lowback pain of thoracic lumbar origin (Maigne) associated witha cellulalgia of the lumbar or superior gluteal region.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

•

Atypical low back pain

whose most frequent causesare ankylosing spondylitis, discitis with Koch’sbacillus or other organisms, compression fracture,metastatic lesion, or multiple myeloma with lowback pain as its first symptom; or

• C

ommon low back pain,

which can be – Low back pain linked to dysfunction of one of

the lower lumbar segments; in general, it is asso-ciated with unilateral or bilateral gluteal triggerpoints; we call it

lumbosacral lumbago

(LS)

– Low back pain linked to dysfunction of the seg-ments of the thoracolumbar junction is associatedwith pain on pinch-rolling and with a cellulalgicthickening of the subcutaneous tissues of the iliaccrest; we call it

low back pain of thoracolumbarorigin

(TL)– A form with the association of the two origins,

LS and TL:

mixed low back pain

– More rarely, low back pain of musculolig-amentous origin, cellulalgic edema, or sprain ofthe false ribs.

281

40

LOW BACK PAIN

OF LUMBOSACRAL ORIGIN

Disk lesions at L4–5 or L5–S1 are traditionally heldresponsible for low back pain. The role of the facet jointswas considered for a long time to be insignificant, but itseems now to be a major question. Certain authors considerligamentous or muscular origins to be possible sources ofpain, but most frequently, it seems that low back pain is theconsequence of

a painful minor intervertebral dysfunction

affecting one of the inferior lumbar segments.

LOW BACK PAIN DUE TO DISK LESIONS

For many years, the intervertebral disk was thought tobe the only source of low back pain, and very few authorsdisputed this exclusivity. Discovery of the discogenic ori-gin of sciatica, the role of the disk in spinal mechanics,its frequent involvement in pathology of the lower lumbarlevels, and other often repeated arguments have contrib-uted to diagnostic importance bestowed upon it. Thesearguments were as follows.

• Chronic low back pain often follows an episode ofacute low back pain, often considered to be an acci-dent of “blockage” during disk degeneration. It isoften associated with episodes of sciatica, the knownconsequence of a radicular impingement by a diskfragment.

• Chronic low back pain that develops in a patientwith no prior history of low back pain or sciaticahas the same characteristics as one whose disco-genic origin is proved by the association with lowback pain or sciatica.

• Patients who were operated on for refractory sciat-ica, in whom a herniated disk was found at surgery,suffered also from tenacious low back pain.

It is easy to counter these arguments with the mediocreresults of disk surgery as done up to now in cases of pure

low back pain. Some of the newer innovative techniquesmay change that. However, disk surgery that sufficientlyrelieves the radicular pain of patients with sciatica oftenleaves a persistent low back pain. Still, we must admit thateven if the disk does not play a direct role as has frequentlybeen asserted, its lesions result in dysfunction of themobile segment, including the posterior elements. Thus,both the facet joints and the interspinous ligament can besources of low back pain. Among the low back pain syn-dromes in which the disk plays a role are the following:

• Discogenic low back pain in which a disk lesionsuch as internal disk disruption is directly responsi-ble for pain; this is the true discogenic low backpain.

• Low back pain due to segmental instability causedby disk degeneration. This pain has different clinicalaspects and variable severity. The facet joints andpossibly the interspinous ligaments become sourcesof associated or isolated pain.

Discogenic Low Back Pain

In true discogenic low back pain, the discogenic lesionresults in irritation of the posterior superficial annularfibers and the posterior longitudinal ligament, the onlyelements of the region that are richly innervated(Fig. 40.1A).

Clinically, discogenic low back pain

is rarely isolated.The patient has episodes of acute low back pain or sciaticathat occur intermittently. The low back pain can be epi-sodic or somewhat permanent and is exacerbated bycoughing, sneezing, defecation, straining, and sudden ges-tures. Certain positions are not well tolerated or are impos-sible; according to Troisier, they are immediately painful,while other positions relieve them. These are the usualfeatures, but they are not specific to discogenic low backpain. On the other hand, epidural injection by thesacrococcygeal hiatus, which is inefficient in low back

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

pain of thoracolumbar or facet joint origin, usually bringsclear relief, even if it is only transient.

In refractory cases, CT or discography, or better, both,can visualize the discogenic lesion responsible for thepain; but many disk protrusions and herniations areasymptomatic and often ignored by the patient.

Low Back Pain Due to Segmental Instability following Disk Degeneration

Disk degeneration modifies the normal biomechanicsof the mobile segment and affects the facet joints, whichmay also start to deteriorate. Dysfunction of the posteriorelements then plays a significant role in the clinical courseof low back pain.

Farfan observed two mechanisms:

1. Initially, there is excessive axial loading whichresults in rupture of the cartilaginous endplateand intravertebral herniation. Then anteropos-terior translation results during extreme flexionor extension.

2. Secondarily, excessive rotation results in radialfissuring of the disk and increased facet jointpressure on one side, with a herniated disk onthe opposite side. This evolves toward aspondylolisthesis due to facet joint arthrosis,and a narrow canal. Often the facet joint dys-function is dominant.

This severe evolution is seen from time to time, butcases in which disk degeneration does not bring suchserious disorders are much more frequent. It is not uncom-mon to see an almost silent evolution, even if there issignificant radiologic evidence of disk degeneration andfacet joint arthrosis.

Usually the evolution is moderate, which can be diffi-cult for the patient and handicapping nevertheless, result-ing in low back pain in various positions and with exertion.Sometimes this evolution is completely silent, as demon-strated by Wiesel et al. They found significant discogenicor facet lesions in radiographic imaging studies, consistentwith those thought to produce low back pain syndromesin patients who never experienced pain.

Dupuis et al. describe the evolution of the degenerativeprocess in three successive phases.

1. Dysfunction, in which the initial lesion altersthe normal segmental biomechanics.

2. Instability, which results in excess and abnormalsegmental mobility.

3. Restabilization by fibrosis and osteophytes,which results in a decrease in intervertebralmovement.

During the instability phase, abnormal segmentalmobility occurs both in quantity and quality. This is bestappreciated by dynamic radiologic examinations. It canbe asymptomatic or symptomatic without having a directlink between the degree of instability and the severity ofsymptoms.

ROLE OF FACET JOINT IN LOW BACK PAIN

As we have seen, segmental instability linked to diskdegeneration fosters facet joint lesions that contribute tothe low back pain. But there are cases in which these facetjoint lesions seem to be the principal cause.

Before 1930, facet joint lesions were considered to beone of the principal causes of low back pain and sciatica.Then, after the publications of Mixter and Barr, lesions ofthe disk were held responsible. Except for a few authors,facet joint lesions were completely forgotten before mak-ing a comeback. Certain authors even denied any role ofthe lesions in low back pain. In 1927, Putti attributed lowback pain and sciatica to facet joint lesions of the inferiorlumbar segments (essentially arthritic lesions) as well asto the asymmetry of the orientation of their articular pro-cesses. Ghormley (1933) used the term

facet syndrome

todescribe the compression of the sciatic nerve (lumbosacralnerve root) in the intervertebral foramen narrowed by facetjoint arthrosis. He presented the first radiographic studiesdepicting this narrowing of the foramen intervertebralis.

In 1971, Rees published, in Australia, an impressiveseries of approximately 3000 cases of low back pain inwhich he “denervated” the inferior lumbar facet joints bydebriding them with a scalpel, blindly (percutaneously).He reported a success rate of 98%. But did Rees in factproduce a denervation or a myofasciotomy? It seems thatthe procedure described did not allow contact between thescalpel and the articular pillars of the posterior elements.

Maigne (1971) brought attention to the role of the facetjoints in spinal pathology and insisted on their frequentinvolvement not only at the lumbar level, where they couldbe the origins of low back or pseudoradicular pain, butalso at the thoracic and cervical levels. He emphasizedtheir treatment by injection or manipulation (report pre-sented at the 3rd Congress of the International Federationof Manual Medicine in Monaco in 1971) (see p. 10).

He also proposed “segmental examination” to exposeclearly the dysfunction of the facet joint. The responsibil-ity of that articulation is proved by relief brought by itsanesthetic injection. Facet joint pain can be due toinflammation, but most often it is the consequence of apainful segmental dysfunction without any radiologicabnormality, which the author calls “painful minor inter-vertebral dysfunction” (PMID).

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Shealy (1975) suggested the use of rhizotomy, per-formed by thermocoagulation, analogous to that used inthe treatment of neuralgia of the trigeminal nerve. Ther-mocoagulation rhizotomies were performed systemati-cally on the articulations of the three last lumbar segmentson both sides. The first published results were excellent,80% and more; but it was soon apparent that these figureshad to be modified. In most present reports, they are about40% (Lora and Long, 40%; MacCulloch, 40%; Privat,40%; Ignelzi, 41%; Y. Lazorthes, 39%).

Burton diagnoses “facet syndrome” by the clinicalexamination and radiologic findings (the term

facet syn-drome

has a different meaning here than the one used byGhormley). According to Burton, pain of facet joint originis increased by activity and relieved by rest; “getting outof bed is painful, the sitting position is not well tolerated,straightening out after total flexion of the flank can resultin sharp pain, but coughing and sneezing are painless.”The best candidates for thermocoagulation (still accordingto Burton) are patients with radiological evidence of con-genital abnormalities of the lumbar spine: “a deembeddedL5 (the iliac line passes through the body of L5), facettropism and spina bifida occulta.”

All these signs seem a bit nonspecific. To verify theconnection between the articulation and the pain syn-drome, Mooney and Robertson (1975) proposed also usingthe test of articular anesthesia; thermocoagulation isapplied to the articulation in question as well as the supra-and subjacent articulations to obtain as complete a dener-vation as possible. The author thinks that one can considera facet joint origin for low back pain under the followingconditions.

1. If segmental examination reveals segmentaltenderness at L4–5 or L5–S1 (L3–4 is rarelyaffected), with a particularly clear facet jointpoint

2. If there are trigger points in the muscles of theexternal iliac fossa ipsilateral to the facet jointpoint

3. (Especially) if a discogenic origin does notseem to be likely

The role of the facet joint will be affirmed only if epiduralinjection does not modify any of the signs and if the facetjoint injection, on the contrary, brings even momentarydisappearance of the signs and relieves the patient.

LOW BACK PAIN OF LIGAMENTOUS ORIGIN

The origin of low back pain can be ligamentous(Fig. 40.1C). According to Hackett, ligamentous “laxity”causes most articular or spinal pain. He treats low back

pain syndromes by injecting sclerosing agents into theinterspinous, sacroiliac, and iliolumbar ligaments. Barborhas accepted a part of these theories and has proposed asclerosing solution that is better tolerated than the oneused by Hackett. The interspinous ligament is painful inspinal instabilities of discogenic origin (described above),but its role in the pain syndrome seems weak in general.It is also often painful in PMIDs, but usually the paindisappears or decreases with manipulation.

Occasionally, ligamentous tenderness may be the prin-cipal origin of low back pain. An anesthetic injection ofthe ligament demonstrated its role by momentarily sup-pressing the painful syndrome.

LOW BACK PAIN SYNDROMES OF LUMBOSACRAL ORIGIN AND PAINFUL MINOR INTERVERTEBRAL DYSFUNCTION

To classify a low back pain syndrome according to awell defined origin, as discogenic, facet joint, or ligamen-tous, is convenient but only applicable to a minority ofcases. In most of the low back pain syndromes seen dailyby physicians, the pain is due to a PMID (see “Definition”in Chapter 17). Indeed, lumbar segmental dysfunction issimilar to that seen at other levels of the spine, and it isgenerally reversible. Moreover, the concept of PMID thatwe propose is independent of the radiologic state of thesegment in question, which could be normal or show somesigns of degeneration.

Figure 40.1

Low back pain of lumbosacral origin can havethree origins that involve the mobile segment:

A.

Superficialfibers of the annulus fibrosus, and the posterior longitudinalligament.

B.

Facet joints.

C.

Interspinous ligament. Addition-ally, both the muscles that directly power the segments inquestion and pressure by the disk lesion on the dura may besources of pain.

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However, even in a patient with low back pain withmarked radiologic lesions and significant postural asym-metries, it is not uncommon to achieve lasting relief by asimple medical treatment such as manipulation that isidentical to the one that relieves the same pain in a personwith a radiologically normal spine. Conversely, a patientwho presents initially with a PMID that responds well to theusual treatments may eventually not be relieved by thesetreatments, suggesting possibly that a disk, facet, or liga-mentous lesion may become the dominant cause of pain.

LOW BACK PAIN OF LUMBOSACRAL ORIGIN AND CELLULOTENOPERIOSTEOMYALGIC SEGMENTAL VERTEBRAL SYNDROME

Periosteomyalgic manifestations of the segmental ver-tebral syndrome are, as we have seen, always present in

low back pain syndromes of lumbosacral origin, as triggerpoints of the gluteal muscles. The latter can play an impor-tant role in low back pain, for these cellulotenoperiosteo-myalgic (CTPM) reflex manifestations can maintain reflexloops that perpetuate the pain (Fig. 40.2).

Treatment

The treatments must first relieve the responsible segmen-tal dysfunction, then the CTPM reflex manifestations that itproduced, which often persist and perpetuate the pain. Somepostural precautions will avoid some recurrences, and ther-apeutic exercise will stabilize the result.

Spinal Treatment

Manipulation —

If manipulation is possible, it is agood treatment for segmental dysfunction. Its result canbe appreciated immediately at the first session. On aver-age, two to six manipulations are sufficient. However, ifthree sessions do not bring any improvement, it is betternot to persist.

The basic technique is a lumbar manipulation per-formed in lateral decubitus, and depending on the case,done in relative degrees of spinal flexion or extension(Fig. 40.3, left). Other maneuvers are tailored to the par-ticular needs of each patient: the belt and astride tech-niques (Fig. 40.3, right), etc. (see “Manipulation” in Chap-ter 67).

Mobilization —

Mobilization is an excellent methodto prepare for a manipulation and sometimes even toreplace it. In difficult cases, mobilization techniques areof first choice. The most useful maneuvers are describedon page 462, but all methods described as techniques ofmanipulation can be used in mobilization. The maneuversare pushed until there is tension without giving the termi-nal thrust, and they are repeated.

Epidural injection —

When there is a discogenic com-ponent, epidural injection is indicated. It relieves the patientand often facilitates incorporation of other treatments such

Figure 40.2

Low back pain of lumbosacral origin is almostalways associated with trigger points of the gluteal muscles(L5, S1) and sometimes with hypersensitivity of the trochanterto palpation (L5) (Maigne).

Figure 40.3

Two manipulative techniques used in the treatment of low back pain of lumbosacral origin.

Left,

manipulationwith rotation to the left in kyphosis.

Right,

manipulation with rotation to the left and lateral flexion to the left.

CHAPTER 40 LOW BACK PAIN OF LUMBOSACRAL ORIGIN

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as manipulation and a therapeutic exercise prescription(see Chapter 26, “Therapeutic Injections”).

Facet joint injection —

The only treatment for facetjoint inflammation is facet joint injection (Fig. 40.4). It isalso indicated in chronic articular dysfunction linked to aPMID or to discogenic pathology and when manipulationis contraindicated or will not normalize facet joint func-tioning.

Rhizotomy —

If an articular injection consistently pro-duces definite but temporary relief, a percutaneous ther-mocoagulative rhizotomy may be indicated.

Injection of interspinous ligament —

When the inter-spinous ligament seems to be the source of pain, injectionof a mixture of local anesthetic and corticosteroid is indi-cated. This is used only in a limited number of cases. Ifthe relief is definite but temporary, then sclerosing agentsrecommended by R. Barbor and O. Troisier (Fig. 40.5) areindicated for use by injection (see “Ligamentous Injec-tions” in Chapter 26).

Intradiscal injection —

In certain cases of discogeniclow back pain that do not respond to treatment, intradiscalinjections of aprotinin (Kraemer et al., Degrave), hexatri-one (triamcinolone hexacetonide), and hexamethasoneacetate have produced good results.

Physical modalities —

Electrotherapy (pulsed shortwave diathermy, ultrasound, TENS, high-voltage pulsedgalvanic stimulation, etc.) is an effective adjunct inchronic cases, in elderly patients, and when other treat-ments are contraindicated.

Cryotherapy, Thermotherapy, and Hydrotherapy

These well known therapeutic modalities still havetheir place in the therapy of low back pain. The use of

sauna baths associated with hydrotherapy often helps todecrease chronic protective muscle guarding and CTPMmanifestations.

Treatment of Manifestations of Segmental Vertebral Syndrome

CTPM manifestations that persist despite spinal treat-ment can be effectively treated by massage, stretching,injection, or ultrasound.

Massage —

Massage is used on the taut bands in thegluteal muscles and should consist of deep, slow, progres-sive kneading maneuvers (Fig. 40.6).

Stretching —

Stretching that takes advantage of pos-tural or postfacilitation techniques can be used effectivelyto treat the affected muscles and is complementary tomassage.

Injection —

The injection of the trigger points is some-times sufficient, but it can also complement massage andstretching.

Ultrasound —

Ultrasound has been used effectivelyon trigger points, and the reaction to treatment is usuallyrapid.

Figure 40.4

Injection of facet joint.

Figure 40.5

Injection of interspinous ligament.

Figure 40.6

Petrissage of gluteal muscles containing triggerpoints is often useful.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Postural Re-education and Corrective Actions

Often-neglected postural re-education and correctiveactions are essential and must be introduced to a patient

at the beginning

of treatment. If the patient suffers frommorning stiffness, a firm bed is advised; a plywood board,1 cm thick, can be placed beneath a good quality mattress.The patient must learn to bend at the knees (both or onlyone) rather than stoop. Training to bend at the knee is thefirst step in re-education. It can start at the beginning ofthe treatment. If the patient is symptomatic while sittingor standing after sitting for a time, the height of the seatmust be adjusted. A seat should have a firm cushion andlumbar support at home as well as in the workplace andin the car.

In many cases, a few treatments such as manipulationand/or injection associated with postural re-education andcorrective actions will be enough to give a patient lastingrelief. A booster treatment is often useful, such as manip-ulation performed two or three times a year. It is best toend the treatment with an exercise prescription thatincludes two or three stabilization techniques a patientwill perform carefully a few times each day.

Lumbosacral Corsets and Rigid Lumbar Orthoses

The reinforced lumbosacral corset is indicated forpatients who have pain when standing or with prolongedsitting. It is worn until treatment, especially therapeuticexercise, precludes its continued use. Then it is worn onlyoccasionally. It should be worn permanently by elderlypatients for whom it is the only convenient solution andby patients with atonic abdomens who, for various rea-sons, cannot tolerate reconditioning.

A low back pain syndrome that is difficult to treat andhandicaps a patient sometimes necessitates wearing a rigidlumbosacral orthosis during the day. It is taken off for thenight, and used for 3 to 6 wk. If it relieves pain, the orthosiscan be replaced by a reinforced lumbosacral corset witha closed cage. Then, depending on the case, the treatmentsdescribed above can be started.

Therapeutic Exercise

Therapeutic exercise is the fundamental treatment ofchronic low back pain, especially low back pain syn-dromes that tend to recur (Fig. 40.7). Therapeutic exerciseis prescribed after thorough patient evaluation, in keepingwith the rule of no pain. Its aim is to restore normalmuscular balance and to develop a dynamic muscularcorset (abdominal, gluteal, and spinal extensor mecha-nism) that will protect the spine in concert with the acqui-sition of new habits that will enable the patient to respondto imposed demands.

The following are necessary to reach these objectives.

• The lower limb muscles must be sufficiently devel-oped to enable the patient to squat and rise and torotate the body while maintaining the trunk in neu-tral position. Mobilization techniques and soft tissuerelease treatments are used to ensure optimum flex-ibility at the hips, knees, and ankles, and a homemaintenance program is reinforced.

• The patient is taught how to avoid extreme move-ments and to “lock” the spine in neutral positionwhile changing positions. Neutral spine is definedas the position of modified lumbar lordosis that pro-duces optimal symptom relief. Neutral spine posi-tion, the foundation of most of the exercises taught,varies from patient to patient.

• The patient is taught how to stretch the muscles,especially the hamstring group, which is often con-tracted in patients with low back pain. Spinal exten-sor stretching is also taught.

• Abdominal exercises are taught. They are importantbecause of the role of the abdominal muscles inunloading the spine; isometric exercises are taughtinitially, followed by isotonics when appropriate.Finally, exercises that condition the muscles of theperineum and the diaphragm are taught.

• Paraspinal muscle strengthening exercises are intro-duced. These muscles play an essential role because,depending on their state of relaxation or contraction,they can transform the spine from a rigid cylinderto a flexible series of links that permit force absorp-tion. A well developed spinal extensor mechanismis necessary to allow one to assume the infinitenumber of positions constantly imposed on thespine. The patient must acquire habits that allow themuscles to dynamically respond to any and all sit-uations of imbalance while protecting the spine.

Surgery —

Surgery is rarely necessary for low backpain and is reserved for cases involving total failure of

Figure 40.7

Once the patient shows improvement, a thera-peutic exercise prescription is essential in the managementof low back pain of lumbosacral origin. It should be adaptedto the particular needs of each patient.

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medical management. Spinal fusion has some rare butgood indications. The pain must indeed come from theregion to be fused (be careful in low back pain syndromesof thoracolumbar origin). Low back pain must be relievedby a rigid lumbar orthosis. Before the decision, a carefulpsychologic examination is necessary.

Discectomy performed by means of classic techniqueshas resulted in many disappointments and has no definiteindication. However, many of the newer techniques thatare still in the developmental stage, (e.g., percutaneousdiscectomy and microdiscectomy) may show promise incertain refractory discogenic low back pain syndromes.

LOW BACK PAIN OF EXTRASPINAL ORIGIN

Low Back Pain of Myofascial Origin

Certain authors, especially J. Travell, have attributedmyofascial causes to low back pain. In these cases, carefulpalpation of the paraspinal muscles reveals one or severalparticularly painful points that are located in firm tautbands. Pressure on these points reproduces the usual pain.Their injection with local anesthetic relieves pain, and theresult can be lasting. The trigger points that are responsiblefor low back pain are most often located in the iliocostalismuscle at the level of the last ribs. Pain is felt in the lumbarfossa or in the gluteal region. The longissimus and quadra-tus lumborum muscles can sometimes be affected.

J. G. Drevet studied similar trigger points located inthe lumbar paraspinal region with ultrasonography. Henoticed that they often correspond to a hypoechoic zone(41 of 62 patients), sometimes are hyperechoic (4 of 62patients), but do not show any abnormal echoes in somepatients (17 of 62). Certain patients had pain for a longtime and many treatments without success; most wererelieved with local treatment.

In four patients with hypoechoic zones, a biopsy wasdone, and it showed that these muscular bundles werebrownish and retracted. Microscopic examination revealedsignificant endo- and perimysial adiposis, fibrosis, andsome atrophic muscular lesions; the muscular fibers wereof irregular diameter and angular. It is difficult to under-stand these lesions, as they could be of neurogenic origin.In three cases of the four, surgical excision of this zone(in patients who were not relieved by local injections andelectrotherapy) brought a total disappearance of the lowback pain.

Low Back Pain of Cellulalgic Sheeting

After observing about 30 patients, we believe we canisolate this particular form of low back pain. In general,

this low back pain is refractory to treatment. It is increasedby fatigue, by certain movements, and by exertion, but itis not always decreased by rest. Forward flexion, usuallylimited and painful, is done with a “fixed” lumbar lordosis.The patient cannot round the back.

Examination by palpation reveals the characteristic fea-tures of this low back pain syndrome. Maneuvers of thesegmental examination seem painful at all lumbar levels;transverse pressure is painful on both the right and theleft, as is the facet joint.

The diagnosis is made with the pinch-roll test. It isimpossible to grasp a skin fold between the thumb andindex finger. The superficial soft tissues seem to cling tothe underlying fascial planes in a solid block, forming atrue symmetric cellulalgic sheeting overlying the lumbarregion that is especially marked in the midline. Thesesubcutaneous tissues do not seem to extend during flexion;they cannot creep freely with segmental motion, as shownby a positive Schober’s test (see “Active Motion Testing”in Chapter 21). The tension produced by forward flexionis painful.

Treatment

Treatment consists of injecting the layers of the regionwith dilute local anesthetic, followed immediately bymobilization of the superficial planes on the deep planes,followed by kneading maneuvers that help to mobilizethem and make the tissues more supple. The second stepis lumbar segmental mobilization. This seems to be a localneurotrophic reaction promoted by certain organisms.

Low Back Pain and Iliolumbar Ligament

According to certain authors (Hackett, Hirschberg etal.), the iliolumbar ligament is responsible for certain uni-lateral low back pain syndromes. Diagnosis is made byfinding a painful point under pressure on the iliac crest,at 7 to 8 cm lateral to the midline, a site that seems tocorrespond to the iliac insertion of the superior fibers ofthis ligament. An anesthetic injection at this point oftenrelieves the patient.

In fact, this point located on the

posterior surface

of theiliac crest cannot correspond to the iliolumbar ligament,which inserts on the anterior surface of the crest and thus isseparated by thickness of the iliac crest. We shall see below(Chapter 41) that this point corresponds to the cutaneousbranch of the posterior ramus of L1 (60% of cases) or L2(40% of cases), which crosses the iliac crest at that preciselevel as it traverses a fibro-osseous tunnel (R. and J. Y.Maigne). This point disappears if the superior branch isinfiltrated with an anesthetic at its emergence from the spineat the level of L1 and L2, which could not happen if thepoint was in fact the iliolumbar ligament.

289

41

LOW BACK PAIN OF THORACOLUMBAR

ORIGIN (T11–T12–L1)

Low back pain of thoracolumbar origin (TL) is the mostfrequent manifestation of the “thoracolumbar junctionsyndrome” (Maigne) that also includes pseudovisceralabdominal pain and pubic and trochanteric tenderness (seeChapter 60, “Thoracolumbar Junction Syndrome”). Forthe sake of clarity and because the low back pain is oftenthe only symptom that patients complain about, it isdescribed here. It is also the first of the painful manifesta-tions that have been attributed to the TL junction (Maigne,1972). As we have shown, low back pain can have its originat one or more segments of the TL junction, usually T11–12and T12–L1, and occasionally T10–11 or L1–2.

Low back pain of TL origin can be acute or chronic.It is common, and the pain is very similar to that of lowback pain of lumbosacral origin with which it is often

confused. Patients never complain of spontaneous pain atthe TL junction (Fig. 41.1 and Fig. 41.2).

This form of low back pain is more frequent in peopleover 45 years of age, but it can also be seen in youngpeople. It can be associated with low back pain of lum-bosacral origin (LS) in variable proportions.

TL low back pain shows some precise and constantclinical signs that must be sought thoroughly, whichrequires a certain level of experience. The diagnosis isconfirmed by response to an injection or manipulationperformed on the responsible thoracic or TL segment thatis sometimes spectacular and immediate.

After a short anatomic review of the particular charac-teristics of the TL junction, we describe the clinical signsand treatment of this syndrome.

Figure 41.1

Low back pain can have a thoracolumbar junc-tional origin (Maigne). It may only be felt at the lower lumbarlevel and gluteal region.

Figure 41.2

Pain of the cutaneous branch of the posteriorramus of the thoracolumbar junction.

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ANATOMIC REVIEW

Facet Joints

The form and orientation of facet joints change at everylevel of the spine, which facilitates certain movements andprevents others. The thoracic articular processes are ori-ented at an angle of 60° from the horizontal, while thelumbar processes are oriented at 90° (Fig. 41.3). In thethoracic spine, the articular processes lie more or less inthe frontal plane; in the lumbar spine, they are in thesagittal plane. This means that the thoracic spine allowsmobility in rotation, while at the lumbar spine, this rota-tion is essentially impossible (Fig. 41.3). It follows, there-fore, that the TL junction is a transitional zone subjectedto significant rotational strains. It is also a common sitefor vertebral compression fractures.

Transitional Vertebra

Anatomically and physiologically, T12 is a transitionalvertebra. Its superior articular processes behave like theadjacent thoracic ones, while its inferior articular pro-cesses behave like those of the lumbar spine. Thus, thereis a certain disruption in the harmony of movement thatcould lead to segmental dysfunction. Normally, most ofthe trunk rotation occurs at the TL junction, as this motionis limited above by the ribs and made difficult or impos-sible below by the orientation of the lumbar articular pro-cesses (Fig. 41.4).

This role of transitional vertebra can be played by T11in certain people. In a CT study of 32 patients with TLlow back pain, T12 was transitional in 25 cases, T11 in6, and L1 in only one patient. Interestingly, in the 32patients, the lower ribs articulated with the T12 vertebralbody (J.Y. Maigne et al.). In fact, this region appears to

Figure 41.3

Facet orientation of thoracic (T) and lumbar (L) vertebrae.

Figure 41.4

T12 is a transitional vertebrae.

1.

Superior articular facet.

2.

Inferior articular facet.

3.

Articular rib facet. Thesuperior articular processes (1) have the same orientation as the thoracic spine articulations (up to T11). The inferior articularprocesses (2) are oriented in a lumbar fashion.

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be associated with a certain degree of anatomic variationthat may impact on the biomechanics of the region andon its pathology. In a Finnish study, T11–12 was found tobe the most frequent transitional segment (Malmivaaraet al.).

Posterior Rami of Thoracolumbar Spinal Nerve Roots

At the superior lumbar and inferior thoracic level, theposterior ramus emerges from the mixed spinal nerve rootat almost a right angle. It courses around the articularpillar, pressing its path on the prominence of the superiorarticular process of the subjacent vertebra (G. Lazorthes).It divides immediately behind the interior portion of theintercostalis muscle into lateral and medial branches. Thelateral branch has both motor and sensory fibers andbecomes subcutaneous approximately three vertebraebelow its origin. The medial branch is composed almostexclusively of motor axons and courses inferiorly, poste-riorly, and medially before terminating in the multifidusand spinalis muscles and supplying them.

Innervation of Subcutaneous Tissues

Classically, the cutaneous and subcutaneous tissues ofthe superior half of the buttock are innervated by theposterior rami of L1, L2, and L3. Some authors like Kee-gan and Garrett even attribute part of this innervation toL4 and L5 in their dermatome maps. However, all the

anatomists agree that the posterior rami of L4 and L5 haveno cutaneous branches.

Therefore, to confirm our clinical findings, we reliedon studies performed by Hovelacque that clearly revealthat the innervation of the subcutaneous tissues of thesuperior part of the buttock is innervated by T12, L1, andL2. A few dissections that we performed with Le Correand Rageot confirmed that these rami indeed cross theiliac crest at a right angle.

In 1976, Barrie and R. Maigne noticed in 25 dissectionsthat the primary cutaneous innervation of the superiorgluteal region was provided by L1 and T12; these tworami that are very close to each other often cross the iliaccrest at a distance of 7 to 8 cm from the midline, corre-sponding to the usual location of the crestal point. Morerecently, J.Y. Maigne and R. Maigne went back to thesestudies so that we could better describe the entire superiorgluteal cutaneous innervation. The study involved 30 dis-sections and showed the following (Fig. 41.5 throughFig. 41.7).

• In 19 cases, T12 and L1 accounted solely for theinnervation of the gluteal area. L1 crosses the iliaccrest 7 to 8 cm lateral to the midline, and T12 crossesit 1 to 3 cm more laterally.

• In 8 cases, the innervation was provided by L2 medi-ally and L1 and T12 laterally.

• In 3 cases, the picture was the same as the above,but L2 received a branch arising from L3 prior tocrossing the iliac crest.

Figure 41.5

In this example (dissection J.Y. Maigne), innervation of the skin overlying the superior gluteal region is suppliedby T12 and L1. One can see the crossing over the iliac crest of these nerves. It should be noted that in this case L1 dividesjust before crossing over the iliac crest. This diagram demonstrates the actual paths of the nerve branches. The iliac crest isrepresented by dark dots.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Figure 41.6

Individual variations are frequent. In this case, the cutaneous branch of T11 takes a medial direction exactlywhere it crosses over the iliac crest and thus innervates the more medial aspect of the gluteal skin region. The iliac crest isdemonstrated by the black dots.

Figure 41.7

The three principal distributions of the cutaneousbranches of the nerves that cross over the iliac crest (J.Y.Maigne). The medialmost branch always crosses over the iliaccrest at a distance of 7 to 8 cm. This corresponds to L1 (

a

), L2(

b

), or a branch composed of both L2 and L3 (

c

). It goes througha fibro-osseous tunnel in which there is only slight mobility.Occasionally, it can be compressed. The cutaneous branch ofT12 does not generally cross over the iliac crest in type c. Itcrosses irregularly in type b. These distributions essentiallyrepresent 60% (

a

), 25% (

b

), and 15% (

c

) of the cases noted.

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293

This confirms that there are no cutaneous branches ofthe posterior rami of L4 and L5, and they are rare in L3.

Iliac Crest Crossing Point

We have noticed that the most medial cutaneous branch(L1 in 19 cases, L2 in 11 cases) always crosses the iliaccrest at a point 7 to 8 cm lateral to the midline after havingperforated the aponeurosis of the latissimus dorsi near itsinsert on the iliac crest. At this point, the nerve passesthrough a fibro-osseous tunnel restricting the nerve’s freemovement when traction is applied to it. This tight passageis a potential site of entrapment and may be a source ofdiscomfort in some cases (Fig. 41.6). During some dissec-tions, J.Y. Maigne noticed a typical case: the nerve ramusuncovered at that level demonstrated evidence of a severestenosis with supra- and substenotic swelling.

CLINICAL SIGNS

In acute and chronic cases, pain is always felt in thesacroiliac joint, low lumbar, or gluteal region. Sometimes,it refers to the thigh laterally or posteriorly. It is practicallynever felt at its origin, that is, at the TL junction. It isgenerally unilateral but sometimes bilateral. This pain canbe acute (see Chapter 42) and occurs often after exertionor forced rotation. Most often, it is chronic. It seems thatnothing can differentiate it from chronic LS low back pain,with which it is often confused.

Clinical Examination

Clinical examination reveals the physical signs of thisdisorder and demonstrates the relationship between lowback pain and its TL origin (T11–12, T12–L1, or L1–2;exceptionally, T9–10 or T10–11). When the patient isstanding, it is common to see that lateroflexion on the sideopposite the low back pain produces or increases the pain.The examination should be performed with the patientlying forward flexed across the table, with a cushion underthe abdomen (Fig. 41.8).

Examination of Lumbogluteal Region at Iliac Crest

The index finger of the physician follows the iliac crestfrom medial to lateral, rubbing it over the skin with smalltransverse and vertical movements in a back-and-forthmanner. At an exact point, usually 7 to 8 cm lateral of themidline, the examiner’s finger encounters a very tenderpoint that corresponds to the site of compression of theirritated cutaneous branch. This point is referred to as the

crestal point

(Fig. 41.8 and Fig. 41.10) (Maigne). It maybe absent if the concerned ramus does not cross the iliaccrest (T11, sometimes T12). It is usually unilateral.

Adjacent to that point, the subcutaneous tissues of thebuttock or lumbar region are painful to pinch-rolling(Fig. 41.9). They are infiltrated by cellulalgia, which isthick and extends over an area usually about the size ofthe palm of the hand, sometimes covering almost all ofthe superior part of the buttock or the inferior part of thelumbar region, or covering only a few square centimetersover the iliac crest (Fig. 41.10 and Fig. 41.11).

The degree of skin fold thickening varies greatly fromone subject to another. Sometimes it is mild; sometimesit is very thick, tight, granular, and impossible to fold. Inall cases, the pinch-roll test is very painful, compared withthe opposite side and the adjacent zones. The cellulalgiczone often seems to be common to the different levels ofthe TL junction, probably because of the frequent anasto-moses that exist and the mechanism of the cellulalgia.

Examination of Thoracolumbar Region

At the TL junction, the sensitivity of one or moresegments appears clearly. For this segmental examination,the patient assumes the prone position across the table,

Figure 41.8

Evaluation of the posterior crestal point. Theexaminer slides slowly along the iliac crest exerting a mildfrictional pressure, evaluating each centimeter. Note that thepatient is lying forward flexed across a table.

Figure 41.9

Pinch-roll test examining superior gluteal region.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

with a cushion under the abdomen. The two essentialmaneuvers are transverse pressure against the spinous pro-cesses and the search for the facet joint point. The facetjoint pain is unilateral and is always located on the sideof the low back pain (Fig. 41.12, top and bottom). It canbe bilateral if the low back pain is so.

The segmental tenderness that is uncovered is usuallyseen on one segment (60%), sometimes on two (25%) orthree segments (15%). With rare exceptions, these seg-ments are adjacent to each other. Tenderness to PA pres-sure on the spinous process and over the interspinousligament may also be noticed, but is not as consistent.

Confirmation of Thoracolumbar Origin of Low Back Pain

Confirmation is obtained by anesthetic injection per-formed at the facet joint point of T11–12 or T12–L1,

where it was found to be tender on examination. Thisinjection results in the disappearance of the pain as wellas the clinical signs.

The needle is advanced perpendicularly about 1 cmlateral to the midline until contact is made with perio-steum. After verification by aspiration, 1 to 2 mL oflidocaine is injected. This can be performed under fluoro-scopic guidance. With experience, it will be noticed thatthe point that is painful on palpation corresponds as a ruleto the facet joint (Fig. 41.13, left). In a few moments, thefollowing can be observed:

• Disappearance of pain and stiffness with restorationof pain-free range of motion

• Disappearance of the crestal point• Decrease or even the disappearance of the cellulal-

gic zone that has become painless to pinch-rolling

During this injection, which affects the posterior ramusas well as the facet joints, the needle should remain inplace for 1 min, while waiting for the disappearance ofthe sensitivity of the crestal point on palpation and of thepain to pinch-rolling (Fig. 41.13, right).

If this does not

Figure 41.10

The zone that is characteristically painful to thepinch-roll test and low back pain of TL origin usually overliesthe iliac crest. If the T9 and T10

segments are involved, thecellulalgic pain will be located above the crest.

Figure 41.11

The cellulalgic zone corresponds to the terri-tory of the posterior rami of the TL junction. This zone maybe supplied by two or three segments from this region of thespine.

Figure 41.12

Segmental examination of the TL junction forfacet joint tenderness should be performed from the rightand the left. As a rule, it is found on the same side as thelow back pain. It is sometimes found bilaterally (as in thefollowing case).

Top,

Transverse pressure against the spinousprocess. This is systematically performed from right to left,and from left to right (

bottom

)

.

CHAPTER 41 LOW BACK PAIN OF THORACOLUMBAR ORIGIN

295

happen, placement of the needle should be modifiedslightly upward, downward, or laterally to render theinjection useful. One should be sure that the injection hasaffected the appropriate level, as two levels can beaffected, but rarely three.

When examination has revealed dysfunction of two orthree segments, it may be necessary to inject all of them.This depends on the result of the procedure. In recurrentcases, it is a good idea to mark the point of injection thathelped, to verify whether the same segment is affected. Iftwo or three painful TL segments are noted on examina-tion, it is not uncommon to find that only one isresponsible for the referred pain.

Placebo injection —

If the injection of lidocaine orsaline is performed at a distance from the facet joint pointor on an insensitive segment (with the patient unaware),there should not be any modification of the crestal point,the zone of cellulalgia, or the spontaneous pain.

RADIOLOGIC EXAMINATION

In most cases of low back pain of TL origin, the stan-dard radiologic examination of the affected zone is unre-markable or demonstrates only minor degenerativechanges. From time to time, sequelae of spinal apophysitisare observed. At that level, they are a cause of fragilityfor that overexerted zone and foster refractory or recurrentlow back pain. In women over 60, some degree of diskdegeneration can be seen, sometimes with retrolisthesisof L1 or L2 or a compression fracture of T11, T12, or L1that was ignored earlier is sometimes found. CT exami-nation has shown us lesions that are not well revealed by

conventional radiography, such as facet joint spondylosis,periarticular calcifications, and calcifications of the liga-mentum flavum.

Malmivaara et al. studied 24 cadavers with degenera-tive lesions of the lumbar spine. They noted the relativefrequency of degenerative changes at the TL junction andfound T11–12 to be the most frequent transitional seg-ment. They noted that the degeneration at that level wason the

• Whole segment (intervertebral disk, facet joints,costovertebral articulations)

• Anterior part (intervertebral disk) for the supra-adjacent segment (T10–11)

• Posterior part (facet articulation) for the subjacentsegment T12–L1

Radiologic examination can reveal uncommon pathol-ogy that may be the first sign of a spondyloarthropathy orof an infectious spondylodiscitis. Even a metastasis ormultiple myeloma can, for some time, be manifested onlyby low back pain with mild discomfort. We should empha-size that many patients with low back pain of TL originshow LS radiologic lesions such as discopathy, articularspondylosis, and spondylolisthesis that are asymptomatic,while the responsible TL region is radiologically normalor has only benign discrete lesions.

INCIDENCE

The incidence of low back pain of TL origin is 30%of all cases of common low back pain. The LS originrepresents 40% of cases, and 30% are of mixed origin

Figure 41.13

Injection of local anesthetic at the facet joint tenderness can relieve the discomfort, tenderness on pinch-rolling(

right

)

,

the cellulalgic zone, and crestal point pain. The needle (

left

)

should remain in place until the signs disappear and bemoved only slightly if there is no improvement.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

(personal statistical study of 500 cases). Our first statisticsdid not take enough notice of the mixed forms in whichthe primary responsibility for the pain could sometimesalternate between one origin or another at intervals of afew weeks. A patient with low back pain of TL origin thatwas perfectly relieved by the specific treatment could verywell consult us a few months later for a recurrence of whatseemed to be the same pain, but whose origin this timewas the LS spine. The following case is an excellentillustration.

Case History 1

— Mr. X., a 52-year old patient hadtwo successful operations for discogenic sciatica, 10and 15 years previously. After the second operation,however, he developed a low back pain that becamehandicapping in a few years. After numerous treatments,he came to our department where the diagnosis of lowback pain of T12–L1 origin was made. The treatmenthad a spectacular result, to the point that he couldresume his athletic activities. During one of these, therewas a recurrence, but this time it was a low back painaccompanied by acute sciatica. A diagnosis of recurrentdisk herniation was made. Treatment of the new condi-tion rendered a perfect result.

After a successful treatment of chronic severe low backpain of TL origin, often the patient, free from its incon-venience and pain and happy to feel at ease, undertakesactivities that are not well tolerated by the LS spine withdisk degeneration and completely lost or faulty coordina-tion, and the activities release LS low back pain or sciatica.Statistically, depending on when the patient is seen, it canbe put in the LS or TL category; but it is also common tosee both categories simultaneously in the same patient.

Age also plays a role. TL low back pain can be seenin the young, but it is much more frequent in people over45 years of age. The young subject with low back pain ofLS origin will later show low back pain of mixed origin,LS and TL; with time, it will tend to have a TL origin.

ATYPICAL FORMS

Ectopic Referral Patterns

Some patients with low back pain of TL origin havereferral patterns that appear to be sciatic and disappearwith treatment that is strictly localized to the TL zone.This referral pattern can be reproduced by injection of thefacet joint at T12–L1 or L1–2 or by injection of the crestalpoint. The two following cases are good examples.

Case History 2

— D.G., a 50-year-old physician, whileplaying golf 2 years previously, felt a lumbogluteal painradiating to the posterior aspect of the leg and the righttesticle. The pain decreased in a few days. One yearlater, while lifting a child several times, he felt a low

back pain that increased in the following days. The painradiated up to the posterior aspect of the right thigh andoccasionally as far as the heel. Bed rest and medicalmanagement improved it slightly. However, a wrongmovement precipitated an acute attack that persisted,resulting in lumbogluteal pain referring to the posterioraspect of the right leg and under the heel. Pain wasincreased by prolonged standing and especially bysitting. There was no significant change after 20 days.

Treatment with anti-inflammatory medications, a rein-forced LS corset, and injections did not help. The patientconsulted a friend, a well known rheumatologist whodiagnosed “atypical sciatica” and prescribed epiduralinjections and different medical treatments. After numer-ous injections, rest, and traction, there was no change.The rheumatologist and two neurosurgeons advisedradiologic studies. Then a neurologist requested a myel-ogram. At this point the low back pain was the dominantfeature, with a mild S1 radicular component.

Before this examination, he sent the patient to us forour opinion. The spine was very stiff; anterior flexionwas very limited (fingers to ground, 50 cm). The topo-graphy of pain was S1, but there was no Lasegue’ssign. At 80°, a slight exaggeration of the gluteal painoccurred. This had already been noted by the differentspecialists consulted. At the examination, the crestalpoint was very sharp, and pressure on it reproducedthe lumbogluteal pain, and curiously, referred it to theS1 region. There was a thick cellulalgic patch on thesuperior aspect of the right buttock and none on theother. Thoracic examination revealed the relative dys-function of T12–L1 with tenderness to transverse pressureon the right side of the spinous process. Radiographyshowed a moderate discopathy at L5–S1 but nothingat the TL junction. Injection of the facet point at T12–L1,which was very tender to palpation, resulted in imme-diate improvement (that no epidural injection ever gave)in flexion and resolution of the pain. After the thirdinjection, the relief was complete, and the patient wentback to his usual activities, which had been interruptedfor 6 months. Manipulation of the T12–L1 segmentcompleted this result, which was maintained for 3 years.

Case History 3

—

Mr. D.,

a 45-year old patient, wasoperated on unsuccessfully 6 months previously for apersistent left S1 sciatica. At surgery, the surgeon founda disk protrusion that did not compress the nerve root.The pain was mostly lumbar, with some referral underthe heel and to the posterior aspect of the thigh andcalf. Pain at the heel was manifested, especially whenpressed on, and became very sharp when it was struck.The patient could not tap on the ground.

Local injections of the heel and epidural injectionsmet with no success. When the patient came to ourdepartment for consultation, examination revealed a leftlow back pain of TL origin. A facet joint injection imme-diately relieved the low back pain, while his anteriorflexion went from 50 to 10 cm distance, fingers toground. Curiously, it also relieved the heel pain. Afterinjection, he could tap and strike the ground.

CHAPTER 41 LOW BACK PAIN OF THORACOLUMBAR ORIGIN

297

This favorable result lasted a few days and disap-peared. Several manipulations and injections were per-formed with the same momentary result. Two placeboinjections that were performed two levels higher withoutthe knowledge of the patient brought no relief. A surgicalcapsulectomy (T10–11, T11–12, T12–L1) was per-formed and produced an excellent result, with disap-pearance of low back and heel pain.

TREATMENT

Manipulation

If the state of the spine allows and the rule of no painis respected, manipulation is the treatment of choice forthis low back pain in young or average age persons; butit must be performed with impeccable technique. Ill per-formed or performed in the wrong direction, it aggravates,which is a true experimental test of the low back pain.Usually, the most helpful maneuvers are the astride tech-nique (Fig. 41.14), the epigastric technique, the supinetechnique (Fig. 41.15, bottom), and the knee technique(Fig. 41.15, top).

Facet Joint Injection

One mL of a long acting corticosteroid derivative isinjected at the affected facet joint. It is a good idea toleave the needle in place after the lidocaine test has beenperformed. Just as the pain on pinch-rolling disappears,the corticosteroid derivative should be administered. Mostoften, two or three injections at 2-wk intervals give anappreciable result, even disappearance of pain in chronicpatients.

Depending on the case and the patient’s age, it may benecessary to repeat similar injections two or three times peryear. The result of the injection is particularly spectacularin the acute or subacute form, in which only one injectionmay bring immediate relief (Fig. 41.13,

left).

Electrotherapy

Short wave diathermy applied to the TL junction cangive good results in patients to whom the two precedingtreatments cannot be applied.

Treatment of Cellulalgic Lumbogluteal Region

Usually, the lumbogluteal cellulalgic zone will disap-pear with spinal treatment. Sometimes relief is total with-out having this zone completely eliminated although it isdecreased. When relief is incomplete and local treatmentdoes not eliminate the zone, kneading maneuvers afterinjection with lidocaine over the crestal point or veryprogressive massage with or without subcutaneous injec-tion of diluted lidocaine can also be of help.

Physiotherapy (iontophoresis, in particular) can be effec-tive in refractory cases. Injection of the crestal point withlidocaine mixed with hydrocortisone can decrease or elim-inate the pain in some patients, probably in cases in whichthe nerve is compressed and irritated in the fibro-osseoustunnel as described above (R. and J.Y. Maigne). This entrap-ment phenomenon is added to the spinal irritation, as in a“double-crush syndrome,” but sometimes it seems to be theonly cause, with no spinal component. The need for surgicalrelease is exceptional; we have performed it twice.

Surgical Capsulectomy

In 1975, we tried surgical capsulectomy of the respon-sible articulation in very severe cases that were handicap-ping, relieved by manipulation or injection, but in whichresults did not last. The capsulectomy was extended to thelevel above and the level below, which destroyed the pos-terior ramus of the spinal nerve attached to it. Henri Judetperformed the surgery. We followed 16 patients who hadbeen operated upon, from 4 to 10 years. Most operationshad been done by Judet; the rest were done by other ortho-pedic surgeons who, after our publication, diagnosed lowback pain of TL origin and consulted us about the surgicalindication. Results were excellent or good in 10 patients,fair in 3, and nil in 3. We should emphasize that these patientshad refractory, chronic, and very incapacitating low backpain, usually due to workplace injuries, and they had alreadybeen operated upon once or twice for sciatica.

The protocol was as follows. Notwithstanding thebenign nature of the intervention, we were very restrictive.Only patients in whom only one level was responsible andin whom injection of lidocaine at the articular pillarresulted in clear relief of pain and temporary resolution

Figure 41.14

Technique for producing rotation with patientsitting astride.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

of the crestal point and the sensitivity of the lumboglutealsubcutaneous tissues to pinch-rolling were operated on.The point of injection was marked, and the test wasrepeated three times. Unknown to the patient, a placeboinjection was performed with saline injected 2 cm aboveand outside the facet joint point. No relief resulted.

Surgery was abandoned with the advent of percutane-ous thermocoagulative rhizotomy. However, one of ourpatients who was relieved only momentarily with twothermocoagulative rhizotomies achieved a lasting resultwith surgical intervention.

Percutaneous Rhizotomy

The protocol is the same as that described above. Oneshould be sure that the same segment is dysfunctional indifferent examinations at different times. Percutaneousrhizotomy is reserved for patients who are relieved bymedical treatment, injection and possibly manipulation,but for whom the result does not last.

Indication for thermocoagulative rhizotomy is infrequentbecause most patients with low back pain of TL origin havegood results with medical means. When medical treatmentyields only temporary results, rhizotomy may give a numberof patients lasting results. After our publications describingthis form of low back pain, Y. Lazorthes used thermocoag-ulative rhizotomy to denervate the facets at the TL levels inrefractory cases of low back pain. According to him, it isthe best indication for this technique, consistent with ourown experience (70% of good results).

Corrective Actions

To avoid recurrences, patients should (a) avoid all trunkrotation and learn to turn with the feet, not the thorax; (b)avoid trunk twisting when sitting, as for instance, whilespeaking to somebody behind him or her or taking some-thing from the back seat of a car while driving; (c) avoidseats that are too low or too soft; and (d) avoid cold inthe lumbar region.

Therapeutic Exercise

In most cases, corrective actions are sufficient to pre-vent recurrences in a patient who has been relieved bymedical treatment, but therapeutic exercise is necessaryfor patients with recurrences and athletes (such as golfers)who stress their TL junctions. Ledoux and Halmagrandstudied the various therapeutic modalities in our depart-ment at the Hotel Dieu. The aims of the therapeutic exer-cise prescription are to:

• Increase the flexibility of the back, which oftenexhibits facet joint stiffness

• Normalize muscle balance by stretching tight mus-cles and reconditioning weak ones

• Restore normal proprioceptive balance

Increased flexibility helps to reduce articular stiffness(through mobilization and postural re-education, so thatthe strains of rotation and lateroflexion do not adverselyaffect the TL junction) and to distribute these forces morewidely. Muscular stiffness can also be alleviated by pos-tural techniques or stretching of the spinal extensor muscles(latissimus dorsi, thoracolumbar, and hamstrings) and thehip flexor muscles (rectus femoris and psoas). Dependingon the results of examination, muscle groups that tend tobecome deconditioned (abdominal, diaphragm transverse,psoas, and muscles of the thoracolumbar extensor group)can be reinforced.

Proprioceptive reflexes are stimulated by teaching thepatient to control movements on a very limited zone ofthe back and flank, which are best performed in sitting orquadruped position and completed by lumbopelvic adjust-ment exercises while sitting or standing. The patient istaught to use the legs to their best mechanical advantagein bending and turning by reinforcing the quadriceps andhip rotator muscles.

Figure 41.15

Top,

manipulation using both knees in extension.

Bottom,

in the supine position in flexion.

299

42

ACUTE LOW BACK PAIN

As in the case of chronic low back pain, it is commonto attribute acute low back pain to the lumbosacral region(L4–5 or L5–S1), and like chronic low back pain, acutelow back pain can also be due to dysfunction of the tho-racolumbar junction (Maigne). Furthermore, some painsmay have myofascial origins.

ACUTE LOW BACK PAIN OF LUMBOSACRAL ORIGIN

Clinical Picture

Acute low back pain of lumbosacral origin occurs mostoften after exertion, although it can occasionally occurspontaneously. The pain is usually described as sharp andis exacerbated by even the slightest movement. It is usu-ally located in the low lumbar or sacroiliac region. Duringan acute episode, the patient remains stiff, even at rest,and is frequently unable to straighten up completely. Oncepatients are able to lie down and find a comfortable posi-tion, they prefer not to move any more than is requiredbecause any attempt to move reproduces the pain.

In less acute cases, the patient moves en bloc, withgreat caution, and bent forward. The lumbar region is stiff,and the pelvis is often tilted to one side because of theantalgic attitude. The patient fears even the slightest move-ment, the least shaking, or coughing, for example. Theselow back pain syndromes come with an antalgic list thatis generally quite pronounced, although it may sometimesbe mild, revealed only when the patient bends the trunkslightly.

In 50% of cases, the patient can laterally flex freelyaway from the painful side but not toward it; the antalgicscoliosis is then convex to the side of pain (Fig. 42.la). In40% of cases, the patient can side bend freely toward thepainful side, and the scoliosis is concave on the side ofthe pain (Fig. 42.1b). In 10% of cases, the antalgic list isin flexion (Fig. 42.1c).

The segmental examination performed on the patientsupine across the table demonstrates dysfunction of a lum-bosacral segment: L5–S1 or L4–5, more rarely L3–4.

The acute attack usually lasts 2 to 4 days and decreasesprogressively. It can last longer, especially when there isan antalgic attitude in flexion. Pain is usually relieved insupine, which is an often-prescribed treatment. In somecases, a persistent low back pain can propagate to involvethe buttock and the leg, and sciatica develops.

Mechanism

Acute low back pain is produced by a posterior intra-discal blockage, according to de Séze. A fragment of thenucleus, which has entered an annular fissure, distends thesuperficial fibers that are the only ones that are innervated.This distention seems to be the principal cause of painthat can also be due to the sudden pressure exerted by thebulging disk on the posterior longitudinal ligament.

Mac Nab thought that the facet joints were the mostcommon sources of acute low back pain, but it seems thatboth origins can be seen and even coexist. We can differ-entiate them with an epidural injection test performed viathe sacrococcygeal hiatus. Assuming sound technique, thepain is immediately relieved if a discogenic mechanismis responsible and is not relieved if the origin is the facetjoint. Conversely, injection of the lumbosacral facet foundto be tender on examination results in relief only if it isresponsible for the lumbar pain.

Treatment

Periodic bed rest may relieve the spinal pain andshorten the acute episode; however, more rapid results canoften be obtained by other means.

Manipulation

Acute low back pain has enhanced the reputation ofmanipulators and manipulations. Half of the patients areinstantly relieved by the first manipulation. A second ses-sion performed 48 hr later relieves 25% more.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Figure 42.1

Three forms of acute low back pain of lumbosacral origin and their correspondingstar diagrams.

a.

With antalgic scoliosis convex to the side of the pain.

b.

With antalgic scoliosisconcave to the side of the pain.

c.

With antalgic scoliosis in flexion.

CHAPTER 42 ACUTE LOW BACK PAIN

301

Not all forms of acute low back pain respond to themanipulative treatment in the same way. Forms with anta-lgic attitude in flexion are generally not good indications.Most often, this treatment cannot be applied because therule of no pain cannot be respected, since all directionsare painful (Fig. 42.1c).

Low back pain with antalgic list, convex to painfulside (Fig. 42.1a) —

This is the most common form. Thepatient lies on the painful side (side of the lumbar con-vexity), and the physician performs a lumbar manipulationin flexion (Fig. 42.2). Other techniques are possibleincluding the astride technique, with lateroflexion towardthe pain-free side and a rotation in the same direction asthe lateroflexion, or the belt technique if the patient cantolerate the prone position; the operator can be on the sideof the free lateroflexion.

Low back pain with antalgic list, concave to painfulside (Fig. 42.1b) —

The patient lies on the table on thepain-free side. The operator performs a manipulation inextension, thrusting on the iliac crest (Fig. 42.3). Thistechnique allows the application of the rule of no pain andopposite movement in most cases. Occasionally, the oppo-site works well; that is, the patient lies on the concaveside of the antalgic list (painful side) and is manipulatedaccordingly (i.e., either in extension, or in flexion).

Low back pain with antalgic attitude in flexion(Fig. 42.1c)

—

This can be pure, the lateral flank concav-ity replaced by a convexity, with or without a scoliosis;the form is always severe. Manipulation is rarely possiblebecause all directions are painful. If two directions arefree, repeated mobilizations in these directions should betried to see whether they free other movements; then pro-ceed by successive approaches. Epidural injection is usu-ally the only useful treatment (Fig. 42.4). Periodic bed restis often necessary.

Relaxation Techniques in Acute Low Back Pain Syndromes

Whether manipulation is possible or not, mobilizationcan bring an appreciable relief. The patient is positionedin supine, on a firm base, with the hips and knees flexed(Fig. 42.5, left). Both knees are grasped under the opera-tor’s axilla, and gradually, the hip flexion upon the trunkis passively increased, bringing the knees toward thepatient’s head with a slow, insistent movement, withrepetition if the technique is painless. The operator canalso pick the knees up on the shoulder (Fig. 42.5, right).

The operator takes one knee in the hand and brings itslowly toward the ipsilateral shoulder (Fig. 42.6, left).This maneuver is performed several times, then the kneeis directed toward the contralateral shoulder (Fig. 42.6,right), taking care that there is no pain with these maneuvers.The operator can thus obtain progressive mobilization.

Figure 42.2

(See Fig. 42.1a). Manipulation in flexion. Thepatient is lying on the left side for a manipulation and rightrotation in flexion.

Figure 42.3

(See Fig. 42.1b). Manipulation in extension. Thepatient is lying on the left side for a manipulation with leftrotation and extension.

Figure 42.4

(See Fig. 42.1c). No manipulation is possible;the rule of no pain and opposite movement cannot beapplied. Epidural injection is the best treatment if there is nocontraindication.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

These maneuvers are usually painless on one side only;this is the one that is used.

Another maneuver (described in Chapter 67, “LumbarTechniques”) is useful in most cases of low back painsyndromes with antalgic attitude, direct or crossed(Fig. 42.7). The patient lies on the most comfortable side,while the operator performs gentle progressive maneuversin lateroflexion in the pain-free direction.

Injection

Epidural injection of corticosteroids can bring remark-able relief in acute low back pain of discogenic origin. Insevere cases, an intrathecal injection of corticosteroids,using the technique of Luccherini, can yield a spectacularresult. The patient must remain in strict supine positionfor 24 hr.

Figure 42.5

Left:

mobilization in lumbar flexion.

Right:

mobilization with stretching of the lumbar musculature in flexion.

Figure 42.6

Mobilization in flexion with mild rotation. The knee is first flexed toward the shoulder in a manner similar to thatof the first mobilization and then progressively toward the opposite shoulder.

Figure 42.7

Mobilization in lateral flexion and rotation to theright.

CHAPTER 42 ACUTE LOW BACK PAIN

303

Rigid Lumbar Orthosis

A rigid lumbar orthosis may obviate the need for bedrest and can sometimes replace it when a patient’s activ-ities cannot be interrupted. It is very useful for patientswith severe forms that are relieved by manipulation orinjection, who cannot rest, or are required to travel.

Medication

From the beginning of the attack, anti-inflammatoriesshould be prescribed if there is no contraindication, andthey should be given for a few days. Muscle relaxants maybe efficacious in certain cases. We find them to be moreuseful for the sequelae of an attack than for the attackitself. Analgesics are often useful.

Prevention (Prehabilitation) and Rehabilitation

A patient with acute recurrent low back pain has a goodchance of progressing to a chronic stage. An appropriatetherapeutic exercise program is the best way to avoid this,and it can limit the frequency and severity of recurrencesas well as the risk of sciatica. Correcting poor posturalhabits and improving the ergonomics of the workplace aredecisive elements in prevention.

ACUTE LOW BACK PAIN OF THORACOLUMBAR ORIGIN

This is the acute form of the low back pain of thora-columbar origin of Maigne, described in Chapter 41. Dur-ing a torsional movement (e.g., turning the shoulderswhile sitting in a car, to take something from behind oron the side) and sometimes after an exertion or a chill, apatient often feels an acute pain in the low lumbar region,resulting in a generalized stiffness. Flexion is usually verylimited and painful, and extension is difficult; the reversecan also happen. In addition, lateroflexion away from thepainful side is limited. Unilateral trunk rotation is alsopainful, sometimes bilaterally. Protective paraspinal muscleguarding can be present, but the antalgic attitude is not asmarked as it is in the acute low back pain syndromes oflumbosacral origin. This form of acute low back pain ismore frequent in people over 40 years of age, but it canbe seen in younger persons.

Clinical Signs

Clinical signs are the same as those in the chronic formdescribed above (see “Clinical Signs” in Chapter 41).

At Inferior Lumbar Level

Clinical signs include the crestal point produced bycompression of the affected posterior ramus against theiliac crest; pain on the pinch-roll test of the skin overlyingthe gluteal region adjacent to the crestal point, and apossible cellulalgic thickening of the subcutaneous tis-sues.

At Thoracolumbar Junction

Segmental examination reveals pain of one and some-times two segments (T12–L1 most often). If it is due toT11–12, there is no crestal point, the cutaneous branch ofT11 does not cross the iliac crest, and the zone that ispainful on the pinch-roll test is located above the iliaccrest.

Treatment

Manipulation

Manipulation is very useful if possible according to therules. Depending on the case, the methods most commonlyused are the astride technique in rotation (Fig. 41.14); theepigastric technique, the supine technique (Fig. 41.15, bot-tom), and the knee technique (Fig. 41.15, top). Facet jointinjection replaces manipulation if the latter is impossible orcomplements it if it is insufficient. The following observationis characteristic of this form of acute lumbar pain.

Case History

— Mrs. C.V., 60 years old, felt a leftacute low back pain while taking a flower pot from awindow. The pain was sharp. She was very stiff, very“blocked.” The attack lasted 10 days and was persis-tent. Three epidural injections of cortisone were per-formed without improvement, but the pain was partiallyimproved by anti-inflammatories, which she did not tol-erate well. She had had the same kind of attack 2 yearspreviously; it dragged on for more than a month, leavinga kind of discomfort that finally disappeared. Radiogra-phy showed advanced degenerative changes of L4–5and L5–S1 that seemed responsible for the low backpain. In fact, these two levels were only slightly sensitiveon segmental examination that revealed, however, sharpsensitivity of T12–L1, with a precisely localized pain onpressure over the right facet joint. Radiographs of thatregion were totally normal. An injection of 1 mL of acorticosteroid derivative with lidocaine was performedat the T12–L1 facet. There was nearly immediate relief,and the patient could bend. Manipulation was thenpossible, and one maneuver in left rotation relieved hercompletely.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

ACUTE LOW BACK PAIN OF CALCIFYING DISCOPATHY

Isolated or integrated in the multiple tendinous calcifi-cations, calcifying discopathy at the lumbar level, as atthe thoracic level, can be responsible for a severe attack.Pain is induced rapidly. The slightest movement producesan extremely violent recurrence on a permanent basis,which is so painful that a patient cannot sleep. This painis usually well localized and does not radiate very much.Fever of 38.5°C is present, and there is an elevated sedi-mentation rate. Examination is very difficult because thepatient fears the slightest change of position; the abdomenis distended, the lumbar spine is stiff, and the paraspinalmuscles are firm, with contracture.

Diagnosis is made by radiographs that demonstratecalcification of the intervertebral disk and the integrity ofthe vertebral endplates and the vertebral body. The attacklasts several days and decreases with nonsteroidal anti-

inflammatories. Spontaneous resolution occurs in about10 days. With such a picture, some other possibilitiescome to mind, especially an infectious discitis or an occultmetastasis.

ACUTE LOW BACK PAIN OF MYOFASCIAL ORIGIN

Some chronic low back pain syndromes can originateat a trigger point, as described previously. In some cases,pain can be acute, and the attack can look like a low backpain of spinal origin. The painful muscular point is foundon examination, when pressure reproduces the sponta-neous pain. Trigger points can be found in the paraspinalmuscles between L1 and the sacrum, in the lumbar ilio-costal muscle, or in the longissimus. In these cases, thetrigger point is localized over the lower ribs. Injection ofa few milliliters of lidocaine or procaine produces relief.

305

43

SCIATICA

Common sciatica is the most frequent radicular painsyndrome of spinal origin. It is usually linked to irritationof a spinal nerve root associated with disk herniation atL4–5 or L5–S1.

ONSET AND TOPOGRAPHY

The onset is often traumatic. Exertion or a forced move-ment results in acute low back pain, followed by referralto the leg. Often this is exacerbated by standing, sitting,exertion, coughing, and sneezing, and relieved by lyingdown. Its referral pattern follows that of the L5 or S1territory: for L5, the buttock, anterior aspect of the thigh,lateral malleolus, dorsum of the foot, great toe or the threefirst toes (Fig. 43.1); for S1, the buttock, posterior aspectof the thigh, knee, leg and heel, to the sole or lateral sideof the foot, up to the fifth toe (Fig. 43.3). In the distallimb, pain may be replaced by tingling or numbness.

CLINICAL EXAMINATION

There is usually an antalgic attitude with scoliosis,either convex (often L5) or concave (often S1) to the sideof pain. If the patient tries to overcome the antalgic attitudeby compensating for the lumbar shift, a relative blockingof spinal motion is encountered, manifested by a break inthe normally smooth C-shaped curve formed by the lineof the spinous processes. With antalgic kyphosis, if thepatient tries to straighten up, the movement is alsoimpaired. Forward flexion in standing, with the legsextended, is limited and often exacerbates the pain. Thestraight leg raise test, performed either sitting (so that thepelvis is fixed) or supine (where the pelvis is free to move),often reproduces the referral pattern to the buttock and legas a result of the dural irritation produced by the disco-genic lesion. This is Lasegue’s sign and is useful forfollowing changes and assessing the efficiency of treat-ment. The neurologic examination is frequently negativeor reduced to minor signs including:

• Hypesthesia or hyperesthesia of the leg or the footin the L5 or S1 distribution.

• Diminished or absent Achilles reflex in S1 sciatica.• Occasionally, a subtle decrease in the motor power.

For S1, the plantar flexors may be weak, and thepatient may have difficulty performing heel raises(in subtle cases, it is only appreciable when thepatient is asked to perform a series of heel raises,alternately on each side, to see whether the involvedside fatigues sooner); for L5, the extensor of thegreat toe and, more rarely, the dorsiflexors.

Examination for Cellulotenoperiosteomyalgic Manifestations

It was with cases of sciatica that we first drew attentionto the simultaneous presence of cellulalgic manifestations,trigger points, and tenoperiosteal tenderness located in theterritory of the involved nerve root, and their role in certainpersistent pain syndromes (Maigne, 1961). These cellulo-tenoperiosteomyalgic manifestations exist in all cases(Fig. 43.2 and Fig. 43.5), and include the following:

• Trigger points are constant in the gluteal musclesand often present in the inferior part of the bicepsfemoris, in S1 sciatica. They are much less commonin L5 sciatica (extensor of the great toe).

• In 50% of cases, a cellulalgic zone is found overly-ing the posterior calf for S1 and at the superioranterolateral aspect of the leg for L5. It is usuallymore marked for S1 than for L5.

• Trochanteric tenderness to palpation is frequent inL5 sciatica. These manifestations may persist foryears after the attack. They either become latent orresponsible for residual and annoying pain. It is thenpossible to make a retrospective diagnosis of theinvolved segmental level.

Most often, trigger points are responsible for local orreferred pain that persists and is reproduced by musclefatigue or certain positions. For example, when com-pressed between the femur and the edge of a seat, the

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

trigger point of the short head of the biceps femoris makesthe sitting position painful; a trigger point of the lateralgastrocnemius (left leg) can be painful when the legs arecrossed (left leg on right leg) as it can be compressedbetween the left shin and the right knee. A trigger pointcan also be a source of cramps during the night. Often thecellulalgic zone, which is usually latent, can be responsi-ble for persistent moderate pain and, exceptionally, acutepain, as in the following case.

Case History

— Mrs. Z., a 48-year old patient, had L5sciatica not relieved by bed rest or by medical treatment.Myelographic studies confirmed the presence of a herni-ated disk at L4–5. She was operated upon, and thesurgeon found a large herniation that he removed easily.The antalgic attitude then disappeared, the spine becamesupple, and Lasegue’s sign disappeared. However, thepatient continued to complain that she had more pain thanbefore, especially when in bed, which was not made

Figure 43.1

Topography of pain in L5 sciatica.

Figure 43.2

Manifestations of cellulotenoperiosteomyalgicsyndrome in L5 sciatica.

Figure 43.3

Topography of pain in S1 sciatica.

Figure 43.4

Manifestations of cellulotenoperiosteomyalgicsyndrome in S1 sciatica.

CHAPTER 43 SCIATICA

307

worse by activity. She was rehospitalized, but no causecould be found for her refractory pain. She was giventricyclic antidepressant medication and anxiolytics, butwas not relieved. We then decided to examine her,although the pain had lasted for 5 months. The clinicalexamination (spinal examination, Lasegue’s sign) was

unremarkable. There were only two trigger points of thegluteus medius, minimally painful on examination, and acellulalgic zone of a few square centimeters on the lateralaspect of the leg, which was extremely painful to pinch-rolling. Injection of local anesthetic throughout this smallzone, on two separated occasions, resolved the pain.

Figure 43.5

Examples of manipulations used in two cases of right sciatica with opposite antalgic scoliosis.

A.

The pain isconvex to the side of the pain.

B.

The pain is concave to the side of the pain. The maneuvers performed are consistent withthe rule of no pain and opposite movement and are thus performed in opposite directions in the two cases. (The star diagramscorresponding to

A

and

B

are shown).

From upper diagram to lower diagram: manipulation in rotation to the left (subject onthe left); manipulation in rotation to the right (subject on the right); manipulation in left lateral flexion (subject on the left);manipulation in right lateral flexion (subject on the right); manipulation in left rotation and flexion (subject on the left); manipulationin right rotation and extension (subject on the right).

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

IMAGING

Radiography

The standard radiograph is useful to assess the state ofthe spine, but there is no relationship between the pictureand the clinical state. The picture can be normal in apatient with acute severe sciatica and, in other subjects,can show significant degenerative lesions that have noth-ing to do with the sciatica. The other examinations areonly indicated when a surgical intervention is being con-sidered or when the diagnosis is difficult.

Computed Tomography

Computed tomography (CT) is a noninvasive modalitythat can readily demonstrate morphologic abnormalitiesrelating to a herniated disk, including the relative impacton the adjacent soft tissues and whether there is any neu-roforaminal or extraforaminal encroachment. CT is usefulfor demonstrating central and lateral recess stenosis aswell as lesions of the facet joints. In cases of recurrentdisk herniation and especially in those patients who havealready undergone surgical procedures, CT with intrave-nous contrast can be used to differentiate between a recur-rent disk herniation and perineural fibrosis because theformer takes up contrast, while the latter does not.

Myelography

Myelography is excellent for assessing the entire sub-arachnoid space from the cervical spinal cord to the sacralroots and allows dynamic examination that can revealcertain impingements that are only visible in standingposition or in extension. It is also useful in the assessmentof spinal stenosis. It has the same disadvantages as diag-nostic lumbar puncture, including headaches, nausea, etc.(in approximately 35% of cases). Problems of neuro-toxicity of the contrast agent have now been eliminatedthanks to modern products.

Myelography is insensitive to far lateral herniationsincluding both foraminal and extraforaminal encroach-ments. Epidural lesions are visualized only if they haveleft an impression on the dural sac. A central disk herni-ation at L5–S1 in a patient with a short thecal sac with athick epidural fat pad will not be readily seen (Bard andLaredo).

Discography

Discography, an often neglected modality, is an excel-lent means of assessing disk pathology because of bothits morphologic depiction and its provocative properties.Contrast injected into an intervertebral disk can demon-strate the following:

• Whether the disk is of normal morphology• Whether there is evidence of annular or radial fis-

suring• Protrusion within the confines of the posterior lon-

gitudinal ligament• Extrusion beyond the confines of the posterior lon-

gitudinal ligament, with or without sequestration• Whether the “end feel” of the injection is firm or

whether the disk accepts an abnormally large vol-ume of contrast (e.g., when the annulus has rup-tured)

• Whether the patient’s typical pain is reproducedexactly

When followed immediately by CT, discography canprovide an excellent three-dimensional morphologic analy-sis that is often indispensable in the preoperative evaluation.

Magnetic Resonance Imaging

MRI is the study of choice for a recurrence followingdiscectomy, to differentiate recurrent herniation fromperineural fibrosis. It can also detect other lesions such asa neuroma that is located higher than the supposed causeof the sciatica.

CLINICAL FORMS OF SCIATICA

Hyperalgic Sciatica

Hyperalgic sciatica is characterized by the severity ofthe pain. The patient prefers to remain in bed and ishesitant to move even slightly. These patients are oftenextremely difficult to examine. If the pain does not respondquickly to the treatment, sciatica can set in.

Of particular interest is a specific form of hyperalgicsciatica called myalgic sciatica. It is seen most commonlyin disk herniations affecting the S1 nerve root, and theneuralgic pain is associated with intense and often con-tinuous muscular pains and cramps affecting especiallythe biceps femoris, triceps surae, and, occasionally, thegluteal muscles. There is often a mild motor deficit. Fas-ciculations are usual.

Once the acute attack is over, moderate pain persistsfor months or years, with periodic cramps, often duringthe night or with certain positions. The segmentalcellulotenoperiosteomyalgic syndrome is much accentu-ated; the trigger points of the gluteal muscles, biceps fem-oris, and triceps surae are very taut and very painful. Theyplay an important role in the acute and chronic pain.

Paralytic Sciatica

On examination, a slight motor deficit can be detected.It is more frequent in L5 sciatica than in S1. In the lattercase, however, the damage can be severe if the subject

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309

cannot perform a heel raise on the affected side. Thisdeficit can be unmasked by applying pressure to the shoul-ders of a patient who is attempting to perform a heel raiseagainst resistance.

Subtle motor deficits that always recover are not to beclassified as paralytic sciatica. Only sciatica that has func-tional deficits (1% of cases, approximately) deserves thatname. Most often, paralytic L5 sciatica leads to footdrop,which forces the patient to modify the gait pattern byincreasing the amount of hip and knee flexion during theswing phase to avoid catching the toe on the ground atmidswing. This deficit is readily detected by the examinerbecause an audible foot “slap” is heard when the involvedfoot makes its initial contact with the ground as it beginsa new stance phase.

There is a great difference between a motor deficit thathas been graded 0 or 1 compared to those graded 3 or 4(Held et al.). Motor deficits of paralytic sciatica oftenaffect more than one nerve root, even when the painfultopography affects only one.

Sciatica in the Young

Sciatica is rather rare in persons under 20 years of age.The antalgic attitude is generally quite marked, with asignificant lumbar shift. Lasegue’s sign is usually positiveat 20° of leg elevation. If forward flexion of the trunk istested with the legs extended, it is surprising to find thatthis flexion is quite impossible; only the superiormostportion of the spine goes into flexion; the lumbar spineremains as rigid as an iron bar. This contrasts with thepossibilities of movement or of activities of the youngpatient who manages to “fake” remarkably well.

In children under 14 years of age, sciatica is rare. Theantalgic scoliosis is marked in flexion, occasionally result-ing in antalgic kyphoscoliosis. Most children with spon-taneously painful scoliosis are seen by their physicians,and rarely is their presentation acute (Fauchet). Sciaticain these cases is generally due to large disk herniations.Spondylolisthesis is still the most frequent cause of sciat-ica in this age group.

Sciatica in the Elderly

Sciatica is uncommon in persons over 60 years old. Iffacet joint spondylosis and spinal stenosis often play arole, herniated disk is not exceptional. Interestingly,Lasegue’s sign decreases in intensity with age. In theyoung, the sign at 10 or 20° is usual, and the patient hasmoderate pain and adapts well to it. The sign at 30° in aperson of 40 years of age means a severe sciatica andconfines the patient to bed. In an elderly patient, the signsof sciatica, although genuine, can be quite mild.

Sciatica and Spinal Stenosis

Verbiest pointed out the significance of congenital spi-nal stenosis in the development of compression of thecauda equina. Later, it was found that this condition, eitheracquired or congenital, could cause sciatica.

Two situations can occur:

1. When the spinal canal is narrow, especially atthe lateral recess, the slightest disk or articularalteration is capable of irritating the nerve root.

2. A spinal canal of normal dimensions candevelop acquired narrowing by the simultane-ous action of disk protrusions, hypertrophy ofthe ligamentum flavum, and facet joint spondy-losis. This acquired narrowing can produceradicular pathology without necessarily causinga localized compression. The stenosis can beglobal or central, lateral or foraminal.

Central Spinal Stenosis

A chronic evolving sciatic pain can be present. It cansometimes be replaced by paresthesia. It can be monorad-icular, often bilateral or alternating, or it can be polyradic-ular. Its physical signs are discrete. Symptoms of neuro-genic claudication are pathognomonic but exist in only50% of cases (Deburge, Lassale et al.) and can havediverse clinical aspects including premature muscularfatigue that forces the patient to stop walking or sensoryclaudication with paresthesia and pain. Forward flexion ofthe trunk relieves this pain.

Sometimes the picture is less typical. There is a per-sistent sciatic pain, generally of L5, worsening progres-sively, often in a solidly built man who bends slowlyforward when walking to feel relieved. Hyperextension ofthe trunk increases the pain, which evolves progressivelytoward chronicity with improvement and aggravationphases, influenced by fatigue and relieved by rest.

Myelography reveals characteristic images, especiallythinning of the epidural space; disappearance of the epi-dural fat pad; a festooned look like a string of the intra-dural opacity in lateral view; and decreased contrast in thenarrowed zones. CT/myelography is especially useful indemonstrating the morphology of the canal so that thestenosis is recognized.

Lateral Recess Stenosis

Lateral recess stenosis produces a monoradicular sci-atica, most commonly at L5, with a very strong mechan-ical component. Occasionally a degree of motor deficitoccurs, usually in relation to the degree of facet hypertro-phy, and occasionally there is an associated disk bulging.

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Foraminal Stenosis

L5–S1 disk degeneration leads to a relative superiordisplacement of the articular process of S1, which narrowsthe intervertebral foramen without necessarily havingspondylosis present.

DIFFERENTIAL DIAGNOSIS

Certain sciatic pains due to inflammatory, infectious,or tumoral causes can simulate common sciatica. In theyoung, there is the possibility of a spondyloarthropathy.Pain usually does not refer distal to the knee, is oftenbilateral or alternating, occurring episodically, and is notmodified by activity. Nocturnal pain is common, keepingthe subject awake much of the night.

Diagnosis can be made by PA views of the pelvis orspecialized Hibbs views of the sacroiliac joints as well asby an elevation in the sedimentation rate. It can be con-firmed by rapid response to medication. The HLA B27haplotype is commonly associated with this group of con-ditions and may be helpful diagnostically.

Intramedullary tumors, especially gliomas can producea sciatica that does not quite follow a radicular topography.Nocturnal pain is common, and the patient will stand orwalk to bring relief. Physical activity has no influence atall on the pain. The spine is sometimes very stiff. Radio-graphic studies are usually normal; it is rare to see theenlargement of the foramen intervertebralis because of thethinning of the pedicle. Diagnosis is made by lumbarpuncture and CT/myelography. Surgical interventionrelieves the patient.

Metastatic lesions or a multiple myeloma can result inintense refractory sciatic pain. Infectious discitis and sac-roilitis can also be manifested by sciatic pain.

Pseudosciatic Syndromes

Some disorders can simulate sciatic pain, such as peri-arthritis of the hip (tendinitis of the gluteus medius), butare rarely confusing. On the other hand, dysfunction ofthe lateral perforating branch of the abdominal genitalnerve or the subcostal nerve (ramus cutaneous lateralisand abdominalis) can sometimes appear to be a “mixed”or polyradicular sciatica (R. and J.Y. Maigne) (see Chapter47, “Perforating Branch Syndrome of T12 and L1”).

A trigger point of the gluteus minimus can cause a verymisleading referred pain that refers distally to the foot.Pressure on this point reproduces the radiating pain, whichdisappears with an anesthetic injection. As we have seenabove, certain low back pains of thoracolumbar origin cancause ectopic and pseudosciatic referral patterns (see“Ectopic Referral Patterns” in Chapter 41).

TREATMENT

Treatment of Attack

Initial management of the acute episode should includeback first aid, of which a component is helping the patientto find a pain-free position. Intermittent bed rest withmovement for short periods in between is probably thesingle most effective self-treatment the patient can imple-ment. The patient should lie on a firm mattress in theposition that feels most comfortable: lying supine, withhips and knees flexed, most often alternating with lyingon the side occasionally. In milder cases, a rigid lumbarorthosis can shorten the duration of or obviate the needfor bed rest.

Medication

Pain relief is of paramount importance to the patientwith sciatica. An epidural injection is often useful. In thehyperalgic forms, intrathecal injection of corticosteroidsby Luccherini’s technique can produce a remarkablereduction in pain. Anti-inflammatory medications andanalgesics are the usual treatment.

Manipulation can decrease or shorten an acute attack,but it is usually performed in moderate or persistent formswhen the acute phase is over. It can produce an excellentresult, sometimes even spectacular, if it is technically pos-sible and well executed. Patients believe they are cured,although they are only relieved, with little or no pain; sothey forget about caution, then face recurrence. For apatient who will not or cannot interrupt activities, a rigidlumbar orthosis is best. In fact, the best treatment of acutesciatica is all of the above together, adjusted according toresults and changes.

Surgery: Chemonucleolysis

For forms that are resistant to treatment and rest, addi-tional examinations, such as CT or myelography, oftenreveal a herniated disk for which surgical interventionsincluding chemonucleolysis or percutaneous discectomymay be considered. Sciatica caused by acute inflammatoryarthritis of the facet joint can be successfully treated withone to three local injections of corticosteroids.

Treatment by Manipulation

The useful maneuvers (the same as those for the acutelow back pain syndromes) are determined by the antalgicattitudes. However, even if the antalgic attitude is charac-teristic, careful study of muscle stretching during tests offree and painful movements (Fig. 43.5) is always best.It happens (rarely), especially in sciatica, that there isnot perfect coincidence between what is revealed by the

CHAPTER 43 SCIATICA

311

antalgic attitude and the study of passive movements exe-cuted on the lower lumbar region.

Sciatica, whose star diagram has three free orientations,is a good indication for manipulation; this is the most fre-quent case. If there are only two free orientations, maneuversof relaxation may be sufficient, and their result can be care-fully monitored. In general, sciatica is not a good indication.If there is no pain-free orientation, manipulation is contrain-dicated, as is the case in hyperalgic sciatica.

After each manipulation, the result should be retested:Lasegue’s sign and pain of the gluteal trigger points onpalpation; the subjective impression of the patient; and afunctional activity (e.g., putting on a sock). No maneuvershould be a setback. This cannot occur, of course, if therule of no pain is applied, the maneuver is perfectly exe-cuted in the pain-free direction, the patient position isoptimal, and the force used is adequate. In general, eachmaneuver has a positive effect; sometimes it producesnothing; but it should never cause aggravation.

The session should include well organized and welldosed maneuvers of relaxation, then mobilization, andfinally, the fewest manipulative maneuvers necessary(never more than three). Otherwise, there may be furtherexacerbation. The patient should be forewarned, however,of the possibility of a temporary exacerbation that nor-mally follows some manipulative sessions. After the reac-tion is over, there is generally an improvement, which isslight or significant, momentary or lasting. The secondsession is usually 3 to 4 days later. There is generally noflare-up after the second session. If the patient demon-strates good improvement after the first session, subse-quent sessions can be spaced at longer intervals. Mostpatients are relieved after three sessions. In some difficultcases, two or three more might be necessary. However, ifno partial or temporary improvement occurs during thefirst three sessions, the treatment should be stopped.

Treatment of Sequelae

In persistent sciatica, particular attention must be givento cellulotenoperiosteomyalgic manifestations that are fre-quently responsible for refractory pain. They can betreated locally, but the responsible spinal segment shouldnot have sufficient facet joint or ligamentous pain (inter-spinous ligament) to maintain them.

Trigger points should be treated by stretching and slow,deep, and progressive kneading massage. Acute triggerpoints can be injected with procaine or lidocaine, followedby stretching of the muscle; ultrasound often producesgood results. Trochanteric pain (L5) will be relieved bythe spinal treatment, but it occasionally requires localtreatment. Cellulalgic manifestations are treated by anes-thetic injection of the subcutaneous tissues followed bykneading. A stay at a spa for hydrotherapy can also havea very good effect in chronic cases.

Rehabilitation

Once the attack is over, therapeutic exercises can beintroduced in cases involving a true low back pain afterdysfunction of thoracolumbar origin has been ruled out oraddressed.

Paralytic Sciatica

Certain authors (e.g., G. Lazorthes et al.) prefer an earlysurgical intervention, as soon as the first signs of neuro-logic deficit are noted. Others (e.g., Held et al.) attest thatsurgical intervention does not result in a more completeor more rapid recovery, especially when the original neu-rologic deficit is complete (as in such axonal lesions asaxonotmesis or neurotmesis). Surgical interventions areusually reserved for patients without total neurologic def-icit, who seem to have the potential to recover normalneuromuscular function in the same manner and timecourse as nonoperated patients. Sany et al. believe thatfactors indicating a good prognosis are early treatment,the topography of pain, age of the patient (less than 40years old), absence of any lumbalgic or sciatic antecedentand absence of any sensory or motor deficit. Therapeuticexercise will hasten recovery and should be continued longafter the symptoms have resolved. Later-stage recovery,over 3 or 4 years, is not uncommon. The use of anankle–foot orthosis can temporarily relieve the foot drop,as well as improve lateral instability.

Sciatica in the Young Patient

Most authors prefer early intervention. The clinicalsigns and the duration of progression are deciding factors.Medical treatment is efficacious; there is no indication formanipulation. Cases in which the lumbar shift is moderateseem to us to be the most amenable to improvement.Treatment should be limited to the relief of the patient;dramatic improvements in spinal mobility or in Lasegue’ssign are rarely attainable goals. Sometimes young patientswill declare that they feel better when the Lasegue’s signis still at 30° and anterior flexion of the trunk is stillvirtually impossible. If the relief is satisfactory and thereis minimal lumbar shift, it is better to wait because thisstiffness will generally decrease progressively and disappearafter several months without any other treatment. The bestadvice is to avoid overexertion and sports during that period.

However, if the pain is sharp and the lumbar shift issignificant, these young patients should be operated uponas soon as possible, which means that, in general, surgeryis more common in the young than in the adult.

Sciatica in the Elderly

Medical treatment is the same as that for the adult, exceptthat manipulation is to be avoided in most cases. If thistreatment is not efficacious and the patient is in great pain,

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then surgical treatment is necessary, whatever the age of thepatient, if the diagnosis is disk herniation. In patients withspinal stenosis, the medical treatment is injection and com-plete rest in recumbent position for 2 weeks, followed by arigid lumbar orthosis worn for 15 to 20 days, and then areinforced lumbosacral corset and rehabilitation.

A flexion exercise program is usually prescribed, withparticular attention to hip joint flexibility. The aim is to

relieve the lumbosacral spine, which is often in hyperlor-dosis (Troisier, Rabourdin).

Surgical intervention is considered only after a wellplanned medical treatment fails, as it is indicated only forsciatica associated with intermittent weakness and not forthe associated low back pain. It consists of a laminectomyfor central stenoses and a partial facetectomy in the lateralrecess stenoses.

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44

FEMORAL NEURALGIA

Femoral neuralgia is much less common than sciatica.It is most often due to irritation of the L3 or L4 nerveroots by a disk herniation. Facet joint spondylosis narrow-ing the intervertebral foramina can also be a source ofaggravation. Femoral neuralgia is more often seen in menover 40 years of age. Besides common femoral neuralgia,there are other symptomatic femoral neuralgias that areuseful to understand.

INITIAL SYMPTOMS AND TOPOGRAPHY

Femoral neuralgia frequently starts with physical exer-tion. The pain is initially felt in the low back, followed byreferral to the anterior thigh, toward the knee. If L3 isaffected, pain is felt over the anteromedial thigh and stopsat the patella. If L4 is affected, the pain may descend asfar distally as the anteromedial leg to the ankle (Fig. 44.1aand b). Mixed or overlapping topographies are common.Pain is internal, deep, and shooting, and nocturnal flare-ups are frequent.

CLINICAL EXAMINATION

On examination, the spine is stiff, but the possibleantalgic attitude is less marked than it is in sciatica. The“sign of Leri” or the “inverse Lasegue sign” is character-istic of femoral neuralgias. This sign is elicited with thepatient in the prone position. The physician fixes the pelviswith one hand while hyperextending the thigh with theknee flexed. This maneuver stretches the femoral nerveand, when it is irritated, produces or increases the painand the referral pattern. The following can be found:

• Hypoesthesia or hyperesthesia in the L3 or L4 region(medial aspect of the knee, medial aspect of the leg)

• Blunting of the patellar reflex• Decrease in the strength of the quadriceps, which

become hypotonic and often amyotrophic

L3 contributes to the innervation of the psoas, adductor,and quadriceps muscles and, with its posterior ramus, thespinal muscles. The L4 root contributes to the innervationof the gluteal, adductor, quadriceps, tibialis anterior, andextensor digitorum and, with its posterior ramus, the spinalmuscles. When the quadriceps is involved, the patientcannot raise the heel from the supine position. In a severeattack, the lower limb gives way and causes falls.

According to Godebout et al., sartorius weakness is aconstant sign in femoral radiculopathy. They note theabsence of the “band of sartorius” that can only be con-firmed in lean or muscular persons.

CelIulotenoperiosteomyalgic Manifestations

The midpoint of the rectus femoris is often the site ofone or two firm trigger points. These points can be a source

Figure 44.1

Topography of pain in L3 femoral neuralgia onthe left (

a

), and L4 on the right (

b

).

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

of chronic pain and even exacerbate it in the acute phase.Their injection often decreases the pain. They are lessfrequently seen in the vasti medialis and lateralis, butwhen present, they may be a source of pseudopatellofem-oral pain and pseudoblockage.

Cellulalgia is practically constant. It is found at thethigh (L3, L4, over the medial knee, where it is oftenpersistent) and in the region of the pes anserinus (L4).Pain with palpation in the superior medial aspect of thetibial periosteum (L4) is frequent (Fig. 44.2).

DIFFERENTIAL DIAGNOSIS

Nerve impingement due to disk herniation is not theonly possible cause of femoral neuralgia. The nerve couldbe impaired along its path by sacroiliac arthritis or as aresult of an appendicular or colitic disorder. There canalso be infection, spinal metastases, or neuroma, which isalways a possibility with any radicular pain. The nervecan be compressed at the hip by a truss or a large ganglion.

In some cases, a viral origin has been proposed. Inhemophiliacs or in patients on anticoagulants, a retropsoashematoma can result in motor deficits that are often sig-nificant. An antalgic posture in psoasitis is the rule. Thefemoral nerve might also be the victim of compression bythe retractors during pelvic surgery. It can also be irritatedby the cement of a hip prosthesis (methyl methacrylate).

TREATMENT

Treatment is the same as for true sciatica. Rest, injec-tions, and anti-inflammatories are the essential modes oftherapy. Manipulation, as in sciatica, can be very useful,especially in the moderate and chronic forms. The mostused manipulations are those involving the lateral decu-bitus, astride, and knee techniques, which are, of course,tailored to each case according to the rule of no pain andopposite movement.

Treatment of the cellulalgic, tenoperiosteal, and myal-gic manifestations can shorten the persistent pain. Oncethe attack is over, reconditioning of the quadriceps mech-anism is necessary. Priority is given to isometric exercises,with particular attention to good stability during singlesupport.

Figure 44.2

Manifestation of the cel lulotenoperios-teomyalgic syndrome of L3 and L4: cellulalgic zones (gray);trigger points (quadriceps and vastus medialis); tenoperi-osteal pain (circle).

315

45

MERALGIA PARESTHETICA

Meralgia paresthetica was described by Roth, whoobserved it in 1895 in German riders wearing tight abdom-inal belts that compressed the emergence of the femoro-cutaneous nerve at the level of the ilioinguinal angle,below the anterior superior iliac spine. They complainedof curious symptoms characterized by bizarre feelingsover the lateral thigh. Meralgia paresthetica is in fact char-acterized by paresthesia along the anterolateral side of thethigh, corresponding to the distribution of the femorocuta-neous nerve (Fig. 45.1, left).

Exquisitely sensitive, this nerve comes from the ante-rior rami of the second, and occasionally from the third,lumbar spinal nerve roots. It becomes superficial at a pointlocated 2 cm anteromedial to the anterior iliac spine, thengoes down along the anterolateral side of the thigh.

Meralgia paresthetica is almost always unilateral. Thepatient complains of a feeling of “dead skin” in that zone,

with tingling (pins and needles) or prickling. The skin ishyperesthetic and contact with clothes can be disa-greeable. Most often, these feelings are triggered by walk-ing or prolonged standing and are soothed by rest.

Sensory disorders are frequent but not constant: loss ofpain and temperature sensation, hypesthesia, and pain oncontact. In all cases, there is an unrecognized sign, a sharppain of the skin (often thickened) on pinch-rolling (Maigne).

Meralgia paresthetica is perhaps not as rare as isthought, but when it is mild and intermittent, it is only amoderate inconvenience. The different therapeuticapproaches tried at the onset of this disorder are often oflittle benefit, causing the patient to simply accept thissmall annoyance and not always mention it to a physician.During a systematic examination of a patient presentingwith another painful disorder, it is not rare to find a zoneof hyperesthesia and cellulalgia over the lateral side of the

Figure 45.1

Left

, lateral femoral cutaneous nerve (gray).

Right

, painful zone on the pinch-roll test in meralgia pares-thetica.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

thigh, discovered by pinch-rolling (Fig. 45.1, right). Whenasked, the patient recognizes having had disagreeable feel-ings in that region for a long time, separated by longintervals of relative calm in which a prolonged walk doesnot produce any disagreeable feeling. With a more pro-nounced form, the daily discomfort motivates the patientto look for a solution and seek some opinions.

CANALICULAR ORIGIN

Meralgia can be due to the irritation of the femorocu-taneous nerve at its emergence near the anterior superioriliac spine. There can be microtrauma (e.g., weight bearingon the thigh, hernial bandages). In some rare cases, meral-gia is symptomatic (e.g., abscess, tumor). Most often, itis caused by a fibro-osseous entrapment mechanism.Between its abdominal path, which is horizontal, and itsfemoral path, which is vertical, the nerve undergoesangulation, putting it under particular stress. At that level,it can be compressed by the thickening of the fascia iliaca(Stookey, Dupont et al.). When decompressed surgically,there is a prestenotic swelling (Claustre et al.). This abnor-mality was also found at autopsy in subjects who neverhad any meralgia. In 60 autopsies, Nathan found 36 casesof enlargement of the nerve and 10 cases in which thatnerve showed a fusiform “pseudoganglionic” aspect. Ifthis anatomic factor predisposes, it is thus not sufficient;an additional factor, usually spinal, is necessary.

SPINAL ORIGIN

A spinal origin is sometimes considered when the seg-ment L2–3 demonstrates disk degeneration or spondylo-sis. This presumptive sign is of no more value than is alow lumbar discopathy seen in radiographic studies to alumbar pain. In fact, systematic use of the segmental

examination enabled us to learn that meralgia is veryfrequently of spinal origin, by revealing a pain in segmentL2–3, while this segment is most often radiologically nor-mal. The patient sometimes complains of low back painipsilateral to the meralgic symptoms, but the pain is notnecessarily concomitant, and is usually left in the back-ground.

The pinch-roll test is painful on all or part of the ante-rolateral side of the thigh and, in some cases, in the medialiliac crest region 7 or 8 cm lateral to the midline. Thiscorresponds to the crestal point where the posterior ramusof L2 can be compressed against the iliac crest. Accordingto our anatomic findings, this ramus passes at this pointin one third of cases (in two thirds it is L1) (J.Y. and R.Maigne; see Chapter 41).

MIXED ORIGIN

As is the case with many pains of spinal origin, mer-algia paresthetica seems generally to have a dual origin.

• Dysfunction of spinal segment L2–3• Irritation of the femorocutaneous nerve in its course

along its abdominal and femoral paths

These contributors are of variable importance, depend-ing on the case. Suppression of one of the two factorsusually suffices to suppress the symptom. Spinal treatmentalone (manipulation and/or facet joint injection) yieldedexcellent responses in 30 of the 42 patients we studied.Most of these patients had been suffering for several years(20 years for the oldest). Sometimes, an occasionalmanipulation (once or twice yearly) is necessary becausethe causative PMID tends to recur.

N.B.

As we shall see in Chapter 47, meralgia paresthetica canbe simulated by irritation of a nearby nerve: the lateral cutaneousperforating branch of the abdominogenital and iliohypogastricnerve (L1) or the subcostal nerve (T12) (R. Maigne).

317

46

COCCYGODYNIA

Coccygodynia is a benign disorder, often refractory,and “wearisome for the patient and for the physician”(Louyot). It can be a simple inconvenience or a handicap-ping disorder with strong psychologic effects; it affectswomen slightly more than men. We propose here a tech-nique that can give quick, sometimes immediate, relief incoccygodynia of mechanical origin.

The usual cause of traumatic coccygodynia is a fall onthe buttocks, which occurs, according to authors, in 60 to70% of the cases. The coccygeal pain is generally imme-diate, but in some cases, it may remain latent for 1 or 2years between the fall and establishment of the coccygo-dynia. In the meantime, there is generally a slight painwith prolonged sitting or at contact.

Coccygodynia may occur on recovery after givingbirth. Some cases seem to be linked to lumbosacral prob-lems; they come after or with low back pain, and they candisappear after lumbosacral manipulation or epiduralinjection. Others result from anorectal infections and areseen especially by proctologists. We observed a chordomathat was manifested for 2 years by coccygeal pain. Finally,some others are called essential, since no cause can befound. Psychologic causes are classic, with coccygodyniaappearing, for example, after the loss of a loved one or adivorce.

DIAGNOSIS

Pain of the sacrococcygeal region is too easily calledcoccygodynia. To arrive at this diagnosis, the characteris-tic sign of pain on pressure of the tip of coccyx should befound.

Occasionally, pressure on the sacrococcygeal articula-tion is painful. In some cases, we have observed triggerpoints at the level of the sacrococcygeal insertions of thegluteus maximus or a trigger point of the pyriformis.Occasionally, one can detect a significant unilateral para-coccygeal cellulalgic zone. Most often, there is only pain

on the tip of the coccyx. On rectal examination, there aretaut bands in the levator ani and the pyriformis.

TREATMENT

In general, coccygodynias have the reputation of beingrefractory to treatment. Massages of the levatores andinjections yield only irregular success. Almost always,coccygodynia occurring after a fall or labor and deliveryis immediately cured by the maneuver that we proposebelow. Other cases are cured much less often.

Massage of Levatores

Thiele proposed this massage. Francon considered it arather efficient maneuver, but its action is far from con-sistent; a certain number of sessions are generally neces-sary. We have abandoned this technique because the onewe propose appears to be faster and more frequently effi-cacious, at least in our hands.

Osteopathic Technique

The manipulation (Fig. 46.1) involves mobilization ofthe coccyx by grasping it between the thumb (external)and the index finger (intrarectal) and applying flexion,extension, and rotation. Performed this way, we find themanipulation to be very unreliable.

Authors’ Technique

The patient is in a prone position (Fig. 46.2). The phy-sician introduces the right index finger in the rectum (withpalmar side of the finger applied against the inferior aspectof the anterior sacral surface). The examiner maintains thecoccyx in hyperextension, rather than pulling strongly on it.

Then the physician places the heel of the left hand onthe superior aspect of the posterior sacral surface andapplies firm and progressively increasing pressure. Pres-sure is maintained for 20 to 30 sec while the right indexfinger maintains the coccyx in hyperextension. Without

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ever pulling back, the operator, at a given moment, hasthe impression of a sudden release, which is probably fromthe levatores. The maneuver is over. Pressure on the tipof the coccyx is usually asymptomatic, allowing thepatient to sit without inconvenience. Sometimes, repeatingthe maneuver two or three times over several days isnecessary for a lasting result.

This maneuver seems to stretch the levator, whichrelieves the spasm and the essential element of the coc-cygodynia. Indeed, the “cord” of the levatores disappearsas soon as the maneuver is successful. For some, thismaneuver acts on the sacroiliac, whose blocking in the“posterior sacrum” according to osteopathic terminology(Renoult) may play a role in this disorder. An L5–S1segmental dysfunction seems to be responsible forreferred pain to the coccyx. Lumbosacral manipulationand epidural injection can then be useful.

Figure 46.1

Osteopathic technique. The operator introducesthe index finger into the rectum and pinches the coccyxbetween the index finger and the thumb. The coccyx canthen be mobilized in extension or in lateral flexion and rota-tion. This is the technique proposed by J.B. Mennell.

Figure 46.2

Authors’ technique. See description in text.

319

47

PERFORATING BRANCH SYNDROME

OF T12 AND L1

Irritability of the lateral perforating cutaneous branchesof T12 and L1 is part of the “syndrome of the thoracolum-bar junction” of Maigne (see Chapter 60). There is a spinalcause (T12-L1 or L1-2) that requires spinal treatment. Butthese branches are also susceptible to entrapment as theytraverse the iliac crest (R. and J.Y. Maigne). These twoetiologies can be associated.

ANATOMY

Classic Studies

According to the classical notions, the iliohypogastricnerve (or abdominogenital nerve) (L1) gives off a branchnear the midaxillary line. It courses downward prior tocrossing the obliquus muscles above the iliac crest, whichit crosses. It then supplies the cutaneous surface of thebuttock (according to Testut); it innervates the superiolat-eral part of the buttock and the thigh (according to G.Lazorthes, it is the lateral cutaneous perforating branch)(Fig. 47.1).

Similarly, another perforating branch, the glutealramus, comes off laterally from the 12th intercostal nerve(T12). It traverses the iliac crest in front of the precedingbranch and innervates the cutaneous surface of the lateraland superior buttock (Testut) (Fig. 47.1). In the anatomicdrawings that show them, these nerves stop above thetrochanter.

Maigne Study

Our anatomic study done with J.Y. Maigne involved20 subjects studied bilaterally (i.e., 40 dissections). Itdemonstrated that

• The perforating branch of the subcostal nerve (T12)becomes superficial 1 to 2 cm above the iliac crestin perforating the internal and external lateraloblique muscles of the abdomen, and it crosses the

iliac crest 5 to 8 cm behind the anterior superioriliac spine (Fig. 47.5).

• The perforating branch of the iliohypogastric nerve(L1) becomes superficial slightly lower, 1 to 2 cmbehind the preceding one. It often leaves the impres-sion of a small bony gutter on the iliac crest, throughwhich it passes. This gutter (which has not beendescribed, as far as we know, but which is palpablein the living) is transformed into a fibro-osseoustunnel by the oblique muscles of the abdomen andtheir aponeurosis (Fig. 47.6). This passage is rela-tively narrow and can sometimes compress the nervealong its course, as we saw in one dissection thatdemonstrated pre- and poststenotic swelling, which

Figure 47.1

The lateral perforating cutaneous branchesoriginate from the subcostal nerve (T12) and the iliohypogas-tric (or abdominal–genital) nerve (L1). These branches mayvary in size.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

opens the possibility of an entrapment syndrome.(We made the same observations during some sur-gical decompressions to free the nerve.) The cross-ing point with the iliac crest is not a right angle; thetwo branches lie on it for 1 to 2 cm and then resumetheir vertical path.

After traversing the iliac crest, these nerves supply theskin overlying the lateral aspect of the hip. The iliohypo-gastric nerve (L1), which is usually the longer of the two,then passes 2 to 3 cm anterior to the greater trochanter.Three variations were noted: short (Fig. 47.2, left),medium (Fig. 47.2, middle), and long (Fig. 47.2, right).In the short variety (8 cases), it does not reach the tro-chanter. In the medium variety — the most frequent (22cases), it branches out at that level. In the long variety (6cases), it can be dissected up to 7 to 9 cm distal to thegreater trochanter and branches out below. In 4 cases, thisnerve did not exist. Its homologue arises from the subcos-tal nerve, which occasionally anastomoses with it, and canpresent the same variations: short, 28 cases; medium, 8cases; and long, 4 cases. In summary, the results of ourstudy show that:

• The lateral perforating cutaneous branches, in manycases, terminate much more distally on the thighthan the classical descriptions mention.

• An entrapment syndrome is possible at the crossingpoint of the iliac crest.

CLINICAL EXAMINATION

Pressure over the iliac crest on a line passing throughthe trochanter reveals a very tender point, the “lateral

crestal point.” One is often able to palpate a small notchon the iliac crest that corresponds to the bony “notch”noted in the cadaver (Fig. 47.3, left and right).

The skin overlying the trochanter that corresponds tothe territory of the lateral perforating branch is painful topinch-rolling and is often thickened. It can cover a narrowband which, especially for L1, can go down to midthighand sometimes lower, following the path of the seam ofthe trousers (Fig. 47.2, right, and Fig. 47.4).

When the syndrome manifests with neuralgic pain orparesthesia, lateral stretching in forced adduction of thelower limb (with patient in supine) can sometimes repro-duce the pain, analogous to a lateral Lasegue’s sign. Allexamination signs and spontaneous discomfort disappeartransiently with anesthetic injection at the level of thelateral crestal point.

CLINICAL PRESENTATION

We have seen three clinical presentations involving thedysfunction of these branches.

1. The first is associated with periarthritis of thehip and is by far the most frequent (90 of 103cases).

2. The second is meralgia paresthetica (7 of 103).3. The third is a truncated sciatica (6 of 103).

Pseudoperiarthritis of Hip

Most often, pain simulates periarthritis of the hip,such as tendinitis of the gluteus medius. The patientcomplains of pain along the lateral aspect of the hip,

Figure 47.2

According to classic description, the perforating cutaneous branches only go as far as the trochanter. In fact,we have been able to demonstrate three varieties (J.Y. Maigne): the short variety that corresponds to the classic description(see Fig. 47.1); the median variety that overlies the trochanter; and the long variety that descends to midthigh.

CHAPTER 47 PERFORATING BRANCH SYNDROME OF T12 AND L1

321

radiating sometimes toward the groin and lateral thigh.Pressure on the trochanter is very painful, but localinjection does not bring any relief. Indeed, pain is causedby compression of the cellulalgic subcutaneous tissuesagainst the trochanter, which is painful to pinch-rolling.Anesthetic injection of the lateral crestal point relieves ordecreases the pain to pinch-rolling as well as the sponta-neous pain from pressure on the trochanter. This injectioncombined with a few milliliters of a corticosteroid deriv-ative and repeated two or three times often results in

lasting relief. The following case history is typical. Itinvolves a patient believed to have an entrapment syn-drome of this perforating branch, the first patient for whomwe prescribed surgery to release the nerve; a PMID atL1–2 was also partially responsible.

Figure 47.3

Left

, examination for the lateral crestal point. The patient is lying on the right side and is seen from above.The finger is often able to feel a small notch over the iliac crest, in which one can find nerve branches.

Right

, the sameposition as noted in the prior patient. L = lateral crestal point. P = posterior crestal point, the point where compressionof the posterior ramus of T12 or L1 can occur.

Figure 47.4

Topography of the cellulalgic zone is variablylimited through the trochanteric and intratrochanteric regions.It presents as a narrow straight vertical band following thelateral crease of the pants. In fact, it corresponds to theterritory of the perforating branches (Fig. 47.2).

Figure 47.5

Perforating branches of lateral thigh. This is amedium-length variety: the branches descend slightly belowthe trochanter (T). EI = anterior superior iliac spine; the darkspot follows the iliac crest. Arrows show the crossing pointsof the branches in relation to the iliac crest:

1

, perforatingbranch of the iliohypogastric nerve (L1);

2

, perforating branchof the subcostal nerve (T12).

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Case History

—

Mrs. P.M., a 30-year old athleticwoman, suffered for years from pain over the righttrochanter, radiating toward the anterolateral thigh. Itrestricted her greatly. Pain started after a motocross race.The diagnosis of tendinobursitis of the gluteus mediuswas made. Several injections were performed withoutany success. Radiographs demonstrated two lacunas atthe level of the right femoral neck. She was hospitalizedin an orthopedics department, and a biopsy of the neckwas performed. Nonspecific bony lesions were foundbut were not felt to be responsible for her pain. Othertreatments yielded no results. She was followed for 2years in a pain center. She wore a stimulator for a yearwith mediocre results.

When we saw her, she could not remain in a sittingposition for more than a few minutes, especially if theseat was hard. Standing was also painful, extension ofthe trunk (position in lumbar hyperlordosis) wasunbearable, as was left lateroflexion. Pinch-rolling wasvery painful on a narrow vertical zone, going from thesupratrochanteric region to the inferior third of the lateralside of the thigh. A lateral crestal point was particularlyclear in the trochanteric line. The spinal segmental exam-ination revealed sensitivity of L1–2, with right facet jointtenderness. Radiographic studies showed an old fractureof the superior endplate of L2 (result of a fall from astool 10 years before) and lesions from sequelae ofspinal apophysitis at T12–L1 and L1–2. Thus, it was atraumatic PMID on a segment that had become fragile.The first session was a spinal manipulation and injectionof the crestal point, which brought distinct relief for thefirst time since the start of her pain.

After a few more treatments on the spine and thelocal cellulalgia, she could resume a nearly normal life.However, prolonged sitting was still very difficult for her,and spinal treatments during a systematic examinationno longer improved the situation. Because of our ana-tomic discoveries (i.e., the possibility of entrapment com-pression), we proposed surgical intervention. The sur-geon, Dr. Touzard, discovered that the perforatingbranch was being compressed at the level of the iliaccrest with a prestenotic dilation. Decompression com-pletely relieved the patient; 5 years later, the result ismaintained.

Pseudomeralgia Paresthetica

The patient has dysesthesia of the lateral thigh suggest-ing paresthetic meralgia paresthetica, but the topographyis higher and more lateral than in meralgia paresthetica,which the painful zone on pinch-rolling reveals very well.

Pseudosciatica

Pain radiates toward the gluteal region, down the lateralthigh to the knee. It occurs in attacks that persist, likeepisodes of truncated sciatica. In one of our patients, thesymptomatology was particularly painful; the origin wasmixed, spinal, and local simultaneously.

Case History

—

Mrs. S., an active 50-year old woman,experienced very painful episodes for the last 6 years.They required prolonged periods of bed rest that didnot completely relieve her pain. The pain was locatedover the lateral left buttock and radiated toward thelateral side of the knee.

She traveled a great deal and was hospitalizedseveral times in different countries. The diagnosis of L5sciatica was made, although Lasegue’s sign was absent.Epidural and even intradural injections had no effect.The attacks lasted about 2 weeks and were recurringmore frequently (six in the last year). Several CT scanswere done at different times. All were normal for theinferior lumbar levels explored. An American orthopedisttook out a large, calcified, gluteal hematoma, but thisdid not relieve the patient.

We saw her during an acute phase which, like thepreceding ones, occurred suddenly during a very smallmovement. She suffered a great deal and held herselfvery stiffly. Any trunk movement exacerbated the painradiating along the lateral side of the thigh.

Lasegue’ssign was negative, and there were no cellulotenoperi-osteomyalgic manifestations. A narrow cellulalgic bandthat was very painful to pinch-rolling went from thetrochanter to the thigh. A lateral crestal point was par-ticularly sharp. Its anesthetic injection brought apprecia-ble relief, which made the examination easier andrevealed the sharp pain of segment T12–L1. Radio-graphic studies performed immediately showed nolesions at that level. In the hours following the injection,pain reappeared, slightly diminished. The next day, a

Figure 47.6

The perforating branch of the iliohypogastricnerve (L1) crosses over the iliac crest in a small bony notch,which is palpable and which passes through a fibro-osseoustunnel where it can sometimes be compressed in an entrap-ment syndrome (R. and J.Y. Maigne).

CHAPTER 47 PERFORATING BRANCH SYNDROME OF T12 AND L1

323

manipulation performed at T12–L1 resulted in rapidimprovement, allowing her to move. A few other treat-ments, including manipulation, facet joint injection, andinjection of the lateral crestal point, brought a total relieffor 1 year. A recurrence was provoked by a forcedrotation of the trunk. The same signs, though decreased,were again found; 1 year later, she had had no furtherattacks.

In this form, very sharp pain is rare; it is usually sub-acute.

N.B.

During a systematic examination, it is common to find acellulalgic band along the lateral thigh in a patient who does notsuffer spontaneously. Like all latent cellulotenoperiosteomyalgicmanifestations, this can last a long time before pain occurs, forwhatever reason, isolated or associated with lumbar or abdominalpain (see Chapter 60).

TREATMENT

Treatment can be spinal, local, or both, depending onthe patient. With a spinal origin and thoracolumbar junc-tion syndrome, treatment can consist of manipulation,articular injection, and electrotherapy. For an entrapmentsyndrome, an injection of the lateral crestal point with amixture of a local anesthetic, 0.5% lidocaine, and a cor-ticosteroid derivative can be tried. When relief is insuffi-cient or only temporary, surgical decompression may beindicated (5 patients in our series of 103 cited above wereoperated upon). In mixed cases, local and spinal treat-ments can be used together.

In chronic cases, the cellulalgia should also be treated(tracing injections and massages with progressive kneading).

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48

HEADACHE OF CERVICAL ORIGIN

In the presence of chronic headache, a cervical originis generally considered only if the pain has a posteriortopography and if the superior cervical spine demonstratessome signs of radiologic abnormalities (especially facetjoint spondylosis). For most authors, the cervical spinedoes not play a major role in common headaches (1% forNick). Muscular, cervical, static, or postural origins aresometimes alluded to, but in general, common headachesare attributed to a psychologic origin (80% for Wolf andWolff) that manifests with protective guarding of the neckand shoulder girdle muscles. This type is commonlyreferred to as a “tension headache.”

The superior cervical spine seems to us to play a fre-quent role in common headaches. We have observed afaciocraniocervical semiology that makes it easy to rec-ognize them and to find useful treatments. If psychologicfactors are frequent in common headaches, they are per-haps sequelae, while the real cause of the headache isoften cervical.

Headache is a very nonspecific symptom with multiplecauses. Statistics show that 2 to 3 of 1000 headaches arecaused by serious disorders (Nick). Therefore, before aheadache is classified as common, a detailed and thoroughhistory and physical examination of the patient are nec-essary. If there is still any doubt, ancillary studies shouldbe performed and advice from specialists sought.

COMMON CHARACTERISTICS OF CERVICAL HEADACHES

Cervical headaches have their own semiology (Maigne,1968, 1976, 1981). They are most often unilateral. In allcases, there is tenderness to palpation of the C2–3 articularpillars ipsilateral to the headache (Fig. 48.1, left and right

).

During the different acute episodes, their topography isfixed, always right or always left for a given patient. Withtime, it can become bilateral, as can the physical signselicited.

For a given patient, the cause triggering the attack canalways be the same or vary from one attack to the other:postural, psychologic, digestive, menstrual period, etc. Itis sometimes impossible to determine the exact nature ofthe trigger. The attacks may vary in frequency and inten-sity and may last a few hours to a few days.

It is important to note that the cervical and craniofacialsigns of examination described below are constant andpermanent and can be found even between acute attacks.Suitable cervical treatment is regularly useful. Attacks andclinical signs of the examination disappear, even if theusual triggering factors persist.

Cervical Semiology

For us, the only spinal sign showing the cervical originof a headache is tenderness to palpation of the C2–3 facetjoint on the affected side. In 20% of cases, that pain isbilateral. A possible decrease in active or passive mobilityhas no particular value; it certainly demonstrates the exist-ence of a cervical problem, but it does not establish thecervical origin of the headache. It is unusual to provokethe headache by various cervical maneuvers. However,pressure maintained on the facet joint point can reproducethe usual referral pattern (Fig. 48.1, left and right).

In most cases, radiographic studies of the superior cer-vical spine are normal. The existence of arthritic lesionsdoes not automatically imply that they are responsible forthe headaches. In a patient having repeated attacks, facetjoint (C2–3) palpation is tender ipsilateral to the headacheand is found even between acute attacks. In general, it isthe result of a PMID. Occasionally, it can be due to syn-ovitis.

DIFFERENT ASPECTS OF HEADACHE OF CERVICAL ORIGIN

Three forms of cervical headaches can be distin-guished, each with its own semiology.

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1. Occipital (Fig. 48.2a)2. Occipitotemporomaxillary (Fig. 48.2b)3. Supraorbital, the most frequent, which cor-

responds to a projection of the cervical pain inthe territory of the ophthalmic division of thetrigeminal nerve (Fig. 48.2c)

Occipital Headache

Occipital headache is felt at the occiput and can radiateto the vertex. It corresponds to the territories of the posteriorrami of C2 and C3 (Fig. 48.3). Isolated, it represents 20%of headaches of cervical origin, but it is often associated

with other forms. The acute form is Arnold’s neuralgia; itis rare and its paroxysms are generally provoked by force-ful or strenuous movements of the neck. The chronic formis frequent. It is responsible for episodic occipital head-aches of variable duration and intensity. In both cases, the“friction sign of the scalp” (Maigne) can be found.

Friction Sign of the Scalp (Maigne)

Friction applied to the scalp replaces the pinch-roll test.It consists of pressing firmly with the pad of the fingersagainst the scalp and mobilizing it with small to-and-fromotions (Fig. 48.4). This maneuver is painless on a normal

Figure 48.1

Left

, cervical segmental examination for facet joint tenderness.

Right

, in all cervical headaches, the segmentalexamination demonstrates facet joint C2–3 tenderness on the side where the headache usually presents. The C2–3 facet jointis the highest that can be palpated. Stress on this facet joint translates to a dysfunction of C2–3 and eventually to segmentsthat are supra-adjacent, including C0–1 and C1–2.

Figure 48.2

Three types of cervical origin headache (Maigne).

a.

Occipital form.

b.

Occipital temporal maxillary form.

c.

Supraorbital form (most frequent). These forms can exist as mixed types.

CHAPTER 48 HEADACHE OF CERVICAL ORIGIN

327

scalp, but it is very disagreeable and even painful in thecase of an occipital headache of cervical origin. Ipsilateralto the C2–3 facet joint, tenderness is found.

The territory that is painful to friction can correspondto the posterior ramus of C3, which innervates the para-median zone, or to the posterior ramus of C2, whichinnervates the lateral part of the occiput (Fig. 48.3). It canbe more diffuse, but it does not go beyond the biauricularline. The periauricular region also receives innervationfrom C2 or C3, but it comes from their anterior rami.

Occipitotemporomaxillary Headache

The occipitotemporomaxillary headache is located inthe retroauricular, mastoid, and parietal region and radi-ates toward the inferior maxilla. Pain is found ipsilateralto the facet joint tenderness at C2–3, with a positive fric-tion sign over the painful scalp in the retroauricular terri-tory that is innervated by branches arising from the super-ficial cervical plexus (anterior ramus of C2, sometimes ofC3; Fig. 48.5).

Pain with pinch-rolling at the angle of the jaw is seen(Fig. 48.6). A fold of the skin is pinched firmly betweenthe thumb and index finger and rolled between these two

Figure 48.3

Posterior primary rami of C2 and C3 (C2P andC3P) and anterior primary rami of C2 and C3 (C2A and C3A)according to G. Lazorthes.

Figure 48.4

Friction sign of Maigne. The fingers rub thescalp against the skull. This maneuver is painful in territoriesthat are irritated. This test replaces the pinch-roll test in thisarea.

Figure 48.5

Topographies of innervation. C2P = posteriorramus of C2. C2A = anterior ramus of C2. C3A and C3P =anterior (A) and (P) posterior rami of C3.

Figure 48.6

Pinch-roll sign of skin overlying the angle of thejaw (Maigne).

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fingers. The maneuver should be controlled and be com-pared with the opposite side. It requires practice, as do allthe maneuvers that we propose here. The sign is positiveif the maneuver is painful (the fold can be thickened). Itis painless on the contralateral side if the impairment isunilateral.

The discomfort elicited at the angle of the jaw isreferred to as “the angle of the jaw sign” (Maigne). Thisskin region at the angle of the jaw is innervated by theanterior ramus of C2 and not by the trigeminal nerve.Isolated, this form comprises about 5% of headaches ofcervical origin, but it is often associated with another formof headache, presenting with mild features.

Supraorbital Headache

Supraorbital headache is the most frequent headacheof cervical origin (67% of cases in our statistics). Thetopography of the pain is usually supraorbital, sometimesoccipitosupraorbital, and in a few cases, retro-orbital. Italways carries with it the “eyebrow sign.”

Eyebrow Sign (Maigne)

The eyebrow is pinched between thumb and index fin-ger and kneaded and rolled like a cigarette. It is exploredfrom one end to the other, going over the skin of theforehead (Fig. 48.7). When the sign is positive, the foldis painful and often thickened throughout all or part of thelength of the brow. This sign is found only on the side ofthe usual headache, which is generally the side of the C2–3articular pain. The maneuver is painless on the other eye-brow, except in cases of bilateral headache.

The link between this sign and an origin in the cervicalspine is shown by the response to injection of local anes-thetic at the C2–3 facet joint. A few moments after the

injection, the eyebrow is no longer painful to pinch-rolling(Fig. 48.8). The fold becomes supple and thin. The sameresult can be obtained with any manual therapy maneuverthat renders the C2–3 articulation painless (Fig. 48.9).Conversely, a poorly performed manipulation thatincreases C2–3 tenderness also increases the sensitivity ofthe eyebrow and usually results in headache.

We did not find this sign in the true migraines, evenwhen they had a dominant radiation toward the eye, norin the other forms of headaches (sinusitis, psychologicheadache, etc.). On the other hand, the supraorbital cer-vical headache can have a migrainous character (see Chap-ter 49, “Cervical Migraine”).

Cheek Sign (Maigne)

Some patients with the eyebrow sign also have sometenderness to pinch-rolling the skin of the cheek, locatedbelow the maxilla (cheek sign). This maneuver is partic-ularly painful in some facial pain syndromes that arerelieved by cervical treatment.

Figure 48.7

Eyebrow sign of Maigne. The pinch-roll eyebrowsign is painful, and the skin is thickened on the side of thecervical origin headache. This is essentially the sign ofsupraorbital headache of cervical origin. It disappears withanesthetic injection of the C2–3 facet.

Figure 48.8

Injection of C2–3 facet joint.

Figure 48.9

Example of manipulation of superior cervicalspine in the treatment of cervical origin headache.

CHAPTER 48 HEADACHE OF CERVICAL ORIGIN

329

Different Aspects of Supraorbital Headache of Cervical Origin

The supraorbital type represents 67% of headaches ofcervical origin. It can have three clinical presentations:simple form (85% of cases), vascular form (10% of cases),and migrainous form (5% of cases). These are personalstatistics from 162 cases of cervical headache. The break-down may vary, depending on the recruitment. For allthese forms, frequency, intensity, and duration of the epi-sodes of headache are extremely variable from case tocase, spanning a spectrum from mild low-frequency head-ache to the intense, daily, incapacitating headache.

Simple form —

The most common form, it involvessupraorbital or occipitosupraorbital pain. It is alwayslocated on the same side for a given subject. It can migrateto the other side if an episode is severe, but its examinationsigns remain unilateral. It can be truly bilateral in somecases. Some patients describe it as the pain of a frontalsinusitis. It is sometimes felt as a retro-orbital pain;the patient has the impression that his eye is “pulledbackward.”

Vascular form —

In this less frequent form withsupraorbital pain, the patient also has nasal congestion(the nostril is clogged with or without rhinorrhea) andoccasionally a unilateral tearing. These manifestations arealways ipsilateral to the C2–3 facet joint tenderness, andthe eyebrow sign is always positive on the same sideduring successive attacks. The efficacy of medications forthe headache is generally poor, whether antiserotonin oran ergotamine derivative is used. The cervical treatmentis the only one that is useful. The following case is typical.

Case History

— A 42-year old woman suffered fromheadaches for 13 years. They had become progres-sively worse during that time, with increasing frequencyand duration, without any precipitating cause. Whenshe consulted a physician, the attacks occurred three tofour times a month, lasting 2 to 3 days. Topographywas supra- and retro-orbital, always on the left, withswelling of the left nostril, then rhinorrhea and wateringof the left eye. She was followed in two departments ofneurology, and their diagnosis was vascular headache.She was not relieved by ergotamine tartrate, dihydroer-gotamine, or antimigraine medication but was wellrelieved with amidopyrine (6 tablets/day of Optalidon).On examination, the left eyebrow was thickened andvery painful to pinch-rolling, and sharp pain was notedat the left C2–3 facet joint. Cervical radiographs werenormal. Four manipulative treatments and two injectionsrelieved her. She did not have any more attacks for thenext 12 months. This form of headache represents 8.5%of cases of cervical headaches in our statistics (14 casesof 162).

Migrainous form —

In

some cases, the migrainousform has the characteristics of true migraine. It is a non-

alternating migraine, localized always on the same sideduring successive attacks. It often responds poorly to anti-migraine medications, but cervical treatment is very useful(see Chapter 49, “Cervical Migraine”).

TRIGGERING FACTORS

Whatever its variety, headache of cervical origin canbe episodic, with variable intervals between attacks. It canbe mild or severe, but as stated above, the examinationsigns that we describe persist beyond the attacks.

The triggering factor can be cervical. It is often pos-tural, such as improper neck positioning on the pillow(sleeping prone) or improper workplace ergonomics thatput patients in strained positions. These headaches canalso be provoked by cold drafts on the neck or triggeredby gynecologic, dietary, or psychologic factors. Often theheadache is fallaciously attributed to these factors withoutconsidering a cervical etiology, despite the fact that cer-vical treatment is the only one that is efficacious and longlasting.

These headaches can also be triggered by minor factorsin persons whose tolerance threshold is very low. Theslightest articular dysfunction is then felt even while thephysical or psychologic state is good. This is consideredto be the mechanism in slightly depressed or anxiousindividuals and spasmophiles (M. Duc, M. Janel), etc. Inthese people, the psychologic factor is often, wrongly, theonly one tended to.

FREQUENCY OF CERVICAL HEADACHES

Cervical headaches are frequent. The frequency foundin various studies depends on the recruiting; in our statis-tics, they represented 80% of unscreened headaches (162cases on a known sampling of 200 cases). J.L. Garcia(1977) used our semiology and diversified its recruiting;he obtained identical figures for 110 cases. His studiesdemonstrated the efficiency of the cervical treatment thatwe propose. He studied three groups of patients with com-mon headaches. The first group was recruited frompatients referred for neurologic consultation. The secondgroup was recruited from patients referred for rheumato-logic consultation. The third group was recruited amongpatients in general medicine selected from a populationthat was easy to follow (military personnel and their fam-ilies). A total of 110 patients was recruited; 87 met thecriteria for cervical headache as we have defined them;78 were followed up and seen regularly. Treatment bymanipulation and sometimes by articular injection brought90% good results with 1 year of follow-up.

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Frequencies of Different Forms

All the forms described above can be seen in isolatedor mixed forms. However, a painful topography is mostoften dominant. In the 162 cases of our study, the domi-nant pain was:

Frontosupraorbital or supraorbital 110 casesOccipital 35 casesOccipitomaxillary 7 casesDiffuse 10 cases

There was always a correlation with the examinationsigns. However, the signs can be present without the painof the attack occupying all the painful territories at exam-ination. For example, the eyebrow sign can be positive ina cervical headache that is painful only in the occipitalregion, but in this case, the friction sign is always positive.

Remarks

Persons showing C2–3 facet joint tenderness on examina-tion do not all have headaches. Those who present othersigns of the craniofacial semiology that we propose arerarely without any episodes of headache, at least mildheadaches of low frequency.

PATHOPHYSIOLOGIC MECHANISMS

There are two questions about the mechanisms of theseheadaches: the first relates to the cause of the C2–3 facetjoint tenderness, the second concerns the supraorbital pro-jection of pain and the eyebrow sign.

C2–3 Facet Joint Tenderness

Facet joint tenderness is a constant sign of PMIDs atall levels of the spine. C2–3 facet joint tenderness is foundon palpation in all cases of cervical headache. Does itexpress only the dysfunction of the C2–3 segment? Prob-ably not. C2–3 is the highest cervical facet joint that ispalpable. It is at the junction of the two functional unitsof the cervical spine:

• Inferior part, with the last five vertebrae, whosebiomechanical characteristics are the same and thatfunction in a synchronous manner

• Superior part, with atlas and axis, whose greatmobility allows precise adjustment of the finest andmost varied movements of the head

The possible isolated dysfunctions of the occiput–atlasaxis cannot be clearly shown. Some signs of palpation orradiologic examination have been proposed; they seem tous to be only presumptive.

Any isolated dysfunction eventually affecting C0–1 orC1–2 also perturbs all of the superior cervical spine, whichfunctions as a unit. This perturbation is reflected at the

junction of the latter with the inferior cervical spine thathas different biomechanical characteristics than C2–3.Tenderness to palpation at C2–3 seems to us to reflect allmechanical perturbations of the superior cervical spine.

Disappearance of this tenderness after treatment meansthe return to normal of the musculoskeletal functions ofthe whole. The small suboccipital muscles that arestretched on palpation are probably essential to maintainthese dysfunctions. They also play a role in the productionof pain, through the formation of taut bands that persistsometimes in spite of the spinal treatment; a local treat-ment then becomes necessary.

Craniofacial Signs

Some signs that we describe correspond anatomicallyto the territory of the anterior and posterior rami of C2and C3 (Fig. 48.5). This is the case with the friction sign,which reveals the hypersensitivity of the scalp in the C2–3region. It is also the case with the angle of the jaw sign,which corresponds to the cutaneous region of the anteriorramus of C2 (masseter notch).

On the other hand, the supraorbital projection and espe-cially the eyebrow sign are more unexpected. The zone ofthe eyebrow is innervated by a branch of the trigeminalnerve (ophthalmic division) and seems to have no ana-tomic connection with the cervical spine. However, theirclinical link is easy to demonstrate.

In a previous study (1981), we had 50 patients withunilateral supraorbital headaches for more than 2 yearsand C2–3 facet joint tenderness and the eyebrow sign onthe same side. In 47, we were able to eliminate the ten-derness to pinch-rolling of the eyebrow by injection of0.5% lidocaine in the tender C2–3 facet joint. Not onlydid the fold become painless, but it was supple after a fewminutes, although it was thickened prior to injection.

Hypotheses about Mechanisms

The observations outlined can be explained by someconnections between the nucleus of the trigeminal nerveand the cervical spinal cord. The gelatinous nucleus of thetrigeminal nerve descends very low and becomes contin-uous with the posterior column of the spinal cord. Ana-stomoses of branches from Cl, C2, and even C3 probablyunite with the ophthalmic division of the trigeminal nerve,as Kerr has demonstrated. It is generally accepted that thefibers carrying nociceptive information have more inferiorlocations in the inferior parts of the gelatinous nuclei,descending as far distally as the second or third cervicalsegment of the spinal cord. The ophthalmic fibers projectto the inferior and anterior part of the trigeminal nucleus(Lazorthes). These common anastomoses explain thepainful supraorbital projection that we have noted.

Another mechanism may also be at work here. Sym-pathetic fibers are carried by branches of the trigeminal

CHAPTER 48 HEADACHE OF CERVICAL ORIGIN

331

nerve and go to the cutaneous regions along with thesensory nerves. These fibers come from the periarterialsympathetic nerves of the internal carotid. After a relayin the superior cervical ganglion, they arrive at the gan-glion of Gasser through the internal pericarotid plexus,but this classic cervicogasserian anastomosis was neverreally shown by anatomists.

On the other hand, numerous peripheral anastomosesunite the trigeminal branches and the vascular plexus ofthe collateral of the external carotid (Lazorthes). In itsintracranial segment, the internal carotid receives from thesuperior pole of the superior cervical ganglion two nervesthat anastomose in the plexus and are distributed to thecollaterals and the terminals of this artery and, therefore,to the supraorbital artery that goes out by the supraorbitalforamen. The superior (Cl, C2, C3) cervical ganglion isbound to the spinal nerves by communicating branches.

Whatever the actual cause of the eyebrow sign, it is acommon sign of the dysfunction of the first three cervicalsegments, as appears to be the case with C2–3 facet jointtenderness.

TREATMENT OF HEADACHE OF CERVICAL ORIGIN

Treatment confirms the cervical origin of the headachebecause the examination signs disappear, and the patientis relieved.

Manipulation

The basic treatment is manipulation if it is not con-traindicated because of the vascular or spinal state (pos-tural tests) and when it is technically possible, respectingthe rules of application. It should be very precise andperfectly executed. If it is performed correctly, it relievesor cures; performed incorrectly, it aggravates and can cre-ate a local perturbation that could make any other treat-ment difficult. Application of the rule of no pain andopposite movement is sometimes difficult at the superiorcervical spine. To determine the direction of the maneuverto be performed, it is often better to perform repeatedstretching in the different orientations. Performed in favor-able directions, stretches definitely decrease facet jointtenderness on palpation and relax the suboccipital muscles(Fig. 48.9).

Depending on the patient, two to five sessions are nec-essary. Soon after the first maneuvers, the result on thefriction sign or the eyebrow sign allows the diagnosis tobe made. A reaction occurring during the night followingthe first session is not rare, and the patient should expect it.

Facet Joint Injection (C2–3)

If manipulation is contraindicated or insufficient, facetjoint injection is useful. For the injection, the patient isseated on a stool, with the forehead resting on a table. Thepoint of injection is at the painful facet joint point, C2–3,about 1 cm lateral to the spinous process of C2, which iseasily found (Fig. 48.8).

A corticosteroid derivative, 0.25 mL, is injected strictlyon contact with the bone, after checking by aspiration thatthere is neither blood nor spinal fluid. To avoid any acci-dent, it is better to use a corticosteroid derivative that issafe for intrathecal use without producing any disturbance.No local anesthetics should be used.

Other Treatments

Massage can be a very useful adjunct (even if thepatient has been relieved of the headache), when appliedto suboccipital trigger points or to the subcutaneous tis-sues of the neck if they are cellulalgic.

The patient should learn to avoid extreme rotation ofthe neck (prolonged backing up in a car, for example).Patients with morning headaches should remove or modifytheir pillow, depending on the case. Sleeping in proneplaces with the neck in extreme rotation can be harmfuland cause morning headaches. Patients should not sleepin that position.

CERVICAL MUSCLES AND HEADACHES

Some headaches seem to be provoked by trigger pointsthat can have several origins.

• They can be postural.• They may result from articular dysfunctions. The

masseter or temporal muscle (Fig. 48.10, left andright)

is

disturbed in the syndrome of temporoman-dibular joint dysfunction. The trigger points provokepains that radiate to the supraorbital and temporalregions, and to the teeth (dental pseudopain) (J.Travell, D. Simons).

• Some of these trigger points can be localized to ataut band that is part of a cellulotenoperiosteomy-algic syndrome of cervical origin (Maigne). Theyaffect especially the suboccipital muscles, the tra-pezius and the sternocleidomastoid (Fig. 48.11).Some can cause headaches. When they are linkedto a cervical PMID, they disappear or become inac-tive after treatment of the PMID; but they can persistif they also have postural origins, and local treatmentis necessary.

The trapezius and the sternocleidomastoid are inner-vated by the cranial accessory nerve, which receives a

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contribution from C2 and C3 as the spinal accessory nerve.The latter participates to a variable degree with the motorfibers of this nerve and assures the proprioceptive inner-

vation of the muscle (Winckler). That explains the possi-bility of having taut bands with a segmental C2 or C3syndrome. For the sternocleidomastoid, the trigger pointusually is located at the junction of the superior one-thirdand the inferior two-thirds, but it can be higher or lower.The pain is projected toward the mastoid or the orbitalregion. It can be provoked by compression of the triggerpoint between thumb and index finger and maintained forabout 15 sec (Fig. 48.11).

With the trapezius, the upper fibers are generally affectedalong its superior border. Pain referral is in the temporalregion. The trigger points of the suboccipital muscles (rectusand obliquus posterior) have occipitotemporal projections(J. Travell, D. Simons). The treatment consists of two tothree trigger point injections of 0.5% lidocaine.

Studies have been performed in normal volunteersdemonstrating lateral axial joints (C1–2) causing pain inthe occiput. A recent clinical study demonstrated that insuch cases nerve blocks are able to demonstrate therapeu-tic value in approximately 60% of patients, possiblyreflecting a mislocalization of painful origin (Aprill et al.).

Figure 48.10

Trigger points either involving the temporalis (

left

) or the masseter (

right

) can be responsible for persistent cervicalheadaches. They are often due to problems with the temporomaxillary joint (due to poor dental articulation).

Figure 48.11

Sometimes the sternocleidomastoid musclehas a taut band that plays a role in cervical origin headache.It is often attenuated by cervical treatment. However, localtreatment may be necessary.

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49

CERVICAL MIGRAINE

TRUE MIGRAINE

Far too many headaches are categorized as migraines.True migraine is frequent and affects women more thanmen. It occurs by paroxysmal attacks that last a few hoursand is usually preceded by signs that are well known tothe patient. Symptoms include unilateral pain, photopho-bia, pallor, nausea, and vomiting. Most often, it goes fromright to left or vice versa from one attack to the other (80%of cases). The first attack often occurs before the age of10. A familial or genetic pattern is usual. Although avascular origin has been proposed, the etiology ofmigraine has not yet been clearly delineated. It can presentin various clinical forms such as ophthalmic migraine,mixed migraine, and migrainous equivalents.

Classic migraine has nothing to do with the cervicalspine. However a patient with a definitive diagnosis ofmigraine can also have headaches of cervical origin. Thepatient can usually distinguish the two types of headaches.However, there are headaches with migrainous character-istics that have cervical components or cervical origins.The first type of cervical migraine was described byBartschi-Rochaix. Below we describe a second one basedon our semiology of cervical headaches.

CERVICAL MIGRAINE

Bartschi-Rochaix described a migrainous syndrome ofcervical origin and noted that cervical osteophytes andepisodic synovitis of cervical elements result in vertebralartery vasospasms. According to Taptas, Ricard, Girard,and Dupasquier, cervical discopathies act essentially onthe preganglionic fibers of the white rami communicantsthat join the cervical sympathetic chain to the cere-brospinal axis while following the path of the last fivecervical roots. Irritation of these elements seems to causevasomotor problems in the whole carotid system, bothextracranial and intracranial.

MIGRAINE AND SUPERIOR CERVICAL SPINE

There is another form of cervical migraine whose ori-gin is in the superior cervical spine (Maigne). Supraorbitalheadaches of cervical origin can, as we have seen above(“Different Aspects of Headache of Cervical Origin,”Chapter 48), have clear vasomotor characteristics associ-ated with nausea in some patients. In others, the migrain-ous character is clearly so prominent that most of thepatients we examined had consulted in other departmentsor in specialized centers and been given diagnoses ofmigraine. However, their responses to treatment weresuboptimal or nonexistent, even with treatments that usu-ally help those suffering from migraine. These cervicalmigraines that we isolate have many other characteristics:

• They do not alternate; they are located always onthe same side, right or left.

• They show the usual signs of cervical headachesdescribed; the eyebrow sign is always present, as istenderness of the C2–3 articulation on the side ofthe usual attack.

• Their response to the treatment is good (manipulationand possible posterior articular injection).

The following observation is typical.

Case History

—

A 41-year old woman, a storekeeper,had unresponsive migraine-like headaches for 10 years.Eight years earlier, she underwent a minor cervicaltrauma in a motor vehicle accident. She subsequentlydeveloped temporary frontal headaches that decreasedprogressively after 1 year. Ten years ago, without anyapparent cause, attacks of frontal headaches occurred,always on the left, with a feeling of a retro-orbitalstretching. These headaches were accompanied bynasal obstruction on the same side and, when the painwas severe, with abundant rhinorrhea and watering ofthe left eye. She looked for calm darkness and sometimes

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vomited. Attacks quickly increased in frequency andbecame daily.

Different sedatives were tried to no avail. After someophthalmologic and ENT examinations were negative,a first consultant physician prescribed Niamid for a yearwithout success. An orthodontist then extracted a wisdomtooth on the left, with no effect on the headaches. Thepatient was seen by a neurologist and the diagnosis oftrue migraine was made. Different medications such asdihydroergotamine, caffeinated Gynergen, and dimetio-tazine were tried but had no effect. Only amidopyrinein high dosage had a mildly positive effect. Finally, shewas hospitalized in a neurology department where(among other examinations) she underwent an arterio-gram that was normal. Dihydroergotamine was triedwithout effect. Attacks became more severe and hand-icapped her at work. She was then hospitalized in asecond department of neurology. A pneumoencephalo-gram was performed and was normal. A third neurolo-gist, a well known headache specialist, ordered anallergy panel. Tests were positive to dust and mildew.After 1 year of desensitization, she noted no effect, andthe migraine remained unchanged. She then saw a faithhealer who prescribed hand baths with plants and sitzbaths without result. She consulted in another departmentof neurology where the diagnosis of migraine wasmade. She was treated with methysergide, which pro-duced a slight improvement. Every 6 months, an intra-venous pyelogram was performed. The third onerevealed the beginnings of retroperitoneal fibrosis andthe treatment was stopped. High dosages of pyramidonwere tried and to some extent relieved her. Upon herreturn, she consulted in the same department of neu-rology, and after all these failures, she was told that allof her problems were probably of psychologic origin.She was told that perhaps the problem was having hermother live with her; however, the patient thought thiswas not a major problem. For some reason her motherhad to leave, but this did not change the headaches.

Then a physician that the patient saw in the Southwestsent her to us. She was described as a “woman whocannot stop her work (she works in a store alone) andwho is very handicapped by quasi-daily attacks.” Thefixed topography was always on the left. Her negativeextensive work-up allowed us to concentrate on exam-ining the cervical spine. X-rays had already been per-formed, and since they were normal, a cervical originwas not considered. With the patient in supine position,palpation of the suboccipital region revealed markedtenderness of the left C2–3 facet joint. Pressure evenreproduced the retro-orbital radiation that she felt duringthe attacks.

The remaining cervical segments — above, below,and on the right — were unremarkable. On palpation,the left suboccipital subcutaneous tissues were thickened,infiltrated, and very sensitive to pinch-rolling. Pinch-roll

of the right eyebrow was painless, but the left wasthickened, infiltrated, and very painful. A diagnosticinjection of the left C2–3 facet joint was performed,and in a few minutes both the sensitivity to pinch-rollingand the left eyebrow sign decreased. Manipulation wasperformed, combined with a left C2–3 corticosteroidinjection. After the third treatment, attacks were lessfrequent and severe, and the pinch-roll test was muchless sensitive. After the fifth treatment, the migraines andpositive clinical findings disappeared. A recurrenceoccurred 4 months later, after the patient carried asuitcase. The left pinch-roll tenderness and the left C2–3sensitivity returned. One treatment was enough to puteverything in order and 2 years have passed withoutan attack.

This is an example of a cervical headache with a typ-ically migrainous aspect. In summary, this women suf-fered from severe migraines for 10 years. She was hospi-talized three times and underwent an angiogram, apneumoencephalogram, and multiple investigationsrepeated many times. Treatment with methysergideresulted in the beginning of retroperitoneal fibrosis. OnlyPyramidon resulted in improvement. The patient wasrelieved by a few manipulations and cervical injection.

The following case is similar.

Case History

—

Mrs. C.L., a 39-year old bookkeeper,had migraines since the age of 16. In the beginning,they were linked to her menstrual periods. Then theyoccurred outside the cycle, with increased frequency forthe last 5 years, following a motor vehicle accident.Pain was always on the right, never the left.

She was hospitalized twice in a department of neu-rology. All investigations were negative (includingangiography and pneumoencephalography). Special-ized examinations (e.g., ENT, orthodontic, ophthalmol-ogy, allergy) were all negative. She consulted manyspecialists, and the diagnosis of true migraine wasalways made because the clinical picture was typical.Treatment with antimigraine medications provided noresults. She had partial relief with Optalidon (usually 30to 40 suppositories a month), the only treatment thatallowed her to continue her work.

When we saw her on referral by her physician, wenoticed marked tenderness over the right C2–3 articularpillar, with a clear eyebrow sign. On radiologic evalu-ations, the cervical spine was normal except for a slightloss of cervical lordosis. After three treatments consistingof two facet corticosteroid injections and a manipulation,there was clear relief, which was definitive after threemanipulations done 15 days apart. In 1 year after thetreatment, she had only two mild attacks of short durationafter a long trip.

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50

CERVICAL SYNDROME

In 1925, Barre and his student Lieou (thesis, 1928)brought attention to the cervical origins of a certain num-ber of headache syndromes, vertigo, tinnitus, etc. Theythought the mechanism was irritation of the “sympatheticsystem by a cervical rheumatism” and therefore describedthe “posterior cervical sympathetic syndrome.”

The existence of this syndrome is now very controver-sial. Most authors attribute its manifestations to circula-tory disorders of the vertebrobasilar system due to insuf-ficiency or psychologic problems. While knowledge ofvertebrobasilar insufficiency brought many clarificationsto these problems, it did not explain everything. In apreceding chapter, we noted the frequency of cervicalheadaches and showed that they have their own clinicalsigns. They are relieved by cervical treatments. Thesepatients often present also with vertiginous sensations ortrue vertigoes, visual problems, difficulties in concentra-tion, and memory loss that usually disappear (like theheadaches) after cervical treatment or, conversely, areaggravated by poorly performed manipulations.

If one thinks that the essential merit of Barre was toaffirm the cervical origin of the manifestations of his syn-drome, these results confirm his opinion. Those who donot agree with Barre’s thesis of a “sympathetic mecha-nism,” disputed by most authors, can say that the syn-drome of Barre and Lieou does not exist. To avoid con-fusion, we use the term

cervical syndrome,

after others(Toussaint), to refer to all the manifestations in which thecervical spine plays a dominant role. We should emphasizethe complexity of the problem and note that multiplecauses — some benign, some serious — can create symp-toms whose frequency and benign nature constitute theessential trap.

ELEMENTS OF CERVICAL SYNDROME

The elements of this syndrome include headache, dis-equilibrium, visual and auditory dysfunction, laryngopha-ryngeal problems, vasomotor problems, and psychologicproblems.

Headaches

Headache is by far the most common manifestation ofthis cervical syndrome. It is treated in Chapter 48, “Head-ache of Cervical Origin.”

Vestibular Symptoms

Some patients complain of poor balance and are afraidto cross a street. Others have the impression of being drunk.Most often, these patients have vertiginous symptoms, usu-ally triggered by rotation of the head to one side or cervicalextension. Sometimes, these are true rotary vertigoes. Ves-tibular symptoms show only minor abnormalities in mostcases, with hypoexcitability of the labyrinth. Spontaneousnystagmus is very rare, but electronystagmography can showinteresting results (Waghemacker).

Auditory Symptoms

Tinnitus, ringing, whistling in the ear, and hyperacusisconstitute the auditory symptoms.

Visual Symptoms

Some patients complain of visual fatigue, floatingspecks, tingling, or a feeling of dust in the eyes.

Pharyngolaryngeal Symptoms

Symptoms include pharyngeal paresthesia (feeling aforeign body) and for singers, difficulties with high notes.

Vasomotor and Secretory Symptoms

Symptoms include rhinorrhea and watery eyes, gener-ally affecting only one nostril or eye.

Psychologic Symptoms

Patients often complain of intellectual fatigue, diffi-culty concentrating, and memory loss. They have a ten-dency toward depression and anxiety. A history of mentalillness can perpetuate the problem. Often, symptoms occur

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in patients without any antecedent history. Because thesesymptoms frequently manifest after cervical trauma anddisappear after cervical treatment, they are considered anintegral part of the syndrome, rather than a psychologicreaction to an accident.

All these symptoms are rarely seen together. Occur-rence, expression, and intensity vary. They are not alwaysthe consequences of a minor cervical trauma. They arealso seen in patients over 50 years old who have someneck stiffness due to spondylosis and who present with aPMID of the superior cervical spine provoked by spondy-losis or synovitis. Often, the symptoms are transitory, butthey are persistent in a few cases, with little tendency tospontaneous regression.

External perpetuating factors include cold drafts, pos-tural factors (e.g., poor posture during sleep or work,driving the car for too long), and especially psychologicfactors. The psychologic factors are manifest by a feelingthat cognitive function (memory, concentration) is declin-ing and not improving after treatment. Patients often havemedicolegal issues and become very vulnerable. A per-sonal problem or a professional setback is taken very badlyat this point, and the depressive reaction becomes theessential therapeutic problem.

DIAGNOSIS

A diagnosis is sometimes difficult to make because thesymptoms of patients with cervical syndromes can be verysimilar to those seen in psychiatric patients. In the anxious,depressed patients, one should differentiate a true cervicalpain and hypochondriacal neck pain. Vertebrobasilarinsufficiency (VBI) should be evaluated by Doppler stud-ies of the carotid arteries. Rancurel’s maneuver is an excel-lent means of uncovering a hemodynamic VBI that maybe present (see “Vertebrobasilar Insufficiency” in Chapter22).

EXAMINATION OF CERVICAL SPINE

Examination of the cervical spine does not differ fromthe examination described in Chapter 48, “Headache ofCervical Origin.” The important thing to look for is ten-derness of the C2–3 facet joint ipsilateral to the supposedproblems. This sensitivity is generally the result of aPMID, although occasionally posterior element inflamma-tion can be the causative factor. Other common physicalsigns ipsilateral to the symptoms include the eyebrow sign,friction sign over the scalp, and tenderness to pinch-rollingat the angle of the jaw. The sternocleidomastoid and tra-pezius muscles should be examined very thoroughly todetermine whether there are trigger points that can be

treated. They can play a role in the painful manifestations(headache, pseudovertigo).

MECHANISM

Chapter 48, “Headache of Cervical Origin,” discussesa mechanism for the headaches. Disorders of equilibriumin the absence of any other lesion can be explained byperturbation of articular and muscular receptors that arevery numerous at the superior cervical level. They playan important role in the control of equilibrium and posture.When there are lesions, afferent misinformation can berelayed to the central nervous system. This is well knownin cases that involve the superior cervical segments. How-ever, irritation of certain taut cervical muscles can alsoproduce the same sympathetic phenomena with visual andvestibular dysfunction (J. Travell).

Trigger points can have a postural origin; however, wehave frequently found them associated with a PMID ofthe superior cervical spine and have frequently seen themdisappear after treatment of the cervical spine. The ster-nocleidomastoid is innervated by the cranial accessorynerve as well as by branches of C2 and C3 (Winckler) orthe spinal accessory nerve. Thus, nociceptive informationarriving from the muscles can induce the disturbances thatare commonly seen with the cervical spine syndrome.

TREATMENT

Manipulation can be performed with the usual precau-tions, and it is often effective. At each session, one shouldevaluate the results of the manipulation and reexamine thespine for pain and associated signs (see Chapter 48,“Headache of Cervical Origin”) such as eyebrow pain, ifit is present. If one can make these various signs disappearwithout the patient feeling better, then one should assumethat there is no relationship between the cervical spine andthe patient’s complaints. Usually the response to treatmentis positive and rapid, especially in those who have head-aches and vertigo.

If manipulation is contraindicated or if the results arepoor, one can try injecting corticosteroid at the painfulC2–3 articulation. Three to four injections should be suf-ficient. One can also try soft tissue release techniques forthe neck, without any mobilization. Petrissage of the sub-cutaneous tissues, if they are injected subcutaneously, canalso be useful. Trigger point injection is a complementarytreatment that is often very effective. Electrotherapy canbe of use in those whose conditions are the sequelae ofold traumas and especially in those with arthritic spines.

Cervical treatment usually gives excellent results inthose with cervical headaches and those with vertigo. It issomewhat less useful in those who complain of difficulty

CHAPTER 50 CERVICAL SYNDROME

337

with hearing or tinnitus (less than 10%). It can be goodfor complaints of visual fatigue and pharyngolaryngealcomplaints. We have seen many singers with acute diffi-culties after cervical traumas who regain their normalvoices after several manipulations.

Some patients require cervical collars during the night,particularly if they sleep in prone and produce extremetorsion because of their nocturnal postures. This extremetorsion can result in facet joint irritation. Such individualsshould be counseled about neck movement and taught toavoid extreme torsion.

Physical Modalities

Physical modalities are rarely useful in the cervicalsyndrome, especially when it is of traumatic origin. Some-times they may further irritate the articular discomfort. Inaddition, the repetitive sessions can condition the patientpsychologically. This is particularly seen in post-traumaticsyndromes that involve medicolegal issues.

When improvement in the condition is noted, oneshould lengthen the time between treatments and reassurethe patient. The patient should also be taught how toprevent future trauma to the cervical spine.

Remarks

R. Waghemacker made interesting observations regardingvictims of minor cervical trauma, their complaints, andthe efficacy of their treatment. He and Decroix performedelectronystagmography before and after cervical treat-ment. In 40 patients with cervical syndromes, usually ofpost-traumatic origin, they noted that manipulative treat-ments tended to normalize the abnormalities, while sub-jective improvement tended to follow objective graphicimprovement in complaints such as vertigo and headaches.Their work helped to identify the complaints of thepatients, show the role of the cervical spine, and documentthe efficacy of manipulative therapeutic approaches andthe good results that could be obtained with them.

339

51

LEVATOR SCAPULAE SYNDROME

The levator scapulae is attached distally at the superiormedial angle of the scapula and to the superior part of thespine of the scapula and proximally to the transverse pro-cesses of cervical vertebrae 1 through 5 (Fig. 51.1). It hasa dual action: when the cervical spine is fixed, it elevatesthe scapula; if the scapula is fixed, it produces ipsilateralrotation and a lateral bending of the cervical spine. Ten-derness to palpation of its scapular attachment is foundvery frequently on systematic examination. It is some-times sufficiently sharp to cause spontaneous pain(Fig. 51.2).

CLINICAL PICTURE

Different Aspects of Pain

Dysfunction of the levator is expressed as:

• Upper thoracic or periscapular pain• Chronic low cervical pain with limitation of move-

ment to the opposite side or an acute pain like atorticollis (wryneck)

• Pain radiating in some cases to the arm; it can bedull and poorly localized or acute, mimicking cer-vicobrachial neuralgia

In all cases, anesthetic injection of the scapular attach-ment of the muscle immediately suppresses the pain andrelieves the limitation of movement.

Mechanism

Tenderness of the levator attachment can be due to alocal cause, a vertebral cause, or both.

Figure 51.1

Levator scapulae (

1

) and rhomboideus (

2

).

Figure 51.2

Palpation of scapular attachment of levatorscapulae.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Local Cause

Muscle fatigue can be due to overworked muscles orstrenuous postures (e.g., turning the head for a prolongedtime while backing a car, speaking to someone seated onthe side, typing while reading text on the side, holding atelephone receiver between shoulder and neck, using toolong a cane as a support). Prolonged or repeated fatigueof the muscle produces taut bands at its inferior part.

Cervical Cause

As we have seen, tenoperiosteal hypersensitivity of thesuperior medial angle of the scapula is usually found inthe cellulotenoperiosteomyalgic syndrome of C4, some-times of C5. The segmental examination reveals dysfunc-tion of C3–4 or C4–5, with ipsilateral facet joint tender-ness and often cellulalgia of the ipsilateral supraspinousfossa.

Mixed Causes

Local and cervical factors are often found in combina-tion. Generally superimposed on this background is recentmuscle fatigue, postural stress, or another irritant, whichthen provokes a cervical or thoracic PMID.

TREATMENT

If there is a cervical element, such as a C3–C4 or C4–5PMID or synovitis, it can be treated, depending on thecase, by facet joint injection or manipulation. Usually thiswill suppress the spontaneous pain. Sometimes an injec-tion of the scapular attachment followed by physiotherapymay be necessary. Trigger points should be looked for,one or two finger breadths above the scapular insertion.If found, an injection of xylocaine should be tried.

341

52

ACROPARESTHESIAS OF UPPER LIMBS

AND CERVICAL SPINE

Acroparesthesias of the arms are characterized by feel-ings of pins and needles, tingling, numbness, and pinchingthat can affect all fingers or be localized to only some ofthem. Acroparesthesias can be unilateral or bilateral.Depending on their topography and character, one candistinguish:

• Global acroparesthesias, affecting the whole handand occurring usually during the night

• Acroparesthesias with radicular topography• Acroparesthesias with entrapment topography

They may originate from lesions in the spinal cord(syringomyelia) or the cerebrum. Multiple causes can pro-voke a feeling of numbness, of a swollen hand, or of adead finger that characterizes this syndrome. The leadingpathologic cause of this syndrome by far is carpal tunnelsyndrome.

ACROPARESTHESIAS WITH RADICULAR TOPOGRAPHY

A form of cervicobrachial neuralgia, acroparesthesiawith radicular topography is linked to irritation of a cer-vical root, producing paresthesia in the thumb (C6), mid-dle finger (C7), or ring and little fingers (C8) (Fig. 52.1).

NOCTURNAL GLOBAL ACROPARESTHESIAS

Especially frequent in women during menopause, noc-turnal global acroparesthesias occur between 2 and 4 a.m.,awakening the patient with a feeling of numbness, theimpression that the hands are dead or swollen, and intenseprickling in the whole hand. The patient wakes, shakesher hands, rubs them, and sometimes gets up, hoping thatthese disagreeable feelings will disappear. The acropares-thesia is usually bilateral, but it can be unilateral.

Figure 52.1

Radicular topography of C6, C7, and C8.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

First, one should ascertain that the hand and all fingersare affected. For example, upon awakening, when thepatient feels the symptoms coming, she should softly rubthe affected hand with a clothes brush. This will determinewhether the fifth finger is involved or not. Usually it isnot, which may be consistent with a carpal tunnel. If allthe fingers are affected, the diagnosis of a bicanalar syn-drome can be made (carpal tunnel syndrome with thesyndrome of Guyon’s tunnel). As we shall see below,participation of the cervical spine should not be excluded.

ACROPARESTHESIAS WITH ENTRAPMENT

Acroparesthesia with entrapment is the most frequentform and the consequence of an entrapment syndrome(Fig. 52.2 through Fig. 52.4). Entrapment of the palmarbranch of the median nerve as it traverses the carpal tunnelis the most common syndrome. Although less common,the ulnar palmar branch can also become entrapped at thewrist in Guyon’s canal. Nerve conduction studies andneedle electrode examination are the fundamental tests.They can localize the site of the entrapment, measure thedegree of conduction block, assess the amplitude of theevoked response, and measure the velocity of the motorand sensory fibers that comprise the nerve.

The median nerve can also be compressed between thetwo heads of the pronator teres or at the fibrous edge ofthe flexor digitorum superficialis. Compression of theanterior or posterior interosseus nerves in the midforearmis less common. The ulnar nerve can be compressed inthe cubital tunnel. When the proximal nerve fibers at thelevel of the brachial plexus are (occasionally) compressedat the thoracic outlet, the term

thoracic outlet syndrome

is applied. In this case, the origin is often postural, locatedin the C8–T1 or lower trunk territory, and is rarely iso-lated.

Carpal Tunnel Syndrome

Compression of the median nerve at the wrist as ittraverses the carpal tunnel is the most frequent cause ofacroparesthesia. The symptoms are classically nocturnalbut may occur during the day. The topography is that ofthe median nerve; that is, it involves the first three fingersand the medial half of the fourth finger. In some cases, itmay only involve one or two fingers. Tapping over thewrist (Tinel’s sign) and sustained passive wrist flexion(Phalen’s test) can trigger the usual pain. In severe cases,there is hypesthesia over the tips of the involved digitsand wasting of the thenar eminence with weakness of themuscles innervated by the median nerve, including theopponens pollicis and the abductor pollicis brevis.

Electrodiagnosis may reveal decreased sensory nerveconduction velocity across the wrist compared with themedian nerve on the opposite side or with the ipsilateralulnar and radial nerves over equidistant segments. Theremay be evidence of either conduction block across thewrist or, in severe cases, axonal loss manifested bydecreased amplitude of the evoked response. Motor stud-ies may show a prolonged wrist latency; the needle elec-trode examination is abnormal only in severe cases.

Figure 52.2

Sensory territories.

a.

Radial nerve.

b.

Ulnar nerve.

Figure 52.3

Anterior view of median nerve in carpal tunneland ulnar nerve in Guyon’s canal.

1.

Median nerve.

2.

Ulnarnerve.

3.

Annular ligament.

4.

Anterior ulnar expansion.

CHAPTER 52 ACROPARESTHESIAS OF UPPER LIMBS AND CERVICAL SPINE

343

The diagnosis is confirmed by injection of the carpaltunnel with anesthetic and corticosteroid and treated withsurgical release in refractory cases. A hypertrophic syno-vitis of the tendons is usually responsible for the compres-sion. The cause can also be traumatic: a Colles fracturewith an imperfect callus, intracarpal fracture and disloca-tion, contusion or sprain of the wrist, or retractable scarof the anterior side of the wrist. Muscular abnormalitiescan also play a role and, rarely, lipomas of the carpaltunnel.

Treatment

In the purely sensory forms, injections are usually suf-ficient, but one should not resort to them frequently. If thedisorders persist, only surgical intervention can avoidmotor lesions and sensory problems. Jesel has shown thatif the injections relieve low back pain of thoracolumbarorigin, the objective electrical signs of nerve compressioncan remain unchanged.

Guyon’s Canal Syndrome

The ulnar nerve can sometimes be affected by anentrapment syndrome at Guyon’s canal. It is really ratherrare, and its causes are variable: vascular, muscular, ortendinous abnormalities; synovial cysts of the carpus;fractures of the pisiform bone or the hook of the hamatebone, etc. The clinical picture is characterized by par-esthesia in the small and ring fingers. Atrophy of the firstdorsal interosseous space is usually the first clinical signof a motor damage.

CERVICAL SPINE AND ACROPARESTHESIA

If the role of the cervical spine seems evident in acro-paresthesias with radicular topographies, it seems that nosuch role exists if the acroparesthesias are global or in the

case of carpal tunnel syndrome. However, in both cases,if cervical manipulation is possible and justified by aninferior cervical PMID, it can often bring appreciablerelief or even the disappearance of all symptoms.

The explanation for this is not clear, although thisobservation is frequent enough to be more than mere coin-cidence. Thus, unless contraindicated, when a patientdemonstrates acroparesthesia and an inferior cervicalPMID with facet joint tenderness on the side of the par-esthesia, a trial cervical treatment is justified. If successful,the local treatment may be unnecessary or more effica-cious. To determine cervical participation and thus a rolefor manipulative treatment, we use the “arm elevation” or“arms up” test (Maigne).

Arm Elevation Test

A patient is asked to hold his arms up for 1 minute.Often, not always, after 20 to 30 sec, the activity elicitsthe usual numbness and paresthesia.

• The time it takes to happen is noted.• The exact topography of the numbness and pares-

thesias is checked by rubbing the fingers softly witha small dry brush to better detect sensory problems.

• If the examination reveals cervical signs (PMID atC5–6 or C6–7), manipulation can be performedaccording to the usual rules.

• The time of appearance of the acroparesthesia withthe arms up is measured again. If the time is length-ened, cervical treatment will bring an improvement,sometimes even the disappearance of the paresthe-sias, in two to four sessions. This result can beobtained in the global forms and in some moderateforms of the carpal tunnel syndrome in which thenerve conduction velocity is only slightly impaired.If there is an inferior cervical segmental dysfunc-tion, the cervical treatment can suppress the symp-tomatology.

Figure 52.4

a.

Section of the wrist at the second carpal row: 1. Median nerve. 2. Palmaris longus tendon. 3. Flexor digitorumsuperficialis. 4. Flexor digitorum profundus. 5. Hamate. 6. Capitate. 7. Trapezoid. 8. Trapezium. 9. Flexor retinaculum.

b.

Sectionthrough Guyon’s canal: 1. Tendon of the flexor carpi ulnaris. 2. Pisiform. 3. Ulnar nerve. 4. Ulnar artery.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

All this indicates that the painful phenomena were dueto local and cervical factors together. If one or the otheris decreased, the paresthesias can disappear.

DOUBLE CRUSH SYNDROME

Cases in which a favorable result can be obtained byeither a local treatment or a vertebral treatment (if there

is a PMID) represent the “double crush syndrome”described by Upton and Comas; the combination of thetwo factors creates the syndrome. This phenomenon isfound in many painful disorders with vertebral compo-nents that we describe in this book (e.g., syndrome of theperforating branches, of the twelfth intercostal nerve andof the first lumbar nerve; pain in the knee; and some lowback pain of thoracolumbar origin).

345

53

SHOULDER PAIN AND THE CERVICAL SPINE

The most common presentation of shoulder pain istenderness at the tendinous insertion. It is frequentlylinked to degenerative lesions, whose frequencies are wellknown. However, a few painful shoulders are remarkablyrelieved by cervical treatment only. They are the resultsof cellulotenoperiosteomyalgic manifestations of segmen-tal dysfunctions at C4–5 or C5–6 (by PMID or synovitis),which may simulate tendinitis or exacerbate it. Thesetotally or partially “cervical” shoulders should be recog-nized so they can be treated efficiently.

GENERALITIES ON TENDINOUS AND CAPSULAR LESIONS

Common shoulder tenosynovitis has been well studiedand this allows investigation and classification of lesionsthat were not usually held responsible. Rev. Rhum et al.(1951) classified these conditions as

scapulothoracic peri-arthritis

as follows:

1. Simple painful shoulder linked to a tendinitisaffecting most often the long biceps and thesupraspinatus

2. Frozen shoulder due to adhesive capsulitis3. Acute hyperalgic shoulder, part of the evolution

of a calcific tendinitis, a microcrystalline acuteattack

4. Pseudoparalytic shoulder due to rupture of therotator cuff tendon

In 1972, Neer highlighted the role of impingementbetween the rotator cuff tendon and the coracoacromialarch, known as the

subacromial impingement syndrome.

Subacromial Impingement (Neer)

Subacromial impingement syndrome is a term used todescribe compression of the soft tissues between thegreater tuberosity of the humerus and the undersurface ofthe acromion and the coracoacromial ligament, especially

during shoulder abduction and flexion. The subacromialimpingement syndrome has three phases that reveal theprogression of the lesions.

Stage 1 —

Edema, hemorrhage, and acute tendinitisdue to excessive physical exertion: patients are usuallyyoung.

Stage 2 —

Tendinitis and fibrosis; patients are older,but under 40; overworking the shoulder produces pain;the shoulder is not painful in mild activities.

Stage 3 —

Tendinous ruptures of the rotator cuff andbony modifications; patients are over 40; the supraspinatusis most often affected; radiologic lesions appear.

On examination, the characteristic sign is the painfularc produced by passive shoulder abduction. Between 60and 90°, this movement produces a sharp pain, increasedby the least resistance. This pain disappears with injectionof local anesthetic into the subacromial bursa at the zoneof impingement. This sign cannot be considered specific.

Neer’s concept based on anatomic and clinical findingsis very interesting. It is useful in refractory cases, in med-ical treatments in which physical therapy has an essentialrole, and in cases in which patients will not or cannotundergo corrective surgery.

More recently, the impingement has been shown to bemore a dynamic dysfunction of shoulder mechanics thana static problem reflecting unfavorable anatomy. Dynamicimpingement is the result of abnormal energy and forcedistribution across the rotator cuff and labrum, which canaccount for the pathoanatomic findings described for thiscondition. The presence of structural injury does notnecessarily imply that a decompressive procedure (whichattempts to modify a structural lesion without adequatelyidentifying the dysfunctional elements producing theimpingement) is a valid approach. The source of the dys-function is the muscle imbalance altering the various forcecouples that control shoulder motion, including the rotatorcuff and scapular rotator muscles, and, to some extent, thecervicothoracic muscles as well. Treatment of this dys-function is necessary to avoid recurrent attacks.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Asymptomatic Lesions

Codman demonstrated the frequency of degenerativelesions in the supraspinatus tendon (focus of fibrillarnecrosis, calcifications, microruptures, etc.), but there isno correlation between the severity of these lesions andthe pain and dysfunction felt by patients. Many of themare asymptomatic.

Subcoracoid Impingement Syndrome

In addition to the anteroposterior and subacromialimpingement, there can be impingement of the anterolat-eral subcoracoid (subcoracoid impingement syndrome)evidenced by pain on internal rotation of the shoulderwhen the arm is in horizontal abduction (Gerber’s sign).

EXAMINATION OF SHOULDER

Each painful shoulder should be thoroughly examined,both clinically and radiologically. Ultrasonography maybe useful (especially for post-traumatic shoulders) and, ifnecessary, arthrography with or without CT. A systematicexamination of the cervical spine should always accom-pany the examination of the shoulder and should be per-formed as follows:

• Assessment of active range of motion• Assessment of passive range of motion• Assessment of resisted range of motion• Assessment of tender sites• Palpation of subcutaneous tissues, muscles, and ten-

dons• Examination of acromioclavicular and sternoclavic-

ular joints• Assessment of scapular mobility• Assessment of glenohumeral joint and signs that

could reveal a lesion of the glenoid labrum

Assessment of Active Range of Motion

Active range of motion assessment allows better eval-uation of the mobility of the shoulder and the discomfortof the patient. The patient is asked to perform the follow-ing movements:

• Vertical elevation of the arm in the sagittal, frontal,and scapular planes

• Hand behind the back (combined adduction andinternal rotation)

• Hand behind the head (combined abduction andexternal rotation)

Assessment of Passive Range of Motion

The same movements are used, but they are pushed toa maximum by the physician.

Muscles of Shoulder Girdle

A complex coordination of prime movers, stabilizers,agonists, synergists, and antagonists is required for opti-mal shoulder function. It can be schematized in the fol-lowing way:

• Abduction: deltoid (C5, C6) supraspinatus (C5–6)• Adduction: teres major (C5, C6), latissimus dorsi

(C6, C7, C8), pectoralis major (C5–T1)• External rotation: infraspinatus (C5, C6), teres minor

(C5, C6)• Internal rotation: subscapularis (C5, C6, C7)• Accessory internal rotators: teres major, latissimus

dorsi, pectoralis major• Vertical flexion: anterior head of deltoid, clavicular

head of pectoralis major and coracobrachialis (C6)• Extension: posterior head of the deltoid, teres major,

latissimus dorsi

Assessment of Resisted Range of Motion

In this phase of the examination, the patient is directedto perform a specific active movement with maximal forcewhile the physician simultaneously applies an equal andopposite resistance. Contraction of a muscle–tendon unitagainst resistance increases the pain of tendinitis becauseof the increased tensile load imposed upon the inflamedtissue. Each specific maneuver can detect the muscle ormuscles that are affected.

Supraspinatus (Abduction)

The arm is positioned in about 30° of horizontal abduc-tion and full internal rotation and raised vertically in theplane of the scapula. The physician applies a downwardtorque on the outstretched arm, while instructing thepatient to resist isometrically (Fig. 53.1).

Figure 53.1

Examination of shoulder: abduction againstresistance.

CHAPTER 53 SHOULDER PAIN AND THE CERVICAL SPINE

347

Infraspinatus (External Rotation)

Maneuver 1 —

The arm is kept against the body inslight internal rotation, the elbow flexed at a right angle.The examiner opposes the external rotation performed inslight abduction (Fig. 53.2).

Maneuver 2 —

The arm is kept horizontal; the forearmis vertical at 90°. The examiner opposes the external rota-tion with the hand at the wrist.

Subscapularis (Internal Rotation)

The arm is kept against the body, forearm flexed at aright angle, and a slight internal rotation is started. Thepatient tries to bring his hand toward the abdominal wallwhile the examiner opposes the movement. This maneuvercan also be performed with the arm horizontal and theforearm at a right angle.

Biceps

When the long head of the biceps is affected, it is rareto evoke pain with resisted elbow flexion, with or withoutassociated resisted forearm supination. In this case, directpalpation renders the best information.

Pectoralis Major, Latissimus Dorsi, and Teres Major

These are adductors and tested by resisted adduction.

Painful Arc

On occasion, a shoulder may not be painful when cer-tain selective maneuvers are performed against resistance.However, a painful arc of motion may be detected duringactive or passive range of motion assessment. Forexample, in some supraspinatus tendinopathies located inhypovascular zones (Codman) within 1 cm of insertion,pain can be evoked at a precise point during active motionat end range in flexion, abduction, or horizontal adduction

(Cyriax). Sometimes, a painful arc is noted with abductionof the arm to about 80°, especially if the arm is in internalrotation. This painful arc means that there is impingementof the affected tendon between two obstacles.

Neer proposed provocative testing of this impingementby passively flexing the arm in internal rotation in anattempt to impinge the rotator cuff attachment betweenthe greater tuberosity beneath and the coracoacromialarch. Hawkins proposed a similar test, with the arm pas-sively flexed at the shoulder and elbow at 90° (the90/90/90 position). The examiner increases the amount ofinternal rotation at the shoulder, attempting to impinge therotator cuff attachment to the greater tuberosity beneaththe coracoacromial arch. Both of these provocativemaneuvers produce pain in shoulders with rotator cufftendinopathies due to impingement.

Palpation

Subcutaneous Tissues

Some falsely localized shoulder pain syndromes arelinked to tenderness of the subcutaneous tissues of thesupraspinous fossa and lateral shoulder. A very painfulcellulalgic zone is often found at the deltoid insertion.This zone can have a local or a cervical reflex origin (C5).Local treatment is sometimes necessary.

Muscles

Palpation of the muscles, particularly the infraspinatus,often reveals very painful trigger points even when manualmuscle testing against resistance is painless. These triggerpoints can play a role in the painful shoulder. They canhave cervical or local origin due to overuse (Fig. 53.3).The deltoid can also be affected.

Tendons

Examination against resistance imparts some limita-tions. In some painful shoulders, movements performedagainst maximal resistance are painless, while direct pal-pation reveals pain of the tendon involved. This is par-ticularly true for the biceps.

Indeed, a movement against resistance performed totest the biceps (flexion of the forearm plus supination) israrely painful although its tendon is very tender to palpa-tion. Injection of local anesthesic around the tendon tem-porarily relieves the habitual shoulder pain, demonstratingits involvement in the pain syndrome.

To palpate the tendon of the supraspinatus, the arm isinternally rotated (back scratch test), which brings thetendon into a subacromial position under the anteromedialedge of the acromion. The arm should be in externalrotation to palpate the tendon of the infraspinatus. It isbetter to have the elbow held by the examiner’s other hand(or resting on a table of the correct height) and placed in

Figure 53.2

Examination of shoulder: external rotationagainst resistance.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

slight adduction and flexion. The tendon is then palpableunder the edge posterior to the acromion.

The tendon of the long head of the biceps is easilypalpated at the deltopectoral groove in the deltopectoralsulcus (Fig. 53.4). It is first palpated statically, and then

while subjecting the arm to small repeated movements ofrotation with the hand holding the elbow. The best positionfor palpating the biceps tendon is with the shoulder andelbow in extension. The tendon is then pulled on thehumeral pulley. So sensitized, its dysfunction is clearer.

The tendon of the subscapularis muscle is palpated inthe deltopectoral groove, just lateral to the coracoid pro-cess. The patient is positioned in supine, with the arm inslight external rotation. The coracoacromial ligament canbe palpated just below the coracoid, with the patient insupine and the arm in external rotation.

All these maneuvers should be compared with maneu-vers on the healthy side.

Assessment of Clavicular Joints

Acromioclavicular Joint

Dysfunction of the acromioclavicular joint often resultsin shoulder pain, poorly localized by the patient, and feltduring flexion and abduction to 120° and internal rotation(back scratch test). Horizontal adduction is limited andsometimes painful against resistance. The diagnosis ismade by the pain felt on palpation and confirmed by ananesthetic injection that relieves it.

The joint line is palpated while the scapula is mobilizedby grasping it between thumb and index finger, laterally,like a piano key. Normally painless, these maneuvers arepainful if the joint is injured (Fig. 53.5).

This joint has a small meniscus that can be torn orsubluxed during rapid and violent movements or evenduring simple forced movements; it undergoes degenera-tive changes in 9 of 10 patients over the age of 50. Acutejoint blockage is rare, but there is often a chronic dysfunc-tion of the joint.

Radiography sometimes demonstrates joint space nar-rowing with sclerosis, osteophytes and in some cases,

Figure 53.3

Palpation of supraspinatus for trigger points.

Figure 53.4

Palpation of biceps tendon.

Figure 53.5

Examination of acromioclavicular joint.

CHAPTER 53 SHOULDER PAIN AND THE CERVICAL SPINE

349

remodeling and deformations of the involved bonyextremities. Initially, widening of the superior part of thejoint space is noted. This degenerative arthropathy is oftensilent; it can become painful after forceful physical move-ments.

Particular Cases

Overhand athletes (e.g., pitchers or tennis players) candevelop microtraumatic arthropathies seen on radiographsas subchondral cysts in the lateral thirds of their clavicles.Resting the joint is the best treatment. In a few cases,Simon (1984) observed osteonecrosis of the distal clavicleseveral months after trauma.

Sternoclavicular Joint

Whatever the nature of the injury, it is generallyrevealed by swelling and always by tenderness on palpa-tion (Fig. 53.6). Pain from the sternoclavicular joint israrely felt at its level; it is often referred toward the shoul-der, the supraspinous fossa, or the neck. This joint alsohas a small meniscus that (rarely) can produce a mechan-ical pathology characterized by painful swelling.

Manipulation can be useful with or without corticos-teroid injections. Degenerative arthropathy of the sterno-clavicular joint occurs later than acromioclavicular degen-eration, but it is practically constant at 60 years of age.Radiographs demonstrate narrowing of the joint space,with subchondral sclerosis and osteophytosis. Theselesions can cause acute inflammation, but they also fosterpainful dysfunction that can be treated successfully bymanipulation. They are usually asymptomatic. Generally,the acromioclavicular joint is spared in inflammatory andrheumatic conditions; the sternoclavicular joint, in con-trast, is frequently affected.

Assessment of Scapular Mobility (Scapulothoracic Joint)

Free mobility of the scapula upon the rib cage is essen-tial for normal glenohumeral range of motion. The mobil-ity of the joint is examined with the patient lying on theside opposite the one to be examined. The examiner graspsthe shoulder tip in both hands, pulling it backward whilesimultaneously taking hold of the medial edge of the scap-ula with the fingers of both hands (Fig. 53.13); in this way,the examiner can mobilize the scapula in all directionsand evaluate any limitation of glenohumeral mobility.

Glenohumeral Mobility and Assessment of Glenoid Fossa

Various maneuvers are used to test the anteroposteriorjoint play of the humeral head on the glenoid fossa. Thepatient is sitting or lying down.

Testing Joint Play

The pylon or hammerhead technique allows testing ofthe separation of the humeral head from the glenoid cavityand at the same time moving it in all directions. Whenpain or limitation precludes maintaining the humerus atan elevation of 90° as shown in Fig. 53.7, the maneuvercan be adapted by maintaining the humerus at 30 to 40°of abduction. Thus, the two shoulders can be comparedwith respect to joint play and pain. Joint play is absent incapsulitis. It is very limited in the rare glenohumeralspondylosis, and there is painful crepitus. Joint play isincreased in lesions of the glenoid fossa.

Glenohumeral play can also be tested with the patientcompletely relaxed in supine. The examiner grasps thehumeral head with the hand contralateral to the side beingassessed, with four fingers posteriorly and the thumbanteriorly, while the opposite hand applies pressure to theclavicle.

Humeral head mobility can also be tested with thepatient seated and bending slightly forward (Fig. 53.8).With one hand, the examiner fixates the shoulder, whilethe other hand grasps the upper part of the arm and appliesslow anteroposterior movements (Rodineau).

Glenohumeral arthropathies are characterized byshoulder pain, with restrictions in both active and passivemotion. Diagnosis is completed by appropriate radio-graphic views to rule out other entities such as spondylo-sis, necrosis, arthritis, benign tumors (chondromas, osteo-mas, osteoid, osteochondromatosis), or malignant tumors(primary or secondary).

Glenoid Fossa

Some shoulder tenderness may be due to a lesion of theglenoid fossa and labrum from athletic trauma or without

Figure 53.6

Examination of sternoclavicular joint.

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clear cause. Such lesions can become progressively morepainful and lead to shoulder instability. These lesions areespecially seen in overhand athletes, whose shoulders aresubmitted to violent and repetitive anteroposterior shearforces associated with internal and external rotation.Injury to the anterior labrum, the most common site ofinjury, is improved by local warm compresses. The patientsometimes senses an abrupt alteration in joint mobility ortransient locking of the shoulder.

Manual muscle testing against isometric resistance isnormal. The back scratch test (adduction plus internalrotation) is limited by pain. Palpation of the glenohumeralfossa cavity at its anterior border is painful. If the patientis asked to simulate the motion of throwing a javelin; itis noted that the range of motion is greater on the affectedside than on the normal side. At maximal external rotationin this position, the examiner exaggerates the movementby applying a posteroanterior shear to the humeral head

with one hand and pulling the patient’s wrist backwardwith the other. This maneuver, similar to the dislocation–relocation test performed in the supine position, repro-duces the usual pain.

Radiographic studies can show a fracture of the inferiorglenoid labrum, a flattening of the glenoid cavity, or ablunted aspect of the rim. Lateral views performed withBernageau’s technique are useful ways to demonstrateglenoid lesions. In difficult cases, CT arthrography, MRI,and possibly arthroscopy complete the examination.

If pain is improved by medical management, the patientshould be rehabilitated by working the internal rotators(subscapularis) in a program similar to those used forpatients with recurrent dislocations of the shoulder. Ifthere is any failure, then surgery is indicated if theinstability is not well tolerated. The techniques used arethe same as those used for recurrent dislocations.

Figure 53.7

This pylon maneuver permits the examiner to assess the mobility between the humeral head and the glenoidfossa. It can also be used to mobilize the shoulder, allowing separation. If the patient is unable to abduct beyond 90°, thismaneuver can be modified by placing the patient’s arm in less adduction.

Figure 53.8

Examination of anteroposterior mobility and glenohumeral joint. This movement is often increased in lesions ofthe glenoid labrum. The patient should be relaxed and bent forward slightly.

CHAPTER 53 SHOULDER PAIN AND THE CERVICAL SPINE

351

Examination of Cervical Spine

After a thorough shoulder examination, the origin ofthe shoulder pain can be diagnosed, and the treatment canbe tailored to the diagnosis. However, sometimes a thor-ough examination will find no lesion to explain the shoul-der pain. Often examination of the cervical spine will thenreveal the answer, as the pain can be due to the cellulo-tenoperiosteomyalgic syndrome, C5 or C6 (tendinalgias,trigger points, periosteal tenderness).

The “cervical shoulder” can present with symptomsconsistent with tendinitis, including pain on movementagainst resistance and motion restriction. Often the cervi-cal and local factors are additive; thus, lesions that wouldbe latent in isolation become painful.

CERVICAL SHOULDER

Often a patient with a painful shoulder, with or withoutmotion restriction, for whom a diagnosis of tendinitismight be made, will obtain immediate relief from manip-ulation of the cervical spine, which may restore pain-freemovement as well (Fig. 53.10). Here it is important todemonstrate the segmental dysfunction of the midcervicalsegments (C4–5 and C5–6) with facet joint tendernessipsilateral to the painful shoulder. This segmental dys-function is almost always the result of a PMID and occa-sionally is due to synovitis (Fig. 53.9a and b).

Radiologic examination of the cervical spine andshoulder is indispensable for diagnosis. However, radio-graphic examinations have high incidences of both false-positive and false-negative findings. The presence of spon-dylosis at C4–5 or C5–6 or the existence of multilevel diskdegeneration is only presumptive. They neither affirm norinvalidate the possible cervical origin of the painful shoul-der. The following case is typical of cervical shoulder.

Case History

— Mr. P., a 56-year old athletic male, wasan accomplished tennis player who played regularly. Aftera fall down some stairs, he began complaining of right

shoulder pain with limitation of movement into abductionand behind the head. The diagnosis of rotator cufftendinitis was made, and a few subacromial injectionsresulted in partial improvement. His condition remainedunchanged in spite of anti-inflammatory treatments, moreinjections, and physical therapy trials. This lasted for 4months, with persistent painful motion restriction. Abduc-tion and rotation against resistance were impossible, asthey produced a very sharp pain. Both the infra- andsupraspinatus muscles as well as the tendon of the rightbiceps were tender to palpation.

Examination of the cervical spine did not reveal anylimitation of movement. Radiographic studies showedonly minor spondylosis, but palpation revealed markedtenderness over the right C4–5 facet joint on the sideof the affected shoulder. Soon after, a manipulation inleft rotation, followed by a manipulation in left latero-flexion was performed. After the manipulation, thepatient was able to lift his arm freely without the leastdiscomfort and the tests against resistance in abductionand external rotation were much improved. Two moresessions of manipulation at weekly intervals were per-formed and improvement of the tests against resistance

Figure 53.9

a.

Cervical segmental examination for facet joint tenderness in the lower cervical spine.

b.

C4–5 and C5–6segments can produce pain in the shoulder through intermediary cellulalgic, tenoperiosteal, or myalgic manifestations.

Figure 53.10

Immediate reduction in pain and increase inshoulder mobility with cervical manipulation supports the par-ticipation of the cervical segment as the origin and cause ofthis dysfunction. Here the manipulation in right rotation isdemonstrated on C5–6.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

improved at every session. After the third session, themovements were free and contraction against maximalresistance was painless.

The patient took up tennis with-out the least inconvenience.

In summary, in this case, the diagnosis of tendinitiswas considered, but on closer examination the pain turnedout to be of cervical origin. Even when pain seems to beundeniably linked to a lesion of the biceps tendon or therotator cuff, the cervical factor, if it exists, can play adeterminant or facilitating role.

Diagnosis of Cervical Shoulder

When a patient presents with shoulder pain accompa-nied by features of tendinitis such as pain with or withoutmotion restriction, two diagnostic possibilities may beconsidered.

1. Cervical facet joint tenderness at C4–5 or C5–6is not found on palpation. In this case, the cer-vical factor may be eliminated.

2. There is facet joint tenderness C4–5 or C5–C6ipsilateral to the painful shoulder. It is thenpossible, but not certain, that the cervical spinemay be totally or partially responsible for theshoulder pain. To make this determination, thefollowing therapeutic tests should be per-formed.a. If it is an acute synovitis, injection of cor-

ticosteroid can be performed, withoutmanipulation.

b. If it is due to a PMID and manipulation ispossible, a test of manipulative treatment canyield an instant answer.

The first manipulation should be performed (e.g., inrotation), then testing of the painful movements should berepeated. If the cervical spine is involved, as is frequentlythe case, a well performed manipulation should result inappreciable improvement; for example, a patient unableto abduct his arm can do it soon after manipulation andwithout pain, even against increased resistance.

After the first manipulation, one or two more manipu-lations may be performed, for example, in lateroflexionand then in chin pivot. The examination should be repeatedafter each of these maneuvers. Thus, from the first sessionon, when manipulation can be done without any difficulty,one knows whether there is a link between the cervicalspine and the painful tendon or tendons.

If the result obtained with manipulation is not satisfac-tory with respect to facet joint sensitivity, an injection withcorticosteroid can be tried. If the shoulder pain does notimprove after the first treatment, there is little chance thatfurther cervical treatment will be useful.

In some cases, the patient may come back a few dayslater and report a painful 24 hours associated with a tem-porary or persistent improvement in the condition. Thisresult helps to confirm that the pain syndrome originatedin the cervical spine. Two or three more sessions of cer-vical treatment will often bring complete and lasting relief.

Sometimes it is necessary to inject a residual triggerpoint. Depending on which segment is involved, C5 orC6, the corresponding cellulotenoperiosteomyalgic syn-drome can be seen involving the infraspinatus (Fig. 48.11),the supraspinatus, or the teres minor.

MIXED SHOULDER PAIN SYNDROMES

In some cases, local treatment produces incompleteimprovement. Cervical treatment produces total relief or,on the contrary, it clearly improves the pain and the testsagainst resistance, but relief is incomplete and injectionof the tendon results in complete relief. In these “mixedshoulder” cases, the contributions to the painful syndromemade by the two components can vary from case to caseand over time in individuals.

Taut Bands, Trigger Points, and Atypical Shoulder Pain

We have already emphasized the role in shoulder ten-derness of some active trigger points belonging to acellulotenoperiosteomyalgic C5 or C6 syndrome, but atthe shoulder especially, certain trigger points can havelocal origins. They can result from excessive exertion:carrying too heavy a suitcase in the case of the supraspina-tus; repeated maneuvers in a car without power steeringfor the teres major; working with the arms held horizon-tally for the deltoid, etc. A forceful, strenuous, or overlywide movement can also be responsible, as can prolonged,sustained, stressful postures.

Taut bands often harbor trigger points that are oftenthe sources of referred shoulder tip tenderness and refer

Figure 53.11

Injection of infraspinatus trigger point.

CHAPTER 53 SHOULDER PAIN AND THE CERVICAL SPINE

353

in a consistent pattern: to the anterior shoulder forinfraspinatus, the lateral shoulder for supraspinatus, andthe posterior shoulder for teres minor.

One often finds trigger points along the lateral borderof the subscapularis. They can be palpated along the lateralborder of the scapula with the patient supine. Severe casescan limit shoulder movement and mimic adhesive cap-sulitis.

The trigger points of the coracobrachialis interfere withthe ability to reach behind the back. Trigger points of thedeltoid are frequent, easy to find, and are more often linkedto nonvertebral causes (trauma, exertion). They cause dis-comfort with abduction. The trigger points of the tricepsprevent complete arm flexion. The treatment is injectionof xylocaine followed by stretching of the affected muscle(Fig. 53.11).

MANUAL THERAPY FOR PAINFUL SHOULDER

Theoretically, manual therapy does not have a domi-nant place in the treatment of shoulder tenderness linkedto rotator cuff pathology. Rotator cuff tendinitis needsspecific treatment (essentially medical), includinginjections in acute cases, provided they are used judi-ciously. Electrotherapy and ultrasound can be recom-mended.

A therapeutic exercise prescription is the best treatmentin total or partial ruptures of the rotator cuff as well as intendinitis caused by subacromial impingement. The basicprinciple of the program is to teach the patient to depressthe humeral head during abduction, thereby decreasingthe subacromial impingement. Physical therapy can start

with passive mobilization of the humeral head into adepressed position that will free external rotation. Thishumeral head depression is performed first with the helpof the physiotherapist, then performed actively andrepeated frequently so that the patient can automaticallydepress the humeral head at all times with flexion orabduction of the arm. It is also necessary to strengthen theadductor muscles, pectoralis major and latissimus dorsi,because they also participate in humeral head depression.There are also cases in which some manual techniqueshave their indication.

Mobilization of Glenohumeral Joint

The technique shown in Fig. 53.7 allows glenohumeralmobilization and separation of the articular surfaces. Thetechnique shown in Fig. 53.12 also permits efficient gle-nohumeral distraction.

Mobilization of Scapulothoracic Joint

Full mobility of the scapulothoracic joint can help tocompensate for inadequate mobility of the glenohumeraljoint in adhesive capsulitis or in spondylosis. Mobiliza-tions shown in Fig. 53.13 (see also Fig. 54.13) are veryuseful. They also allow for good stretching and relaxationof the muscles of the scapula.

Manipulation of Acromioclavicular Joint

The acromioclavicular joint is often affected in shoul-der tenderness associated with other conditions. Injectioncan prove its involvement and often relieve it, but it is notalways sufficient, and manual techniques can be of help.Fig. 53.14 and Fig. 53.15 show two usual techniques.

Figure 53.12

Demonstration of glenohumeral distraction. The examiner, standing in front of the patient, places the arm underthe patient’s axilla with the patient’s arm dangling at the side. With the left hand, pressure is applied rhythmically to the lateralinferior aspect of the arm, using it as a lever to produce progressive glenoid humeral distraction. This maneuver stretches thelateral joint capsule to permit distraction.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Lesage uses a slightly different technique from the oneshown in Fig. 53.15. For a right acromioclavicular joint,the patient sits on a stool, right hand on the hip and thumbforward. This point can be the pivot point. The examinerstands behind with the left foot slightly forward and rightfoot back, legs bent. The examiner’s left side flank isagainst the lumbar region of the patient. The examiner’sleft arm rests on the right clavicle of the patient; the righthand grasps the patient’s right shoulder. The examiner’sright forearm rests on the lateral side of the patient’s arm.Manipulation is performed by suddenly bending the twolegs with an elbow motion that brings the shoulders intoretraction.

Manipulation of Sternoclavicular Joint

The sternoclavicular joint is manipulated with the tech-nique shown on Fig. 53.16. The technique shown inFig. 53.17 simultaneously mobilizes the three joints of theshoulder: sternoclavicular, acromioclavicular, and gleno-humeral. A direct manipulation is possible. The patient is

Figure 53.13

Mobilization of scapulothoracic joint withstretching of scapular rotators.

Figure 53.14

Acromioclavicular manipulation. The left handfixes the lateral surface of the clavicle, while the right handplaces pressure at the base of the neck, applying lateraltension to the axis of the clavicle to take up the slack. A briefthrust is then applied with the left hand on the acromioclav-icular joint.

Figure 53.15

Acromioclavicular manipulation (second tech-nique). The patient is sitting on a table with the right armhanging slightly posteriorly and the hand in supination. Thedoctor, standing behind, presses with the left hand over themedial surface of the clavicle and places the right hand overthe acromion. Then while firmly maintaining pressure with thesternum and left hand, the examiner progressively appliesposterior lateral traction with the right hand to take up theslack and then applies a manipulative thrust.

Figure 53.16

Sternoclavicular manipulation. The patient issupine. The examiner takes the left arm of the patient andpulls it outward and in abduction, slowly applying pressureon the axis of the clavicle so that the heel of the right handapplies pressure to the median clavicle. The examiner takesup the slack while applying pressure to the medial aspect ofthe clavicle. Repeated mobilizations are performed.

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355

supine, arms along the body. For a right sternoclavicularmanipulation, the examiner stands on the right side of thepatient and presses on the medial part of the right cla-vicular head with the heel of the right hand and applies acounterpressure with the left hand on the left clavicle. Theexaminer takes up the slack by pressing downward andlaterally (in the direction of the acromioclavicular joints)then applies a thrust of the right hand in the same direction.

In some cases, the sternoclavicular and acromioclavic-ular joints are painful at the same time (syndrome of bothends of the clavicle [Troisier]). This is often a post-traumaticsequela, but in these cases, there is never a local pain, butrather, radiating tenderness (e.g., supraspinatus fossa, ear).The usual treatment is the injection of the two joints, butmanipulative treatment (Fig. 53.17) can be useful in somecases.

Figure 53.17

The examiner stands behind the seatedpatient, with the forearms flexed and placed over the anterioraspects of both humeral heads. Counterpressure is thenapplied with the sternum against the patient’s back. Posteriorlateral tension is progressively increased rhythmically or witha thrust to mobilize or manipulate the glenohumeral, acromi-oclavicular, and sternoclavicular joints.

357

54

LATERAL EPICONDYLAR PAIN

Lateral epicondylar pain or epicondylitis refers to painlocalized to the lateral epicondyle in which some move-ments (e.g., turning a doorknob and pouring a drink) arevery painful or even impossible if the disorder is severe.It is often called “tennis elbow,” since it is common amongtennis players. Workers whose jobs require repetitivepronation and supination (e.g., using a screw driver) areoften affected, as are people who are neither athletes normanual laborers.

Pain is generally attributed to tenoperiosteal irritationof mechanical origin caused by overwork of the long wristand finger extensors that have a common origin on thelateral epicondyle (hence the name, lateral epicondylitis).However, the efficiency of treatment by cervical manipu-lation demonstrates that “insertion tendinitis” is not theonly process involved in the lateral epicondylar pain.

Six muscles have their proximal attachment on thelateral epicondyle including the:

• Supinator• Extensor carpi radialis longus and brevis (ECRL,

ECRB)• Extensor digitorum communis (EDC)• Extensor digiti minimi• Extensor carpi ulnaris

Among those muscles originating from the epicondyle,the surface of attachment of the extensor carpi radialisbrevis represents half of the total surface of attachment ofall the epicondylar muscles.

CLINICAL EXAMINATION

Elbow

Palpation

Tenderness to palpation over the lateral epicondyle isthe characteristic sign of the condition (Fig. 54.1). It isperformed with the elbow flexed at a right angle. Thecommon extensor tendon, the radiohumeral joint line, the

circumference of the radial head, and the point of emer-gence of the posterior interosseous branch of the radialnerve are also palpated. One or two trigger points in thesupinator or in the radialis muscles are often palpated also.Sometimes, a cellulalgic zone painful to pinch-rolling isfound at the lateral side of the elbow.

Manual Muscle Testing against Resistance

Pain produced by resisted isometric contraction of theepicondylar muscles is a quasiconstant sign. This shouldbe assessed by first having the patient extend the wristagainst resistance, with fingers clenched, and then extendthe fingers against resistance, usually directed at the mid-dle finger.

Examination of Active and Passive Range of Motion

Mobility is normal in general, but extension may belimited on occasion. More rarely, the limitation involvesboth flexion and extension. Passive mobility is tested inflexion–extension, then in pronation–supination. It can

Figure 54.1

Lateral epicondyle tenderness is an essentialsign of this disorder.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

sometimes give the impression of “hooking” in cases ofradiohumeral subluxation, but as we have already empha-sized, the lateral joint play should be studied.

Lateral Joint Play of Elbow

The elbow is extended. With the physician facing thepatient, the affected forearm is held under the examiner’saxilla, in supination. The lateral elbow is then graspedwith both hands. Then, while firmly grasping the patient’sforearm, the examiner applies gradual varus and valgusstresses to the elbow to assess the passive range and endfeel. The joint play varies from one patient to another butis readily appreciated in the intact patient. The physiciancompares both sides, knowing that the lateral play isalways a little less free in the dominant elbow (Fig. 54.2).In some lateral epicondylar pain syndromes, this play isglobally decreased, and elbow mobilization is painful; itis painless in the normal state. Sometimes, this maneuveris very painful in abduction or in adduction, giving theimpression of joint blockage.

Joint Play of Distal Radioulnar Joint

In some persistent lateral epicondylar pain syndromes,there is a decrease in the passive mobility of the distalradioulnar joint together with a decrease of the lateralmobility of the elbow. The examiner grasps the distalradius with the thumb and index finger of one hand andgrasps the distal ulna with the thumb and index finger ofthe other. Gliding mobilizations can be performed toassess joint play. Mobility of both sides is compared. Thistest can be disagreeable for the patient.

Radiography

Radiography can reveal small periarticular calcifica-tions that indicate joint overuse and are usually not thecauses of the pain.

Cervical Spine

The patient is in supine position, and the physicianexamines for tenderness over the C5–6 or C6–7 facetjoints ipsilateral to the lateral epicondylar pain. Tender-ness suggests that there may be a cervical component tothe elbow pain, and the cervical spine should be carefullyexamined with the usual techniques. Radiographic studieswill be necessary.

EVALUATION OF LATERAL EPICONDYLAR PAIN

It is important to be able to evaluate lateral epicondylarpain, not so much to compare the lateral epicondylar painof a patient with the one of another patient, but to appre-ciate the evolution of the condition and the efficiency ofa therapeutic treatment in a given patient. In 1975, weproposed a series of maneuvers performed with the phy-sician applying isometric resistance in two different elbowpositions.

1. Extension of hand and fingers with (a) theelbow flexed at a right angle and the armadducted at the side (Fig. 54.3, left) and (b) theelbow extended (Fig. 54.3, right).

2. Pronation: the physician grasps the patient’shand and instructs the patient to turn the palmto the floor (pronate) against isometric resis-tance supplied by the examiner. The elbow is(a) flexed at a right angle (Fig. 54.4, left) and(b) extended (Fig. 54.4, right).

3. Supination: same maneuver as above, exceptthe patient is asked to turn the palm up (supi-nate) against isometric resistance. The elbow is(a) flexed at a right angle (Fig. 54.5, left) and(b) extended (Fig. 54.5, right).

Each maneuver is rated as follows:

0 No pain1 Some resistance, but painful2 Some weak resistance, with marked pain3 Resistance impossible, pain too severe

If there is pain at rest, it is rated from 0 to 2. Thus, thetotal range is between 0 and 20 (3 points for each of thesix maneuvers plus 2 for pain at rest), but it is not absolute.One cannot conclude that a patient with a score of 14 ismore affected than a patient with a score of 10, but thisscoring system allows one to reliably judge the evolutionof pain and the response to treatment. It is particularlyuseful in lateral epicondylar pain syndromes with cervicalinvolvement in which a suitable cervical maneuver can,

Figure 54.2

Examination of lateral mobility of lateral epi-condylar joint.

CHAPTER 54 LATERAL EPICONDYLAR PAIN

359

for example, improve and sometimes even render the testsnegative.

Classification

The examination allows the examiner to classify thepain syndrome with respect to the underlying pathophys-iologic mechanism. It may be

• Lateral epicondylar pain of local origin

• Lateral epicondylar pain of tenoperiosteal, muscu-lar, articular, or neurogenic (due to compression ofthe posterior interosseous branch of the radial nerve)origin

• Lateral epicondylar pain of cervical origin

• Lateral epicondylar pain of mixed origin

Figure 54.3

Wrist extension against resistance.

Left.

With forearm flexed to 90°.

Right.

With forearm extended.

Figure 54.4

Pronation against resistance.

Left.

With forearm flexed to 90°.

Right.

With forearm extended.

Figure 54.5

Supination against resistance.

Left.

With forearm flexed to 90

°

.

Right.

With forearm extended.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Periarthritis of the elbow and sometimes also adecrease in the range of motion of the distal radioulnararticulation can be associated with each of these forms.

Lateral Epicondylar Pain of Local Origin

Lateral Epicondylar Pain Due to TenoperiostealIrritation.

Most authors believe that lateral epicondylarpain is due to irritation of the tendinous attachment to theperiosteum caused by overuse of the epicondylar muscles.This seems to be confirmed by the often favorable resultsof only local treatment. The diagnosis is based on:

• Pain on palpation of the common extensor tendon• Pain on resisted contraction of the epicondylar

muscles (ECRB, EDC)• Pain caused by forced varus and hyperextension

In our experience, a purely local origin accounts foronly a fraction of the cases because the pain of tendinousinsertion is often facilitated or even caused by a cervicalfactor that responds to cervical treatment. If the cervicalfactor is moderate or transient, local treatment can besufficient. If not, the result can be temporary or insufficient(see “Lateral Epicondylar Pain and Cervical Spine”below).

Treatment.

Treatment consists of injection of the pain-ful site on palpation, using a corticosteroid derivative, withor without a local anesthetic. Physiotherapeutic modali-ties, including electrical stimulation and ultrasound, canalso be most useful.

In refractory cases of tendinitis, deep transverse mas-sage has been recommended by Cyriax. Transverse fric-tion massage of the tendon is a painful treatment, demand-ing three to six sessions of about 15 min each. It does notseem very logical if the tendon is thought to have inflam-matory or necrotic lesions, but it is useful in some cases.

In very refractory cases, Troisier, after Cyriax, advo-cated the technique of subcutaneous tenotomy of the com-mon extensor tendon, followed 6 weeks later by one ortwo injections of corticosteroid; the patient is relievedafter the injections. Troisier reported 34 good results outof 39 with this technique. The steps are as follows.

Using sterile technique, the operator inserts a short-blade scalpel under the skin and detaches the commonextensor tendon from the lateral epicondyle. The tenotomyis followed by a Mill’s manipulation: the operator main-tains the patient’s hand and fingers in maximal extension,with the forearm in abduction, and then forces extensionof the elbow. Six weeks later, the patient, who generallyis still in pain, is reexamined and receives one or twoinjections of corticosteroid that usually bring relief.

Epicondylalgia of Muscular Origin.

During epi-condylitis, it is common to palpate a few trigger points inthe body of the epicondylar muscles (Fig. 54.6). They canbelong to a cellulotenoperiosteomyalgic segmental verte-

bral C6 or C7 syndrome, have a local origin such asmuscular fatigue or articular pain, or can be of mixedorigin.

Treatment.

If a cervical origin is suspected, spinal treat-ment should be performed first; often it is sufficient. Theresult is immediately noted on the rating tests.

If the origin is local or mixed, local treatment is indis-pensable. The trigger points are usually found in the supi-nator muscle and occasionally in the extensor carpi radi-alis longus and brevis muscles. The trigger points shouldbe injected with 1 mL xylocaine or 0.5% lidocaine. Pres-sure should be maintained for 90 sec on the trigger pointsand repeated several times. Ultrasound is often useful inthese forms.

Radiohumeral Articular Blockage (Locking).

Sometimes testing the lateral joint play of the elbowreveals that it is impaired and very painful in some direc-tions while free in others. This usually corresponds to amechanical pain of the articulation; it is related to eitheradduction, abduction, or hyperextension. The oppositemovement is usually free and painless. Most often, thereis exquisite pain on palpation of the radiohumeral jointline. This lateral epicondylar pain often starts rapidly dur-ing a certain movement.

Frequently, an appropriate manipulation or a series ofmobilizations performed in the pain-free direction, some-times with intra-articular injection, relieves the patient.Does this “radiohumeral disturbance” (Maigne, 1959) cor-respond to the impingement of a synovial fringe or afragment of the radiohumeral pseudomeniscus? Both havebeen found in surgical interventions. In 1959, De Goesopted for the pseudomeniscus, and Benassy’s operativefindings suggested the same thing. In other cases, chon-dromalacia lesions of the radial head have been found.

A test that we trust seems to confirm the existence ofan intra-articular factor: the transient disappearance ofpain after the intra-articular injection of local anesthetic.In chronic cases, there is an associated periarticular reac-tion resulting in restricted elbow range of motion withpain increasing markedly in a given direction. This can be

Figure 54.6

Palpation of supinator trigger points.

CHAPTER 54 LATERAL EPICONDYLAR PAIN

361

tested by oscillating the joint at end range in all directions.In our experience, a radiohumeral origin accounts for 8%of all the lateral epicondylalgias.

Treatment.

In

acute cases, manipulation of the elbowis often useful. The technique to be used depends on thetype of blockage. The rule of no pain always determineswhich manipulation can or should be used. In chroniccases, it has to be performed progressively and, in somecases, may require an intra-articular injection of corticos-teroid and anesthetics prior to manipulation.

Manipulation in adduction —

This technique is usedwhen there is a blockage in abduction, which is the mostfrequent cause (Fig. 54.7).

First technique.

The patient’s forearm is positioned inextension and full supination. The operator grasps thepatient’s wrist with the opposite hand (operator’s left handfor the patient’s right and vice versa) and grasps the medialelbow with the other hand, keeping the forearm perpen-dicular to the patient’s arm. Manipulation consists of abrief thrust that exaggerates elbow adduction, followingseveral maneuvers that take up the slack.

Second technique.

The operator is on the right side ofthe patient (for a right elbow). The elbow is extended, withthe forearm in supination. The examiner’s left arm isflexed around the patient’s elbow with the fist tightenedto make that position rigid. The operator’s forearm is incontact with the medial side of the patient’s elbow. Theoperator’s right hand grasps the wrist, maintained in supi-nation. This hand will give the manipulative thrust inforced adduction (Fig. 54.8).

Manipulation in abduction

—

This manipulation isthe opposite of the above.

First technique.

The right hand takes the right wrist ofthe patient, while the left hand grasps the lateral elbow,with the left forearm of the operator kept perpendicularto the patient’s arm (Fig. 54.9).

Second technique.

The operator blocks the patient’sextended right elbow in the V formed by the operator’sflexed right arm. The forearm is in contact with the lateralaspect of the patient’s elbow. The left hand grasps thewrist, which is maintained in supination. It gives themanipulative thrust in abduction after several maneuversto take up the slack (Fig. 54.10).

Manipulation in extension

(Fig. 54.11)

—

Thismanipulation is performed in anterior or anterolateralblockage of the radiohumeral joint. The forearm of thepatient is extended and supinated; the thumb applies pres-sure to the posterior radial head, while the operator

Figure 54.7

Manipulation of elbow in adduction (first tech-nique).

Figure 54.8

Manipulation of elbow in adduction (secondtechnique).

Figure 54.9

Manipulation of elbow in abduction (first tech-nique).

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

exaggerates the extension of the elbow with a brief pushon the wrist.

Manipulation in pronation (Fig. 54.12) —

Thepatient’s arm is extended. The operator’s right hand graspsthe right wrist of the patient in forced pronation. Theelbow is held by the operator’s left hand, with the thumbagainst the posterior radial head. The maneuver consistsof inducing a hyperextension and forced pronation of thepatient’s elbow while the thumb keeps the pressure againstthe radial head. Then, while maintaining this pressure, theelbow is brought back slowly to the starting position. Thismaneuver is performed several times, progressively.

Manipulation in flexion–supination (Fig. 54.13)

—

This maneuver is used for “pediatric pulled elbow” inchildren but can also be applied to certain epicondylalgiasof adults. Pediatric pulled elbow is generally caused whena child is lifted by pulling his or her hand to step up to asidewalk or stairway. The operator supports the patient’selbow with the right hand and presses with the right thumbon the anterior part of the radial head. The operator graspsthe patient’s wrist with the left hand, the thumb pressingon the back of the patient’s hand. A strong traction is thenapplied on the forearm, and while maintaining the wristin supination, the elbow is brought in forced supinationand in complete flexion. This maneuver is simple to applyto a child because traction is not necessary, should usuallybe repeated in an adult to be useful. Its indication is rarerthan that for the maneuver in pronation.

N.B.

The operator can also apply pressure on the radial headwith the pad of the fingers of the right hand while the left handencloses the patient’s wrist. The execution of the maneuver isthe same.

Periarthritis of Elbow.

A certain number of epi-condylalgias of local origin or with a cervical factorpresent with a global decrease in the lateral joint play ofthe elbow when tested by the above technique (Maigne;Fig. 54.2). The test is a little painful, but it is perfectlyfree and painless on the other elbow. This seems to cor-respond to a periarticular reaction that can be responsiblefor the persistence of pain. Indeed, in some cases, thelateral epicondylar pain is decreased by either local treat-ment or cervical treatment and disappears completely onlywhen the lateral joint play of the elbow is reestablished.

Treatment.

To free lateral play, we use the same maneu-vers used for assessment. They are repeated progressivelyand insistently, 10 to 20 times. The periarticular reactionseems to be the consequence of an articular dysfunctioncaused by the lateral epicondylar pain.

Lateral Epicondylar Pain Due to Compression ofRadial Nerve.

Irritation of the posterior interosseousbranch of the radial nerve as it passes through the twoheads of the supinator into the radial tunnel can causelateral epicondylar pain (Koppel and Thompson, 1963). Itis refractory to local treatment, is often increased duringthe night, and can radiate toward the anterior forearm.According to Roles, the characteristic sign is the increasedpain with contraction against resistance of the ECRB(resisted extension of the third ray). This sign lacks spec-ificity. Electromyography confirms the diagnosis (Roles,Bence, and Commandré).

If local injections do not bring any improvement, asurgical decompression should be considered. At surgery,a fibrous arcade (arcade of Frohse) that is often seenincreases the irritation of the nerve. In pronation, the supi-nator is stretched and compresses the posteriorinterosseous branch of the radial nerve (80 of 90 cases,[Werne]). In chronic cases, lesions of the nerve are noted.Moreover, the roof of the radial tunnel is formed by thefibrous edge of the ECRB, which can be a source ofirritation. In their examination of 36 cases of chroniclateral epicondylar pain, Jesel et al. showed compressionsof the posterior interosseous branch of the radial nerve in

Figure 54.10

Manipulation of elbow in abduction (secondtechnique).

Figure 54.11

Manipulation of elbow in extension.

CHAPTER 54 LATERAL EPICONDYLAR PAIN

363

5 cases. Local injections are the best treatments. Whenthey fail, a patient should be considered for surgery.

Remark

In most epicondylalgias, whatever the mechanism, palpa-tion of the epicondylar muscles reveals the presence ofpainful taut bands that may have a cervical origin(cellulotenoperiosteomyalgic syndrome C6 or C7) orcould result from a radiohumeral articular dysfunction ormuscular strain. Under favorable anatomic conditions,

these trigger points might be able to cause a functionalentrapment syndrome that could be another factor in thedevelopment of lateral epicondylar pain.

DISTAL RADIOULNAR DYSFUNCTION

Certain patients with persistent lateral epicondylar painalso have decreased passive mobility of the distal radioul-nar joint. To test for this, the distal end of the radius is

Figure 54.12

Three phases of manipulation of elbow in pronation. This is actually more of a mobilization because the movementperformed is repeated several times.

Figure 54.13

Manipulation of elbow in flexion and supination.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

grasped between the examiner’s thumb and index finger,and the distal ulna is grasped between the thumb and indexfinger of the other hand while applying opposite move-ments from front to back, like playing the piano. Mobilityis compared with that of the opposite side. This maneuvercan be disagreeable on the affected side. Treatment con-sists of repeating this maneuver several times and tryingprogressively to free the movement.

This distal radioulnar block can perpetuate a persistentlateral epicondylar pain (Fig. 54.14). In several cases, wehave been able to eradicate chronic refractory epicondyl-algia. The patients had no pain at the wrist, but passivemovements of forced supination were painful.

LATERAL EPICONDYLAR PAIN AND CERVICAL SPINE

Most authors agree that common lateral epicondylarpain is caused by an insertional tendinitis due to overuseof the epicondylar muscles. This opinion seems to beconfirmed by the favorable results of local treatment(injections), but many cases involve a cervical factor

(C5–6, C6–7) whose treatment can also ease the lateralepicondylar pain, often immediately. This factor may pre-cipitate and perpetuate the lateral epicondylar pain. Themore prominent the cervical factor is, the more likely itis that lateral epicondylar pain will result with minimaleffort or routine movements.

J. Lacapére (1950) first considered the cervical originof lateral epicondylar pain. Renoult (1955) and Maigne(1955) found that cervical manipulation produced favor-able results. A semiologic and statistical study of 150 cases(Maigne, 1959) indicated that two of three cases of epi-condylitis showed variable degrees of cervical participa-tion. The mechanism can be understood in terms of aPMID and segmental vertebral cellulotenoperiosteomyal-gic syndrome (Maigne). Hypersensitivity of the lateralepicondyle to palpation is common in dysfunction of theC5–6 and C6–7 segments. The slightest overuse can causelateral epicondylar pain (Fig. 54.15 and Fig. 54.16).

The origin or facilitation of lateral epicondylar pain bycervical factors should be considered when the examina-tion demonstrates ipsilateral tenderness to palpation of theC5–6 or C6–7 facet joints. Of course, it is definite iftreatment produces amelioration, which is usually rapidwith a manipulation. The result of each treatment can beshown by evaluation tests; it can be shown immediatelywith manipulation.

We drew attention a long time ago (1959) to the fre-quent hypersensitivity of the lateral epicondyle in patientswith a segmental dysfunction of C5–6 or C6–7 due to aPMID or facet joint spondylosis. Recently, with J.C. Gous-sard, we examined patients with minor cervical pain inwhom the segmental examination revealed a contributionof C5–6 or C6–7. None of them complained about thelateral epicondyle. In 80 selected patients, the lateralepicondyle was found to be tender to palpation, and in 53cases, it was ipsilateral to the facet joint tenderness andpainless on the other side. In a control group of 40 patientswith no cervical signs on examination, the lateral epi-condyle was painful in only 3 patients.

Figure 54.14

Assessing mobility of distal radioulnar joint.

Figure 54.15

a.

Cervical segmental examination: palpation of facet joints.

b.

Lateral epicondylar pain can be related todysfunction of the C5–6 or C6–7 segments found ipsilateral to the facet joint tenderness.

CHAPTER 54 LATERAL EPICONDYLAR PAIN

365

In patients with cervical signs, the examination fre-quently showed some manifestations of the segmental C6or C7 cellulotenoperiosteomyalgic syndrome. In anunpublished study, we found the same results in patientswith no cervical pain but whose routine examinations alsoshowed latent PMID at C5–6 or C6–7. American osteo-paths have studied the origins of some lateral epicondylarpains. However, Steiner (1976), in an article published inthe

Journal of the American Osteopathic Association,

wrote about all the pathogeneses proposed for lateral epi-condylar pain without mentioning the cervical causes.

Certain authors, with the help of electromyographicexamination, have looked for evidence of neural dysfunc-tion in the C6 or C7 territory to invalidate or confirm thecervical thesis of diverse epicondylalgias: Illouz andLimon (1974) and Bence et al. (1978). In 40% of cases,the latter found a narrow relationship between lateral epi-condylar pain and cervical radiculopathy.

Canadians Gunn and Milbrandt suggest cervical originsin 42 patients with lateral epicondylar pains that wereresistant to local treatment (1976). In an electromyo-graphic study involving 36 patients with refractory epi-condylalgias, Jesel et al. (1986) found that 8 showed evi-dence of nerve dysfunction from C5 to C7. A cervicalspine origin is generally considered only when there areradiologic lesions of spondylosis that prove nothing orwhen there are electromyographic signs that are very con-clusive but can only be applied to a portion of the cases.Indeed, given the present state of affairs, we cannot expectto find objective signs of neural irritation in all patients

with only PMID and reflex cellulotenoperiosteomyalgicmanifestations. The following case is typical.

Case History 1

— A 35-year old female ranked tennisplayer experienced pain for 2 years and had to stopplaying. She had 36 consecutive local injections. Shewas relieved for a while in the beginning but laterinjections had no effect. Then she showed a PMID atC5–6 on examination. After the third session of cervicalmanipulation, she was clearly improved and wasrelieved after the sixth. She then resumed her normalcompetition.

The following case is more interesting because thepatient, after the failure of medical treatments and unsuc-cessful surgery, was then relieved by cervical treatment:

Case History 2

—

A 45-year old male manual laborerhad lateral epicondylar pain for 2 years prior to con-sulting us. His pain, after having been partially relieved,was refractory to medical treatments. He was operatedon (lengthening of ECRB) but the intervention did notrelieve him. A few months later, he was examined inour department at Hotel Dieu. The cervical examinationdemonstrated a PMID at C6–7. Three sessions of cer-vical manipulation relieved him completely, and he wasable to resume his work.

In chronic cases, if the improvement brought by thecervical treatment is clear but incomplete, a local treat-ment generally acts very quickly, even if it had been inef-fective earlier. It consists of injection of the lateral epi-condyle or the trigger points and/or electrotherapy.

Figure 54.16

Manifestations of segmental vertebral cellulotenoperiosteomyalgic syndrome of C6.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Treatment

The proof of the cervical origin is the success of thetreatment. C5–6 or C6–7 facet dysfunction is usually theconsequence of a PMID, but it can be due to acute syno-vitis. In the first case, manipulation can be used for treat-ment (Fig. 54.17) if it is technically possible and there isno contraindication. In favorable cases, cervical maneu-vers can result in clear improvement on evaluation tests,sometimes even the disappearance of any pain againstresistance. In persistent cases, two or three sessions andsometimes five or six may be necessary.

When the articular pain does not disappear after a wellperformed manipulative treatment, injection of the cervi-cal articulation with a corticosteroid derivative is useful.This can be the first treatment if manipulation is con-traindicated or in cases of synovitis. To be effective,the manipulation should be technically possible, precise,and rather forceful. Cervical electrotherapy (short-wave

diathermy, ultrasound) can be useful when the above treat-ments cannot be used.

In chronic cases, patients often show limitation in thelateral joint play of the elbow. This should be treated bythe above described mobilizations. Surgery is reserved forcases refractory to medical treatment. They are relativelyrare. Most lateral epicondylar pain resistant to classicaltreatment (injections) shows cervical or articular factors,and suitable treatment relieves them. Nevertheless, insome resistant cases, relief is impossible with medicaltreatment, and there is no great need to defer action, espe-cially if a simple extra-articular intervention is considered.The proposed interventions are numerous. Some authors(Narakas) classify them according to the type of painpresent. The principal interventions are:

• Denervation of lateral epicondyle (Kaplan, Wilhelm)• Excision of inflamed tendinous tissue• Tenotomy with debridement of lateral epicondyle

(Hohmann) together with annular ligament release(Bosworth)

• Lengthening of ECRB (Garden)• Excision (ablation) of pseudomeniscus or synovial

fringes (de Goes, Benassy)• Release of posterior interosseous branch of the

radial nerve (Roles and Maudsley)

According to Saillant et al., most of the proposed tech-niques have common denominators, principally the lateralepicondylar muscles. They propose systematic and com-plete detachment of all epicondylar muscles with (possi-bly, and only if clinically warranted) a radiohumeralarthrotomy. Results are good when a true entrapment syn-drome of the posterior interosseous branch of the radialnerve exists (87% for Narakas) and a little poorer in othercases.

Figure 54.17

Example of cervical manipulation in lateral flex-ion useful for treating an inferior cervical PMID. When the Cspine plays a role in lateral epicondylar pain, amelioration ofthe pain (Fig. 54.3 through Fig. 54.5) is often immediate aftera properly performed cervical manipulation.

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55

MEDIAL EPICONDYLAR PAIN

Medial epicondylar pain is much less frequent thanlateral epicondylar pain. In fact, on examination, palpationoften demonstrates a particular sensitivity of the medialepicondyle, while the patient has no spontaneous pain. Itis generally caused by repetitive activity of the forearm inflexion and in pronation. It is frequent in manual therapists.

Often, it is noticed only when the patient leans on atable with the elbows apart; the medial epicondyles arethen directly in contact with the table and become verypainful. At the next level of activity, the patient complainsof pain over the medial elbow, increased with exertion,especially by movements such as the forceful shaking ofhands in flexion and pronation of the forearm.

A cervical element (PMID at C7–T1) that facilitates itmay exist. In those cases, the neck should be treated. Localinjection is performed in the same manner as for lateralepicondylalgias. Frequently, injection of trigger pointsfound in the body of some epitrochlear muscles is moreuseful if it is combined with the stretching of these muscles.

Rest is necessary in difficult cases. Patients at risk fordeveloping this condition should be instructed in stretch-ing techniques for the common flexor muscles that origi-nate from the medial epicondyle: with the elbow extended,the wrist and fingers are extended with the palm andfingertips pressed on a table, for example, to increase thestretching.

369

56

PUBIC PAIN AND SPINAL FACTORS

Pubic pain, or pubalgia, is currently common becauseit frequently strikes athletes, especially tennis and soccerplayers. This pain is due to mechanical stresses peculiarto these sports that affect the pubis. The pain is promotedby some morphologies (hyperlordosis and anteversion ofthe pelvis) associated with abdominal insufficiency. Someauthors (Durey) think that overtraining can also be a cause.Pain in the pubis is generally attributed to:

• Arthropathy of symphysis (osteitis pubis)• Tendinitis of adductors• Tendinitis of abdominal muscles

Arthropathy of the symphysis is associated with lesionsthat progressively worsen and are classified in four stages(Luschnitz). The initial period is followed by a period ofa progressive healing that lasts several years. The painfulperiod lasts only a few months and responds well to restand anti-inflammatory medications. However, similarradiologic abnormalities can be found in individuals whodo not complain of pain.

THEORIES

Nesovic’s Theory

According to Nesovic, the essential cause of pubalgiais a musculoaponeurotic disequilibrium between weakabdominal muscles and hypertonic adductors. It is com-mon, particularly in pubalgic soccer players, to see adehiscence of the obliquus superior in a prehernial stateand pain in the internal opening of the inguinal tunnel.

Nesovic’s procedure consists of putting the large musclesof the abdomen in tension. It is indicated in patients whoare not relieved by medical treatment that usually consistsof rest, injection, physiotherapy, and therapeutic exercise.

Spinal Factor (Maigne)

Nesovic’s theory describes well the local conditionsthat can promote and result in the decompensation that

maintains the pubic pain. Our observations indicate thatanother factor affects pubalgia and is probably the first toappear — the spinal factor. Thus we would add to Neso-vic’s theory a reflex spinal origin of pubalgia (Maigne,1981).

We had noticed that pain on palpation of the hemipubisis found in one third of patients with PMID of the thora-columbar junction (T11–12, T12–L1; Fig. 56.1). Theaffected hemipubis is ipsilateral to the articular pain ofthe PMID. In chronic cases, the condition may becomebilateral (see Chapter 60, “Thoracolumbar Junction Syn-drome”). These patients are usually unaware of havingpubic sensitivity, and they are very surprised when it isdiscovered at the insertion of the rectus abdominis muscleor on the whole surface of the bone (Fig. 56.2). Frequently,a cellulalgic zone painful to pinch-rolling, overlying theipsilateral groin and superomedial thigh, is detected onexamination. Sometimes, one or two small trigger pointsare found in the inferior aspect of the rectus abdominisand are very painful to palpation (Fig. 56.3).

Most of these patients will never experience pain in thepubis. They usually complain of low back or abdominalpain which is the most frequent manifestation of the tho-racolumbar junction syndrome, but if a patient with a“sensitized” pubis subjects the muscles that are insertedon it to excessive use, they will reproduce the pubic painand periosteal tenderness during a sudden movement orphysical effort.

Soccer players frequently strike the ball with theirtrunks in extension. This imparts a strong rotatory torqueto the thoracolumbar junction. Indeed, rotation at the lum-bar spine is minimal under tension because of the lockingof the facet joints.

At the onset of this condition, spinal treatment sufficesto bring relief. In our first publication, we successfullytreated a number of diverse patients with pubalgia, includ-ing a few soccer players. After that, Zimmermann, one ofour students and a soccer player, conducted a study ofsoccer players.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Zimmermann had followed several soccer teams,including teams of young players, regularly for manyyears as a consulting physician. His findings confirmedour hypothesis; he even found a spinal factor at the tho-racolumbar junction in all pubalgic patients. For the last6 years, no player on the teams he took care of had to beoperated on for pubalgia, thanks to prevention based onsystematic spinal and pubic examination and spinal treat-ment applied as soon as the first signs of thoracolumbarPMID were noted.

This very interesting experiment should be developedfurther, but it demands a high quality segmental examina-tion — not as simple as it seems if one is not used to thattype of examination — and extensive experience in manip-ulative treatment. If it is done inexpertly, the results canbe very poor. A. Gourjon made the same observationsand relates the following observation (personal communi-cation).

Case History

—

X., a 24-year old rugby player, hadhead trauma and loss of memory following a motorvehicle accident. After hospitalization for a few days,he left the hospital complaining of pain in the groin.Radiographs revealed a pubic diastasis. He was treatedwith six local injections, bed rest, and electrotherapybut was not relieved. Two months later, radiographswere repeated, and osteophytes were noted on thesymphysis pubis. Pain continued to increase, and surgerywas proposed. The patient then consulted Dr. A.G. whonoticed a typical thoracolumbar junction syndrome onthe side of the pubalgia, with a PMID at T12–L1. Afacet joint injection was performed at this level, and thepatient was able to move his thigh without pain. Threemanipulations at the thoracolumbar junction brought totalrelief and the patient was able to resume rugby. Seenagain 1 year later, he did not suffer any longer and theradiologic image was unchanged. This does not implythat all pubalgias are of spinal origin. However, thespinal factor should be considered in the diagnosis andtreatment of pubic pain.

CLINICAL STAGES OF PUBIC PAIN WITH SPINAL FACILITATION

Zimmermann classified the clinical stages of pubic painwith spinal facilitation into four stages.

Stage I

In the subclinical stage, there is no spontaneous pain,but palpation reveals hypersensitivity of the pubis on oneside. There is often a discrete, intermittent, well toleratedlow back pain. In all cases, thoracolumbar examinationreveals dysfunction of the thoracolumbar junction in theform of a PMID affecting one or two segments. The

Figure 56.1

Territory of the posterior and anterior rami of T12and L1 including the lateral cutaneous branch that arisesfrom the anterior ramus.

Figure 56.2

The hemipubis is tender to friction rubbing inone third of cases of thoracolumbar junction syndrome (PMIDat T11–12, T12–L1). This is a facilitating factor for pubalgia.

Figure 56.3

The anterior cellulotenoperiosteomyalgic mani-festations are related to segmental dysfunction of the thora-columbar junction: zone of cellulalgia, trigger points of therectus abdominis, and hemipubic tenderness to palpation(seen in one third of cases).

CHAPTER 56 PUBIC PAIN AND SPINAL FACTORS

371

affected hemipubis is on the side of the facet joint tender-ness.

Stage II

The patient complains of unilateral pubic pain afterprolonged physical exertion, usually not severe enough torestrict the activities. Low back pain is constant but oftenunrecognized, mildly inconvenient, and considered by thepatient to be a minor problem.

Stage III

Pubic pain is confirmed and is diffuse and bilateral.Pain on exertion is increased and may bring a temporaryhalt to competition. There is a specific sign: the patientfinds that sitting while resting on both hands is particularlypainful, if not impossible. Low back pain is more pro-nounced, with pains projected to the muscles of the legs(quadriceps, hamstrings, calves).

Stage IV

The pain is sufficiently severe to make participation inathletic activities impossible. All tests are painful, and thereis always weakness of the abdominal obliquus muscles,with pain and widening of the inguinal ring, sign of Mal-gaigne, etc.

Zimmerman also noted that at stages I and II, spinalperturbations are occasionally located at the thoracolum-bar junction and on one or two intervertebral segments,generally T11–T12 or T12–L1. The cellulotenoperiosteo-myalgic syndrome is usually well represented and local-ized to the territory of the posterior or anterior rami of thecorresponding spinal nerve root.

During stages III and IV, the spinal dysfunction reachesthe subjacent lumbar and intervertebral segments, result-ing in dysfunction in the region of L3–4. This explainsthe pain referral to the anteromedial thighs that is fre-quently observed. At the back, a cellulalgic zone of the

entire lumbosacral region is seen, but the mobility of thespine remains normal.

TREATMENT

Stage I

In most cases, it is sufficient to treat the thoracolumbarPMID or PMIDs and the related possible cellulalgic man-ifestations. Activities that involve significant spinal rota-tion must be limited, and the abdominal muscle balancemust be restored.

Stage II

Spinal treatment is by manipulation, combined if nec-essary with thoracolumbar facet injections and local treat-ment of the cellulomyalgic manifestations that persist afterthe spinal treatment. Abstinence from competition or sportis not compulsory. The player is relieved in fewer than 6weeks.

Stage III

Same treatment as above, but competition must stopfor 2 months.

Stage IV

Surgical intervention is required. This stage should beseen rarely. Nesovic’s technique is used most commonly.It strengthens and shortens the obliquus muscles to rebal-ance the forces that act on the pubis; but it may alsodenervate the pubic region.

N.B.

Pubic pain or tendinitis of the rectus abdominis musclecan be caused or precipitated by a spinal factor (PMID of thethoracolumbar junction) (Maigne). This concept is of therapeuticinterest because spinal treatment at the first stage can suffice torelieve the patient. At a more advanced stage, it can contributeto the cure. It also has a preventive effect. Supervision of thespine should help to avoid a certain number of pubalgias.

373

57

FALSE HIP PAIN OF SPINAL ORIGIN

Certain pain syndromes of spinal origin can mimic hippain. The pain is felt over the lateral aspect of the hip,sometimes with pain in the groin and in the buttocks.Mobility of the hip is normal; extreme movements aresometimes slightly limited and painful. This pictureresembles periarthritis of the hip, especially when thepalpation of the trochanter is painful (Fig. 57.1), but localinjections have no effect or (sometimes) act only briefly.

This false pain of the hip can have

two origins.

Exam-ination shows a different picture in each of these cases.

• Tendinitis of the gluteus medius with periosteal sen-sitivity of the trochanter in relation to an L5 cellu-lotenoperiosteomyalgic syndrome

• Cellulalgia (producing pain that feels deep) related tothe thoracolumbar junction syndrome, with involve-ment of the iliohypogastric nerve (L1) or subcostalnerve (T12) lateral perforating branches; the nervesare usually found to be subject to entrapment as theycross over the iliac crest (R. and J.Y. Maigne).

TROCHANTERIC PAIN AND L5 SEGMENTAL VERTEBRAL SYNDROME

Pain on palpation of the greater trochanter and triggerpoints in the gluteus medius is regular when the L4–5segment pain is due to a PMID, a herniated disk, or facetjoint synovitis (Fig. 57.2). Generally, the picture is of hipperiarthritis. Injection of the trochanter or the triggerpoints of the gluteus medius can relieve the patient if thespinal factor that is responsible is sufficiently decreased,but there is recurrence. If segmental spinal pain persists,only spinal treatment can bring lasting relief.

FALSE HIP PAIN AND T12–L7 SEGMENTAL VERTEBRAL SYNDROME

False hip pain can be caused by irritation of the lateralperforating branches coming from the subcostal (T12) or

Figure 57.1

Pressure over the greater trochanter is painful.This can be due to a painful trochanter or a tendinobursitisof the gluteus medius. It can also represent pain due to apainful cellulalgic zone compressed between the examiner’sfinger and the trochanter.

Figure 57.2

Cellulotenoperiosteomyalgic L5 syndrome con-sists of taut bands in the gluteus medius and hypersensitivityof the trochanter to palpation.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

iliohypogastric nerve (L1). See Fig. 57.3a. Irritation of thelatter can be part of a thoracolumbar junction syndrome (seeChapter 60), arise from entrapment at the iliac crest, or beof mixed origin. In the thoracolumbar junction syndrome,the picture may include pain in the buttock and the groin.

Generally periarthritis of the hip is diagnosed. Thetrochanter seems tender to palpation and injections haveno effect, even temporarily. In fact, the trochanter is notpainful, but the subcutaneous tissues pressed against it atthe hip are (Fig. 57.3b). External rotation of the hip canbe impaired in severe cases, but it disappears quickly aftera spinal treatment.

ENTRAPMENT SYNDROMES OF PERFORATING CUTANEOUS BRANCHES OF T12 AND L1

The picture is the same as above, but there is no spinalfactor. Branches of the subcostal or iliohypogastric nerve

can be entrapped at the iliac crest and show the samesymptomatology (R. and J.Y. Maigne; see Chapter 47). Itis common to find some mixed pictures in which the spinalfactor is associated with a local factor.

TOTAL HIP ARTHROPLASTY AND FALSE HIP PAIN

These falsely localizing pains are seen particularly inpatients with total hip arthroplasties. Chronic pain oftenoccurs, even when the technical result of the operation isgood and there is no infection or technical problem withthe joint. When these patients recover mobility of theirhips, they modify their usual postures and gesturesbecause of the pain. Generally, in older patients, the spinedoes not adapt well to the new constraints; thus, dysfunc-tion of the thoracolumbar junction is frequently seentogether with pain referred to the trochanter and groinsimulating pain arising from the joint (see Chapter 60).

Figure 57.3

a.

Posterior and anterior branches of T12 and L1 with the perforating branches (circled in one and on the otherin gray).

b.

Lateral cutaneous perforating branches of the subcostal nerve (T12) and of the iliohypogastric nerve (L1). Thepain can be projected toward territory beyond the thoracolumbar junction (R. Maigne). It can also be involved in an entrapmentsyndrome at the iliac crest (R. and J.Y. Maigne).

375

58

KNEE PAIN OF SPINAL ORIGIN

Some pain syndromes of the knee that seem to be dueto tendinitis, cruciate ligament sprain, or meniscal block-age may instead have its origin at the lumbar spinal level.These pains originating at the lumbar level are associatedwith cellulotenoperiostalgic manifestations of L

3

or L

4

origin. (Fig. 58.1).

EXAMINATION

The segmental examination reveals pain at the L2–3 orL3–4 level. Some patients report having had femoral neu-ralgias in the past, but usually no previous history is noted.Often, there is cellulalgia over the medial aspect of theknee (L4; Fig. 58.2), tenoperiosteal tenderness of thesuperior medial aspect of the tibia (Fig. 58.3), and triggerpoints of the vastus medialis (L3, L4; Fig. 58.4). A min-imal entrapment syndrome affecting the saphenous nerve

Figure 58.1

Cellulotenoperiosteomyalgic syndrome of L3and L4.

Figure 58.2

Pinch-roll test.

Figure 58.3

Palpation tenderness.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

seems to occasionally exacerbate the cellulalgic manifes-tations.

CLINICAL PICTURE

Cellulalgia of L3 or L4

The observation of this young classical dancer is typical.

Case History

— A.C., 24 years old, had been com-plaining of pain in the right knee for the previous 3months. She was able to do all the dancing exercises,but especially when she was tired or stretching, she felta diffuse, poorly localized pain at the anteromedialregion of the knee. She was examined several times bydifferent specialists. A sensitivity of the pes anserinustendon was found; two injections did not result in anychange. On the other hand, the knee was strictly normal.When we examined her, we found the same thing. Weperformed the pinch-roll test of the skin and noticed thatthe pes anserinus ligament was not sensitive, but asensitive cellulalgic zone overlying the ligament coveredan area as large as the palm of the hand. The pinch-roll test was very painful at that level and painless onthe other knee. The skin was thickened and lumpy.

The segmental examination demonstrated L3–4 seg-mental dysfunction; spinal radiographs were normal.Three lumbar manipulations were performed on theaffected segment and the pain disappeared. The cellu-lalgia decreased. After two local injections with dilutelocal anesthetic, followed immediately by a brief knead-ing massage on the affected tissues, the pain completelydisappeared. She complained only of a few episodesof low back pain that caused little inconvenience anddisappeared after the spinal treatment.

Tenoperiosteal Tenderness (L4)

Tenoperiosteal tenderness is easily confused with pesanserinus bursitis, but it does not respond well to local

injection. On the other hand, it is generally relieved byspinal treatment (L4). It can be associated with cellulalgia.

Trigger Points of Vastus Medialis and Pseudoblockage of Knee

The patient complains of pain localized to the medialknee, which increases with walking and prevents running.Sometimes a real blockage limits the total extension ofthe leg, simulating a blockage of the meniscus, which(amazingly) can yield immediately after a lumbar manip-ulation. Injection of local anesthetic into the trigger pointof the vastus medialis can have the same effect, but isoften transient.

Case History

— L., 24 years old, while running 6months earlier, felt pain on the medial side of the leftknee and limped for a few days. It recurred severaltimes during diverse activities until the day 2 monthsearlier when the pain became sharper, making stretchingthe knee impossible. A meniscal lesion was suspected,but arthroscopy was normal. Injections, electrotherapy,and massages did not result in any relief. Upon exam-ination, an extension lag was noticed and any attemptto force it was very painful. There was no joint linetenderness and Apply’s grind test was negative. Palpa-tion of the vastus medialis was painful and revealed ahypersensitive trigger point. Spinal examination revealedsegmental pain at L3–4; the radiograph was normal. Areferred pain of spinal origin was suspected and wasconfirmed by a lumbar manipulation that brought rapidclear relief. After the second session, the patient couldjump, run, and extend the knee against resistance with-out pain. One year later, there had been no recurrence.

Such cases are not rare. Recurrence can occur follow-ing exertion or a false lumbar movement. This is not toofrequent in our experience.

Entrapment Syndrome of Saphenous Nerve

The saphenous nerve can be entrapped in its coursewhere it crosses Hunter’s canal. The patient feels a diffusepain in the medial region of the knee. Initially some dis-comfort while running may be felt, then walking becomesvery difficult. To decrease pain, the patient starts to walkwith the knee partially flexed and with the foot equinus.Pain increases with hyperextension of the hip. It is exac-erbated with pressure over the nerve at about four fingerbreadths above the medial condyle, at the anterior edgeof the sartorius muscle. Treatment can consist of injectionof the point with local anesthetic mixed with corticoster-oids. In severe cases, the nerve must be released surgically.

The nerve can also be entrapped at the medial aspectof the leg by the saphenous vein, usually in women witha history of thrombophlebitis. In certain cases, there canbe two origins: an entrapment syndrome and a spinal

Figure 58.4

Palpation of trigger points of vastus medialis.

CHAPTER 58 KNEE PAIN OF SPINAL ORIGIN

377

problem at L3–4, each one contributing in variable pro-portion.

Case History

— M.C., 25 years old, complained ofpain in the medial knee for about a year. She was ableto run and even to walk quickly. The knee was examinedseveral times. Arthroscopy was normal and nothingcould explain her discomfort. When examined in thedepartment, there was significant cellulalgia of themedial knee and L3–4 segmental tenderness with normalradiographs. A few lumbar manipulations broughtenough relief to enable her to resume playing tennis;but 8 months later, the identical pain reappeared, withthe same cellulitic infiltrate. This time, neither pain norinfiltrate yielded to spinal treatment. However, injectionof the saphenous nerve resulted in temporary relief. Thediagnosis of an entrapment syndrome was made. Thepatient was completely relieved by surgical release ofthe entrapment in Hunter’s canal.

This observation shows that certain false knee painscan have dual origins: spinal and local entrapment. Whenthe entrapment is mild, the spinal treatment suffices. Atthe next stage, a few injections can be added, performedat the point of entrapment. At a more severe stage ofcompression, surgical intervention is indicated.

KNEE PAIN AND PROXIMAL TIBIOFIBULAR JOINT

The proximal tibiofibular joint only moves in relationto the subtalar joint. The presence of cartilage proves theexistence of the movement. Flexion–extension at the ankleis transmitted automatically to the two tibiofibular joints.The talus is wider anteriorly than posteriorly. It is insertedlike a coin in the tibiofibular notch, which it widens duringdorsiflexion of the foot.

When the tibiofibular joint diverges or converges, thereis a simultaneous associated axial rotation. The amplitudeof movement is 30°. Simultaneously, the fibula pistons upand down because, when it diverges from the tibia, theinterosseous membrane draws it upward. Conversely, it isdrawn downward during ankle plantar flexion. Thesemovements have repercussions on the proximal tibiofibu-lar joint. During ankle dorsiflexion, the fibula slidesupward; it slides downward with plantar flexion.

The joint also glides anteroposteriorly because of itsorientation. Gliding backward is easier than gliding for-ward because the articular facet is at the back of the tibia,and its obliquity outside and backward does not facilitategliding forward.

In the normal state, joint play is palpable. It is testedwith the patient supine. The knee to be examined is flexedto 90°. The physician grasps the head of the fibula between

the thumb and index finger (left hand for the right kneeand vice versa) and slowly performs to-and-fro move-ments. It is a good idea to sit on the patient’s foot tostabilize it on the table. Joint play should be comparedwith that of the knee on the other side (Fig. 58.5).

Isolated dislocation or fracture–dislocation of the tibiais seen in children and adolescents (Sirbrandij). They com-plain that the knee hurts and that it seems to give way orthat there is a “click” in the knee with a vague pain thatseems to come from the knee. Since this lesion is notfound in adults, it seems to improve spontaneously.

On the other hand, one can see cases in which mobilityis difficult and painful in the tibiofibular joint. The paindoes not occur spontaneously, but it can happen afterflexion or extension. Sometimes it looks like a joint peri-arthritis. Pain with mobilization is often seen as a mani-festation or sequela of sciatica.

Proximal Tibiofibular (PTF) Blockages

A minor mechanical dysfunction of the PTF joint canexist without radiographic abnormality and can be con-sidered a blockage of the fibula. It results in knee pain or,more surprisingly, pain along the instep; on examination,there is a precise tender point on the talus at the talarinsertion of the anterior talofibular ligament (Maigne;Fig. 58.6).

This pseudoblockage occurs most often after prolongedsquatting, but it can also be seen in subjects who havestood on tiptoes for a long time or did series of jumpswithout having been trained to do so (e.g., volleyball onthe beach) or after a long drive in the car, with the legsoverly bent or a seat that is too soft or too low. It is as ifthe joint being used in its maximal course in elevation orin lowering the head of the fibula has been blocked in thatposition. But the anteroposterior joint play, which is theonly one that can be tested, decreases or disappears. Thetherapeutic maneuver should attempt to restore the antero-posterior mobility.

Figure 58.5

Examination of proximal tibiofibular joint.

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Proximal Tibiofibular Arthritis and Sciatica

Dysfunction of the PTF joint sometimes follows anepisode of sciatica. The patient complains of lateral legpain and instep pain, which is sometimes sharp. In somecases, the instep pain can exist alone.

Anteroposterior mobilization of the PTF joint is usedto assess whether the joint play is limited or painful.Manual therapy using mobilization treatments usuallyproduces good results, in some cases, immediately. If aperiarticular pain is present, one must consider the possi-bility that it could be part of the segmental cellulotenope-riosteomyalgic syndrome or the mechanical consequenceof a gait that is altered by sciatic pain.

Treatment

Mobilization is performed exactly as in the examination.The knee is flexed to 90°, and the head of the fibula isgrasped between the thumb and index finger and mobilized

from front to back progressively. If mobilization is insuf-ficient, manipulation can be performed. Depending on thecase, it can be performed by pushing the fibula toward thefront or the back (according to the rule of no pain andopposite movement).

First Technique (Left Leg): Leg at 90°.

The righthand is placed on the popliteal surface so that the meta-carpophalangeal joint of the index finger is on the headof the fibula. The left hand grasps the inferior part of theleg and progressively flexes the knee until the hand is wellwedged, the support against the fibular head is firm, andthere is some tension. The manipulation is then performedwith a sharp exaggeration of the left hand, whichexaggerates the flexion of the knee. The head of the fibulais pushed forward with a cracking sound (Fig. 58.7).

Second Technique.

The patient is supine with legsextended. The operator pushes on the fibular head withthe heel of the hand applying a progressive downwardpressure that is suddenly exaggerated. When these maneu-vers are insufficient (which is rare), injection or electro-therapy can be used.

Figure 58.6

In cases of blockage of the proximal tibiofibularjoint, there is often marked tenderness to palpation at theinsertion of the anterior talofibular ligament.

Figure 58.7

Manipulation of proximal tibiofibular joint.

379

59

PSEUDOVISCERAL PAIN OF SPINAL ORIGIN

Certain types of pain originating in bony structures cansimulate visceral pain. They often have a spinal origin thatis confirmed by the effectiveness of the spinal treatment.However, finding objective spinal manifestations does noteliminate the subjacent viscera as the painful sourcebecause there is often an association between certain vis-ceral conditions and a reflex cellulalgia that is painful tothe pinch-roll test.

ORIGIN OF PAIN

Role of Cellulalgia

It has been known for a long time that pseudoanginalpain can be linked to cellulalgia overlying the chest wall.Laroche, Debray, and May have drawn attention to thediagnostic errors brought about by a cellulalgia of theabdominal wall.

On the other hand, the spinal origin of these cellulalgiczones is rarely considered. However, these zones are foundrather frequently during systematic examinations of thechest wall. They are not always the causes of the painfulsymptoms, but they could become so. Nearly all belong tothe cellulotenoperiosteomyalgic syndrome (Maigne), andthe responsible spinal segment is demonstrated with regu-larity. Usually, it is a PMID, but all possibilities can occur.

Frequently, a second cellulalgic zone is found in theregion of the corresponding posterior ramus. These cellu-lalgic zones, unknown by the patient, are very painful topinch-rolling. The pain elicited is felt curiously as deepor burn-like. Pain is generally chronic and sometimessharp. Anesthetic injection of the affected cutaneous zonerelieves it momentarily and confirms that it is not theviscera that is painful on palpation.

Trigger Points

In certain cases, small trigger points are responsible forthe pseudovisceral pain. They are rather rare in the abdom-inal muscles but more frequent in the muscles of the thorax

(pectoralis major). They can have a local origin or belongto a segmental cellulotenoperiosteomyalgic syndrome.These misleading pains can be found at all levels, but theyare particularly frequent at the inferior abdominal regionin the territory corresponding to the thoracolumbar junc-tion.

THORACIC PAIN

Pseudocardiac Pain

Pseudocardiac pains are the most common pseudovis-ceral pains. Precordial cellulalgia that can mimic anginalpain can have a cervical (C4) or thoracic (T2–5) origin(Fig. 59.1). Trigger points of the left pectoralis minor ormajor can also be implicated (C6–7).

False Breast Pain

Certain pain syndromes felt as breast pain can havespinal origins. They can be due to a cellulalgic zone butgenerally are due to trigger points of the pectoralis majoror minor that can be of spinal or local origin (overworkof muscle). See Fig. 59.2.

Pseudopleuropulmonary Pain

Pseudopulmonary pain can be simulated by interscap-ular pain of cervical origin (see Chapter 36, “ChronicThoracic Pain”), which is sometimes felt as an intratho-racic pain and is increased by deep breathing or by triggerpoints of the iliocostalis muscle.

ABDOMINAL PAIN

Cellulalgia, usually of spinal origin, can simulate gas-trointestinal, urologic, testicular, and (especially) gyneco-logic pain. At the abdominal level, these pseudovisceralpains are generally due to a very localized cellulalgia, whichcan be misleading because during the abdominal palpation,

380

SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

the cellulalgic skin is compressed between the hand of theoperator and the subjacent viscera, so that the pain seems tocome from those viscera (Fig. 59.3 and Fig. 59.4).

Abdominal pain can be minor, intermittent, barelynoticeable, or blamed for minor gastrointestinal or gyne-cologic problems. It can also be chronic and tenacious aswell as distressing and alarming because no cause is foundduring the multiple necessary examinations. In somecases, the presentation is acute, simulating a surgicalemergency.

These abdominal pains can be seen at all levels of theabdomen, but they are particularly frequent in the lowerquadrants supplied by T12 and L1. They are then part ofthe thoracolumbar junction syndrome of Maigne (seeChapter 60). The observations below will show moreclearly what we mean.

Pseudogastrointestinal Pain

The following case is a good example of a pseudogas-trointestinal pain syndrome.

Case History

—

A 67-year

old man had suffered forthe past 35 years from refractory epigastric painoccurring without any cause. During certain particularlypainful attacks, he had to interrupt any activity and liedown. He had found that using hot water bottles short-ened and notably decreased these attacks. The manyinvestigations over these years had always been nega-tive. In fact, he had right epigastric cellulalgia linked toa PMID at T7. Several spinal treatments brought totalrelief.

Cellulalgic zones linked to PMIDs can simulate painof the entire digestive system. They are common in theepigastric region and subcostal zones, but they are morefrequent at the inferior part of the abdomen (thoracolum-bar junction syndrome).

Figure 59.1

Precordial cellulalgia (often of spinal origin) canmimic pain of cardiac origin.

Figure 59.2

A trigger point of the pectoralis major can beresponsible for falsely localized chest pain.

Figure 59.3

Abdominal cellulalgia of spinal origin can pro-duce a sense of profound pseudovisceral pain that can bemisleading.

Figure 59.4

Myalgic pain along the border of the erectorspinae can produce abdominal or low back pain.

CHAPTER 59 PSEUDOVISCERAL PAIN OF SPINAL ORIGIN

381

Pain can be moderate and episodic —

In these cases,the pains do not result in anxiety or in visits to physicianslooking for a diagnosis.

Pain can be more severe and more tenacious —

These pains can lead to distressing situations for thepatient and difficulty for the physician, as can be seen inthe following case.

Case History

— M.X., 50 years old, complained of aleft-sided abdominal pain that was low, dull, continuous,and soothed by bed rest. The intensity of this pain (lastingfor a year) led to several hospitalizations in such spe-cialized departments as urology, gastroenterology, andrheumatology; all investigations were negative.

This persisted until, during a new hospitalization,gastrointestinal radiologic examinations led to the suspi-cion of a carcinoid tumor of the small intestine. After amesenteric arteriography and other intestinal imagingstudies, this diagnosis was discarded. He was trans-ferred to the department of neurology, where he under-went the usual examinations, including myelography,which was normal. A lymphangiogram and a laparos-copy were also negative. A psychiatrist found the patientsomewhat depressed (!) and prescribed a treatment thatwas not well tolerated and was quickly stopped.

All this lasted a year; then the patient’s own physi-cian, suspecting a spinal origin, sent him to us. Exami-nation of the abdominal subcutaneous tissues revealeda very painful zone of cellulalgia in the region of theiliac fossa and the left groin. The ipsilateral pubis waspainful to palpation. The lumbar examination revealed acrestal point on the left and gluteal cellulalgia. The patientalso complained of low back pain, but he believed it wasradiating abdominal pain. Segmental examinationshowed pain at T12–L1. The radiographic examinationwas unremarkable. A PMID at T12–L1 was diagnosed.

After the first manipulation, he was relieved. After thesecond, palpation of the cellulalgic zone was less pain-ful. After the third, he had no further pain. After a fewsessions of massage, the residual cellulalgia disap-peared. Seen 2 years later because of moderate recur-rence of the low back pain, he declared that he hadno more abdominal pain.

Acute Pain

Acute pain can lead to useless interventions.

Case History

— M.C., 38 years old, was an avidcyclist who frequently took long rides during his leisuretime. One day, during a strenuous workout, he felt avery sharp pain in the right inferior abdominal regionand had to stop. With difficulty, he arrived at a neigh-boring town and went directly to the hospital emergencydepartment. The diagnosis of acute appendicitis wasmade. He underwent a laparotomy, but the appendixwas normal. Pain decreased over the following days.From time to time afterward, he felt a disagreeable

sensation. Then he had another acute attack that disap-peared spontaneously. This happened several times.

Right-sided low back pain brought him to our depart-ment for examination. A diagnosis of low back pain ofT12–L1 origin was made. A cellulalgic zone sensitiveto palpation, yet previously asymptomatic, was discov-ered over the right lower quadrant of the abdomen,which was responsible for the false appendicitis. Spinaltreatment completely relieved this patient; on follow-upafter 6 months, he had no further abdominal pain.

In most cases, intermittent abdominal pain is thoughtto be due to irritable bowel syndrome because thesepatients have flatulence with periods of constipation thatalso responds to spinal treatment.

Pseudogynecologic Pain

In the gynecologic domain, pain of spinal origin is par-ticularly misleading and frequent. During the examination,the painful subcutaneous tissues are compressed betweenthe intravaginal fingers and the adnexa. The pain that iselicited reproduces the usual pain; to both patient and phy-sician, it seems to come from the organ that is palpated.

This pain is especially frequent at the inferior abdom-inal region innervated by the anterior rami of T12 and L1or the thoracolumbar junction — a zone that is subject tooveruse and is a frequent site of PMID. We have observednumerous patients who were operated upon because ofsharp pains attributed to PMIDs (some histories are col-lected in the thesis of J.C. Goussard). Endometriosis wassuspected and verified at OR, but no relief resulted fromtreatment. The pain was coming through the wall from thespine and was relieved by spinal treatment.

Case History

—

Mrs. Z., 40 years old, had severeright-sided abdominal pain with each menstrual period,which increased on the second day. This started at firstmenstruation at the age of 14. Failure of medical treat-ment led to surgical intervention when she was 17.Endometriosis of the right broad ligament was detectedand it was resected, but the pain was unchanged. For10 years, other medical treatments failed. One day,exertion resulted in acute low back pain of thoracolum-bar origin and abdominal pain. We examined her atthat time. Her examination confirmed low back pain ofthoracolumbar origin without any radiologic lesion. Herpain complaints disappeared after the first manipulation.

We saw her again 12 years later. She came to askfor pain relief as in the past for her “endometriosis.” Thepain attributed to this disorder had totally disappearedwith the low back pain. The pains then reappearedacutely a few months later, after she had engaged inphysical activities. First she had severe low back pain;later, the abdominal pain reappeared with menstruation.

A manipulation done by an orthopedist had aggra-vated both pains. Examination revealed sensitivity topinch-rolling over the inferior right iliac fossa, tenderness

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

of the right hemipubis, and pain at T12 to transversepressure from right to left. Radiographs of the spine werenormal. Three manipulations again relieved the abdom-inal pain and the low back pain.

The point in this case history is that the abdominal painoccurred only during menstruation. The findings weresimilar in other patients with abdominal pain of spinalorigin. Generally, the pain is more constant, with episodicattacks having no clear precipitating cause.

When the gynecologic examination is normal, it limitsthe value of other investigations and surgical proceduresand often leads to a diagnosis of psychosomatic origin.Occasionally, the investigations discover abnormalitiesthat mislead the gynecologist to falsely attribute causation,particularly if the pain is severe. More rarely, the pain isstrictly vulvovaginal, usually unilateral. The skin of thegroin and the labia majora is painful to pinch-rolling, andthe hemipubis is tender to palpation. It is usually due toa PMID at T12–L1 or L1–2.

Pseudourologic Pain

Pseudourologic pains lead to fewer interventions thando the gynecologic ones, as the examinations are usuallynormal. They are rather frequent and may mimic renalcolic and testicular pain.

Case History

— Mr. C., 42 years old, had right lowback pain chronically for 15 years, with occasionalperiods of exacerbation. An orthopedist prescribed phys-ical therapy, which continued for a long time with nonoticeable result. After that, the patient had severalpainful attacks of the right lumbar fossa, radiating to theright testicle. The first attack was considered to be renalcolic, but the patient always pretended that it was theresult of exertion in rotation. The second acute episodehappened a few months later. Hospitalized in the depart-ment of urology, he had three intravenous pyelograms(IVPs) that were all normal. He was then referred toorthopedics and rheumatology.

Nothing abnormal was found that could explain theseattacks. After 12 years, a particularly severe attack broughthim to the urology department as an emergency. Again,the IVP was normal. He was then hospitalized underrheumatology. Two spinal injections of corticosteroid failedto relieve either the low back pain or the right testicularpain that persisted since the attack. A myelogram wasdone and was normal. The attack gradually subsided.

At the end of another acute attack, he came to usfrom another department of urology for his refractoryright-sided low back pain and the unexplained testicularpain. On examination, he showed right low back painof typical thoracolumbar origin with a crestal point,gluteal cellulalgia, and a PMID of the T12–L1 segment.There was also a cellulalgic zone above the right groinand medial side of the thigh. Pressure on the right

hemipubis was painful. Radiographs showed a com-pletely normal thoracolumbar junction.

After three manipulations, he was considerablyimproved. The low back and testicular pains were lessintense and episodic rather than constant. A T12 facetjoint injection along with an anesthetic injection of theresidual cellulalgic zone ended the treatment.

These pains of spinal origin are generally unilateral,but they can be bilateral, as in the following case.

Case History

— M.T., 65 years old, was operated uponfor a prostatic adenoma 2 years previously with excellentresults. Since that time, he complained of bilateral testicularpain that increased with any pressure, for example, thighadduction or crossing his legs. The urologic examinationwas unremarkable. His surgeon sent him to our depart-ment. He also had bilateral low back pain that appearedsoon after surgery, just as his testicular pain had. TheT11–12 segment was painful with transverse pressure inboth directions, and the two facet joints were painful.Palpation revealed bilateral cellulalgic bands over theinferior part of the iliac fossa, and the pubis was painfulon both sides. Several radiologic examinations were nor-mal. The result of the spinal treatment was excellent.

Sprain of the false ribs

can also simulate renal painbecause it is felt in the lumbar fossa and sometimes radi-ates toward the groin. One of our patients was hospitalizedthree times and underwent five IVPs (all negative) forattacks that were attributed to renal colic. He had an unrec-ognized sprain of the twelfth rib.

CASE EXAMPLE

Abdominal Pain and Lumbar Herniated Disks

Inguinal pain is often seen in sciatica. It is rarely signif-icant, and the patient has to be questioned to have him noticeit. In certain cases, the inguinal pain can be more severe,isolated (i.e., without low back pain), or associated withsciatica, making the diagnosis difficult (Fernstrom). Halma-grand and Seror reported a case of lumboabdominal painoccurring with acute attacks, associated with an anteriorL5–S1 herniated disk revealed by discography and cured bychemonucleolysis. An identical observation was reported byLelong et al. These authors emphasize the importance ofdiscography, which reproduces the usual abdominal pain.

TREATMENT

Treating the responsible PMID usually removes thepseudovisceral pain, and the cellulalgic zone disappearsor decreases considerably. In certain chronic cases, theimprovement obtained by spinal treatment is only partial,and an additional local treatment of the cellulalgia is nec-essary, such as massage or possibly local injections.

383

60

THORACOLUMBAR JUNCTION SYNDROME

The term

thoracolumbar junction syndrome

(TLJS)(1981) was coined to refer to all the painful manifesta-tions, combined or isolated, that are the consequences ofdysfunction of segments of the thoracolumbar junction:T12–L1 and, more rarely, T11–12 and L1–L2 (Fig. 60.1a).TLJS includes:

• Low back pain — the most frequent manifestation• Lower abdominal pseudovisceral pain• False hip pain• Pubic tenderness• Irritable bowel symptomatology

Figure 60.1

a.

Three pain referral patterns of the thora-columbar junction syndrome (Maigne): 1, posteriorly — lowback pain; 2, anteriorly — pseudovisceral pain, pubic ten-derness; 3, laterally — pseudotrochanteric pain, false meral-gia paresthetica. Patients with these syndromes often do notcomplain of pain at the level of the thoracolumbar junction.

b.

Three branches of the divisions of the T12 and L1 spinalnerve: 1, anterior ramus; 2, posterior ramus; 3, lateral perfo-rating branch.

384

SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

Pain distribution and the clinical signs found on exam-ination correspond to the branches of the T12 and L1spinal nerve roots (Fig. 60.1b). Their posterior rami inner-vate the superior gluteal and inferior lumbar subcutaneoustissues. Their anterior ramus innervates the inferior partof the abdomen and the groin region. A perforating lateralcutaneous branch arising from the anterior ramus inner-vates the trochanteric region.

Low back pain, the most frequent manifestation of thesyndrome, is often the patient’s only complaint. It is thetopic of a special chapter (see Chapter 41) and is describedwith the other low back pain syndromes. When we firstisolated low back pain of the thoracolumbar origin (1974),we brought attention to its frequent association withabdominal pain on the same side.

TLJ ANATOMY AND PHYSIOLOGY

The lumbar spine has only a limited amount of rotationavailable, especially when it is in extension. On the otherhand, the thoracic spine is very free in rotation. T12 (andsometimes T11) is a transitional vertebra. The TLJ is thusa zone that is particularly used in all efforts of everydaylife and sports.

PHYSICAL SIGNS

Dysfunction of one or more segments of the TLJ isrevealed by segmental examination. Usually, it concernsT12–L1, sometimes T11–12 or L1–2. Among the referredsigns are:

• Cellulotenoperiosteomyalgic manifestations locatedin the regions corresponding to one of the posterioror anterior rami or one of the lateral perforatingcutaneous branches.

• Tender points palpable on the iliac crest, includingthe posterior crestal point and the lateral crestalpoint corresponding to the site of compression of anirritated nerve branch — the posterior ramus and/orlateral perforating cutaneous branch.

Examination of Thoracolumbar Junction

The segmental examination reveals dysfunction of onlyone segment in 6 of 10 cases, of two in 3 of 10 cases, andof three in 1 of 10 cases. For this examination, it is bestto have the patient prone, across the table or at the end ofthe table (Fig. 60.2).

Segmental dysfunction is generally related to a PMID,sometimes to an episode of facet joint arthritis, and veryexceptionally to discogenic pathology. Radiographicexamination is usually unremarkable, but sometimes anold and unrecognized compression fracture of T12 or L1

is found. It is quite unusual for a patient to complain ofpain at the level of the TLJ.

Cellulotenoperiosteomyalgic Manifestations

Cellulotenoperiosteomyalgic manifestations are unilat-eral, located ipsilateral to the facet joint tenderness. If thepain is bilateral, the manifestations are also bilateral. Cel-lulalgic zones are a constant finding, whereas the ten-operiosteal tenderness to palpation of the pubis is ratherfrequent.

Zones of cellulalgia are found uniformly in the cuta-neous region of the three terminal branches of T12 andL1. The cellulalgia manifests the cutaneous territory of asingle nerve or region common to two levels. This can bedue to the presence of numerous anastomoses but also tothe physiopathologic mechanism of the cellulalgia itself.In practice, there is usually concordance with what weknow of the cutaneous distribution of these nerves.

The TLJS has two characteristics frequently seen incellulotenoperiosteomyalgic manifestations:

Figure 60.2

Two maneuvers that are essential in the seg-mental examination of the thoracolumbar region.

a.

Examina-tion for facet joint tenderness. Generally, it is unilateral,involving one or two segments. The painful manifestationsare always on the painful side.

b.

Transverse pressure againstthe spinous process.

CHAPTER 60 THORACOLUMBAR JUNCTION SYNDROME

385

• The spontaneous pain linked to the cellulalgia is feltby the patient as a deep intense pain, and (veryexceptionally) as a superficial burn-like pain.

• These manifestations can also be found on the sys-tematic examination when they do not cause anypain (they are then called

latent).

In the TLJS, one can find, for example, cellulalgiasimultaneously in the anterior, posterior, and lateralregions, while the patient complains only of low back orabdominal pain.

Cellulalgia

1. The posterior region corresponds to the territoryof the posterior ramus, inferior lumbar and supe-rior gluteal (Fig. 60.3), and is practically constant(97%). Only in 3 cases out of 100 was it missing.

2. The anterior region corresponds to the territoryof the anterior ramus; it was found in 60% ofcases: inferior abdominal region (Fig. 60.4, topleft and top right) and the superomedial part of

Figure 60.3

Posterior cellulalgic zone (

left

)

and its examination (

right

).

×

= posterior crestal point.

Figure 60.4

Top left:

anterior cellulalgiczone.

Top right:

abdominal examination.

Bottom right:

medial examination.

Topleft:

hypersensitivity of hemipubis exam-ined by friction rubbing.

386

SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

the thigh (Fig. 60.4, top left and bottom right),forming a triangle with an inferior apex withvery clear limits.

3. The lateral region covers the trochanter andsometimes extends as a narrow band followingthe “seam of the trousers” up to the PMID thighand even beyond (56% of cases). See Fig. 60.5.This territory corresponds to the lateral perfo-rating cutaneous branch coming from the ante-rior rami of T12 and L1.

Trigger Points

Trigger points are infrequent and small. They can befound along the inferior border of the rectus abdominismuscle and occasionally in the quadratus lumborum muscle(Fig. 60.4, top left).

Tenoperiosteal Tenderness

Tenoperiosteal tenderness to friction rubbing is foundon the ipsilateral hemipubis, compared with the oppositeside (32% of cases). See Fig. 60.4, top left, and Fig. 60.6).

Crestal Points

Painful points can be noticed on palpation of the iliaccrest.

A posterior crestal point is detected at the site of pres-sure by the physician’s finger over the traversing posteriorramus of T12 or L1 (Fig. 60.7, left). It is generally located7 to 8 cm lateral to the midline (see “Clinical Signs” inChapter 41).

A lateral crestal point on a line passing through thetrochanter corresponds to the pressure over the lateralperforating branch of the iliohypogastric nerve (L1) or thesubcostal nerve (T12) (Fig. 60.7, right).

The iliac crestoften has a small notch in which the first of these tworami goes (J.Y. Maigne), and which can be palpated duringthe clinical examination (see Chapter 47).

CLINICAL SYMPTOMS

Clinical symptoms may appear in isolation or in mul-tiple combinations.

Low Back Pain

Low back pain of thoracolumbar origin of Maigne canbe acute or chronic and is by far the most frequent man-ifestation (Table 60.1). It is felt in the sacroiliac or glutealregion and is often isolated or dominant. When the othersymptoms (e.g., previous pains or pains of the externalside of the hip) are moderate, they are generally not men-tioned right away by the patient. (A detailed descriptionof this lumbar pain is given in Chapter 41.)

Pseudovisceral Pains

Pseudovisceral pains are located at the inferior part ofthe abdomen and simulate gynecologic pains or low gas-troenterologic, urologic, or even testicular pains. Whenpseudovisceral pain is the dominant pain, the patient does

Figure 60.5

Lateral cellulalgic zone (

left

)

and its examination (

right

).

×

= lateral crestal point.

Figure 60.6

Hemipubic tenderness to friction rub examina-tion is found in one third of cases.

CHAPTER 60 THORACOLUMBAR JUNCTION SYNDROME

387

not report the associated moderate low back pain that isless handicapping. These pains are misleading and oftenlead to consultation with a general physician, internist, orgynecologist rather than a specialist in musculoskeletalconditions. If the pains are discrete and moderate, theyare attributed to colitis or a minor gynecologic disorder.If they are sharp and severe, diagnostic errors can be made.(They are described in Chapter 59, “Pseudovisceral Painof Spinal Origin,” where they are well demonstrated byour observations.)

False Hip Pain

Pain is localized to the lateral side of the thigh, some-times the groin. It feels deep and is sometimes accompa-nied by sudden sharp stabs toward the groin during certainmovements or with a sudden increase in pace while walk-ing. It can mimic periarthritis of the hip but can alsoresemble a truncated sciatica or even meralgia paraesthet-ica. It often is exacerbated by wearing a belt or clothingthat is too tight. A detailed description can be found inChapter 47, “Perforating Branch Syndrome of T12 andL1” and Chapter 57, “False Hip Pain of Spinal Origin.”

Pubic Tenderness

Pubic tenderness to palpation is frequently found in thethoracolumbar junction syndrome — up to 32% of cases.It is most often unilateral and is found only on examina-tion. Sometimes it is only inconvenient, but it can be ofprime importance, especially if the subject uses the adduc-tor muscles or the rectus abdominis (e.g., in soccer), asboth are inserted on the sensitized pubis. When the TLJis affected, it presents a form of pubic tenderness thatreadily responds to treatment (see Chapter 56, “Pubic Painand Spinal Factors”).

Functional Disorders

Functional disorders show the participation of the vis-ceral sympathetic system, but they do not have the samesystematic clinical character as the manifestations dis-cussed above. Nevertheless, in certain patients, they aresufficiently pronounced and stereotypic to be noticed,especially since they disappear with the spinal treatment.There are feelings of bloating, of abdominal meteorism,and sometimes constipation. Certain patients complain ofa strong need to urinate, without any evidence of otherorganic lesions.

Table 60.1 is based on 100 cases of TLJS that we havestudied and shows the frequencies of the different signsand their correlations with patient entrance complaints.The figures may vary, depending on the patient sample.There were only 4 complaints of pubic pain among the100 cases, probably due to the fact that the study includeda number of athletes.

N.B.

On examination, a patient having only low back pain mayvery well have a very painful abdominal cellulalgia that doesnot cause abdominal pain.

Figure 60.7

Left:

examination of the posterior crestal point where the posterior ramus crosses the iliac crest.

Right:

exami-nation of the lateral crestal point where the lateral perforating branch crosses over the iliac crest.

Table 60.1Frequency of Signs and Correlation

with Patient Complaints

SignPresent on

ExaminationPresentingComplaint

Lumbogluteal cellulgia

97 Low back pain, 89

Abdominal cellulalgia

60 Pseudovisceral pain, 16

Lateral hip cellulalgia

56 Pseudohip pain, 14

Pubic tenderness

32 Pubic pain, 4

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

TREATMENT

The first treatment is spinal and is generally sufficient.Sometimes it is necessary to treat the cellulotenoperios-teomyalgic manifestations.

In most cases, the spinal treatment consists of mobili-zation and manipulation of the affected segment. Some-times manipulation can be replaced by a facet joint injec-tion (with corticosteroids) after the joint or joints involvedare accurately located. For patients who are clearlyrelieved but not cured, a percutaneous rhizotomy

shouldbe considered. When manipulation and injection arecontraindicated, electrotherapy (e.g., pulsed short wave

diathermy) is very beneficial. Global treatments (e.g., anti-inflammatories, analgesics) are sometimes effective forlimited periods.

In certain cases, local cellulomyalgic manifestationscan be treated by injections of the cellulalgic zones fol-lowed by progressive maneuvers of kneading of the cuta-neous surface by pinch-rolling. Injection of anesthetic pluscorticosteroids into the posterior or lateral crestal pointsis useful, especially when an entrapment syndrome ispresent. Intervention is rarely necessary to free a laterperforating branch involved in an entrapment syndromeor, rarely, a posterior ramus.

Therapeutic exercise is prescribed for recurrent cases.This is discussed in Chapter 41.

389

61

TRANSITIONAL ZONE SYNDROME

The spinal transitional zones (TZs) are located at thejunction of two adjacent spinal regions with various dif-ferences in posterior element orientation and differingdegrees of mobility. There are four TZs, top to bottom(Fig. 61.1): cervico-occipital (CO), cervicothoracic (CT),thoracolumbar (TL), and lumbosacral (LS). While theymay differ significantly, vertebrae of the same region (cer-vical, thoracic, or lumbar) have common characteristics.Vertebrae of a junction or TZ have intermediate charac-teristics.

The CO junction is interposed between the cervicalspine that has great mobility and the occiput that it sup-ports. The CT junction is located between the superiorthoracic spine that has limited mobility because of thethoracic cage and the cervical spine that is free in alldirections. The TL junction links the lumbar spine thathas limited capacity for rotation and the thoracic spinewhere such motion is easy. The LS junction articulates thespine with the pelvis. This zone has a considerable numberof constraints to mobility, which explains the frequencyof its mechanical pathology.

A PMID may be the source of simultaneous and diversesymptoms. The TL junction syndrome, the topic of thepreceding chapter, is a good example.

Another kind of association of symptoms and pain ofspinal origin can exist. Located at different levels, but allon the same side, right or left, they are the consequencesof the simultaneous presence of PMIDs localized to thetransitional zones and the cellulotenoperiosteomyalgicmanifestations that they develop. These are the transitionalzone syndromes (Maigne). The result is a distinct clinicalpicture, with a curious interdependence between thesePMIDs that reflects on the way they must be treated(Fig. 61.2).

Figure 61.1

Transitional zones: 1, cervico-occipital (CO); 2,cervicothoracic (CT); 3, thoracolumbar (TL); 4, lumbosacral(LS).

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

CHARACTERISTICS OF TRANSITIONAL ZONE SYNDROME

The TZ syndrome has distinct semiologic, clinical, andtherapeutic characteristics.

Semiologic Characteristics

There is a PMID on each of the transitional zones(initially two of three). On examination, these PMIDsreveal themselves with ipsilateral facet joint tenderness,right or left. The cellulotenoperiosteomyalgic manifesta-tions caused by these segmental dysfunctions are alsounilateral and on the same side. They can be active (i.e.,responsible for pain complaints) or latent.

Clinical Characteristics

The patient complains of pain at one or several levels:lumbar, cervical, or cephalic; usually unilateral and alwayson the same side. Occasionally, the pain is described asdiffuse and even as bilateral although the clinical signsare unilateral. The patient may complain of only oneregion. Examination reveals the involvement of the othertransitional zones with PMIDs and latent cellulotenoperi-osteomyalgic manifestations.

Treatment

There seems to be true interdependence of the PMIDsof the different transitional zones. Sometimes treating themost irritable PMID causes the others to disappear as well.But often all the PMIDs of the different transitional zones,even the latent ones, must be treated to produce a lastingresult on the one that is most inconvenient for the patientand which is often the only reason for consultation. Incertain cases, it is good to treat the residual celluloteno-periosteomyalgic manifestations locally as well.

The patient’s general condition has an important rolein the expression of these common pains. Pain will persistin a subject with a low tolerance threshold, who is anxious,tired, or spasmophilic. In such cases, the slightest pertur-bation may result in acute diffuse pain, especially in adepressed patient. In these instances, psychologic treat-ment is necessary. Finally, when the PMIDs have beentreated, and the causative factors have been recognizedand corrected, therapeutic exercise will stabilize the result,and recurrences will be avoided.

PERPETUATING AND PRECIPITATING FACTORS

In refractory or recurrent cases, the perpetuating orprecipitating factors must be sought. They are sometimesquite evident: compensatory postures, repetitive rotation,etc. Occasionally, none are found.

Compensatory Postures

There is a possible interrelationship between the dif-ferent TZs: a static disequilibrium results in repercussionsfrom the base to the top, and any functional perturbationof one of them has its repercussion on the others, whetherthey are super- or subjacent. The antalgic attitude of sci-atica demands a compensatory adjustment from the TL,TC, and CO TZs. This compensatory adjustment can bewell tolerated without creating PMIDs if the junctionalzones are supple and tolerant. If not, the zones can fosterand aggravate preexisting PMIDs.

Figure 61.2

Transitional zone syndrome (Maigne) is charac-terized by the presence of a PMID at each level. The facettenderness in a patient with a PMID is always located on thesame side.

CHAPTER 61 TRANSITIONAL ZONE SYNDROME

391

Daily experience shows that a marked antalgic attitudeis not necessary for a lumbar mechanical problem to haverepercussions at a distance. A chronic low back pain canlead to functional adaptations that can persist beyond theresolution of symptoms. A patient needs horizontal visionand any postural deviation of the trunk is compensated atthe cervical or CO level to maintain the eyes at the samelevel. The modifications imposed on the spine by a changein a given region readily result in PMIDs in the transitionalzones; it is different with static problems that have existedsince childhood or adolescence.

Repetitive rotation from a seated position in a car, atthe office, or elsewhere is an example of a typical move-ment expected of the CO, CT, and TL junctions. In repet-itive activities, the dominant side of the subject (right orleft) seems sometimes to play a role. Right-handed per-sons who must rotate frequently to the left do it in a lesscoordinated manner and more awkwardly than if theywere rotating from the right side and therefore more easilyproduce some PMIDs in the involved zones.

Postural habits play a frequent role. Sleeping on theabdomen creates excessive stress on the CO and CT TZs.A seat that is too low or too soft results in lumbar kyphosisand a cervical hyperlordosis.

CLINICAL PICTURE

Typical Clinical Picture

The most commonly seen clinical picture of the tran-sitional zone syndrome has the following presentation:

• Supraorbital headache (CO TZ)• Interscapular pain (TC TZ)• Low back pain that can be of thoracolumbar origin

(TL TZ), lumbosacral origin (LS TZ), or both(Fig. 61.3).

These pains are all localized on the same side, right orleft. Sometimes the patient notices the consistent laterality,sometimes not. Symptoms that the patient cannot analyzevery well can seem confusing: “I have the impression Iam aching all over.” The facet joint tenderness of theresponsible PMIDs and pain of the subcutaneous tissuesto pinch-rolling show the usual unilaterality and the clearsystematization of the symptomatology.

In certain cases, a patient complains only about one ofthe three symptoms: headache, thoracic pain, or lumbarpain, but a systematic examination reveals some latentPMIDs with the usual cellulotenoperiosteomyalgic mani-festations on the other transitional zones. With excessivefatigue or for any other cause, the latent PMID and thecellulotenoperiosteomyalgic manifestations can becomeactive.

Other Clinical Features

The association between headache and thoracic or lum-bar pain on the same side is by far the most usual, as eachof these manifestations is the most frequent combinationfor each of the corresponding TZs. Other associations arepossible. There can be several symptoms for the sametransitional zone; for example, low back pain and abdom-inal pain for the TL junction and cervical pain and shoul-der pain for the CT junction.

During a systematic examination, it is common to seetenoperiosteal or tendinous hypersensitivity as a conse-quence of a PMID localized to the TZs. With the CT TZ,one sees pseudotendinous pain of the shoulder or hyper-sensitivity of the lateral epicondyle, which is found in 6of 10 cases if the segments C5–6 or C6–7 are affected(Fig. 61.4). With the TL TZ, tenderness to palpation ofthe hemipubis is found in one case out of three. When theLS junction is affected, the trochanter can be painful onexamination if the segment L4–5 is affected.

Usually, the subject does not get any pain spontane-ously; only palpation reveals the hypersensitivity of thesezones of insertion. But if repeated violent movementsstress the tendons too much, the patient can easily causea refractory pain. The simultaneous damage of the TZ ina patient who exercises excessively favors the associationof these insertional pains (Fig. 61.5).

Figure 61.3

The most common form of the transitional zonesyndrome is associated with a low back pain overlying theiliac crest (of thoracolumbar origin [TL]); interscapular pain(of cervicothoracic origin [CT]); and headache, usuallyoccipitosupraorbital (of cervical occipital origin [CO]). Thepains are unilateral and always located on the same side.

392

SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

The TL junction syndrome and the TZ syndrome dem-onstrate well the multiplicity of clinical manifestationsthat benign spinal dysfunction or PMIDs can produce.These syndromes also show the interrelations between thePMIDs and the cellulotenoperiosteomyalgic manifesta-tions they produce and emphasize the interdependencebetween PMIDs located at different levels of the spine,particularly if they are at the spinal TZs.

Figure 61.4

A C5–6 or C6–7 PMID is often characterized byinterscapular pain. It can also produce cervical pain orpseudotendinous pain of the shoulder or elbow.

Figure 61.5

A transitional zone syndrome can present astenoperiosteal insertional tenderness. The transitional zonePMID syndrome, whether CT, TL, or LS, is often associatedwith tenoperiosteal tenderness to palpation, noted at theshoulder and elbow (C6–7), pubic region (L1, T12), and thetrochanter (L5). It can be latent (not noted by the patient) andbecome active because of the stress of repetitive activities.

393

62

FAILED BACK SYNDROME

By definition, failed back syndrome is pain that persistsinto the postsurgical period. In one series, it was seen todevelop in 10 to 15% of patients who underwent spinaldecompressive surgery and in 15 to 20% in the ensuing 3to 5 years after fusion (Diwan et al). Although the numbersof such patients appear to be small, they comprise a sig-nificant portion of patients who attend pain managementclinics.

The causes of failed back syndrome are variable andinclude infection, stabilization failure in cases in whichcages are used, and insufficient removal of herniated discmaterial. In most cases, however, the diagnostic cause offailed back syndrome remains elusive in spite of the MRIand EMG studies.

The primary management aim of failed back syndromehas been to contain pain. Treatments have included phys-ical therapy, intrathecal drug administration systems, spi-nal cord stimulation, repeated surgery, and analgesic andmuscle relaxant use. Analgesics frequently include opioids,and their use subjects these patients to the dangers ofdependence.

All cases of failed back syndrome warrant full reexam-ination for the development of centers of pain not due tothe lumbar surgery itself in effect: false failed back syn-drome as a result of altered musculoskeletal mechanicalrelationships of the spine that may lead to the activationof sites of pain unrelated to the original surgery involvingthe vertebral spine.

Frequently seen syndromes associated with false failedback syndrome include the thoracolumbar junction syn-drome that may be related to increased mechanical strainimposed on the upper lumbar thoracic vertebral region asa result of surgical procedures focusing on the lower lum-bar spine that alter the normal mechanical relationshipsof the thoracolumbar junction.

A study of the frequency of thoracolumbar junctionsyndrome as a cause of false failed back syndrome amonga selected population of 52 severely incapacitated post-surgical patients demonstrated that in 32 patients (62%),pain was attributable to the T11–12, T12–L1, and L1–2

facets with pain primarily referred to the lateral buttocksand lower lumbar regions, not the thoracic region(Maigne, 1978). The high frequency of this syndromeshould foster a high degree of clinical suspicion in casesof persistent postsurgery pain as other PMID syndromesmay also present.

In some cases of false failed back syndrome, persistentpain may spread and go on to produce other syndromesincluding false hip pain, spinal pubic pain, lower extremityjoint pain, and pseudovisceral pain. It may trigger a fulltransitional zone syndrome associated with unilateralheadaches, unilateral cervical pain, and unilateral paininvolving the lower extremity having as its origin thelumbar junction. These patients frequently demonstratecellulotenoperiosteomyalgic syndrome tenderness andmuscular alterations consistent with PMID on full exam-ination. Other causes of false failed back syndrome notdue to surgical failure may include myalgic sources asso-ciated with taut bands and trigger points that should alsobe sought and treated if found.

Since the presentation of false failed back syndromemay be pleomorphic, treatment should be directed at thesyndrome uncovered and should not be based on theassumption that pain must originate at the site of surgicalintervention.

FAILURE-TO-IMPROVE SYNDROME

As with failed back syndrome, the failure-to-improvesyndrome is defined as failure to improve with therapy.Diagnostic entities typically associated with failure toimprove often include lumbar stenosis, spondylosis,spondylolisthesis, spodylitic instability, nonsurgical lum-bar herniated discs, recent or old vertebral compressionfractures, and medical conditions such as arthritis,osteoporosis, facet arthropathy, and scoliosis. Such casesoften have their therapies dictated by their primary diag-noses, regardless of accompanying clinical findings and

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SECTION VI CLINICAL ASPECTS OF PAIN OF SPINAL ORIGIN

may undergo surgery for the primary diagnosis that doesnot result in pain control.

Failure to improve is often attributed to psychologicalissues including depression, anxiety, malingering, drugseeking behavior, or lack of inherent responsiveness of theunderlying diagnosed condition. Thus, both the patient andthe diagnosis are held responsible for failure to improve.

Examination of these cases often reveals, as in the caseof false failed back syndrome, overlooked sources of pain,some of which may be myalgic in origin and some ofwhich may be due to activated PMIDs presenting withcellulotenoperiosteomyalgic findings appropriate to thelevels involved that are triggered as a result of mechanicaland muscular strain; the original primary diagnosis, attimes, plays the role essentially of an innocent bystander.

As in failed back syndrome, the thoracolumbar junctionis a frequently overlooked and underexamined source of

pain. The frequency of thoracolumbar junction syndromein cases of failure to improve is high and should be con-sidered when painful symptoms persist in spite of treat-ments aimed at the primary diagnosed condition.

Treatments for failure to improve should be appropriateto the clinical findings on examination. In cases wherePMIDs are uncovered or where symptom complexes suchas thoracolumbar junction syndrome are found, appropri-ate treatments including facet injections and manual tech-niques along with properly chosen medications should betried regardless of the primary diagnosis provided that theclinical features are supportive of the diagnosis and notcontraindicated by the diagnosis.

The coincidence of features of pain related to bothprimary diagnosed causes and triggered PMIDs shouldalso be considered prior to the initiation of any therapy asthe ignoring of either site may lead to therapeutic failure.

VII

MANUAL TECHNIQUES

397

63

INTRODUCTION TO

MANIPULATIVE TECHNIQUES

EQUIPMENT

For the practice of manual therapy, certain basic equip-ment is necessary:

• Examining/treatment table (Fig. 63.1 and Fig. 63.3)• Stool with crossbars (Fig. 63.2)• Firm pillow for patient comfort• Two or three small firm bolsters that can be replaced

by terry towels that can be folded or rolled if necessary• For certain techniques, a wide belt (5

×

200 cm)with Velcro closure (see Fig. 67.47)

Figure 63.1

The best height for the treatment table justreaches the fingers of the examiner’s hands while resting atthe sides. It is best to have a table that can adjust to differentheights to best accommodate the morphology of the patientand all techniques. It should not be too wide (about 60 cm)and should taper in width to the foot of the table, allowingthe patient to sit astride without difficulty for the performanceof certain techniques.

Figure 63.2

A stool is necessary for certain techniques. Thestool should have bars at three levels that can serve assupport for the examiner’s feet in certain maneuvers.

Figure 63.3

The upholstery of the table should be comfort-able, but firm, and have rounded edges. An opening shouldbe provided for the patient’s face (15

×

7 cm) so that thepatient can lie comfortably in the prone position.

398

SECTION VII MANUAL TECHNIQUES

In the following chapters, we describe in detail, regionby region, the techniques for soft tissue mobilization,stretching (when possible), and manipulation. Sincenumerous manipulative techniques are possible, weconcentrate only on the indispensable ones that includeseven basic techniques and seven accessory techniques.

BASIC MANIPULATIVE TECHNIQUES

Seven Basic Techniques

One should first learn and master the seven basic tech-niques of manipulation. The study of manipulation shouldnot be started until mobilization is understood. With theirvariations, mobilizations can be adjusted to a great numberof circumstances. All manipulative techniques make useof mobilization to take up the slack. These seven tech-niques include two cervical, two thoracic, one thoracolum-bar, and two lumbar.

Cervical Spine: Techniques 1 and 2

The chin-free technique can be used at all levels of thecervical spine by varying the point of application. It ismostly a technique of rotation, but it can accommodateall combinations with lateroflexion, flexion, or extension(Fig. 63.4; see description in Chapter 64).

The second technique is a maneuver performed in lat-eroflexion (Fig. 63.5). It is most often used at the cervi-cothoracic junction. While it can be mastered quite wellin its simplest form (pure lateroflexion), it can be com-bined easily with all the available degrees of freedomincluding lateroflexion, rotation, flexion, or extension, toimpart a triplanar manipulative thrust (see description inChapter 65).

Thoracic Spine: Techniques 3 and 4

The epigastric (Fig. 63.6) and supine (Fig. 63.7) are theclassic techniques used for the middle and inferior regions(see description in Chapter 66). Technique 3 is performedwith the patient seated, using a rolled towel or bolster asthe contact point; the latter is performed in prone, withthe point of contact made by the examiner’s hand.

Figure 63.4

Technique 1.

Figure 63.5

Technique 2.

Figure 63.6

Technique 3.

CHAPTER 63 INTRODUCTION TO MANIPULATIVE TECHNIQUES

399

Thoracolumbar Junction: Technique 5

The astride technique is ideal for rotational manipula-tion of this region (Fig. 63.8). It allows numerous combi-nations with flexion, extension, and lateroflexion.

Lumbar Spine: Techniques 6 and 7

The lateral decubitus techniques impart rotation to thelumbosacral spine, either in flexion (Fig. 63.9) or in exten-sion (Fig. 63.10; see description in Chapter 67). In bothvariations, the examiner fixates or blocks the patient’sshoulder while applying the manipulative thrust to thepelvis.

The basic maneuvers, like all manipulative techniques,are routinely effective only if they are executed perfectly.These techniques have the advantage of permitting someimperfection in technique, which makes them somewhatless effective without rendering them systematically dan-gerous. This is not true for the accessory techniques,described below. They require more technical expertise,may be painful to the patient if performed incorrectly, andcarry a degree of risk if they are not executed correctly.

These basic and accessory techniques are the ones thatare routinely used. There are many other interesting tech-niques, and the principal ones are described. They can beadapted to an examiner’s own capabilities. An examinercan even “invent” a new technique that is personally morecomfortable or efficient. The most important point is tobe certain of the indication for the technique and to acton the appropriate segment in the pain-free direction, gentlyand with precision.

We insist on the use of mobilization and stretchingtechniques that are gentle and progress gradually, yetfirmly, in all phases of treatment. These techniques thatare imperative in older patients are to be used initially inmost cases. They often can produce very good resultsalone and may also indicate the best way to execute amanipulative thrust if it is necessary.

Manipulation, like all complex manual acts, needs alengthy apprenticeship to be well executed. The practitionermay be more or less gifted to succeed. One does not learnto play tennis or golf in a few weeks, and in each of theseactivities, there are obvious differences between amateursand professionals. The same can be said for manipulation.

Manipulation as a form of treatment is only useful inthe context of a sound understanding of all the clinicalconditions that bring patients for consultation. Each appli-cation must be carefully planned, must be tailored to theparticular patient, and must respect the various indicationsand contraindications particular to the patient. The entirespectrum of manipulative techniques represents a wholearmamentarium of tools from which the physician maydraw, and with experience these techniques prove to beinvaluable. Although a novice may initially meet withsuccess, it is the experienced manipulator who regularlyfinds these techniques to be efficacious while at the sametime avoiding the many possible adverse effects.

Seven Accessory Techniques

In general, the accessory techniques require greaterprecision to execute correctly than the basic techniquesdo, and most have less tolerance for error.

Cervical Spine: Technique I

The chin grasp technique allows very precise maneu-vers, but it is powerful and must be done with the tips ofthe fingers (Fig. 63.11; see detailed description in Chapter64).

Figure 63.7

Technique 4.

Figure 63.8

Technique 5.

400

SECTION VII MANUAL TECHNIQUES

Figure 63.9

Technique 6.

Figure 63.10

Technique 7.

Figure 63.11

Technique I.

CHAPTER 63 INTRODUCTION TO MANIPULATIVE TECHNIQUES

401

Cervicothoracic Junction:

Techniques II and III

The transverse thrust (Fig. 63.12) and chin pivot

(Fig. 63.13) are two excellent techniques that also require

great precision (see description in Chapter 65).

Thoracic Spine: Technique IV

The knee technique is very precise (Fig. 63.14) but can

be very painful for the patient if performed incorrectly.

False Ribs: Technique V

The manipulation shown in Fig. 63.15 is the most fre-quent indication for costal manipulations (see Chapter 68).

Lower Thoracic and Lumbar Levels: Techniques VI and VII

The double knee technique uses both knees as the con-tact points (Fig. 63.16) and is an excellent maneuver forextension manipulation of the lower thoracic and lumbarspine (see Chapter 67). The belt technique is a very precise(Fig. 63.17) and powerful maneuver (see Chapter 67).

Figure 63.12

Technique II.

Figure 63.13

Technique III.

Figure 63.14

Technique IV.

Figure 63.15

Technique V.

402

SECTION VII MANUAL TECHNIQUES

Figure 63.16

Technique VI.

Figure 63.17

Technique VII.

403

64

CERVICAL TECHNIQUES

MASSAGE

RELAXATIONAL MANEUVERS

Figure 64.1

The pinch-roll test that we use for examinationcan also be used as a therapeutic maneuver in the treatmentof cellulalgic zones. It should be performed in a measuredand progressive manner, with the patient sitting on a stool,arms crossed and resting on a table, and the head restedon the arms.

Figure 64.2

Stretching and distraction of subcutaneous tis-sues and skinfolds. Same position as in Fig. 64.1.

Figure 64.3

Kneading suboccipital muscles. The examinerstands or sits at the head of the supine patient. Deep knead-ing of the suboccipital muscles is executed with the fingertipsof both hands. This maneuver is very relaxing.

Figure 64.4

Stretching of lateral cervical paraspinal muscles.The patient is supine. The examiner stands at the head,grasps the neck with the fingertips along each side of theparaspinal muscles, and stretches them alternately from oneside to the other, pulling them toward him or her as if tryingto detach them slowly from the spine and then releasing themrhythmically from one side and then the other.

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SECTION VII MANUAL TECHNIQUES

Figure 64.5

Kneading suprascapular fossa. The same posi-tion as in Fig. 64.1.

Figure 64.6

Transverse stretching of paraspinal muscles.The fingertips grasp the taut muscular bands and stretchthem to the other side of the spinous process. Same positionas in Fig. 64.1.

Figure 64.7

Kneading–stretching. The patient is supine. Theexaminer grasps the left paracervical muscles with the righthand and pulls them toward him or her, while the heel of theleft hand prevents the head from turning to the right. Thesemovements are to be performed slowly and rhythmically.

Figure 64.8

Kneading–stretching of suprascapular fossa.Same principle as in Fig. 64.7. The left hand fixates the lateralside of the head of the patient while the right hand stretchesthe muscles, with the fingers in a “hook” position.

Figure 64.9

Suboccipital stretching. The patient is lyingsupine. The backs of the examiner’s hands and wrists reston the table, with the fingers strongly maintained in a hookgrasp-like position along the inferior edge of the occiput. Thewrists pushing firmly on the table allow the hands to act likea lever in stretching the occiput and the suboccipital muscles.

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405

MOBILIZATION AND MANUAL TRACTION

These techniques include mobilization in rotation, lat-eroflexion, flexion, and extension. They are useful formuscular stretching.

Mobilization

In Rotation

Patient is in supine position.

First Technique

—

This example is in right rotation.The physician supports the head of the patient with the

right hand over the right occipitomaxillary region. The lefthand, with the fingers flat against the neck, brings thespine into right rotation until end range is reached. At thispoint, the pressure is maintained for a few seconds, thenthe examiner releases and starts again with slow, rhythmic,and oscillating movements. Depending on the position ofthe left hand, the action will be applied to the middle,superior, or inferior cervical spine (Fig. 64.10).

Second Technique

—

For right rotation, the examinerfixates the patient’s left shoulder with the right hand whileimparting right rotation to the cervical spine with the lefthand applied to the patient’s occiput and superior cervicalsegments (Fig. 64.11).

Figure 64.10 Figure 64.11

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SECTION VII MANUAL TECHNIQUES

In Lateroflexion

In Flexion

Patient is supine. The operator’s forearms are crossedbehind the patient’s neck, blocking the patient’s shoulderswith the hands (Fig. 64.14). By gently alternating betweenflexion and extension of the wrists, the operator acts as a

lever and pushes (Fig. 64.15) the neck into flexion, thenreleases (Fig. 64.15). This maneuver is powerful, to bedone very slowly, with great caution. It must be repeatedseveral times.

Patient is in supine position; see Fig. 64.12. Patient is in lateral decubitus position; see Fig. 64.13.

Figure 64.12

The patient and the physician are positionedas in the preceding techniques. However, the physician’s lefthand makes contact with the parietal region and stretchesthe cervical spine in lateral flexion.

Figure 64.13

Mobilizations in right lateral flexion. The patientlies on the left side, firmly maintained in that position with theright shoulder under the physician’s axilla. The movement isrepeated slowly in stretching and in an “elastic” manner inan upward direction and then letting go.

Figure 64.14

Start.

Figure 64.15

Finish.

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407

Superior Cervical Spine

—

This maneuver is for thesuperior cervical segments, especially the atlanto-occipitaljoint. The patient is supine. The physician, standing at thehead, grasps the base of the occiput with the thumb and tipsof the third, fourth, and fifth fingers of one hand, while the

other hand pushes on the forehead (Fig. 64.16). With theoccipital hand, the physician applies traction while the fron-tal hand applies simultaneous downward pressure, whichresults in hyperflexion on the upper neck. The movement,as always, is slow, rhythmic, and repetitive (Fig. 64.17).

Manual Traction

Several methods can be used for cervical traction, amaneuver of stretching and relaxation that is often useful.It is also a necessary test before deciding on treatmentwith mechanical cervical traction. The head is supportedin one of three ways. In the first technique, the examinergrasps the base of the occiput with both hands placed oneach side (Fig. 64.18). In the second technique, the exam-iner simulates a Sayre’s collar by grasping the chin withone hand and the occiput with the other (Fig. 64.19). Inthe third technique, the examiner holds the occiput andthe forehead. The occipital hand applies traction, whilethe other hand maintains the forehead (Fig. 64.20).

Figure 64.16

Start.

Figure 64.17

Finish.

Figure 64.18

First method.

Figure 64.19

Second method.

Figure 64.20

Third method.

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SECTION VII MANUAL TECHNIQUES

The first method is an easier means of applying manualtraction in extension. With the second technique, tractionin flexion can also be performed. The third method avoidsthe possibility of discomfort with mandibular contact thatoccurs with certain patients with dental apparatus. Thisprinciple has been applied in our apparatus for cervicaltraction (see Chapter 23, “Spinal Traction”). The operatorpulls slowly, regularly, progressively, and firmly towardhimself, maintains the traction for about 10 sec, thenreleases and starts again. This is repeated about ten times.In doing so, the examiner should lean backward with armsoutstretched because it is better to use the weight of thebody than to rely on the strength of his arms.

Suboccipital Traction (Fig. 64.21)

With the fingertips, the operator grasps the occiput,maintains it in traction for several seconds, releases it, andstarts again. This is a soft, relaxing maneuver of the sub-occipital muscles.

Traction with Towel (Fig. 64.22)

A very good system for maintaining traction of thecervical spine is as follows: the examiner places thepatient’s head in a folded towel that is passed like a slingunder the occiput.

Traction with Belt (Fig. 64.23)

The patient is supine. A 5-cm wide belt is passed underthe patient’s occiput, forming a long loop passing behindthe physician’s back. By leaning backward, the examinerapplies tension to the belt and produces cervical tractionthat is easy to measure and to control and much lessfatiguing for the examiner. The examiner can either simplymaintain the traction while maintaining the position of thehead with the hand or perform a manipulation in rotationunder traction or simply mobilizations. With a step to theleft or to the right, the examiner can apply right or leftlateroflexion.

Figure 64.21

Figure 64.22

Figure 64.23

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409

MANIPULATION

Basic Technique: Chin Free

The example chosen is a manipulation of the middlecervical spine in pure rotation. In this example, left rota-tion is used. The chin free technique is used more fre-quently than the chin grasp technique described later.

Example (Fig. 64.24a and b)

Manipulation into left rotation is performed with thepatient supine. The physician stands at the end of the tableand slightly to the right. The patient’s head, placed in leftrotation, is supported with the left hand, while the physi-cian applies pressure with the radial edge of the right indexfinger to the lateral aspect of the target vertebra. Thephysician then brings the cervical spine to end range inleft rotation to take up the slack. With end range wellassured, a brief and brisk thrust of the right index fingerexaggerates the left rotation resulting in a manipulation

,

accompanied by the usual cracking.The right forearm is maintained in a vertical plane

perpendicular to the plane of the table throughout theentire movement. This implies that the examiner’s shoul-ders play an important role in the execution of the manip-ulative thrust. In this example, the right shoulder goes upwhile the left one goes down (Fig. 64.25, left).

The left hand supports and maintains the head through-out the movement and assists the right hand to take up theslack and apply the terminal phases of the manipulation.The left forearm is nearly horizontal (Fig. 64.25, right),the right forearm remains perpendicular to the patient’s

Figure 64.24

a.

Start.

b.

Finish.

Figure 64.25

Positions of examiner’s arms.

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SECTION VII MANUAL TECHNIQUES

neck (Fig. 64.25, left and right). The thumb of the righthand does not play a role and should not apply pressureto the patient’s cheek (Fig. 64.25, left).

The part of the index finger that contacts the vertebralsegment is the fleshy part located between the lateral edgeand the palmar surface of the finger (full stroke in Fig. 64.26)rather than the bony edge of the phalanx (hatched inFig. 64.26). The fingers should not be tightly adducted as inFigure 64.27a. The active index finger overlaps the dorsalaspect of the middle finger (Fig. 64.27b). The index finger

plays the role of shock absorber. Even though the manipu-lative thrust is brisk, it is painless. However, if the fingersare held too firmly, the pressure of the soft tissues againstthe vertebra is very painful.

To properly position the fingers, the hand must first beplaced flat on the neck (Fig. 64.28, top); then, while thecontact is maintained with the index finger, pronation ofthe wrist is performed (Fig. 64.28, middle and bottom).With a few minor adjustments in position, this manipula-tion can be executed at all levels of the cervical spine. The

Figure 64.26

Figure 64.27

a.

Incorrect.

b.

Correct.

Figure 64.28

CHAPTER 64 CERVICAL TECHNIQUES

411

active index finger is placed at the level of the segment tobe manipulated:

• Superior cervical spine (Fig. 64.29)• Middle cervical spine (Fig. 64.30) • Inferior cervical spine (Fig. 64.31)

These maneuvers can be executed on the spine:

• In neutral position (without flexion or extension)• With flexion or extension• With or without associated lateroflexion (Fig. 64.26

and Fig. 64.27)

Remarks

We have chosen to describe the technique in which theexaminer keeps the forearm (here the right one) perpen-dicular to the axis of the patient’s neck. We consider thisbest for a precise and well measured maneuver, but thetechnique can also be done with the forearms parallel tothe ground, in the axis of the neck of the patient. Move-ment is then essentially at the forearms, wrists, and hands.

Figure 64.29

Manipulation in left rotation of superior cervicalspine.

Figure 64.30

Manipulation in left rotation on midcervicalsegment.

Figure 64.31

Manipulation in left rotation on segment of infe-rior cervical spine.

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SECTION VII MANUAL TECHNIQUES

Pure Rotation (with or without Flexion or Extension)

Superior Cervical Spine

Figure 64.32

Starting position for manipulation in left rotationin neutral position (neither in flexion nor extension).

Figure 64.33

Final position.

Figure 64.34

Starting position for a manipulation in left rota-tion on the superior cervical spine placed in extension.

Figure 64.35

Final position.

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413

Middle Cervical Spine

Figure 64.36

Starting position for manipulation in left rotationon a spine in flexion.

Figure 64.37

Final position.

Figure 64.38

Manipulation in right rotation on a spine in neu-tral position of midcervical segment.

Figure 64.39

Manipulation in right rotation on spine in exten-sion (with head of patient maintained over the end of thetable).

Figure 64.40

Manipulation in right rotation of midcervicalspine in flexion.

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SECTION VII MANUAL TECHNIQUES

Inferior Cervical Spine

Figure 64.41

Manipulation in right rotation on segment ofinferior cervical spine in neutral position.

Figure 64.42

Manipulation in right rotation on inferior cervi-cal spine in flexion.

Figure 64.43

Manipulation in right rotation on the inferiorcervical spine (starting position).

CHAPTER 64 CERVICAL TECHNIQUES

415

Accessory Technique (Chin Grasp)

Manipulation with Combined Rotation and Lateroflexion

Superior Cervical Spine

Both hands combine to impart lateroflexion to thespine. The apex of the lateroflexion is the site where themanipulation is performed.

Figure 64.44

Right lateral flexion on inferior cervical spine.

Figure 64.45

Left lateral flexion on superior cervical spine.

Figure 64.46

Left rotation without lateral flexion.

Figure 64.47

Left rotation with right lateral flexion. The rightlateral flexion is produced by simultaneous action of the handand left forearm of the examiner and the countersupport ofthe right hand.

Figure 64.48

Left rotation with left lateral flexion. Here theaction of the two hands is opposite. Their simultaneousactions put the head in left lateral flexion.

416

SECTION VII MANUAL TECHNIQUES

Middle and Inferior Cervical Spine

Chin Grasp Technique

The chin grasp technique can be very powerful whenthe head is used as a lever. The maneuver must beextremely precise and perfectly controlled from beginningto end (Fig. 64.51). This technique allows manipulationof the superior, middle, and inferior cervical spine withall the desired combinations. The patient lies supine. Forleft rotation, the examiner grasps the chin of the patientwith the left hand. The top of the patient’s head is sup-ported against the arm or the thorax of the examiner,similar to carrying a football. This hand assures the desireddegree of flexion or extension. The other hand contactsthe target vertebra. Both hands must move in perfect syn-chrony to properly take up the slack and then perform themanipulative thrust.

Figure 64.49

Right rotation and left lateral flexion.

Figure 64.50

Right rotation and right lateral flexion.

Figure 64.51

CHAPTER 64 CERVICAL TECHNIQUES

417

Manipulation in Rotation with or without Flexion/Extension

Superior Cervical Spine

Middle and Inferior Cervical Spine

Figure 64.52

Manipulation in left rotation in neutral position.

Figure 64.53

Manipulation in left rotation on spine in flexion.

Figure 64.54

Manipulation in left rotation on superior cervi-cal spine in extension.

Figure 64.55

Manipulation in right rotation in neutral positionof midcervical spine.

418

SECTION VII MANUAL TECHNIQUES

Variation

Manipulation in Rotation and Lateroflexion

Figure 64.56

Variation. Manipulation in right rotation of supe-rior cervical spine in neutral position. Instead of providing themanipulative thrust with the radial edge of the index finger, itis provided by the thumb.

Figure 64.57

Manipulation of superior cervical spine in leftrotation and right lateral flexion. Lateral flexion is applied bythe left forearm of the examiner. The patient lies on the leftside. The pressure of the right index finger is directed on theocciput. The “chin” hand performs the right lateral flexion.The manipulative thrust is performed downward and forward.

CHAPTER 64 CERVICAL TECHNIQUES

419

Anterior Hand Technique

Manipulation in Left Rotation

Middle Cervical Spine

The patient is seated, with legs dangling over the edgeof the table. The physician, standing beside the patient (onthe side of the rotation), places the middle finger in contactwith the right transverse process of the vertebra on whichthe maneuver will be executed, while the right handpushes on the left frontoparietal region and brings the neckto end left rotation. Once the slack has been taken up, thephysician pulls toward the left and anteriorly with themiddle and index fingers as they “hook” the vertebrae andexaggerate the left rotation to execute the manipulation.

Figure 64.58

Figure 64.59

Rotation with neutral flexion/extension performedon middle cervical spine.

Figure 64.60

Manipulation in rotation with flexion. Note directions of the forearms of the examiner.

Figure 64.61

Manipulation in rotation with extension. Notedirections of the forearms of the examiner.

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SECTION VII MANUAL TECHNIQUES

Superior Cervical Spine

Inferior Cervical Spine

Figure 64.62

Manipulation in pure left rotation performed onC2. The active finger is the index, which contacts the occiput.

Figure 64.63

Manipulation in left rotation and flexion on C2.

Figure 64.64

Manipulation in left rotation and extension on C2.

Figure 64.65

The inferior cervical spine is subjected to a leftrotation, and it is always the left hand that puts the cervicalspine in position. The middle finger is active. To effect amanipulative thrust at C7, it is generally more comfortable touse the fourth or fifth finger as the active finger, with the handflattened against the neck. Shown is a left rotation on a spinein flexion.

N.B.

This technique can include a component of lateroflexion.

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421

Posterior Hand Technique

This personal technique is closely related to the pre-ceding one. The patient is seated. The physician does notput the active hand in front of the patient’s neck, but inthe back, with the active finger (usually the index ormiddle finger) applied at the level of the vertebra to be

manipulated (here the right middle finger for left rota-tion) to assist the manipulation. The other hand placesthe patient’s head and neck in position by contact withthe temporal region (Fig. 64.66) or the inferior maxilla(Fig. 64.68).

There is choice of movement because only one fingerguides the rotation and the maneuver is well localized toa specific segmental level. Moreover, as the slack is taken

up, the head and neck are positioned very precisely by thecombined action of the two hands (Fig. 64.67 andFig. 64.68).

Figure 64.66

For a left rotation, the left hand of the examinergrasps the right side of the patient’s forehead or chin. Withthis hand, the physician positions and then takes up the slack.To give the manipulative thrust, the physician suddenly exag-gerates the rotation, helped by a synchronized pressure withthe right middle finger. This technique allows all maneuversof lateroflexion, flexion, and extension, all combined.

Figure 64.67

Manipulation of superior cervical spine in leftrotation. Note the position of the examiner’s hands.

Figure 64.68

Manipulation of inferior cervical spine in leftrotation. Note the position of the examiner’s hands.

423

65

CERVICOTHORACIC JUNCTION TECHNIQUES

MASSAGE OF SUBCUTANEOUS TISSUES

The pinch-roll (Fig. 65.1) and skin fold (Fig. 65.2)maneuvers are used for petrissage of cellulalgic skin andsubcutaneous tissues. They must be very progressive.

RELAXATIONAL MANEUVERS

Patient Seated

Figure 65.1 Figure 65.2

Figure 65.3

The patient is seated on a stool, arms crossedin front and resting over a table, and the head resting on thearms. The maneuver is performed with the thumbs, whichform a deep petrissage of the muscles and apply tractiongoing from the midline and directly, obliquely, superiorly, andlaterally. The same maneuver can be performed with thepatient supine.

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SECTION VII MANUAL TECHNIQUES

Figure 65.4

Same patient position. The examiner’s fingersin a hook position grasp the muscles of the supraspinousfossa and pull them backward and inward, maintaining them,then releasing them, and starting again in a slow rhythmicpattern.

Figure 65.5

The physician is on the opposite side of thepatient to be treated. The right hand grasps the mass of thelateral muscles of the neck at their inferior attachment andpulls them toward the physician, releasing them in a slowrepeated rhythmic fashion. The other hand applies counter-pressure to the shoulder.

Figure 65.6

Massage and deep gliding are performed withthe thumbs of each side of each hand along the sides of thelines of the spinous processes. The examiner glides parallelto that line, slowly, progressively modifying the pressureapplied.

CHAPTER 65 CERVICOTHORACIC JUNCTION TECHNIQUES

425

MOBILIZATION

In Extension

Patient Seated

The patient is seated, with the head resting on crossedforearms. The physician, standing in front, places forearmsunder the patient’s forearms and the hands over the thoracic

region on each side. By lifting the arms slowly and pullingtoward himself or herself, the physician is able to mobilizethe superior thoracic spine in extension. (Fig. 65.7).

Figure 65.7

426

SECTION VII MANUAL TECHNIQUES

In Flexion

Patient Supine

With the patient lying supine, the examiner’s forearmsare crossed behind the patient’s neck, with the hands onthe patient’s shoulders to block them. With light alternat-ing flexion and extension movements of the wrist, theexaminer acts as a lever to bring the neck into flexion andrelease it. The maneuver is powerful and must be per-

formed slowly with great caution. It must, of course, berepeated several times (Fig. 65.8).

For a lateroflexion maneuver, the hand is placed on theparietal region as support, while the other hand fixates theshoulder. Movement is slow, rhythmic, and tailored to theneeds of the patient. The maximum time that stretchingshould be maintained is 2 to 3 sec (Fig. 65.9).

In Rotation

Patient Supine

Figure 65.8 Figure 65.9

Figure 65.10

CHAPTER 65 CERVICOTHORACIC JUNCTION TECHNIQUES

427

MANIPULATION: BASIC TECHNIQUES

Cervicothoracic Technique in Lateral Decubitus Position

In Pure Lateroflexion (without Rotation)

Preparation —

The patient is lying in lateral decubi-tus, with both legs and thighs slightly flexed. Manipulationinto right lateroflexion is pictured, so the patient is lyingon the left side (Fig. 65.11, left).

Execution —

Manipulation in right lateroflexion inneutral flexion/extension.

Placing in position —

The examiner is standing semi-upright, with the left thigh resting against the table. Theupper part of the patient’s body is slowly brought over theedge of the table (Fig. 65.11, right) until the patient’s headand neck are practically perpendicular to the axis of thetable (Fig. 65.12, left). The physician’s right hand supportsthe patient’s head at the ear, taking care not to compressit, which would be uncomfortable for the patient. Thefingertips have contact with the skull (Fig. 65.12, right).

Figure 65.11

Figure 65.12

428

SECTION VII MANUAL TECHNIQUES

The patient’s superior shoulder must be fixated firmlyunder the examiner’s axilla. The examiner pushes it pos-teriorly and, by so doing, verifies that the scapula is pulledupward and outward, not pushed back toward the spine(Fig. 65.12, right). The examiner presses the left thumbagainst the right edge of the spinous process of the sub-jacent vertebra of the segment that is to be manipulated(Fig. 65.12, left).

In this position, the examiner is nearlylying on the patient. The patient should not be crushedbut must be firmly fixated. Only the neck remains mobile.

Taking up slack —

The right hand of the physician thatsupports the patient’s head brings the neck into lateroflexion

toward the physician’s left. Taking up the slack, assuredwhen the physician feels the “break” (which depends on thegiven lateroflexion), is done at the height of the segment tobe manipulated; it locks the subjacent segments.

Thrust —

From the point of taking up the slack, themanipulative thrust is delivered by a brief ascent of theexaminer’s right hand (Fig. 65.12, right)

.

This manipulation can be done on the thoracolumbarjunction in neutral position (no flexion, no extension) asshown in Fig. 65.12. It can also be done on the spinepositioned in extension (Fig. 65.13) or flexion (Fig. 65.14).

Figure 65.13

Manipulation in lateral flexion on spine inextension.

Figure 65.14

Manipulation in right lateral flexion on spine inflexion.

CHAPTER 65 CERVICOTHORACIC JUNCTION TECHNIQUES

429

In Lateroflexion Associated with Rotation

This manipulation in lateroflexion can be associatedwith:

1. Rotation in the same direction as the lateroflex-ion — right lateroflexion with right rotation(homologous lateroflexion); see Fig. 65.15.

2. Rotation in the opposite direction — right lat-eroflexion with left rotation (heterologous lat-eroflexion); see Fig. 65.16.

All of these maneuvers can be performed on segmentsof the cervicothoracic junction in neutral position, inextension, or in flexion. Figure 65.17 shows left lateralflexion combined with right rotation of the C6–7 segment(note support of the thumb on the spinous process of C7)in the spine in extension.

Figure 65.15

Manipulation in right lateral flexion and rightrotation.

Figure 65.16

Manipulation in right lateral flexion and leftrotation.

Figure 65.17

Manipulation in left lateral flexion, extension,and right rotation.

430

SECTION VII MANUAL TECHNIQUES

Chin Pivot (Accessory Technique)

Patient in Prone

The patient is prone, with arms apart, hanging on eachside of the table (Fig. 65.18 and Fig. 65.20). The chin restson the table. It is often more comfortable for the patientto rest the chin on the hands resting flat on the table(Fig. 65.19). This position puts the spine in slight extension.

The physician stands (on the left side of the patient inillustration) at the corner of the table and places the thenareminence over the right transverse process of the first,second, or third thoracic vertebra (Fig. 65.19 and

Fig. 65.20). The hand grasps the patient’s right temporo-maxillary region, taking care not to compress the ear. Thepatient’s neck is brought into right rotation with stretchingtoward the left (Fig. 65.21).

When taking up of the slack is assured, the manipula-tive thrust is given by accentuating the action of the handtaking support on the head, while the counterpressure isfirmly maintained on the transverse process by the thenareminence of the other hand, which remains fixed.

Figure 65.18 Figure 65.19

Figure 65.20

Placing in position.

Figure 65.21

Taking up slack.

CHAPTER 65 CERVICOTHORACIC JUNCTION TECHNIQUES

431

Variant —

The maneuver can be done by taking upthe slack in the same manner as above (Fig. 65.23, left),but at the terminal thrust, pressure on the head is the fixedpoint. The thrust is given by the sudden increase in pres-sure on the transverse process of the thoracic vertebra(Fig. 65.23, right).

Same maneuver on spine in flexion —

The maneuvercan be done on the spine in flexion. The head of the patientmust be over the edge of the table. It is supported by theexaminer’s knee (Fig. 65.24); the counterpressure is sup-plied by the thumb against the transverse process of thevertebra subjacent to the segment to be manipulated. Thisdelicate and powerful maneuver has only rare indications.

Figure 65.22

Same maneuver shown in Fig. 65.19, but theexaminer uses the thumb to assure counterpressure.

Figure 65.23

Variation of basic technique. The manipulative thrust is performed by the dorsal hand (thick arrow).

Left,

start.

Right,

taking up slack; thrust.

Figure 65.24

432

SECTION VII MANUAL TECHNIQUES

Same maneuver associated with lateroflexion —

Theleft hand takes a slightly different support. It is placed infront of the patient’s ear, on the temporomaxillary region.The examiner brings the neck into right lateroflexion,while the counterpressure on the thenar eminence (or thethumb) of the left hand is applied to the left transverseprocess of the first, second, or third thoracic vertebra,depending on which segment will bear the maximumeffect. The neck is then in strong right lateroflexion withslight left rotation (Fig. 65.25). The manipulative thrust isgiven by sudden and limited accentuation of the exam-iner’s right hand on the transverse process. Its directionis slightly caudal.

Lateral Pressure against Spinous Process (Accessory Technique)

Patient Seated

The physician stands behind the patient and places theleft hand over the patient’s left parietal region and bringsthe neck into right lateroflexion. The right thumb appliespressure against the right lateral part of the vertebra sub-jacent to the joint to be manipulated (Fig. 65.26). Thephysician gradually increases the right lateroflexion of theneck, until the left thumb senses that the flexion hasreached end range (i.e., the point at which the peak of thelateroflexion reaches the vertebra on which it rests). Themanipulative thrust is given by increasing the pressure ofthe thumb with a small brief movement directed down-ward and to the left, in the direction of the line that bisectsthe angle formed by the neck and the shoulder of thepatient. The examiner’s wrist and forearm are maintainedfirmly throughout the maneuver.

To execute this maneuver and have it strictly painlessfor the patient, both patient and physician should be per-fectly positioned, with lateral inclination of the trunk ofthe patient. Two techniques can be used.

Figure 65.25

Patient is prone, with arms on either side ofthe table.

Figure 65.26

CHAPTER 65 CERVICOTHORACIC JUNCTION TECHNIQUES

433

Technique A (Fig. 65.27).

The patient’s body ismaintained slightly to the left. The physician’s elbowgrasps the patient’s left shoulder, like a pair of pliers. Thephysician’s chest is flat against the back of the subject,forming a kind of block. The patient’s trunk is broughtinto slight left inclination, and the cervicothoracic junctioninto slight right inclination. The right thumb applies pres-sure against the spinous process; the right forearm is ori-ented obliquely, with the elbow raised superiorly. Whenthe examiner senses that end range has been reached, theterminal thrust is applied; the direction is given by theobliquity of the forearms, which practically bisect theneck–shoulder angle.

Technique B (Fig. 65.28).

The physician’s foot isplaced on the table, against the left hip of the patient. Thepatient’s left axilla rests on the physician’s left knee. Theinclination of the knee gives the inclination of the patient’strunk.

N.B.

Note in all cases the strict parallelism of the two forearmsof the operator.

When the manipulation is applied on the sixth cervicalvertebra, the active pressure is not provided by the thumbagainst the spinous process (as it is too small) but withthe thumb and the index finger which are half-folded,forming pliers. The so-formed pliers take the lateral partof the spinous process and the posterolateral part of the

Figure 65.27

Figure 65.28

435

66

THORACIC TECHNIQUES

MASSAGE

Techniques for this region are identical to those for thecervicothoracic junction (see Chapter 65).

RELAXATIONAL MANEUVERS

The patient is prone.

Figure 66.1

The patient is prone with the head turned to thedirection opposite to the side being treated. The examinerstands at the side opposite the one to be treated and appliesthe hands with the fingers spread apart to the paraspinalregion. The thumbs are together at their extremities, forminga line parallel to the line of the spinous processes.

With the “bar” formed by the thenar eminences andthumbs, the examiner pushes the paraspinal muscles slowly,as if trying to pull them away from the spinous process anddetach them from the deep planes. When maximal tensionis reached, the examiner pauses, increases the pressureslightly, and then releases it. This should be done in a rhyth-mic, well controlled way, without losing contact, even duringthe release.

In many conditions, this is a relaxing and useful maneuver,particularly in the treatment of acute and chronic thoracicpain. At the start of the massage, the elbows of the examinerare partially flexed, and during the maneuver, they areextended. The examiner finishes with the elbows fullyextended, permitting a strong tangential pressure to be trans-mitted to the thorax and allowing good stretching of theparaspinal muscles.

Figure 66.2

The patient is in lateral decubitus (here on theright side), with the arm resting on the head. The examinerstands facing the patient. The examiner’s two hands are sideby side, and the fingers in a claw-like position can grasp theparaspinal muscles at the spinous process. The examinerpulls the muscles, with hands slightly apart, and then releasesthem in a slow and rhythmic fashion, allowing an elasticmovement that is firm at the moment of maximal stretching.At that moment, there is a brief pause.

Figure 66.3

The patient is prone. The examiner stands atthe head, and places the hands flat on each side of the spinenear the midline over the superior thoracic vertebrae. Theforearms are partially flexed. The examiner slides the handsalong the spine, downward in a parallel fashion, stretchingthe forearms. The maneuver should be performed slowly andrhythmically, applying pressure in a constant manner accord-ing to the results that are desired.

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SECTION VII MANUAL TECHNIQUES

Scapular Muscle Stretching

The patient is positioned in side lying. The examinerfaces the patient and grasps the medial scapular edge withthe fingertips. The scapula is circumducted slowly, stretch-ing the soft tissues in the different directions while knead-ing the muscles laterally (Fig. 66.4); inferiorly (Fig. 66.5);and superiorly (Fig. 66.6).

Note the variations in the position of the patient’supper limb. The different maneuvers are performedslowly and rhythmically, stretching to end range andpausing as maximal tension is reached. These maneuversalso provide an excellent way to mobilize the scapulotho-racic joint.

Figure 66.4 Figure 66.5

Figure 66.6

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437

MOBILIZATION

Mobilization can be performed in extension, lateroflex-ion, rotation, and occasionally flexion.

In Extension

The patient is seated. The upper thoracic spine is shownin Fig. 66.7 and Fig. 66.8, and the midthoracic spine isshown in Fig. 66.9 through Fig. 66.13.

N.B.

Because the patient has a tendency to slide forward withthese maneuvers, the examiner uses his knees to block the patientand prevent sliding (Fig. 66.8 through Fig. 66.13).

Figure 66.7

The patient is sitting on the table with handsfolded behind the neck. The examiner, in front, passes theforearms between the forearms and the shoulders of thepatient and applies the hands at each side of the line of thespinous process at the first thoracic vertebrae. The examinerpulls the arms back, bending slightly backward, while theforearms act as levers on the patient’s forearms. The handsact on the back of the patient while supporting the patient’sforearms (pressing them upward) to bring the affected regioninto extension.

Figure 66.8

This variant is also useful for the inferior thoracicspine. The patient’s two stretched arms are rested verticallyon the examiner’s right shoulder. The examiner, in front,crosses the hands over the segment to be treated andpresses on it, while pushing the shoulder forward. With back-ward and forward movement of the trunk, the examiner canexecute repeated mobilizations in extension.

Figure 66.9

The patient, with arms crossed over the fore-head, rests on the physician’s chest in front. The physician’shands are placed on each side of the region to obtain mobi-lization in extension and pulls, while going back slightly. Thephysician then releases the pressure, going a little forward,and starts again gently.

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SECTION VII MANUAL TECHNIQUES

Figure 66.10

through

Figure 66.12

The patient is seated on the tablewith the feet on the bar of the stool and the arms stretched forward.The examiner is at the side, with the outer foot on the stool and theforearm holding the stretched arms of the patient. The physician reststhe forearm on the knee and, with the other hand, presses the thoracicregion that must be mobilized. While increasing the pressure, theexaminer bends the knee outward, thus lengthening the thoracic spinein extension. The examiner then releases, puts the foot back at thestarting position, and does a series of alternating slow, rhythmic, andelastic movements.

Figure 66.11

Positioning.

Figure 66.12

Taking up slack.

Figure 66.13

The patient is sitting with arms crossed behind thehead. The physician, from behind, passes the left forearm in front ofthe chest and grasps the patient’s right arm. The physician, with rightelbow on the right hip, presses with the right hand on the zone to bemobilized in extension. By rotating the pelvis and advancing the hip,the physician transmits increased pressure through the right forearmto the spine while applying counterpressure with the left forearm asit pulls the upper thorax into extension.

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439

In Lateroflexion

The patient is seated astride the end of the table. Thismaneuver is performed slowly, with counterpressure wellmaintained by the operator’s right hand by placing the

right elbow against the iliac crest. At maximum tension,the pressure is gradually released and reapplied severaltimes.

In Rotation

The patient is seated astride the end of the table inrotation.

Figure 66.14

Left lateral flexion. The subject is seatedastride at the end of the table, arms crossed over the head.The examiner stands to the left and grasps the patient’s rightelbow. The examiner’s left forearm rests on the patient’s rightforearm. The examiner then applies the right hand to thepatient’s left lateral thorax and bends patient’s thoracic spineto the left by pulling back with the left hand. The examinercan vary the degree of bending by changing the position ofthe right hand. The maneuver is performed slowly, with counter-pressure from the right hand as the examiner’s right elbowrests on the iliac spine. At the point of maximal tension, thepressure is relaxed. The movement is performed severaltimes.

Figure 66.15

The patient is astride the end of the table, back to the examiner, and hands crossed behind the neck. Theexaminer grasps the patient’s right arm with the left hand. The right hand grasps the region to be mobilized, with the heel ofthe hand overlying the right transverse process. The examiner’s right elbow is at a 90° angle, and the forearm is parallel tothe ground. The examiner brings the thoracic spine into left rotation with the left hand, while the right hand applies pressureon the transverse process in a synchronous manner, which increases the rotation on the affected vertebrae. The examinertakes up the slack, maintains it for a moment, and then returns to the starting point. This maneuver is repeated several times.

440

SECTION VII MANUAL TECHNIQUES

MANIPULATION

(Basic) Epigastric Technique

Two patient hand positions are utilized: hands foldedbehind the neck (hands-on-neck) and hands placed ante-riorly across the thorax (hands-front).

Hands-on-Neck Position (Fig. 66.17 and Fig. 66.18)

Positioning —

The patient is seated on the table, withlegs dangling over the edge and hands folded behind theneck. The physician, standing behind, passes the forearmsunder the patient’s axilla and grasps the wrists. The phy-sician’s sternum is applied to the patient’s midthoracicregion with a tightly rolled towel (or bolster) interposedbetween examiner and patient (Fig. 66.16).

Taking up slack —

The examiner takes a deep breathwhile elevating the patient by the axillae, taking care that

no downward pressure is applied to the wrists (this wouldproduce neck hyperflexion). Simultaneously, the sternalpressure against the patient’s spine is increased by eleva-tion of the examiner’s chest at end inspiration with aValsalva maneuver. Sternal pressure is further augmentedby compressing the patient’s thorax between the two fore-arms (Fig. 66.17).

Manipulative thrust —

The examiner briefly exagger-ates the forward and upward sternal movement, withoutapplying tension to the patient’s neck, while the exam-iner’s forearms elevate the patient’s thorax posteriorly(Fig. 66.18).

Figure 66.16

Positioning.

Figure 66.17

Taking up slack.

Figure 66.18

Taking up slack; manipulative thrust.

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441

Hands-Front Position (Fig. 66.19 through Fig. 66.22)

This position is generally more efficacious than thehands-on-neck position, especially for the middle andinferior thoracic spine. It is also more comfortable for thepatient.

Positioning —

The patient is seated. A tightly rolledtowel or bolster is placed between the examiner’s lower

sternum and the segment to be manipulated. To adjust tothe various vertebral levels, either a table with a variableheight adjustment should be used or the examiner mustadjust to the patient by bending the knees and keeping thechest straight (although the examiner always keeps thelegs bent).

The examiner’s right arm is passed under the patient’sright axilla, with the hand on the patient’s neck. This handdetermines and maintains the degree of neck and backflexion. Its pressure must not vary because it maintainsthe chosen position throughout the maneuver, even duringthe terminal manipulative thrust.

With the left hand, the examiner then grasps thepatient’s right wrist (or hand) and firmly places it againstthe patient’s chest immediately in front of the thoracicpoint of contact. The left arm of the patient remains freeat the side (Fig. 66.19).

Taking up slack —

The examiner simultaneouslyincreases the sternal pressure against the patient’s spineby elevating the chest at end inspiration with a Valsalvamaneuver. Sternal pressure is further augmented byincreasing the traction on the patient’s forward arm, pull-ing the patient posteriorly.

Manipulative thrust —

As in the preceding technique,the manipulative thrust originates from the sternal pressure(Fig. 66.21) while the patient’s upper thorax is elevatedupward and backward.

Figure 66.19

Placement is now completed (Fig. 66.20); sub-ject and examiner must move together

en bloc

, as the exam-iner firmly maintains the pressure against the sternum.

Figure 66.20 Figure 66.21

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SECTION VII MANUAL TECHNIQUES

Localizing Manipulation to Specific Spinal Segment

Depending on the level chosen, the position of thepatient is modified by varying the degree of posteriorinclination so that the segment to be manipulated is situ-ated at the apex of the curve formed.

Hands-Front Position

For the midthoracic region, the patient sits normally onthe table, with the chest vertical (Fig. 66.22, top).

For the upper segments, the examiner must pull thepatient backward so that the plane of the shoulders fallsbehind the table (Fig. 66.22, middle).

For the lower segments, the examiner positions thepatient in slight forward bending, rounding the patient’sback (Fig. 66.22, bottom).

Figure 66.22

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443

Hands-on-Neck Position

The principle is the same as above: midthoracic spine(Fig. 66.23); superior thoracic spine (Fig. 66.24); inferiorthoracic spine (Fig. 66.27).

The positions of the patient’s arms and the examiner’shands are important for the successful execution of themaneuver. The positions can vary depending on thepatient’s or physician’s size, but in general, the followingtechniques can accommodate:

• The midthoracic spine (Fig. 66.23 and Fig. 66.25).The patient’s arms are positioned horizontally orslightly lower. The examiner’s hands are applied tothe patient’s wrists.

Figure 66.23 Figure 66.24

Figure 66.25

Figure 66.26 Figure 66.27

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SECTION VII MANUAL TECHNIQUES

• The superior thoracic spine (Fig. 66.24 andFig. 66.26). The patient’s arms are positioned morevertically and are abducted and externally rotated.The examiner’s hands overlap those of the patient.

• The inferior thoracic spine (Fig. 66.27). Thepatient’s arms rest below the horizontal. The exam-iner’s hands grasp the patient’s forearms, proximalto the wrists.

Variations in terminal manipulative thrust —

Analternative technique of administering the manipulativethrust modifies the manner in which the examiner elevatesthe patient. This modification involves the sudden exten-sion of the semiflexed knees or rising up on the toes whilethe examiner’s trunk and lower limbs are maintained rig-idly.

First MethodPositioning —

The patient is positioned as above. Thephysician’s knees are

partially flexed

because the musclesof the thighs and the legs are contracted.

Taking up slack —

There is no change from above.The physician’s chest is inflated at end inspiration, and thesternum is pushed forward and upward while firmly main-taining the patient. Physician and patient move

en bloc

.

(Basic) Sitting Astride Technique

Designed for manipulation in rotation, this techniqueis applicable at all levels, from the midthoracic to the lowlumbar spine, in neutral position, flexion or extension. Therotation can be pure or combined with lateroflexion(Fig. 66.28)

Manipulative thrust —

The physician begins bybriefly externally rotating the hips and spreading the par-tially flexed knees, which suddenly stretches them a fewdegrees. This results in a sudden elevation of the exam-iner’s upper body (which remains stiff throughout) includ-ing the thorax and sternal pressure. Contrary to what onemight think, when performed with precision, this maneu-ver is not traumatic.

Second Method

This method is quite similar to the first.

Positioning —

As above.

Taking up slack —

As above.

Manipulative thrust —

Although the principle is thesame, the examiner’s technique is modified slightly. Theexaminer’s entire body becomes blocked and stiff, holdingthe subject firmly against it, while firmly maintaining thepressure of the hands on the patient’s neck and sternum.The examiner’s feet are flat on the floor, and the knees areslightly flexed. The manipulative thrust is executed bysuddenly raising the heels from the floor while maintain-ing the knees in their semiflexed position. This movementmust be very rapid. The cervicothoracic segment must beperfectly fixated, without any loosening, throughout themaneuver.

Figure 66.28

CHAPTER 66 THORACIC TECHNIQUES

445

In Pure Rotation (Fig. 66.29).

The technique is performed according to the usual threephases: placing in position, taking up the slack, and ter-minal thrust.

Example: Manipulation in Left Rotation

Positioning —

The patient is seated astride the end ofthe table with the physician standing behind. The patient’sarms are crossed in front of the chest, with each handgrasping the opposite arm (Fig. 66.29, left). The physi-cian’s left arm passes in front of the patient’s thorax and

grasps the patient’s right arm to bring the trunk into leftrotation. The physician’s right thenar eminence (orhypothenar eminence) is placed over the transverse pro-cess of the target vertebra (Fig. 66.29, right).

Taking up slack

—

This is assured by the action ofthe physician’s left arm as it brings the patient’s trunk toend range. This movement is assisted by the palm of theright hand.

Manipulative thrust —

The physician uses a briefsimultaneous action of both hands.

Figure 66.29

Left,

start of the maneuver (taking up the slack).

Right,

end of the maneuver (taking up slack and manipulativethrust).

446

SECTION VII MANUAL TECHNIQUES

Variations of Patient’s Arm Position

Several arm positions can be assumed by the patient.The choice depends on the size of both the examiner andthe patient and especially on the level to be treated: hands-on-neck (Fig. 66.30, top left); arms crossed (Fig. 66.30,top right); mixed position, one hand behind the neck, theother grasps the elbow (Fig. 66.30, bottom left).

Positions of Examiner’s Arms and Feet

Position of arms (Fig. 66.30) —

Independent of theposition chosen for the patient’s arms, the examiner’s rightforearm must remain perpendicular to the spine during themanipulation (Fig. 66.31 and Fig. 66.32). The height ofthe table must be adjusted if possible to accommodatethis. When using a table without a variable height adjust-ment, the physician varies the degree of knee flexion toadjust the position of the arms. The left forearm must alsobe horizontal. The technique is more efficient if the exam-iner’s elbow is against the iliac crest (for the lower andmidthoracic segments) See Fig. 66.32. The thoracic pres-sure is then applied by a pelvic thrust anteriorly. Themanipulation is therefore due to a vast rotation of theexaminer’s entire body to the left, while the forearms aremaintained parallel to the floor and each other, subtendinga horizontal arc (Fig. 66.31 through Fig. 66.35).

Position of feet —

To perform the horizontal circlewith the arms, the examiner must turn around the patient,in small steps. As the slack is taken up, the physicianplants the foot ipsilateral to the contact hand and shiftsthe weight to that side. The pelvic rotation is thus trans-mitted to the elbow and contributes to the manipulativethrust of the forearm.

Example.

For a manipulation in left rotation, the exam-iner’s weight is shifted somewhat to the left, with the rightfoot positioned slightly behind the left (Fig. 66.32 andFig. 66.35, left,

starting position; Fig. 66.34 andFig. 66.35, right, finishing position). The movements ofthe feet (white asterisk) and the pelvis (black asterisk) areshown by the arrows.

Figure 66.30

CHAPTER 66 THORACIC TECHNIQUES

447

Figure 66.31

Starting position of arm.

Figure 66.32

Positioning.

Figure 66.33

Intermediate phase.

Figure 66.34

Taking up slack; manipulative thrust.

448

SECTION VII MANUAL TECHNIQUES

In rotation combined with other directions —

Theneutral position technique (pure rotation) described above

can be combined

with flexion, extension, or lateroflexion(Fig. 66.36 through Fig. 66.40).

Figure 66.35

Examiner’s foot position during maneuver.

Left,

start.

Right,

finish.

Figure 66.36

Manipulation in left rota-tion of the inferior thoracic spine in neu-tral posit ion, without flexion orextension (crossed arms position). Theplane of the shoulders is horizontal.

Figure 66.37

Manipulation in left rota-tion of the inferior thoracic spine withleft lateral flexion (crossed arms posi-tion), without flexion or extension. Theplane of the shoulders is inclinedtoward the left.

Figure 66.38

Manipulation in left rota-tion of the middle of the inferior midtho-racic spine in left lateral flexion and inextension (crossed arms position).

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449

Resisted manipulation —

The previously describedtechniques are assisted manipulations, in which themanipulative thrust of the right hand is in the same direc-tion as the trunk and the left hand. In the assisted tech-nique, pressure is applied to the transverse process of thesupra-adjacent vertebra of the segment to be manipulated(see Fig. 66.34). In certain cases, the resisted maneuvermay be used (Fig. 66.41).

For example, to produce left rotation of T11, the exam-iner can apply counterpressure to the left transverse pro-cess of T12 with the heel of the right hand, while the lefthand takes up the slack in left rotation and applies themanipulative thrust. The examiner’s right elbow is firmlyin contact with the right iliac crest.

Figure 66.39

Manipulation of midthoracic spine in left rota-tion in neutral position (hands-on-neck position). Comparewith Figure 66.40.

Figure 66.40

Manipulation of midthoracic spine in left rotationand in flexion without lateral flexion (hands-on-neck position).

Figure 66.41

Manipulation in counter-rotation.

450

SECTION VII MANUAL TECHNIQUES

(Accessory) Knee Technique

This is an extremely precise technique for manipulationof the thoracic spine.

Positioning (Fig. 66.42)

—

The patient is seated on astool, with hands folded behind the neck. The examinerstands behind, with a foot on the bar of the stool, whoseheight is adjusted to the thoracic level to be manipulated.The examiner then grasps the patient’s wrists with bothhands, after passing the forearms under the patient’s axil-lae. The knee is then placed in contact with the spinousor transverse process (the latter introduces a rotationalcomponent to the thrust) of the vertebra on which themanipulation will be performed. The contact point is pad-ded by a folded thick towel or bolster.

Manipulative thrust —

With the knee well fixed, thephysician takes up the slack by elevating the patient’saxillae upward and toward the physician, without applyingdownward leverage on the patient’s wrists. The manipu-lative thrust consists of exaggeration of this tractionslightly, without the least effort.

This maneuver can be performed at all levels of thethoracic spine, but it is technically more difficult at thesuperior thoracic level. Notwithstanding its appearance,this maneuver is not at all uncomfortable for the patient.It must be executed with the fingertips and with welltrained hands, so that it is soft and precise. Depending onthe spinal level (midthoracic, Fig. 66.44; upper,Fig. 66.45; or lower, Fig. 66.46), the examiner positionsthe patient’s trunk in neutral, flexion, or extension, so thatthe apex of the curve formed is over the segment to bemanipulated (Fig. 66.44 through Fig. 66.47).

Figure 66.42

Positioning.

Figure 66.43

Taking up slack; manipulative thrust.

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451

Localizing Manipulation to Specific Spinal Segment

• Midthoracic spine (Fig. 66.44 and Fig. 66.47A).• Superior thoracic spine (Fig. 66.45 and Fig. 66.47B).• Inferior thoracic spine (Fig. 66.46 and Fig. 66.47C).

Mechanisms of action of the maneuver on the spineare shown in Fig. 66.48 and Fig. 66.49.

Figure 66.44 Figure 66.45 Figure 66.46

Figure 66.47

Figure 66.48

The contact point of the knee (G) is applied to the spinous process of A. The global movement imparted bythe examiner’s arms results in flexion (F). This movement is maximal between A

and B because of the position of the knee.

Figure 66.49

If the spine was initially in extension (which is not possible with all patients), the pressure applied here on Bwould facilitate the extension of B on the subjacent vertebrae (A). It should be considered an assisted maneuver. The segmentAB would be manipulated in extension and no longer in flexion.

452

SECTION VII MANUAL TECHNIQUES

(Basic) Supine Technique

Hands-on-Neck Position (Fig. 66.50 through Fig. 66.53)

The patient is supine, with the hands folded tightly behindthe neck, elbows adducted forward, and the forearms restingunder the chin. The physician stands to the right and graspsthe patient’s elbows with the left hand. The physician willact as a lever on the elbows. The patient places a hand inthe “gutter” (here the right one) over the segment to be

manipulated, while the left hand applies pressure to theelbows, to vary the degree of flexion necessary to place thesegment to be treated under maximal tension. Once the slackhas been taken up, a brief manipulative thrust of the left armwill suffice to obtain the manipulation, as it directs forcetoward the right hand (countersupport).

Figure 66.50

Preparation.

Figure 66.51

Execution.

Figure 66.52

Method of achieving manipulation of the upper(a), mid or lower (b) thoracic spine according to the positionof the thoracic hand and the degree of flexion imposed onthe spine.

Figure 66.53

Demonstration of action of manipulation on thespine. M = counterpressure of the hand. P = pressure pro-vided by the weight of the physician. A = segment on whichthe action is performed. F = force of flexion imposed by elbowpressure.

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453

Crossed Arms Position (Fig. 66.54 through Fig. 66.58)

The patient’s arms are crossed in front of the chest(Fig. 66.54) while the examiner’s thoracic spine appliespressure in a protected manner, using a cushion. The

examiner’s left forearm and hand maintain the thoracicspine in the necessary position of flexion. The fixed pointof contact is provided (as in the above technique) by theright hand placed flat in the gutter on the table.

Note the position of the examiner’s left arm (Fig. 66.55),which envelops the head in line with the axis of the body.This technique is especially useful for mid and inferiorthoracic spine problems. The manipulative thrust is givenby a sudden but measured accentuation of the thoracicpressure.

Figure 66.56 shows a manipulation performed on amidthoracic spine (patient: hands on neck); start of themaneuver.

Figure 66.57 shows a manipulation performed on theinferior thoracic spine (patient: crossed arms); start of themaneuver.

Figure 66.58 shows a manipulation of the superior tho-racic spine (patient: hands on neck); end of maneuver,moment of manipulative thrust.

Figure 66.54 Preparation. Figure 66.55 Taking up slack.

Figure 66.56 Figure 66.57

Figure 66.58

454 SECTION VII MANUAL TECHNIQUES

Direct Technique

This apparently easy technique readily produces thefamiliar cracking sound. In reality, it is difficult to measureit well.

In Figure 66.59, pressure on the left transverse processof B gives the vertebra B a rotation to the right in relationto C. Counterpressure on the right transverse process ofC will add precision to the movement (Fig. 66.60). Pres-sure is applied with the pisiform of each hand (Fig. 66.61and Fig. 66.62).

An analogous technique, done in a particular way, wasone of the essential chiropractic maneuvers: the “recoil”of Palmer. The principle is shown in Fig. 66.63. Pressureis maintained by the examiner’s hand contact, with armsslightly flexed. The manipulative thrust is performed bythe rapid contraction of the triceps, which relax immedi-ately. This type of maneuver requires that the patient’sbody and head rest on a support that absorbs a part ofmanipulative force and offers a counter-resistance to thesegment treated.

Figure 66.59 Figure 66.60

Figure 66.61 Figure 66.62

Figure 66.63

455

67

LUMBAR TECHNIQUES

MASSAGE

Superficial petrissage is used in the treatment of cellu-lalgic subcutaneous tissues. The maneuver is adjustedaccording to the severity and degree of induration. Thereare two typical cases.

The first type is a global cellulalgia of the lumbarregion. The thickened subcutaneous tissues are sometimesdifficult to mobilize on the deep fascial planes and difficultto pleat. In these patients, the superficial fascial planesmust be mobilized on the deep planes. This is followedby maneuvers of progressive pleating (or folding?) of theskin and superficial soft tissues. The skin folds are verythick at first, but they become more pliable as the treatmentprogresses.

The second type is a localized cellulalgia, often unilat-eral, usually corresponding to dysfunction of the thora-columbar junction (Maigne’s low back pain). It is the mostfrequent possibility (Fig. 67.1). Variable techniques canbe used: pinch-rolling, Wetterwald’s maneuvers, brokenfold, etc. The maneuvers are always somewhat uncomfort-able. They must be well measured so that they are notpainful; otherwise, the pain must stop at the same time asthe maneuver.

RELAXATIONAL MANEUVERS AND MUSCLE STRETCHING

Relaxational Maneuvers

Buttock and Lower Limb Muscles

These techniques are used in the treatment of triggerpoints, often associated with segmental cellulotenoperio-steomyalgic syndrome of low lumbar origin.

Petrissage (Fig. 67.2) —

The treatment of gluteal trig-ger points associated with a lower lumbar PMID or adiscogenic problem is important in the treatment of lowback pain and the sequelae of sciatica. Slow deep pet-rissage of muscles with taut bands is generally effective.It must be performed in a rhythmic and progressive fashion.

When muscle involvement is very severe, petrissagecan be contraindicated. This is often the case when thespine is the origin of the problem. Attention must be givenfirst to that problem.

Slow pressure maintained for 30 to 60 sec on the mostsensitive trigger points can also be effective.

Figure 67.1

Figure 67.2

456

SECTION VII MANUAL TECHNIQUES

Paraspinal Muscles

The patient is prone (head turned away from the sidebeing treated; Fig. 67.3).

Patient Supine.

(Fig. 67.4 through Fig. 67.6.)

Figure 67.3

The examiner stands opposite the side to betreated, hands applied to the paraspinal region, with thefingers apart and the thumbs touching each other in a lineparallel to the line of the spinous processes. With the “bar”formed by the thenar eminence of the thumbs, the examinerslowly pushes the paraspinal muscles, as if trying to pushthem away from the spinous process and detach them fromthe deeper fascial plane. When maximum tension is reached,the examiner pauses, slowly exaggerates the pressure, andthen releases it. This gesture is performed in a rhythmic andcontrolled manner, without losing contact, even during theperiod of relaxation.

Figure 67.4

The examiner’s thumbs are placed on each sideof the line of the spinous process and perform slow, deep,gliding maneuvers that are very relaxing and should be per-formed slowly and rhythmically.

N.B.

These maneuvers often serve as an indispensable start tospinal mobilization and manipulation.

Figure 67.5

The physician places both hands under thepatient’s flank, with the fingertips nearly in contact with thetransverse processes. The physician then pulls back on theclosest lumbar muscles while the wrists act as a lever pushingthe fingers upward. The pressure–traction is maintained fora while, relaxed, and then the movement is repeated. Themaneuver is very sedating and is performed for acute lowback pain.

Figure 67.6

The physician stands to the right of the patient,whose legs are flexed. With the right hand, the physiciantakes the patient’s knees while the left hand grasps thepatient’s left lumbar muscles. The knees are maintained inposition, while the examiner pushes them back and pulls theerector spinae mass upward. This is performed slowly andrhythmically.

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457

Patient lying on side: fanning maneuver (Fig. 67.7) —

The patient lies on the right side with knees and hipsflexed. The physician stands in front and rests the rightforearm on the iliac crest, while the left forearm restsagainst the patient’s axilla. The hands are placed side byside over the patient’s flank. Using the fingertips in a claw-like fashion, the examiner grasps the left erector spinaemass and pulls the mass upward and back, while pullingthe forearms apart, like a fan, which distracts the shouldergirdle away from the pelvic girdle.

Stretching

These techniques constitute efficacious means of treat-ing trigger points.

Gluteus Medius and Tensor Fascia Lata

The patient is prone.

Figure 67.7

Fanning technique is used.

Figure 67.8

The physician grasps the distal leg above theknee and crosses it over the other leg, while applying coun-terpressure on the iliac crest with the other hand. This positionis maintained for a few seconds, with stretching progressinga little more for each maneuver.

Figure 67.9

The examiner’s knee can be used for thismaneuver. The flexed knee rests on the superior part of theleg of the patient near the knee, and by pressing downward,stretches the gluteus medius and the tensor fascia lata.

458

SECTION VII MANUAL TECHNIQUES

External Rotators of Hip

Internal Rotators of Hip

This maneuver, the opposite of the preceding one, canact especially on the gluteus minimus. A component ofadduction incorporated into the technique increases theeffectiveness of this maneuver on this muscle, which actsas an internal hip rotator as well as an abductor.

Extensors of Hip and Spine

At the start, the patient is supine, with the lower limbsextended. The physician squats and places both of thepatient’s legs on the shoulder. With the right hand, thephysician dorsiflexes the feet. The dorsiflexion is main-tained and slightly increased during the maneuver. Withthe left hand, the physician locks the knees in extension,and progressively stands up. In doing so, the physicianslowly raises the patient’s lower limbs until pain isreported (i.e., to the limit of what is bearable), then stops,lessens the tension slightly, and maintains this new posi-tion for 15 to 30 sec (sometimes more). The tension isgradually increased in a stepwise fashion and interspersedwith periods of relaxation, until the maximum length pos-sible is reached. With each step, the initial painful feelingmust dissipate gradually while the tension is maintained.Throughout the maneuver, the patient is encouraged tobreathe regularly and deeply (Fig. 67.11).

Figure 67.10

The patient is prone with the leg flexed 90° onthe thigh (to the left). The examiner stands opposite the sidebeing treated. The right hand blocks the pelvis, while the lefthand pushes the sacrum and pushes the left foot of thepatient outward, which causes internal rotation of the hip andstretches the external rotator muscles. This maneuver is per-formed progressively and interspersed with stretching in aslow, rhythmic pattern tailored to the reaction of the muscle(usually the pyriformis). A maneuver with the same effect canbe performed with the patient supine, thighs and legs flexedat 90°.

Figure 67.11

This maneuver stretches the triceps surae,hamstrings, and gluteus maximus. If the only aim of themaneuver is to stretch these muscles, the patient’s handscan be crossed behind the neck (as shown). If the intent isto act on the paraspinal muscles as well, then the patient’sarms should be kept along the body, with the shoulders downin a caudal direction and the chin in to eliminate the cervicallordosis.

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459

Axial Traction of Leg

This maneuver must be executed in three phases: (a)the examiner firmly grasps the patient’s foot; (b) with thelower limb completely relaxed, the slack is taken up pro-gressively; and finally (c) a sudden traction. The exam-

iner’s feet must be well under control. This maneuver canalso produce good relaxation of the gluteal muscles(Fig. 67.12). It is contraindicated in sciatica, which couldbecome serious.

Figure 67.12

460

SECTION VII MANUAL TECHNIQUES

MOBILIZATION

These maneuvers act on the spine by mobilizing to endrange and including the affected segments in the chosendirection. They also gradually lengthen the muscles. Themovements must be applied slowly, repeatedly, and pro-gressively. When muscular stretching is desired, the musclesshould be maintained in tension for several seconds.

In Flexion

Contact on Both Knees (Fig. 67.13 and Fig. 67.14)

The patient is supine, with both knees and hips flexed(Fig. 67.13). The physician applies the hand and forearmto the patient’s flexed knees and exaggerates pressure inthe direction of the patient’s head, bringing the lowerlimbs into hyperflexion. This maneuver must be repeatedslowly, insisting a little more each time.

Variation —

The examiner’s shoulder holds thepatient’s legs. The examiner then bends forward andincreases the lumbar flexion to take up the slack, and thenreleases and starts again slowly (Fig. 67.14).

Contact on One Knee (Fig. 67.15)

The physician stands beside the table (e.g., at right)and faces the head of the table. The left hand is appliedto the patient’s right shoulder while the right hand graspsthe flexed knee. The degree of hip and knee flexion is thenexaggerated, pushing the lower limb toward the ipsilateralshoulder (Fig. 67.15). This maneuver is gradually releasedand repeated. This is a mobilization in pure flexion. How-ever, if the physician pushes the thigh toward the con-tralateral shoulder, flexion and slight rotation result(Fig. 67.16).

Figure 67.13

Figure 67.14

Figure 67.15

Figure 67.16

CHAPTER 67 LUMBAR TECHNIQUES

461

In Lateroflexion

The patient is lying on the side. This maneuver isexcellent, but powerful; it must be done with great care,progressively, and must be repeated slowly (Fig. 67.17 andFig. 67.18).

Figure 67.17

This maneuver mobilizes the patient into left lateral flexion. The patient lies on the right side, with legs and hipsflexed 90

°

. The physician stands, hips and knees partially flexed, facing the patient. The physician’s left elbow blocks thepatient’s left shoulder, and the right hand grasps the patient’s ankles and places the knees on the physician’s thighs. Thephysician then pulls the patient’s ankles upward while pushing anteriorly with the abdomen. This produces left lateral flexionof the patient’s lumbar segments. The pressure is then released and returned to the starting position.

Left,

positioning.

Right,

taking up slack.

Figure 67.18

Same maneuver shown from another angle reveals the position of the examiner’s left arm.

Left,

positioning.

Right,

taking up slack.

462

SECTION VII MANUAL TECHNIQUES

In Extension

The patient is prone. The physician stands beside thetable and grasps the patient’s distant thigh just proximalto the knee, while the other hand is applied to the lumbarregion. The examiner then rhythmically extends the hipwith counterpressure applied to the lumbar region(Fig. 67.19). With this technique, a certain degree of lat-eroflexion can be combined with extension by combininghip adduction with hip extension. A similar maneuver canbe done by simultaneously extending both of the patient’sthighs (Fig. 67.20).

In Rotation

The patient is seated astride the end of the table, armscrossed on the chest. The physician stands behind andgrasps the patient’s right forearm with the left hand, whilethe right hand is applied to the paraspinal region. Theexaminer then gradually increases the degree of lumbarrotation imparted by the left arm. As in the thoracic tech-niques, the examiner’s right elbow is held firmly againstthe iliac crest to transmit the force of pelvic rotation tothe patient’s lumbar spine. Mobilization is applied prima-rily by rotation of the examiner’s pelvis, while the left armacts in synchrony to bring the patient’s trunk into leftrotation (Fig. 67.21). This maneuver is identical to thatdescribed for the thoracic spine.

N.B.

From the astride position at the end of the table, allaccessory orientations are possible (flexion or extension, ipsilat-eral or contralateral lateroflexion). It is the position that we usefor examining the mobility of the lumbar spine as well as forcertain manipulations.

Figure 67.19 Figure 67.20

Figure 67.21

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463

MANIPULATION

(Basic) Lateral Decubitus Technique in Flexion (Fig. 67.22)

Positioning —

The patient lies on the right side, withthe head resting on a pillow, and the top lower limb flexedat the hip and knee (in this example, the left one). Theexaminer faces the patient and pulls the patient’s lowerarm (here, the right one) so that the plane of the shouldersis 45° to the plane of the table. The lower leg is extendedat the knee, with the thigh in very slight flexion. The footis positioned off the edge of the table at the corner andfacing downward (Fig. 67.23).

Figure 67.22

This maneuver imparts left rotation (

a

) to the lumbosacral segments by exaggerating the flexion (

b

).

Figure 67.23

The lower leg (here the right one) is kept in extension at the knee during the entire maneuver. The foot is pointeddown.

464

SECTION VII MANUAL TECHNIQUES

The examiner’s left hand is placed on the patient’s leftshoulder and firmly maintained; this is the fixed point(Fig. 67.24, top left),

and it does not move during themanipulative thrust. The physician then places the rightforearm against the patient’s upward facing ischium. Thevector of manipulation applies a downward and distractiveforce to the patient’s left hemipelvis, resulting in tractionin flexion, with slight left rotation. During this procedure,the physician stands close to the table. The physician’sright knee blocks the patient’s left thigh to maintain itfirmly and to assuage any patient fear of falling off thetable.

Taking up slack —

Once in position, the physicianrotates the patient’s body (which must move as a block)

anteriorly (Fig. 67.24, top right). The ischial pressure is

then increased to produce pelvic rotation (from right to

left) while the left hand firmly fixates the shoulder

(Fig. 67.24, bottom left).

Manipulative thrust —

Once the slack has been taken

up, the examiner suddenly increases the pelvic rotation

with the right elbow on the ischium. The manipulative

thrust is applied downward and to the right (Fig. 67.24,

bottom right).

N.B.

The anterior rotation of the patient’s trunk is well shown

in Figure 67.26, as is the blocking of the patient’s left thigh by

the right knee of the examiner.

Figure 67.24

Different phases of manipulation.

CHAPTER 67 LUMBAR TECHNIQUES

465

The technique shown in Fig. 67.25 and Fig. 67.26 canbe compared with the movements used in archery. Theleft hand pushes back the left shoulder while remainingfixed at the time of manipulative thrust. At the same time,the right forearm pulls in the opposite direction, downwardon the pelvis (Fig. 67.25, Fig. 67.26a and b, andFig. 67.22b).

Variation of Manipulation in Flexion (Fig. 67.27)

The patient lies on the right side. The physician doesnot use the hand to fixate the patient’s shoulder, butinstead, passes the forearm under the patient’s axilla. Theleft hand now approximates the right one. This technique

allows better control of the segment to which the rotation

is applied. By varying the amounts of shoulder inclination,

thigh flexion, and the direction of the manipulative thrust

by a few degrees, the physician can execute a precise and

effective manipulation, but this maneuver does not allow

as forceful an axial traction as the preceding one.

Figure 67.25

Figure 67.27

Figure 67.26

466

SECTION VII MANUAL TECHNIQUES

(Basic) Lateral Decubitus Technique in Extension

Positioning —

The patient lies on the side (on the rightside for left rotation). For extension of the lumbar spine,the left leg is flexed at the knee, and the dorsum of thefoot rests against the right popliteal fossa. The plane ofthe shoulders is perpendicular to the plane of the table.The lower leg is placed on the table in extension to facil-itate the spinal extension. The examiner, standing in frontof the patient, fixates the patient’s shoulder with the lefthand and maintains it during the entire maneuver

(Fig. 67.28). The examiner’s right hand is the active hand.

It makes contact with the lateral iliac crest. The forearm

is perpendicular to the plane of the back.The iliac hand brings the patient’s body into rotation

around an axis that passes from head to toes, while the

left hand, opposing the global movement, maintains the

left shoulder of the patient in the position it had at the

start (Fig. 67.28b and Fig. 67.29).

Figure 67.28

This maneuver imparts left rotation to the lumbosacral segments (

a

) by forcing extension (

b

). The iliac positionthus differs from that used in the flexion technique.

Figure 67.29

Contact with the iliac position can also be made with the forearm.

CHAPTER 67 LUMBAR TECHNIQUES

467

The aim of the maneuver is to produce rotation of thelumbosacral spine (in this example, left rotation) and forcethe extension. The iliac placement thus differs from theone described in flexion (Fig. 67.28 through Fig. 67.30).

Note the difference between the positions of the exam-iner in Figure 67.30, left and right, showing the momentof the forward manipulative thrust and the arm that isperpendicular to the axis of the patient’s body.

Taking up slack —

The physician then progressivelyrotates the left iliac crest anteriorly, bringing the lumbosac-ral spine into extension and left rotation (Fig. 67.28a).

Manipulative thrust —

The thrust is applied perpen-dicular to the axis of the spine, inferiorly and anteriorly(Fig. 67.30). The patient’s left shoulder is firmly fixatedby the examiner’s left hand throughout the maneuver.

N.B.

During the entire maneuver, the physician’s thighs mustmaintain pressure against the patient’s left thigh and knee, sothat the patient is not concerned about falling from the table(Fig. 67.31).

Variation

The technique shown in Fig. 67.32 is sometimes morecomfortable for the examiner. The superior (right) leg ofthe patient is placed between the examiner’s thighs. Thetechnique is then the same as that described above.

Figure 67.30

Left,

positioning.

Right,

taking up slack; manipulative thrust.

Figure 67.31

Figure 67.32

468

SECTION VII MANUAL TECHNIQUES

Lateral Decubitus Technique in Neutral Position (without Extension or Flexion)

First Technique (Fig. 67.33, left)

The positions for both patient and physician are thesame as in the technique described above. The active(right) hand is applied to the left edge of the sacrum. Asin the technique in extension, the forearm is perpendicularto the plane of the patient’s back. Thus no component ofthe thrust produces anterior pelvic rotation, as in the exten-sion technique, nor any posterior rotation, as occurs withthe flexion technique.

Second Technique (Fig. 67.33, right)

The patient is supine, with arms crossed anteriorly andleft leg flexed at the hip and knee. From the patient’s rightside, the examiner’s left hand grasps the patient’s wristsfirmly to block trunk movement. The examiner’s righthand then grasps the patient’s left leg, distal to the kneeto bring the hip into 90° of flexion. The examiner thenpulls in the thigh with a thrust directed downward.

Fig. 67.34 summarizes the various permutations andcombinations of the lumbar lateral decubitus technique(described above and shown in Fig. 67.22 through Fig.67.33). Much of what distinguishes these techniques isdue to the angle and direction of the manipulative thrustexecuted.

Figure 67.33

CHAPTER 67 LUMBAR TECHNIQUES

469

Figure 67.34

Starting from the same patient position (lyingon side, superior leg flexed at hip and knee), it is possibleto obtain a different orientation of the manipulation.

A.

Theforearm is applied to the sacrum parallel with the axis of thespinal column. The resultant movement is essentially tractionin flexion; there is practically no rotation.

B.

The contact pointis the distal forearm on the ischium. There is still manipulationin flexion with segmental traction, but already a certaindegree in rotation.

C.

The contact point is the inferior buttock.There is notable rotation with the lumbar spine in slight flexion.

D.

Same point of contact, but the manipulative force is per-pendicular to the spine. Significant rotation of the lumbosacraljunction is produced, in neutral position.

E.

The contact pointis the superior iliac crest. This produces rotation, but with thespine in extension.

F.

Same point of contact, but the manip-ulative force is perpendicular to the spinal column, producingrotation in significant extension.

470

SECTION VII MANUAL TECHNIQUES

(Basic) Astride Technique

This maneuver has already been described for the tho-racic spine. It is the technique of choice for rotationalmanipulation of the thoracolumbar junction and can beutilized for the lower lumbar spine as well. It may also becombined with other coordinates including flexion, exten-sion, rotation, or lateroflexion. It can be used in mobili-zation or in manipulation, and permits both assisted andresisted manipulative techniques. Moreover, this is anexcellent position for examining and testing lumbarmotion and detecting subtle degrees of painful limitation.

Manipulation in Pure Rotation

Positioning —

The patient is seated astride the end ofthe table, back to the examiner. Several arm positions arepossible, including hands folded behind the neck(Fig. 67.35, bottom left); arms crossed anteriorly(Fig. 67.35, top right); and one hand behind the neck, withthe other grasping the opposite elbow (Fig. 67.35, bottomright). The hand-on-neck position is generally preferableif significant lateroflexion or rotation is desired, but theposition chosen will depend on the size of both patientand examiner [see “(Basic) Epigastric Technique” inChapter 66].

Figure 67.35

Different patient arm positions.

CHAPTER 67 LUMBAR TECHNIQUES

471

For left rotation, the examiner passes the left forearmin front of the patient’s thorax and grasps the right armnear the elbow. The examiner’s right thenar eminence isapplied to the right transverse process of the vertebra tobe manipulated. The forearm is held horizontally,perpendicular to the patient’s trunk. However, if a vari-able-height table is not available, the examiner’s legs areflexed to adjust the position. The right elbow may remainfree, but it is best to place it against the anterior iliac crest(Fig. 67.36).

Taking up slack —

At the start of the maneuver, thephysician is slightly to the patient’s left. The physician’s

left hand brings the patient’s trunk into left rotation.Simultaneously, the examiner uses small gliding steps topivot around the patient, while firmly maintaining thecontact on the transverse process and progressively takingup the slack to end range in rotation. At that moment, mostof the examiner’s weight has been shifted to the right foot.

Manipulative thrust —

With the elbow still in contactwith the iliac crest, the manipulative thrust is executed bytransmitting pelvic rotation to the right forearm. (Fig. 67.36).This technique is described in detail in Chapter 66,“(Basic) Sitting Astride Technique.”

Figure 67.36

Three phases of manipulation.

Top left,

posi-tioning.

Top right,

taking up slack.

Bottom left,

manipulativethrust. Top left and top right show the patient in the arms-crossed position, while to the bottom left, the hands-on-neckposition is shown. The rest of the maneuver follows the usualtechniques.

472

SECTION VII MANUAL TECHNIQUES

Manipulation in Rotation Combined with Lateroflexion, Flexion, or Extension

This technique allows one to combine rotation withlateroflexion, flexion, or extension. For example:

• Manipulation in left rotation and left lateroflexion(Fig. 67.37).

• Manipulation in left rotation, flexion, and left later-oflexion (Fig. 67.38). In this variation, the thumb isapplied to the patient’s spinal segment.

• Manipulation in left rotation, extension, and leftlateroflexion (Fig. 67.39).

The manipulation can also be executed with combinedcontralateral lateroflexion. Certain authors consider thisto be a sacroiliac manipulation because the spinal segmen-tal motion is blocked by the lateroflexion. The maneuveracts on the ipsilateral sacroiliac joint (Fig. 69.8).

Figure 67.37

Figure 67.38

Lower lumbar manipulation into left rotation, with the spine in left lateral flexion and forward flexion.

Figure 67.39

Manipulation at L3 into left rotation to the left,with the spine in extension and left lateral flexion.

CHAPTER 67 LUMBAR TECHNIQUES

473

(Accessory) Double Knee Technique (Fig. 67.40)

Positioning —

The patient is seated on a stool, fingerscrossed behind the neck. The physician is seated behindon the table, at a slightly higher level than the patient,with the balls of the feet resting on a bar of the stool sothat the two knees are in contact with the segment to bemanipulated. The heels are lowered as the examiner passesthe forearm under the patient’s axillae and grasps thewrists (Fig. 67.40).

Taking up slack —

This is executed in two steps. First,the examiner slightly flexes the arms, pulling the patientback by the shoulders until a firm resistance is felt. Careis taken not to increase pressure on the patient’s neck toavoid altering the flexion applied at the start. The patient’shands must be tightly clasped. Second, the examiner thenlifts the heels. This increases the pressure of the kneesagainst the spine and takes up the slack (Fig. 67.41).

Manipulative thrust —

The examiner briefly pullsboth arms slightly upward and back. This powerfulmaneuver must be executed gently. As with all manipula-tion, it must be strictly painless. Fig. 67.40 shows thestarting position; Fig. 67.41, the intermediary position;and Fig. 67.42, the position at the end. Fig. 67.41 showstaking up the slack (first step); Fig. 67.40, positioning; andFig. 67.42, taking up the slack (second step) and manip-ulative thrust.

Figure 67.40

Positioning.

Figure 67.41 Taking up slack (first technique).

Figure 67.42 Taking up slack (second technique) andmanipulative thrust.

474 SECTION VII MANUAL TECHNIQUES

(Accessory) Belt Technique

This technique allows one to perform manipulation inpure rotation, rotation with ipsilateral lateroflexion, androtation with contralateral lateroflexion. It is a powerfuland delicate maneuver. The arms act as such powerfullevers that the risk of patient injury is significant in anuntrained examiner’s hands.

In Pure Rotation

Right rotation is illustrated in Fig. 67.43 through Fig.67.46. The effect of the maneuver is on the thoracolumbarjunction.

Positioning — The patient is prone and is attached tothe table with a large belt over the sacrum. For a manip-ulation in right rotation, the physician squats on thepatient’s right side, facing the shoulders (Fig. 67.43). Thepatient’s right arm is on the physician’s right shoulder.The physician’s right hand grasps the patient’s left shoul-der, while the patient’s left hand, flat, is placed against theexaminer’s back (Fig. 67.43). During the positioning, thepatient must remain in the center of the table. The physi-cian must rise and move forward over the examining table(Fig. 67.43). Finally, the examiner places the left hypo-thenar eminence over the transverse process of the targetvertebra (Fig. 67.44).

Taking up slack — The physician gradually leansforward, moving the patient with the shoulder, and slowlyrises halfway up on the knees (Fig. 67.45). This impartsa degree of rotation to the patient’s trunk, acting maxi-mally on the thoracolumbar junction.

Manipulative thrust — A slight push forward of theright shoulder gives the manipulative thrust (Fig. 67.45and Fig. 67.46). This manipulative thrust must be mea-sured. During the entire maneuver, the patient’s chest

Figure 67.43

Figure 67.44 Positioning.

Figure 67.45 Taking up slack.

Figure 67.46 Manipulative thrust.

CHAPTER 67 LUMBAR TECHNIQUES 475

should not move excessively on the table. The lumbarhand assists the movement by applying pressure over theleft transverse process of the vertebra to be manipulated(Fig. 67.46). The patient’s right shoulder should never losecontact with the table. The patient must not be lifted whenthe physician rises. During the maneuver, the examinermust maintain the patient on the table and ensure that thepatient does not rise. The patient is simply turned on theaxis. As the physician’s shoulder drives forward andslightly downward, the patient’s lower shoulder is pulledtoward the examiner (Fig. 67.43). The lumbar spineshould not be in extension.

In Rotation with Ipsilateral Lateroflexion

A component of ipsilateral lateroflexion allows themanipulation to act on the lumbosacral and lower lumbarsegments. Fig. 67.47 illustrates right rotation and latero-flexion.

Positioning — The physician pulls in the patient andbrings the head and shoulders off the end of the table(Fig. 67.47). The rest of the maneuver is applied as above.Fig. 67.47 shows the different actions. The right arm ofthe examiner must assure that the patient remains “glued”to the table. The patient must not, in any case, be lifted.When the top of the patient’s chest comes over the end ofthe table, the examiner must pull it downward when press-ing with the right shoulder.

Taking up slack and manipulative thrust — Theseare executed as in the preceding maneuver.

In Rotation plus Contralateral Lateroflexion

Figure 69.9 shows an example of left rotation and rightlateroflexion. This maneuver acts on the lower lumbarsegments, and the proponents of sacroiliac joint dysfunc-tion also consider it to act on the S1 joint. It is describedin Chapter 69.

Figure 67.47 Manipulation with lateral flexion performed onthe lumbosacral spine.

477

68

RIB TECHNIQUES

The techniques used in the treatment of the costalsprains are often the same as those used for examination.When examining, the aim is to try to evoke tendernesscaused by either rib elevation or depression. The samemaneuvers are utilized for treatment, with the addition ofa thrust at end range in the pain-free direction.

(ACCESSORY) FIRST TECHNIQUE (FOR INFERIOR RIBS)

In Fig. 68.1A, the 12th rib is painful when depressedand pain-free when elevated. Therefore, manipulation isperformed in elevation. The patient is seated astride theend of the table with arms crossed overhead. The examinerpositions the patient’s trunk in left lateroflexion. Thepatient is instructed to breathe calmly as the examinergrasps the rib to be manipulated with the fingertips of theright hand and maintains it in traction. At the end inspi-ration, the pressure is suddenly increased with a very slightthrust.

In contrast, if the rib is painful with elevation, it mustbe manipulated in depression (Fig. 68.1B). The patient ispositioned in left lateroflexion. The examiner’s thumb isapplied to the superior edge of the rib to be manipulated.At end expiration, the manipulative thrust is appliedlightly.

SECOND TECHNIQUE (FOR INFERIOR RIBS)

This maneuver is similar to the preceding one. To facil-itate lateroflexion of the patient’s trunk (in this example,to the left), the examiner’s left foot is placed on the tableso that the left knee rests under the patient’s left axilla.The rest of the maneuver is performed as in the precedingtechnique (Fig. 68.2).

Manipulation for Last Ribs: Second Technique

The patient is seated astride at the end of the table oron a stool. The physician’s knee passes under the patient’saxilla contralateral to the side of the rib to be manipulated.This induces trunk lateroflexion, which opens up theregion to be treated. The principle is the same as in thepreceding technique. Depending on the case, one musteither (a) slowly elevate the affected rib by grasping itsinferior border with the fingertips (Fig. 68.2, left) or (b)slowly depress the affected rib with maintained pressurethat is exaggerated at end expiration (Fig. 68.2, right).

Figure 68.1

Manipulation of lower ribs: first technique.

478

SECTION VII MANUAL TECHNIQUES

Variation: Patient Standing (Fig. 68.3)

In certain difficult cases, the technique shown inFig. 68.3 is used. The physician has one foot on the manip-ulation table, the other on the stool. The patient, standingin front, rests the axilla on the physician’s knee (right kneein illustration). The left arm is raised vertically with theelbow flexed and the hand placed behind the neck. Thephysician applies traction to the patient’s left elbow andthus increases the right trunk lateroflexion to open up thecostal region on which the manipulation will be per-formed, according to the same principles outlined for thetwo techniques (A and B) above.

Figure 68.2

Manipulation of lower ribs: second technique.

Figure 68.3

CHAPTER 68 RIB TECHNIQUES

479

THIRD TECHNIQUE (FOR MIDDLE AND INFERIOR RIBS)

The patient is seated astride the end of the table, handscrossed behind the neck or arms crossed on the chest(depending on morphology). To manipulate a right rib, theexaminer grasps the patient’s right arm with the left handand applies the right hand, flat, on the thorax, parallel tothe ribs (Fig. 68.4 and Fig. 68.5).

Figure 68.4

Manipulation in elevation. The examiner appliesthe lateral aspect of the index finger against the inferior bor-der of the rib to be manipulated. The upward pressure ismaintained throughout the entire maneuver. With the left arm,the patient’s trunk is placed into combined left rotation andleft lateroflexion. The right hand assists the movement. At endrange, the patient is instructed to breathe slowly and deeply.At end inspiration, a brief and light thrust is given, synchro-nously, with the left hand (which accentuates the trunk rota-tion) and the right index finger (which accentuates thepressure upward). This is done while the thumb appliesdownward pressure against the superior border of the angleof the posterior rib.

Figure 68.5

Manipulation into depression. This maneuver isperformed in a similar manner to that used with rib elevation.In this case, the palmar aspect of the index finger is appliedto the superior edge of the rib. With this finger, the examinerapplies constant downward pressure to the rib while the leftarm brings the trunk into rotation and left lateroflexion. Theactive finger maintains the downward rib pressure. At thesame time, the thumb applies upward counterpressure tothe inferior edge of the posterior angle of the rib, elevatingit. At end expiration, the pressure is gently and preciselyincreased to perform the manipulation, while a slight thrustis applied with the left hand to increase the rotation of thetrunk to the left.

480

SECTION VII MANUAL TECHNIQUES

TECHNIQUE FOR FIRST RIB

The patient lies on the back, with the arm on the sideof the rib to be treated lying along the body. For a left rib,the examiner, on the right side of the patient, places theright hand flat on the table, palmar side up, the thenareminence resting on the posterior part of the first or secondrib at the level of its angle. The other hand rests on theanterior part of the rib, near the sternum. This hand willexecute the manipulative thrust downward or upwardwhile the thoracic hand applies counterpressure(Fig. 68.6). This maneuver is delicate, requiring closeattention when taking up the slack and precision whenapplying the terminal thrust.

TECHNIQUE FOR ANTERIOR COSTAL SPRAIN

The patient is supine. The examiner places the thumbon the superior edge of the rib to be manipulated andassists the downward movement of the rib during expira-tion. The pressure is maintained and is gently but pro-gressively increased (Fig. 68.7). For this maneuver, it ismore comfortable to position the patient’s ipsilateral armas shown in the figure. The maneuver is reversed whenrib elevation is indicated (Fig. 68.8), applying the thumbto the rib’s inferior edge with both thumbs opposed endto end.

Figure 68.6

Figure 68.7 Figure 68.8

481

69

SO-CALLED SACROILIAC

JOINT TECHNIQUES

GENERALITIES

In the early 1900s, in the English-speaking world,joint sprains were thought to be responsible for mostcases of lumbosciatic pain. The first published case ofpost-manipulative paraplegia resulted from a manipula-tion performed under general anesthesia by an orthopedicsurgeon to treat “SI joint sprain” (Goldthwait).

When Barr and Mixter discovered the herniated diskin 1930, it appeared in a young patient with a refractoryacute sciatica attributed to “SI joint sprain.” They thoughtthat the source of the sciatic pain might be a tumor. Mixteroperated and discovered a “tumor” compressing the S1root. This tumor, thought first to be a chondroma, was aherniated disk. Micromechanical pathology of the SI jointhas been forgotten for quite a long time in traditionalmedicine but still has a place for most manipulators.Important for chiropractors and osteopaths, the principlevaries for manipulative physicians, depending on theschool. After having believed that SI joint microdisplace-ments were frequent, J. Cyriax later thought they wererare, then concluded that they did not exist (1976).

Although the slight but real joint mobility has beenproven, the existence of micromechanical pathology hasnot yet been validated. On the other hand, the techniquesused to unblock these joints are perfectly effective forcertain lumbar and lumbosacral dysfunctions. The ques-tion then is whether these so-called SI joint techniques acton the lumbosacral spine or on the SI joints themselves.

Semiology of SI Joint Disorders in Traditional Medicine

The clinical signs diagnostic of SI joint problems(inflammatory or infectious) in traditional medicine arefar from specific, but it is interesting to recall them. Theprincipal ones are:

• Posterior pain caused by gapping or compressingthe iliac wings with the patient supine (Fig. 69.1,top left and top right) or by compression of thesuperior iliac crest with the subject side lying, whichgives a similar result.

• The tripod sign (Coste et al.): the patient is proneand the examiner applies pressure on the sacrumwith the heel of the hand, which irritates the SI jointsand causes pain if they are affected.

• Gaenslen’s maneuver: the patient is supine and theexaminer leans on the patient’s flexed hip and knee(in this example, the right one), bringing them intohyperflexion. The patient’s other leg hangs over theend of the table while the examiner exaggerates thismovement by pushing the contralateral thigh down-ward into extension. This maneuver induces maxi-mal SI joint nutation on one side (Fig. 69.1, bottomleft) with counter-nutation on the other.

• This maneuver has the same aim. The patient ispositioned in side lying (in this example on the left)and is instructed to bring the downward-facing hipand thigh into full flexion with the arms. The exam-iner grasps the patient’s left (upward-facing) kneeand brings the thigh into hyperflexion. After apply-ing the left hand to the right iliac crest, the examinerhyperextends the upward thigh (Fig. 69.1, bottomright).

These maneuvers have both poor specificity and poorsensitivity, even in cases of inflammation of the SI joints.They can also be painful in some cases of lumbosacraldysfunction.

Semiology Proposed by Supporters of SI Joint Blockage

Certain authors and most of the school of manual med-icine believe that SI joint blockages are possible and evenfrequent. The diagnostic criteria are based on a certainnumber of signs that vary considerably depending on theschool or author. They are numerous and include:

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• Positions and variations of gaps of different land-marks: posterior superior iliac spines, sacral apex,tubercle of S2, ischium, etc. when the subject bendsforward, stands on one leg, or raises the knee to thechest.

• Modifications in tissues of the regions close to theSI joint and the influence of certain maneuvers onthese modifications.

• Joint mobility tested by palpation.

We now review these proposed signs.

J.B. Mennell’s Signs

Mennell believed that these “blockages” or “SI jointup-slips” were frequent. Among the numerous causes ofSI joint sprains, movements such as getting out of the tubor turning back suddenly when seated in a chair are themost frequent. Mennell recommended a series of exami-nation maneuvers, for the most part osteopathic tech-niques, that would rotate the iliac crest either forward orbackward to test the blockage and freedom of movement.Note that it was presumed that these maneuvers selectivelymobilized the SI joint and the SI joint only. However, thisis not certain.

In case of blockage, the following signs should befound:

• With the patient seated, the posterior superior iliacspine (PSIS) is lower than the one on the oppositeside if the iliac wing is blocked in posterior rotationon the sacrum. It comes back to the same level afteran adequate manipulation (this sign is described bythe osteopaths).

• There is an antalgic attitude in case of “acute SIjoint sprain” (antalgic scoliosis concave at theblocked side).

• A false Lasegue’s sign can exist. Contrary to whathappens with discogenic sciatica, dorsiflexion of thefoot does not increase pain if the condition is an SIjoint sprain.

• Lateroflexion is not painful in patients with SI jointsprain (unless it is acute).

• In cases of pure sciatica, it has a nerve root topo-graphy. To demonstrate clinically the mobility of theSI joints, Mennell measured the distance betweenboth PSISs of a patient, first sitting, then prone. Inthe latter position, he noted that the processes are1.5 cm closer. We tried to find this sign and did notsucceed. This measurement technique is quite diffi-cult and subject to significant error. Colachis et al.,using pins inserted in the iliac bones, found theopposite of Mennell’s results; that is, the processeswere slightly closer in the sitting position. Among12 cases, the maximum closeness was 1.5 mm,which is not clinically detectable.

Figure 69.1

Classical maneuvers for SI joint examination.

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Osteopathic Signs

As always in osteopathy, SI joint dysfunction isdetected by palpation techniques. According to M.C. Beal,the diagnosis of “anterior sacrum” (i.e., blockage in nuta-tion) or “posterior sacrum” (blockage in counter-nutation)is made according to classical osteopathic palpation.

Blockage in Nutation

• Local modification of the soft tissues with hyper-sensitivity to palpation over the superior part of thejoint.

• “Strained” gluteal muscles in the part adjacent tothe superior pole of the joint.

• “Tension” in the adductor magnus (both superiorheads), rectus femoris, and sartorius muscles.

• The interval between the median part of the sacrumand the ilium at the level of the superior pole seemsincreased in relation to the other side and to thenormal.

• The anterior superior iliac spine (ASIS) is higher onthe blocked side than on the other.

• The PSIS is felt relatively lower on the blocked side(sign noticed by Mennell and Piédallu).

• There is an apparent ipsilateral leg length shortening(false short leg) noticed on examination in supine.

• Finally, palpation reveals loss of mobility in the SIjoint that is blocked, at its superior pole.

Blockage in Counter-Nutation

• Local modification of the soft tissues with hyper-sensitivity to palpation over the inferior part of thejoint.

• “Strained” gluteal muscles over the inferior part ofthe joint.

• “Tension” to palpation of the inferior heads of theadductor magnus and pyriformis muscles.

• The interval between the median part of the sacrumand the ilium is decreased in relation to the oppositeside and to the normal.

• The ASIS seems relatively lower.• The PSIS seems relatively higher than the contralat-

eral one.• Palpation reveals loss of mobility in the SI joint at

the level of its inferior pole.

Motion testing is performed as follows. The patient isprone as the examiner passes the hand under the iliac creston the side opposite. The pelvis is gently rocked, whilethe examiner places the other hand over the SI joint regionto assess the degree of joint play that is present or lacking.In addition, the source of the motion restriction is deter-mined to be at either the superior or the inferior pole ofthe joint.

Signs Based on Alterations in Bony Landmarks

The various bony landmarks change position when thesubject moves from sitting to standing, bends the trunkforward, stands on one foot, or raises the knee to 90°. Bestknown in France is Pascal Piédallu’s test that seems tohave been developed especially in the chiropractic group.The tests most used seem to be the ones perfected byGillet, Liekens, and Gitelman. The bony location pointsare the PSIS, the sacral apex, the tubercle of S2, and theischium (Fig. 69.2).

Piédallu’s Test (Fig. 69.3)

Piédallu, speaking about the osteopathic arguments,finds that they are “indisputable but too subjective”:

The tactile changes in the periarticular tension correspondto reality. Probably one day, an appropriately sensitiveapparatus will be able to record them. But as long as theresearcher will have only his training and his tactile sub-jectivity to detect them, the personal bias and subjectivitymakes a truly objective assessment impossible. The samecan be said for the control of the joint mobility which,however, in difficult cases, remain the principal criteria.

He proposed a test that evaluated the “upward migra-tion of the posterior superior iliac spine” for blockage innutation (Fig. 69.3).

Figure 69.2

Contact points for motion testing performed onthe SI joints.

A,

tubercle of S2.

B,

tubercle of S5 (lowest).

C,

ischium

. D,

posterior superior iliac spine.

Figure 69.3

PSIS upward migration sign of Piédallu.

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• The PSIS is lower on the blocked side of the patientsitting on a hard surface (in standing position also,but that can be due to a real short leg on that side).

• If the patient is asked to bend forward at the waist,sitting or standing, the PSIS goes up during flexion,while the PSIS on the normal side (higher at thestart) is pulled to a much lesser extent and is lowerthan that on the blocked side at the end of the flexion.

This could be explained by the blockage and the con-tractures making the sacrum interdependent on the iliacon the blocked side, while there is a certain “play” on thefree side.

Other Tests

• The standing patient, facing a wall, leans forwardagainst it with arms extended. The examiner placesa thumb on each of the PSISs. The subject raisesthe right knee as high as possible to assess the rightSI joint (certain authors think that 90° is ideal).Normally, the PSIS on the side of the raised kneegoes down more than that on the stationary side. Ifthere is blockage, it does not descend (Fig. 69.2).

• The patient stands with the legs extended andslightly apart. The examiner places a thumb on eachPSIS and grasps the iliac crest with the other fingers.The patient is asked to laterally flex slowly to theright and to the left. Normally, the PSIS remains atthe same level.

• The patient stands with legs extended. The exam-iner’s thumb is placed on the lowest posterior tuber-cles of the sacrum, with the index finger on the PSIS.The patient bends forward. Normally, flexion resultsin divergence of the two fingers by 12 mm. Thesame maneuver is repeated on the other side. In caseof blockage, diversion no longer occurs.

• The patient stands with the legs extended. Theexaminer places the left thumb on the sacral tubercleof S2 and the right thumb on the PSIS. The patientraises the right leg with knee flexed. If the right SIjoint is free, the iliac spine goes down 5 mm inrelation to the sacral point location; if the right SIjoint is blocked, it does not go down. The test isrepeated on the other side. Normally, the sacrummust be felt moving forward and downward,whereas the ilium moves backward and upward. Themovement detected would be 6 to 12 mm. If thereis blockage, the sacrum and ilium move together;there is no separation. Note the similarity of thesetests to Piédallu’s test.

Tests of Sell and Neumann

The German School of Manual Medicine also examinesfor SI joint dysfunction. Neumann selected the tests that

seemed to him to be the most reliable and the most sen-sitive for revealing SI joint blockage. He describes twopathologic situations in the SI joint: (1) loss of normalplay (hypomobility), and (2) excess of movement in rela-tion to normal play (hypermobility). Only the first case isamenable to manipulative treatment. The tests of SI jointblockage, according to Neumann, are:

• Decrease in joint play• Reflex dysfunction in the S1, S2, and S3 regions

Decrease in joint play —

This is evaluated by maneu-vers called spring tests. The first test is similar to theosteopathic test discussed above. The patient lies proneand the examiner palpates the SI joint with one hand. Thefinger used for palpation is placed over the SI joint space,with the fingertip touching the sacrum and the ilium. Withthe other hand, the examiner grasps the anterior part ofthe iliac crest and gives rapid vibrating thrusts to the iliaccrest. If the vibrations are properly transmitted to thepalpating hand, the conclusion is that there is blockage,and if they are poorly transmitted, it means that the artic-ulation is free.

In the second test, the SI joint is also palpated, withthe subject and the examiner’s hand in the same positionswhile the other hand exerts spring pressures on the caudalpart of the sacrum. If the SI joint that is tested is free, asmall part of the thrust is transmitted to the sacrum. If thearticulation is blocked, it is felt completely.

For the third test, the patient is supine. The finger usedfor palpation is in the same position as for the precedingtests. The hand used for mobilization grasps the leg belowthe knee, flexes the hip to 90°, and adducts the leg untilthe slack is taken up in the SI joint. The joint is repetitivelymobilized at end range with a gentle repetitive springingmovement. The finger palpating the SI joint feels whetherit moves or not.

Neumann insists on the difficulty of palpating a jointwhose mobility is subtle.

Reflex signs —

The muscles receiving their innerva-tion from S1, S2, and S3 — the glutei, hamstrings, calfmuscles, and some adductors — are affected and presentwith taut bands with or without trigger points. Taut musclebands have been found one finger breadth outside the PSISin the medial part of the gluteus maximus while the restof the muscle is hypotonic. These cords are good signs ofSI joint blockage according to Sell and Neumann.

These signs decrease if traction is applied to the leg onthe locked side, associated with a caudal support on thesacrum. On the other hand, they increase with the oppositemaneuver, that is, support on the base of the sacrum withtraction to the contralateral lower limb (Sell).

Other Signs.

Neumann also looked for:

• A sign similar to Piédallu’s sign with the patientstanding, then sitting. If it was positive, it might

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mean there was a blockage of the SI joint; but itcould also result from a reflex blockage of superiorcervical origin or of Ll–2 (Gutmann).

• The pseudo-Lasegue sign (after Mennell).• A decrease in the adduction of the thigh on the side

of the blocked SI joint.

Palpation of the iliopsoas muscle below ASIS in theinguinal canal is tender. In fact, Neumann declares thatthe diagnosis of SI joint blockage is made on the conver-gence of several signs, as they are rarely present together.

Personal Opinion

The diverse signs that are proposed to demonstrate SIjoint blockage are subtle as Piédallu and Neumann note.When they are clear, they certainly correspond to a dys-function, but it is unclear whether it arises from blockageof the SI joints. In almost all cases in which theresponsibility of the SI joint seems possible, clinicalexamination of the spine on the basis of segmental pain(PMID), as we do it, shows the probability of the lum-bosacral or thoracolumbar origin of the problem. Theimpairment of these segments also explains the tissuechanges that are perceptible to palpation (cellulotenope-riosteomyalgic syndrome):

• In the thoracolumbar junction syndrome, the tissuedysfunction involves the subcutaneous tissues over-lying the SI joints, with pain and thickening onpalpation (pain and perturbations that one would betempted to assign to the subjacent articulation).

• Irritation of the lower lumbar facets and posteriorrami brings perturbations in the retrosacral muscu-loligamentous tissues.

• The posterior ramus of S1 contributes to the inner-vation of the SI joint.

The perturbations in texture and sensitivity of the tis-sues found on palpation make it difficult to appreciate SIjoint mobility by palpation, if it is in any way possible.Piédallu’s sign seems often, like the other signs, to indicateonly a slight antalgic attitude. SI joint sprains can certainlybe seen in particular cases (e.g., end of pregnancy, a fallon the ischium, or a fracture of the pelvis), but even inthese cases, the clinical picture is not very specific. Thosewho think that SI joint blockages are possible use palpa-tion tests to diagnose them, as they use palpation tests todiagnose segmental vertebral dysfunctions, focusing onlyon the mobility, not on the provoked pain that we believeis essential to the concept of PMID that we propose toexplain pain coming from the spine.

The problem can be summed up as follows. In certaincases, subtle signs on examination lead to the diagnosisof SI joint blockage. The improvement of these signs bymaneuvers that are considered to produce specific actionson these joints is taken as confirmation of that diagnosis.

Unfortunately, no diagnostic sign is specific for SI jointdysfunction, and no manipulation acts only on the SI joint.Thus, it seems difficult to describe in the present state, a“syndrome of SI joint blockage” that would be welldefined, with clear and objective signs of examination.

N.B.

A very interesting study was done by B. Sturesson et al.involving the movement of the SI joints in 25 patients who wereconsidered to have problems at that level (according to Lewit’scriteria, similar to Neumann’s). The movements were studiedwith radiologic stereophotogrammetric instrumentation atextreme range and under the influence of loads. The authorsnoticed that the mobility of the joint was limited, even in youngpatients. Rotation of 2.5° between the extreme positions andtranslation of 1 mm was measured (0.1 to 1.6 mm). There wasno difference between symptomatic and asymptomatic SI joints.The authors remarked that their measures were far from the 6°of Weisl and the 9 or 10° estimated by Grieve. If these resultsare confirmed, it would greatly relieve our doubts about thereality of the blockages of this joint and the possibility of testingits mobility by palpation.

SO-CALLED SI JOINT MANIPULATIVE TECHNIQUES

The techniques that we describe here or that we recallare considered by proponents of SI joint blockages to bemaneuvers capable of treating them; they also act stronglyon the lumbar spine and even the thoracolumbar region.

Two types of blockages in general are considered, onein nutation, the other in counter-nutation. The maneuversthus are aimed at freeing the blocked movement by mov-ing the iliac crest forward in relation to the sacrum for ablockage in nutation (Fig. 69.4a), or by moving the sacrumforward in relation to the iliac crest for a blockage incounter-nutation (Fig. 69.4b). Some authors consider onlythe global loss of mobility of the SI joint and do notdifferentiate these two types (Neumann). For others, thereare an infinite number of ways in which the SI joint canbe blocked and as many tests to differentiate them.

First Technique

The lateral decubitus maneuver in extension, asdescribed for the lumber spine (Fig. 69.5), is often pro-posed as manipulation of the SI joint destined to correcta blockage in the “anterior sacrum” or a blockage innutation.

Second Technique

The aim of the second technique is anterior rotation ofthe iliac crest (Fig. 69.6). The patient is prone. The exam-iner stands on the side opposite the target SI joint (in thisexample, the left one). The left lower limb of the patientis placed in extension, and the examiner then steps over

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it so that the patient’s left leg is held against the examiner’spopliteal crease. This pulls the patient’s left lower limbinto extension and adduction. The examiner then graspsthe anterior part of the patient’s iliac crest with the lefthand and reinforces this action with the right hand.

He then takes up the slack with the left leg, whichincreases the adduction while firmly maintaining thecounterpressure of the hands on the iliac crest. Once theslack has been taken up, a sudden thrust of the handsdownward and slightly outward on the iliac crest willresult in manipulation.

Third Technique

Fig. 69.7 shows a maneuver in flexion with contact onthe right PSIS. The examiner applies a posterior rotationto the ilium capable of treating a blockage in the “posteriorsacrum” (blockage in counter-nutation).

Fourth Technique

This astride technique (Fig. 69.8) with combined rightlateroflexion and left rotation is considered to act on theright SI joint whose blockage in “posterior sacrum” wouldbe corrected. The heel of the right hand is applied to theright superior part of the sacrum.

Fifth Technique

Fig. 69.9 shows a maneuver in left rotation and rightlateroflexion of the lumbosacral spine. The belt is fixedabove the PSISs. It is also a manipulation for blockage in“left anterior sacrum” (in nutation). The examiner’s righthand presses on the right PSIS.

Sixth Technique

Traction on Leg

Certain American osteopathic doctors, especially Fry-ette, consider sudden axial traction of the lower limb oneof the best techniques of SI joint manipulation. According

Figure 69.4

a.

Nutation.

b.

Counter-nutation.

Figure 69.5

Figure 69.6

Figure 69.7

CHAPTER 69 SO-CALLED SACROILIAC JOINT TECHNIQUES

487

to him, it must be applied with precision so that its actionis precisely localized on the SI joint.

With one examiner —

The patient is supine. Theexaminer grasps the patient’s leg above the malleoli. Thepatient is asked to relax and to keep the leg well relaxed.The examiner slowly swings the leg with small and slowmovements and then leans progressively backward, witharms slightly bent. Slowly the leg is pulled toward theexaminer, applying axial traction. With the slack taken up,the examiner applies strong and brief traction. Two posi-tions of the lower limb are possible:

1. The leg is level with, or slightly below, the levelof the table. This partially takes up the slack ofthe anterior muscles (Fig. 69.10).

2. The leg is above the table, taking up the slackof the hamstring muscles (Fig. 69.11). In thefirst case, it would produce an anterior rotationof the iliac crest, thus unblocking a sacrumblocked in nutation (anterior sacrum) and in thesecond case, would act on a sacrum blocked incounter-nutation (posterior sacrum).

Figure 69.8 Figure 69.9

Figure 69.10

Manipulation of SI joint blockage in nutation according to Fryette.

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This maneuver can be useful in certain lumbar prob-lems not necessarily of SI joint origin. It is delicate in itsapplication because taking up the slack can be painlesswhile the sudden traction can cause a sharp pain and could

seriously aggravate a discogenic problem that it can some-times relieve.

With two examiners —

A similar technique can bedone with two examiners (Fig. 69.12 and Fig. 69.13).

Figure 69.11

Manipulation of SI joint blockage in counter-nutation according to Fryette.

Figure 69.12

Manipulation for blockage in nutation: anterior rotation of iliac spine. The patient lies on the side. The firstexaminer maintains the ilium in rotation anteriorly, and in so doing presses on the iliac spine, which is pushed forward towardthe ischium, which is pushed cephalad. At the same time, the second examiner pulls briskly, with the leg slightly elevatedand slightly extended (see Fig. 69.10), while the first examiner firmly maintains that pressure.

Figure 69.13

Manipulation for blockage in counter-nutation: posterior rotation of iliac spine. The patient is lying on the side.The first examiner maintains the iliac in rotation posteriorly, placing one hand on the anterior iliac crest and the other at thelevel of the ischium so that the two hands exert a force that results in a posterior rotation. The second examiner pulls brisklyon the leg, which is slightly elevated and in flexion (see Fig. 69.11), while the first examiner maintains the pressure firmly.

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TECHNIQUES NOT REQUIRING

VERTEBRAL MANIPULATION

The fundamental principle underlying these techniquesis that they do not require vertebral manipulation. This ismost useful in conditions in which vertebral manipulationis contraindicated, as in cases of vertebral fragility as aresult of arthritis, osteoporosis, etc. These techniques canalso be useful in patients in whom these conditions arenot present. To be successful, these techniques must bemastered and executed correctly. On the whole, these tech-niques may not be as effective as techniques alreadydescribed but, in some cases, may be as efficacious if notmore so with a rapid onset of effect. In summary, theyconstitute useful methods complementary to other manualtechniques.

The basic maneuver that characterizes these techniquesand is tailored to the region involves a stretching of muscleand ligamental fibers performed perpendicularly to theiralignment which places them under tension somewhat asone might do in plucking the strings of an instrument suchas a guitar. The fingers firmly hook onto the muscle groupdemonstrated to be under tension. The muscle group isstretched until it escapes in the way a string of a musicalinstrument escapes when pulled to the side. This maneuveris facilitated and made easier in areas where there is anosseous prominence against which one can perform themaneuver. There are many different approaches to thisprocedure, depending on the muscle and the region con-cerned. The maneuver can be performed slowly using along trajectory with a gentle sweeping movement, or con-versely, it can be performed with a brief rapid locallyapplied movement. The experience of the physician willdetermine which maneuver will be performed.

TECHNIQUES APPLICABLE TO GLUTEAL REGION PAIN

This maneuver can be very useful in cases of lumbar orsciatic or joint pain. It is performed on myalgic cords thatare usually found in painful conditions involving the lastthree lumbar segments (cellulotenomyalgic syndrome).

These taut bands and trigger points play a variable role inthe overall pain of the patient. In certain cases, particularlythose that are chronic, the role played may be primary asdemonstrated by the response to this maneuver. The fol-lowing maneuvers can be highly efficacious in trainedhands.

The patient is seated or is leaning slightly with handspressing against the examining table. The physician, hook-ing onto the gluteus maximus muscle at its inferior borderwith his thumb firmly holding on in a hook-like fashion,pulls in an upward and outward movement which in asweeping fashion stretches the muscle toward the iliaccrest, along the way seizing the gluteus medius. At thispoint, the physician applies a degree of tension as ifattempting to stretch the muscle just under the iliac crest(Fig. 70.1). The second part of the maneuver at times mayfeel somewhat painful particularly in cases where sciaticamay be present and may sometimes trigger pain in theinvolved extremity which has been painful. The samemaneuver is repeated in a slightly different direction.Starting from the same point, it is directed upward andmore laterally and involves the gluteus minimus muscle.

Figure 70.1

The patient, standing, leans slightly forward withhands pressing against the examining table. The physicianhooks onto the gluteus maximus muscle with the thumb firmlyholding on in a hook-like fashion, which is pulled upward andoutward in a sweeping fashion stretching the muscle alongthe way, seizing the gluteus medius, and stretching it also.

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Maneuvers similar to these can be applied to the peritro-chanteric muscles.

After a transient sensation of swelling, the patient willfeel resolution of the pain if the maneuver has been suc-cessful. These maneuvers can be repeated many timesaccording to the results obtained and can complementother treatment schemes and, at times, replace them.

TECHNIQUES APPLICABLE TO THORACIC REGION

Muscle techniques —

The fundamental maneuverhere is also the perpendicular stretching of painfullyinvolved muscles. In some cases, the maneuver can beexecuted at a slight angle to the muscle axis forming an

×

. It can be performed gently in a brushing fashion orperformed with the thumb using it to hook onto the muscleand stretch slowly, eventually allowing the muscle toescape, as one would allow a guitar string to escape.

A related maneuver can be utilized at all paravertebrallevels. The thumb (always held in a hook-like fashion),holding onto the tight paravertebral myalgic cord whichhas been identified, is stretched in an oblique and upwardfashion medially to the spinal process, at which point, itfeels as though it were going to spring away. To performthis maneuver, the physician uses the right hand for theleft back and the right hand for the left back.

TECHNIQUES FOR PERISPINAL AND INTERSPINAL REGION PAIN

This maneuver consists of a short brief muscle stretch-ing generally performed with the knuckles of the middleor index fingers according to the muscle involved. Some-times the pulp of the index finger can also be used. Twotechniques are available.

The first concerns paravertebral muscles. It is per-formed with the patient seated or standing with handsleaning against the examiner’s table. With the thumb againin a hook-like position, the physician hooks onto theparavertebral muscles 2 to 3 cm from the median line andstretches them toward the crest of the spinal process, againstretching as one would stretch the string of an instrumentwith the thumb.

The second technique concerns interspinal ligamentsand the small interspinal muscles. This technique is per-formed with the knuckle of the index or middle finger,which is firmly applied laterally against the spinal process.The knuckle under pressure glides slowly into the spacebetween the spinal processes and with a brief swift move-ment downward, applying maximal pressure, goes over tothe inferior spinal process (Fig. 70.2).

CERVICAL REGION TECHNIQUES

It is in the cervical region where this maneuver is mostinteresting because it can be demonstrated to be useful ina number of conditions with the advantage that cervicalmanipulation is avoided. The maneuver can be performedwith the patient seated or recumbent.

With the patient seated, the physician holds thepatient’s head firmly with one hand. With the index ormiddle finger of the other hand, he hooks onto the lateralborder of the concerned muscle and stretches it towardthe vertebral process, acting as if again, pulling on a string,allowing the muscle to jump out once it is under sufficienttension. The maneuver can be performed several ways.

1. Repeatedly performed gently and progressively.2. In certain cases, however, as described earlier,

brief stretching, utilizing pressure friction onparaspinal and vertebral process ligaments, isperformed with the knuckles of the index and/ormiddle finger (Fig. 70.3). It is performed byapplying firm pressure against the spine asclosely as possible to the base by creating a slid-ing movement progressing toward the interspinal

Figure 70.2

The patient is seated or standing. The physi-cian’s knuckle of the index or middle finger is firmly appliedlaterally against the spinal process. The knuckle under pres-sure glides slowly into the space between the spinal pro-cesses and with a brief swift movement downward, applyingmaximal pressure, goes over to the inferior spinal process.

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491

subadjacent space, utilizing a brief firm shortfrictional impulse. This maneuver is terminatedat the lower spinal process and can be highlyeffective for segmental pain.

PATIENT RECUMBENT

These related maneuvers can be performed with thepatient lying recumbent. The head of the patient is cradledin the right palm of the physician with the left handapproaching from the left under the neck reaching to theright side of the neck, hooking onto the muscles there(Fig. 70.4a and b). The maneuver can be performedinversely to reach the muscles of the left side of the neck.The muscles are stretched with the distal fingertips form-ing a hook-like position. The muscles involved are gentlystretched toward the spinal process. This process isrepeated progressively, slowly. If the maneuver is thera-peutic, the tight cords become supple and much less tenderfor the patient. One can perform this maneuver on all ofthe muscles and tight bands of the posterior neck.

Figure 70.3

The seated patient has firm pressure appliedagainst the spine as closely as possible to the base. Themaneuver is performed by creating a sliding movementtoward the interspinal subadjacent space using a brief, firm,short frictional impulse. The maneuver is terminated at thelower spinal process.

Figure 70.4a

The patient lies recumbent with his or her headin the physician’s right palm. The physician’s left hand, usingthe fingertips, comes under the neck and hooks onto themuscle which is gently stretched toward the spinal process.

Figure 70.4b

The patient lies recumbent with his or her headin the physician’s right palm. The physician’s left hand, usingthe index or middle finger, hooks onto the muscles involved,stretching them toward the process.

VIII

THE PHYSIOLOGY OF PAIN

495

71

THE NEUROPHYSIOLOGY OF PAIN

OVERVIEW

The rigid conceptual framework provided by past ana-tomic and pathology studies, the framework in which theaction of pain is understood, has broadened to incorporatea greater appreciation of the plasticity of anatomic orga-nization and pathologic consequences (Woolf, Parker).This is in large part due to a better understanding of theplastic nature of the physiology of nociception and itsunderlying organization, manner of maintenance, and con-trol. Muscular and autonomic accompaniments of painhave also been clarified by a better understanding of theinherent plasticity of nociception.

Studies performed in the past, attempting to correlatenociceptive states with pathology, particularly that involv-ing the vertebral spine, by means such as x-ray, magneticresonance imaging (MRI), computer-assisted tomography(CAT), radionuclide scanning (bone scan, etc.), ultra-sound, and electromyographic (EMG) studies have metwith relatively uniform failure (Schwarzer). This failureindicates clearly that nociceptive states are heavily outsidethe purviews of these types of procedures. The dependenceof nociception on objective physiologic mechanisms thatdemonstrate significant plasticity has been confirmed byadvanced techniques such as positron emission tomogra-phy (PET), single-photon emission computer tomography(SPECT), and event related functional MRI (Davis, Dolanet al., Price et al.). With these techniques, along withadvanced genetic probes, nociception has been removedfrom the realm of subjective reportage to an objective statedemonstrable to have the capacity to alter neural organi-zation in a profound and permanent manner and which ismeasurable and imageable.

PHYSIOLOGIC SYSTEMS

The notion of rigidly definable physiologic systems orsubsystems such as a central nervous, musculoskeletal,

endocrinologic, or other system assumed to be self-contained and mutually exclusive is no longer tenable inview of recent studies by Maier (2003).

The physiology of nociception has similarly beenshown not to be in the domain of any one system. Rather,the emerging picture of the physiology of pain can belikened to that of a nonlinear continuum of functional inter-plays of several systems, among which are the neural, mus-cular, endocrinologic, and inflammatory systems to namebut a few. This interplay bears strong resemblance concep-tually to a matrix field out of which borders are carvable andwhich serve only the purpose of facilitating discussions, butare not necessarily fixed properties of the system.

NOCICEPTION

Nociception can be defined physiologically as a fieldhaving cognitive, phenomenologic, and biologic dimen-sions as well as purely physiologic dimensions that maynot linearly correlate with behavioral or cognitive states.

The stimulus to nociceptive states is often assumed tobe due to an external pathologic condition and correlatablewith severity of pathology, i.e., worse pathology is equalto worse pain. That nociceptive stimuli need not be exter-nal and can be internal and integral to the physiologicnociceptive system has been amply demonstrated (Agug-gia, Amir et al., Devor, C.N. Liu et al. 2002, Quintner).

Numerous studies have demonstrated that nociceptivestimulation can induce changes in sensorial thresholds,neuronal excitability, and inhibition along with long-termpotentiation and inhibition (Rygh, Sandkühler). Thesource of the stimulation does not bear on the degree ofplastic effect on the system. In some cases, internal stimulimay induce a more intense quality of pain than that whichan external trauma, lesion, or inflammation might be ableto trigger. Furthermore, sustained nociceptive stimuli ofany source, cognitively appreciated or not, may becomesufficient triggers to the induction of classic neuronallymediated muscle, autonomic, and visceral reflexes, and

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may also trigger classic inflammatory cascades and elab-orate referred pain patterns with their own associatedreflex changes once thresholds are reached.

Nociceptive states prior to reaching of the point ofcognitive appreciation can interact with compensatory andnoncompensatory mechanisms capable of altering theoverall matrix in which nociception is operant. The noci-ceptive response is not at all times a proportionateresponse as one might expect assuming a linear reactionsystem, but rather demonstrates a significant capacity fordisproportionate response typical of a system demonstrat-ing a significant degree of plasticity and capacity for bothaugmentation and inhibition (Cervero). Typical experi-ments demonstrating how trivial stimulation may beexpressed by ever-increasing pain demonstrate well thelack of nonlinearity within the nociceptive system (Sand-kühler, Arendt-Nielson et al.).

Nociception is not a psychological state although cer-tainly its perception and phenomenologic appreciation andthus its communicated aspects are indicators of corticalprocessing. Recent studies of nociceptive states have dem-onstrated clearly the involvement of numerous cortical andsubcortical regions such as the anterior cingulate gyruswhich, when facilitated by non-nociceptive influences, cansignificantly alter the nociceptive inexperience.

PHYSIOLOGIC PLASTICITY OF PAIN

Advanced imaging techniques and DNA probing havedemonstrated a marked plasticity of the physiologic sys-tems activated during nociceptive experiences. The foun-dations of that plasticity appear at multiple levels includ-ing the genome.

The Genome

The human genome is the sum of heritable informationheld in chromosomes that govern how an organism devel-ops and is able to express itself. Protein-coding genesmake up less than 2% of the total DNA of the human cell.Human DNA is coated with at least an equal mass ofprotein forming a complex referred to as chromatin, whichcontrols gene activity and the inheritance of traits.

The principal protein components of chromatin are pro-teins called histones. The histones facilitate gene activa-tion by promoting specific structural interactions betweendistant sequences or repression by occluding binding sitesfor transcriptional activators.

The fundamental subunit of chromatin is the nucleo-some consisting of DNA wrapped around a core of his-tones. Regulatory signals entering the nucleus encounterchromatin, not DNA, and the rate-limiting biochemicalresponse that leads to activation of gene expression inmost cases involves alterations in chromatin structure.

Epigenetic Inheritance

An epigenetic trait is inheritable independently of DNAsequence and can appear at the level of cell division or atthe generational level when an offspring inherits a traitfrom its parents. The mechanism by which a parentalinheritance is accomplished involves in part DNA meth-ylation on the paternal allele. The methylation state of anallele is linked inextricably with patterns of histone mod-ification. Epigenetic inheritance involves the maintenancepatterns of histone modifications and/or association ofchromosomal proteins correlated with specific expressivestates. The maintenance of repressed or activated tran-scription states represents an efficient mechanism for pro-gressive cellular differentiation. In such a model, funda-mental decisions regarding turning genes on or off needbe made only once. At subsequent stages of development,the maintenance of gene expression is associated withspecific histone modifications and chromatin remodelingactivity (Felsenfeld et al.).

GENOMIC ACTIVATION AND REPRESSION

The stimuli to genomic activation and repression tran-scription functions are largely unknown, although they areassumed to be varied and have multiple components.Among those components is intracytoplasmic Ca

2+

, underthe control of Ca ion channels, which has been demon-strated to play a key role through its interactions withintracytoplasmic proteins, which in turn are able to inter-act at the genomic level to induce specific transductionchanges.

Genomic transcription studies specific to nociceptionhave focused on several systems including the regulationof opioid transmitter and receptor systems, systems largelyconcerned with the regulation of pain thresholds, and non-opioid systems having similar functions. These studieshave highlighted the complexity of genomic expressionassociated with nociceptive states.

Recently studied in connection with the opioid systemhas been the protein DREAM (Downstream RegulatoryElement Antagonist Modulator), a calcium-activated sen-sitive protein capable of activating the transcriptionalrepressor of DNA associated with prodynorphin expression.On activation by calcium, dissociation of DREAM fromthe DNA repressor site has been demonstrated to result inprodynorphin expression (Cheng et al.). It is the first tran-scription factor known to be regulated by calcium. InDREAM knockout mice, increased dynorphin expressionresulting in a strong reduction in pain-associated behaviorhas been demonstrated (Carrion et al., Costigan et al.).

While DREAM regulation can play a role in the plas-ticity of response to pain, it is not always easy to determine

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what direction the response will take as exemplified inrecent experiments involving knockout mice for prodynor-phin in which normal responses to acute non-noxiousstimuli and mild increased sensitivities to some noxiousstimuli were demonstrated. Knockout mice lacking pro-dynorphin expression after nerve ligation demonstrated areturn to baseline status in 10 days. In non-knockout mice,ligation was capable of decreasing the threshold for nox-ious and innocuous stimuli. The decrease was sustainedand reversed with the administration of antidynorphin,thus demonstrating that the absence of dynorphin wasassociated with a lower pain threshold while the upregu-lation of dynorphin in pathologic states could paradoxi-cally play a pronociceptive role by maintaining a lowerthreshold for pain (Wang). This contrasts with its suppres-sion of noxious input in the non-upregulated state whenresponding to mild stimuli.

The balance between dynorphin pro- and anti-nociceptiveactivity may depend on affinities for nonopioid receptorsin the upregulated state, in particular for glutamate recep-tors where glutamate activity may be enhanced.

It is interesting to note that upregulation of dynorphinhas been demonstrated in sustained nociceptive states asseen in neuropathic states related to nerve injury that canundergo block with antidynorphin or block at the NMDAreceptor (Lai et al., 2001).

Catechol-o-methyltransferase (COMT), an enzymethat metabolizes and terminates the activities of the epi-nephrine, norepinephrine, and dopamine neurotransmit-ters upon presynaptic reuptake is an example of a systemin which a genetic variation can produce a specific impacton nociception. In individuals, homozygous for the met158 allele of COMT polymorphism (val 158 met) showeddiminished regional µ-opioid system responses to paincompared with heterozygotes. These effects were accom-panied by higher sensory and affective ratings of pain anda more negative internal affective state. Thus, individualdifferences in adaptation and response to pain can havegenomic bases that can be of great subtlety (Zubieta et al.2003).

Genomic expressions that are assumed to be long termcan be surprisingly short term under the influence of acti-vating and deactivating transduction signals that haveeffects that last only seconds or go on to produce long-lasting alterations in overall function. This in turn canlead to increased complexity of interactions and greaterpleomorphism of expression than might be expectedassuming a static picture of genomic function and celldifferentiation.

Cellular Plasticity

The production of cell surface and intracytoplasmicreceptors, their activation, facilitation, and production ofexport regulatory and cell surface ligand proteins, having

metabolic and electrotonic effects, are under multiple con-trols, some of which are external such as neurotransmittersor cytokines and some of which are intracytoplasmicand/or intranuclear. The summation effects of all inputshave convergence effects with both short- and long-termconsequences on cellular activity. Intracytoplasmic mes-senger activity for the purposes of genomic transductionis performed by various functional proteins including ade-nylyl cyclase and/or by ions including calcium and potas-sium (Onyike).

The change in intracytoplasmic Ca

2+

ion activitybrought about by Ca

2+

ion channel opening does not actas a direct messenger but rather has been shown to bemediated by the presence of a calcium-sensing proteinknown as calmodulin which is found both attached to ionchannels at the intracytoplasmic ends and free within thecytoplasm. Calcium ions entering through calcium chan-nels are able to bind to free calmodulin and cause it tomove to the nucleus where it influences genetic expression(Masayuki). It is suspected that calmodulin associatedwith calcium channels may be an initial trigger linkinglocal calcium influx to the activation of cyclic AMPresponse element binding (CREB) protein to the regula-tion of calcium channel activity — an event that can belikened to neuronal memory.

Cellular Communication and Synaptic Plasticity

The singular cell model of cellular activity can be con-ceptualized best by thinking of the cell as if it were withina matrix field of incoming information to which the cellresponds either as a transducer or integrator of activity,responding with an output having simple linear or nonlin-ear characteristics. The behavior of two- or three-cell mod-els differs from that of single-cell models in that the effec-tiveness of intercellular communication characterized byeither facilitation or inhibition becomes an essential char-acteristic of the system.

The organization of multicell systems characteristic ofthe physiology of pain is dominated by our conceptualunderstanding of cellular communication as a function ofsynaptic activity of neurons that are under the influenceof neural, glial, hormonal, and immunologic elements.

THE NEURON

A neuron is a cell characterized by a central cell bodythat has a singular axon at one end and a dendriticarborization at the other end. The axon can be furtherbroken down into its proximal segment associated withthe generation of an action potential and a distal segmentthat makes contact with other neurons in regions termed

synapses

. The neuron is further characterized by the

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maintenance of a transmembrane potential voltage arisingfrom activities at ion pumps that are responsible for main-taining ion gradients across membranes, and ion channelsthat can rapidly reverse established gradients upon opening.

The change in the transmembrane potential in the caseof the axon is produced by the opening of ion channelsas mentioned. This is accomplished through triggeredchanges in conformations of protein structures that allowselected single ions to move down their gradients for abrief period of time while the channel is open. As a resultof the movement of ions down their gradients, a rapid shiftin transmembrane ion concentrations results in a trans-membrane voltage reversal or change up or down. Thechange in transmembrane potential of the axon is charac-terized by a change in polarity propagated as an actionpotential in a wave-like manner to the distal segment ofthe axon where its arrival triggers the opening of calciumchannels resulting in an influx of Ca

2+

and subsequentbinding with synaptotagmin (Tucker et al.), which inducesthe release of neurotransmitters and neuroactive sub-stances stored in vesicles.

Upon the release of neurotransmitters at what aretermed the presynaptic ends of axons, neurotransmittersdiffuse across small synaptic spaces to the postsynapticends where they interact briefly with neural transmitterreceptors. Termination of neural transmitter function isaccomplished by either reuptake by the presynaptic endwhere metabolic degradation further occurs, as in the caseof the neurotransmitter epinephrine, norepinephrine, anddopamine, or by local degradation, as in the case of ace-tylcholine by acetylcholine esterase. Some neurotransmit-ter receptors may also be located at the presynaptic endsof synapses.

The dendritic arborization consisting of thousands ofbranch-like structures receives the inputs of thousands ofother neurons at regions called synapses. At the dendriticend of the synapse (postsynaptic region), alterations oftransmembrane potential induced by the arrivals of neu-rotransmitters are produced which, unlike in the axons,do not propagate any great distance. However, they areable to temporally and spatially summate local voltagechanges. The changes, upon reaching threshold, are ableto induce the firing of a volley of action potentials startingat the proximal segments of the axons.

Some neurons demonstrate specializations containingsensory endings capable of inducing action potentialsupon threshold stimulation by mechanical, thermal, ornoxious stimuli. Other neurons (termed

unipolar

)

act asone large axon having a sensory end and terminating at adendritic arborization.

GLIA

Glia are groups of cells with common precursorsclosely associated with neurons to which they give rise.They are grouped into macroglia: astrocytes, oligodendro-glia, oligodendrocyte precursor cells (OPCs), Schwanncells; and microglia that have macrophage-like character-istics. Astrocytes, oligodendrocyte precursor cells, and oli-godendroglia along with microglia are found in the centralnervous system. OPCs can be converted to multipotentstem cells capable of differentiating into both neurons andglia including oligodendrocytes. They form directglutamatergic synapses with neurons in the hippocampus,suggesting that glutamate receptors are used as a pathwayfor signaling the state of neural activity to these immatureoligodendrocytes (Liu and Raou). Schwann cells ensheaththe peripheral nervous system to myelinate axons. Astro-cytes and oligodendroglia have been demonstrated to havemetabolic support functions and are closely associatedwith neurons. Astrocytes in the central nervous systemalso ensheath most synapses and make active contact inthose areas. In the dentate gyrus of the hippocampus, theyalso give rise to new neurons throughout life in manyvertebrates including man (Seri et al.). In the central ner-vous system, the ratio of glia to neural elements is 10:1.

In addition to their metabolic support functions, astro-cytes also undergo transmembrane potential shifts second-ary to ion channel (Na

+

, Cl

–

, Ca

2+

) activation due to acti-vation of cell surface receptors for glutamate, GABA (

γ

-aminobutyric acid), serotonin, acetylcholine, dopamine,and neurepinephrine. The sources of the transmitters areboth neural and glial (Gilbert, Hosli et al., Kettenmann).In addition to transmembrane potential shifts triggered byneurotransmitters, ATP released by both neurons and gliacan interact with glial ATP receptors to induce Ca

2+

chan-nel ion activity and membrane shifts in potential.

Glia are capable of and do participate in neurotrans-mitter release (Kurosinski et al.) including GABA (Albrechtet al.) and glutamate (LoTurco).

Glia have also been demonstrated to participate in therelease of neuroexcitatory factors: nitric oxide, prostag-landins, excitatory amino acids, and proinflammatorycytokines; tumor necrotizing factor (TNF), and interleukin-1 and interleukin-6 (LoTurco).

Unlike neurons, glial communication does not occurthrough the propagation of action potentials, but ratherthrough calcium waves associated with ATP and otherneural transmitter releases, thus forming glial–neural net-works. The initiation and conformation and maintenanceof these waves are under numerous controls includingdirect synaptic communication with neurons andglial/glial, glial/immunologic, and glial/hormonal receptorinteractions.

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THE SYNAPSE

The classic neuronal circuit is characterized by a neu-ronal axon making contact with the dendritic arborizationof another neuron at a site called a synapse. Generally,the dendritic arborization of a neuron receives tens ofthousands of synaptic inputs from other neurons. Thespace between the axon contact end and dendritic contactis known as the synaptic clef.

At synapses, neurotransmitters such as acetylcholine,serotonin, dopamine, GABA, glutamate, glycine,

β

-alanine,taurine, endogenous opiates, and substance P on releaseat the axon associated end into the synaptic clef are ableto diffuse to the postsynaptic dendritic contact sites wherethey are able to induce or facilitate, depending on theneurotransmitter and receptor combination, local hyper-polarization leading to inhibition or hypopolarization pro-ductive of excitatory postsynaptic potentials, (EPSP).Graded polarizations are accomplished by means of neu-rotransmitter action on receptors coupled to ion channelsthat are opened or closed to specific ions (Ca

2+

, Na

+

, Cl

–

,K

+

). The activity at the synapses is capable of undergoingspatial and temporal summation and can be expressed bythe firing of a neuronal action potential, depending on thesetting of the firing threshold (Hosli 1981).

In addition to the release of classic neurotransmitters,the concurrent release of neural modulators, such as cyclicAMP and substance P, can have significant effects onneural transmitter uptake mechanisms and neurotransmit-ter metabolism, and can induce glial activity capable ofenhancing, facilitating, or inhibiting neurotransmittereffects in highly localized areas, depending on the agentreleased. The quality of transmission at specific synapsescan undergo modification, leading to facilitation by severalmechanisms. One mechanism involves the influx of cal-cium at dendritic spines that can trigger changes in recep-tor densities through interaction with nucleosomes. Ingeneral, such synaptic changes may not be long term andare thus dependent on persistent local stimulation.

Another proposed theoretical mechanism of interestbecause of its capacity to produce long-term local synapticfacilitation involves a role of prion-like proteins. Prionsare proteins that exhibit two forms, one of which is self-propagating. In Aplysia, this protein, known as cytoplas-mic polyadenylation element binding protein (CPEB),connected to mRNA regulation, has been demonstrated tohave such isoforms with conversion to a prion-like statein synapses undergoing stimulation, resulting in increasedlocal mRNA activity with associated synaptic facilitation.The presence of a self-replicating protein resulting in localsynaptic enhancement results in a form of epigenetic per-manence functioning locally which has the capacity

for synapse-specific long-term potentiation (Si et al.,2003).

In addition to anterograde information transfer, basedon neurotransmitters, gap junctions can also form physicalconnections allowing for electrical synapses. Both electri-cal and neurotransmitter gap junctions can and do dem-onstrate retrograde information transfer utilizing bothsmall molecules, such as NO, and large polypeptide factors,such as nerve growth factor. Such factors are felt to playsignificant roles in enhancing neuronal signaling, thus pro-viding bases for long-term plastic alterations of neuronalcircuitry (Jessell, Kandel ).

Neurotransmitters

Neurotransmitters are able to influence the efficiencyof synaptic transmission and therefore the probability ofsuprathreshold firing in a dynamic manner. The path bywhich neurotransmitters influence synaptic modelingincludes a system of intracytoplasmic messengers capableof acting both on neuronal and glial elements and capableof inducing genomic transcription and downstreamenhancement of neurotransmitter production and receptorproduction and distribution. Reciprocal interactions ofneuroreceptors have also been demonstrated recentlybetween NMDA receptors and D

1

dopamine receptorsaffecting further signaling, demonstrating an area of plas-tic potential (Salter).

Neurotransmitters principally involved in nociceptioninclude at the segmental spinal level GABA andglutamate, and at the suprasegmental level, the opioidsystem.

Both GABA and glutamate function at ionotropicreceptors where activation leads to either activation orinhibition, and at metabotropic receptors that modulatenuclear translation. As a result of the modulation ofnuclear translation, effects such as long-term synapticpotentiation and depression occur along with the modula-tion of the transcriptions of other proteins. These diversefunctions are not always possible to separate into ionotro-pic and metabotropic activities on the basis of receptortype alone, and some receptors can demonstrate bothactivities (Huettner et al.).

GABA of neural and glial origin is primarily active atthe GABA receptor where its function is primarily inhib-itory to neuronal and glial function. It can act at both pre-and postsynaptic locations. GABA receptors are of twotypes: GABA-A and GABA-B. Autoradiograph tech-niques have demonstrated GABA-A receptors on neurons,whereas GABA-B, a metabotropic receptor, has beenfound on neurons and glia (Hosli 1990 and 1991). Cou-pling of the GABA receptor to chloride channels has beendemonstrated (Gallagher et al.).

Glutamate of both neural and glial origins (Ferking)associated with neuronal excitation and inhibition is noted

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to function through its affinity for pre- and postsynapticNMDA, AMPA, and kainate receptors (Huettner et al.).These receptors found both on neural and glial elementsall share common basic structures but differ in ionotropicactivity (Brand-Schieber, Liu, Q. S. et al.). Glutamate isalso associated with metabotropic effects mediated by alarge class of metabotropic receptors found pre- and post-synaptically. It is important to note that the distinctionbetween ionotropic and metabotropic effects is neitherhard nor fast, and multiple effects are possible at singleionotropic receptors (Huettner et al.). The complex roleplayed by metabotropic receptors is demonstrated by thenecessity to activate metabotropic receptors to maintainrhythmic motor output (Takahashi).

The AMPA receptor on activation allows for fast depo-larization associated with Na channel properties and actsas the predominant mediator of excitatory transmissionfor glutamate. The receptor is also associated with NMDAreceptor modulation resulting in long-term potentiation ordepression (Lüthi)

The kainate receptor has been demonstrated to modu-late inhibitory synaptic transmission in the hippocampusand in dorsal root ganglion (DRG) neurons. This is ofparticular importance to the transmission of nociceptiveinformation. Both ionotropic and metabotropic functionshave been noted to be localized at presynaptic sites andto mediate, by way of depolarization, inhibition ofglutamate expression and NMDA excitation (Kerchner).

The NMDA receptor is associated with a high conduc-tive calcium channel that, in a resting nondepolarized con-dition, is blocked by magnesium in a voltage-dependentmanner. Immunocytochemical studies of the distributionof cortical NMDA receptors have shown that NMDAreceptors are preferentially localized on dendritic spinespostsynaptically and at presynaptic locations on both exci-tatory and inhibitory axon terminals and on cortical astro-cytes. Thus, the effects of the NMDA receptor are not onlyat the postsynaptic site, but must take into account pre-synaptic and glial receptor effects (Conti).

The physiologic role of the NMDA receptor is associ-ated with synaptic plasticity. Working with metabotropicglutamate receptors, it ensures the establishment of long-term potentiation, a process responsible for the acquisitionand retention of information. These functions are mediatedby calcium entry through the NMDA receptor-associatedchannel. Calcium activates a number of calcium-dependentenzymes that influence a wide variety of cellular compo-nents such as cytoskeletal proteins or secondary messen-ger synthesis.

The NMDA receptor has also been associated with long-term depression (LTD), particularly in hippocampalregions. In general, the determination whether long-termpotentiation as opposed to long-term depression will bedominant depends on the subtype of NMDA receptor stim-ulation and its effect on cellular calcium entry kinetics

(Liu et al. 2004). It is also interesting to note that the ratioof NMDA receptors associated with LTP as opposed toLTD increases with age and that, in older test animals,LTD is difficult to induce (Bliss, Schoepfer).

In the spinal cord, the NMDA receptor is located post-synaptically in neurons of the dorsal horn. It is importantto note that nerve injury has been shown to result insignificant increases in spinal glutamate which can resultin significant calcium influx at NMDA receptors and, bythis mechanism, produces reinforcement of synaptic activ-ity leading to prolonged nociceptive behavior. This, insome ways, resembles the LTP seen at hippocampalregions.

The NMDA receptor has also been shown to be asso-ciated with cellular damage as a result of a triggeredexcessive influx of calcium, which in turn initiates a seriesof cytoplasmic and nuclear processes that promote neu-ronal cell death.

Neuromodulators

Neuromodulators are also found at synaptic sites wherethey act to facilitate or inhibit neurotransmitter function.Of the neuromodulators, substance P has attracted a greatdeal of attention in regard to its role in the neurophysiol-ogy of nociception. It is a polypeptide formed by elevenamino acids of the tachykinin family that has been foundto play a major role in the transmission of nociceptiveinformation in the CNS and to act also in the peripheralnervous system. In addition, it has been found to be ubiqu-itous throughout the body and is found in many tissuesinvolved in the inflammatory response (Cesaro).

In the peripheral nervous system, it is found principallyin small diameter myelinated and nonmyelinated afferentfibers and is concentrated at both proximal and distal endsof sensory neurons. In the CNS, it is also found concen-trated in the substantia nigra, basal ganglia, brain stem,and hypothalamus (Cuello, Ribeiro-da Silva).

In the spinal cord, it is found in lamina I and II of thespinal dorsal horn. In addition, it is found in high concen-trations in the substantia gelatinosa of the trigeminal nerveand the skin of the trigeminal territory. Neurons containingsubstance P may also contain neurotransmitters. Sub-stance P is also found freely in spinal fluid.

The components of the enteric nervous system, alongwith vascular endothelial cells, macrophages, eosinophils,lymphocytes, and platelets are also sources and sites ofhigh substance P concentration (Milner et al., O’Connoret al.). Both neuronal and glial elements have been dem-onstrated to harbor substance P. Substance P has beendemonstrated to exert its effects both pre- and postsynap-tically, mediated through the activation of NK-1 receptors(McLeod).

The anatomic localization of the NK-1 receptor has beendemonstrated to be localized in the CNS to the prefrontal

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501

and visual cortex involving both neuronal and astrocyticelements as well as microglial elements (Tooney et al.).Outside of the CNS at the spinal cord level, NK-1 recep-tors have been demonstrated in the dorsal horn spinal cordneurons at dendritic sites in close apposition to substanceP containing butons. These neurons are noted to projectrostrally. Astrocytes in these regions have similarly dem-onstrated high specificity for NK-1 receptors.

Sympathetic neurons have also been shown to expressNK-1 receptors thought to respond to endogenouslyreleased substance P. NK-1 receptor in this case has beennoted to be expressed almost entirely by noradrenergicneurons that contain somatostatin (Messenger). NK-1receptors have also been demonstrated in the GI tractinvolving the lamina propria, epithelium, and submucosalvasculature along with smooth muscle, myenteric plexus,platelets, and microglia (Goode et al.).

The effect of the activation of the NK-1 receptor iscomplex, and depending on its cellular localization, reg-ulation of smooth muscle contractility, epithelial ion trans-port, vascular permeability and immune function of thegastrointestinal tract, release of cytokines, and plateletaggregation have been demonstrated (O’Connor). Thesetypes of activities have been referred to as neurogenicinflammation as opposed to inflammation due to directinjury or infection.

The NK-1 receptor has been demonstrated to be ableto potentiate NMDA-activated current in rat primary sen-sory neurons. Substance P has also been demonstrated toelevate intracellular calcium by promoting Ca

2+

entry intothe dorsal horn neurons. In glia, a similar elevation ofcalcium has been noted, but was noted to occur as a resultof the release of internal stores (Wu et al., Heath et al.).

In astrocytoma cell lines, activation of NK-1, inducingthe subsequent activation of the nuclear transcription fac-tor NF-

κβ

receptors requiring intracellular mobilizationof calcium, has been demonstrated (Lieb 1997). This wasshown to be associated with increased expression andsecretion of IL-8 and IL-6, granulocyte macrophage colony-stimulating factor, and leukemia inhibitory factor (Gitteret al., Palma and Manzini, Lieb et al., 2003). In addition,NF-

κβ

is noted to target the gene for the expression ofthe NK-1 receptor and provides a mechanism for increasedavailability of NK-1 receptors in responsive cells. Theplurality of potential responses of this system is high-lighted by the demonstration that the IL-1B pro-inflam-matory cytokine has been shown to increase the expres-sion of NK-1 receptor at the mRNA and protein levels.This has been postulated to occur through the activationof the NF-

κβ

transcription factor (Simeonidis et al.). The function of substance P has been demonstrated in

the CNS at the spinal cord level to be significantly tied tonociceptive response. In studies ablating lamina spinalneurons in rats expressing substance P receptors, inhibition

of the nociceptive hyperalgesic response has been dem-onstrated. The specificity of this response is highlightedby the projection neurons in lamina I of rat spinal cordwith NK-1 receptors selectively innervated by substanceP-containing afferents responsive to noxious stimuli(Mantyh et al., Todd et al.).

The complex role played by substance P in the spinalcord has been demonstrated by the finding that NK-1receptor activation leads to enhancement of inhibitorydescending neurotransmission in the spinal substantiagelatinosa, lamina II neurons in the mouse model, and inthe absence of this descending influence, does not alterreceptive responses (Vergnano et al.). Similarly, vagalstimulation has been noted to induce dynorphin releaseand suppress substance P release from a thoracic spinalcord preparation during cardiac ischemia, demonstratingthe nociceptive activity of substance P both to excitatoryand inhibitory circuits (Hua et al.).

NK-1 receptors have been demonstrated to colocalizewith GABA- B receptors in the dorsal horn, which furtherdemonstrates multiple pathways for nociceptive modula-tion (Castro). In one recent study, ablation of the substanceP nociceptive pathway did not suppress nocioceptionentirely, but rather limited nociception, reducing thedegree of severity of pain noted. The pleural nature ofsubstance P activity was shown in studies demonstratingthe release of cytokines from glial cells stimulated bysubstance P. Outside of the central nervous system, sub-stance P has been noted in models of the lungs to bereleased by allergens, histamines, and prostaglandins andcan result in neurogenic sterile inflammation.

In addition to its function in inflammatory, neural, glial,and nociceptive pathways, substance P functions as a cen-tral pattern generator for locomotion when injected intothe brainstems of mammals, particularly the reticulospinalcells, as has been clearly demonstrated. Substance P wasfound to be released in the medial amygdala during stress-related situations, and an association with IL-6 elevationwhich is responsive to block by valporate through inhibi-tion of kinase-C activation has been demonstrated (Ebneret al., Lieb). In cases of fibromyalgia, elevations of spinalcord substance P with reduction in substance P levelsassociated with blocking were noted (Stratz et al.). In arat model of complex regional pain syndrome type I, sub-stance P blockade was able to reverse vascular and noci-ceptive changes (Guo et al.).

Platelet substance P was shown to be elevated in head-ache disorders both of the migraine and tension types,suggesting a possible pool for nociception sensitization inindividuals prone to headache and a possible mechanismfor sensitization.

In summary, substance P demonstrates a highly com-plex role in the regulation of nociception. Its close rela-tionship to inflammatory cytokines and NMDA receptors

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and its presence in neuronal, glial, and other cell elementsallow it to function locally and participate in CNS signalamplification processing. These functions taken togetherdemonstrate the complex nature of CNS sensitization andits relationship to self-sustained neurogenic inflammation.

Synaptic Field Plasticity

Multineuronal cell models have largely ignored the roleplayed by astrocytic elements, but recent work on neuron–glia two-way communication has demonstrated that gliaplay a significant role in synaptic plastic modeling andmaintenance and are intimately associated with inflamma-tory responses (Fields et al., LoTurco). Glia have beendemonstrated to express cell surface receptors essentiallyof the same classes as those associated with neurons andto undergo changes in transmembrane potentials.

Ion channels on astrocyte testing have been demon-strated to respond to classic neurotransmitters and respondwith calcium channel activity productive of intracytoplas-mic changes in calcium fluxes. Calcium-dependentgenomic transductive responses resulting in classic neu-rotransmitter export, including the capacity to releaseGABA and glutamate along with proinflammatory cytok-ines, has been demonstrated, as has K-dependent GABArelease (Albrecht).

Intimate relationships of glia to axonal and dendritictrees have been demonstrated to be necessary to inducesynaptic plasticity and to produce inhibitory and facilita-tive synaptic transmission of a nonlinear type. Glial cellsmay also induce propagating cellular signals termed “cal-cium waves” based on communication utilizing cyclicAMP derived from neuronal activity, thus modulating syn-aptic activity and receptive field conformation.

NOCICEPTIVE SENSITIZATION

In studies of the nociception of neurally mediated pain,“central sensitization” and “long-term potentiation” (LTP)are terms used in reference to an increase in synapticefficacy in the dorsal horn of the spinal cord followingintense, noxious stimuli inducing increased synaptic activ-ity in the dorsal horn. The process of LTP is seen at thelevels of both the brain and spinal cord. In the brain, LTPis closely associated with the formation of memory. Themechanisms of LTP in the brain and spinal cord are cur-rently being studied and seem to have a great deal incommon (Ji).

Two major mechanisms appear to contribute to increas-ing synaptic efficacy: alterations in ion channel and/orreceptor activity owing to post-translational processingand trafficking of receptors to membranes.

Two types of nociceptive sensitization have beendescribed:

allodynia

, defined as a nociceptive sensation

evoked by stimulation intensities that do not normallyevoke pain, and

hyperalgesia

, an increase in pain sensiti-zation to normal painful stimuli.

Neurotransmitters closely associated with LPT includeglutamate and its effect at the NMDA receptor which iscoupled at the level of the CNS hippocampus at post-synaptic sites with brain derived neurotrophic factor(BDNF), a neurotrophin that can induce enhanced synap-tic transmission over seconds to minutes through its actionat the tyrosine kinase receptor (Kovalchuk).

In addition to neurotransmitters, prostaglandin, PGE

2

produced by cyclo-oxygenase in the spinal cord, acts ontransmembrane receptors expressed by dorsal horn andprimary sensory neurons and can facilitate transmitterrelease from nociceptor central terminals and reduce gly-cine receptor activity and direct depolarization (Ji).

The process of central sensitization as applied to noci-ception also involves the long-term potentiation of entrylevel segments and also the manner by which severalsegments associated with nociceptive input participate inlong-term potentiation processes. That this is common tonociception was demonstrated in experimental modelsstudying the dorsal horn. Nociceptive stimuli are noted tobe able to activate several segmental levels above andbelow the root entry zone, as opposed to non-noxiousstimuli that are more limited to the segmental root entryzone (Coghill 1993).

The sources of nociceptive stimuli capable of acting toinduce central sensitization can be internal or external, asin the case of injury. Studies have demonstrated thatectopic spike activity, generated at low levels in intactsensory dorsal root ganglia and intensified following axo-tomy, is an important cause of neuropathic pain related inpart to oscillatory subthreshold membrane potentials thatare normally present and reach threshold following axo-tomy (Amir). This condition has been noted more withmuscle afferents than cutaneous afferents (C.N. Liu 2002).The process of central sensitization is thus both a matterof facilitation and anatomic spread of spatial recruitmentwhich, as processes, are highly interactive and not mutu-ally exclusive. Central desensitization or long-term depo-tentiation, a counterprocess to central sensitization, differsfrom reflex analgesia, a known process, in that desensiti-zation remodeling, rather than reflex activity, occurs whichassumes a return to a homeostatic norm.

REFERRED HYPERALGESIA

In models of neural cellular function, the cellular activ-ity of a group of closely associated cells is dominated bysynaptic, electrotonic, hormonal, or inflammatory mech-anisms. Within a group of cells, there is generally a subsetof cells that operate primarily as receptors to stimuli andact as conduits for afferent information. Another group of

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cells within the group has a primary efferent functionacting on other cells, muscles, or endocrine organs. Thereceptivity function need not be relegated to a single setof cells but may rather be characterized by groups of cellsspecifically organized to receive particular stimuli.

The apparent in-tandem facilitation of receptivity todifferent stimuli contributes to the situation referred towithin the study of nociception as “referred hyperalgesia.”In the case of referred hyperalgesia, afferent input arisingfrom different fields, other than that which is the sourceof the noxious sensory input and has produced a centralsensitization, is identified as the active source of pain.Although it is not the original source of pain, it can activatemuscle reflex arcs, inflammatory reactions, and autonomicchanges. These reactions are associated with lowerednociceptive thresholds in fields not originally involved butintimately associated with spinal segments that are receiv-ing nociceptive input (Vecchiet).

“Referred pain” is also related to cognitive limitationsof localization of pain origin as a result of convergentinput to groups of cells that have limited output, thusresulting in cognitive bias, which will be discussed later.

Referred pain reflects the segmental embryologicdevelopment of a given segment. During embryologicdevelopment, osseous, muscular, and cutaneous sensoryrepresentations related to a single segment occur (Inmanet al.). The sensory information derived from the converg-ing of these sources upon a single segment is relayed tothe central nervous system. Cognitive localization isdependent upon cortical representation that does not, forthe most part, include muscular or osseous critical local-ization. Instead, pain interpreted to be from these areas isexperienced as diffuse and difficult to localize. Regionsinvolved in painful referred patterns can themselvesbecome targets of neural reflexes characterized by inflam-mation, swelling, muscle spasm, and cutaneous reaction(Maigne 1972).

In animal experiments, it has been demonstrated thatreferred hyperalgesia can follow as a result of centralsensitization after repeated visceral stimulation and is afunction of the number of stimulus episodes (Roza, Giam-berardino et al. 1997).

Somatic receptive field areas have been shown exper-imentally to increase with stimulation and to undergo adecrease in threshold for convergence for somatic receptorfields, resulting in facilitated referred expanded hyperal-gesia.

In human repetitive tap experiments, for example, sum-mation effects indicating facilitation of nociception andalteration of receptive field activity have been demon-strated (Arendt-Nielsen et al.). This demonstrates that,although apparent in-tandem augmentation of facilitationbased on convergence (i.e., a small group of cells in ahyperexcited state will respond to external stimuli withexaggerated responses) may be applicable in some sys-

tems, spread is also an important feature of central sensi-tization that can interact with convergence.

Referred pain or hyperalgesia from deep somatic struc-tures is not explained by the central sensitization of con-vergent neurons, as there is little convergence from deeptissues in dorsal neurons. It has been proposed that theseconnections may not be present from the beginning andare opened as a result of viscerally triggered reflex musclecontractions that lead to the sensitization of nociceptiveinputs from skeletal muscles, and are thus referred tomyotomes outside the lesion resulting from the spread ofcentral sensitization to the adjacent spinal segment (Giam-berardino et al. 1997). Referred hyperalgesia is thus aplastic response related to the interplay of central sensiti-zation and spread and inhibitory analgesic systems.

NOCICEPTIVE DESENSITIZATION

In most models of nociceptive desensitization, refer-ence is made to the endogenous opiate system first dis-covered in 1976. The system consists of anocortin, proen-kephalin, prodynorphin, their receptors

µ

,

δ

,

κ

and thatmodulate pain, producing analgesia, and also have cogni-tive, cardiovascular, neuroendocrine, and neuroimmunefunctions.

Electrophysiologic evidence supports a

κ

-mediatedinhibitory effect of dynorphin on synaptic transmission ofnociceptive neurons in the spinal dorsal horn by way ofhyperpolarization. It has been suggested that dymorphinmay play a role in antinociception during inflammationand may mediate cannabinoid-induced analgesia.

Beyond the endogenous opiate system that is organizedsupersegmentally, local factors play active roles at thesegmental level. Such factors include the activities of localreflex arcs. In animal experiments, it was shown that Cfiber stimulation with high frequency burst generation ofthe sciatic nerve can result in long-term potentiation (LTP)of C fiber fields. The A

δ

fiber, but not the A

β

fiber, stim-ulation strength has been shown to induce long-termdepression (LTD) of C fiber-evoked field potentials of thedorsal horn. This difference between LTP and LTD mayunderlie some forms of prolonged analgesia induced byperipheral nerve stimulation (Liu 2002).

Other studies noted that cutting spinal nerves just distalto the dorsal root ganglia (DRG) triggered with rapid onsetmassive spontaneous ectopic discharges in axotomizedafferent A neurons, and at the same time induced tactileallodynia in the partial denervated hindlimb. A secondarytransection of the dorsal root (rhizotomy) of the axoto-mized DRG or topically applied local anesthetic elimi-nated or attenuated the allodynia. Thus, local sustainingmechanisms can be demonstrated under circumstancesinvolving acute local neural injury (Sukhotinsky).

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SECTION VIII THE PHYSIOLOGY OF PAIN

The depotentiation of enhanced synaptic response andfield characteristics also comes under the influence ofsuprasegmental influences including evidence of a corticalspinal inhibition of Renshaw cells via a short interneuronalchain in both the upper and lower limbs (Mazzocchio,Bonnet). Bonnet et al. demonstrated that even mental sim-ulation of muscle activation had the capacity to enhancethe excitability of spinal reflex pathways in humans, thusdemonstrating the capacity for supersegmental enhance-ment or depotentiation of muscle reflex pathways inhumans.

The capacity for active tendon reflexes and nociceptivestimuli to produce inhibition of muscle reflexes has beendemonstrated; they are task and anatomically organizedand may influence nociceptive states (Burne et al., Kofler).Studies of human subject reflex activities of the tibialisanterior and soleus demonstrated that inhibitory reflexreceptive fields are organized in a highly functional, asopposed to an anatomical manner supporting the actionof the excitatory reflex. Together, the two reflexes resultin an optimal withdrawal from stimulus. In the case of thetibialis anterior, low stimulation intensity has been dem-onstrated to be sufficient to elicit the inhibitory reflexwhile high stimulation intensity causes a reversal of inhi-bition to excitation. This is in contrast to the soleus musclein which inhibition has been demonstrated to be facilitatedby stronger intensities (Sonnenborg).

The issue of the relationship of spinal reflex pathwaysto central sensitization and desensitization is particularlypertinent when noting the interaction of convergent inputof low threshold mechanoreceptors and nociceptors intospinal neurons that are felt to play a role in the pathophys-iology of the clinical signs of allodynia. In particular, insecondary hyperalgesia, data suggest the convergence oflow threshold mechanoreceptive and nociceptive inputsinto spinal reflex pathways in humans, probably at aninterneuronal level, that contributes to the phenomenon ofmutual facilitation (Ellrich et al., Cervero et al.).

Electrical stimulation over selected muscle tendons inalert human subjects has been demonstrated to produce areflex inhibition of muscle activity that may arise fromGolgi tendon organ afferents (Burne).

A further connection between the state of the motorreflex arc and the state of nociception is noted in the workof Chan et al., who noted a linear relationship of thepresence of low level voluntary muscle contraction, theresponse to painful electrical stimuli, and the estimate ofperceived pain intensity reported on a visual analog scale,suggesting that the sensory components of nociceptivestimuli may already be set largely by levels of muscularactivity at the spinal interneuronal levels.

Studies using subthreshold magnetic vertex corticalstimulation have demonstrated facilitation of monosynap-tic reflex arcs produced by corticospinal inhibition of Ren-shaw cells via a short interneuronal chain in both upper

and lower limbs. This clearly demonstrates that reflexmodulation can be cortically generated and thus can beexpected to play a role in nociception, sensitization, anddesensitization (Mazzocchio et al.).

PHASIC DETERMINANTS OF NOCICEPTION

The role played by reflex activity in the maintenanceof nociceptive states is assumed to be of central impor-tance. However, the Sherrington reflex arc (defined in itssimplest form as a monosynaptic reflex having as its originlow threshold, muscle spindles sensitive to sudden stretchand having as its efferent arm the motor neuron) is not atall typical of physiologic reflex patterns that, as a rule,subserve the highly complex functions of ambulation, pos-ture, and sequential activity. Physiologic reflexes are notstatic or localized; they are rather temporally and anatom-ically sequenced within the entire spinal cord and typicallyinvolve facilitory and inhibitory activity timed with recip-rocal contralateral facilitation and inhibition of all limbsand axial musculature. The primary benefit of such anarrangement is the avoidance of global burst activityinvolving either a single limb and/or contralateral homo-logous regions that may, through facilitory or inhibitoryactivity, make phasic motor function impossible to main-tain as seen in the simple acts of walking and swimming.Phasic activation has been shown in animal models to beunder the control of local neuronal networks comprisedof commisural interneurons whose neurons traverse themidline to innervate contralateral neurons and also func-tion as central pattern generators (CPGs) for left–right androstral–caudal coordination (Butt et al. 2003, Butt et al.2002).

Although it is accepted that central pattern generatorsdominate phasic activity, the system is plastic and not“hard wired.” It allows for movements such as walking,climbing, swimming, etc. through mechanisms that aresensitive to feedback from afferent sources such as muscleproprioceptors that establish the timing of major phasetransitions in motor patterns, generate certain features ofthe motor patterns, and are required for adaptive modifi-cation of motor patterns (Pearson 2004, Pearson 2000).Inhibition of afferent impulses has been noted to be animportant characteristic of the system (DiCaprio), withafferent discharges having been shown to be able to blockor reset generated patterns and interfere with coordinatemuscular activity (Perrins et al., MacKay-Lyons, McCrea,Squalli-Houssaini et al.).

It is interesting to note that small axial muscles havebeen noted to have higher muscle spindle densities whencompared to paired large muscles across the same joints(Peck et al., Nitz et al.). Such an arrangement would be

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505

able, under normal circumstances, to provide afferent mod-ulable information for coordinated phasic axial activity.

It is reasonable to speculate that axial nociceptive affer-ent input could alter normal mechanical axial phasic activ-ity, resulting in conditions propitious to the developmentof mechanical strain, particularly at active joints resultingin nociceptive activity. Along these same lines as the lossof phasic activity, local reflexes not generally active couldbecome activated and play important roles.

It is intriguing to further speculate what role might beplayed by the occasioning of these local reflex-basedautonomous motor activities escaping CPU surveillanceas a result of nociceptive sensitization and spread. It mightbe reasonably speculated that any interruption or break inthe sustaining reflex arc might lead to the cessation of paindue both to a reduction in muscular mechanical and jointstrain and a reduction in nociceptive facilitation of mus-cular origin. It would be reasonable to imagine that areturn to CPU direction could be maintained unless thecondition that resulted and sustained the mechanism thatled to escape were to remain present. The delicate balancebetween CPU direction and escape clearly under a multi-tude of influences might determine why some pain statesmay have intermittent or chronic presentations.

Central pattern generators have been demonstrated tohave activity levels that are genetically determined and toselectively interact with motor neurons whose identitiesare marked by transcriptional repressors (Bonnot et al.,Lanuza et al.). The activities of CPUs are triggered bymultiple mechanisms including sensory inputs with aminor role for motor neuron feedback loops. It is reason-able to speculate that, as a result of feedback loops,derangements of phasic activation in the form of nonpha-sic or out-of-phase, chaotic or burst activation from anycause could occur and result in significant postural ambu-latory and complex motor phasic activity dysfunction onboth small and large scales.

The cause of CPU derangement could reasonably betheorized to have pathology referable to the spinal cord.However, it is also reasonable to consider that suchderangement could originate on the basis of purely phys-iologic mechanisms that may produce and be responsiblefor nonsequential activity as a result of local sensitizationor spinal cord nociceptive spread that could recruit furtherphasic derangement, resulting in a downward spiral ofgradually increasing dysfunction that could go on toinduce or sustain local and satellite painful conditionsresulting from mechanical muscle and joint strain. Supra-segmental factors could be expected also to influence ten-dencies toward CPU dysfunction. The role of CPUs isparticularly interesting when considering the interactionsbetween muscle activation and sustaining nociceptivereflex mechanisms.

It is reasonable at this point to consider manual tech-niques that may derive some of their efficacy as a result

of being able to block, by way of the production of anappropriate, non-nociceptive afferent volley, inappropriatemuscle phasic activity long enough for normal phasicactivity to take over the system and, in essence, reset it toits proper mechanical settings. That this can be achievedin milliseconds is not incompatible with the rates at whichphasic activity is modified by everyday activity. Facetblocks and nerve blocks, by reducing uninhibited afferentactivity, could also allow normal phasic activity to takeover and could explain the general rapid resolution ofnociceptive states when facet blocks are properly per-formed.

Taut Bands

It is interesting to note that sustained nonphasicallygoverned muscle contraction of a highly localized nature,as often seen in conditions productive of muscle spasmand cramps associated with pain, is commonly noted clin-ically in isolated muscle areas that are felt to have under-gone overload or direct mechanical injury. These findingsof “taut bands and muscle trigger points” have generatedsignificant interest. Taut bands and muscle trigger pointsare defined as localized regions of muscle that demonstrateabnormal shortening with increased tone and tension. Inaddition, myofascial pain disorders have also been definedclinically as characterized by the presence of tender firmnodules called trigger points. Each trigger point is accom-panied by irritable regions or taut bands composed ofhypercontracted extrafusel muscle fibers that demonstratelow voltage spontaneous activity resembling normal,spontaneous endplate activity. This is characteristic of, butnot restricted to, the area of the trigger points or taut bands,suggesting that this may be a region of hyperactivity(Wheeler, Simons et al., Hong et al. 2002, Hong et al.1997).

The physiologic mechanism underlying the finding oftaut band spontaneous activity found in endplate zonesmay be related to increased spontaneous acetylcholinerelease, although other influences, including mechanical,chemical, and immunologic factors, may also participate.Definitive evidence that spontaneous endplate noise intrigger points and taut bands, in the absence of EMGneedle exploration, needs further research (Simons et al.2002, Hong et al.).

Clinical interpretations suggest that myofascial painand dysfunction with characteristic trigger points and tautbands represent a spinal reflex disorder caused by a rever-berating circuit of sustained neural activity in a specificcord segment. The observation that mechanical, thermal,and chemical treatments that are assumed to neurophysi-ologically or physically deactivate the neural loops of thetrigger points may explain the resultant reduction in painnoted to be associated with restoration of normal musclelength and proper biomechanical orientation of myofascial

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SECTION VIII THE PHYSIOLOGY OF PAIN

elements (Simons and Mense ). To date, taut bands andtrigger points remain clinical entities of unclear cause andunderlying physiology. That does not prevent their pres-ence from being of use in explaining certain nociceptivestates.

The bilateral activation of motor unit potentials withunilateral stimulation of active painful myofascial triggerpoints, but not with nonpainful taut bands, suggests thata threshold of activation exists (Audette et al., Hong et al.1997). As a result of this threshold, it can be expected thatthe plastic impact both at primary and referred sites maywell depend on mechanisms that inhibit or facilitate aconversion of potentially painful sites to active painfulones. The possibility that CPU derangement may facilitateconversion from nonpainful to painful conditions andenhance the possibility of the development of reverbera-tory reflexes warrants serious exploration.

Sensory motor reflexes are certainly not the onlyreflexes under CPU governance. Multiple CPU gover-nances involving autonomic and similar activities existand may, as a result of nociceptively induced derange-ment, explain various autonomic complaints and findingsthat frequently accompany nociceptive states such as nau-sea, vomiting, blurred vision, sweating, and abdominalcomplaints such as bloating.

ANATOMIC DETERMINANTS OF NOCICEPTION

When dealing with very large assemblies such as thosethat have efferent and afferent arms, nociceptive thresh-olds can be seen to differ according to the site of thelocalization of the stimulus. In the case of the trapeziusmuscle, when compared to the anterior tibial muscle, forexample, it has been shown that nociceptive thresholdsdiffer with the trapezius muscle demonstrating a lowerthreshold than the anterior tibial muscle (Ashina et al.),suggesting the possibility of greater potential for plasticeffect on the neural network from stimuli originating inthe trapezius muscle as compared to the tibial. Similarexperiments using ultrasonic stimulation of the skin, muscle,and joints have noted a higher threshold for muscle com-pared with skin and joints, particularly involving the fin-gers (Wright et al.). This in turn suggests a higher capacityfor plastic modeling impact on the neural system for stim-uli originating in joints.

The capacity for a particular site to exert an effect onthe development of supersensitivity when compared toother sites can be disproportionate. The reasons for sen-sory disproportionality may rest on anatomic and physio-logic mechanisms.

In the case of the facet joint, it has been demonstratedthat the joint can carry a significant amount of total com-pressive load on the spine when the human is hyperex-tended. Extensive stretch of the human facet capsule alsooccurs when the spine is in physiologic range of extremeextension. An extensive distribution of small nerve fibersand free and encapsulated nerve endings exists in thelumbar facet joint capsule including nerves containingsubstance P, a neuromodulator. Low and high thresholdmechanoreceptors fire when the facet joint capsule isstretched and/or is subject to localized compressive forces.Sensitization and excitation of nerves in facet joints andsurrounding muscles occur when the joint is inflamedand/or exposed to certain chemicals released during injuryand inflammation. Marked reduction in nerve activityoccurs in facet tissues injected with hydrocortisone andlidocaine (Cavanaugh et al.).

HORMONAL DETERMINANTS OF NOCICEPTIVE PLASTICITY

Much of the work regarding sensitization has focusedon closed loops including neuronal, neuronal muscular,and neuronal articular. Receptors for external humeralinfluences have been noted to result in significant changesin synaptic transmission efficiency of an inhibitory andfacilitory type. Estradiol in animal models has been dem-onstrated to decrease the number of inhibitory synapticinputs, increase the number of excitatory synapses, andenhance the frequency of neuronal firing (Parducz et al.).In humans, estrogen has been noted to produce a similareffect and induce synaptic plastic effects (Foy et al.).

SUPRASEGMENTAL DETERMINANTS OF PLASTICITY

A number of supersegmental influences on nociceptionhave been identified including serotonogenic, dopaminer-gic opiate, and nonopiate influences (Basbaum and Fields,Fields). Opiodergic systems in particular have been highlystudied. The opiodergic system also has the capacity tointeract with other systems involved in producing analge-sia and can demonstrate a characteristic termed

collateralinhibition

. The collateral inhibition model suggests thatmultiple mechanisms of pain inhibition are activatedselectively to respond to or avoid noxious stimuli in themost appropriate and parsimonious manner. This systemof producing parallel enhancements and reductions of dif-ferent forms of analgesia may allow an animal to continueresponding actively or passively to its environment in away that befits the organism as a whole (Bodnar).

CHAPTER 71 THE NEUROPHYSIOLOGY OF PAIN

507

IMMUNOLOGIC DETERMINANTS OF NOCICEPTION

Chronic pain can occur after peripheral nerve injury,infection, or inflammation. Under such neuropathic painconditions, sensory processing in the affected body regionbecomes grossly abnormal. Immune cells are natural andinextricable parts of skin, peripheral nerves, dorsal rootganglia, and spinal cord.

There is ample evidence for bidirectional immune braincommunication. Anatomically, the vagus nerve has beendemonstrated to have receptors for inflammatory cyto-kines and to have direct CNS-communicated effectsincluding fever and inflammation-related behavior thatcan be terminated with vagus nerve transection (Maier andWatkins).

Immune and glia activation may participate in the eti-ology and symptomatology of diverse pathologic painstates in both humans and laboratory animals and showsignificant overlap of functions. A variety of substancesare released on activation by both activated immune andglia cells including pro-inflammatory cytokines (tumornecrosis factor [TNF], interleukin-1, and interleukin-6)that are of importance in the development of peripheralnerve and neuronal hyperexcitability (Maier and Watkins,Watkins et al.). Furthermore TNF receptors are noted tobe expressed on cells such as chondrocytes and undergoupregulation under conditions of stress related to load,with or without osteoarthritis although the response ismore marked by the presence of osteoarthritis (Westacottet al. 1994, Westacott et al. 2002).

Studies in rats demonstrated that both ipsilateral andmirror image sciatic inflammatory neuropathy-inducedallodynias are reversible by intrathecal (perispinal) deliv-ery of fluorocitrate, a glial metabolic inhibitor. Allodyniashave also been prevented and reversed by the use of anintrathecal inhibitor of mitogen-activated kinases impli-cated in proinflammatory cytokine production and signal-ing; and prevented or reversed by an intrathecal pro-inflammatory cytokine antagonist specific for interleukin-1, TNF, or interleukin-6. Reversals of ipsilateral and mir-ror image effects were shown to be rapid and completeeven when the noxious stimuli were maintained for 2weeks (Milligan et al.).

The involvement of glia in creating mirror imageeffects is intriguing. Glia are well suited for creating anexpansion of the body region from which pain is perceivedfor two reasons: (1) proinflammatory cytokines act in aparacrine manner to excite distant cells; this would poten-tially allow the cytokine to reach spinal terminations ofneighboring nerves, causing hypersensitivity of pain trans-mission neurons; and (2) glia are organized as widespreadnetworks at glia gap junctions and can propagate calcium

waves. Excitation of glia at one site can activate distantglia, causing them to release pain-enhancing substancesas well (Milligan et al.).

The method by which glia activation occurs is stillunknown. One possibility is that glia are directly activatedby neurotransmitters released by the dorsal horn by theinflamed sensory neurons. Indeed, astrocytes and microgliamay be activated by pain neurotransmitters including sub-stance P, ATP, calcitonin gene-related peptides (CGRPs),and glutamate. Spinal cord astrocytes are activated bysubstance P binding neurokinin (NK-1) endocrine recep-tors. Microglia also express nonclassic NK-1 receptors.

Substance P has been noted to synergize with interleukin-1 and TNF, enhancing the release of interleukin-6 andprostaglandin from human spinal cord glia. It also syner-gizes with oligosaccharide, enhancing interleukin-1release. Astrocytes in the spinal cord, but not astrocytesisolated from various brain regions, release prostaglandinsin response to substance P, suggesting that glia areuniquely responsive to neurotransmitters in the dorsalhorn. Extracellular ATP and ATP metabolites also stimu-late astrocytes to release prostaglandins and microglia torelease TNF and interleukin-6 (Milligan et al.).

Further experiments have demonstrated that glia acti-vation is both necessary and sufficient for enhanced noci-ception in every animal model tested. Activated gliaenhanced pain via the release of a variety of neurointer-active substances. Central to these effects is glial releaseof proinflammatory cytokines including TNF, interleukin-1, and interleukin-6. These in turn activate a cascade ofevents leading to release of a host of neuroexcitatory sub-stances such as nitrous oxide, prostaglandin, growth fac-tors, and excitatory amino acids. Thus, evidence is accu-mulating that glia play a profound role in relation to noci-ception by means of immunologic and neuronal interac-tions (Watkins et al., 2001; 2003).

It is interesting to note that prostaglandin PGE

2

in miceblocked the inhibitory action of the glycine spinal neu-rotransmitter by blocking its action at the glycine receptorsubtype (GlyR 3) through inducing receptor phosphory-lation. Blocking of these receptors, found primarily in thesubstantia gelatinosa of the dorsal horn, led to nociceptivesensitization. Knockout mice lacking the receptor demon-strated reduced sensitization. This further demonstrateshow products of inflammation may shape the nociceptiveresponse through neural interaction (Harvey et al.).

Other evidence implicating a significant role for micro-glia in the development of allodynia is noted in the workof Tsuda et al. They noted that the pharmacologic block-ade of spinal P2X

4

receptor, a subtype of inotropic ATPreceptor-reversed tactile allodynia caused by peripheralnerve injury, did not affect acute pain behavior in animals.After nerve injury, P2X

4

expression increased strikinglyin the ipsilateral spinal cord, and P2X

4

receptors wereinduced in hyperactive microglia but not in neurons or

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SECTION VIII THE PHYSIOLOGY OF PAIN

astrocytes. Both these results demonstrate that the activa-tion of P2X

4

R in the hyperactive microglia is necessaryfor tactile allodynia after nerve injury and is sufficient toproduce tactile allodynia in normal animals (Tsuda et al.).

SUPRASEGMENTAL DETERMINANTS OF NOCICEPTION

The cognition of pain of the chronic and acute typeshas been imaged via PET scan and functional event-related MRI. In the case of chronic neuropathic pain stud-ied by PET scan techniques, a significant decrease inthalamic activity contralateral to the symptomatic side wasdemonstrated (Iadarola et al.). In acute pain states, thesituation was different. In studies utilizing event-relatedfunctional MRI techniques, acute pain was noted to beassociated with secondary somatosensory cortex and tha-lamic activation.

In addition to the finding of thalamic modeling, othercentral areas have also been found to play central roles innociceptive anticipation, processing, and reflex activity(Porro et al.). The high degree of intraindividual sensitivityto pain is well known. It has now been shown that indi-viduals who are highly sensitive to pain exhibit morefrequent and more robust pain-induced activations of theprimary somatosensory cortex, anterior cingulate cortex,and prefrontal cortex (Coghill et al. 2003).

The variability of individual differences in both thesubjective experience of pain and activation of somatosen-sory, anterior cingulate, and frontal cortices is likely attrib-utable to factors other than differential sensitivity of spinalor peripheral afferent mechanisms. Therefore, supraspi-nally mediated factors that fall into the cognitive domainmay account for significant variations in the subjectiveexperience of pain and differences in the activation ofsuprasegmental influences on the involved segments.

Cognitive manipulations such as hypnotic manipula-tion for the purpose of reducing the perceived unpleasant-ness of pain, i.e., the subjective experience of pain, havebeen shown to produce significant changes in the activitylevels of the somatosensory and anterior cingulate corticeswith activation when subject to pain without hypnoticsuggestion and lack of activation when hypnotic sugges-tion is utilized. The thalamus and somatosensory cortexunder these conditions demonstrate similar levels of acti-vation in hypnotized and nonhypnotized subjects. How-ever, hypnotized subjects not undergoing activation of theanterior cingulate cortex reported reduced unpleasantness ofpain, underscoring how these cerebral cortical regions maybe involved in enhancement or suppression of nociceptivecognition and behavior (Coghill et al., 2003, Rainville et al.,1997, Rainville et al. 1999).

Other studies demonstrated via PET scans that bothopioid and placebo analgesics are associated with

increased activity of the anterior cingulate cortex, suggest-ing an overlap of neuromechanisms involved in placeboand opioid analgesia (Petrovic et al.).

A study of placebo-induced changes associated withnociceptive experience utilizing functional magnetic res-onance noted that placebo analgesia is related to decreasedbrain activity in pain-sensitive regions including the thal-amus, insula, and anterior cingulate cortex, and is associ-ated with increased activity during anticipation of pain inthe prefrontal cortex, providing evidence that placeboalters the experience of pain (Wagner et al.).

Studies of social distress utilizing neuroimaging tech-niques have demonstrated the activation of the anteriorcingulate cortex, indicating a close analogy to neuralchanges associated with physical pain (Eisenberger et al.).This suggests an objective physiologic basis for theenhancement of nociceptive sensitivity during stressstates. Studies of conflict have demonstrated that anteriorcingulate cortex activity predicts both greater prefrontalcortex activity and adjustments of behavior, supporting arole of the anterior cingulate cortex in conflict monitoringin the engagement of cognitive control (Kerns et al.).

A study examining the role of affective conditions andthe regulation of responses involving the anterior cingulateand limbic opioid neural transmission noted that sustainedsadness as a condition is associated with a statisticallysignificant deactivation in

µ

opioid neurotransmission inthe rostral anterior cingulate cortex, ventral pallidum,amygdala, and inferior temporal cortex. This deactivationis reflected by increases in µ opioid receptor availability

in vivo

. The deactivation of µ opioid neurotransmission inthe rostral anterior cingulate cortex, ventral pallidum, andamygdala was felt to be correlated with the increase innegative affective ratings and the reductions in positiveaffect ratings during sustained sadness. This demonstra-tion of the dynamic changes in µ opioid neurotransmissionin response to an experimentally induced negative affec-tive state provides further objective evidence of physio-logic plasticity at suprasegmental levels connected to cog-nitive states (Liberzon et al., Zubieta et al.).

NOCICEPTIVE RATIONALIZATION

Nociception, or the knowing that one has pain, is sub-ject numerous controls that have characteristics particularto its mode of inception, processing, and the cognitivestate of the individual. The process of nociceptive ratio-nalization also takes into account the bias of the individ-ual, from stoic to extreme cases of “catastrophizing” —a situation marked by heightened anticipation of pain andheightened emotional response to pain.

In studies of catastrophization of pain, Gracely et al.demonstrated increased activation in subjects catastroph-izing in the medial frontal cortex and cerebellum with

CHAPTER 71 THE NEUROPHYSIOLOGY OF PAIN

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anticipation of pain and in the dorsal anterior cingulategyrus and dorsal lateral prefrontal cortex with attention topain. The overlap and segregation of areas activated sug-gest multiple possibilities for interaction and modulationof pain and, when combined with spinal segmental, super-segmental, and intracerebral processing, sufficient plastic-ity to allow a wide variety of responses can be demon-strated.

The role of nociceptive rationalization in the modula-tion of the nociceptive chain can cover extremely shorttime spans reminiscent of reflex arcs or can induce long-term changes that bear striking resemblance to intracorti-cal memory. The timeframe in which nociceptive process-ing and nociceptive chain modulation occur can be influ-enced by numerous mechanisms that are inhibitory orfacilitory; the contribution of cognitive activity is notalways taken fully into account during the nociceptivestate.

NOCICEPTIVE LOCALIZATION

The study of the physiology of nociception demon-strates clearly that it is a highly dynamic process that isboth plastic and diffusely located, further complicating thecognitive perspective expectations involving localization.The process of nociceptive cognitive localization is com-plicated by a perceptual bias imposed on nociceptiveinformation as a result of the limited anatomic represen-tation in cortical parietal lobe processing and the spreadof central sensitization so that pain that has a referredcharacter may be misidentified as a primary source of painby the observer. Thus, the presence of nociceptive ration-alization bias and localization bias must also be consid-ered within the worldview of the nociceptive experienceand can help to explain the phenomenologic diversity ofdescriptions of the nociceptive experience.

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Maigne, R. Manipulations of the spine, manipulations and mobilisationof the limbs, in Basmadjian J.V., Ed., Manipulation, Traction andMassage, Baltimore, Williams & Wilkins, 1980, 1985.

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Painful Minor Intervertebral DysfunctionMaigne, R. Semiologie des derangements intervertebraux mineurs.Ann. Med. Phys., 1972, 15, 275–293 (Lire la page 281, apreslapage 276, et avantla page 278).

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Segmental Vertebral SyndromeMaigne, R. Le massage dans les sciatiques. Communication au Con-gres National de Medecine Physique, Nice, 1961.

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Maigne, R. Articulations interapophysaires et pathologie douloureusecommune du rachis. Ann. Med. Phys., 1972, 15, 262–275.

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Maigne, R. Origine dorso-lombaire de certaines lombalgies basses.Role des articulations interapophysaires et des branches posterieuresdes nerfs rachidiens. Rev. Rhum., 1974, 41, 12, 781–789.

Maigne, R. Responsabilite du rachis cervical clans les cephaleescommunes. Cinesiologie, 1972, 73, 73–84.

Maigne, R. en coil. avec Maigne, J.Y. and Lazareth, J.P. Etude del’innervation cutanee lombo-sacree: application a la physiopathologiede certaines lombalgies. Rev. Rhum., 1988, 55, 2, 107–111.

Interscapular Pain of Cervical OriginMaigne, R. Dorsalgies, sequelles des traumatismes cervicaux mineurs.Communication au 3e Congres de Therapie Manuelle, Nice, 1962.

Maigne, R. La dorsalgie benigne interscapulaire. Son origine cervicalefrequente. Rhumatologie, 1964, 14, 457.

Maigne, R. Sur l’origine cervicale de certaines dorsalgies benigneset rebelles de I’adulte. Rev. Rhum., 1964, 31, 497–503.

Maigne, R. A propos du mecanisme de la douleur dans les dorsalgies.Le point interscapulo-vertebral. Rev. Rhum., 1967, 34, 636–641.

Maigne, R. La dorsalgie interscapulaire. Manifestation de la souffrancedu rachis cervical inferieur. «Le point cervical du dos». Sem. Hop.Paris, 1977, 53, 1067–1072.

Maigne, R. Dorsalgie commune et derangement intervertebral mineurcervical. Rhumatologie, 1977, 29, 23–34.

Low Back Pain of Thoracolumbar OriginMaigne, R. Articulations interapophysaires et pathologie douloureusedu rachis. Ann. Med. Phys., 1972, 15, 262.

Maigne, R. Origine dorso-lombaire de certaines lombalgies basses.Role des articulations interapophysaires et des branches posterieuresdes nerfs rachidiens. Rev. Rhum., 1974, 41, 781–789.

Maigne, R. Une origine meconnue et frequente de lombalgies basses:les articulations interapophysaires de la charniere dorso-lombaire.Rô1e des «posterior rami» des nerfs rachidiens D11, D12, L1. UnionMed. Can., 1975, 104, 1676–1684.

Maigne, R., Le Corre, F., and Judet, H. Lombalgies basses rebellesd’origine dorsolombaire. Traitement chirurgical par excision des cap-sules articulaires posterieures. Nouv. Press. Med., 1978, 7,565–568.

Maigne, R. Les lombalgies apres chirurgie discale. Leur origine dor-solombaire frequente (etude de 52 cas). Rhumatologie, 1978, 30,329–335.

Maigne, R., Le Corre, F., and Judet, H. Premiers resultats d’un traitementchirurgical de la lombalgie basse rebelle, d’origine dorso-lombaire.Rev. Rhum., 1979, 46, 177–183.

Maigne, R. Low back pain of thoracolumbar origin. Arch. Phys. Med.Rehabil., 1980, 61, 389–395.

Maigne, R. Lombalgies et branches posterieures des nerfs rachidiensde la charniere dorso-lombaire. Ann. Med. Phys., 1980, 23,150–168.

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Maigne, R. Lombalgies et branches posterieures des nerfs rachidiens.Med. Hyg., 1984, 42, 3281–3288.

Thoracolumbar Junction SyndromeMaigne, R. Un syndrome nuevo y frequente: el sindrome D12–L1(lumbalgias bajas, dolores seudoviscerales, falsos dolores de la cad-era). Rehabilitacion, 1977, 11, 197–210.

Maigne, R. Le syndrome de la charniere dorsolombaire. Lombalgiesbasses, douleurs pseudoviscerales, pseudo-douleurs de hanche,pseudotendinite des adducteurs. Sem. Hop. Paris, 1981, 57,545–554.

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Maigne, R. Pubalgies, pseudo-tendinite des adducteurs et charnieredorso-lombaire. Ann. Med. Phys., 1981, 24, 313–319.

Shoulder Pain and Cervical SpineMaigne, R. Pseudo-tendinites d’epaule et rachis cervical. Ann. Med.Phys., 1975, 18, 196–203.

Maigne, R. Douleurs d’epaule et rachis cervical, in Simon, L., Ed.,Epaule et medecine de reeducation, Paris, Masson, 1984, pp.98–100.

Headache of Cervical OriginMaigne, R. La cephalee sus-orbitaire. Sa frequente origine cervicale.Son traitement. Ann. Med. Phys., 1968, 11, 241–246.

Maigne, R. Un signe evocateur et inattendu de cephalee cervicale:«la douleur au pince-route du sourcil». Ann. Med. Phys., 1976, 19,416–434.

Maigne, R. Signes cliniques des cephalees cervicales. Leur traitement.Med. Hyg., 1981, 39, 1174–1185.

Maigne, R. and Maigne, J.Y. Semiologie des cephalees cervicalesou diagnostic clinique des cephalees cervicales, in Simon, L., Ed.,Actualites en reeducation fonctionnelle et readaptation, Paris, Masson,1982, pp. 123–130.

Epicondylar PainMaigne, R. Le traitement des epicondylites. Rhumatologie, 1957, 9,293–295.

Maigne, R. Epicondylalgies, rachis cervical et articulation humero-radiale. A propos de 150 cas. Ann. Med. Phys., 1960, 3, 299–311.

Maigne, R. Cotation et diagnostic dune epicondylalgie. Cinesiologie,1975, 56, 113–114.

Maigne, R. Evaluation et orientation therapeutique des epicondylalg-ies, in Simon, L., Ed., Coude et medecine de reeducation, Paris,Masson, 1979, pp. 123–128.

Maigne, R. Les manipulations dans le traitement des epicondylites. Lefacteur cervical. Le facteur articulaire. Ann. Readapt. Med. Phys.,1986, 29, 57–64.

Maigne, R. Douleurs de sein d’origine vertebrale ou parietale. Seno-logia, 1980, 5, 287–292.

Maigne, R. Pathologie mecanique de l’articulation tibioperonieresuperieure, in Simon, L., Ed., Actualites en reeducation fonctionnelleet readaptation, Paris, Masson, 1981, pp. 112–118.

Maigne, R. Douleurs et pseudo-blocages du genou d’origine verte-brale. Ann. Med. Phys., 1981, 3, 320–325.

Maigne, R. Das Syndrom der Ubergangszonen der Wirbelsaule.(syndrome des zones transitionnelles). Man. Med., 1984, 22,122–124.

Maigne, R. and Maigne, J.Y. Le syndrome du ligament ilio-lombaire.Mythe ou realite? Ann. Read. Med. Phys., 1987, 30, 439–446.

PubalgiaMaigne, R. Pubalgies, pseudo-tendinite des adducteurs et charnieredorso-lombaire. Ann. Med. Phys., 1981, 24, 313–319.

Maigne, R. La pubalgie peut titre une douleur tenoperlostee d’originerachidienne. Cinesiologie, 1982, 21, 213–220.

Maigne, R. Pubisschmerzen and Tendiniden der Adduktoren verte-bralen Ursprung. Man. Med., 1986, 24, 109–113.

ManipulationMaigne, R. Manipulations vertebrales et manipulateurs. Sem. Hop.Paris, 1953, 29, 1944–1949.

Maigne, R. Les manipulations vertebrales: indications, contre-indications,techniques et resultats. J. Med. Paris, 1955, 11, 405–418.

Maigne, R. Les manipulations vertebrales. Paris, Expansion ScientifiqueFrangaise, 1960.

Maigne, R. L’application rationnelle des manipulations vertebrales, inProceedings of the IV International Congress of Physical Medicine.Paris, 1964, Amsterdam, Excerpta Medica, 1966, pp. 145–149.

Maigne, R. The concept of painlessness and opposite motion in spinalmanipulations. Am. J. Phys. Med., 1965, 44, 55–69.

Maigne, R. Le choix des manipulations cans le traitement des scia-tiques. Rev. Rhum., 1965, 32, 366–372.

Maigne, R. Une doctrine pour les traitements par manipulations: laregle de la non-douleur et du mouvement contraire. Ann. Med. Phys.,1965, 8, 37–47.

Maigne, R. Fundamentos fisiopatologicos de la manipulacion verte-bral. Rehabilitacion, 1976, 10, 427–442.

Maigne, R. Manipulations vertebrales et thromboses vertebro-basilaires.Angeiologie, 1969, 21, 287–288.

Perforating Branch Syndrome of T12 and L1Maigne, R. and Maigne, J.Y. Syndrome des branches perforanteslaterales des nerfs sous-costal et abdominogenital (D12 et L1): unecause meconnue de douleurs de hanche d’origine vertebrale ou locale.Ann. Read. Med. Phys., 1986, 29, 29–37.

Maigne, R. and Maigne, J.Y. Syndrome des branches perforanteslaterales des nerfs sous-costal et ilio-hypogastrique. Rev. Rhum., 1986,53, 307–301.

MiscellaneousMaigne, R. Les entorses costales. Rhumatologie, 1957, 1, 35–41(voir aussi J.Y. Maigne, R. pour articles faits en collaboration). sur lespresses Acheve d’imprimer.

de l’Imprimerie Soulisse et Cassegrain 79000 NIORT en octobre1989 No. d’imprimeur: 2727.

531

INDEX

A

Abdominal pain, pseudovisceral, 379acute, 381lumbar herniated disk and, 382pseudogastrointestinal, 380pseudogynecologic, 381pseudourologic, 382role of cellulalgia in, 379treatment of, 382

Acetylcholine, 44, 226, 498Achilles tendon rupture, 225Acromioclavicular joint

assessment of, 348dysfunction of, 114 manipulation of, 353

Acroparesthesias of upper limbs and cervical spine, 341–344acroparesthesias with entrapment, 342–343

carpal tunnel syndrome, 342–343Guyon’s canal syndrome, 343

cervical spine and acroparesthesia, 343–344double crush syndrome, 344nocturnal global acroparesthesias, 341–342with radicular topography, 341

Acute cervical pain,

see

Torticollis and acute cervical painAdrenalin, 44, 225Aging spine, 69–72

effects on facet joints, 70–72intervertebral foramen, 71–72trophostatic syndrome of menopause, 70–71

effects on intervertebral disk, 69formation of osteophytes, 69nucleus pulposus, 69

effects on vertebral body, 69Anatomy

arterial supply, 31autonomic nervous system, 43cervical spine, 17intervertebral disk, 36lumbar spine, 21muscles, 27–30perforating branch syndrome, 319–320sacroiliac joint, 23thoracic spine, 21thoracolumbar junction syndrome, 384venous supply, 31

Angle of the jaw sign, 146, 328, 330Annulus fibrosus, 7

concentric splits of, 83radial tears of, 83

Anomaliesof facet joints, 86in frontal plane, 120

antalgic posturing, 120scoliosis and pseudoscoliosis, 120

of occipitocervical junction, 19in sagittal plane, 121

Antalgic posturing, 120Anterior cervical doorbell sign, 262Arm elevation test, 343Artery(ies)

intercostal, 31lumbar, 31mesenteric artery compression syndrome, 234radicular, 31 vertebral, 18

in cervical spine, 18compression of, 86injury of, 19spinal nerve with, 20transverse processes and, 19

Arthrosis, 70facet joint, 71, 86, 101, 282thoracic, 268

Articular receptors, 40Atlanto-axial articulation, 52

flexion/extension at, 52lateral inclination at, 52pressure on, 67rotation at, 52

Atlanto-occipital articulation, 52flexion/extension at, 52lateroflexion at, 52pressure on, 67

Atlas (C1), 11Auditory symptoms, 335Automotor frame, 203Autonomic nervous system, 43–45

parasympathetic system, 44–45sympathetic system, 43–44

Autoregulation, 49Axial pressure maneuver, 136Axial traction maneuver, 136, 204, 459Axis (C2), 11

B

Backcervical point of, 246, 260examination of, 120, 132, 275, 305muscles of, 27, 28, 30zones of hyperesthesia, 79

BDNF,

see

Brain derived neurotrophic factorBelt technique, 474

for cervical traction, 408for lumbar manipulation, 301

Biomechanicsaging spine, 69–72disk degeneration and, 282forces acting on vertebral column, 65–67

532

INDEX

of sacroiliac joint, 59–63spinal kinematics, 49–57

Brain derived neurotrophic factor (BDNF), 502Breast pain, false, 379Buffalo’s hump, 248, 250

C

Calcium waves, 502Calmodulin, 497Cardiac disorders, 259Carpal tunnel syndrome, 111, 341, 342Causalgia, 45Cellulalgia, 103

electrotherapy for, 231examination for, 141, 143

cheek sign, 142, 145eyebrow sign, 145friction maneuver for scalp, 145in lumbar region, 455pinch-roll test, 106–107, 145, 375in thoracic region, 150

of L3 or L4, 376low back pain and, 287midthoracic cellulalgic band, 260role in pseudovisceral pain, 379in thoracolumbar junction syndrome, 373topography of, 106, 107

Central pattern generators (CPGs), 504Cervical collars, 239–240

indications, 239acute cervical pain, 239cervical trauma, 239cervicobrachial neuralgia, 239chronic cervical pain, 239

types of collars, 239collars with rigid reinforcement, 239flexible collars, 239mini Minerva collars, 239

Cervical lordosis, 3Cervical migraine, 333–334

cervical migraine, 333migraine and superior cervical spine, 333–334true migraine, 333

Cervical point of the back, 246, 253Cervical syndrome, 335–337

diagnosis, 336elements, 335–336

auditory symptoms, 335headaches, 335pharyngolaryngeal symptoms, 335psychologic symptoms, 335–336vasomotor and secretory symptoms, 335vestibular symptoms, 335visual symptoms, 335

examination of cervical spine, 336mechanism, 336treatment, 336–337

Cervical techniques, 403–421manipulation, 409–421

accessory technique (chin grasp), 415–416anterior hand technique, 419–420basic technique (chin free), 409–414chin grasp technique, 416–418posterior hand technique, 421

massage, 403mobilization and manual traction, 405–408

manual traction, 407–408mobilization, 405–407

relaxational maneuvers, 403–404Cervicobrachial neuralgia, 253–257

clinical examples be segmental level, 254differential diagnosis, 255–256

entrapment syndromes, 255referred pain syndromes, 255–256

etiologies, 254–255examination of neck, 253

examination of affected level, 253test of manual traction, 253

interscapular pain, 253pain, 253treatment, 256–257

manipulation, 256, 257spinal traction, 257

Cervicobrachial radiculitis, 188Cervicothoracic junction techniques, 423–433

manipulation, 427–433cervicothoracic technique in lateral decubitus position,

427–432lateral pressure against spinous process, 432–433

massage of subcutaneous tissues, 423mobilization, 425–426

in extension, 425in flexion, 426in rotation, 426

relaxational maneuvers, 423–424Chamberlain’s line, 20, 21Cheek sign, 142, 145, 328Chemonucleolysis, 310, 382Chin free technique, 398, 409Chin grasp technique, 399, 409Chin pivot technique, 266, 352Cholinergic fibers, 44Chromatin, 496Clinical history, 119, 275Cobb angle, 121Coccygodynia, 196, 317–318

causes of, 317diagnosis, 317traumatic, 317treatment, 317–318

authors’ technique, 317–318massage of levatores, 317osteopathic technique, 317

Coccyx, 11, 24, 60, 188, 317Cold pulverization, 228Collagen, maturation of, 69Computed tomography (CT), 85, 182, 308Corsets,

see

Lumbosacral corsetsCorticosteroid injections, 217,

see also

Injections, therapeuticcontraindications to, 217therapeutic complications of, 225

Costal sprains, 271–273clinical picture, 271clinical presentation, 271

direct trauma, 271faulty movement or forceful effort, 271

diagnosis, 271–272anterior costal sprains, 272posterior costal sprains, 271–272

false ribs, 188

INDEX

533

hooked rib, 272treatment, 272

Counternutation, 59CPEB,

see

Cytoplasmic polyadenylation element binding proteinCPGs,

see

Central pattern generatorsCracking, 168

articular gapping and, 199mechanism of, 168time of recharging after, 168

Cranial settling, 20, 21Crestal points, 386, 388Crossed antalgic attitude, 152Cryotherapy, 228

cold pulverization, 228ice application, 228ice massage, 228

CT,

see

Computed tomography Curvatures, 3–6

accentuated, 5embryology, 3evolution of, 6keystone vertebrae of, 24scoliotic, 89, 120, 124spinal curves and resistance to loading, 3types, 3

Cysts, synovial, 87Cytoplasmic polyadenylation element binding protein (CPEB), 499

D

Delmas index, 3Dermatomes, 33, 36, 76, 82, 105, 139, 158, 263Diathermy treatment, 98, 231, 285, 388Diffuse idiopathic polyalgic syndrome,”115Direct antalgic attitude, 152Discal osteophyte, 72Discal pathology, 99Discography, 77, 84, 92, 279, 308Disco-osteophytic nodule, 19Doorbell sign, 262Dorsal root ganglia (DRG), 500, 503Double crush syndrome, 111, 297, 344Double knee technique, 401DREAM protein, 496DRG,

see

Dorsal root gangliaDrop attacks, 192Dynamic spine of Delmas, 3

E

ECT,

see

Electroconvulsive therapyElbow pain, 358,

see also

Lateral epicondylar painElectroconvulsive therapy (ECT), 191Electronystagmography, 193, 335Electrotherapy, manifestations of neurotrophic spinal segmental

syndrome, 231cellulalgia, 231periosteal pain, 231tendinous pain, 231trigger points, 231

β

-Endorphins, 75

Enkephalins, 75Enthesites, 110Entrapment syndrome(s), 255

consequence of, 342

at Guyon’s canal, 343knee pain due to, 375of perforating cutaneous branches of T12 and L1, 374of saphenous nerve, 376treatment, 323

Epidural injectionvia first sacral foramen, 217, 218for low back pain, 284, 299patient position for, 217via sacrococcygeal hiatus, 217via translumbar route, 219

Epinephrine, 44, 497EPSP,

see

Excitatory postsynaptic potentialsExcitatory postsynaptic potentials, (EPSP), 499Experimentally provoked pain, 75–82

dermatomes, 82disk, 76–77facet joints, 77interspinous ligaments, 78–79ligamentum flavum, 80muscles, 80–82posterior and anterior longitudinal ligaments, 79–80spinal nerve root, 76

motor root, 76sensory root, 76

vertebral body, 80Extension of spine, 50, 53

assessment of, 124cervical, 17, 53lumbar, 56

Eyebrow sign, 142, 145, 328

F

Facet block, 101, 505Facet joints

anomalies of, 86arthrosis of, 86articular malformations and, 99cervical, 17, 221discal pathology and, 99 experimentally provoked pain and, 77inflammatory involvement of, 248innervation of, 37lesions, 86, 197longitudinal friction overlying, 129, 155low back pain and, 281, 299of lumbar spine, 56meniscoid formations of, 87periarthritis of, 87

Failed back syndrome, 393–394False hip pain of spinal origin, 373–374

entrapment syndromes of perforating cutaneous branches of T12 and L1, 374

false hip pain and T12–L7 segmental vertebral syndrome, 373–374

total hip arthroplasty and false hip pain, 374trochanteric pain and L5 segmental vertebral syndrome, 373

Fanning maneuver, 457Femoral neuralgia, 313–314

causes of, 314cellulotenoperiosteomyalgic manifestations of, 313clinical examination, 313–314clinical symptoms of, 313differential diagnosis, 314

534

INDEX

initial symptoms and topography, 313topography of, 313treatment, 204, 314

Fibromyalgia, 115Fibrositis, 113, 115Fischgold’s line, 21Flexion of spine, 17

assessment of, 123lumbar, 21, 56thoracic, 55

Flurimethane spray, 214Foot drop, 311Forces acting on vertebral column, 65–67

disk, 65pressure, 65–66role of abdominal wall, 66role of sacroiliac joints, 67role of vertebral body as shock absorber, 66–67

Free nerve endings, 36, 38, 40Friction sign test, 247Frozen shoulder, 345

G

Gaenslen’s maneuver, 481Gamma loop, 40

inverse myostatic reflex, 40myostatic reflex, 40

Ganglion, 43cervical, 331lumbosacral, 43ophthalmic, 44optic, 44sphenopalatine, 44stellate, 45submaxillary, 44

Gate control theory, 75Gerber’s sign, 346Glenohumeral joint

assessment of, 346examination of, 350mobilization of, 353

Glenoid fossa, 349Golgi tendon organs, 37Growth apophysitis,

see

Scheuermann’s disease

H

Headache(s)case history of, 329cheek sign, 328eyebrow sign, 328, 329, 330migrainous form of, 329simple form of, 329vascular form of, 329

Headache of cervical origin, 325–332cervical muscles and headaches, 331–332common characteristics of cervical headaches, 325different aspects of headache of cervical origin, 325–329

occipital headache, 326–327occipitotemporomaxillary headache, 327–328supraorbital headache, 328–329

frequency of cervical headaches, 329–330pathophysiologic mechanisms, 330–331

craniofacial signs, 330

facet joint tenderness, 330hypotheses about mechanisms, 330–331

treatment, 331facet joint injection, 331manipulation, 331

triggering factors, 329Head support, 3, 18, 134Heat baths, 227Herniated disk, noncontained, 83Hip

entrapment syndromes, 320, 321false hip pain of spinal origin, 374L5 segmental vertebral syndrome, 160periarthritis of, 228, 310total hip arthroplasty, 374

Histones, 496History taking, 119, 246Hollow round maneuver, 153Hooked rib, 272Hotel Dieu method, 227Hydrotherapy, 227–228

contraindications, 228Hotel Dieu method, 227results, 227–228

Hyperacusis, 335Hyperalgesia, referred, 502, 503Hyperkyphosis, thoracic, 89

due to dystrophic spinal growth, 90posture in adolescent, 89–90

Hyperlordosis, 70, 86, 125, 312, 322, 369

I

Ice application, 228Ice massage, 228Imbibition pressure, 13Implantable devices, 229Injections, therapeutic, 217–226,

see also specific types

accidents associated with injection of local anesthetic, 225

allergic reactions, 225diffusion of local anesthetic toward neuraxis, 225toxic accidents, 225

botulinum toxin injections, 226complications of steroid injection, 225–226injection of scars, 225medications and complications of medication use, 226selective neural blockade, 223–224spinal injections, 217–223

epidural injection, 217–219facet joint injections, 220–222intrathecal injection, 219–220ligamentous injections, 222–223

trigger point injections, 224Innervation of vertebral structures, 33–41

articular receptors, 40–41disk, 36–37facet joints, 37ligaments, 38muscle and tendon receptors, 38–40

free nerve endings, 40Golgi tendon organs, 40neuromuscular spindles, 38–40

posterior primary rami, 33–35sinovertebral nerve, 35

INDEX

535

spinal musculature, 38vertebral periosteum, 38

Intervertebral disk(s), 11–13aging effects on, 69calcification of, 304hydrophilic properties, 12infectious discitis, 245inhibition factor, 13lesions, 83, 281mobile segment and, 49ratio of disk to vertebral body height, 11separation, 204Sharpey’s fibers, 12shock-absorbing function of, 65

Intramedullary tumors, 255, 310Intrathecal injection, 219, 220, 310Inverse Lasegue sign, 313Inverse myotatic reflex, 40Iontophoresis, 231, 250, 297Irritable bowel syndrome, 381

J

Joint blockage, 165Joint play, 102

of distal radioulnar joint, 358lateral, of elbow, 358testing of, 349

K

Kissing spine, 70Knee pain of spinal origin, 375–378

clinical picture, 376–377cellulalgia of L3 or L4, 376entrapment syndrome of saphenous nerve, 376–377tenoperiosteal tenderness, 376trigger points of vastus medialis and pseudoblockage of knee, 376

examination, 375knee pain and proximal tibiofibular joint, 377–378

Knee technique, 297, 303, 314, 401Kyphosis, 89, 241

L

Lasegue’s sign, 184, 213, 279, 313, 482, 485Lateral epicondylar pain, 357–366

cervical spine and, 364–366classification of, 359clinical examination, 357–358

cervical spine, 358elbow, 357–358

distal radioulnar dysfunction, 363–364evaluation of, 358–363lateral joint play of elbow, 358manipulation in abduction, 361manipulation in adduction, 361manipulation in extension, 361manipulation in flexion-supination, 362manipulation in pronation, 362manual muscle testing against resistance, 357palpation, 357radiography, 358range of motion, 357

Lateral Lasegue’s sign, 320Lesion in flexion, 102Levator scapulae syndrome, 339–340

clinical picture, 339–340different aspects of pain, 339mechanism, 339–340

treatment, 340Ligament(s)

iliolumbar, 57, 223, 287innervation of, 38interspinous, 78, 99, 268posterior and anterior longitudinal, 79therapeutic injection of, 222

Ligamentous system, 15–16anterior longitudinal ligament, 15interspinous ligament, 15ligamentum flavum, 16posterior longitudinal ligament, 15

Linea alba, 29Local anesthetic injections,

see also

Injections, therapeuticallergic reactions, 225diffusion of anesthetic toward neuraxis, 225muscular lesions and, 87toxic accidents, 225

Local twitch response (LTR), 224Locked-in syndrome, 194Lordosis

cervical, 3hyperlordosis, 70, 391lumbar, 3

Low back painclinical signs of, 293discogenic, 281epidural injection for, 284facet joint injection for, 285functional assessment, 277intradiscal injection for, 285Lasegue’s sign, 279 lumbosacral corsets used for, 235mobilization for, 284muscle examination, 278myofascial, 287neurologic examination, 279physical modalities for, 285radiologic examination, 279, 295rhizotomy for, 285segmental examination, 277 spinal manipulation for, 284therapeutic exercise for, 286

Low back pain, acute, 233, 299–304of calcifying discopathy, 304of lumbosacral origin, 299–303

clinical picture, 299mechanism, 299treatment, 299–303

of myofascial origin, 304of thoracolumbar origin, 303

clinical signs, 303treatment, 303

Low back pain, chronic, 275–280conclusions of clinical examination, 279–280examination of patient, 275–275

active range of motion assessment, 275–277clinical history, 275examination of muscles, 278–279examination of subcutaneous tissues, 278

536

INDEX

Lasegue’s sign, 279neurologic examination, 279physical examination, 275radiographic examination, 279segmental examination, 277–278

Low back pain of ligamentous origin, 283Low back pain of lumbosacral origin, 241, 281–287

cellulotenoperiosteomyalgic segmental vertebral syndrome, 284–287

low back pain due to disk lesions, 281–282discogenic low back pain, 281–282low back pain due to segmental instability following disk

degeneration, 282low back pain of extraspinal origin, 287

cellulalgic sheeting, 287iliolumbar ligament, 287myofascial origin, 287

low back pain of ligamentous origin, 283painful minor intervertebral dysfunction, 283–284role of facet joint in low back pain, 282–283

Low back pain of thoracolumbar origin, 242, 289–298anatomic review, 290–293

facet joints, 290posterior rami of thoracolumbar spinal nerve roots, 291–293transitional vertebra, 290–291

atypical forms, 296–297clinical signs, 293–295

clinical examination, 293–294confirmation of thoracolumbar origin of low back pain,

294–295incidence, 295–296radiologic examination, 295treatment, 297–298

corrective actions, 298electrotherapy, 297facet joint injection, 297percutaneous rhizotomy, 298surgical capsulectomy, 297–298therapeutic exercise, 298treatment of cellulalgic lumbogluteal region, 297

LTR,

see

Local twitch responseLumbar lordosis, 3Lumbar orthoses, 233–234

fabrication of rigid lumbar orthosis, 233–234indications, 233

acute low back pain, 233chronic low back pain, 233sciatica, 233

mode of action, 234Lumbar techniques, 455–475

manipulation, 463–475astride technique, 470–472belt technique, 474–475double knee technique, 473–474lateral decubitus technique in extension, 466–467lateral decubitus technique in flexion, 463–465lateral decubitus technique in neutral position, 468–469

massage, 455mobilization, 460–462

in extension, 462in flexion, 460in lateroflexion, 461in rotation, 462

relaxational maneuvers and muscle stretching, 455–459relaxational maneuvers, 455–457stretching, 457–459

Lumbosacral corsets, 235–237contraindications, 237indications, 235mode of action, 237types, 235

M

Magnetic resonance imaging (MRI), 84, 182, 308, 495Maigne collar, 202Manipulative techniques, introduction to, 397–402

basic manipulative techniques, 398–402accessory techniques, 399–402basic techniques, 398–399

equipment, 397–398Manipulative thrust, 166Manual therapy techniques

accessory techniques, 399–402 basic techniques, 398–399 cervical spine, 398, 399cervicothoracic junction, 401 equipment, 397 false ribs, 401 lower thoracic and lumbar levels, 401lumbar spine, 399thoracic spine, 398thoracolumbar junction, 399

Massage, 207–211, 403acute muscle spasm, 207cellulotenoperiosteomyalgic manifestations,

207–210cellulalgia, 208tenoperiosteal pain, tenalgias, and tendinitis, 210trigger points, 208–210

chronic muscle spasm, 207 deep transverse massage, 210–211paraspinal muscle relaxation, 207

Maturation of collagen, 69Medial epicondylar pain, 367Menisci, 9Meralgia paresthetica, 157, 315–316

canalicular origin, 316mixed origin, 316spinal origin, 316

Mesenteric artery compression syndrome, 234Migraine,

see

Cervical migraineMini Minerva collar, 239MRI,

see

Magnetic resonance imagingMuscle(s), 27–30

abdominal muscles, 29–30biceps, 347

brevis, 357, 360deltoid, 27erector spinae, 29extensor carpi radialis longus and brevis, 357extensor carpi ulnaris, 357extensor digiti minimi, 357extensor digitorum communis, 357hamstrings, 298 iliocostalis, 27, 28infraspinatus, 346intercostal, 28intertransversarii, 33 intrinsic vs. extrinsic, 27 latissimus dorsi, 347

INDEX

537

levator scapulae, 28, 29, 142, 188, 247, 268, 339–340longissimus thoracis, 28, 29longus colli, 27lumbar region, 30masseter, 331multifidus, 28, 29neck and back, 30obliquus capitis inferior, 29 obliquus capitis superior, 29 obliquus externus abdominis, 29 obliquus internus abdominis, 29paraspinal muscles, 27–29

erector spinae muscles within vertebral sulcus, 29muscles located anterior to plane of transverse process,

27muscles located between transverse processes, 28–29

pectoralis major, 347psoas, 27

quadratus lumborum, 28 rectus abdominis, 28rectus capitis anterior, 27rectus capitis lateralis, 27rectus capitis posterior, 29relaxants, 303 rhomboideus, 28sacrospinalis, 27, 33scalenus anterior, 28scalenus medius, 28scalenus posterior, 28semispinalis capitis, 29serratus anterior, 28serratus posterior, 27small deep muscles at craniocervical junction, 29 splenius, 29 sternocleidomastoid, 29, 30, 142, 224suboccipital, 142, 330, 403subscapularis, 347supinator, 357, 360supraspinatus, 346temporalis, 226, 332teres major, 142, 346, 347transversus abdominis, 29trapezius, 27, 30, 142, 250vernier, 29

Muscle and tendon receptors, 38–40 Myelography, 255, 308Myofascial pain of nonvertebral origin, 113–115

cellulalgia or panniculalgia, 113fibromyalgia, 115muscle trigger points, 114–115tendomyosis, 113–114

Myotatic reflex, 40

N

Nalorphine, 75 Naloxone, 75 Neck pain, chronic, 245–250

clinical signs of neck pain syndromes, 245–247evaluation of cellulotenoperiosteomyalgic manifestations of

segmental vertebral syndrome, 246–247history, 246radiographic examination, 247range of motion assessment, 246segmental examination, 246

diagnostic errors to be avoided, 245origins of neck pain and treatment, 248–250

cervical pain of muscular, subcutaneous, or ligamentous origin, 250

cervical pain and psychologic disorders, 250cervical spondylosis, 248–249painful minor intervertebral dysfunctions, 249–250

Nerve(s)anterior primary rami of, 29, 223, 263 articular receptors, 40–41 autonomic nervous system, 43–45 compression of, 342dermatomes, 33, 36, 82, 139dorsal rami of, 26entrapment syndromes of perforating cutaneous branches of TI2 and

LI, 374 experimental irritation of motor root of, 76experimental irritation of sensory root of, 76facet joints, 37 ganglia for, 43, 44iliohypogastric, 319, 321, 373, 374, 386ligaments, 38 muscle and tendon receptors, 38–40posterior gluteal, 35 posterior primary rami of, 33–35, 38, 223 saphenous, entrapment syndrome affecting, 375–376sinovertebral, 35 spinal muscles, 38 ulnar, 255, 342, 343vertebral periosteum, 38

Neural arch, 7Neuralgia

cervicobrachial, 19, 76, 183femoral, 76, 83

Neurogenic inflammation, 501Neuromodulators, 500Neuromuscular spindles, 38

afferent fibers, 39efferent fibers, 39gamma loop, 40Renshaw loop, 40

Neurophysiology of pain, 495–509anatomic determinants of nociception, 506genomic activation and repression, 496–497

cellular communication and synaptic plasticity, 497cellular plasticity, 497

glia, 498hormonal determinants of nociceptive plasticity, 506immunologic determinants of nociception, 507–508neuron, 497–498nociception, 495–496nociceptive desensitization, 503–504nociceptive localization, 509nociceptive rationalization, 508–509nociceptive sensitization, 502overview, 495phasic determinants of nociception, 504–506physiologic plasticity of pain, 496

epigenetic inheritance, 496genome, 496

physiologic systems, 495referred hyperalgesia, 502–503suprasegmental determinants of nociception, 508suprasegmental determinants of plasticity, 506synapse, 499–502

neuromodulators, 500–502

538

INDEX

neurotransmitters, 499–500synaptic field plasticity, 502

Neurotransmitters, 44, 499Neutral spine, 286NMDA receptors, 499Noncontained herniated disk, 83Nucleus pulposus, 11, 51

aging effects on, 69during spinal motion, 53hydrophilic properties, 12

Nutation, 59Nystagmus, 195, 335

O

Obsessional neurosis of the spinal displacement, 191Occipital headache, 326Occipitocervical junction, anomalies of, 19 Odontoid process, in cranial settling, 20 Orthoses

plaster orthosis syndrome, 234 rigid lumbar, 233

Osteopathic lesions, 165Osteophyte formation, 18, 69Osteoporosis, 183, 226, 268, 393, 489

P

Pacchionian corpuscles, 37 Pain

acute, 252 cervical, 241cervicobrachial neuralgia, 231, 239, 253–257chronic, 268 coccygodynia, 197, 317–318entrapment syndromes, 255experimentally provoked, 75–82 facet joints, 86 false hip pain of spinal origin, 373–374 femoral neuralgia, 245, 313–314gate control theory of, 75 headaches, 325–334 knee, 375–378 ligamentum flavum, 80of lumbosacral origin, 241 meralgia paresthetica, 322pathways, 44 physiologic plasticity of, 496postural disorders and, 89–93 pseudovisceral, 379–382psychological component of, 119pubic, 369–371radicular, 76, 103, 204, 305referred, 44, 76, 95, 108, 187, 225, 255, 503rule of no pain, 178sciatica, 305–312scoliosis and, 89segmental vertebral cellulotenoperiosteomyalgic syndrome,

103–112of thoracolumbar origin, 242 torticollis, 252, 269

Painful minor intervertebral dysfunction (PMID), 75, 95–102, 196association of PMID at different levels, 98definition, 95diagnosis, 95–96

differential diagnosis, 96–97acute synovitis, 96–97PMID and herniated disks, 97

facet syndrome and, 101hypothesis on mechanism of, 99–101

possible role of discal or facet joint pathology, 99–100reflex mechanism, 100–101

localization and number, 97–98osteopathic lesions and, 102pain threshold and, 98thoracic pain due to, 267torticollis due to, 251treatment, 98–99

acute cases, 98chronic cases, 98latent PMID, 99recurrent PMID, 98–99

types, 97active, 97acute, 97chronic, 97latent, 97

visceral repercussions, 99Pancoast tumor, 256Pancreatic lesions, 259Percutaneous radiofrequency rhizotomy, 101Perforating branch syndrome, 319–323

anatomy, 319–320classic studies, 319Maigne study, 319–320

clinical examination, 320clinical presentation, 320–323

pseudomeralgia paresthetica, 322–323pseudoperiarthritis of hip, 320–322

treatment, 323Periarthritis

of elbow, 362 of hip, 320 scapulothoracic, 345

Petrissage, 208, 285, 423Phalen’s test, 342 Pharyngeal paresthesia, 335Pinch–roll test, 79, 106, 107, 142, 149, 261, 375Platybasia, 20 Pleuropulmonary disorders, 271 PMID,

see

Painful minor intervertebral dysfunctionPMSWs,

see

Pulsed magnetic short wavesPolyenthesopathy, 115Polysaccharides, depolymerization of, 13Position set, 166Postural disorders and pain, 89–93

asymmetry of lumbar transverse process orientation, 92scoliosis, 89short leg syndrome, 92–93

evidence, 92–93false and true short leg, 93procedural considerations, 93

spondylolisthesis, 90–92thoracic hyperkyphosis, 89–90

hyperkyphosis due to dystrophic spinal growth, 90hypnotic posture in adolescents, 89–90

transitional zone abnormalities, 90Pseudotendinitis, 110Pseudovisceral pain of spinal origin, 379–382

abdominal pain, 379–382acute pain, 381

INDEX

539

pseudogastrointestinal pain, 380–381pseudogynecologic pain, 381–382pseudourologic pain, 382

case example, 382origin of pain, 379

role of cellulalgia, 379trigger points, 379

thoracic pain, 379false breast pain, 379pseudocardiac pain, 379pseudopulmonary pain, 379

treatment, 382Pubic pain and spinal factors, 369–371

clinical stages of pubic pain with spinal facilitation, 370–371theories, 369–370

Nesovic’s theory, 369spinal factor, 369–370

treatment, 371Pulsed magnetic short waves (PMSWs), 248Purpura, 195Pylon technique, 349

R

Rachiometer, 276 Radiofrequency denervation, 228Radiohumeral articular blockage, 360

abduction, 361adduction, 361extension, 361–362flexion–supination, 362pronation, 362

Radiologic evaluation, of short leg syndrome, 92Rami

abdominal cutaneous reflexes of, 150 abdominal muscular reflexes of, 150 cervical posterior, 38communicantes, 43, 110cutaneous territory of, 150cutaneous topography of, 138 point of emergence of cutaneous branches of, 149 posterior primary, 33, 34thoracolumbar posterior, 150

Rancurel’s test, 196 Range of motion, assessment of, 52, 133Referred hyperalgesia, 502, 503Referred pain, 255, 503Reflex(es)

abdominal cutaneous, 150abdominal muscular, 150Achilles, 157biceps, 139 brachioradialis, 139 finger flexor, 139, 254inverse myotatic, 40mechanism, 100medial hamstring, 156myotatic, 40patellar, 156pronator, 139spinal, 39 triceps, 139

Renshaw cells, 40Rhinorrhea, 329

Rhizotomy, 228Rib techniques, 477–480

for anterior costal sprain, 480for first rib, 480 for inferior ribs, 479

first technique, 477second technique, 477–478third technique, 479

for middle ribs, 479

Ring epiphysis, 7Rotator cuff tendinitis, 210, 353 Ruffini’s corpuscles, 37 Rule of no pain and opposite movement, 176–181

in direct manipulation, 181 particular cases, 179–181 practical application of, 178–179

S

Sacrococcygeal hiatus, 217 Sacroiliac joint, biomechanics of, 59–63

joint motion, 59–63interpretations of axis of movement, 59–62motion evaluation, 62–63

types of articulations, 59Sacroiliac joint techniques, so-called, 481–488

generalities, 481–485blockage in counter-nutation, 483blockage in nutation, 483Mennell’s signs, 482osteopathic signs, 483personal opinion, 485semiology proposed by supporters of SI joint blockage, 481–482semiology of SI joint disorders in traditional medicine, 481signs based on alterations in bony landmarks, 483–485

manipulative techniques, 485–488Sayre’s collar, 202, 407Scapulothoracic joint

assessment of, 349 mobilization of, 353, 354

Scheuermann’s disease, 89, 262, 268Schober’s test, 123, 152, 153, 276Sciatica, 305–312

clinical examination, 305–308clinical forms, 308–310

central spinal stenosis, 309foraminal stenosis, 310hyperalgic, 308lateral recess stenosis, 308paralytic, 308–309sciatica in the elderly, 309sciatica in the young, 309spinal stenosis, 309

differential diagnosis, 310imaging, 308

computed tomography, 308discography, 308magnetic resonance imaging, 308myelography, 308radiography, 308

onset and topography, 305treatment, 310–312

of attack, 310by manipulation, 310–311paralytic sciatica, 311–312

540

INDEX

rehabilitation, 311of sequelae, 311

Scoliosisbalanced vs. unbalanced, 120idiopathic, 121 minor, 89painful, 122

Segmental vertebral cellulotenoperiosteomyalgic syndrome (SVCPMS), 103–112

active and latent, 110cellulalgia, 106–108hypotheses on pathophysiology of manifestations, 110–12myalgic indurated cords, 108–109tenoperiosteal hypersensitivity, 110

Septic arthritis, 225 Sharpey’s fibers, 12Shiatzu, 210 Short leg, 92–93 Shoulder pain and cervical spine, 345–355

cervical shoulder, 351–352examination of shoulder, 346–351

assessment of active range of motion, 346assessment of clavicular joints, 348–349assessment of passive range of motion, 346assessment of resisted range of motion, 346–347assessment of scapular mobility, 349examination of cervical spine, 351glenohumeral mobility and assessment of glenoid fossa, 349–350painful arc, 347palpation, 347–348

generalities on tendinous and capsular lesions, 345–346manual therapy for painful shoulder, 353–355

manipulation of acromioclavicular joint, 353–354manipulation of sternoclavicular joint, 354–355mobilization of glenohumeral joint, 353mobilization of scapulothoracic joint, 353

mixed should pain syndromes, 352–353Sign

angle of the jaw, 146, 328, 330of Cassure, 126cheek, 142, 145, 328doorbell, 262eyebrow, 145friction sign, 109, 247Gerber’s, 346Lasegue’s, 184, 213, 279, 313, 482, 485Tinel’s, 342

Skin folding, 209 Soft herniations, 85Somatic dysfunction, 102, 188Spasmophilia, 98 Spinal characteristics by region, 17–26

cervical spine, 17–21anomalies of occipitocervical junction, 19–21facet joints, 17spinous processes, 17supraspinous ligament, 18transverse processes and vertebral artery, 19uncinate processes, 18–19

lumbar spine, 21–22spinous processes, 22transverse processes, 23

sacroiliac joint, 23–26thoracic spine, 21

Spinal examination, general principles, 119–132clinical history, 119–120

physical examination, 120–132dynamic inspection, 123–127segmental examination, 127–131static inspection, 120–123

radiographic and advanced studies, 132Spinal examination, regional applications, 133–161

cervical spine, 133–144examination of cervical spinal nerve roots, 138–140examination for manifestations of segmental vertebral

neurotrophic syndrome of Maigne, 140–144range of motion assessment, 133–136segmental examination, 136–138

lumbar spine, 152–161examination of lumbar spinal nerves, 156–157examination for manifestations of segmental vertebral

neurotrophic syndrome of Maigne, 157–161examination of mobility, 152–154segmental examination, 154–156

thoracic spine, 144–151examination for manifestations of segmental vertebral

neurotrophic syndrome of Maigne, 150–151examination of mobility, 144–147examination of thoracic spinal nerves, 150segmental examination, 147–150

Spinal kinematics, 49–57mobile segment, 49–50regional spinal motion, 50–57

cervical motion, 51–55lumbar motion, 56–57thoracic motion, 55–56

Spinal manipulation, 165–199,

see also

Manual therapy techniques

accidents and incidents, 193–196dramatic, 194–195incidents, 195medical responsibility, 196prevention of accidents, 196serious accidents, 195

contraindications to manipulation, 189–190clinical, 189technical, 189–190

errors of manipulation, 190–193diagnosis, 190neurology, 190–191rheumatology, 190vertebrobasilar insufficiency, 191–193

general concepts, 166–168basic principles, 166–167definitions, 167–168

general indications, 187–189cervical region, 187–188coccyx, 188lumbar region, 188thoracic region, 188visceral and functional disorders, 188–189

indications for manipulation, 173–175components of manipulative movement, 173–174description of manipulation, 174–175

localization of manipulation, 172–173mechanism of action of manipulation, 196–199

effects of manipulation on normal spine, 197possible mechanical factors, 197–198reflex factor, 198–199

protocol of manipulative session, 181–187age considerations with respect to manipulation, 186evaluation of response to treatment, 184–185

INDEX

541

evolution of pain after manipulation session, 185–186justification of manipulative treatment, 182–183management of treatment, 183manipulation session, 183–184number and frequency of sessions, 186possibility of manipulative treatment, 183quality of results, 186–187

rule of no pain and opposite movement, 176–181cases, 179–181direct manipulation and, 181practical application, 178–179technical contraindications to manipulation, 179

types of manipulation, 168–172direct, 168–169indirect, 169–170semi-indirect, 170–172

Spinal stenosis, 309 Spinal traction, 201–205

application of, 203 in bed, 203with belt, 408 cervical traction, 202

application, 202sitting, 202traction on inclined plane, 202traction on special table, 202

for cervicobrachial neuralgia, 204–205 indication for traction, 204–205

cervical spine, 204–205lumbar spine, 205

lumbar traction, 202–203application of traction, 203fastening pelvis, 203fastening thorax, 202–203traction in bed, 203

mode of action of traction, 204mechanical action, 204reflex action, 204

mode of application, 201suboccipital, 408with towel, 408traction table for, 201

Spinous process(es)applying pressure over, 155 applying transverse pressure against, 148, 155contralateral pressure, 128in thoracic spine, 21

Spondylolisthesis, 77, 89, 90, 152, 282, 393 Spondylosis, 18, 99

arthrotic stiffening due to, 248 cervical, 187, 248, 254painful minor intervertebral dysfunction and, 249

Spring tests, 484 Sternoclavicular joint

examination of, 349 manipulation of, 354

Steroid injection complications of, 225Stretching, 213–215

longitudinal, 213–214global stretching of extensor muscles, 213–214manual stretching, 213postural stretching, 214stretching exercises, 214

transverse stretching, 214–215vapocoolant spray, 214

SVCPMS,

see

Segmental vertebral cellulotenoperiosteomyalgic syndrome

Swimming, 267 Sympathetic nervous system, 43Symphysis pubis, 23, 150Synapse, 498, 499Synaptic clef, 499Synaptic field plasticity, 502

T

Taking up the slack, 166Taut bands, 505 Techniques not requiring vertebral manipulation, 489–491

cervical region techniques, 490–491patient recumbent, 491techniques applicable to gluteal region pain, 489–490techniques applicable to thoracic region, 490techniques for perispinal and interspinal region pain, 490

Tender points, 115Tennis elbow,

see

Lateral epicondylar painTenoperiosteal hypersensitivity, 110Therapeutic exercise, 241–242

cervical pain, 241low back pain, 241–242

lumbosacral origin, 241–242rehabilitation of lower limbs, 242thoracolumbar origin, 242

thoracic pain, 241Thermal therapy, 227–228

contraindications, 228Hotel Dieu method, 227results, 227–228

Thermotherapy, 227–228Thoracic outlet syndrome, 255, 342Thoracic pain

diagnostic errors to avoid with, 259 due to disk calcification, 269 examination of back for, 259–261 examination of neck for, 261–262interspinous ligaments and, 268 osteoporosis and, 268pathogenic mechanism of, 263 pseudocardiac, 379psychologic factors and, 266 treatment of, 269

Thoracic pain, acute, 269–270of cervical origin, 269due to disk calcification, 269of muscular origin, 269–270of thoracic origin, 269

Thoracic pain, chronic, 259–268interscapular thoracic pain of low cervical origin, 259–266

clinical examination, 259–263clinical picture, 259posterior primary rami of second thoracic nerve root, 263–266treatment, 266–267

of muscular origin, 268of thoracic origin, 267–268

of discogenic origin, 267–268due to thoracic arthrosis, 268due to thoracic PMID, 267interspinous ligaments and, 268osteoporosis and, 268Scheuermann’s disease and, 268

542

INDEX

Thoracic spine examinationextension, 124, 146flexion, 123, 145lateroflexion, 146 of mobility, 144–147pressure on spinous process, 137rotation, 124segmental, 127, 136–138, 147–150of spinal nerves, 138–140 transverse pressure against spinous process, 137

Thoracic spine manual techniquesin lateroflexion, 406 massage, 403mobilization, 405 relaxational maneuvers, 403–404

Thoracic techniques, 435–454manipulation, 440–454

epigastric technique, 440–441knee technique, 450–451localizing manipulation to specific spinal segment, 442–449supine technique, 452–454

massage, 435mobilization, 437–439

in extension, 437–438in lateroflexion, 439in rotation, 439

relaxational maneuvers, 435–436Thoracolumbar junction, 150

calcification at, 87examination of, 384 low back pain originating at, 188, 242, 290, 303pure rotation, 474radiographic examination of, 279tenoperiosteal tenderness and, 150

Thoracolumbar junction syndrome (TLJS), 383–388anatomy and physiology, 384clinical symptoms, 386–387

false hip pain, 387functional disorders, 387low back pain, 386pseudovisceral pains, 386–387public tenderness, 387

physical signs, 384–386cellulotenoperiosteomyalgic manifestations, 384–386crestal points, 386examination of thoracolumbar junction, 384

treatment, 388Thoracolumbosacral orthosis, 233 Tibiofibular joint, proximal, 377–378

blockages of, 378examination of, 377knee pain and, 377manipulation of, 378mobilization of, 378sciatica and arthritis of, 378

Tietze’s syndrome, 272Tinel’s sign, 342Tinnitus, 192, 335TKJS,

see

Thoracolumbar junction syndromeTNF,

see

Tumor necrotizing factorTorticollis and acute cervical pain, 251–252

acute cervical pain, 252due to acute synovitis, 252as result of herniated disk, 252

benign acute torticollis, 251–252torticollis due to PMID, 251

torticollis of mixed origin, 252torticollis of muscular origin, 251–252

Traction,

see

Spinal tractionTransitional zones (TZs), 389, 390Transitional zone syndrome, 389–392

characteristics, 390clinical characteristics, 390semiologic characteristics, 390treatment, 390

clinical picture, 391–392compensatory postures, 390–391 perpetuating and precipitating factors, 390–391

Transverse foramen, 19Transverse process(es), 7, 23

of cervical spine, 19 paraspinal muscles in relation to, 27of thoracic spine, 21 vertebral artery and, 19

Transverse thrust technique, 401 Trauma, cervical, 190, 239, 249, 336 Trigger points, 87, 99, 103, 142, 150, 505

cervical headaches and, 331injections, 224, 252, 285knee pain and, 375, 376 lateral epicondylar pain and, 360massage of, 207, 208muscular, 114, 250, 279, 347neurotrophic spinal segmental syndrome and, 231referred pain and, 80, 108role in pseudovisceral pain, 379sciatica and, 308 shoulder pain and, 352target muscles for, 108thoracic pain and, 268 in thoracic region, 82

Tripod sign, 481 Trochanteric pain, 311, 373

L5 segmental vertebral syndrome, 373 T12–L1 segmental vertebral syndrome, 373–374

Trophostatic syndrome of menopause, 70Tumor necrotizing factor (TNF), 498TZs,

see

Transitional zones

U

Ulcers, 259Ultrasound therapy, 98, 231, 248, 285Uncinate processectomies, 72Unipolar neurons, 498

V

Vapocoolant spray, 214Vascular supply of spine, 31–32

arterial supply, 31venous supply, 31

intraspinal venous plexus, 31perispinal venous plexus, 31

Vasomotor symptoms, 335VBI,

see

Vertebrobasilar insufficiencyVein(s)

azygos, 31basivertebral, 31hemiazygos, 31intraspinal venous plexus, 31

INDEX

543

lumbar, 31perispinal venous plexus, 31 posterior intercostal, 31vertebral, 19

Vernier muscles, 29Vertebra(e), 7–10

architecture of posterior arch, 8cartilaginous endplates, 8different groups of vertebrae, 7structure of vertebral body, 7–8vertebral endplate, 7zygapophyseal joints, 8–10

joint capsule, 9meniscoids, 9–10

Vertebral endplate, 7Vertebral lesions and common pain syndromes, 83–87

intervertebral disk lesions, 83–86lesions of facet joints, 86–87

anomalies, 86degenerative lesions, 86–87

objective muscular lesions, 87Vertebrobasilar insufficiency (VBI), 191Vertical trabeulae, function of, 7Vestibular symptoms, 335Visual symptoms, 335

W

Wallenberg syndrome, 192, 194Wryneck,

see

Torticollis and acute cervical pain

Z

Zygapophyseal joints,

see

Facet joints