acupuncture, trigger points and musculoskeletal pain (elsevier 3rd ed)

To Oina, my wife, for her patience and forbearance during the writing of this book.

The phenomena of pain belong to that borderland between the body andsoul about which it is so delightful to speculate from the comfort of anarmchair, but which offers such formidable obstacles to scientific inquiry.

J. H. Kellgren (1948)

Extracts from reviews of the first edition:

‘…I warmly recommend this book to anyone who wants to learn more about thisoften neglected area of common musculoskeletal pain conditions…’Journal of the Royal College of Physicians of London

‘This is a book that should belong to physicians, neurologists, rheumatologists andteachers of medical students…’Pain

Endorsements of the new edition:

‘Peter Baldry is one of the most respected practitioners of Medical Acupuncture inthe UK. This new edition is yet another first-class book, which adeptly combinesthe theory and practice of treatment of trigger points for musculoskeletal pain. An eminently readable and informative text; this is a tour du force and an essentialacquisition for those practitioners who want a clear practical guide for thetreatment of musculoskeletal pain using trigger point treatment and the scientificunderstanding that underpins the treatment.’Jacqueline Filshie, Consultant in Anaesthesia and Pain Management, RoyalMarsden Hospital, London and Surrey; Secretary of the British MedicalAcupuncture Society

‘In this fine comprehensive book, Dr Baldry removes much of the mystique from acupuncture as a technique for musculoskeletal pain relief. Using a fullyscientific integration of Eastern and Western knowledge, coupled with the relevant literature on clinical effectiveness of acupuncture, he provides an ideal,evidence-based text for the practitioner.

From the beginner to the expert, anyone with an interest in the nature ofmuscle pain, its pathophysiology and treatment will be informed by this book: theentry-level therapist will gain a better understanding based on sound scientificevidence, while the experienced clinician will be rewarded with a well-writtenguide to what is significant in everyday clinical practice. Clinicians of severalmedical specialties (neurologists, orthopaedic surgeons, general practitioners, painspecialists, physiatrists) and other practitioners (acupuncturists, physiotherapists,nurses, occupational therapists) will find this book an indispensable reference intheir daily work. For those who wish to implement acupuncture in the clinic, thistextbook is an invaluable resource for responsible practice.

In total, this book offers an innovative approach to the diagnosis,understanding and treatment of myofascial trigger point pain using acupuncturethat integrates all current concepts of neurophysiology and neuroanatomyprinciples. Dr Peter Baldry is to be congratulated for conceptualizing, editing andwriting such a truly valuable asset for every clinical practice.’Dr George Georgoudis, Research Physiotherapist, University of Manchester, UK;Lecturer, Technological Educational Institute of Athens, Department ofPhysiotherapy, Greece; “Tzanio” General Hospital of Pireaus, Greece

For Elsevier Ltd

Commissionning Editor: Karen MorleyProject Development Manager: Kerry McGechieProject Manager: Derek Robertson

Distributed in the United States of America by RedwingBook Company, 44 Linden Street, Brookline, MA 02146.

© Longman Group UK Limited 1993© Harcourt Brace and Company Limited 1998© Harcourt Publishers Limited 2000© Elsevier Ltd 2005

No part of this publication may be reproduced, stored in a retrieval system, ortransmitted in any form or by any means, electronic, mechanical, photocopying,recording or otherwise, without either the prior permission of the publishers or alicence permitting restricted copying in the United Kingdom issued by theCopyright Licensing Agency, 90 Tottenham Court Road, London W1T 4LP.Permissions may be sought directly from Elsevier’s Health Sciences RightsDepartment in Philadelphia, USA: phone: (�1) 215 238 7869, fax: (�1) 215 2382239, e-mail: [email protected]. You may also complete yourrequest on-line via the Elsevier homepage (http://www.elsevier.com), by selecting ‘Customer Support’ and then ‘Obtaining Permissions’.

First edition 1989Second edition 1993Third edition 2005Translated into Japanese 1995Translated into German 1996

ISBN 0 443 06644 2

British Library Cataloguing in Publication DataA catalogue record for this book is available from the British Library.

Library of Congress Cataloging-in-Publication DataA catalog record for this book is available from the Library of Congress

NoteKnowledge and best practice in this field are constantly changing. As new researchand experience broaden our knowledge, changes in practice, treatment and drugtherapy may become necessary or appropriate. Readers are advised to check themost current information provided (i) on procedures featured or (ii) by themanufacturer of each product to be administered, to verify the recommended doseor formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience andknowledge of the patient, to make diagnoses, to determine dosages and the besttreatment for each individual patient, and to take all appropriate safetyprecautions. To the fullest extent of the law, neither the Publisher nor the authorassumes any liability for any injury and/or damage.

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Quod est ante pedes nemo spectat: coeli Scrutantur plagas. (What is before one’s feet no one looks at;they gaze at the regions of heaven.)Ennius, quoted by Cicero, De Divinat., 2, 13.

This is an important and valuable book thatneeded to be written. Musculoskeletal or myofas-cial pain is an all too common and extraordinarilyneglected subject of medicine; it is barely men-tioned in many textbooks of medicine. In reality itis a ubiquitous condition that causes a great dealof pain and suffering and one which, unfortu-nately, either slips by unrecognized or is passedoff as trivial or untreatable. In this book Dr PeterBaldry has shown how musculoskeletal pain canbe simply and effectively treated by acupuncture.But this book is much more than that because it isreally three books in one.

The first part presents an interesting historicalbackground to Chinese acupuncture and its spreadto the outside world, particularly to the West. Thesecond part deals with the principles of triggerpoint acupuncture wherein, over the course of sixchapters, the reader is presented with a detailedand critical account of the evidence for and thenature of trigger points and the way in which acu-puncture can be used to deactivate them. Dr Baldryspares no effort to provide the reader with an up-to-date and accurate account of the neurophysiologyof pain and the possible ways in which acupunc-ture can be used to control it. He also grasps the dif-ficult and important nettle concerning the scientific

evaluation of acupuncture. The results of properlycontrolled experiments and trials demonstratingthe efficacy of acupuncture are slowly but surelyaccumulating and Dr Baldry discusses these criti-cally and points the way to the further rigorousstudies that are urgently needed. The third part ofthe book gives a detailed and splendidly practicalaccount of the many different forms of muscu-loskeletal pain and the way that these can be treatedwith acupuncture.

Even for the reader who does not intend to useacupuncture, this book still serves a most valuablepurpose by drawing attention to the very largenumber of common musculoskeletal pain condi-tions that are all too commonly overlooked. A par-ticularly helpful feature of Dr Baldry’s book is therich admixture of case histories of his ownpatients, from which the medical reader can learnthe correct way to diagnose and subsequently totreat these painful conditions.

There seems little doubt that, through unfamil-iarity with this condition, much time and effort areoften expended unnecessarily both by the medicalprofession and by patients seeking the cause andtreatment of pain problems that are, in fact, mus-culoskeletal in origin. Dr Baldry has performed amost valuable service in writing this eminentlyreadable book and I wish it the very considerablesuccess that it richly deserves.

John W. Thompson

vii

Foreword

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The aims of this book

It is because traditional Chinese acupuncture is per-force inextricably bound up with archaic conceptsconcerning the structure and function of the bodythat most members of the medical profession in theWestern world view it with suspicion and scepti-cism and assign it, together with various otherseemingly esoteric forms of therapy, to what iscalled alternative or complementary medicine.Moreover, it is evident that attempts during the past40 years to place Chinese acupuncture on a morerational and scientific basis have done little to dispelthis attitude.

My reason for writing this book is to bring to theattention of doctors and physiotherapists a 20th-century-evolved scientific approach to acupunc-ture for the relief of pain emanating from triggerpoints in the myofascial pain syndrome and fromtender and trigger points in the fibromyalgia syn-drome, and to take acupuncture (so far as the alle-viation of nociceptive pain of this type is concerned)out of the category of alternative or complementrymedicine by describing a method of employing itthat has been developed as a result of observationsmade by physicians during recent years and isnow fast becoming incorporated within the frame-work of present-day orthodox medical practice.

It is because there have been so many advancesin our knowledge concerning the pathophysiology,diagnosis and treatment of the myofascial trigger

point and fibromyalgia syndromes since the 2ndedition of this book was published, that in this edi-tion four chapters in Part 2 (Principles of TriggerPoint Acupuncture) have had to be replaced byentirely new ones. In addition to these changesmost of the other chapters in Part 2 and Part 3 (The Practical Application of Trigger PointAcupuncture) have had to be extensively revised.

It is hoped that as a result of reading this bookmany more anaesthetists, rheumatologists, ortho-paedic specialists, general physicians, general prac-titioners and physiotherapists than at present maynot only be led to search for trigger points in theirroutine clinical investigation of pain, but may alsobe persuaded to include dry needling at thesepoints in their therapeutic armamentarium.

Case histories

I offer no apology for having included case histor-ies in this book. They are, of course, by their verynature essentially anecdotal and certainly no infer-ence is meant to be drawn from them concerningthe effectiveness of trigger point acupuncture, forany conclusions about that can only come fromclinical trials. The sole purpose of including thesevignettes is to provide illustrations from everydayclinical practice that serve to highlight certainimportant principles underlying the diagnosis andmanagement of various painful musculoskeletaldisorders.

ix

Preface

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My very sincere thanks are due to Professor JohnThompson for the meticulous manner in which heread the manuscript of this book and then gave memuch valuable advice and constructive criticismbesides kindly writing a foreword.

I wish to express my gratitude to Dr AlexanderMacdonald for it was he who, some years ago, firstdrew my attention to the aetiological importanceof trigger points in the pathogenesis of mus-culoskeletal pain and introduced me to triggerpoint acupuncture as a method of alleviating it.

I thank Dr Felix Mann for having initially broughtto my notice the close relationship between triggerpoints and traditional Chinese acupuncture points.

I wish to say how indebted I am to the late Drs Janet Travell and Dr David Simons for thevery considerable contribution they made to my knowledge of specific patterns of myofascialtrigger point pain referral. It has largely been fromstudying their descriptions and illustrations of these patterns in various publications referredto later in this book that I am now able to recog-nize them in my own patients.

I also wish to say how very grateful I am to Dr David Bowsher, for it has been from him in parti-cular that I have learnt so much about what is currently known concerning the mechanisms respon-sible for the pain-relieving effect of acupuncture.

I have to thank Professors Peter Williams andRoger Warwick, the editors of Gray’s Anatomy(36th edition 1980) and its publishers ChurchillLivingstone for giving me permission to repro-duce Figures 12.1, 12.5, 12.9, 12.14, 13.12, 15.1, 15.2,

15.17, 15.23*, 16.8, 16.9, 16.10, 18.1*, 18.6, 18.7*,18.9*, 18.11*, 20.1, 20.2, 20.5*, 20.6. The illustrationsfrom Gray’s Anatomy marked with an asterisk orig-inally appeared in Quain’s Anatomy 11th edition.

Finally, I have to thank the following: Dr J. H. Kellgren and the editor of Clinical Sciencefor permission to publish Figures 4.1 and 4.2; Dr Kellgren and the editor of the British MedicalJournal for permission to publish Figure 4.3; Dr Howard Fields and McGraw Hill, New York forpermission to reproduce Figures 6.1, 6.2, 6.3 and7.3 from Pain 1987; Dr David Bowsher and the edi-tor of Acupuncture in Medicine – The Journal of theBritish Medical Acupuncture Society for permissionto reproduce Figures 6.5 and 9.1; Dr David Simonsand Haworth Press for permission to reproduceFigure 7.2; Dr Alexander Macdonald and GeorgeAllen & Unwin, London for permission to repro-duce Figures 7.4 and 7.5 from Acupuncture – fromAncient Art to Modern Medicine 1982; Mr R. J.D’Souza for providing me with Figure 7.6;Professor Yunus and Lea & Febiger, Philadelphiafor permission to reproduce Figure 7.7; Dr J. Parkand the editor of Acupuncture in Medicine for per-mission to reproduce Figure 11.1; Dr David Simonsand Churchill Livingstone, Edinburgh for permis-sion to reproduce Figure 16.6 from Textbook of Pain (Wall P., Melzack R., eds) 2nd edition 1989;Professor R. W. Porter and Churchill Livingstone,Edinburgh for permission to reproduce Figures17.2 and 17.3 from The Lumbar Spine and Back Pain(Jason M. I. V., ed) 3rd edition 1987.

P.E.B. ([email protected])

xi

Acknowledgements

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For reasons to be explained later in this book, theearly 1970s saw the dawn of an era when people inthe Western world began taking an increasing inter-est in the ancient oriental mode of therapy knownas acupuncture, with lay practitioners of it leadingthe public to believe that it has such wide ranginghealing properties as to be an effective alternativeto orthodox medicine in the treatment of a largenumber of diseases.

There is clearly no justification for such extra-vagant claims and it has to be said that, at the onsetof this era, the medical profession in Europe andAmerica viewed this form of therapy with consid-erable suspicion and continued to do so for so longas explanations as to how it might work remainedinextricably bound up with abstruse concepts for-mulated by the Chinese 3000 years previously.This reluctance to believe in these long-establishedbut somewhat esoteric hypotheses was, of course,because they had been conceived at a time whenideas concerning the structure and function of thebody together with those concerning the nature ofdisease belonged more to the realms of fantasy thanfact, and for this reason it was difficult to reconcilethem with the principles upon which the present-day Western system of medical practice is based.

During the latter part of the 20th century, how-ever, there has been a considerable increase inknowledge concerning the neurophysiology ofpain and because of this there is now a scientificexplanation for acupuncture’s ability to alleviatepain. It has become apparent that this technique,which involves the use of dry needles (acus (Latin),

needle) for the purpose of stimulating peripheralnerve endings, achieves its pain-relieving effect by virtue of its ability to evoke activity in pain-modulating mechanisms present in the peripheraland central nervous systems.

In the light of this discovery and a number ofothers the public in general and the medical pro-fession in particular have had to revise their atti-tudes towards acupuncture.

Furthermore, when the House of Lords selectcommittee in science and technology (2000) took aclose look at various types of treatment at presentincluded within the ambit of complementary/alternative medicine, it divided them into threegroups and placed acupuncture in the one con-taining therapeutic procedures deemed to be themost organized and regulated.

The committee, in addition, considered that theresearch bases of these procedures are of suffi-ciently high standards to allow them to be usedwithin the UK’s National Health Service.

Prior to the publication of this report the BritishMedical Acupuncture Society (1997) had publisheda discussion paper entitled ‘Acupuncture’s PlaceWithin Mainstream Medicine’. In this it was stated:

‘… Medical acupuncture practice depends onthree important principles: an orthodox Westerndiagnosis needs to be made for every patient;acupuncture should be integrated with conven-tional medicine; and it must be appreciated thatthe traditional Chinese view of acupuncture is beingreplaced in many areas by an approach based onmodern physiology and neuroanatomy. …’

xiii

Introduction to the third edition

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In accordance with the above, in 2000 The RoyalCollege of Physicians of London set up a subcom-mittee to assist with the present task of bringingacupuncture and a strictly selected number of otherhitherto somewhat pejoratively called complemen-tary or alternative therapeutic procedures withinthe framework of orthodox medical practice.

Lewith et al (2003), moreover, during the courseof discussing the current status of certain thera-peutic procedures in the Journal of the Royal Collegeof Physicians of London, including acupuncture, madethe following two apposite comments concerningthe latter: (1) ‘needling trigger points is particu-larly effective in the treatment of pain’; (2)‘acupuncture is currently used in at least 84% ofpain clinics in the UK …’

A paucity of suitably funded research has beenthe principle hindrance to getting certain therapeut-ic procedures including acupuncture integratedwithin the fabric of conventional medical practice.This has prompted Lesley Rees, Director of Edu-cation at the Royal College of Physicians of Londonand Andrew Weil, Professor of Medicine at the Uni-versity of Arizona (Rees & Weil 2001), to emphasizethe need for the NHS research and developmentdirectorate and the Medical Research Council tonow help correct this unfortunate state of affairs.

The purpose of this book is to discuss the scien-tific aspects of acupuncture in general and triggerpoint acupuncture in particular and to show howthis latter type of therapy can readily be used bydoctors and physiotherapists in the treatment ofthe myofascial pain and fibromyalgia syndromes.

For those trained in the Western system of medi-cine there are obvious advantages in using thisparticular method rather than the traditionalChinese one, but clearly these advantages cannotbe fully appreciated without knowing somethingabout the latter. This book is, therefore, divided intothree parts with Part 1 containing a brief accountof traditional Chinese acupuncture. It also givesreasons as to why doctors in Europe on first learn-ing about this type of treatment in the 17th centuryrejected it, and describes how certain 19th-centuryEuropean and American doctors, having put onone side what they considered to be unacceptableChinese concepts concerning this mode of therapy,

devised a method of practising it principally forthe relief of musculoskeletal pain that may be con-sidered to be a forerunner of the somewhat moresophisticated one developed in recent years anddescribed in this book. It is also pointed out that,although physicians who advocated the use ofacupuncture in the Western world during the lastcentury wrote enthusiastically about it, it was neverwidely practised by their contemporaries, mainlyit would seem because at that time there was nosatisfactory explanation as to the manner in whichit might work.

In Part 2 attention is drawn to fundamental lab-oratory investigations into the phenomenon ofreferred pain from musculoskeletal structures car-ried out by J. H. Kellgren at University CollegeHospital, London, in the late 1930s. In addition itis explained how these investigations promptedmany physicians during the 1940s, in particularthe late Janet Travell in America, to study the clin-ical manifestations of this particular type of pain,and how, as a result of this, she came to recognizethe importance of what she termed trigger pointsas being the source of pain in many commonlyoccurring musculoskeletal disorders.

It is also shown how once it had been discover-ed that it is possible to alleviate such pain byinjecting trigger points with a local anaesthetic orwith one or other of a variety of different irritantsubstances, it was found that this could be accom-plished even more simply, as well as more safelyand equally effectively, by means of the carryingout of needle-evoked nerve stimulation at triggerpoint sites.

Part 2 also contains a brief account of advances in knowledge concerning the neurophysiology ofpain during the 1960s and 1970s and describes thevarious pain-modulating mechanisms now consid-ered to be brought into action when acupuncture iscarried out. In addition, it includes a discussion ofsome of the difficulties so far encountered in scien-tifically evaluating the pain-relieving efficacy of thisparticular type of therapy and in determining itsplace relative to other forms of treatment in the alle-viation of musculoskeletal pain.

Part 3 is devoted to the practical applications oftrigger point acupuncture.

INTRODUCTION TO THE THIRD EDITIONxiv

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British Medical Acupuncture Society 1997 Acupuncture’splace within mainstream medicine. Acupuncture inMedicine 15(2): 104–107

House of Lords Select Committee on Science andTechnology 2000 6th report, Session 1999–2000.Complementary and alternative medicine. StationaryOffice, London

Lewith G T, Breen A, Filshie J, Fisher P et al 2003Complementary medicine: evidence base, competence topractice and regulation. Clinical Medicine (Journal of theRoyal College of Physicians of London) 3(3): 235–240

Rees L, Weil A 2001 Integrated medicine. British MedicalJournal 322: 119–120

Introduction to the third edition xv

References

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The Chinese first carried out acupuncture, thatseemingly strange practice whereby needles areinserted into people for therapeutic purposes, atleast 3000 years ago. News of this, however, did notreach the Western world until about 300 years agowhen European medical officers employed by theDutch East Indies Trading Company in and aroundJava saw it being used there by the Japanese, andwhen at about the same time Jesuit missionariescame across it whilst endeavouring to convert theChinese to Christianity.

From their writings it is clear that both thesegroups found the concepts upon which the Chinesebased their curious practice difficult to comprehend,due to the fact that these appeared to be completelyat variance with what Europeans by that time hadcome to know about the anatomy and physiologyof the human body. And it has been this inabilityto reconcile the theoretical concepts put forward bythe Chinese in support of acupuncture with thoseupon which modern scientific medicine is basedthat has for so long been the cause of such little interest being taken in it in the Western world.During the past 30 years, however, attitudes towardsacupuncture in the West have been changing sinceresearch into the mechanisms of pain has provideda certain amount of insight as to how possibly itachieves its effect on pain. These, as might beexpected, are entirely different from those origi-nally put forward by the Chinese.

The prime purpose of this book is to describe arecently developed method of practising acupunc-ture in which dry needles are inserted into the tis-sues overlying what have come to be known as

3

Chapter 1

Traditional Chinese acupuncture

CHAPTER CONTENTS

Ancient Chinese concepts concerning thepractice of acupuncture and moxibustion

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ACUPUNCTURE, TRIGGER POINTS AND MUSCULOSKELETAL PAIN4

each time of extensive commentaries by a variety ofdifferent people. This prompted Ilza Veith to say:

It is obvious that any work that has undergonethe fate of the Yellow Emperor’s Canon of InternalMedicine contains but little of its authentic originaltext; it is also clear that its various commentatorshave frequently obscured rather than elucidatedits meaning. It seems impossible to determine nowhow much of the original text remains; especiallysince in former times it was difficult to distinguishtext from commentary.

Nevertheless, in spite of all these difficulties it isgenerally agreed that from a study of this work itis possible to gain a clear idea as to how the prac-tice of acupuncture had developed in China by the2nd century BC.

Acupuncture and a related form of heat ther-apy and counter irritation known as moxibustionalmost certainly had their origins long before this,as may be seen from recently discovered medicalmanuscripts written on sheets of silk in the tomb ofthe son of the Lord of Tai, a young man who died in168 BC. As Lu Gwei-Djen & Joseph Needham pointout ‘the style and contents of the texts is similar tothat of the Nei Ching but more archaic, so that theypresent a picture of Chinese medical thought dur-ing the two or three centuries preceding the compil-ation of that great classic’.

It is interesting to observe that these manu-scripts, whilst certainly referring to the practice ofacupuncture with needles made of stone, discussmoxibustion in even greater detail and there arereasons for believing that that technique may havebeen introduced even longer ago than acupunctureitself.

MOXIBUSTION

This is a process by which heat is applied to thebody by the burning of Artemisia leaves that havebeen dried to a tinder. This Artemisia tinder hascome to be known in the West as moxa – a word ofJapanese derivation (mogusa, herb for burning)because it was from Japan that the Western worldfirst heard about this technique in the 17th century.

The classical method of performing moxibus-tion is to make the tinder into a cone and apply itto the skin at points identical to those used for

trigger points as a means of alleviating muscu-loskeletal pain. Before turning to this, however, itis necessary to give a brief account of the discov-ery and development of the traditional practice of Chinese acupuncture as it is only by having aproper understanding of this that the merits of the trigger point approach to acupuncture can befully appreciated. For an explanation as to how theChinese came to discover the therapeutic proper-ties of acupuncture in the first place it is helpfulto turn to an early Chinese medical book entitledHuang Ti Nei Ching and known in the English-speaking world as The Yellow Emperor’s Manual ofCorporeal Medicine. This is a most unusual textbookof medicine as it is written in the form of a dialoguebetween the Emperor Huang Ti and his ministerChhi-Po. It is a work which incorporates much con-cerning the philosophical thoughts of the ancientChinese, their religious beliefs with particular ref-erence to Taoism, their observations concerning theworkings of the universe in general, and the appli-cation of all this to their practice of medicine.

The Western world is much indebted to theAmerican scholar, Ilza Veith, who, in February 1945at the Institute of the History of Medicine at JohnsHopkins University, undertook the extremely dif-ficult task of translating this important treatise intoEnglish. This translation together with her owninvaluable introductory analysis of the work wasfirst published in 1949. Also, for those who wish toread a detailed account of how the Chinese prac-tice of acupuncture has gradually evolved over thecenturies, there is much of considerable interest in Celestial Lancets, an erudite study of the subjectwritten by the two distinguished Cambridge his-torians, Lu Gwei-Djen and Joseph Needham (1980).

It is by no means certain that Huang Ti everlived, with the general consensus of opinion beingthat he is a legendary figure, but nevertheless he isto this day worshipped as the father of Chinesemedicine. It is very difficult to determine with anydegree of accuracy the date the Nei Ching firstappeared, but it seems likely that Part I, the Su WEn(Questions and Answers), originated in the 2ndcentury BC and that Part II Chen Ching (NeedleManual) first appeared in the 1st century BC.However, not only was the latter re-named theLing Shu (Vital Axis) in about AD 762, but both partshave been repeatedly revised with the addition

Chap-01.qxd 11*10*04 10:11 Page 4

acupuncture. Sometimes it is used as a counter irri-tant by being allowed to blister and scar the skin.At other times it is used as a milder form of heattreatment, by applying it to the skin with a layer ofvegetable material interposed between this and thecone in order to protect the former from damage.Yet another method is to combine moxibustion withacupuncture by placing a piece of moxa on top of aneedle inserted into the body, and igniting it, whenthe heat from the moxa is conducted down the needle to the surrounding tissues.

ACUPUNCTURE

The concepts which prompted the ancient Chineseto use acupuncture for therapeutic purposes werecomplex and to the modern Western mind difficultto comprehend. They were intricately bound upwith their views concerning all aspects of the living world, including in particular their belief in the existence of two cosmic regulators known asYin and Yang.

The supremacy of power and influence accordedto these two forces in the creation of the world iswell illustrated by the following quotations fromthe Nei Ching.

The principle of Yin and Yang is the basis of theentire universe. It is the principle of everythingin creation. It brings about the transformation toparenthood; it is the root and source of life anddeath …

Heaven was created by an accumulation ofYang; the Earth was created by an accumulationof Yin.

The ways of Yin and Yang are to the left and tothe right. Water and fire are the symbols of Yinand Yang. Yin and Yang are the source of powerand the beginning of everything in creation.

Yang ascends to Heaven; Yin descends to Earth.Hence the universe (Heaven and Earth) repre-sents motion and rest, controlled by the wisdomof nature. Nature grants the power to beget andto grow, to harvest and to store, to finish and tobegin anew.

Further, the Chinese considered that, followingthe creation of the world, Yin and Yang continued toexert a considerable influence, and that indeed thepreservation of order in all natural phenomena,

both celestial and terrestial, was dependent on themaintenance of a correct balance between them. It should be noted in this connection that neitherof these two opposing forces were ever envisagedas existing in pure form but rather that each con-tained a modicum of the other. And moreover,there was the belief that all events, both in natureand in the human body, were influenced by a con-stantly changing relationship between them.

Yin and Yang were thus said to be ubiquitousessential components of all things, with in somecases Yang being predominant and in others Yin.In the universe for example, phenomena such as thesun, heaven, day, fire, heat and light were all con-sidered to be predominantly Yang in nature, whereastheir opposites, the moon, earth, night, water, coldand darkness were considered to be predominantlyYin. The individual structures of the body werealso thought to have either Yang or Yin qualities.For example, five hollow viscera – the stomach,small intestine, large intestine, bladder and gallbladder – were said to be Yang organs because lyingnear to the surface on opening the body they getexposed to light. In contrast, five solid viscera – theheart, lungs, kidneys, spleen and liver – were saidto be Yin organs due to their being in the darkrecesses of the body.

The conclusion reached by the Chinese that fiveorgans had Yang and five had Yin characteristicswas apparently not a fortuitous one but seeminglybecause five was considered to be a dominantnumber in their conception of the universe. Thisstemmed from their fundamental belief in the the-ory of the five elements, which stated that Yin andYang consist of five elements, namely water, fire,metal, wood and earth, and that man and, indeed,all natural phenomena are products of an inter-action between these two opposing forces.

The theory of the five elements was extremelycomplicated and there is little to be gained bygoing into it in detail except to say, in view of itsrelevance to the traditional practice of Chineseacupuncture, that in its application to the organs ofthe body the Nei Ching teaches that:

The heart is connected with the pulse and rulesover the kidneys. The lungs are connected withthe skin and rule over the heart. The liver is con-nected with the muscles and rules over the lungs.

Traditional Chinese acupuncture 5

Chap-01.qxd 11*10*04 10:11 Page 5

The spleen is connected with the flesh and rulesover the lungs. The kidneys are connected withthe bones and rule over the spleen.

With this background it is now possible to seehow these various considerations concerning Yinand Yang came to be applied to matters concern-ing the maintenance of health and the develop-ment of disease. It was considered that in order tobe healthy these two opposing forces have to be ina correct state of balance (crasis) and that it iswhen this is not so that disease occurs (dyscrasia).

Further, it was considered that this health-givingbalance between Yin and Yang only exists when aspecial form of energy, known as chhi, flows freelythrough a system of tracts. And, as a corollary tothis, that disease develops when a collection of ‘evilair’ in one or other of the tracts obstructs the flow of chhi through it as this leads to an imbalancebetween Yin and Yang. It was in attempting to dis-pel this ‘evil air’ or wind that the Chinese were firstled to insert needles into these tracts, and then fromthis, over the course of centuries, to develop a some-what complex system of therapy now known to theWestern world as acupuncture (from the Latin acus,a needle; and punctura, a prick).

As it is only possible to understand how theChinese developed their system of acupuncture byhaving some knowledge of their original, somewhatprimitive ideas concerning the anatomy and physi-ology of the body, these will now be discussed.

The knowledge of anatomy and physiology possessed by the Chinese when they first started topractise acupuncture was obviously both scantyand inaccurate. It is, therefore, surprising to findthat from an early date and certainly by the time theSu WEn was compiled in the 2nd century BC theyhad with considerable perspicacity come to realizethat blood circulates continuously around the body.For in this manuscript Chhi-Po says:

The flow (of blood) … runs on and on, and neverstops; a ceaseless movement in an annular circuit.

Chhi-Po is here showing remarkable intuitionespecially when it is remembered that it wasanother 1700 years before the Western world cameround to this view. This tardy realization of thetrue state of affairs in the West was of coursebecause Galen, that remarkably influential earlyGreek physician, had categorically stated that the

movement of blood in the vessels of the body is bymeans of a tidal ebb and flow. This remained theofficial view for centuries and anyone who dared toquestion it was considered a blasphemous heretic.Indeed, it was not until 1628 that William Harveywith considerable courage published his proof thatblood moves around the body in a continuous circle in his Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus.

The ancient Chinese admittedly had no scien-tific evidence to support their belief in the circu-lation of the blood but because of their inherentconviction that the workings of the body are amicrocosmic representation of those to be found inthe macrocosm or universe itself, they may havecome to this conclusion from observing the meteoro-logical water-cycle that occurs in nature.

It should be noted that the Chinese at an earlydate not only correctly concluded that blood circu-lates around the body but also that this is effectedby a pumping action of the heart, for in the Su WEnit says ‘the heart presides over the circulation ofthe blood and juices and the paths in which theytravel’. Moreover, they were quick to appreciatethat the action of the heart is reflected in move-ments of the pulse felt at the wrist, and were ableto measure the pulse rate by using an instrumentcapable of measuring time by a regulated flow ofwater, an apparatus similar to that used by theancient Greeks for timing speeches in their lawcourts and called by them a clepsydra.

The ancient Chinese also with much ingenuityattempted to estimate the time it takes for blood tocirculate around the body and to assist with this calculation measured the approximate total lengthof the great blood vessels. Although their conclusionthat the circulation time is 28.8 minutes was about60 times too slow, modern methods having nowshown it to be only 30 seconds, it was neverthelessa praiseworthy effort, especially when it is remem-bered that even William Harvey several hundredyears later got the calculation wrong!

The Chinese whilst realizing that blood circu-lates around the body in specially designed ves-sels also believed, as did the ancient Greeks, thatthere is a separate substance very difficult to definein modern terms but which could perhaps best bedescribed as a vital force or special form of energy,that also circulates around the body.


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The Greeks referred to it as pneuma and con-sidered it to be present with the blood in arteries.The Chinese called a substance of similar naturechhi, with part of it having Yang properties and theother part Yin properties. Following the appear-ance of the Ling Shu in about 762 AD it has alwaysbeen said that the Yin chhi circulates around thebody in the blood vessels, whilst the Yang chhitravels outside them in a completely separate sys-tem of channels or tracts.

This system of tracts, which anatomically is not demonstrable, has nevertheless always beenvery real to the Chinese who from the beginningbelieved it to consist of an intricate network of main channels, connecting channels and tributariessimilar to the rivers, tributaries and canals whichtogether make up the waterways of the earth. The idea is to be found clearly expressed in a bookentitled the Kuan Tzu written about the late 4thcentury BC where it says ‘one can say water is theblood and the chhi of the earth, because it flowsand penetrates everywhere in the same manner asthe circulation … in the tract and blood vessel systems’.

A belief in the existence of such tracts was vitalto the Chinese in developing their practice ofacupuncture and it is because of the essential partthese channels play in this that they are specific-ally known as acu-tracts. Nonetheless, it must beemphasized that it is the lack of any tangible proofof their existence that has been one of the mainreasons why the Western world has viewed thetraditional Chinese method of practising acupunc-ture with such considerable suspicion since firsthearing about it 300 years ago.

The Chinese have always visualized anddescribed these tracts in a three-dimensional formand considered them to be at variable depths alongtheir individual courses. Clear descriptions of thisare given in their writings, although their illustra-tions merely give the impression that the tractsrun in a relatively straight line along the surface ofthe body. It should be noted that modern Westernwriters often refer to the Chinese acutracts asmeridians but this is better avoided because as LuGwei-Djen & Joseph Needham in the Celestial Lancetspoint out ‘the analogy with astronomical hour-circles or terrestrial longitude is so far-fetched thatwe do not adopt the term’.

The Chinese described 12 main acu-tracts corres-ponding in number with the months of the yearwith each one being considered to have a connec-tion with and taking its name from an organ of the body. However, as already stated, the Chinesewere of the opinion that there were only ten prin-cipal organs, five with Yin characteristics and fivewith Yang characteristics. Therefore, in order thatthe 12 tracts could be linked with 12 organs theyfound it necessary to include the pericardiumamongst the Yin organs, and to invent a structurewith no known equivalent in modern anatomy,which they called the san chiao (triple warmer)and included this amongst the Yang organs.

It is of interest to note that because the brain wasconsidered to be nothing more than some form ofstorage organ it was not included amongst theprincipal organs. The Nei Ching in fact states that itis the liver that ‘is the dwelling place of the soul orspiritual part of man that ascends to heaven’.

Those who pioneered the development ofacupuncture in ancient China believed that acu-tracts for most of their course are situated in thedepths of the body’s tissues, but that at certainpoints, now known in the West as acu-points, theycome to lie immediately under the skin surfacewhere needles can readily be inserted into them.

It will be remembered that, according to trad-itional Chinese teaching, the purpose of insertingneedles into acu-points in disease is to release nox-ious air or ‘wind’ (malignant chhi) that impedesthe free flow of chhi in acu-tracts and thereby dis-turbs the balance between Yin and Yang.

It is possible to gain some idea as to how theChinese have always thought about acu-points bystudying the various names they use to describethem in their writings. One of the commonest ofthese being chhi hsüeh – hsüeh being a word mean-ing a hole or minute cavity or crevice; in the SuWên, chhi hsüeh are described as pores or inter-stices in the flesh that are connected to the naturallyoccurring Yin and Yang forms of chhi in the acu-tract and blood vessel systems. It is also said thatthese ‘holes’ in the flesh are open to invasion bymalignant chhi from outside the body but that ifand when this onslaught occurs it is readily repelledby acupuncture!

The Nei Ching in several places says that thereare 365 acu-points. A figure no doubt arrived at


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because of its symbolic association with the num-ber of degrees in the celestial circle, the number ofdays in the year and the number of bones in thehuman body. This, however, was only the numberof points supposed to be present in theory, as evenin the Nei Ching itself only 160 points actuallyreceive names, and with the passage of time evenfewer have remained in regular use.

The Chinese have given each of their acupointsa specific name and just as they have named acu-tracts after various rivers so they have incorp-orated into the names of acu-points references tosuch parts of nature’s waterway system as tanks,pools and reservoirs. Also, during the course of time,acu-points along the length of each tract have beenindividually numbered, and, as every tract bearsthe name of the organ to which it is supposed to belinked, it necessarily follows that each point maybe identified by reference to the name of the tractalong which it is situated and its number on thistract. For example, the point on the gall bladdertract situated half-way between the neck and thetip of the shoulder at the highest point of the shoul-der girdle has been named by the Chinese Jianjingbut is more commonly referred to as Gall Bladder21 (GB 21); the point situated between the head of the fibula and the upper end of the tibia calledby the Chinese Zusanli is more usually known asStomach 36 (St 36); and the point just above theweb between the first and second toes known asTaichong is more often referred to as Liver 3 (Liv 3).

In the recently developed Western type ofapproach to acupuncture to be described in thisbook, acu-tracts and their alleged links with inter-nal organs are not of themselves of any practicalimportance. However, because most of the triggerpoints employed in this Western form of acupunc-ture have been found to have a close spatial cor-relation with many of the traditional Chineseacu-points, some of the latter will be referred to inthe text as a matter of interest.

In traditional Chinese acupuncture it is from anexamination of the pulse that disease is mainlydiagnosed. The Nei Ching contains a clear accountof how, from a detailed study of the pulse at thewrist, it is possible to establish the nature of a dis-ease, its location in the body and where best toinsert needles to combat it.

The reason why the Chinese have placed suchimportance on examining the pulse is becausethey have always considered that it is at that sitethat the Yin chhi in the blood vessels and the Yangchhi in the tracts converge, and the pulse in someof their writings is referred to as The Great MeetingPlace.

In the Nan Ching – The Manual of Explanationsof Eighty-one Difficult Points in the Nei Ching – a work that first appeared some time around the1st century AD it says:

The Yin chhi runs within the blood vessels, while the Yang chhi travels outside them (in thetracts). The Yin chhi circulates endlessly, nevercoming to a stop (save at death). After fifty revolu-tions the two chhi meet again and this is called a‘great meeting’. The Yin and Yang chhi go alongwith each other in close relation, travelling in cir-cular paths which have no end. So one can see howthe Yin and Yang mutually follow one another.

The Chinese method of examining the pulseconsists of placing three fingers along the length ofthe radial artery at both wrists and by first apply-ing superficial pressure to these points and thendeep pressure 12 separate observations can bemade. From this it is said to be possible to ascertainthe state of chhi in the 12 main tracts, and whendisease is present, to tell which organ is affectedand into which tract needles have to be inserted.

Chinese sphygmology is therefore basicallycomplicated and has been made even more com-plex over the centuries by the laying down of rulesas to when the examination might most profitablybe carried out, including the taking into account ofcertain astrological considerations in determiningthe best day for it. Next, the right time of day hasto be selected for according to the Nei Ching theexamination must be done very early in the morn-ing ‘when the breath of Yin has not yet begun tostir and when the breath of Yang has not yet begunto diffuse, when food and drink have not yet beentaken, when the twelve main vessels are not yetabundant, … when vigour and energy are not yetexerted’.

It is clear that the technique of pulse diagnosismust always have been extremely difficult to mas-ter and yet it would seem that those who devisedthe procedure must have achieved some measure


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of agreement as to the significance of the variousnuances that they considered they could detect atthe wrist. Nevertheless, their diagnostic interpret-ation of these was of necessity expressed in noso-logical terms quite irreconcilable with those basedon our present-day knowledge of pathology, and,therefore, it is surprising to find that certain Western-trained doctors even to this day still try to base theirpractice of acupuncture on this archaic approachto diagnosis, and are quite unwilling to accept thatsuch an anachronistic procedure should long agohave been relegated to the realms of history.

As the practice of acupuncture has of necessityalways depended on the insertion of needles intothe body it is of considerable interest to discoverhow primitive Asiatic man found objects of suf-ficient tensile strength and sharpness for this purpose.

Thorns of various plants, slivers of bamboo, andneedles fashioned from bone have always beenavailable. Bone needles have in fact been found inrecent years in tombs from the neolithic age, andby the 6th century, which is about the date of theoldest existing reference to acupuncture, it wouldhave been technically possible to make needlesfrom bronze, copper, tin, silver and even gold. And certainly gold needles have recently been dis-covered in the tomb of the Han Prince, Liu-ShÊng(113 BC). It is therefore somewhat surprising tofind that seemingly needles in the early days ofacupuncture were commonly made of stone, for inHuang Ti Nei Ching (2nd century BC), Chhi-Po says:

In the present age it is necessary to bring forwardpowerful drugs to combat internal illnesses, andto use acupuncture with sharp stone needles andmoxa to control the external ones.

Also, in manuscripts written on silk before thisand found in the tomb of the son of the Lord of Tai,there are two separate specific references to theuse of stone needles.

It seems difficult to conceive how needles madeof stone could have been sharpened sufficiently topenetrate the tissues of the body, but, of the variousmineral substances available in those far off days, it has been suggested that the following mighthave been employed: flint, mica, asbestos and jade.However, there is no confirmatory evidence thatany of these were utilized and the exact nature of

the type of stone originally used still remains amatter for conjecture. The only certainty is that asiron and steel did not become available to theChinese until the 5th century BC and as the prac-tice of acupuncture was started long before this, itnecessarily follows that materials other than ironmust have initially been employed.

It is impossible in this brief review to mention allthe various stages in the development of this tech-nique over the centuries. Reference will howeverbe made to the Chen Chiu Chia I Ching as this is theoldest existing book entirely devoted to acupunc-ture and moxibustion. It was written soon after theChinese Empire became re-unified in AD 265 byone Huang Fu-mi who apparently became inter-ested in medicine partly because his mother wasparalysed and partly because he himself sufferedfrom rheumatism! In this book Huang Fu-mi forthe first time groups the various acu-points underthe names of the various tracts to which they belongand, after numbering them, gives a detailed descrip-tion of their positions and how to locate them.Further, he names specific acu-points recommendedin the treatment of various illnesses and gives muchadvice as to how he considers acupuncture shouldbest be practised. This is, therefore, an outstandingbook in the history of acupuncture and one whichwas to exert a great influence on the practice of thistechnique throughout the East.

Mention must be made of the eminent phys-ician Sun Ssu-mo (AD 581–673) as it was he whointroduced the so-called module system for deter-mining the exact position of acu-points on people’sbodies irrespective of their various sizes by takingmeasurements using relative or modular inches.He defined a modular inch as being the distancebetween the upper ends of the distal and middleinterphalangeal folds when a person flexes themiddle finger; and recommended that measure-ments should be made by using strips of bamboo,paper, or straw, cut to the length of a person’sindividual modular inch.

Sun Ssu-mo was also the author of two out-standing books on acupuncture and moxibustionand was the first to draw attention to the import-ance of inserting needles into exquisitely tenderpoints, particularly, he said, in treating low backpain. He called these ah-shih (oh-yes!) points, fromthe expletive often uttered by the patient when


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pressure is applied over them! This is of particularinterest as he was clearly practising what is knownnow as trigger point acupuncture, and which hav-ing been rediscovered in recent years is describedin Parts 2 and 3 of this book.

The Imperial Medical College, with a depart-mental professor of acupuncture, lecturers, anddemonstrators, had been founded by AD 618, andby AD 629 a similar college of medicine had beenestablished in each province.

From AD 1027 the teaching of acupuncture atthese institutions was carried out with the help oflife-size bronze figures of the human body. Thewalls of these figures had holes punched in themat the sites of all the known acu-points. The figureswith their holes filled with water and covered bywax were then used for examining medical stu-dents in acupuncture. This was done by makingthe students insert needles into sites on these figureswhere they considered acupoints points might exist,and if, on attempting this, no water poured outthey failed their examination!

The Chinese have always had a deep convictionthat the workings of the body are intimately linkedwith those of nature in general, and that variouscyclical events external to the body have an import-ant influence over matters of health and disease.Further, that for the successful eradication of dis-ease by acupuncture it is necessary to perform thelatter at a propitious time and one that can only bedetermined by taking into consideration the inter-relationship of these various external factors. It is,therefore, not surprising to find that the Nei Chingclearly states that in order to discover the righttime for both the application of acupuncture andmoxibustion the physician must first establish theposition of the sun, the moon, other planets, and thestars in addition to taking into account the seasonof the year and the prevailing weather conditions!

The following is a quotation from Chapter 26 ofthat book:

Therefore one should act in accordance with theweather and the seasons in order to have bloodand breath thoroughly adjusted and harmonized –and consequently – when the weather is cold, oneshould not apply acupuncture. But when the daysare warm there should not be any hesitation. …

In an earlier part of the same book there is astatement that when acupuncture is applied for an

excess of Yang it has a draining effect, and whenfor a deficit of Yin it supplements vigour. Later onin the same chapter it states:

At the time of the new moon one should notdrain, and when the moon is full one should notsupplement. When the moon is empty to the rimone cannot heal diseases, hence one should con-sult the weather and the seasons and adjust thetreatment to them.

This concept that cyclical events have an import-ant controlling influence over matters of healthand disease was still further developed with theintroduction of the wu-yün liu-chhi system (thecyclical motions of the five elements and the sixchhi) in AD 1099, and of the tzu-wu liu-chu system(noon and midnight differences in the following ofthe chhi) in about the middle of the 12th century.

These are complex systems the details of whichwill not be entered into. Suffice it to say that thefirst was based on the conviction that external cyclical, astronomical, meteorological, and climaticfactors influence the workings of the body and thatfrom a study of these the occurrence of disease andparticularly epidemics of it may be predicted. Andthat the second was based on the idea that there areinternal cyclical changes occurring inside the bodyand that these have to be taken into account whendeciding upon ideal times for performing acupunc-ture and moxibustion. It is of great interest that suchideas concerning circadian rhythms in the bodywere put forward so long ago considering that it is only in very recent years that proof has beenobtained of the existence of internal biological clocks.

From this brief review it may be seen that theChinese did not discover the therapeutic effects of acupuncture as a result of some astute clinicalobservation nor alternatively were they inspiredto use it by the logical development of some well-founded hypothesis. On the contrary, it wouldseem that it was very much by luck that they stum-bled upon this valuable form of therapy becausetheir original reasons for using it have subsequentlybeen shown to be entirely fallacious. And further,to a very large extent they succeeded in obscuringthe merits of this therapy by grafting upon it asomewhat esoteric set of rules for its application.The manner in which all this prevented acupunc-ture from becoming readily accepted in the Westernworld during the past 300 years will be discussed


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in detail in the next two chapters but before this itis necessary to say something about its changingfortunes in China itself.

From the time that acupuncture was first usedin China it remained in the ascendance in that partof the world until reaching its zenith at about theend of the 16th century. From then onwards dur-ing the Ch’ing dynasty (1644–1911), when Chinawas under Manchu rule, the practice of it wentinto a gradual decline. This initially was mainlybecause the Confucian religion practised by theManchu people was associated with much prud-ishness so that the baring of the body, as clearly isso often necessary with treatment by acupuncture,was considered to be immoral. And also becausethe religion discouraged the inserting of needlesinto a person’s body for fear that this might dam-age that which was considered to be sacred byvirtue of it having been bestowed on that individ-ual by loving parents. Another important reasonwas that from the 17th century onwards mission-aries from Europe, with initially these mainly beingPortuguese Jesuits, in bringing the Christian religionto China, also brought with them the Western formof medical practice, and this over the next 300 yearsprofoundly influenced the type of medicine prac-tised in the Far East with the practice of acupunc-ture gradually being displaced.

Events moved so quickly that when Hsü LingThai, an eminent Chinese physician and medicalhistorian, wrote about the history of Chinese medi-cine in 1757, he had to report that by that timeacupuncture had become somewhat of a lost artwith few experts left to teach it to medical students.

During the 19th century its status declined stillfurther, with the Ch’ing emperors in 1822 orderingthat it should no longer be taught at the ImperialMedical College. From then on an increasing num-ber of colleges were opened by medical missionar-ies for the express purpose of teaching Chinesestudents Western medicine, until finally this ancientform of treatment reached its nadir in 1929 when

the Chinese authorities officially outlawed thepractice of it in that country.

It has to be remembered, however, that whathas been said only really applied to a minority ofthe population because China has always been a land of the rich and poor, of the rulers and theoppressed, and whilst Western medicine increas-ingly displaced traditional Chinese medicine in thewealthy coastal cities the rural peasants that inhab-ited most of the country continued to depend ontraditional forms of treatment including acupunc-ture, and increasingly, what health care system wasavailable to them became more and more chaoticdue to years of Japanese occupation, civil war, andlack of doctors trained in this type of medicine.

The Chinese communist victory in the so-calledWar of Liberation in 1949, however, changed all thiswith Mao Tse Tung being determined to improvethe health service for the poor by ensuring thatmore doctors became trained in traditional Chinesemedicine; and by ensuring that the practice of thisform of medicine and Western medicine becameclosely integrated with both being taught in themedical colleges.

Following the Great Proletariat Cultural Revolu-tion during the years 1966–69 there was even furtheremphasis placed on the importance of traditionalChinese medicine including acupuncture with the result that most hospitals offered both forms of treatment to their patients. It is therefore not surprising that when President Nixon and hisentourage visited China in 1972, with acupunctureby then having been fully restored to its formerprestigious position, its use in the treatment of dis-ease and in particular as an anaesthetic was demon-strated to them with considerable pride. And it wasbecause his personal physician was so impressedwith what he saw that, on returning to America,he generated a wave of enthusiasm for it in theWestern world that advances in knowledge con-cerning the neurophysiology of pain since thattime have helped to sustain.


ReferencesLu Gwei-Djen, Needham J 1980 Celestial lancets. A history

and rationale of acupuncture and moxa. CambridgeUniversity Press, Cambridge

Veith I 1949 Huang Ti Nei Ching Su Wen The YellowEmperor’s classic of internal medicine. University ofCalifornia Press, Berkeley

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Kaptchuk T J 1983 Chinese medicine: the Web that has noweaver. Hutchinson, London

Macdonald A 1982 Acupuncture from ancient art to modernmedicine. George Allen & Unwin, London

Ma Ran-Wen 2000 Acupuncture: its place in the history ofChinese medicine. Acupuncture in Medicine 18(2): 88–98

Porkert M 1974 The theoretical foundations of Chinesemedicine. MIT Press, Cambridge, Massachusetts


Recommended further reading

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The Chinese had practised acupuncture and moxi-bustion for several centuries before news of itreached the outside world. The first people to hearabout it were the Koreans and then not until aboutthe beginning of the 6th century AD. It was notlong after that, however, that both Chinese andKorean missionaries introduced it to Japan duringthe course of converting the people of that countryto Buddhism.

The Western world, on the other hand, did notlearn about these oriental practices until the 17thcentury when Jesuit missionaries, whilst attempt-ing to convert the Chinese to Christianity, saw thembeing used in Canton, and when European doctorsemployed by the Dutch East Indian Company in and around Java saw them being used by theJapanese in that part of the world. Willem tenRhijne (1647–1700), a physician born in the Dutchtown of Deventer, and who received his medicaleducation at Leyden University, must be given thecredit for being the first person to give the Westernworld a relatively detailed, if unfortunately a some-what misleading, account of the Chinese practiceof acupuncture and moxibustion.

His opportunity to see orientals practising thesetechniques came when, soon after qualifying as adoctor, he joined the Dutch East India Company in1673 and was sent to Java. During the latter part ofhis life there he was to become the director of theLeprosarium but as a young man he had no soonerarrived than he was ordered to go to the island ofDeshima in Nagasaki Bay. It was during the 2 yearshe was stationed there that he first saw the tech-niques of Chinese acupuncture and moxibustion

13

Chapter 2

How news of acupuncture andmoxibustion spread from China to the outside world

CHAPTER CONTENTS

How the Western world learned about theChinese practice of acupuncture in the 17thcentury when physicians working for the DutchEast India Trading Company saw it beingpractised by the Japanese in and around Java atthat time

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which he included with essays on other subjects inhis book Dissertatio de Arthritide; Mantissa Schematica;de Acupunctura …, written some time after he hadleft Nagasaki on 27 October 1676 and returned toJava, and which was published simultaneously inLondon, The Hague, and in Leipzig in 1683.

In the introduction to this essay on acupunc-ture, in which he also included comments on moxi-bustion, he gave reasons why the Chinese andJapanese preferred these two particular forms oftherapy to the therapeutic form of bleeding (phle-botomy; venesection) that was so widely practisedin Europe in his time, by saying:

Burning and acupuncture are the two primaryoperations among the Chinese and Japanesewho employ them to be free from every pain. Ifthese two people (especially the Japanese) weredeprived of the two techniques, their sick wouldbe in a pitiful state without hope of cure or alle-viation. Both nations detest phlebotomy because,in their judgement, venesection emits both healthyand diseased blood, and thereby shortens life.They have, accordingly, attempted to rid unhealthyblood of impurities by moxibustion; and to rid itof winds, the cause of all pain, with moxibustionand acupuncture.

It is interesting to learn from him that in Japan atthat time therapy was mainly carried out by tech-nicians working under the direction of medicalpractitioners, but as ten Rhijne said, ‘For difficultillnesses the physicians themselves administer theneedle.’

These technicians called by the Chinese Xinkieu,and by the Japanese Farritatte, must have had afair degree of independence and clinical freedomfor they had their own establishments with each of the latter having a distinctive sign outside it inthe form of a wooden statue with acupuncture and moxibustion points marked in different col-ours, an eye-catching device, similar to the multi-coloured striped pole often seen outside a barber’sshop in the Western world representing the splintfor which the barber-surgeon in former timesbound the arms of his patients during the processof blood-letting.

From ten Rhijne’s account it would seem thatthe needles used by the Japanese in the 17th cen-tury were made of gold, or occasionally of silver,

being practised by the Japanese, and managed toacquire four illustrations depicting acupuncturepoints lying along channels. He not unnaturallyassumed that the latter must be blood vessels, butfound the matter confusing as the directions inwhich they appeared to run in no way conformedwith those taken by any anatomical structures withwhich he was familiar. He was nevertheless verymuch impressed with the therapeutic effects ofthese two techniques and was therefore determinedto learn more about them and in particular to getsomeone to explain the drawings to him. This how-ever was not to prove easy because as he later saidin his book on the subject:

The zealous Japanese are quite reluctant to share,especially with foreigners, the mysteries of theirart which they conceal like most sacred treasuresin their book cases.

It would seem, however, that the Japanese on theother hand had no such inhibitions when it came tothem wanting to know all about Western medicinefor, on the orders of the Governor of Nagasaki, aChinese-speaking Japanese physician, Zoko Iwanga,was sent to see ten Rhijne in order to question himclosely about the way in which medicine was prac-tised in Europe. Ten Rhijne however seemed to take all this in good part for when writing about it later he refers to the various questions put to himas nothing but ‘bothersome trifles, to be sure’, and moreover in return for the information he gave Iwanga he managed to persuade the latter toattempt to explain to him the drawings in his pos-session. Unfortunately as ten Rhijne later pointedout in his book, in order for him to understandIwanga’s explanations of the notes attached to thedrawings it necessitated one interpreter having to translate the Chinese into Japanese and thenanother interpreter, whose command of the Dutchlanguage was limited, having to translate theJapanese into Dutch. It therefore follows that theinformation ten Rhijne received was of necessityinaccurate and yet he himself then had to do his bestto translate this into Latin, which was the universallanguage in the Western world at that time.

In spite of these difficulties there is no doubtthat ten Rhijne convinced himself that he had suf-ficient understanding as to how the Japanese prac-tised acupuncture for him to write an essay on it

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which is somewhat surprising considering thatsteel must have been readily available to them.The main indication for their use according to himwas for the release of ‘winds’ for as he says:

The Japanese employ acupuncture especially forpain of the belly, stomach and head caused bywinds … They perforate those parts in order topermit the confined wind to exit.

In an attempt to explain this further, he adds thefollowing somewhat homely simile: ‘in the sameway, sausages, when they threaten to explode in aheated pan, are pierced to allow the expandingwind to go out’.

It would seem therefore that although theChinese originally employed acupuncture for thepurpose of clearing collections of ‘wind’ in acu-tracts (p. 7) in due course both they and the Japanesecame to use it for the relief of abdominal painbrought about by the entrapment of a quite differ-ent type of ‘wind’ in the intestinal tract.

It is of particular interest in this respect that theonly case history ten Rhijne includes in his book isof a Japanese soldier with some abdominal pain.The soldier believing this to be due to ‘wind’ pro-duced as a result of drinking an excessive amountof water, is reported to have carried out his owntreatment by inserting an acupuncture needle intohis abdomen. Ten Rhijne was obviously presentwhen he did this for he says:

… lying on his back, he drove the needle into theleft side of his abdomen above the pylorus at fourdifferent locations … while he tapped the needlewith a hammer (since his skin was rather tough)he held his breath. When the needle had beendriven in about the width of a finger, he rotatedits twisting-handle … Relieved of the pain andcured by this procedure, he regained his health.

Ten Rhijne whilst watching this demonstrationof auto-acupuncture must have cast his mind backto his youth for by a strange coincidence the title ofhis dissertation for his doctorate in medicine wasDe dolore intestinorum e flatu … ! In his essay he alsogives a long list of other disorders that the Japanesein those days were treating with acupunctureincluding conditions such as headaches, rheumaticpains, and arthritis that people all over the worldare still using it for. The one notably bizarre and

certainly very hazardous use for it at that time wasin the field of obstetrics with the acupuncturistbeing advised to ‘puncture the womb of a pregnantwoman when the foetus moves excessively beforethe appropriate time for birth and causes themother such severe pains that she frequently is indanger of death; puncture the foetus itself with along and sharp needle, so as to terrify it and makeit cease its abnormal movement fraught with dan-ger for the mother’!

It is very unfortunate considering that ten Rhijnewas sufficiently impressed with the practical valueof acupuncture to feel that he wanted to pass on hisknowledge of the subject to the Western world bywriting an essay on it, that this should have provedto be a totally inaccurate account, due to his failureto understand that the Chinese believed in theexistence of a system of channels (now referred to inthe West as acutracts or meridians) completely sep-arate from and yet closely associated with bloodvessels. His knowledge of anatomy was extensivefor at one stage in his life he taught the subject andtherefore in all fairness there was no reason why itshould have ever crossed his mind that the acu-tracts depicted in the illustrations he acquired couldbe anything but structures already well known tohim from dissecting the human body. As a result herepeatedly refers to them as arteries, and to con-fuse the matter even more insists that the Chineseand Japanese use the terms artery, vein, and nerveinterchangeably and so in some places he evenrefers to them as veins and in others as nerves.

His belief that these tracts were arteries is alsoreadily understandable when it is remembered howmuch importance the Chinese placed on their long-held beliefs concerning the circulation of the bloodin developing their practice of acupuncture. This isclearly expressed by ten Rhijne when he said:

Although Chinese physicians (who are the fore-runners from whom Japanese physicians bor-rowed these systems of healing) are ignorant inanatomy, nonetheless they have perhaps devotedmore effort over many centuries to learning andteaching with very great care the circulation of theblood, than have European physicians, individu-ally or as a group. They base the foundation oftheir entire medicine upon the rules of the circula-tion, as if the rules were oracles of Apollo at Delphi.

How news of acupuncture and moxibustion spread from China 15

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He then goes on to point out how, ‘among theChinese the masters employ hydraulic machines to demonstrate the circulation of the blood to theirdisciples who have earned the title of physician; inthe absence of such machines the masters assistunderstanding with clear figures’. It is obvious thatten Rhijne was under the impression that the draw-ings he possessed were examples of such figures.

Another reason for his confusing acu-tractswith arteries was that he knew that the Chineseplace considerable emphasis on the examinationof the pulse in making a diagnosis before under-taking acupuncture or moxibustion. In referring tothe latter for instance he says:

… wherever pain has set in, burn; burn howeverin the location in which the arteries beat moststrongly. For in that place the seat of the pain islodged, where harmful winds inordinately movethe blood. After prior examination of the pulse ofthe arteries, place the burning tow on the locationmarked with its own sign.

And in another place he says:

… wherever pain has lodged, burn. To which Iadd, when it is necessary puncture, punctureand burn where the arteries beat strongest. Whatthe patient can detect by the sensation of pain thephysician can detect by feeling the pulses in theaffected part.

At the same time he is clearly aware that if thechannels depicted in his illustrations and which hedescribes in the text of his book are arteries thenthey are a very inaccurate anatomical representa-tion of the course known to be taken by such ves-sels. And it would seem that, fearing that for thisreason alone authorities in the Western worldmight reject out of hand the whole system ofacupuncture and moxibustion, he finds it neces-sary to apologize for the apparent ineptness ofthose who drew the illustrations by saying:

In many instances, a person especially skillful at the art of anatomy will belittle the lines andthe precise points of insertion, and will censurethe awkward presentation of the short notes on thediagrams, when these should be more closelyidentified with walls of the blood vessels. But wemust not on this account casually abandon our

confidence in experiments undertaken by thevery great number of superb and polished intel-lects of antiquity. Chinese physicians prefer tocast the blame for a mistake upon their own ignor-ance, rather than diminish in the slightest theauthority of and trust in antiquity …

Although the account of acupuncture in tenRhijne’s book was the first detailed one to appearin the Western world, a passing reference to thesubject had already been made in a book writtenby Jacob de Bondt (1598–1631) who as surgeon-general to the Dutch East India Company in Javahad also seen the technique being used in that partof the world. This book, Historia Naturalis et MedicaIndiae Orientalis, published in 1658, is in the mainan account of the natural history of animals andplants found in the East, but it contains a para-graph about acupuncture.

When ten Rhijne quotes this paragraph in his ownbook he cannot refrain from putting in parentheseshis own critical comments thus causing de Bondt’sdescription of acupuncture to read as follows:

The results with acupuncture in Japan which I willrelate even surpass miracles [without undermin-ing belief in their authenticity]. For chronic painsof the head [and moreover for recent ones, espe-cially those arising from winds], for obstruction ofthe liver and spleen, and also for pleurisy [and forother ailments, as is here made clear] they borethrough [and they perforate] with a stylus [heshould have said, with a needle] made of silver orbronze [more correctly, from gold] and not muchthicker than ordinary lyre strings. The stylus [herethe good author is quite in error] should be drivenslowly and gently through the above mentionedvitals so as to emerge from another part.

One book that presumably ten Rhijne did notread, but which could have been a help to him inunderstanding something about acu-tracts, waswritten anonymously but almost certainly by aFrench Jesuit missionary working in Canton. Thiswork was based on a translation of a 1st-centurymanual, the Mo chüeh (Sphygmological Instructions).This book printed at Grenoble in 1671 clearlyrefers to acu-tracts although admittedly there isvery little detail about them or about the Chinesesystem of pulse-diagnosis in spite of its title Les


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Secrets de la Médecine des Chinois, consistant en laparfaite Connoissance du Pouls, envoyez de la Chinepar un Francois, Homme de grand mérite.

It is more surprising that ten Rhijne did notlearn about the belief of Chinese physicians in asystem of channels or acu-tracts separate from theanatomically demonstrable circulatory system fromthe German Andreas Cleyer as they were togetheras medical officers in the service of the Dutch EastIndia Company on Java. And Cleyer edited a bookgiving clear references to acu-tracts that was pub-lished in 1682, the year before ten Rhijne’s bookappeared.

Cleyer attributes several parts of this bookSpecimen Médicinae Sinicae, sive Opuscula Medica admentem Sinesium to an ‘eruditus Europaeus’ livingin Canton. The possibility therefore exists that thiswas none other than the anonymous author of thebook Les Secrets de la Médecine des Chinois, consis-tant en la parfaite Connoissance du Pouls, envoyez de la Chine par un Francois, Homme de grand méritethat appeared in 1671. Like the latter, Cleyer’sbook also includes translations from the Mo chüeh(Sphygmological Instructions) but is far moreinformative with a lengthy discussion of the vari-ous types of pulse found in health and disease;there are also no less than 30 drawings depictingthe course of acu-tracts. In addition there arenumerous references to acu-tracts, or viae (ways)as they are called in the text but unfortunately, asmight be expected, the author is quite unable toexplain how the Chinese believed that circulatorydisturbances in these invisible tracts could bediagnosed from observations on the pulse.

Nevertheless, the book certainly aroused theinterest of Sir John Floyer (1649–1734) who includedan abridged and paraphrased form of it in his fam-ous two-volume work, The Physician’s Pulse-Watch oran Essay to Explain the Old Art of Feeling the Pulse, andto improve it by the help of a Pulse-Watch, the first vol-ume of which was published in 1707 and the secondin 1710.

Floyer’s pulse-watch was a portable instrumentthat he carried in a box, it having been made underhis direction by a Mr Samuel Watson, a watch-maker in Long Acre, London. Its great virtue wasthat it ran for 60 seconds, and with it he studiedthe effects of a variety of different factors on thepulse rate including food, drink, tobacco, anxiety

and fevers. He implored all young physicians touse the instrument ‘to discern all those dangerousexorbitances which are caused by an irregular diet,violent passions, and a slothful life’.

His reference to Cleyer’s observations onChinese medicine comes in the first part of the second volume under the title of An Essay to makea new Sphygmologia, by accommodating the Chineseand European observations about the Pulse into oneSystem. As may be gathered from the title this onlydiscusses the Chinese method of pulse diagnosisand there is no mention of acupuncture in it. Itwould seem in fact that Floyer had no interest inthe latter believing that the Chinese in the maintreated most diseases pharmaceutically after hav-ing diagnosed them in the first place by means of observations on the pulse. Curiously enough hewas not all that wrong because unbeknown tohim, at the time his book was being written, acu-puncture in China was going through one of itsperiodic phases of being out of fashion.

In spite of Floyer’s enthusiasm for Chinesesphygmology his contemporaries failed to showany real interest in it, or for that matter in the prac-tice of acupuncture itself. This perhaps is surpris-ing considering that in the early part of the 17thcentury William Harvey dramatically changedlong-held ideas in the Western world concerningthe physiology of the circulatory system when in1628 he published his famous book ExercitatioAnatomica de Motu Cordis et Sanguinis in Animalibus.In this he was at last able to refute the hithertoseemingly inviolable but erroneous teaching ofGalen concerning the structure of the heart and the manner in which he had insisted that bloodebbs and flows in the vessels. Harvey proved bymeans of carefully conducted experiments what theChinese had surmised centuries before that bloodflows around the body in a continuous circle.

As might be expected, in view of the manner inwhich Galen’s views had been revered for so manycenturies, there was initially considerable oppos-ition to Harvey’s revolutionary discovery, but, basedas it was on such sound evidence, its gradual accept-ance over the course of years became inevitable.

Considering that the system of sphygmologydevised by the Chinese and their practice ofacupuncture were both firmly founded on theprinciple that blood circulates around the body one


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might therefore have thought that in the climate ofopinion prevailing in the West towards the end ofthe 17th century that more interest might havebeen shown in them. Yet when the book ClavisMedica ad Chinarum Doctrinam de Pulsibus, whichbasically was yet another translation of the Mochüeh, written by Michael Boym (1612–1659) aPolish Jesuit missionary in China, was published in1686, it prompted Pierre Bayle in reviewing it thatyear in Nouvelles de la République des Lettres to say:

The Reverend Father expounds to us the Chinesesystem of medicine very clearly, and it is easy tosee from what he says that the physicians of Chinaare rather clever men. True, their theories andprinciples are not the clearest in the world, but ifwe had got hold of them under the reign of thephilosophy of Aristotle, we should have admiredthem very much, and we should have found themat least as plausible and well based as our own.Unfortunately, they have reached us in Europe justat a time when the mechanick Principles invented,or revived, by our Modern Virtuosi have given usa great distaste for the ‘faculties’ of Galen, and forthe calidum naturalis and the humidum radicaletoo, the great foundations of the Medicine of theChinese no less than that of the Peripateticks.

It should be noted that the Galenic-Aristoteliancalidum naturalis or ‘innate heat’ was widely considered in the 17th century to correspond tothe Chinese yang whilst the Galenic-Aristotelianhumidum radicale or ‘primigenial moisture’ wasconsidered to correspond to the Chinese yin.

It may therefore be seen from the sentimentsexpressed by Bayle that what really deterred mostphysicians in the Western world from taking any particular interest, either in the Chinese methodof pulse-diagnosis, or in acupuncture itself, onfirst learning about them in the 17th century, at atime when they had only recently come to termswith Harvey’s new and enlightened approach toanatomy and physiology after centuries of slavishadherence to Galenic dogma, was that the curi-ously esoteric and nebulous concepts includingyin, yang, chhi and invisible acu-tracts upon whichthese Chinese practices seemed to be based, wereall too reminiscent of some of the bizarre Graeco-Roman beliefs from which they had just been liberated.

Most European physicians also showed little orno enthusiasm for the Chinese practice of applyingheat to the skin by burning moxa on it, when theyfirst heard of this in the 17th century, in spite of thefact that at that time they were still firm believers inblistering their patients with strong irritants, andburning them with boiling oil and red hot irons!One person, however, who did advocate its use wasHermann Buschof, a Dutch Reformed Minister anda friend of ten Rhijne when they worked together inJava. He wrote a laudatory account of its use ingout and other arthritic conditions in a book pub-lished in 1674 entitled Het Podagra … Another pro-tagonist was Sir William Temple the eminent17th-century diplomat who wrote appreciativelyabout it in an essay ‘The cure of Gout by Moxa’ inhis Miscellanea published in 1693, after havingreceived this form of treatment for a painful attackof this affliction during an international conferenceat Nijmegen in 1677. Conversely the eminent physi-cian Thomas Sydenham (1624–1689), when writingabout gout some time earlier, had referred dis-paragingly to the use of moxa in its treatment.

The most comprehensive account of moxibustionto reach the West, however, was that written by theGerman physician Englebert Kaempfer (1651–1716).Kaempfer, who was brought up in Germany at atime when it had recently been devastated by theravages of the Thirty Years War (1618–1648), decidedafter qualifying as a doctor that rather than continueto live there he would prefer to seek work abroad.He therefore joined the United East India Companyand became yet another of the surgeons to work atthe Dutch trading station on the island of Deshimain Nagasaki Bay.

His observations on Japanese medical practicein that part of the world led him to write two essays,one ‘Acupuncture, a Japanese Cure for Colic’, andthe other ‘Moxa, a Chinese and Japanese Substancefor Cautery’, which appeared together with a largenumber of essays on other subjects in his Amoeni-tatum Exoticarum Politico-Physico-Medicarum FasciculiV … published in 1712.

The essay on acupuncture is of limited valuebecause as may be seen from the title it confinesitself to the use of this technique in one conditiononly, namely the relief of cramp-like pains occurringin association with a severe type of diarrhoea thatwas endemic in that part of the world at the time


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and known to the Japanese as senki. There is adetailed account of how needles should be insertedin this condition but all reference to acu-tracts isavoided, and it does not really add anything tothat which had by that time already been writtenon the subject.

The essay on moxibustion, however, is far morewide ranging. His description of the sites at whichhe saw a moxa cautery applied, and the reasonsfor doing this make fascinating reading, as may beseen from the following quotation:

Considering the places cauterised, you wouldthink the unexpected successes illusory. Forexample to facilitate birth, the tip of the small toeon the left foot; to prevent conception or to pro-mote sterility, the navel; to relieve toothache, theadducting muscle of the thumb on the same sideas the aching tooth.

The latter is a clear reference to the classicalChinese acupuncture and moxa point Ho-Ku,stimulation of which to this day is widely recog-nized as having a powerful analgesic effect.

From what has been said it will be clear thatmuch information concerning acupuncture andmoxibustion reached Europe during the 17th cen-tury but only limited use was made of these tech-niques either during that century or the followingone because physicians in the Western world werecompletely mystified as to how these particularforms of therapy achieve their effects. One of thefew men to think deeply about this matter wasGerhard van Swieten, the famous Dutch phys-ician, who concluded that any beneficial effectsthat they may have must be for reasons entirelydifferent from those that had been put forward bythe Chinese, for as he said in 1755:

The acupuncture of the Japanese and the cauteryof various parts of the body with (Chinese) moxa

seems to stimulate the nerves and thereby to alle-viate pains and cramps in quite different parts ofthe body in a most wonderful way. It would bean extraordinarily useful enterprise if someonewould take the trouble to note and investigatethe marvellous communion which the nerveshave with one another, and at what points cer-tain nerves lie which when stimulated can calmthe pain at distant sites. The physicians of Asia,who knew no (modern) anatomy, have by longpractical experience identified such points.

It was of course another 200 years before researchinto the neurophysiology of pain provided objectiveevidence in support of van Swieten’s hypothesis.

It is now necessary to consider the attitudes ofdoctors, both in Europe and America, to acupunc-ture during the 19th century as this was a periodwhen a few of the more courageous of them, inspite of not being able to accept the traditional theo-ries upon which the Chinese based their practiceof it, decided to explore empirically its clinicalapplications. And having convinced themselves ofits merits in alleviating musculoskeletal pain, theyattempted to popularize its use for this purpose.They were, however, to find their efforts thwartedby entrenched conservatism. Members of the med-ical profession at that time showed a strangelyinconsistent attitude whereby they were morethan willing to prescribe potentially toxic sub-stances of uncertain efficacy whilst being quiteunwilling to try out the relatively harmless proced-ure of inserting needles into people, presumablybecause they could not bring themselves to believethat anything so simple could have the effectsclaimed for it – an attitude of mind, regretfully, stilladopted by some in the late 20th century!


ReferencesBowers J Z 1966 Englebert Kaempfer; Physician, explorer,

scholar and author. Journal of the History of Medicineand Allied Sciences 21: 237–259

Bowers J Z, Carrubba R W 1970 The doctoral thesis ofEnglebert Kaempfer on tropical diseases, orientalmedicine and exotic natural phenomena. Journal

of the History of Medicine and Allied Sciences 25:270–310

Carrubba R W, Bowers J Z 1974 The Western world’s firstdetailed treatise on acupuncture: Willem ten Rhijne’s DeAcupunctura. Journal of the History of Medicine andAllied Sciences 29: 391–397

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Floyer Sir John 1707 The physician’s pulse watch: or, anessay to explain the old art of feeling the pulse, and toimprove it by the help of a pulse-watch. London

Harvey William 1628 Exercitatio anatomica de motu cordiset sanguinis in animalibus. London – an anatomicaldisquisition on the motion of the heart and blood in

animals. Translated by Robert Willis, Barnes, Surrey,England 1847. In: Willius F A, Keys T E (eds) Classics ofcardiology, Vol 1. Dover Publications, New York, 1961

Lu Gwei-Djen, Needham J 1980 Celestial lancets. A historyand rationale of acupuncture and moxa. CambridgeUniversity Press, Cambridge

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There is good evidence to show that acupuncturecame to be widely practised by the medical profes-sion in Europe during the first half of the 19th century.

Its protagonists, however, turned their backs on the complexities of the traditional Chineseapproach to the subject and, in a determined effortto shed it of all its mysticism, ignored the acu-tractsystem and refused to attempt to use the orientalsystem of pulse-diagnosis. They confined them-selves for the most part to the treatment of painfulconditions and the method adopted was simply astraightforward insertion of needles into painfulareas, similar to the ah shih hsüeh type of acupunc-ture practised by Sun Ssu-mo in China in the 7thcentury (see Ch. 1). Both of these forms of acupunc-ture ‘in loco dolenti’, as Lu GweiDjen & Needham(1980) so aptly call it, were clearly the forerunnersof the more sophisticated type of trigger pointacupuncture recently developed in the Westernworld and described in detail later in this book.

The circumstances leading to this renewal ofinterest were not the same in every country. InGermany the somewhat unlikely source of inspir-ation was a letter published in 1806 by the play-wright, August Von Kotzebue in his magazine TheCandid Observer (Funny and Serious). This letterostensibly from his son travelling in Japan gave asomewhat satirical account of the way acupunc-ture was being practised there. This might haveattracted no more than passing interest if it hadnot been for the fact that it caught the eye of someunknown physician who wrote a long rejoinderurging that the subject be treated with more

21

Chapter 3

The practice of acupuncture inthe Western world during the19th century

CHAPTER CONTENTS

An account of how acupuncture for the relief ofpain came to be employed for limited periods oftime by certain physicians in Germany, France,Britain, America, and Canada during the 19thcentury

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he employed electroacupuncture and used Leydenjars as the source of electricity.

In England the medical practitioner who didmost to interest his colleagues in the clinical appli-cation of acupuncture by writing two books on thesubject was J. M. Churchill. The first, entitled ATreatise on Acupuncturation, being a Description of aSurgical Operation originally peculiar to the Japaneseand Chinese, and by them denominated Zin-King, nowintroduced into European Practice, with Directions forits Performance and Cases illustrating its Success, waspublished in 1821, and the second consisting of anumber of case histories was published in 1828.His treatise on acupuncturation, a modest volumeof only 86 pages, was dedicated to the famous sur-geon Astley Cooper as follows:

To Astley Cooper Esq. the steady friend andpatron of humble merit the author respectfullyinscribes this little treatise. Less from presump-tion of its deserving his approbation than as amark of respect for splendid achievements andof gratitude towards a great master.

Churchill said it was his friend Mr Scott ofWestminster, the first person as far as he knew toperform acupuncture in England, who initiallydrew his attention to the subject by demonstratingto him several successfully treated cases, and it wasthis which led him to study the technique himself.

From reading Churchill’s books it is obviousthat he restricted himself to treating cases of whathe called ‘rheumatalgia’, and judging from thecase histories this was invariably of short dur-ation. This no doubt accounts for his uniformlyexcellent results and clearly because of this he con-sidered it only necessary to present a limited num-ber of cases for as he said:

I would certainly add many others to the list but to minds open to conviction and truth nostronger impression would be made by multi-plying examples, whilst the sceptical would notbe persuaded though one rose from the dead!

He admits that he did not know how acupunctureworks stating:

I have by no means made up my mind as to thenature of its action and rather than venture intospeculations which may be received as doubtful

seriousness. In spite of this it was some timebefore the clinical application of the techniquebecame widely adopted but in 1828 some import-ant papers appeared, including one by Bernsteinand another by Lohmayer, reporting good resultswith this form of treatment in the alleviation ofrheumatic pain.

In France, interest in acupuncture was reawakened in a far more direct manner. When IsaacTitsingh, a surgeon attached to the Dutch East IndiaCompany at Deshima, eventually returned toEurope, he brought with him among the memora-bilia of his travels, an ebony case containing needlesand moxa tinder; and also a teaching-aid in theform of a cardboard doll with acu-points and tractspainted on it that had been presented to him by aJapanese Imperial Physician. His friends in Europeshowed considerable interest in these items, butwhat was to prove to be of even greater importancewas his translation of an 18th-century Japanesetreatise on acupuncture, for when this came to theattention of the Parisian physician Sarlandière hewas so intrigued with it that he began to practiseacupuncture himself and persuaded several otherphysicians in Paris to do likewise. Included amongthese were Berlioz, the father of the composer, whoin 1816 wrote the first book on the subject in France,and Cloquet & Dantu who reported their results oftreating patients with this technique in an articleObservations sur less Effets Thérapeutiques de I’ Acu-puncture in Bayle’s Bibliothèque de Thérapeutiquepublished in 1828.

Sarlandière himself was the first to apply electriccurrents to implanted needles, and his book givingan account of this was published in 1825. This willno doubt surprise anyone who might have thoughtthat electroacupuncture is a recent invention.

From their reports it is clear that these Parisianphysicians were using acupuncture in the treat-ment of many different disorders but that their bestresults, as might be expected, were in the relief ofmusculoskeletal pain and migraine.

In Italy the first book to be published on the prac-tice of acupuncture was that of Bozetti in 1820, butthe one that was to become best known was that ofAntonio Carraro published in 1825. Also of particu-lar interest were two books, the first appearing in1834 and the second in 1837, in which da Camindescribes how following the example of Sarlandière

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by some and visionary by others I prefer to pre-serve a profound silence.

Such honesty has to be admired particularly ashe clearly recognizes that his self-confessed ignor-ance concerning its action could seriously under-mine his efforts to popularize the technique for hesays ‘… if on the other hand, a rational theory, builton sound logical reasons, be the only evidence to which any value can be attached, then will my efforts have been unavailing and fruitless’. Suchfears, however, proved groundless because hisbook undoubtedly aroused much interest with it,not only being translated into German in 1824 andinto French in 1825, but it also inspired many of hisEnglish colleagues to take an interest in the subject.One such person was Mr Wansborough of Fulham,who writing in the Lancet in 1826 says:

As respects the modus operandi I have proceededin every case according to the recommendation ofMr Churchill in his useful little work on acupunc-turation to which I beg the readers of the Lancet toconsult for further information on the subject.

In his paper he describes how by the use of acu-puncture he alleviated the pain of various musculo-skeletal disorders in eight patients. He says thelatter were all so impressed with the result as topronounce them as being magical!

He, like Churchill, was unwilling to commithimself as to how inserting needles into the bodycould have a therapeutic effect, but he clearlythought that the Chinese were wrong in believingthat it was due to noxious air being released fromthe tissues for he says:

I shall not hazard a hypothesis of the modusoperandi of acupuncturation but at the same timeI am free to confess myself sceptical on the creed,that its effects are produced by the escape of airfrom the cellular membranes through the punc-tures made by needles.

He then proceeds to give three cogent reasons forhis incredulity:

1. The very form of the needle is a barrier to theescape of air; 2. the cure is often performedbefore the needles are withdrawn; and 3. the cureis often performed by causing acute pain in theact of introducing them.

His first observation, being self-explanatory,needs no further comment; his second may soundfarfetched to anyone who has not practised acu-puncture but on occasions it is surprising howrapidly pain is relieved in response to needle stimulation; and his third is in line with the cur-rently held view that for acupuncture to be suc-cessful in the relief of chronic pain the needlingitself has to be such as to produce a brief intenselypainful stimulus (see Ch. 8).

Another person whose interest in acupuncturewas aroused by Churchill was John Elliotson, aphysician who was originally on the staff at StThomas’s Hospital, London but who later becameProfessor of Medicine at University College Hos-pital. Elliotson writing in the Medico-ChirurgicalTransactions in 1827 stated that the use of acupunc-ture both in his private practice and at St Thomas’sHospital over several years had led him to agreewith Mr Churchill that it was mainly of value in the‘rheumatism of the fleshy parts’, which he also inplaces referred to as ‘rheumatalgia’.

In view of Elliotson’s high standing as a teacherin a leading medical school it was unfortunate thathis enthusiastic support for animal magnetism, aform of hypnosis introduced by Mesmer, causedhim to suffer professional opprobrium, as this inturn served to undermine any influence he mightotherwise have had in furthering the cause ofacupuncture.

It is clear that in 19th-century Britain any inter-est that may have been shown in acupuncture bothby the medical profession and the general publicwas intermittent, as may be seen from the follow-ing contribution to the subject by Dr T Ogier Wardof Kensington, in the British Medical Journal on 28thAugust 1858:

… acupuncture is a remedy that seems to have itsfloods and ebbs in public estimation; for we see itmuch belauded in medical meetings every tenyears or so, even to its recommendation in neu-ralgia of the heart, and then it again sinks intoneglect or oblivion. And it is not unlikely that its disuse may be occasioned partly by fear of the pain, and partly by the difficulty the patientfinds to believe so trifling an operation can produce such powerful effects. Its use is not asfrequent as it deserves and now that we know

Acupuncture in the Western world during the 19th century 23

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the rationale of its operation I venture to bringforward a few cases in illustration of its remedialpowers in order that others may be induced togive it a more extensive trial, and thus ascertainits true value in the treatment of neuralgia orrheumatic pains.

There then follows six case reports describinghow muscle pain in various parts of the bodyincluding the shoulder, lower back and thigh wasalleviated by inserting needles into the areas wherethe pain was most intensely felt. Acupuncture maynot have been widely adopted by the British med-ical profession during the 19th century but there isevidence to show that at least one large provincialgeneral hospital in this country favoured its use inthe alleviation of musculoskeletal pain. T. PridginTeale, Surgeon to the General Infirmary at Leeds,writing in the Lancet in 1871, states:

In the present essay it is my wish to record somefacts concerning a method of treatment of greatantiquity which seems in a great measure to havedropped out of use, or at any rate to be at thepresent day but little employed or even knownin many parts of the United Kingdom. It hashowever been for years a favourite traditionalpractice at the Leeds Infirmary.

He then goes on to say ‘when it does succeedthe relief it gives is almost instantaneous, gener-ally permanent, and often in cases which forweeks or months have run the gauntlet of othertreatments without benefit’.

He then proceeds to describe five cases includingtwo with pain and restricted movement of theshoulder joint, one with pain around the coccyx fol-lowing labour, one with persistent pain around theos calcis, and one with long-standing pain aroundthe wrist following trauma. He expresses the opin-ion that cases suitable for acupuncture includetrauma to muscle, stretching or tearing of muscle ortendon, and disuse pain. Certainly, even by today’sstandards, this is a reasonably comprehensive list of‘surgical’ indications.

It is interesting to note that Teale, from observ-ing the area of redness that so frequently arises inthe skin around the site where an acupunctureneedle has been inserted, was misled into thinkingthat acupuncture must work by producing someform of temporary congestion.

Another surgeon to write about the use of acu-puncture in hospital practice at Leeds was SimeonSnell. Snell writing in the Medical Times and Gazettein 1880 at a time when he was ophthalmic surgeonto the Sheffield General Hospital says:

At the Leeds Infirmary the use of it is almost trad-itional. It was there that I both saw it employed,practised it myself and witnessed the remarkablebenefits frequently resulting.

He then proceeds to describe five cases of painwith limitation of movement of the shoulder jointhe had treated successfully at Leeds.

Presumably when he became an ophthalmicsurgeon at Sheffield he had little opportunity touse the technique but one can be sure that heencouraged others to do so. And certainly he wasmore enlightened than Teale in his view as to howit works believing ‘it may act as a stimulant to thenerve twigs’.

News concerning the manner in whichacupuncture was being practised in Europe fromthe beginning of the 19th century quickly reachedAmerica. American physicians, however, at thattime viewed this form of therapy with consider-able suspicion and were reluctant to make use ofit. An anonymous reviewer in admitting this,when reviewing Churchill’s Treatise on Acupunc-turation in the Medical Repository in 1822, was forcedto say:

… but we have probably been mistaken. Acu-puncture is likely to become, employed with dis-crimination and directed with skill, a valuableresource.

In spite of these words of encouragement, andalso that during the 1820s American medical jour-nals published a number of European reports onthe subject, the only physicians in the whole ofthat great continent who seemed to take any inter-est in it were a few in Philadelphia, with one of themost enthusiastic of these, as Cassedy (1974) haspointed out, being Franklin Bache.

Franklin Bache was the assistant physician atthe Philadelphia State Penitentiary and in 1825 hedecided to try the effects of acupuncture on pris-oners suffering from various painful disorders,which as he said, when reporting his results a year


Chap-03.qxd 11*10*04 10:12 Page 24

later (Bache 1826), ‘may be arranged into the fourgeneral heads of muscular rheumatism, chronicpains, neuralgia, and ophthalmia’. In his report in which he reviewed the results of the effects ofacupuncture on 29 people, most of whom wereconvicts, he concluded that the treatment hadmuch to offer in removing and mitigating pain,and that it was ‘a proper remedy in almost all dis-eases, whose prominent symptom is pain’.

One cannot help but feel that if only more noticehad been taken of this wise dictum that interest inacupuncture in 19th-century America might havebecome more widespread, but, unfortunately, cer-tain other Philadelphian physicians decided todirect their energies to exploring its use in condi-tions of a far more dubious nature.

These included E. J. Coxe, D. T. Coxe, and SamuelJackson, who having heard reports from Europeabout it being possible to revive drowned kittensby inserting needles into their hearts, decided toinvestigate whether the same procedure had any-thing to offer in resuscitating drowned people!And finding, as might be expected, that it had not,they clearly became disillusioned with the thera-peutic properties of acupuncture in general, for asEdward Coxe (1826) in reporting the results of theirexperiment remarked:

Whatever others may think of the possibility ofresuscitating drowned persons by acupuncture, I can only say that I should think myself highlyculpable, if, called to a case of asphyxia, I were towaste time, every moment of which is precious,in endeavouring to resuscitate by a means whichI sincerely believe to be good for nothing.

This in my opinion is a very good example as to how acupuncture can so readily be brought intodisrepute when it is not employed in a selective anddiscerning manner, and should serve as an objectlesson to all those currently engaged in investigat-ing the clinical applications of acupuncture. Despitethis adverse report the cause of acupuncture inAmerica received a boost when in 1833 the editorsof the Medical Magazine reprinted a paper that John Elliotson, the physician at St Thomas’s Hos-pital, London, had originally contributed to theCyclopaedia of Practical Medicine. Also, in 1836 theeditors of the prestigious and widely read BostonMedical and Surgical Journal reprinted an article that

had appeared shortly before in the Southern Medicaland Surgical Journal. In this paper, William M. Lee ofSouth Carolina reported how he had used acupunc-ture for 6 years in the treatment of rheumatism and concluded that this method of treatment was‘entitled to far more attention than it has yetreceived in the United States’.

Such a view, however, does not seem to havebeen widely shared, for there continued to be apaucity of literature on acupuncture in America atthat time with the only further outstanding contri-bution being that of Robley Dunglison, anotherPhiladelphian physician. This took the form of aneight-page account of the subject in a compendiumof his entitled New Remedies, and published in 1839.The same article was reproduced in subsequenteditions of the book up to the last one whichappeared in 1856, but in spite of this any interestthat there may have been in this type of treatmentwas gradually fading leaving Samuel Gross in hisbook A System of Surgery, published in 1859 to state:

Its advantages have been much overrated andthe practice … has fallen into disrepute.

This certainly may have been true so far asAmerica was concerned but up in Canada noneother than the famous physician Sir William Oslerwas using it in the late 19th and early 20th centuries,for in the eighth edition of his book The Principlesand Practice of Medicine published in 1912 at thetime when he was Regius Professor of Medicine atOxford University he wrote:

For lumbago, acupuncture is, in acute cases, themost efficient treatment. Needles of from three tofour inches in length (ordinary bonnet needles,sterilised, will do) are thrust into the lumbarmuscles at the seat of pain, and withdrawn afterfive or ten minutes. In many instances the reliefof pain is immediate, and I can corroborate thestatements of Ringer, who taught me this prac-tice, as to its extraordinary and prompt effect inmany instances.

He had clearly been in the habit of using the technique for many years because HarveyCushing (1925) in his book The Life of Sir WilliamOsler refers to an unfortunate experience the greatman had when he was a physician at the MontrealGeneral Hospital.


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It would seem that early in Osler’s career at that hospital a certain Peter Redpath, a wealthyMontreal sugar refiner and member of the hos-pital’s board, having suffered from intractable lum-bago for some time, had high hopes that the newlyappointed physician might be able to cure him.

Arrangements were therefore made for him toconsult Osler in his office at the hospital and it isrecounted that Redpath, having arrived exhaustedfrom the effort of mounting the stairs, did not takekindly to being treated with acupuncture, forCushing reports that:

… at each jab the old gentleman is said to haverapped out a string of oaths, and in the end gotup and hobbled out, no better of his pain, this toOsler’s great distress, for he had expected to givehim immediate relief which as he said ‘meant amillion for McGill’.

It should be noted that, unlike the Chinese whohave always attached much importance to mani-pulating needles such as twirling them betweenthumb and finger, once they have been insertedinto the body, most 19th-century European expo-nents of acupuncture were content merely to inserttheir needles and then to leave them withouttouching them again for a short period of time. Theactual time varied considerably and ranged fromMr Wansbrough of Fulham leaving them in situ forfrom 20 seconds to 4 minutes, and Mr Pridgin Tealeleaving them on average for about 1 minute; up toMr Churchill who advised leaving them for about5–6 minutes, and Sir William Osler who recom-mended that they remain for 5–10 minutes.

This was of considerable practical interest dur-ing the resurgence of interest in acupuncture in thelatter part of the 20th century, as many people,including myself, for reasons to be explained inChapter 8, favoured the technique whereby nee-dles, having been inserted, were left in positionwithout any form of manipulation. However, it isalso now realized that it is wrong to stipulate anyparticular period of time for which they should beleft, as this varies widely from a few seconds to 10minutes according to a patient’s individual centralnervous system’s speed of reaction to peripheralnerve stimulation with dry needles.

It is also worth stressing once again that none ofthese physicians put needles into traditionalChinese acupuncture points but so far as muscu-loskeletal disorders were concerned, which verysensibly is what in the main they used it for, theysimply inserted them into the painful areas. How-ever, it is now realized that musculoskeletal paindoes not necessarily originate at the site where it isfelt, but is referred there via the central nervous sys-tem from some focus of neural hyperactivity – nowknown as a trigger point – that is often situatedsome distance away. Therefore, rather than insert-ing a needle into the area where pain is felt, the painis more likely to be relieved if the needle is insertedinto the tissues overlying the trigger point for thepurpose of stimulating Adelta nerve fibres in itsvicinity.

This is the fundamental principle upon whichthe recently developed Western approach to trig-ger point acupuncture is based, and the manner inwhich it was discovered will now be explained.


ReferencesAnon 1822 Review of James Churchill’s treatise on

acupuncturation. Medical Repository (New Series) 7:441–449

Bache F 1826 Cases illustrative of the remedial effects ofacupuncturation. North American Medical and SurgicalJournal 1: 311–321

Berlioz L V J 1816 Mémoires sur les maladies chroniques, lesévacuations sanguines et 1’acupuncture, 2 vols.Croullebois, Paris

Bozetti S 1820 Memoria sull’agopuntura. MilanCarraro A 1825 Saggio sull’agopuntura. UdineCassedy J H 1974 Early use of acupuncture in the United

States. Bulletin of the New York Academy of Medicine 50 (8): 892–896

Churchill J M 1821 A treatise on acupuncturation being a description of a surgical operation originallypeculiar to the Japanese and Chinese, and by them denominated zin-king, now introduced intoEuropean practice, with directions for its performance,and cases illustrating its success. Simpkins & Marshall, London (German trans 1824, French trans 1825)

Churchill J M 1828 Cases illustrative of the immediate effectsof acupuncturation in rheumatism, lumbago, sciatica,anomalous muscular diseases and in dropsy of thecellular tissue, selected from various sources andintended as an appendix to the author’s treatise on thesubject. Callow & Wilson, London

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Cloquet J, Dantu T M 1828 Observations sur les effectsthérapeutiques de 1’acupuncture. In: Bayle A L J (ed)Bibliotheque de Thérapeutique, vol 1, p. 436

Coxe E J 1826 Observations on asphyxia from drowning.North American Medical and Surgical Journal 2: 292–293

Cushing H 1925 The life of Sir William Osler. ClarendonPress, Oxford

da Camin F S 1834 Sulla agopuntura, con alcuni cenni sullapuntura elettrica. Antonelli, Venice

da Camin F S 1837 Dell’agopuntura e della galvano-puntura.Osservazioni, Venice

Dunglison R 1839 Acupuncture. In: New remedies. Waldie,Philadelphia, pp. 23–30

Elliotson J 1827 The use of the sulphate of copper in chronicdiarrhoea together with an essay on acupuncture.Medicochirurgical transactions 13, part 2: 451–467

Elliotson J 1833 Acupuncture. Medical Magazine 1: 309–314Gross S D 1859 A system of surgery, vol 1. Blanchard and

Lea, Philadelphia, pp. 575–576

Lee W M 1836 Acupuncture as a remedy for rheumatism.Southern Medical and Surgical Journal 1: 129–133

Lu Gwei-Djen, Needham J 1980 Celestial lancets. CambridgeUniversity Press, Cambridge, p. 295

Osler Sir William 1912 The principles and practice ofmedicine, 8th edn. Appleton, New York, p. 1131

Sarlandière le Chevalier J B 1825 Mémoires surl’electropuncture … Private publication, Paris Snell S1880 Remarks on acupuncture. Medical Times andGazette 1: 661–662

Teale T Pridgin 1871 Clinical essays no. III. On the relief ofpain and muscular disability by acupuncture. Lancet 1:567–568

Wansborough D 1826 Acupuncturation. Lancet 10: 846–848Ward T Ogier 1858 On acupuncture. British Medical Journal

(Aug 28): 728–729


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INTRODUCTION

The traditional practice of Chinese acupuncturehaving become officially recognized once again inChina during the 1950s, and it having since thenbeen increasingly used by some doctors, and to an even greater extent by non-medically qualifiedpractitioners in the West, there are at present manyacupuncturists throughout the world who claim it is beneficial in the treatment of a wide variety ofdisorders. It is, however, only in the alleviation ofpain, and in particular musculoskeletal pain, thatthere is any scientific basis to its use. And, evenwhen used within these strictly defined limits, thetraditional Chinese approach to this form of ther-apy has serious drawbacks.

The principal disadvantage is that, for mostpractitioners of traditional Chinese acupuncture,needles have to be inserted somewhat arbitrarily inaccordance with the numerous lists of points thatare recommended for use in the treatment of vari-ous rather ill-defined clinical conditions in everystandard textbook on the subject. Moreover, beforea person is able to use these lists, recipes, or pre-scriptions, as they are sometimes called, it is firstnecessary to memorize the course taken by the vari-ous Chinese acu-tracts, and the exact anatomicalposition on them of the various acu-points. It can only be assumed that these traditional guidesto point selection owe their origin to the time-honoured, but highly contentious, Chinese methodof pulse-diagnosis, and for this reason alone they areunlikely to be acceptable to most doctors trained in20th-century scientific Western medicine.

31

Chapter 4

Some basic observations leadingto its development

CHAPTER CONTENTS

Introduction 31A review of John Kellgren’s laboratory and

clinical observations during the 1930s whichestablished that pain which arises from points of maximum tenderness in muscle and certainother structures is referred to distant sites. Also, his injection method of treating this pain 32–35

The relevance of his discoveries to thesubsequent development of trigger pointacupuncture 36

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experimental findings had already received supportfrom the clinical observations made by severalphysicians, who, from 1925 onwards, had notedthat certain painful conditions of the extremities areassociated with tender areas in the muscles of thelimb girdles and because of this had suggested the possibility that in such cases pain arising inmuscle may be of the referred type.

In his experiments that he carried out on himselfand healthy volunteers working in the same labora-tory, he first anaesthetized the skin and then injectedsmall amounts (0.1–0.3 cc) of hypertonic (6%) salineinto various muscles; and then carefully observedthe distribution of pain. For example, in studiesinvolving the gluteus medius muscle the skin of the buttock was first anaesthetized with Novocainat three sites. Then intramuscular needles wereinserted through these anaesthetized areas until theyimpinged upon the gluteal fascia. An injection ofhypertonic saline into this fascia produced localizedpain. The needles were then advanced into the mus-cle itself and a further injection into this produced adiffuse pain felt at some distance from the injectionsite in the lower part of the buttock, the back of thethigh, and on occasions as far down as the knee (Fig.4.1). Injections into the fascia enveloping the tibialisanticus (anterior) muscle and into the muscle itselfproduced similar findings (Fig. 4.2).

However, fortunately for those who wish toavoid this somewhat empirically determined andimpersonal method of point selection and prefer toemploy one based on a carefully conducted clinicalexamination of each individual patient, there isnow a trigger point approach to acupuncture. Thisrecently developed Western approach to acupunc-ture has as its main application the alleviation ofpain that is referred to some part of the body from afocus or foci of neural hyperactivity in one or otherof the structures that together form the muscu-loskeletal system. In order to explain the principlesupon which it is based, it is first necessary to reviewthe outstanding pioneer research into referred paincarried out by J. H. Kellgren at University CollegeHospital Medical School in the late 1930s.

THE REFERRAL OF MUSCULOSKELETALPAIN – SOME EARLY OBSERVATIONS

It was Sir Thomas Lewis, the director of the clinicalresearch department at University College Hospitalwho, because of his particular interest in the subjectof pain in general, prompted Kellgren to carry outclinical observations on the referral of musculo-skeletal pain.

Lewis in his paper Suggestions Relating to theStudy of Somatic Pain published in February 1938states:

As an experimental method of producing musclepain the injection of a minute quantity of a saltsolution is the most satisfactory … In these obser-vations I have noted that muscle pain is referred toa distance. Thus pain arising from the lower partof the triceps is often referred down the inner sideof the forearm to the little finger, from the trapez-ius it is usually referred to the occiput. I have beenfortunate in interesting Dr Kellgren in this matter.In a long series of very careful researches carriedout in my laboratory he has formulated some verystriking principles underlying the reference ofpain from muscle – principles which appear tohave an important practical bearing.

Kellgren, in his paper Observations on ReferredPain Arising from Muscle, published later the sameyear, states that in taking on the task set him by Sir Thomas Lewis he was aware that the latter’s

Points ofinjection

Musclepain

Figure 4.1 The distribution of diffuse referred pain(hatched area) produced by injecting 6% saline into threepoints in the gluteus medius muscle. (Reproduced withpermission of J. H. Kellgren from Clinical Science, vol. 3.pp 175–190 © 1938 The Biochemical Society, London.)

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Kellgren also points out in this paper that aninjection of saline into muscle produces pain atsome distance from the point stimulated and that,in certain cases, the maximal pain is not experi-enced in muscle itself but in other structures. Fromhis experimental work he was able to show, forexample, that when an injection is given into theoccipital muscle, pain is felt diffusely as a headache;when into the masseter muscle, it is felt in themouth as toothache; when into the infraspinatusmuscle, it is felt at the tip of the shoulder; when intothe vastus intermedius, it is felt around the kneejoint; when into the peroneus longus, it is felt at theankle joint; and when into the multifidus muscleopposite the first and second lumbar vertebrae, it isfelt in the scrotum.

His finding that referred pain from a focus of irritation in a muscle may be felt in such struc-tures as joints, teeth, or the testicles is, of course, of considerable importance, and one which hasconstantly to be borne in mind in everyday clinicalpractice.

From these observations he decided that thedistribution of referred pain, induced artificially innormal people, by injecting hypertonic saline intomuscle broadly follows a spinal segmental pattern

but that it does not correspond with the sensorysegmental patterns of the skin.

Kellgren did not confine himself to laboratoryexperiments but applied knowledge gained fromthese to clinical medicine. And his paper, A Prelim-inary Account of Referred Pains Arising from Muscle,published in 1938, is of the greatest possible interestbecause, unbeknown to him, from his study of anumber of cases of what he calls ‘fibrositis’ or‘myalgia’ he laid down certain principles uponwhich the practice of modern Western acupunctureis now based. As his observations are therefore ofsuch fundamental importance, part of his paperwill be quoted in full:

During the last year I have made an extensiveinvestigation of the character and distribution ofmuscular pain produced experimentally in nor-mal subjects … Briefly I find that pain arising frommuscle is always diffuse and is often referred,with a distribution which follows a spinal seg-mental pattern; and that this referred pain isassociated with referred tenderness of the deepstructures.

A number of cases of ‘fibrositis’ or ‘myalgia’have been investigated from this point of view.The distribution of pain was noted as accuratelyas possible, and experience of the distribution of pain provoked from normal muscles guidedme to the muscles from which spontaneous painmight have arisen. Such muscles almost alwayspresented tender spots on palpation. Pressure onthese spots sometimes reproduced the patient’spain; but a method more often successful was theinjection of sterile saline into the tender muscle.The injection of Novocain may also reproducethe pain momentarily.

The search for the source of trouble by defin-ing areas of tenderness is often confused by the patients calling attention to areas of referred tenderness. But referred tenderness is rarely con-spicuous, and I have found it a useful guide toconsider tenderness to be referred unless thepatient winces under the palpation of a givenspot. When these acutely tender spots were nottoo extensive they were infiltrated with 1%Novocain … This infiltration often produced reliefof the symptoms and signs, and sometimes abol-ished them completely.

Some basic observations leading to its development 33

Points ofinjection

Tendon pain

Muscle pain

Figure 4.2 The distribution of referred pain (hatchedarea) from injecting 6% saline into points in the tibialisanterior muscle. Also, the pattern of locally referred pain(stippled area) from injecting saline into the tendon ofthis muscle at the ankle. (Reproduced with permission ofJ. H. Kellgren from Clinical Science, vol. 3, pp 175–190 ©1938 The Biochemical Society, London.)

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Case 1

Case 4

Case 5 Case 6 Case 7 Case 8

Case 2 Case 3

Figure 4.3 The distribution of pain (hatched area) and tender spots (black) in eight cases in which the pain wasabolished by injecting Novocain into the tender spots. (Reproduced with permission of J. H. Kellgren from the British Medical Journal, 1938.)

Chap-04.qxd 11*10*04 10:15 Page 34

It should be noted from this that Kellgren madea clear distinction between certain ‘spots’ in muscleso exquisitely tender that palpation of them makesthe patient wince; and diffuse rather ill-definedareas of referred pain which on palpation are onlyslightly tender. Also, that he realized that such‘spots’ as he called them, or trigger points as theyare now termed, are the cause of this referred pain with it being possible to alleviate the latter by de-activating these acutely tender ‘spots’ ortrigger points by infiltrating them with Novocain (Fig. 4.3).

Kellgren (1939) also investigated referred painarising from experimentally-induced irritant fociin interspinous ligaments, tendons, joints and theperiosteum. Two others who also made a valuablecontribution to our understanding of skeletal pain were Verne Inman, an anatomist, and JohnSaunders, an orthopaedic surgeon working at the University of California Medical School. Intheir paper, Referred Pain from Skeletal Structures,published in 1944, they describe how they studiedexperimentally induced pain in healthy volunteersby artificially stimulating periosteum, ligamentsand tendons by mechanically traumatizing themeither by scratching them with the point of a nee-dle, or by drilling them with a special type of wire;and, secondly, by chemically stimulating them byinjecting into them either normal isotonic Ringer’ssolution, or a weak solution of formic acid orhypertonic saline.

From these experiments they conclude:

Stimulation of the periosteum or the tendinousattachments of ligaments and tendons is accom-panied by an extensive radiation of the pain,which, if sufficiently intense, radiates for consid-erable distances … so constant is the directionand locality to which the pain radiates that it hasbeen found possible to chart and map out theextent of the areas to which the pain radiates,and an attempt has been made to relate them toareas of segmental innervation.

It should be noted that they refer to these areasof segmental innervation in the case of skeletalstructures as sclerotomes in order to distinguishthem from myotomes or dermatomes.

In this paper they also state that for several yearsthey had been making detailed clinical observations

on the radiation of pain from pathological disordersaffecting bony and ligamentous structures. Andthey had found that in every case the type of painwas similar to that produced experimentally andthat, like the latter, its radiation to distant areas hada distinctive pattern but one which could not beaccounted for by reference to the distribution ofperipheral nerves.

The anatomical distribution of referredmusculoskeletal painIt has to be admitted that there is much confusionconcerning the anatomical distribution of referredpain in disorders of the musculoskeletal system. It will be remembered that Kellgren concludedthat pain referred from skeletal muscle usually follows spinal segmental patterns but that this isnot dermatomal, and that he also noted manyexceptions when pain extended over several segments.

Travell & Bigelow (1946) also concluded fromclinical observations on patients with referredpain from skeletal muscle that it does not follow asimple segmental pattern for, as they say, ‘the ref-erence from a single site may comprise fragmentsof several “segmental pain areas” without includ-ing any one entirely, or may take in a whole “seg-mental area,” skip the adjacent one and reappeardistally’.

Hockaday & Whitty (1967) in attempting to clarify the situation studied referred sensationsproduced by injecting 6% saline into interspinousligaments in 28 normal subjects, and concludedthat the:

… site of reference for a given site of stimuluswas constant and replicable in the individual, butwas not always confined to the segment of innerv-ation in which the injection was given. Site of ref-erence within a group of subjects varied widelyand could not be interpreted as segmental or hav-ing a fixed anatomical substrate.

It is difficult, however, to be certain as to howmuch credence should be placed on conclusionsdrawn from any of the experiments carried outover the past 50 years in which hypertonic salinehas been injected into various musculoskeletalstructures in an attempt to map out the distribu-tion of referred pain for as Wyke (1987) says, in

Some basic observations leading to its development 35

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discussing these during the course of consideringvarious aspects of spinal ligamentous pain:

Although such saline solutions provide a veryeffective chemical irritant for connective tissuenociceptive receptors, it must be emphasised herethat because of the diffuse distribution of thisreceptor system through the vertebral connectivetissues, and because of the widespread interseg-mental linkages between their afferent nervefibres, attempts to use such a procedure as a meansof delineating a supposed segmental nociceptiveinnervation of the spinal tissues are clearly falla-cious, especially as it is impossible (even with theintroduction of radio-opaque material into theinjected solution) to be certain just how much ofthe diffuse nociceptive afferent system is beingstimulated by any given volume of hypertonicsaline.

The situation, therefore, is far from straight-forward and Travell & Simons (1983) after years of extensively studying referred pain in patientswith disorders of the musculoskeletal system havebeen forced somewhat negatively to conclude that

referred pain of this type ‘does not follow a simplesegmental pattern. Neither does it follow familiarneurological patterns, nor the known patterns forreferred pain of visceral origin’.

The relevance of these discoveries to thedevelopment of trigger point acupunctureKellgren’s discovery that it is possible to alleviatereferred musculoskeletal pain by injecting a localanaesthetic into what he called tender points hasproved to be an important therapeutic advance.The relevance of this to the recent development oftrigger point acupuncture might however at firstsight seem to be somewhat obscure until it isexplained that there are now sound neurophysi-ology grounds for believing that it is more rationalas well as being simpler, safer and just as effectiveto alleviate this type of pain by stimulating withdry needles, nerve endings in the superficial tissues directly overlying these intramuscularlysituated tender points, or what, for reasons to beexplained in the next chapter, are now called trig-ger points.


ReferencesHockaday J M, Whitty C W M 1967 Patterns of referred pain

in the normal subject. Brain 90: 481–496Inman V T, Saunders J B de C M 1944 Referred pain from

skeletal structures. Journal of Nervous and MentalDiseases 99: 660–667

Kellgren J H 1938 Observations on referred pain arisingfrom muscle. Clinical Science 3: 175–190

Kellgren J H 1938 A preliminary account of referred painsarising from muscle. British Medical Journal 1: 325–327

Kellgren J H 1939 On the distribution of pain arising fromdeep somatic structures with charts of segmental painareas. Clinical Science 4: 35–46

Lewis Sir Thomas 1938 Suggestions relating to the study ofsomatic pain. British Medical Journal 1: 321–325

Travell J, Bigelow N H 1946 Referred somatic pain does notfollow a simple ‘segmental’ pattern. FederationProceedings 5: 106

Travell J, Simons D G 1983 Myofascial pain and dysfunction.The trigger point manual. Williams and Wilkins,Baltimore

Wyke B 1987 The neurology of low back pain. In: Jayson M I V(ed) The lumbar spine and back pain, 3rd edn. ChurchillLivingstone, Edinburgh, p. 78

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INTRODUCTION

Trigger point (TrP) acupuncture is mainly employedfor the alleviation of pain arising from points ofmaximum tenderness in the muscles of patientssuffering from what is now known as the myofascialtrigger point pain syndrome (MTrPPS).

Acupuncture of a similar type, together withother forms of treatment, may also be used to relievethe pain that affects those suffering from what ispresently termed fibromyalgia syndrome (FS).

The purpose of this chapter is to show how ourcurrent concepts concerning these two syndromeshave gradually evolved.

NOSOLOGICAL OBFUSCATION

Before MTrPPS and FS were recognized to be sep-arate disorders, over the past 200 years they wereknown collectively by a variety of different names.The original term was rheumatism, which was first introduced by Guillaume de Baillou in the latter part of the 16th century. Unfortunately, asRuhmann (1940) has pointed out in his introduc-tion to an English translation of De Baillou’s bookLiber de Rheumatismo, de Baillou used the termrheumatism not only when describing clinicalmanifestations of muscular rheumatism, but alsowhen writing about what has since becomeknown as acute rheumatic fever.

Thomas Sydenham then added to this termino-logical confusion when in his Observationes Medicaepublished in 1676 he included a chapter entitled‘Rheumatism’ that dealt only with the characteristic

37

Chapter 5

Evolution of knowledgeconcerning muscle painsyndromes for which it isemployed

CHAPTER CONTENTS

Introduction 37Some 19th and early 20th century observations

concerning a muscle pain disorder initially called muscular rheumatism and subsequentlyfibrositis 37–40

The introduction of a variety of other names forthe disorder during the first half of the 20thcentury 40–41

Observations during the 1950s that led to therecognition of the disorder – myofascialtrigger point pain syndrome. And observationsfrom the 1960s onwards that led to therecognition of the disorder – fibromyalgiasyndrome 41–43

Chap-05.qxd 11*10*04 10:15 Page 37


when in 1915 Llewellyn, a physician at the RoyalMineral Water Hospital in Bath, and Jones, a sur-geon in that city, published a book entitled Fibrositis.In this they included under the term fibrositis avariety of disorders including gout and rheumatoidarthritis. Since that time, the term has been used insuch an imprecise manner as to make it virtuallymeaningless.

A search for a more suitable term for what was originally called muscular rheumatism hastherefore continued, and some of the synonymsemployed during this century include nodularfibromyositis (Telling 1911), myofascitis (Albee1927), myofibrositis (Murray 1929), neurofibrositis(Clayton & Livingstone 1930), idiopathic myalgia(Gutstein-Good 1940), rheumatic myalgias (Good1941) and even myodysneuria (Gutstein 1955).

Simons (1975, 1976) and Reynolds (1983), in theirwide-ranging historical reviews of the subject,have shown that, in addition to this longstandingterminological confusion, there has also been muchdisagreement over the years concerning the diag-nostic significance of the nodules, palpable bandsand tender points found in this disorder.

NODULES AND PALPABLE BANDS

The Edinburgh physician William Balfour (1816), asa result of massaging muscles to relieve the pain ofmuscular rheumatism, was one of the first to reportthe presence of nodules in this disorder. However,it was not until the middle of the 19th century,when the Dutch physician Johan Mezger placedmassage on a sound scientific basis (Haberling1932), and this ‘hands-on’ technique then becamewidely adopted for the treatment of muscularrheumatism, that nodules and the elongated cord-like structures now known as palpable bands,which are found in this disorder, became generallyrecognized.

It was Mezger’s Swedish and German studentswho were particularly influential in disseminat-ing knowledge about these structures. In 1876, theSwedish physician Uno Helleday wrote extensivelyabout nodules occurring in what he called chronicmyitis (Helleday 1876). Following this, the Germanphysician Strauss (1898) distinguished betweennodules – which he described as being small, tender, apple-sized structures – and palpable

migratory type of arthropathy seen in acute rheum-atic fever. This confusion was further compoundedwhen, in 1810, Wells called the carditis that devel-ops in this febrile disorder rheumatism of the heart(Baldry 1971). Fortunately, Jean Bouillau helped toclarify the situation when in 1840 he made a cleardistinction between the arthropathy and carditisof acute rheumatic fever and muscular rheuma-tism (Reynolds 1983).

By that time two British physicians, Balfour(1815) and Scudamore (1827) had put forward theidea that the pain of muscular rheumatism occursas the result of inflammation developing in thefibrous connective tissue in muscle. This conceptdiffered from the one held by 19th-century Germanand Scandinavian physicians who believed that thepain develops as the result of an inflammatoryprocess in the muscle itself. Nevertheless, it wasone that was to persist throughout England andFrance for the rest of that century and in 1904 causedSir William Gowers to recommend that the disorderhitherto known as muscular rheumatism shouldbe called fibrositis.

Gowers did this during the course of a lecture on lumbago at what was then called the NationalHospital for the Paralysed and Epileptic (NationalHospital for Nervous Diseases, London). The argu-ments he put forward in support of his propositionwere, in retrospect, distinctly specious, but never-theless they led him to conclude: ‘We are thus com-pelled to regard lumbago in particular, and muscularrheumatism in general, as a form of inflammation ofthe fibrous tissues of the muscles … (and thus) … wemay conveniently follow the analogy of “cellulitis”and term it “fibrositis.” ’

Ralph Stockman, the then Professor of Medicineat Glasgow University, seemed to provide him withthe pathological confirmation he required when, onexamining microscopically some nodules removedfrom the muscles of patients affected by this dis-order, he reported the presence of ‘inflammatoryhyperplasia … confined to white fibrous tissue’(Stockman 1904).

Although Stockman’s findings have never sub-sequently been confirmed, their publication at that particular time helped to ensure that Gowers’term fibrositis became widely adopted. Any diag-nostic specificity Gowers may have hoped to con-fer upon this term, however, was soon removed

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bands – which he described as being painful, pencil-sized to little finger-sized elongated structures.The identification of these structures requires morethan a cursory examination and, as Müller (1912)pointed out, the main reasons why so many doc-tors fail to identify them is because it requires askilled technique, one that he considered difficultto learn but that could be made easier by the appli-cation of a lubricant to the skin.

He also thought that the reason why his con-temporaries tended to deny the existence of nod-ules and palpable bands was because they did not bother to look for them conscientiously, unlikemasseurs who, according to him, had no difficultyin detecting them from palpating muscles system-atically and then treating them appropriately. Asimilar state of affairs prevails today, with physio-therapists being far more practised in the art ofpalpating muscles than many doctors.

NodulesBy the beginning of this century doctors in Britainwere being taught to regard the presence of nod-ules as essential for the diagnosis of what was thencalled fibrositis. However, it soon became apparentthat not only are nodules not always present in thedisorder, but also they can occasionally be presentin people with no history of it. It is because of theirsomewhat enigmatic and elusive nature, andbecause of their distinctly nebulous morphology(Ch. 7), that over the course of this century theirdiagnostic significance has increasingly come tobe questioned. Despite this, there is no doubt thatwhen nodules are specifically sought they are fre-quently found in the lumbar region in patientswith chronic low-back pain, and also, though lessfrequently, in the neck and shoulder girdle ofthose affected by persistent musculoskeletal painat that site. Moreover, the insertion of dry needlesinto these nodules helps to relieve this pain (Ch. 8).

Palpable bandsUnlike nodules which only develop in muscles inthe lumbar and cervical regions, palpable bands areliable to develop in any muscle of the body. Likenodules, however, they are only discovered if con-scientiously and skilfully looked for. When these

elongated bands are carefully palpated they arefound to contain one or more focal points of exquis-ite tenderness, now known as TrPs, but whichKellgren and others before him called tender points.

Tender points

Balfour (1824a,b) not only found tender nodules in patients with muscular rheumatism, but alsoobserved that, separate from these, there are focalpoints of tenderness in the muscles. However, thefirst person to write at length about these was theFrench physician François Valleix.

Valleix, in his Treatise on Neuralgia published in1841 described a disorder characterized by pain ofa shooting nature and the finding of painful points(points douloureux) on palpation of the tissues. Herealized that the pain emanated from these pointsfor he states:

If, in the intervals of the shooting pains, one asks(a patient with neuralgia) what is the seat of thepain, he replies by designating limited points …It is with the aid of pressure … that one discoversthe extent of the painful points. …

Some of the pain syndromes he described wouldclearly be included in a present-day classificationof neuralgias but others, such as what he termedfemoropopliteal neuralgia, would not. Furthermore,7 years later he somewhat confused the situationby calling muscular rheumatism a form of neural-gia (Valleix 1848). With reference to this he states:

I conclude that pain, capital symptom of neuralgiaexpresses itself … in different ways. If it remainsconcentrated in the nerves one finds characteristic,isolated, painful points; this is neuralgia in the propersense. If the pain spreads into the muscles … thisis muscular rheumatism … an obvious muscularrheumatism can transform itself into a true neuralgia. …

Despite his belief that neuralgia can turn itselfinto muscular rheumatism and vice versa, he mustbe given credit for recognizing that the pain inmuscular rheumatism emanates primarily fromfocal points of neural hyperactivity, and also that ittravels some distance from its source. He waswrong, however, in believing that this is because it is ‘propagated along neighbouring nerves’.

Evolution of knowledge of muscle pain syndromes 39

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Since then many other European physicians haveerroneously subscribed to Valleix’s idea that rheum-atic pain spreads along the course of peripheralnerves, but they have differed in their views as tohow this might occur. Stockman’s (1904) explan-ation was that ‘a branch of a nerve may be pressedupon by a nodule, or may even pass through it,hence the pain often radiates over a wide area perhaps far from a nodule’. Others believed that itoccurred as a result of pressure on a nerve when amuscle goes into spasm. Athird hypothesis, and onewhich was widely held well into the 20th century,was that it is due to rheumatic inflammation of con-nective tissue in or around nerves, and it was for thisreason that the terms neurofibrositis and perineuri-tis were introduced (Gowers 1904, Llewellyn &Jones 1915, Clayton & Livingstone 1930).

Those who put forward such ideas seem tohave been oblivious of the fact that the Britishphysician Thomas Inman, as long ago as 1858, hadshrewdly noted that the radiation of pain in mus-cular rheumatism ‘is independent entirely of thecourse of nerves’. They also seem to have ignoredthe observations made by the German physicianCornelius, who at the beginning of this centurynoted that ‘this radiation often enough absolutelydoes not keep to the individual nerve trunks’ andis bound ‘to no anatomical law’ (Cornelius 1903).

Cornelius not only confirmed Inman’s observa-tion that the radiation of pain is not along the courseof peripheral nerves and, therefore, cannot be dueto compression of these structures, but went fur-ther than this by showing that pressure on tenderpoints in muscles evokes this type of pain and thatthe latter must therefore emanate from these points.He clearly realized that the reason why these pointsare tender is because they are sites where nerveendings are in a state of hyperactivity and for thisreason he called them nerve points (nervenpunkte).He also stated that he thought this neural hyper-activity occurred as a result of external factors suchas changes of temperature, alterations in weatherconditions, physical exertion and emotional upsets,or, alternatively, because of ‘heightened excitability’of the nervous system occurring as the result of suchinfluences as heredity, intemperance and illness ingeneral.

He was, therefore, beginning to formulate ideas concerning the pathogenesis of muscular

rheumatism, which were very much in line withthe modern view that the pain develops as a resultof nerve endings at tender points (or what todayare more often called TrPs) becoming sensitizedfor one or other of a variety of different reasons. Inthe light of all this, it may be seen that Valleix maynot have been so far off the mark as at first sightmight be thought when he called muscular rheum-atism a type of neuralgia. There is also no doubtthat Sir William Osler (1909), with his customaryperspicacity, must have had Valleix and Corneliusin mind when, in writing about what he calledmuscular rheumatism or myalgia in his famoustextbook of medicine, he said:

It is by no means certain that the muscular tissuesare the seat of the disease. Many writers claim,perhaps correctly, that it is a neuralgia of the sensory nerves of the muscles.

Early 20th-century physicians, however, haddifficulty in explaining why pain occurring as theresult of the sensitisation of nerve endings at ten-der points should be felt some distance away fromthem. Cornelius (1903) stated it was due to ‘reflexmechanisms’ but did not enlarge much on thenature of these. Nobody else seems to have beenable to take the matter much further until 1952,when Neufeld attributed the heterotopic nature of rheumatic pain to cortical misinterpretation ofsensation. It was, however, the 3rd decade of the20th century that was particularly notable for stud-ies concerning the clinical aspects of rheumaticheterotopic pain.

Hunter (1933) described cases in which therewas referral of pain from tender points in the muscles of the abdominal wall. Edeiken & Wolferth(1936) described how, in some patients with cor-onary thrombosis who had developed pain in theshoulder during the course of strict bed rest, pres-sure on tender points in muscles over the leftscapula caused the spontaneously occurring shoul-der pain to be reproduced. Then, in 1938 therewere no less than three important contributions tothe subject.

One of these was Kellgren’s experimental and clinical observations concerning the referral ofpain from tender points, which were of such con-siderable importance, both from a diagnostic andtherapeutic point of view, that they have already


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been considered at some length in Chapter 4. Asecond was that of the Czechoslovakian physicianReichart, who was one of the first to describe andillustrate diagramatically specific patterns of radi-ating pains from tender points in muscles. Thethird came from a Polish physician, Gutstein, fol-lowing his arrival in England as a political refugee.

Gutstein, unlike Kellgren, who in 1938 publishedhis clinical observations in the British MedicalJournal, published his findings that year in the lesswidely read British Journal of Physical Medicine,and that is possibly one of the reasons why it didnot receive the attention it deserved. Nevertheless,in an attempt to get the medical profession to takenotice of what he had to say about musculoskel-etal pain, he wrote a number of papers on the sub-ject over the next 10 years. Confusingly, however,during the course of this he changed his name threetimes and even more confusingly kept giving themusculoskeletal pain disorder he was discussing a different name. Thus, in 1938 and again in 1940,under the name of M Gutstein, he wrote about whathe called muscular or common rheumatism. In1940 under the name of Gutstein-Good he calledthe disorder idiopathic myalgia. Then, a year later,by which time he had changed his name yet againto Good, he wrote about rheumatic myalgias! In1950 he called it fibrositis, and in 1951 non-articularrheumatism. To add to the confusion, there was at about the same time an R. R. Gutstein (1955)calling this disorder myodysneuria!

Despite all this, Good made the valuable obser-vation that pressure applied to tender points, orwhat he called myalgic spots in a muscle or ten-don, gives rise to both local and referred pain, andhe must be given the credit for being the first per-son to stress that the patterns of pain referral fromtender points in individual muscles are the samein everyone; these patterns he illustrated in well-executed drawings. In a similar manner to Kellgrenhe alleviated this type of pain by injecting a localanaesthetic into these tender points.

Sadly, the medical profession in Britain largelyignored Kellgren’s and Good’s valuable observa-tions. One reason for this was that by the 1950smany of its leading rheumatologists had come to the conclusion that fibrositis, or non-articularrheumatism as it was by that time more commonlycalled, is not an organic disorder and that a more

appropriate name for it is psychogenic rheum-atism. They were led to believe this because ofdoubts concerning the significance of its physicalsigns, the absence of any characteristic histologicalappearances and the lack of any specific labora-tory tests for it. Typical of this view was the oneexpressed by Ellman & Shaw (1950) who, duringthe course of discussing patients with this dis-order stated:

From the striking disparity between the grossnature of their symptoms and the poverty of thephysical findings … it seems clear that the natureof this often very prolonged incapacity is psychi-atric in the majority of cases … the patient achesin his limbs because in fact he aches in his mind.

Another reason was that by the 1950s specialistsin the field of physical medicine were of the opin-ion that there is no such disorder as muscularrheumatism and that the pain, said to be associ-ated with it, occurs as the result of disorders in thevertebral column with, in particular, degenerativediscs impinging upon nerve roots (Cyriax 1948, deBlecourt 1954, Christie 1958).

Fortunately, there were physicians in other partsof the world who were sufficiently perspicaciousto recognize the merits of Kellgren’s observations.One of these was Michael Kelly in Australia. Kellynot only adopted Kellgren’s methods of diagnos-ing and relieving referred pain from tender pointsin muscles but recorded his clinical observationsin a series of valuable papers published over aperiod of 21 years from 1941 onwards. Referencesto the majority of these are to be found in his lastpaper (Kelly 1962).

MYOFASCIAL TRIGGER POINT PAINSYNDROME

The physician, however, who from the 1940sonwards has done the most to further the subjectis Janet Travell (Fig. 5.1). She first began to take aninterest in it after reading how Edeiken & Wolferth(1936) had been able to reproduce spontaneouslyoccurring shoulder pain by applying pressure totender points in muscles around the scapula, andthen reading about observations made both by Kellgren and by the American orthopaedic surgeon Steindler (1940).


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It was Steindler who, during the course ofreporting how he was able to relieve ‘sciatica’ byinjecting Novocain into tender points in muscles inthe lumbar and gluteal regions, first called thesepoints trigger points (TrPs). It was, however, Travellwho brought this term into general use when, in theearly 1950s, she introduced the adjective myofascialand began to refer to myofascial TrPs and todescribe the pain coming from these as myofascialpain. She adopted the term myofascial as a result ofobserving, whilst doing an infraspinatus musclebiopsy, that the pain pattern evoked by stretchingor pinching the fascia enveloping the muscle is sim-ilar to that when the same is done to the muscleitself. Following this, she realized that each musclein the body has its own specific pattern of myofas-cial TrP pain referral and she introduced the termmyofascial pain syndromes – a term that has sincebeen generally accepted.

By 1951, Travell & Rinzler had had sufficientexperience in recognizing these patterns of painreferral to enable them to give a detailed descriptionof a large number of them at that year’s meeting of

the American Medical Association. In the follow-ing year they published an account of them in aclassic contribution to the subject, ‘The MyofascialGenesis of Pain’, which is particularly notable forthe clarity of its illustrations (Travell & Rinzler1952). Thirty-one years later, Travell and her col-league David Simons (Fig. 5.2) had gained suchconsiderable experience in the diagnosis and man-agement of the myofascial pain syndromes thatthey were able to produce the first authoritativetextbook on the subject (Travell & Simons 1983).

FIBROMYALGIA SYNDROME

In 1965 Smythe, a rheumatologist, and Moldofsky,a psychiatrist in Toronto, Canada, began to take afresh look at so-called fibrositis and investigatedelectroencephalographically sleep disturbances inpatients suffering from this disorder (Moldofskyet al 1975, Moldofsky 1986, Smythe 1986). Theyfound that the rapid 8–10 c/s alpha rhythm nor-mally found in rapid eye movement (REM) sleepintrudes into the usual slow 1–2 c/s delta rhythmof non-REM stage IV deep sleep. It is for this reasonthat 60–90% of patients with fibromyalgia com-plain of a non-restorative sleep that causes them towake feeling tired and with generalized musclestiffness (Goldenberg 1987).


Figure 5.1 Janet Travell. (With permission from VirginiaP. Wilson, USA.)

Figure 5.2 David Simons.

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It was this renewed interest in fibrositis thateventually led to the recognition of a syndromecharacterized by persistent generalized musclepain, non-restorative sleep, early morning stiff-ness, marked fatigue, and multiple tender pointsscattered over the body at certain specific sites.

When Smythe & Moldofsky (1977) (Fig. 5.3) firstdrew attention to this syndrome they somewhatconfusingly referred to it as the ‘fibrositis’ syn-drome, but, for the same reason that made thisterm unacceptable earlier in this century, it wassoon abandoned and in 1981 it was re-named thefibromyalgia syndrome (Yunus et al 1981). Thisterm has since been officially included in theWorld Health Organization’s 10th revision of itsInternational Classification of Diseases, where it has been given the number M79.0 (Consensusdocument on fibromyalgia) (WHO 1993). Beforediscussing present knowledge concerning thepathophysiology of MPS and FS it will be first necessary in the next chapter to consider the various pain-arousing and pain-suppressingmechanisms present in the peripheral and centralnervous systems.


Figure 5.3 Harvey Moldofsky.

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Balfour 1815 Observations on the pathology and cure ofrheumatism. Edinburgh Medical and Surgical Journal 11:168–187

Balfour 1816 Observations with cases illustrative of newsimple and expeditious mode of curing rheumatism andsprains. … Adam Black, Edinburgh

Balfour 1824a Illustrations of the efficacy of compression andpercussion in the cure of rheumatism and sprains. TheLondon Medical and Physical Journal 51: 446–462

Balfour 1824b Illustrations of the efficacy of compressionand percussion in the cure of rheumatism and sprains.The London Medical and Physical Journal 52: 104–115,200–208, 284–291

Christie B G 1958 Discussion on non-articular rheumatism.Proceedings of the Royal Society of Medicine 51: 251–255

Clayton E G, Livingstone J L 1930 Fibrositis. Lancet 1:1420–1423

Cornelius A 1903 Narben und Nerven. DeutscheMilitärärztlische Zeitschrift 32: 657–673

Cyriax J 1948 Fibrositis. British Medical Journal 2: 251–255

de Blecourt J J 1954 Screening of the population forrheumatic diseases. Annals of Rheumatic Diseases 13:338–340

Edeiken J, Wolferth C C 1936 Persistent pain in the shoulderregion following myocardial infarction. American Journalof Medical Science 191: 201–210

Ellman P, Shaw D 1950 The chronic ‘rheumatic’ and hispains. Psychosomatic aspects of chronic non-articularrheumatism. Annals of Rheumatic Diseases 9: 341–357

Goldenberg D L 1987 Fibromyalgia syndrome. An emergingbut controversial condition. Journal of the AmericanMedical Association 257 (20): 2782–2787

Good M G 1941 Rheumatic myalgias. Practitioner 146:167–174

Good M G 1950 The role of skeletal muscle in thepathogenesis of diseases. Acta Medica Scandinavica 138:285–292

Good M G 1951 Objective diagnosis and curability ofnonarticular rheumatism. British Journal of PhysicalMedicine and Industrial Hygiene 14: 1–7

Gowers W R 1904 Lumbago: Its lessons and analogues.British Medical Journal 1: 117–121

Gutstein M 1938 Diagnosis and treatment of muscularrheumatism. British Journal of Physical Medicine 1:302–321

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Gutstein M 1940 Common rheumatism and physiotherapy.British Journal of Physical Medicine 3: 46–50

Gutstein R R 1955 A review of myodysneuria (fibrositis).American Practitioner 6: 570–577

Gutstein-Good M 1940 Idiopathic myalgia simulatingvisceral and other diseases. Lancet 2: 326–328

Haberling W 1932 Johan Georg Mezger of Amsterdam. Thefounder of scientific massage (translated by EmilieRecht). Medical Life 39: 190–207

Helleday U 1876 Nordiskt medicinskt arkiv 6 and 8 Nr 8. P A Norstedtosöner, Stockholm

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Inman T 1858 Remarks on myalgia or muscular pain. BritishMedical Journal 407–408, 866–868

Kelly M 1962 Local injections for rheumatism. MedicalJournal of Australia 1: 45–50

Llewellyn L J, Jones A B 1915 Fibrositis. Rebman, New YorkMoldofsky H 1986 Sleep and musculoskeletal pain. The

American Journal of Medicine 81(suppl 3A): 85–89Moldofsky H, Scarisbrick P, England R, Smythe H 1975

Musculoskeletal symptoms and non-rem sleepdisturbance in patients with fibrositis syndrome andhealthy subjects. Psychosomatic Medicine 371: 341–351

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Neufeld I 1952 Pathogenetic concepts of ‘fibrositis’ – fibropathicsyndromes. Archives of Physical Medicine 33: 363–369

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Reichart A 1938 Reflexschmerzen auf grund von myogelosen.Deutsch Medizinische Wochenshrift 64: 823–824

Reynolds M D 1983 The development of the concept offibrositis. The Journal of the History of Medical andAllied Sciences 38: 5–35

Ruhmann W 1940 The earliest book on rheumatism. TheBritish Journal of Rheumatism II (3): 140–162 (This paperincludes an original translation of de Baillou’s Liber deRheumatismo which, originally written in medieval Latin,was first published by a descendant M J Thevart in 1736,i.e. 120 years after the author’s death.)

Scudamore C 1827 A treatise on the nature and cure ofrheumatism. Longman, London, p. 11

Simons D G 1975 Muscle pain syndromes – Part I. AmericanJournal of Physical Medicine 54: 289–311

Simons D G 1976 Muscle pain syndromes – Part II. AmericanJournal of Physical Medicine 55: 15–42

Smythe H 1986 Tender points: evolution of concepts of thefibrositis/fibromyalgia syndrome. The American Journalof Medicine 81 (suppl 3A): 2–6

Smythe H A, Moldofsky H 1977 Two contributions tounderstanding of the ‘fibrositis’ syndrome. Bulletin ofRheumatic Diseases 28: 928–931

Steindler A 1940 The interpretation of sciatic radiation andthe syndrome of low-back pain. Journal of Bone and JointSurgery 22: 28–34

Stockman R 1904 The causes, pathology and treatment ofchronic rheumatism. Edinburgh Medical Journal 15:107–116, 223–225

Strauss H 1898 Über die sogenannte ‘rheumatischemuskelschwiele’. Klinische Wochenshrift 35: 89–91,121–123

Sydenham Thomas 1676 Observationes medicae. The worksof Thomas Sydenham translated by R G Latham in 1848.Sydenham Society, London

Telling W H 1911 Nodular fibromyositis, an everydayaffliction, and its identity with so-called muscularrheumatism. Lancet 1: 154–158

Travell J, Rinzler S H 1952 The myofascial genesis of pain.Postgraduate Medicine 11: 425–434

Travell J, Simons D G 1983 Myofascial pain and dysfunction.The trigger point manual. Williams and Wilkins,Baltimore

Valleix F 1841 Traité des Neuralgies; ou, affectionsdouloureuses des nerfs. Ballière, Paris.

Valleix F 1848 Études sur le rhumatisme musculaire, et enparticulier sur son diagnostic et sur son traitement.Bulletin général de thérapeutique médicale etchirurgicale 35: 296–307

WHO 1993 Consensus Document on Fibromyalgia: theCopenhagen Declaration 1993. Journal ofMusculoskeletal Pain 1(3/4): 295–312

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INTRODUCTION

This brief and therefore somewhat superficialaccount of the neurophysiology of pain is simplyto provide a certain amount of insight into its complexities. Its purpose is to serve as a basis fordiscussing in subsequent chapters the variousphysiological mechanisms that are involved in thedevelopment of pain in the myofascial pain andfibromyalgia syndromes and the alleviation of thisby means of stimulating peripheral nerve endingswith dry needles.

As space does not permit the neurophysiologyof pain to be considered at length, anyone inter-ested to learn more about this fascinating subject isrecommended to read an extremely lucid accountof it in Melzack & Wall’s book The Challenge of Pain(1988) or an even more detailed presentation of itsvarious aspects by a number of authorities in theirTextbook of Pain (Wall & Melzack 1999).

Modern concepts concerning the transmission ofnoxious impulses from the periphery to the cortexand how the sensation of pain may be modulatedby various physiochemical mechanisms in the cen-tral nervous system have been profoundly influ-enced by the gate-control theory first put forwardby Melzack & Wall (1965). Although this theory, asmight be expected, has had to be revised over theyears in the light of further knowledge, it, neverthe-less, remains a remarkably useful hypothesis and asLiebskind & Paul (1977), when discussing reasonsfor the current interest in pain research, have said:

Probably the most important was the appearancein 1965 of the gate control theory of pain by

45

Chapter 6

Neurophysiology of pain

CHAPTER CONTENTS

Introduction 45The nature of pain 46Types of pain 46–47Nociceptive pain 47–55Advances in knowledge during the 1950s

and 1960s 56Gate-control theory 56

Advances in knowledge during the 1960s and 1970s 58Opiate receptors 58–59Opioid peptides 59–60Descending pain inhibitory systems 61–65

The distinction between nociceptive andneuropathic pain 65

The emotional aspects of pain 66–68

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doctors to seek relief is not the occurrence ofsome minor pain of which they are just awarewhen their pain threshold is reached (we havethis every day of our lives) but is when the limitof their individual pain tolerance is reached.

This, of course, is of considerable practical import-ance when attempting to assess pain and the effectof any particular form of treatment on it, for it isnot changes in pain threshold that have to be meas-ured but rather changes in pain tolerance.

Pain tolerance clearly depends on a person’semotional response to a noxious stimulus. It is veryinteresting with respect to this to note that the 17th-century Dutch philosopher Benedict Spinoza(1632–1677) referred to pain as ‘a localized form ofsorrow’.

It therefore follows that throughout a person’slife the intensity with which pain is felt dependson his or her psychological make-up, culturalbackground, parental influence and ethnic origin(Zborowski 1952, Bond 1979). The manner inwhich perception of, and reaction to, noxiousstimuli is influenced by past experiences has beendemonstrated in ingenious experiments carriedout on various animals, including dogs (Melzack &Scott 1957, Melzack 1969) and monkeys (Lichstein &Sackett 1971).

The reaction to pain at any specific time is alsodependent on an individual’s current mood, withanxiety or depression intensifying it. The experienceof pain also depends upon the prevailing circum-stances so that, for example, a severe wound sus-tained in the heat of battle may hardly be noticed,whereas a similar injury incurred in a less stressfulenvironment may be the cause of severe pain(Beecher 1959). Conversely, the intensity with whichpain is felt is diminished by distraction of attention.It is for this reason that some people find back-ground music helpful whilst undergoing somepainful experience such as at the dentist (Gardner& Licklider 1959). This is also why chronic painsufferers find that their pain is far less intrusive ifthe mind is occupied by carrying out an absorbingtask (Wynn Parry 1980).

TYPES OF PAIN

Pain is of three types. Very occasionaly it is solelydue to a disorder of the mind (psychogenic pain).

Melzack & Wall. This theory, like none before it,has proved enormously heuristic. It continues toinspire basic research and clinical applications.

It will, therefore, be necessary to consider thisparticular theory at some length but, in order fullyto understand its ingenuity and implications, it isfirst necessary to say something about the natureof pain, and the parts of the central nervous systemin which pain-modulating mechanisms are to befound.

THE NATURE OF PAIN

Pain is not a simple, straightforward sensory experi-ence, in the manner of, for example, seeing or hearing, since it has both emotional and physicalcomponents. The definition of pain put forward bythe International Association for the Study of Painis that it is ‘an unpleasant sensory and emotionalexperience associated with actual or potential tissuedamage, or described in terms of such damage’(Merskey 1979).

As Hannington-Kiff (1974) points out, pain hasthree main components: physical, emotional andrational. The physical component is determinedby the responsiveness of an individual’s nocicep-tive system to a given stimulus; the rational com-ponent is derived from an objective interpretationof pain in the cerebral cortex; the emotional com-ponent is determined by the responsiveness of anindividual’s limbic system to any particular nox-ious stimulus.

It, therefore, follows that for a given noxiousstimulus the intensity with which pain is felt variesfrom person to person, and with regard to this adistinction has to be made between an individual’spain threshold and pain tolerance. The pain thresh-old is the least stimulus intensity at which a sub-ject perceives pain and, contrary to popular belief,this is much the same in everyone (Thompson1984a). As Wyke (1979) has pointed out, it is an alltoo common misconception:

… that measuring pain thresholds tells one some-thing about the mechanisms that influence theintensity of a patient’s experience of pain. On thecontrary, of course, what one should assess in thisregard is not a patient’s pain threshold but hispain tolerance, because what brings patients to

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Not infrequently it arises as a result of damage to either the peripheral or central nervous system(neuropathic pain). Most commonly it developsbecause of the primary activation and sensitisationof nociceptors in either the skin, a muscle or a viscus(nociceptive pain).

As will be discussed in Chapter 7, the pain pre-sent in the myofascial pain and fibromyalgia syn-dromes is nociceptive. For that reason pain of thisparticular type will be discussed at some length.

NOCICEPTIVE PAIN

Our understanding of the psychological and phys-ical components of nociceptive pain has been greatlyadvanced by recent detailed studies showing thatthe behavioural and physiological response to it isdependent on a number of facilitatory and inhibitorymodulating mechanisms in various parts of thecentral nervous system. The structures that are ofparticular importance in this complex process aresensory receptors, their associated afferent nervefibres, the dorsal horns, ascending and descendingtracts in the neuraxis, the reticular formation in themidbrain and medulla, the thalamus, the limbicsystem and the cerebral cortex. Each of these will be considered in turn.

Sensory receptors in the skin

A-delta nociceptors These nociceptors are connected to the spinal cord’s dorsal horns viamedium diameter (1–5 �m) myelinated A-deltanerve fibres with a conduction velocity of 12–30 m/s(25–70 mph).

These A-delta nociceptors are activated by anynoxious mechanical stimulus such as that deliveredby a sharp pointed instrument or needle and forthis reason are also known as high-thresholdmechanonociceptors. Approximately 20–50% ofthem, in addition, respond to suddenly applied heatin the noxious range of from 45° upwards and,because of this, are known as mechanothermalnociceptors.

A-delta myelinated nociceptors are found mainlyin and just under the skin and, as will be discussedin Chapters 9 and 10, it is these receptors whichare stimulated when carrying out the acupunctureprocedure known as superficial dry needling.

The receptive field of a high-threshold mech-anonociceptor in the skin (Fig. 6.1) consists of anumber of sensitive spots about 1 mm in diametergrouped together in a cluster covering on averagea total area of 5 mm2 (Georgopoulos 1974).

C-polymodal nociceptors C-polymodal nocicep-tors, are connected to the spinal cord’s dorsal hornsvia small diameter (0.25–1.5 �m) unmyelinated Cafferent nerve fibres. The conduction velocity rateof these is only 0.5–2 m/s (1–4.5 mph). These recep-tors are termed polymodal because under experi-mental conditions it is possible to activate them byapplying either a mechanical, thermal or chemicalstimulus (Fig. 6.2). However, it is somewhat of amisnomer as, clinically, such activation is invariablyonly produced by chemicals released as a result oftissue damage.

The receptive field of C-polymodal nociceptorsis usually a single area rather than a cluster ofspots as in the case of A-delta nociceptors.

Low-threshold mechanoreceptors in the skin

Low threshold mechanoreceptors in the skin areconnected to the spinal cord’s dorsal horns via largediameter A-beta myelinated nerve fibres with adiameter of 5–15 �m and the relatively fast con-duction velocity of 30–70 m/s (70–155 mph).

They are stimulated physiologically when theskin is stretched or lightly touched and also whenits hairs are bent.

Neurophysiology of pain 47

Figure 6.1 The multipunctate receptive field of an A-deltanociceptor. Reproduced with permission from HowardField’s Pain. McGraw-Hill 1987.

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Sensory receptors in muscle

Lloyd (1943) divided muscle sensory afferents intothe following groups:

Groups IA, IB and II Group IA and Group IB,which have a diameter of 15–20 �m and trans-mission velocity of 70–120 m/s (155–270 mph),together with Group II, which have a diameter of3–6 �m and a transmission velocity of 15–30 m/s(35–70 mph), have a proprioceptive function andare attached to annulospiral muscle spindles, Golgitendon organs and flower spray muscle spindlesrespectively (Thompson 1994). Their role is to trans-mit to the brain information about changes in thelength of muscle fibres and the rate at which thistakes place.

Group III and Group IV sensory afferentsMany of a muscle’s Group III sensory afferents and all of its Group IV ones have free nerve endingsthat terminate in arterioles’ adventitia and it is

presumably because of this that they are somarkedly sensitive to chemical stimuli and particu-larly to those accompanying disturbances of themicrocirculation (Mense 2001, p. 31).

Group III small diameter (2–5 �m) myelinatedfibres with a conduction velocity of 12–30 m/s(25–70 mph) are divided (Mense 2001, p. 42) intothose that have contraction sensitive receptors(23%), those that have nociceptive receptors (33%)and those that have low-threshold mechanosensi-tive receptors (44%).

Group IV unmyelinated fibres with an evensmaller diameter (0.4–1.2 �m) and a conductionvelocity of 0.5–2 m/s (1–4.5 mph) are divided(Mense 2001, p. 42) into those that have low-thresh-old mechanosensitive receptors (19%), those thathave contraction sensitive receptors (19%) and the vast majority of them that have nociceptivereceptors (43%).

Muscle nociceptors

Group III nociceptors It has for long beenknown that pain may be produced by the low-intensity stimulus provided by squeezing a mus-cle between the fingers and thumb (Lewis 1942).And it was Paintal (1960) who, from experimentson cats, came to the conclusion that this pressure-evoked pain develops when those sensory afferentsin this group with nociceptive terminals (33%) arestimulated.

Group IV nociceptors It has been shown in ani-mal experiments that the 43% of sensory afferentsin this group that have terminal nociceptors arenot responsive to a low-intensity stimulus such asthat provided by weakly applied pressure orstretching within the physiological range, but areresponsive to high-intensity noxious ones such asthose that cause myofascial trigger points (TrPs) tobecome active (see Ch. 7).

First and second pain (Fig. 6.3)

Stimulation of A-delta nociceptors gives rise to animmediate, sharp, relatively brief pricking sensa-tion – the so-called first or fast pain.This sensationserves to provide a warning of impending tissuedamage and is accompanied by reflex withdrawal


Pressure

Heat

Chemical

Figure 6.2 Sensitivity range of the C-polymodalnociceptor. Its terminals are sensitive to direct heat ormechanical distortion, and to chemicals released fromdamaged cells. Reproduced with permission from HowardField’s Pain. McGraw-Hill 1987.

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movements designed to avoid or minimize suchdamage.

Stimulation of C-polymodal nociceptors in theskin or Group IV nociceptors in muscle leads tothe development of pain that, because its onset isdelayed beyond the first few seconds, is known as‘second’ or ‘slow’ pain. It is because pain of thistype tends to persist for some time that it almostinvariably requires treatment.

Activation of C (skin) and Group IV (muscle)unmyelinated sensory afferent nociceptors

The effect of subjecting skin or muscle to a high-intensity noxious stimulus is to activate C orGroup IV nociceptors respectively and to causethem to become pain-producing.

The mechanisms responsible for this activationare twofold, one being electrical and the otherchemical.

Firstly, the noxious stimulus by deforming anociceptive sensory afferent nerve ending opension channels present in its membrane with, as aconsequence, the development of an ion flux acrossthis membrane and a resultant depolarization of it. The difference in membrane potential betweenthe stimulated depolarized nerve ending and theafferent fibre then causes a current to develop thatdepolarizes the latter and by so doing elicits apropagated action potential in it.

Secondly, the noxious stimulus brings about the release of the neuropeptides Substance P andcalcitonin gene-related peptide stored in vesiclesin nociceptive sensory afferents’ nerve endings.


Intensity

Firstpain

Secondpain

Time

C

B

A

C

A-delta

Figure 6.3 A. First pain – produced by stimulation of A-delta afferent nerve fibres. Second pain – produced bystimulation of C afferent nerve fibres. B. First pain suppressed by the selective application of pressure to the A-deltafibres C. Second pain suppressed by selectively blocking, with low concentrations of local anaesthetic, the C afferentfibres. (Reproduced with permission from Howard Field’s Pain. McGraw-Hill 1987.)

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Both of these have a vasodilatory effect and causean increase in vascular permeability with, as aconsequence, the development of oedema and theliberation of algesic vasoneuroactive substances(Sicuteri 1967) from the blood. These includebradykinin from plasma proteins, serotinin (5-hydroxytryptamine) from platelets, potassiumions from plasma and other tissues, and histaminefrom mast cells.

Sensitisation of C (skin) and Group IV (muscle) unmyelinated sensory afferentnociceptors

Bradykinin not only activates nociceptors but alsoincreases the synthesis and release of prostaglan-dins, particularly prostaglandin E2, from damaged tissue cells (Jose et al 1981). This has a powerfulsensitising effect on nociceptors with a lowering oftheir pain threshold so as to make them responsivenot only to high-intensity noxious stimuli, but alsoto low-intensity ones. One of the consequences ofthis is the development of a zone of primaryhyperalgesia at the injury site.

The dorsal horn

Laminae It was the Swedish anatomist, BrorRexed (1952), who established that the cells of thespinal cord are arranged in layers or laminae.There are six laminae in the dorsal (Lamina I–VI);three in the ventral horn (Lamina VII–IX) and anadditional column of cells clustered around thecentral canal known as Lamina X (Fig. 6.4).

At the outer part of the dorsal horn there is a clearzone visible to the naked eye and it was because ofthis appearance that the Italian anatomist LuigiRolando (1773–1831) in 1824 named it the substan-tia gelatinosa. Some neurophysiologists (Wall 1990)state that the substantia gelatinosa includes bothLamina I and II, whilst others (Bowsher 1990, Fields1987, p. 44) call Lamina II the substantia gelatinosaand Lamina I the marginal zone.

The thin unmyelinated C nociceptive afferentsterminate mainly in Laminae I and II where theiraxon terminals secrete either Substance P orvasoactive intestinal polypeptide (VIP) accordingto whether they arise from somatic structures orvisceral ones respectively (Thompson 1988).

The medium-sized myelinated A-delta noci-ceptive afferents terminate chiefly in Laminae I, IIand V.

In contrast to this, most of the large diametermyelinated A-beta low-threshold mechano-receptive afferent fibres, on entering the spinal cord,pass directly up the dorsal column to end in themedulla oblongata’s gracile and cuneate nuclei.Axons from these nuclei then form the medial lemi-niscus and this, after decussating in the medulla, terminates principally in the ventrobasal thalamus.However, what is of particular importance, as far asthe pain modulating effect of A-beta afferent activityis concerned, is that the medial leminiscus is con-nected, via the anterior pretectal nucleus, to the peri-aqueductal grey area in the midbrain at the upperend of the opioid peptide mediated serotinergicdescending inhibitory system (see p. 61).

Therefore, as a result of these connections, A-betaafferent activity is enabled to block the C afferentinput to the spinal cord by promoting activity inthis descending system (Bowsher 1991). In addition,Todd & Mackenzie (1989) have shown that largediameter A-beta nerve fibres, on entering the spinalcord, give off branches which make contact withgamma-aminobutyric acid mediated interneurons(GABA-ergic interneurons) in Lamina II. These alsoexert an inhibitory effect on the C afferent input tothe cord.

It therefore follows that high-frequency, low-intensity transcutaneous nerve stimulation (TENS),which exerts its pain modulating effect by recruit-ing A-beta nerve fibres (Ch. 9), achieves this effectpartly by these fibres, when stimulated, evokingactivity in the opioid peptide-mediated descend-ing inhibitory system, and partly by them evokingactivity in dorsal horn GABA-ergic interneurons(Fig. 6.5).

Dorsal horn transmission cells The neurons in thedorsal horn responsible for transmitting sensoryafferent information to the brain are of three main types – low-threshold mechanoreceptor cells,nociceptive-specific cells, and wide dynamic rangecells.

Low-threshold mechanoreceptor cells, foundchiefly in Laminae III and IV, transmit to the brain information received via large diameter low-threshold A-beta afferents that have become


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Frontal cortex

Post-central gyrusof the parietal lobe(somatosensory cortex)

Link between NSTpathway and PAG

Periaqueductal grey area(PAG) of midbrain

Red nucleus

Laterally situatedNST pathway

Medially situatedPSRD pathway

Nucleus raphémagnus in medulla

D L Funiculus

DH

A-delta fibres

C-afferent fibres

VIIth nucleus

Vth nucleus

Limbic system

Thalamus

IIIIIIIVVVI VII VIII

IXIX

X

Figure 6.4 Diagramatic representation of the course taken by the two ascending ‘pain’ pathways – the neospinothalamic(NST) pathway carrying A-delta ‘pin prick’ information, and the paleo-spino-reticulo-diencephalic pathway carrying C‘tissue damage’ information. It also shows the descending inhibitory pathway – the dorsolateral funiculus (DLF) which linksthe periaqueductal grey area (PAG) and the nucleus raphé magnus (NRM) with the dorsal horn (DH).

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To thalamus

Pretectalnucleus

PAG

NSTpathway

DLFSG SG

G

ENK ENK

C

NRM

A-beta

A-delta

DCN

ML

Figure 6.5 Tissue damage nociceptive information reaches the substantia gelatinosa (SG) vis C afferent fibres. The onward transmission of this information is inhibited by enkephalinergic interneurons (ENK) which are activated viaA-delta ‘pin prick’ fibres as they enter the cord and via serotinergic inhibitory fibres that descend in the dorsolateralfuniculus (DLF) from the nucleus raphé magnus (NRM) in the medulla and periaqueductal grey area (PAG) in themidbrain (the descending inhibitory system). The descending inhibitory system is brought into action either viacollaterals which link the neospinothalamic ‘A-delta pin prick’ ascending pathway (NST) with the PAG: or via collateralswhich form a link between the PAG and the medial leminiscus (ML), which arises from dorsal column nuclei (DCN)connected to A-beta fibres in the dorsal column. The onward transmission of tissue damage nociceptive information inC afferent fibres is also inhibited by inhibitory GABA-ergic interneurons (G) which are activated by the A-beta fibresthat enter the substantia gelatinosa.

(Based on Dr David Bowsher’s diagram in the Journal of the British Medical Acupuncture Society (1991). Reproducedwith permission).

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activated by some innocuous stimulus such aslight touch to the skin.

Nociceptive-specific cells, principally present inLamina I but also to a lesser extent in Lamina IVand V (Christensen & Perl 1970), as their nameimplies, are only excited by nociceptive primaryafferents. Somewhat paradoxically, a study byMayer et al (1975) suggests that interpretation ofpain is related more closely to activity in widedynamic range cells than it is to that in nociceptive-specific ones.

Wide dynamic range cells, which are present inall laminae but are mainly concentrated in Lamina Vand to a lesser extent in Lamina I, transmit to highercentres information received via A-beta, A-deltaand C afferents. The message they pass on to thehigher centres therefore varies according to whetherthe peripherally applied stimulus is innocuous ornoxious. It thus follows that the sensation ultimatelyexperienced may be one of touch, or the brief local-ized pricking type of ‘first’ pain, or the persistentwide-spread aching type of ‘second’ pain.

The wide-dynamic range cells that receive smalldiameter afferents from the heart and abdominalorgans also receive low-threshold afferents fromthe skin (Cervero 1983). Melzack & Wall (1988, p. 173) suggest that this may be the reason whypain from a pathological lesion in some internalstructure may appear to be coming from the sur-face of the body and why in such circumstancesthe skin is liable to be tender.

It needs to be understood that none of thesetransmission cells possess physiological specificity,as they are capable of changing from one to anotherdepending on the excitability of the spinal cord.For example, animal experiments have shown that,under light barbiturate anaesthesia, nociceptive-specific cells become wide dynamic range ones(Collins & Ren 1987) and that under deeper anaes-thesia the latter become nociceptive specific(Dickhaus et al 1985).

Dorsal horn inhibitory interneurons In LaminaeI and II there are interneurones that containinhibitory neurotransmitters such as enkephalinand gamma-aminobutyric acid (Todd et al 1992).

Dorsal horn neuroplasticity From animal experi-ments it is clear that the effect of prolonged or

repetitious high-intensity stimulation of nocicep-tors is to bring about a progressive build-up ofexcitability in dorsal horn-situated nociceptivetransmission neurons (wind-up) and the eventualsensitisation of them (central sensitisation).

Central sensitisation develops when these neurons’ N-methyl-D-aspartate (NMDA) recep-tors become activated. This is brought about as aresult of the co-release of excitatory amino acids(glutamate and aspartate) and neuropeptides (SPand calcitonin gene-related peptide). The NMDAreceptor channel is normally blocked by a magne-sium ‘plug’. The effect of activating these trans-mission neurons is to remove this ‘plug’ and by sodoing allow an influx of calcium ions into them.This in itself gives rise to considerable cell hyperex-citability. It also leads to the expression of onco-genes such as c-fos which brings about long-termchanges in the responsiveness of these neurons; to the production of nitrous oxide which is nowbelieved to contribute to the maintenance of pain;and to the activation of a number of secondarymessengers including inositol triphosphate anddiacylglycerol that further increase the excitabilityof the cells (Coderre et al 1993).

The effects of this central sensitisation are toincrease the receptive fields of these dorsal hornnociceptive neurons; to bring about the develop-ment of large diameter A-beta sensory afferent-mediated hyperalgesia and allodynia; and to causethe nociceptive pain to persist (Cousins & Power1999; Doubell et al 1999).

As will be discussed in Chapter 7 there aregrounds for believing that central sensitisation notinfrequently takes place in the myofascial pain syn-drome and invariably does so in the fibromyalgiasyndrome.

Ascending pathwaysThe long-held belief that nociceptive informationis transmitted centripetally via a single contra-lateral spinothalamic tract had to be revised in the1950s when it was shown that the transmission isthrough a number of pathways each of which hasits own conduction velocity and termination in thebrain (Kerr et al 1955).

It is now recognized that these pathways havedeveloped over the course of time as part of an


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evolutionary process (Melzack & Wall 1988, p. 125)and that their relative importance varies from onespecies to another (Willis 1989).

Two major ascending systems have been identified, one phylogenetically much older thanthe other. The principal pathway in the newer ofthe two systems is the neospinothalamic pathwayand the main one in the earlier developed systemis the paleo-spino-reticulo-diencephalic pathway(Bowsher 1987).

The neospinothalamic pathway (Fig. 6.4)

The neospinothalamic pathway arises from thedorsal horn’s Laminae I and V, where the majorityof the small myelinated A-delta nociceptive fibresterminate. It ascends in the contralateral anterolat-eral tract to reach the ventrobasal nucleus in thelateral part of the thalamus, and from there it pro-jects to the somatosensory cortex in the postcentralgyrus. This topographically organized lateral path-way subserves the sensory-discriminative processresponsible for the localization and identificationof a noxious stimulus (Melzack & Casey 1968) andfor determining when such a stimulus reaches thepain threshold.

The paleo-spino-reticulo-diencephalic pathway (Fig. 6.4)

This pathway, which Melzack & Casey (1968) call the paramedian pathway, arises from the dor-sal horn’s Laminae VII and VIII and to a lesserextent from Lamina V. As this pathway carriesinformation ultimately interpreted as ‘second’ or‘slow’ pain that is conveyed to the dorsal horn byC afferent fibres, and as these terminate in neuronsin Laminae I and II, it follows that electricalimpulses from these neurons have to pass throughseveral internuncial relays before reachingLaminae V, VII and VIII. From the dorsal horn, itascends in the contralateral anterolateral tractalongside the neospinothalamic pathway until itreaches the base of the brain where it separatesfrom this by passing medially into the brainstem’sreticular tissue. From there, C afferent nociceptiveinformation is projected to the cerebral cortex via

the medially situated intralaminar nuclei of thethalamus.

Brainstem’s reticular formation

The reticular formation that ramifies throughoutthe medulla and midbrain is so-called because itsdense mass of neurons with overlapping and inter-twining dendrites give it a net-like appearance.

As Casey (1980) has pointed out, it is becauseneurons in the reticular formation have bifurcatingaxons that project downwards to the spinal cordand upwards to the thalamus and hypothalamusthat this structure is so extremely well adapted toplaying a major integrating role in pain experienceand behaviour.

Its links with the motor neurons of muscle spin-dles enable it to bring about alterations in muscletone. With respect to this, it is because people whoare psychologically tense have an overactive reticu-lar system that they tend to hold certain groups oftheir muscles persistently taut (Nathan 1982). Whenthis happens, pain is liable to develop in thesemuscles as a result of TrPs in them becoming acti-vated (see Ch. 7). As Mense (1990) has succinctlyput it, ‘skeletal muscle is a tool for expressingemotional state in higher mammals and, thus, psy-chogenic changes of muscle tone may become asource of pain’.

The reticular formation contains several nucleithat make important contributions to the experienceof pain and the behavioural activities associated withthis. One of these is the nucleus reticularis giganto-cellularis situated in the medulla. This nucleus,which receives a large input from the paramedianpathway and that has an upwards projection to theintralaminar part of the thalamus, contains neuronswhose discharge in response to a noxious stimulus,as Casey has shown in a series of experiments oncats, sets off aversive escape behaviour (Casey1971a, b; Casey et al 1974). In addition, serotonin-containing cells in this nucleus and the adjacentnucleus raphe magnus, together with neurons inthe periaqueductal grey area of the midbrain fromwhich they receive an excitatory input, form theupper part of the opioid peptide mediated descend-ing inhibitory system that is of such considerableimportance in the control of pain.


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Most of the fibres in the paramedian pathwayterminate at the reticular formation but some con-tinue upwards to the medially situated intralami-nar nuclei of the thalamus. There are also separateascending projections from the reticular formationthat reach both these thalamic nuclei and thehypothalamus. It is because of this link betweenthe reticular formation and the hypothalamus thatso-called second or slow C afferent tissue damagetype pain has autonomic concomitants.

From the intralaminar nuclei of the thalamusthere are projections to a number of structures clus-tered around the thalamus that collectively form thelimbic system, as well as projections to other parts ofthe brain including, in particular, the frontal lobe.

The limbic system

The limbic system consists of a group of structuresclustered around the thalamus. These include thehypothalamus; the hippocampus (Greek, sea horse);the amygdala (Latin, almond); and the cingulumbundle connecting the hippocampus with thefrontal cortex.

There is evidence that the limbic structures con-trol the motivational or behavioural responses topain together with the emotional response to it or what may be called its affective dimension. Withrespect to the latter, it is the extent to which thelimbic system becomes activated in response toany given noxious stimulus that determines howmuch any particular individual suffers from it – inother words, the degree to which it hurts that per-son. It is therefore activity in the limbic system thatgoverns a person’s pain tolerance.

The frontal cortex

As mentioned when discussing the nature of pain,this physico-emotional experience is considerablyinfluenced by cognitive activities such as memoriesof past experiences, mood and prevailing circum-stances. By virtue of the frontal cortex having a two-way communication system not only with allsensory cortical areas but also with the limbic andreticular structures, it controls both of these cogni-tive activities as well as the paramedian system’smotivational-affective ones (Melzack & Casey 1968).

Knowledge as to exactly where in the brain nox-ious information transmitted to it is processed,with the development of pain as a consequence,has been considerably advanced by recent studiesemploying positron emission tomography to meas-ure the regional blood flow to various parts of thebrain and functional magnetic resonance to meas-ure changes in blood oxygenation (Bushnell et al2002, Ingvar & Hsieh 1999).

From these studies, which have been carriedout both in humans and animals, it is apparentthat when noxious information is transmitted tothe brain a number of cortical and subcorticalregions are activated. These include the primaryand secondary somatosensory cortices (S1 & S2), theanterior cingualate cortex (ACC) and the insularcortex (IC ).

That so many regions are activated is a measureof the complexity of the processes involved in painperception, and a reflection of the fact that painhas three separate components: a sensory, discrim-inative one that provides information concerningthe type of sensation experienced (e.g. aching,burning or stabbing) and the part of the body fromwhich it is arising; an affective (emotional), motiv-ational (behavioural ) one; and an autonomic onethat is responsible for such responses to pain astachycardia, elevation of the blood pressure andsweating.

From studies carried out both on animals andhumans it is now evident that the S1 & S2 corticesare the principal regions involved in the process. It is also evident that ACC activity determinesbehavioural, emotional and autonomic responses,and that IC has a role in associating the immediateaffective response to a pain experience with memories of the suffering caused by a previoussimilar one.

In the past, extensive resections of the frontallobes were performed as a last resort for intract-able pain. Patients who underwent this, becausethe sensory component of pain subserved by thesomatosensory cortex was still present, remainedaware of the pain and often said it was as intenseas before, but they were no longer worried about it and no longer needed medication for it. Theeffect of a lobotomy, therefore, was to reduce themotivational-affective and aversive dimensions


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of the pain experience. As Freeman & Watts (1950)remarked, ‘Prefrontal lobotomy changes the atti-tude of the individual towards his pain, but doesnot alter the perception of pain.’

ADVANCES IN KNOWLEDGE DURING THE 1950S AND 1960S

There were several important advances concern-ing the neurophysiology of pain during the 1950sand 1960s. The Swedish anatomist, Bror Rexed(1952), established that the cells of the spinal cordare arranged in layers or laminae; Hagbarth &Kerr (1954) found evidence of a descending inhib-itory system; and Kerr et al (1955) established thatthere are a number of ascending pathways relatedto pain. In addition, Noordenbos (1959) furtheredthe theory first put forward by Head in 1920 that arapidly conducting afferent fibre system inhibitstransmission in a more slowly conducting one by establishing that the fast system is made up oflarge diameter myelinated fibres and the slow oneby small diameter unmyelinated ones. In referringto the interaction between these two systems, hepithily commented; ‘stated in the most simpleterms, this interaction could be described as fastblocks slow’.

This comment, as Wall (1990) has recentlyadmitted, profoundly influenced Melzack’s andhis thinking when eventually they came to formu-late their gate-control theory. Also influential wasthe fact that Wall (1960), by a series of ingeniousrecordings from single dorsal horn cells, was ableto confirm Noordenbos’s observations concerningthis interaction, and was able to show that it is strongly influenced by descending inhibitorysystems first identified by Melzack et al 1958.

THE GATE-CONTROL THEORY

It was thus in the light of knowledge acquired by a number of different workers during the 1950sthat Melzack & Wall in 1965 developed their nowfamous theory that in each dorsal horn of thespinal cord there is a ‘gate-like mechanism whichinhibits or facilitates the flow of afferent impulsesinto the spinal cord’. The theory, as originally pro-pounded, stated that the opening or closing of the

‘gate’ is dependent on the relative activity in thelarge diameter (A-beta) and small diameter fibres(A-delta and C), with activity in the large diameterfibres tending to close the ‘gate’, and activity in the small diameter fibres tending to open it. Also,an essential part of the theory ever since the time it was first put forward is that the position of the ‘gate’ is in addition influenced by the brain’sdescending inhibitory system.

Substantia gelatinosaFrom the start, Melzack & Wall envisaged the gate as being situated in the substantia gelatinosawhere, as they said, inhibitory interneurons are tobe found in Lamina II. They also premised that theinteraction between the large and small diameterfibres influences activity both in these interneuronsand in the dorsal horn transmission cells (T cells). It was thought and subsequently confirmed thatthe large-diameter myelinated afferents excite theinhibitory interneurons, and that the effect of this isto presynaptically reduce the input to the T cellsand thereby to inhibit pain. They further postulatedthat activity in small diameter unmyelinated fibres,by inhibiting activity in the inhibitory interneurons,facilitates the flow of noxious impulses to the T cellsand by so doing enhances pain.

By the time that Melzack & Wall introducedtheir theory, there was already good evidence tosupport their belief that it is the substantia gelati-nosa (i.e. Laminae I & II) that acts as the ‘gate’.Szentagothai (1964) and Wall (1964) had shownthat it receives axons directly and indirectly fromlarge and small diameter fibres, that it has connec-tions with cells in deeper laminae and, that its cellsconnect with one another and are connected tosimilar cells at distant sites – on the ipsilateral sideby means of Lissauer’s tract and on the oppositeside by means of fibres that cross the cord.

Although it remains reasonable to assume thatit is the substantia gelatinosa that acts as the spinalgating mechanism, Melzack & Wall (1982, p. 236)have found it necessary to emphasize that there is still no absolute proof of this. They also posedthe question rhetorically, ‘If the substantia gelati-nosa is a gate control, why is it so complex?’, andanswered this by saying that it would be wrong toconsider that this structure is only concerned with


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the modulation of nociceptive impulses, but ratherthat it has to monitor all forms of incoming infor-mation and that it is likely to have ‘to control andemphasize different aspects of the arriving mes-sages with the emphasis changing from momentto moment’.

There can be no doubt, therefore, that the sub-stantia gelatinosa has the properties of a complexcomputer and, the greater the detail in which itsstructure and function are studied, the more intri-cate the mechanisms contained in it are found to be. There is now experimental evidence to show thatthe cells that make up this structure, together withthose in the underlying laminae, are somatotopi-cally organized (Melzack & Wall 1982, p. 237) in thesame way as cells in the dorsal column-medial lem-niscus system (Millar & Basbaum 1975) and cells inmidbrain structures (Soper & Melzack 1982).

It is also now known that the afferent nocicep-tive input into the substantia gelatinosa is influ-enced by several descending inhibitory systemslinking cortical and brain-stem structures with thedorsal horn via the dorsolateral funiculus.

It is obvious from the number of peptides foundin the substantia gelatinosa in recent years, that itsfunction must be extremely complicated. It is nowknown that nerve terminals at this site contain atleast five peptides, these being vasoactive intes-tinal peptide, somatostatin, angiotensin, cholecys-tokinin and SP (Jessell 1982). Endogenous opioidsare to be found in the dorsal horn of the spinal cordin the same areas as small diameter primary painafferents containing SP neurons and opiate recep-tors (Clement-Jones 1983). Now that it is knownthat morphine inhibits the release of SP – a primaryafferent nociceptor transmitter – it has been pro-posed that, in addition to the opioid-mediateddescending inhibitory system, opioid-containinginterneurons presynaptically control the afferentnociceptive input (Jessell & Iversen 1977). Such ahypothesis would certainly provide a neurochemi-cal basis for the ‘gate’ theory of pain control.

There are thus strong arguments in support ofMelzack & Wall’s original idea that the substantiagelatinosa acts as a complex ‘gating’ mechanismthat modulates input signals to the spinal cord bymeans of decreasing their effect on other highlyspecialized transmission cells (T cells), the functionof which is to pass on these messages to various

centres in the brain. For a more detailed account ofthe evidence in support of the substantia gelati-nosa’s role as a controlling ‘gate’, reference shouldbe made to Wall’s (1980a, b; 1989) comprehensivereviews of the subject.

Revision of the gate-control theoryAdvances in knowledge since 1965 have inevitablyled to the theory being revised. For example,Melzack & Wall soon came to the conclusion thatthere are excitatory as well as inhibitory interneu-rons in the substantia gelatinosa and that inhib-ition not only occurs presynaptically, as originallythought, but also takes place postsynaptically.

Furthermore, when the gate-control theory wasfirst put forward, it was considered that the flowof centripetal impulses into the dorsal horn, andfrom it up to the brain, was influenced partly by descending inhibitory mechanisms and partlyby the relative activity in small diameter and large diameter afferent nerve fibres, and that it wasalways the net result of these various facilitatoryand inhibitory effects that controlled the activationof T cells. When Wall, however, re-examined thetheory in 1978, he pointed out that the situation wasnot as straightforward as might have appeared at first, and that large diameter fibre activity is, incertain circumstances, capable of firing T cells, sothat the inputs from large and small fibres may attimes summate with each other. He also admittedthat their original ideas concerning the inhibitoryeffects of large diameter fibres was much influ-enced by Noordenbos (1959) who, having shownthat in post-herpetic neuralgia there is a loss oflarge myelinated fibres, generalized from thisobservation by proposing that pain in general isdue to a loss of inhibition normally provided bylarge fibres. As Wall (1978) then goes on to say, ‘Wenow know that loss of large fibres is not necessar-ily followed by pain. In Friedreich’s ataxia there isjust such a preferential large-fibre defect withoutpain’ … (and) ‘the polyneuropathy of renal failurein adults is not associated with complaints of painalthough there is preferential destruction of largefibres.’ He then cites many other examples toshow that ‘any attempt to correlate the remainingfibre diameter spectrum with the symptomatol-ogy of neuropathies is no longer possible’.


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This notwithstanding, it would seem that whenthe central nervous system is intact and unaffectedby disease, the balance between the large andsmall diameter fibres in determining the output ofT cells remains an acceptable hypothesis. The the-ory has also been subjected to criticism by othersfor neglecting the known facts about stimulusspecificity of nerve fibres that have emerged sinceVon Frey first developed his theory about this inthe closing years of the last century (Nathan 1976).

For all these various reasons and others, includ-ing advances in knowledge concerning the relativefunctions of A-delta and C nerve fibres (to be dis-cussed later), Melzack & Wall have had to subjecttheir theory to certain modifications (Wall 1978,Melzack & Wall 1982, p. 260; 1988, pp. 165–193).Nevertheless, it remains remarkably useful andhas been considerably enriched by subsequent biochemical discoveries. Much, however, remains tobe explained. For example, the descending controlsystem has turned out to be not one system but a number of systems involving a complexity ofchemical substances yet to be unravelled. Andwhen enkephalin-containing terminals and opiatereceptor-bearing axons were discovered, it wasassumed that they must make contact but, surpris-ingly, this apparently is not so (Hunt et al 1980).

Despite all this, 20 years after Melzack & Wallfirst put forward their gate-control theory, Verrill(1990) reviewed its influence on current ideas con-cerning pain modulation and was led to concludethat:

… despite continuing controversy over details,the fundamental concept underlying the gatetheory has survived in a modified and strongerstate accommodating and harmonizing with ratherthan supplanting specificity and pattern theo-ries. It has stimulated multidisciplinary activity,opened minds and benefited patients.

The relevance of the gate-control system to the 1st and 2nd phases ofnociceptive painAs stated earlier, when some deep-seated struc-ture such as muscle is damaged, the resultantinflammatory reaction leads to the release ofchemical substances which sensitize A-delta and C

afferents. The outcome of this is that two types ofpain develop one after the other. Initially there is asharp, well-defined sensation – the first pain –brought on as a result of activity in the A-deltaafferent nerve fibres. The pain during this firstphase is only of brief duration and is followed bya less well-defined and more prolonged secondpain, which develops as a result of activity in Cafferent nerve fibres. Melzack & Wall (1988, pp.165–193) have now pointed out that the gate-control pain modulating mechanisms only operateduring the 1st phase and that the prolongation ofthe pain during the 2nd phase is due to C afferentfibres, where they terminate intraspinally, liberat-ing a variety of peptides including substance P,cholecystokinin, neurokinins, vasoactive intestinalpeptide and others, giving rise to immediate neur-onal excitation in the dorsal horn followed by aslow-onset, prolonged facilitation.

It should be noted with respect to this that thepeptide content of unmyelinated sensory afferentsis not the same in every type of tissue. The peptidemake-up of Group IV fibres in muscle, for example,is very different from that of C fibres in the skin.That is why Group IV afferents, unlike C afferents,produce prolonged facilitation.

ADVANCES IN KNOWLEDGE DURING THE1970S AND 1980S

Opiate receptorsDuring the 1970s, biochemists and pharmacolo-gists were becoming increasingly convinced thatthe reason why morphine was such a powerfulanalgesic was because there were highly special-ized chemical receptors in the central nervous system to which this substance could readilyattach itself. In 1973, Solomon Snyder of the Johns Hopkins School of Medicine, Baltimore, and Candice Pert of the U.S. National Institute of Mental Health discovered, during the course ofbasic research on drug addiction, that there areclusters of cells in certain parts of the brain,including the brain stem nuclei, the thalamus andhypothalamus, which serve as opiate receptors(Pert & Snyder 1973). A number of cells in the dor-sal horn were then also found to have the samefunction (Atweh & Kuhar 1977). The finding of


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opiate receptors in the midbrain perhaps was notso surprising as it had already been shown that an injection of only a small amount of morphineinto the area has a considerable analgesic effect.However, of particular interest was the discoverythat there are also cells with the same function inthe substantia gelatinosa of the dorsal horn and thata local injection of a small amount of morphineinto this structure (laminae I and II) has a markedlyinhibitory effect on the response of lamina V trans-mission cells to afferent nociceptive stimuli (Dugganet al 1976); this lent considerable support to theidea that the substantia gelatinosa has an impor-tant pain-modulating function. It is now knownthat there are at least three distinct types of opioidreceptors termed mu, kappa and delta (Paterson et al 1983).

The distribution of opiate receptors in the cen-tral nervous system is of considerable interest.There are numerous ones in the paramedian sys-tem’s intralaminar (medial) thalamic nuclei, reticu-lar formation and limbic structures. In contrast,however, there are only a few in the neospinothal-amic system’s ventrobasal thalamus and post-central gyrus. This explains why a microinjection of morphine into structures in the paramedian system has a powerful analgesic effect but notwhen injected into the ventrobasal thalamus. It alsoexplains why morphine suppresses so-called sec-ond or ‘slow’ tissue damage type of pain but notthe so-called first or ‘rapid’ type of pain produced,for example, by a pinprick.

In the dorsal horn there are large numbers of opiate receptors situated postsynaptically onneuronal membranes. There are also some situatedpresynaptically on the intraspinal part of C affer-ent nerve fibres, but at present the biological significance of these remains unknown (Fields &Basbaum 1989).

It is because of a particularly high concentrationof opiate receptors in the substantia gelatinosa,that a micro-injection of morphine into this struc-ture has a marked pain-suppressing effect. It isalso why lumbar intrathecal injections of opiatesproduce profound analgesia in animals (Yaksh &Rudy 1976) and man (Wang et al 1979).

There is a high concentration of opiate receptorsin the corpus striatum, where their function isunknown. They are also extremely numerous in

the brain stem’s respiratory centre, thus explain-ing why morphine is such a powerful respiratorydepressant.

During the 1990s it was also established thatopiate receptors are present on the peripheral terminals of sensory afferents (Stein et al 1990,Coggeshall et al 1997).

Opioid peptidesOnce these opiate receptors had been located, itwas argued that nature was hardly likely to haveprovided animals, including man, with them forthe sole purpose of having somewhere for opiumand its derivatives to latch on to should they happen to be introduced into the body. It was farmore likely that they are there because morphine-like substances (opioid substances) are producedendogenously.

A search for physiologically occurring morphine-like substances was therefore instituted. Many scientists took part in this, including Snyder andhis colleagues at Baltimore; Terenius & Wahlstromin Uppsala; and Hughes et al in Aberdeen.

The big breakthrough occurred in 1975 whenHughes et al in the Unit for Research on AddictiveDrugs at Aberdeen University in collaborationwith a research team at Reckitt & Colman isolateda substance from the brains of pigs that appearedto act like morphine and that latched onto opiatereceptors in the brain. They named it enkephalin(‘in the head’). It was a major discovery, andLewin (1976) showed considerable prescience bycommenting in the New Scientist:

With the structure of enkephalin now at hand …we are now poised for an exciting breakthroughin the complete understanding of opiate anal-gesia, addiction and tolerance. Probably the mostintriguing aspect of all this is the inescapableimplication of the existence of an unexpectedchemical transmitter system in the brain, a systemwhich may have something to do with dampen-ing pain, but almost certainly has more generaleffects also.

Enkephalin having been isolated, Linda Fothergilat Aberdeen and Barry Morgan at Reckitt & Colmanattempted to analyze its structure and soon


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established that it was a peptide, but came upagainst certain technical difficulties in establishingthe exact sequence of its amino acids. Therefore theyenlisted the help of a spectroscopist, Howard Morrisat the Imperial College, London. Morris was ableto show that in fact there are two enkephalinpolypeptides – leucine (leu) and methionine (met)enkephalin – but for a time the chemical sourcefrom which these substances are made in the bodyremained a mystery.

By a strange chance, about the time that Morris was considering this, he attended a lectureat Imperial College given by Derek Smythe of the National Institute for Medical Research on beta-lipotrophin, a 91 amino acid peptide that hadbeen isolated from the pituitary glands of sheep 10years previously (Li et al 1965). Smythe showed aseries of slides illustrating its chemical structureand as Morris sat there looking at these, he sud-denly saw to his amazement the amino acidsequence of met enkephalin hidden away in the61–65 position of the betalipotrophin structure. It subsequently became apparent, however, thatmet and leu enkephalin are derived by enzymecleavage not from this substance but from the pre-cursor proenkephalin A. Since the discovery of theenkephalins, opioid bioactivity has been found invarious beta-lipotrophin fragments with the mostpotent of these being one in the 61–91 positionknown as beta-endorphin (Fig. 6.6).

It is now known that beta-endorphin, togetherwith beta-lipotrophin and ACTH (corticotrophin)are all derived by enzyme cleavage from a largeprecursor pro-opiomelancortin, but that of thesethree polypeptides only beta-endorphin has knownanalgesic activity, and also that ACTH acts as aphysiological antagonist of this (Smock & Fields1980).

Recently, two other opioid peptides with N-terminals identical to that of leuenkephalin havebeen isolated. These are dynorphin, a 17 amino

acid peptide (Goldstein et al 1979), and the decapep-tide alpha-neoendorphin (Weber et al 1981), both ofwhich are cleaved from yet another precursor pro-enkephalin B (prodynorphin).

These various substances are sometimesreferred to collectively as the endorphins (endoge-nous morphine-like substances) but, as may beseen, there are three distinct families of these peptides – the enkephalins, the dynorphins andthe endorphins – and therefore it is better simplyto call them opioid peptides (Thompson 1984b).

Distribution of endogenous opioid peptides

Studies using radioimmunoassays and immuno-histochemical techniques have demonstrated highlevels of enkaphalins and dynorphins in the limbicstructures, the periaqueductal grey, the nucleusraphe magnus and the substantia gelatinosa of thedorsal horn. From these sites, opioid peptides spillover into the cerebrospinal fluid. In addition, opi-oid peptides are released from the anterior pitu-itary and adrenal medulla into the plasma.

By means of radioimmunoassays and gel filtra-tion techniques, it has been possible to demonstratethe presence of beta-endorphin and metenkephalinin human plasma (Clement-Jones 1983). Beta-endor-phin is found there in association with beta-lipotrophin and ACTH with all three showing thesame pattern of circadian secretion from the anteriorpituitary (Shanks et al 1981). Plasma metenkephalinlevels, however, show no relationship to those ofthe other peptides just mentioned during circadianstudies and corticosteroid suppression tests. It is not derived from the pituitary, as levels aredetectable in subjects with pan-hypopituitarism(Clement-Jones & Besser 1983) but released from theadrenal gland into the circulation (Clement-Jones et al 1980). It is also derived from the gut, sympa-thetic ganglia and peripheral autonomic neurons(Smith et al 1981).


1 91 Beta-lipotrophin

Beta-endorphin9161

61 65 Methionine enkaphalin

Figure 6.6 Schematic representation of the 91 amino acid peptide beta-lipotrophin and otherpeptides structurally related to it.

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Endogenous opioid peptides have also beenfound to be present in macrophages, monocytesand lymphocytes present in inflamed tissues(Przewlocki et al 1992, Stein et al 1990). Schafer et al (1996) have shown that the liberation of theseopioids is induced by corticotrophin-releasinghormone.

When opioid peptides were first discovered, itwas assumed that any structure containing themmust have a pain-modulating function. It is clear,however, that this is not so because there is, forexample, a very high concentration of them in thebasal ganglia where their function has yet to beexplained (Bowsher 1987). They are also present invagal nuclei in the medulla where they presum-ably contribute to various reflexes such as thoseassociated with the control of coughing.

Descending pain inhibitory systemsDuring the 1970s, exciting discoveries were madeconcerning the biochemistry of the descendinginhibitory system, although it was observationsmade in the 1950s, firstly by Hagbarth & Kerr (1954)and then by Melzack et al (1958) – with their unex-pected discovery in experiments on cats that dam-age to the central tegmental tract in the midbrainmarkedly enhances pain in these animals – that setthe stage for these discoveries.

It was because of their observations that DavidReynolds, a young psychologist at the Universityof Windsor, Ontario, decided to investigate whether,by electrically stimulating this central tegmental-lateral periaqueductal grey area, it might be pos-sible to increase the effects of any inhibitory systemthat might be present there to such an extent as tobring about pain suppression. In 1969 he was ableto report that such stimulation did, in fact, producesuch a profound degree of analgesia that it waspossible to carry out surgical operations on con-scious rats without any other form of anaesthesia,and later he reported being able to control pain bythis method during operations on higher speciesof animals.

Unfortunately, although Reynolds’ observa-tions were of the utmost importance, regrettablythey were viewed with considerable scepticism andlargely ignored. It was not until Mayer, Liebeskindand their colleagues (Mayer et al 1971), with no

knowledge of Reynolds’ contributions to the sub-ject, independently carried out similar experimentson rats, that any notice was taken of the remark-able phenomenon, now generally referred to asstimulation-produced analgesia.

Stimulation-produced analgesia

It has been found possible to produce analgesia byelectrically stimulating one or other of severalsites, but the most consistently effective manner ofdoing this is to place electrodes either on the peri-aqueductal grey area in the midbrain or on thenucleus raphé magnus in the medulla (Liebskind &Paul 1977).

Although stimulation-produced analgesia wasfirst demonstrated in experimental animals, it was quickly shown to have considerable therapeuticvalue in relieving humans of persistent severe pain.In fact, man has been shown to obtain more lastinganalgesia using this method than do many types ofanimals (Adams 1976, Hosobuchi et al 1977).

Electrical stimulation of the brain stem for the purpose of suppressing pain had not been inuse for long before it was discovered that its anal-gesic effect could be abolished by the morphine-antagonist naloxone (Akil et al 1976) and that theinjection of a small amount of morphine directlyinto the periaqueductal grey area produces anal-gesia (Herz et al 1970, Mayer & Price 1976, Mayer& Watkins 1981). It was therefore concluded thatthe morphine must act by activating neurons in thedescending inhibitory system situated in the brainstem, and it raised the possibility that stimulation-produced analgesia might also occur as a result of the release of endogenous opioids (Basbaum et al 1976). Melzack & Melinkoff’s observation(1974), that the analgesic effect of electrically stim-ulating the brain stem is enhanced by carrying thisout for several minutes before a painful stimulus isadministered, provided support for this idea.

Opioid peptide-mediated descending inhibitory system

It is now realized that there are several descendinginhibitory systems, but the one about which mostis known and the one that is mainly brought intoaction when acupuncture is employed for the reliefof nociceptive pain is opioid peptide-mediated.


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Periaqueductal grey This opioid peptide-mediateddescending inhibitory system (OPMDIS) has its ori-gin in the midbrain’s periaqueductal grey (PAG).

The PAG is divided into two components: adorsolateral one that projects to the pons and ventrolateral medulla (both of these are involvedin autonomic control) and a ventrolateral one that,together with the adjacent nucleus cuneiformis(NC), forms the upper part of the OPMDIS withdescending projections from these to structures inthe rostral ventromedial medulla (Cameron et al1995).

Rostral ventromedial medulla The rostral ventro-medial medulla (RVM) includes the midline situated nucleus raphe-magnus (NRM) and theadjacent reticular formation in the vicinity of thenucleus reticularis gigantocellularis.

Confirmation that the RVM is an importantrelay station in the OPMDIS comes from the dis-covery that electrical stimulation of or a microin-jection of an opoid peptide into it has an inhibitoryeffect on dorsal horn neuronal responses to nox-ious stimuli (Fields et al 1991).

Dorsolateral funiculus From the RVM axonsproject down the dorsolateral funiculus (DLF) andterminate on nociceptive neurons in the dorsalhorn. Proof of this was obtained when it wasshown that neither opiate – induced nor stimula-tion – produced analgesia occurs when this tract iscut (Basbaum et al 1977).

Spinal terminals The spinal terminals of thesedescending axons are mainly to be found inLaminae I, II, & V (Basbaum et al 1978) the lami-nae to which nociceptive sensory afferents mainlyproject (Willis & Coggeshall 1991).

Serotonin (5-hydroxy tryptamine) There are reasons to believe that serotonin is the main trans-mitting agent in the OPMDIS (Basbaum & Fields1978). These include the discovery that electricalstimulation of the RVM causes this substance to bereleased into the cerebrospinal fluid and the anal-gesia produced by this type of stimulus is reducedby its antagonists (Yaksh & Wilson 1979, Barbaro et al 1985). Also the analgesia produced by a micro-injection of morphine into the PAG is partiallyblocked by intrathecally administered methy-sergide a non-selective serotonin antagonist (Yaksh

1979). Finally, para-chlorophenylalanine, a serotonininhibitor, suppresses analgesia brought about eitherby electrical stimulation of the PAG or the NRM, andby the microinjection of morphine into either ofthese structures (Anderson & Proudfit 1981).

With respect to all this it should be noted that Thompson (1984a) believes that the pain-suppressing effect of certain trycyclic antidepres-sants is probably because of their ability to enhancetransmission down this descending pathway byblocking the re-uptake of serotonin.

Rostral projections to the periaqueductal greyThere are downward projections to the PAG fromthe medial prefrontal and insular cortex (Bandler &Shipley 1994). Also, from the hypothalamus; theelectrical stimulation of or opioid microinjectioninto which has an analgesic effect (Manning et al1994). There are also projections from various otherstructures, including the amygdala, the almondshaped nucleus at the front of the temporal lobe(Gray & Magnuson 1992), the nucleus cuneiformis,the postmedullary reticular formation, and thebluish-grey coloured locus coeruleus in the floor ofthe fourth ventricle (Herbert & Saper 1992).

Caudal projections to the periaqueductal greyNociceptive neurons in the dorsal horn’s Laminae I & V project caudally to the PAG and the adjacentnucleus cuneiformis via the neospinothalamictract, as this not only conveys A-delta nociceptive-generated information to the somato-sensory pari-etal cortex, but also has a collateral at the midbrainlevel that connects with these two structures (Fig. 6.5).

It is because of this collateral that needle stimu-lation of A-delta nerve fibres is able to bring theOPMDIS into action when acupuncture is beingused to alleviate nociceptive pain.

The OPMDIS is also brought into action, asstated earlier in this chapter, when A-beta nervestimulation, such as, for example, by means of high-frequency low intensity TENS, sets up activity inthe dorsal column-medial leminiscus ascendingpathway as this also has a projection to the PAG.

Anti-opioid peptide effect of cholecystokininoctapeptide Cholecystokinin octapeptide is anendogenous opioid antagonist found to be presentin the spinal cord (Yaksh et al 1982). It is also


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liable to be released into the RVM where it has anantagonistic effect on the antinociceptive action of endogenous opioids at that site (Crawley &Corwin 1994).

Opioid peptide-mediated pain modulatingmechanisms in the dorsal horn

The enkephalinergic inhibitory interneurons situ-ated on the border of Laminae I and II of the dorsalhorn not only block C afferent transmission as aresult of A-delta afferent activity causing thedescending inhibitory system to come into action inthe manner just described. These interneurons alsodo this because A-delta nerve fibres make directintraspinal contact with them in the dorsal horn(Fig. 6.5). In addition, enkephalinergic interneuronspresent on the terminals of C afferent fibres exert a presynaptic inhibitory effect (Bowsher 1990). Ittherefore follows that the acupuncture technique ofstimulating A-delta nerve fibres with dry needlesrelieves C-afferent-transmitted tissue damage-typepain as a result of this kind of stimulus evokingactivity in opioid peptide mediated pain modul-ating mechanisms situated at both supraspinal andspinal levels.

These two endogenous pain control mechanismscollectively constitute what Fields & Basbaum (1989)refer to as the opioid-mediated-analgesia system(OMAS).

The physiological activation of the opioid-mediated-analgesia system When opiatereceptors and their opioid peptides were found to be present in the central nervous system it wasassumed, because the administration of naturallyoccurring opium and its derivatives has long beenknown to have an analgesic effect, that the body’sown opioid peptides must be capable of modul-ating pain. Support for this idea came from find-ing that a microinjection of morphine either intocertain midline nuclei in the brain stem or into thesubstantia gelatinosa produces analgesia (Herz et al 1970), and from the fact that the adminis-tration of high doses of beta-endorphin into thecerebrospinal fluid (Oyama et al 1980) and theintravenous injection of an enkephalin analogue(Calimlim et al 1982) has an analgesic effect.

Although it is now accepted that opioid peptidesexert their analgesic effect both at supraspinal and

spinal levels, the question that has to be addressed is:under what circumstances is this OMAS activated?

It was thought that, because naloxone is an opiatereceptor antagonist with a particular affinity for � receptors, that observations on the effects of thissubstance on pain produced by various means mightthrow some light on the matter. Unfortunately, the results of experiments designed to study theeffects of naloxone on pain in man have proved to be bewilderingly conflicting. As Woolf & Wall(1983) point out, ‘each positive result is matchedby negative ones’, and they go on to say:

… the hodge-podge of conflicting results cannotbe explained by the use of inadequate doses sincemany of the negative studies used higher dosesthan the positive ones. It is obvious that there mustbe an uncontrolled naloxone-reversible variableunrelated to pain in these studies, which may wellbe the degree of the subjects’ stress.

Now this would seem to be the nub of the mat-ter – that both noxious inputs and stress activatethe OMAS. Whilst there is no doubt that a noxiousinput brought about by stimulating A-delta affer-ent nerve fibres, with, for example, acupunctureneedles, may activate the system, so also may thisbe achieved either by environmental or surgicalstress (Gracely et al 1983).

Many experiments have been conducted byLewis et al (1980, 1981, 1982) on stress-producedanalgesia in rats. The rats were stressed by havingelectric currents applied to their feet. Lewis and hiscolleagues found that what determines whether ornot the analgesia produced by this type of shock isnaloxone reversible, and therefore opioid peptidemediated or not, depends on its duration. Thus the analgesia produced by foot shock applied for30 minutes is naloxone reversible, whereas thatproduced by foot shock applied for 3 minutes is not.

It is important to note that it was only whenstress, such as that produced in these experimentson rats with an electric shock, is applied for a rela-tively long period that the OMAS is activated,because Levine et al (1979) have similarly shown,with respect to noxious stimuli, that this analgesiaproducing system also only operates when such astimulus is of long duration. They demonstratedthis by showing that naloxone has little or no effect


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on relatively brief, experimentally produced painbut markedly increases the intensity of any pro-tracted pain such as that which may be experi-enced following a dental operation.

In summary, therefore, it has now been estab-lished that the OMAS is physiologically activatedeither by a prolonged, intense, noxious stimulus orsome form of prolonged stress. A briefly appliednoxious or stressful stimulus is also capable of pro-ducing analgesia. However, the question that hasbeen asked is whether they do so by activatingsome less well-understood, non-opioid-mediatedsystem, because as will be discussed in Chapter 10,the possibility that different analgesia-producingsystems are activated according to whether the noxious stimulus is strong or weak is of considerablerelevance when it comes to considering whether ornot the pain suppressing mechanisms involved witheither prolonged or brief stimulation with acupunc-ture needles are different.

Finally, it has to be said that the exact manner inwhich endogenous opioid peptides achieve theiranalgesic effect is not known. It is particularly con-fusing that electrical stimulation, which presumablyhas an excitatory action, and an opiate microinjec-tion, which presumably has an inhibitory action,both produce analgesia when applied to certainmidline brain stem nuclei. Fields & Basbaum (1989)suggest that this is because ‘the opioid peptides may act by inhibiting inhibitory interneurons, thusdisinhibiting the output neurons in these analgesia-producing regions’.

Non-opioid peptide-mediated descendingsystems

For many years now the morphine antagonistnaloxone has been used to investigate brain stemstimulation-analgesia, the action of opiates intro-duced into the central nervous system and the roleof endogenous opioid peptides in suppressing pain.

As long ago as 1965, Lasagna showed thatnaloxone seemed to increase pain when adminis-tered to experimental subjects already experien-cing some level of clinical pain. A more recentdouble-blind clinical study of postoperative den-tal pain (Levine et al 1978) has demonstrated thatcompared with a placebo, naloxone considerablyincreased the intensity of pain.

However, it was not long before contradictoryreports started to appear, with Lindblom & Tegner(1979) even questioning whether the endogenousopioids are active in suppressing chronic pain as theadministration of naloxone in their patients did notmake the pain worse. Also, Dennis et al (1980) foundthat the adminstration of naloxone does not impairthe analgesia produced by midbrain stimulation inrats suffering pain produced by injecting formalinsubcutaneously.

Furthermore, as will be discussed again inChapter 10, despite the fact that there have beenmany reports of acupuncture-induced analgesiabeing suppressed by naloxone, Chapman et al(1980) was unable to confirm this in a trialdesigned to study the effects of acupuncture onexperimentally induced dental pain.

It is now accepted that one of the reasons forthese conflicting reports must be that there are sev-eral descending control systems and that, whereasone of these is opioid peptide mediated, others mustbe mediated by various other transmitters. Most ofthese have yet to be discovered and their transmit-ters identified. However, it is now known that onesuch system has its origin in the dorsolateral ponswhere noradrenalin-containing cells project into thespinal cord (Melzack & Wall 1988, p. 141).

Noradrenergic descending inhibitory systemNoradrenergic axons, which mainly arise in thelocus coeruleus in the pons, descend down thespinal cord to bring about direct inhibition of dorsal-horn-situated nociceptive neurons.

This system, like the OPMDIS, has projectionsto it from the prefrontal cortex and arcuate nucleusof the hypothalamus.

In addition, stimulation of A-delta nerves suchas happens when the skin is penetrated by anacupuncture needle also brings this system intoaction because the neospinothalamic tract up whichA-delta nociceptive information is conveyed has acollateral projection to the locus coeruleus (Craig1992).

It therefore follows that another reason for thecontradictory evidence concerning these variousdescending inhibitory pain-modulating mechan-isms is the likelihood that in some of the experi-ments more than one of these systems is active atany given time (Watkins & Mayer 1982).


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Diffuse noxious inhibitory controls Lebars et al(1979) identified a powerful pain suppressing system that they have called diffuse noxiousinhibitory controls (DNIC). The upper part of thissystem is the subnucleus reticularis in the caudalmedulla (Villanueva et al 1988, 1990). From there,projections descend down the dorsolateral funicu-lus to dorsal horns where they have an opioidergiceffect on wide dynamic range transmission neurons(Bernard et al 1990).

The importance of the DNIC system withrespect to acupuncture is that Bing et al (1991)have shown that it is brought into action whenneedle stimulation of A-delta nerves is carried outanywhere on the body surface.

THE DISTINCTION BETWEEN NOCICEPTIVE AND NEUROPATHIC PAIN

The tissue-damage type of nociceptive paindescribed earlier in this chapter occurring as aresult of the activation and sensitisation of eitherC-polymodal nociceptors in skin or Group IVnociceptors in muscle has to be distinguished fromthe neuropathic type of pain that develops as aresult of malfunction of either the peripheral orcentral nervous system.

One reason for this so far as acupuncture is con-cerned is that neuropathic pain is very much lessresponsive than nociceptive pain is to this form oftherapy that acts by evoking activity in endogen-ous opioid-peptide-mediated pain modulatingmechanisms. This is hardly surprising consideringthat neuropathic pain is extremely resistant to theeffects of opioids (Portenoy et al 1990).

Therefore, before considering the use of acupunc-ture (or for that matter any other form of therapy)for the alleviation of persistent pain, it is essentialto establish whether it is of a nociceptive or neuro-pathic type.

With certain types of pain, such as, for example,post-herpetic neuralgia, trigeminal neuralgia andcentral pain from spinal cord or brain stem dam-age, there is usually no difficulty in recognizing itto be of a neuropathic type. However, when paindevelops during the course of some neurologicaldisorder such as a stroke, multiple sclerosis, or sub-acute combined degeneration, whilst it may be neuropathic, it should not automatically be assumed

to be so, as, not infrequently, myofascial TrP noci-ceptive pain develops in such disorders as theresult of the overloading of weakened muscles.Similarly, with post-herpetic neuralgia, becausethis neuropathic type of pain is difficult to allevi-ate it may cause a patient to tense muscles in thevicinity of the affected area and, as a consequence,acupuncture-responsive nociceptive TrP pain maydevelop as a secondary event.

Cancer is another commonly occurring disorderwhere pain may be either nociceptive or neuro-pathic and it is necessary to take this into consider-ation when deciding how best to alleviate it(Banning et al 1991), including whether or not toattempt to do this with acupuncture (Filshie 1990).

Furthermore, it has to be remembered thatmyofascial TrP nociceptive pain and neuropathicpain may be present concomitantly. This may hap-pen when an active TrP causes the muscle contain-ing it to become shortened with, as a consequence,the compression of underlying nerve roots (see Ch. 7). And, conversely, it may happen when cervi-cal or lumbar nerve root compression, for reasonsto be discussed in Chapter 7, causes TrP activity todevelop.

In order to differentiate between nociceptiveand neuropathic pain it is essential to pay closeattention to the patient’s description of the painand to carry out a carefully conducted clinicalexamination.

Nociceptive pain of myofascial origin takes theform of a widespread dull aching sensation withtenderness of the tissues in the affected area andsystematic examination revealing the presence ofwell-demarcated exquisitely tender TrPs some dis-tance from it.

In contrast to this, neuropathic pain occurringas a result of peripheral nerve injury or dysfunc-tion is commonly described as being of a burningnature or taking the form of shooting electricalsensations that, though not necessarily painful, areextremely distressing.

In addition, there is characteristically a latentinterval between the time that the neural damageoccurs and the onset of the pain. The intensity of the pain usually increases gradually to reach its maximum some weeks or months after onset.During this time, the skin becomes markedlyhypersensitive so that it only requires a slight


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breeze or the rubbing of clothes to bring on anepisode of pain (allodynia).

With neuropathic pain occurring as a result ofnerve injury or dysfunction, there is inevitablysome activation of nociceptors but the reason whythis type of pain differs from that which is entirelynociceptive must be that the structural damage, aspointed out by Fields (1987, p. 216), causes ‘dis-ruption of the sensory apparatus so that a normalpattern of neural activity is no longer transmittedto the perceptual centers’. Melzack & Wall (1988,p. 118), with reference to this, state:

… the presence of peripheral nerve damage issignalled rapidly by nerve impulses and slowlyby chemical transport. The long-term end resultis that central cells whose input has been cut inthe periphery increase their excitability andexpand their receptive fields … The duty of sens-ory cells is to receive information. When cut offfrom the source of their information, the cellsreact by increasing their excitability to such anextent that they begin to fire both spontaneouslyand to distant inappropriate inputs.

From experiments with the C nerve inactivatorcapsaicin, it has been shown that it is due to dam-age to C fibres that the prolonged central effectsdevelop (Melzack & Wall 1988, p. 181). It is thiscentral cell hyperexcitability which is responsiblefor various sensory abnormalities detectable onclinical examination.

When the skin over an area of the body affectedby neuropathic pain and over a non-painful area(preferably the contralateral mirror image region)are in turn gently brushed with strands of cottonwool the sensation produced over the affectedarea is abnormally intense (hyperaesthesia). It mayalso be unpleasant (dysaesthesia) or even painful(allodynia). The noxious sensation produced bysticking a pin into the skin overlying an areaaffected by this type of pain is also far more intensethan when such a stimulus is applied to skin in anon-painful area (hyperalgesia).

In addition, with neuropathic pain the phenom-ena of summation, spatial spread, and after dis-charge are often present. When the skin over anarea affected by neuropathic pain is repeatedlypricked with a pin for 30 seconds or more the

perceived intensity grows with successive stimuli(summation); this unpleasant sensation may alsospread beyond the area stimulated (spatial spread);also, it may persist after the stimulation has beendiscontinued (after discharge).

THE EMOTIONAL ASPECTS OF PAIN

Finally, it is necessary to examine the emotionalaspects of pain and to discuss what influence thesemay have on the assessment and treatment ofchronic pain. Pain is a complex physico-emotionalexperience with its emotional component largelydetermining how much suffering it causes. It is,therefore, not surprising that in describing pain,no matter whether it is nociceptive, neuropathic orentirely of emotional origin, patients are liable toinclude not only adjectives like aching, tingling orburning to describe its sensory qualities, but alsoadjectives like depressing, horrible or excruciatingto convey the suffering caused by it.

Melzack & Torgerson (1971), in recognizing thatthere are three main categories of pain experience –sensory, affective and evaluative – drew up theMcGill Pain Questionnaire and this, together with a subsequently introduced shortened version(Melzack 1987) has been shown to be of consider-able value in the assessment of pain. It is, however,because all types of pain experience have an emo-tional component that it must never be assumedthat pain is due to some primary psychologicaldisturbance simply because a patient uses a predominance of affective terms to describe it.

Pain may very occasionally be a hallucinatorysensation experienced by schizophrenics. It mayalso be a manifestation of conversion hysteria orhypochondriasis. It therefore has to be admittedthat there is such an entity as psychogenic pain(Feinmann 1990) but there are good grounds forbelieving that this is relatively rare and that affect-ive disorders such as anxiety or depression aremostly the result of chronic pain rather than thecause of it.

The relationship of emotional factors to chronicpain can be assessed by giving patients with it spe-cially designed standardized questionnaires suchas the Minnesota Multiphasic Personality Inventory(MMPI). Sternbach et al (1973) used this inventory


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to compare the relative significance of psychologi-cal symptoms occurring in patients with acute (i.e. less than 6 months’ duration) and chronic low-back pain. They found that although those withthe shorter history of pain had elevated scores on the scales for depression, anxiety, hysteria andhypochondriasis, the scores were significantlyhigher in those with chronic pain. The MMPI wasalso used by Sternbach & Timmermans (1975) intheir study of 113 patients with low-back pain of atleast 6 months’ duration. An assessment wasmade before and after either surgery followed byrehabilitation or rehabilitation only. From thisassessment it was found that there was a signifi-cant decrease in the hysteria, depression, anxietyand hypochondriasis scales following successfulalleviation of the pain.

Observations such as these confirm that chronicpain is usually the cause rather than the result ofneurotic symptoms and Melzack & Wall (1988, p. 32) in discussing this conclude:

It is evident from studies such as these that it isunreasonable to ascribe chronic pain to neuroticsymptoms. The patients with the thick hospitalcharts are all too often prey to the physicians’innuendos that they are neurotic and that theirneuroses are the cause of the pain. Whilst psy-chological processes contribute to pain, they areonly part of the activity in a complex nervoussystem. All too often, the diagnosis of neurosis asthe cause of pain hides our ignorance of manyaspects of pain mechanisms.

The error of failing to recognize pain as beingorganic in origin and considering it to be entirelypsychological most commonly occurs in my experi-ence when myofascial TrP activity causes pain topersist long after all clinical evidence of tissuedamage has disappeared (Ch. 7). This error, ofcourse, is particularly likely to be made when thepain has led to the development of appreciableanxiety or depression or both. The reason why thismistake is so frequently made is clearly because ofa widespread failure amongst health professionalsto search for myofascial TrPs when attempting tofind a cause for persistent pain.

It is as a result of this that many injustices arecommitted concerning the cause of protractedpain in accident compensation cases. Accidents

undoubtedly give rise to much psychological dis-tress (Muse 1985, 1986) but this does not mean thatpost-accident pain that does not respond readily tosome of the more conventional methods of treat-ing organic pain is necessarily psychological inorigin and in some way associated with an uncon-scious or even at times a conscious desire for compensation.

Such an assumption is all too prevalent and inthe past has led experienced physicians such asHenry Miller (1961, 1966) to believe that once compensation is awarded, persistent post-accidentpain invariably starts to improve. That this is notso has been demonstrated by Mendleson (1982,1984) who, from a study of accident compensationcases in Australia, concludes that ‘patients are notcured by the verdict’, and that, in general, the painremains as intense after the financial settlement asbefore. This is confirmed by Melzack et al (1985)who, in commenting both on Mendelson’s find-ings and their own psychological studies of acci-dent compensation cases, states:

… the phrase ‘compensation neurosis’ is anunwarranted, biased diagnosis. Not only are thedisability and pain not cured by the verdict butcompensation patients do not exaggerate theirpain or show evidence of neurosis or other psy-chopathological symptoms greater than thoseseen in pain patients without compensation.

From serving on medical appeal tribunals thatdeal with people seeking compensation for post-accident disablement, it has become evident to methat of those who seek financial assistance becauseof persistent pain only relatively few are malinger-ers. This observation is in keeping with that ofLeavitt & Sweet (1986) in their study of the frequency of malingering amongst patients withlow-back pain.

What, however, has become apparent to me isthat a disturbingly large number of these claimantsare allowed to suffer from the myofascial pain syn-drome for unnecessarily long periods of time sim-ply because the dictum laid down by Livingstonas long ago as 1943 is so frequently ignored. Hesaid that in every case of persistent pain followingtrauma it is essential to search for TrPs. It wasbecause Crue & Pinskey (1984) did not do this that


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they failed to find a nociceptive peripheral input ina group of patients with chronic back pain; intro-duced the totally inept diagnostic term ‘chronicintractable benign pain’; and made the unwar-ranted assumption that such pain is a central phenomenon – a polite way of saying ‘it is all inthe mind!’ As Rosonoff et al (1989) have nowshown, in 96–100% of patients with chronic low-back or neck pain of the type studied by Crue &Pinskey, the pain emanates from myofascial TrPs.

Finally, it is necessary to reiterate that whilstanxiety is rarely the cause of pain, persistent pain

is commonly associated with the development ofanxiety. When this happens, the anxiety causesmuscles to be held in a state of tension and withmusculoskeletal pain this results in an increase inTrP activity with a consequent exacerbation of thepain (Craig 1989). In all such cases it is not suffi-cient simply to deactivate the TrPs but it is alsonecessary to reduce the anxiety. My personal pref-erence is to employ hypnotherapy (Orne & Dinges1989, Hilgard & Hilgard 1994) and to teach thepatient how to practise autohypnosis on a regulardaily basis.


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INTRODUCTION

In this chapter there will firstly be an account of cur-rent knowledge concerning what is widely knownas the myofascial pain syndrome, or what will becalled here the myofascial trigger point (MTrP) painsyndrome, in order to draw attention to the all-important source of the pain and the one to whichtreatment with acupuncture has to be directed.

This will be followed by a review of what ispresently known about the fibromyalgia syndrome(FS) because, although due to the complexity of thisdisorder its treatment perforce has to include theemployment of a wide variety of pharmacologicalagents and physical forms of therapy, acupunctureis becoming increasingly often included amongstthese.

MYOFASCIAL TrP PAIN SYNDROME

Nociceptor activity at MTrP sites is one of the com-monest causes for musculoskeletal pain developing(Travell 1976). And yet despite the appearance ofnumerous wide ranging reviews of the MTrP painsyndrome in recent years, including those byBaldry (2001), Gerwin (1994), Hong (1999), Hong &Simons (1998), Mense (1990, 1993 a, b; 1997, 2001),Mense et al (2001), Rachlin (1994), Simons (1996,1999), Simons et al (1999) and Travell & Simons(1992), the importance of searching for MTrPs wheninvestigating the cause of pain of uncertain origin isstill not sufficiently well recognized.

In an attempt to redress this unfortunate state of affairs, the incidence, pathophysiology, clinicalcharacteristics and criteria for the diagnosis of the

73

Chapter 7

Myofascial trigger point pain and fibromyalgia syndromes

CHAPTER CONTENTS

Introduction 73Myofascial TrP pain syndrome 73Fibromyalgia syndrome 90

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nerve endings that have terminal motor endplateswith juxtapositional contraction knots. In add-ition, the bundle contains nociceptive and proprio-ceptive sensory afferents; also, blood vessels withclosely related sympathetic fibres (Fig. 7.1).

Physiological contraction of a muscle fibre

When, as a result of alpha-motor neuronal activityin the spinal cord’s anterior horn, a nerve actionpotential enters the central part of a muscle fibre,acetylcholine becomes liberated from the motorendplate’s synaptic clefts and causes the musclefibre to contract.

Development of contraction knots at MTrP sites

When a MTrP develops pain-producing activity,the release of an appreciable amount of calcitoningene-related peptide from its activated and sensi-tized nociceptor sensory afferents causes an exces-sive amount of acetycholine to be liberated from

MTrP pain syndrome will be discussed at somelength.

IncidenceThere have been no large epidemiological studiesbut as McCain (1994) states, ‘anecdotal evidencefrom expert examiners suggest that MTrP pain syn-drome is a very common condition, particularly inindustry, where it is a frequent cause of disabilityafter trauma’. Confirmation that the incidence ofthis syndrome is high also comes from Fricton et al’s(1985) finding that 54.6% of a large group of patientswith chronic head and neck pain had pain emanat-ing from MTrPs; from Skootsky et al’s (1989) findingthat 85% of patients presenting with low-back painto a general internal medicine practice had MTrPsas the source of their pain; and from Schiffman et al(1990), who in an epidemiological study of orofacialpain in young adult females, found that in 50% ofthem the pain emanated from MTrPs.

MTrP pain mainly affects adults but children mayalso develop it (Aftimos 1989, Bates & Grunwaldt1958, Fine 1987). Unlike the fibromyalgia syndrome,in which over four-fifths of patients are females(Yunus 1989) the incidence of the MTrP pain syn-drome is about the same in both sexes.

Pathophysiology of myofascial TrPs

Myofascial TrP sites

The principal TrPs in a muscle are located at itscentre (central TrPs) in the motor endplate zone.This zone is where the motor nerve on entering amuscle divides into a number of branches with eachof these, as Salpeter (1987) has shown, having a ter-minal claw-like motor endplate embedded in thesurface of a muscle fibre (Fig. 7.1). When a centrallyplaced MTrP becomes active the muscle fibre con-taining it becomes so markedly contracted as toform a taut band and then because of the tension inthis, an enthesopathy may develop at the fibre’s lat-eral attachments with, as a consequence, the produc-tion of TrP activity at these sites (attachment TrPs).

Structures present at a MTrP site

Each MTrP contains a neurovascular bundle. Thiscontains a motor axon with branching motor

MN

NB

MEP

CK

SAs BVsNMF

Figure 7.1 Diagramatic representation of part of amyofascial trigger point showing two motor endplates(MEPs) and juxtapositional contraction knots (CKs); also aneurovascular bundle (NB) containing motor nerves(MNs), nociceptive and proprioceptive sensory afferents(SAs) and blood vessels (BVs) with closely associatedsympathetic fibres. Note: in normal muscle fibre (NMF)the sarcomeres are of equal length. In a muscle fibrecontaining a contraction knot there is a shortening of thesarcomeres at that site and compensatory lengthening ofthem on either side.

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dysfunctional motor endplates so that the musclefibres into which these are embedded then becomeso markedly contracted as to form contractionknots. These were first identified by Simons &Stolov (1976) when during the course of palpatingmuscles in dogs they identified points of tendernesswith characteristics similar to those of humanMTrPs. On examining longitudinal sections ofbiopsy material taken from these sites under themicroscope they found that the muscle fibres con-tained fusiform swellings (contraction knots). Theyalso observed that each of them was located in closeproximity to a motor endplate and was approxi-mately about the same length as it. They concludedthat a knot of this type is a segment of muscle fibre which has become abnormally thickened as aresult of its sarcomeres having become consider-ably shortened; and that the reason why the sar-comeres on either side of it are considerably thinneris because of compensatory stretching (Fig. 7.1).

Electrical activity at myofascial TrP sitesKnowledge concerning motor endplate activity at MTrP sites has recently been considerablyadvanced by electromyographic (EMG) studies. Thefirst to examine a MTrP’s electrical activity wereWeeks & Travell (1957), who recorded a series ofhigh-frequency spike-shaped discharges with anamplitude of approximately 1000 �V and a dur-ation of 1–3 m/s from MTrP sites in the trapeziusmuscle. The next to turn their attention to this wereHubbard & Berkoff (1993) who, from working witha monopolar EMG needle, recorded similar high-amplitude spike activity of about 100–700 �V anda continuous low amplitude potential of about50 �V at active TrP sites in the trapezius muscle.They decided that:

… the activity is not localised enough to be gen-erated in an endplate, nor does it have theexpected location or waveform morphology forend plate activity. We theorize that TrP EMGactivity is generated from sympathetically stimu-lated intrafusal muscle fibre contractions…

A theory that led them to conclude that:

… a MTrP is located in the muscle spindle as theintrafusal fibres of this are sympatheticallyinnervated …

It has to be said, however, that EMG studies car-ried out both in the middle of the 20th century andagain more recently have not provided support for this. Jones et al (1955), using an iron depositiontechnique to confirm the position of their needle,recorded an electrical activity of 50–700 �V whenthey inserted it into muscle at a site which histo-logically was shown to have iron deposited arounda number of small nerve endings. And, althoughthis wave pattern was similar to the one Hubbard &Berkoff believed arose in a muscle spindle, theywere unable to identify such a structure within the vicinity of their recording needle. Furthermore,their observations that denervation abolished theelectrical activity, that the insertion of the needleinto the site gave rise to acute pain and also led to the development of brief muscle twitches (seelocal twitch response p. 86) all strongly suggest, asGerwin (1994) has pointed out, that the plexus ofmotor nerves into which their needle was insertedwas at a MTrP site.

More recent evidence that a MTrP is not locatedat a muscle spindle but rather in the vicinity ofbranches of a muscle’s motor nerve and their ter-minal motor endplates comes from studies carriedout by Simons et al (1995a,b,c,d) who, in the carry-ing out of these, employed a fivefold higher ampli-fication and a tenfold increase in sweep speed fortheir recordings than had been previously used(Simons et al 1999).

With this technique (Fig. 7.2), they recorded fromactive MTrP sites intermittent high-amplitudebiphasic spike potentials (100–600 �V) similar tothose recorded firstly by Weeks & Travell and thenby Hubbard & Berkoff. They also drew specialattention to having in addition to this recordedspontaneous electrical activity (SEA) made up ofconstantly present continuous low-amplitude noise-like action potentials (10–50 �v).

It is now clear from studies carried out by Heuser & Miledi (1971) and others that this SEAfound at a MTrP site corresponds to an abnormalpattern of motor endplate electrical activity broughtabout by an excessive release of acetylcholine(Hong 1999).

Support for the belief that MTrPs are not locatedin muscle spindles but in motor endplate zonesalso comes from the finding made by Cheshire et al (1994) that it is possible to abolish the pain

Myofascial trigger point pain and fibromyalgia syndromes 75

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emanating from a MTrP by injecting the botu-linum A toxin into it as the effect of this substanceis to block the release of acetylcholine from motornerve terminals.

A MTrP’s GroupIV nociceptorsFor reasons stated in Chapter 6, there are groundsfor believing that the pain that develops whenMTrPs become active does so as a result of the acti-vation and sensitisation of Group IV nociceptors.

Activation of a MTrP’s Group IV nociceptors

As discussed at some length in Chapter 6, this isbrought about in two ways. Firstly, by a high-intensity noxious stimulus transiently deformingGroup IV sensory afferent nerve endings and by sodoing causing electrical changes to take place thatculminate in the development of propagated actionpotentials in them. Secondly, by this type of stimu-lus releasing from vesicles in these nerve endingsthe neuropeptides Substance P (SP) and calcitoningene-related peptide that, by having a vasodilatoryeffect and giving rise to an increase in vascularpermeability, cause oedema to develop and algesicvasoneuroactive substances such as bradykinin,serotonin, potassium ions and histamine to be lib-erated (Sicuteri 1967).

With respect to this, however, it is of interest to note that the nociceptive sensory afferents in

muscle contain much less SP and calcitonin gene-related peptide than their counterparts in the skin(McMahon et al 1989).

It has been suggested that the teleological reason for this may be because these neuropep-tides cause the tissues to become oedematous andif this was allowed to become excessive in skeletal muscle, encased as it is in unyielding fascia, itwould be liable to become ischaemic or evennecrotic (McMahon et al 1984).

Sensitisation of a MTrP’s Group IV nociceptors

As also discussed in Chapter 6, bradykinin notonly activates nociceptors but also sensitizes themwith, as a consequence, a lowering of their thresh-old so as to make them responsive not only to high-intensity noxious stimuli, but also to low-intensitymildly noxious or innocuous ones (Mense 1993b).In addition, it has the effect of releasing prosta-glandins of the E type (particularly E2) from dam-aged tissue cells (Jose et al 1981). And these in turnhave a powerful nociceptor sensitizing effect.

It is this sensitisation of its nociceptors thatmakes a MTrP so exquisitely tender that when firmpressure is applied to the tissues overlying it thepatient involuntarily carries out a reflex flexionwithdrawal movement – the ‘jump’ sign (Kraft et al1968) and may, on occasions, utter an expletive – the‘shout ‘ sign. It is this latter vocal reaction that ledthe 5th century Chinese physician Sun Ssu-Mo to


Figure 7.2 Spontaneous electrical activity (SEA) and spike characteristic of an active locus in a human trigger point. Both records are of essentially the same activity; the difference is in the recording speed. A, slow speed which presentsa one-second record that shows the general pattern of activity, but little detail. B, recording at 10 times faster speed (0.1 s record) that shows the noise-like spontaneous activity of low amplitude and two superimposed, intermittent,sharp, initially negative spikes of high amplitude. Amplification is less for the slow record. Reproduced from Simons1996, with permission.

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call these points of maximal tenderness in muscle ahshih (oh yes it hurts) points (Lu & Needham 1980).

Factors responsible for development ofMTrP nociceptor activity

Trauma

The usual reason for MTrP nociceptor activitydeveloping is the subjection of muscle to the high-intensity stimulation provided by trauma.This may be brought about either by a directinjury to a muscle or by the sudden or repeatedoverloading of it. Alternatively, it may developwhen a muscle is subjected to repeated episodes ofmicrotrauma, such as occurs with a repetitivestrain injury (see Ch. 15).

Anxiety

Not uncommonly a patient who, because of anx-iety, holds a group of muscles in a persistently con-tracted state develops MTrP activity in them. Onesuggested reason for this happening is because of sympathetic nerve overactivity (McNulty et al1994). Another possibility is that it is brought aboutas a result of psychologically determined stimula-tion of brain-stem structures. This is because neu-rons in the brain stem’s reticular tissue have axonsthat project upwards to the thalamus and hypo-thalamus, and axons that project downwards to thespinal cord’s alpha motor neurons. These, in turn,have connections with MTrP’s motor endplates.

Radiculopathic compression of motor nerves

Chu (1995, 1997), during the course of carrying out electromyographic studies in patients withpersistent back pain, has observed that when thisoccurs as a result of spinal nerve root entrapment,such as from spondylosis or disc prolapse in thecervical or lumbar region, it may be followed bypain arising as a result of the secondary develop-ment of TrP activity in the paraspinal muscles.With reference to this Simons et al (1999) state that‘there is much clinical evidence that compressionof motor nerves can activate and perpetuate theprimary TrP dysfunction at the motor endplate’.

Muscle wasting

TrP activity may develop in muscles that havebecome weakened and overloaded such as a resultof malignant disease or various neurological dis-orders. Examples of the latter include poliomyelitis,motor neurone disease and strokes.

With respect to strokes, TrP nociceptive pain maydevelop during the recovery stage when weakenedmuscles become overloaded during attempts torestore movements to them. It may also arise in con-junction with glenohumeral joint capsulitis pain incases where following a stroke the joint has notbeen kept adequately mobilized.

This TrP-evoked nociceptive pain of a dullaching character, because it is liable to radiate downa limb affected by a stroke has to be distinguishedfrom post-stroke neuropathic pain that arises as aresult of damage to the central nervous system(central pain). This, however, is not usually difficultas the latter often takes the form of a severe burn-ing, similar to that experienced when a hand isplunged into ice cold water. Alternatively, it may beeither a lacerating, shooting, squeezing or throb-bing type of sensation.

Muscle ischaemia

TrP activity may arise in muscles that have becomeischaemic because of arterial obstruction sufficientto cause the development of intermittent claudica-tion (see Ch. 18). It may also develop in musclesthat have become ischaemic as a result of neuro-logical disease – induced spasticity (Mense 1993b).

Visceral pain referral

Pain arising as a result of visceral disease is fre-quently referred to both skin and muscles. Whenthis happens TrPs in muscles situated in this zoneof pain referral are liable to become active with theproduction of superimposed MTrP pain.

There are grounds for believing that the under-lying reasons for this happening (Gerwin 2002,Giamberardino et al 2002) are because the dorsalhorn neurons activated by a sensory afferent inputfrom visceral nociceptors also have a similar inputfrom muscle nociceptors. And because the centralsensitisation brought about as a result of the sens-ory afferent barrage sustained by these convergent


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viscero-somatic dorsal horn neurons results in anexpansion in the number and size of their receptivefields (see Ch. 6).

An example of when this may happen is TrPactivity developing in anterior chest muscles fol-lowing the referral to them of coronary heart dis-ease pain. Another is TrP activity developing inabdominal muscles following the referral of painto them from a peptic ulcer.

Other causes

TrPs may also become active when the musclescontaining them are exposed to adverse environ-mental conditions such as damp, draughts, exces-sive cold or extreme heat (Melzack & Wall 1988).

Primary, secondary and satellite active MTrPsAn active MTrP is one whose nociceptors havebecome sufficiently activated and sensitized forpain to be referred from it to a site some distanceaway (zone of pain referral). Active MTrPs are ofthree types – primary, secondary and satellite.

Primary MTrPs

These are TrPs whose nociceptor activity in a muscle or a group of muscles is primarily responsi-ble for the development of the MTrP pain syndrome.

Secondary MTrPs

These are TrPs that develop activity in the initiallyaffected muscle or group of muscles’ synergists orantagonists. They develop activity in the synergistswhen these become overloaded as a result of com-pensating for the weakened primarily affectedmuscles and in the antagonists when these becomeoverloaded as a result of combating the tension inand shortening of the primarily affected ones.

Satellite MTrPs

These are TrPs that become active when the musclein which they are present is situated in a primarilyaffected muscle’s zone of TrP pain referral. Painfrom these satellite TrPs is then referred to an even

yet more distant site. For example, it is not uncom-mon for a TrP in the lower part of the posteriorchest wall to refer pain to the buttock and for painfrom satellite TrPs in the gluteal muscles to then bereferred down the leg.

Latent MTrPs

A latent MTrP is one whose nociceptors havebecome activated and sensitised but not enough to cause pain to develop. Nevertheless, the nocicep-tor sensitisation makes it sufficiently tender for a ‘jump’ and ‘shout’ reaction (see p. 85) to be elicitedwhen firm pressure is applied to the overlying tis-sues. It, therefore, follows that latent TrPs are liableto be found when examining the muscles of pain-free people. Sola & Kuitert (1955), during the courseof examining 200 fit young people in the AmericanAir Force (100 males, age range 17–27 years; and 100females, age range 18–35 years) found latent TrPs tobe present in 45 of the males and 54 of the females.

The natural history of MTrP painMTrP pain may disappear spontaneously once theinflammatory reaction responsible for releasingnociceptor activating and sensitizing substanceshas resolved.

Not infrequently, however, the pain persistslong after tissue healing has taken place. This isliable to cause much diagnostic confusion as all toooften it is erroneously concluded that this prolonga-tion of the symptom for months or even years inthe absence of physical signs of tissue damage can-not possibly be organic and that the person com-plaining of it must be neurotic. This may lead to theperson concerned being unnecessarily referred forpsychiatric assessment.

Alternatively, it may mistakenly be assumedthat the pain is being consciously or unconsciouslyallowed to persist in an attempt by the person con-cerned to gain financially from it. The case outlinedbelow typifies this.

A man (27 years of age), whilst at work, fell from aladder on to his back. This caused considerablebruising and pain in the lower lumbar and sacralregions. Radiographs of the spine showed no evidenceof a fracture and all signs of soft-tissue damage fairly


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quickly disappeared. The pain, however, persisted andwhen 6 months later it continued to be disablingdespite intensive physiotherapy an orthopaedicsurgeon expressed the opinion in his report that thismight be due to the patient subconsciouslyexaggerating his symptoms in the hope of claimingindustrial compensation. Nothing, however, could havebeen further from the truth for the patient, frustratedby his poor response to physiotherapy, asked hisgeneral practitioner if he thought acupuncture mightbe helpful and as a consequence was referred to mefor assessment.

On examination, several TrPs were found to bepresent in muscles on both sides of the lower back.The pain from these was alleviated after they had been deactivated with dry needles on four occasions at weekly intervals. He was then only too glad to getback to work with no thought of trying to claimcompensation.

Mechanisms responsible for MTrP pain’s persistenceAs it is not certain why MTrP pain tends to persistlong after all evidence of soft-tissue damage hasdisappeared it is only possible to hypothesize aboutthis (Mense 1990).

The four mechanisms that have to be consid-ered are (1) the development of dorsal horn neuronal plasticity; (2) the development of self-perpetuating ischaemic changes at MTrP sites; (3) the development of self-perpetuating activityin motor efferents; and (4) the development ofsuch activity in sympathetic efferents. Each ofthese will be considered in turn.

Spinal dorsal horn neuroplasticity

As stated in Chapter 6 the sensory afferent barrageset up when nociceptors become activated andsensitized eventually causes dorsal horn transmis-sion neurons to develop the neuroplastic changesknown as central sensitisation. It, therefore, fol-lows that when MTrP nociceptors have been sub-jected to prolonged high-intensity stimulation thiscentral sensitisation must inevitably develop andone of its effects is to cause the pain that emanatesfrom them to persist (Mense 1993b).

Development of self-perpetuating ischaemicchanges at MTrP sites

When the MTrP nociceptor-sensitizing substancesbradykinin and prostaglandins are released intothe tissues as a result of trauma-induced inflam-mation, they give rise to the development of bothvasodilatation and increased vascular permeabil-ity. The effect of this is to cause oedema to developwith compression of veins and resultant tissueischaemia. As a consequence of this a vicious circleis liable to be created because the ischaemia thenleads to the release of still more MTrP nociceptor-sensitizing chemical substances.

Self-perpetuating circuits between a MTrP and the spinal cord motor efferent activity (Fig. 7.3, lower drawing)

Fields (1987) has postulated that the sensory affer-ent input to the spinal cord from activated and sensitized MTrP nociceptors projects not only todorsal horn nociceptive neurons but also to ven-tral horn-situated motor neurons with, as a result,the setting up of motor efferent activity. And it was thought by him that this in turn may cause the muscle containing the TrP to go into sufficientspasm to make it ischaemic with, as a consequence,the release of still more MTrP nociceptor activat-ing substances and the development of a self-perpetuating circuit.

It requires, however, a very considerable amountof spasm to render a muscle ischaemic and themore likely explanation is that it is the effect of this motor efferent activity on a MTrP’s dysfunc-tional motor endplates that leads to the perpetu-ation of its nociceptor activity.

Sympathetic efferent activity (Fig. 7.3, top drawing)

Livingston (1943) was the first to put forward the hypothesis that a self-perpetuating circuit ofthis type may also be set up by the development of efferent activity in the sympathetic nervous system. He did this in an attempt to explain the persistence of pain in his patients with the sym-pathetic disorder currently called the complexregional pain syndrome-type 1 (RSD). With someof them the disorder was of a primary type and


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S

H

SG

IML

Spasm

S

Figure 7.3 Livingston’s viciouscircle. Top: A stimulus delivered at Sactivates a primary afferentnociceptor that, in turn, activatesthe sympathetic preganglionicneuron in the intermediolateralcolumn (IML). The preganglionicneuron activates the noradrenergicpostganglionic neuron in thesympathetic ganglion (SG), whichsensitizes, and can activate, primaryafferent nociceptors (H) which, feedback to the spinal cord, maintainingthe pain. Bottom: Nociceptive inputmay also set in motion anothernociceptive input by activatingmotoneurons that cause musclespasm. Prolonged muscle spasmactivates muscle nociceptors whichfeed back to the spinal cord tosustain the spasm.

In both situations, the originalnoxious stimulus sets in motion aspreading and potentially self-sustaining process. In some cases theprecipitating noxious input may betrivial and short lasting. In such cases,blocking the spasm or interruption ofthe reflex loops may provide long-lasting relief. Reproduced withpermission from Howard Fields’ Pain,McGraw Hill 1987.

or sympathetic involvement to account for thelong-term persistence of MTrP activity. The follow-ing case is a good example of this.

A 65-year-old woman was referred to me with a painin the lateral chest wall that had been present for 31 years! On examination there was no evidence ofsympathetic involvement and no muscle spasm. Therewere, however, three well-defined TrPs in the serratusanterior muscle and despite the exceptionally longhistory it only required the deactivation of these bymeans of dry needling on three occasions for the painto disappear. She stated that the pain had developedas a result of trauma to the chest wall incurred when31 years previously she fell off her bicycle. Shecomplained to doctors on many occasions about thepain but it was not until she eventually had to consult

with others there was concomitant MTrP activity(see Ch 8).

His theory was that a MTrP’s nociceptive sens-ory afferent input to the spinal cord, on reaching it,is in some cases liable to activate sympathetic pre-ganglionic neurons in the intermediolateral columnsituated between the dorsal and ventral horns. Andthat this, in turn, causes noradrenergic postgan-glionic neurons in the sympathetic chain to becomeactivated with, as a consequence, the release ofnoradrenaline (norepinephrine), which then helpsto maintain MTrP nociceptor activity. This hypoth-esis has since received support from in vitro experi-mental rat muscle receptor studies carried out byKieschke et al (1988).

All this notwithstanding, it has to be said thatoften there is no clinically obvious muscle spasm

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a physician about her heart that the TrP origin of this long-standing pain in the lateral chest wall wasrecognized.

MTrP pain referralLewis (1942) was one of the first to point out thatpain that develops as a result of the application ofa noxious stimulus to the skin is accurately locatedby the brain, but that pain that develops as a resultof trauma to muscle is perceived as arising somedistance away from the affected site.

It was also about that time, as discussed inChapter 4, that John Kellgren was able to demonstrate that pain emanating from whatwould now be called a MTrP, is referred to a sitesome distance from it (zone of pain referral). Andthat not only is the MTrP itself exquisitely tender,but that there is also a certain amount of tender-ness of the healthy tissues in the zone of pain referral.

Since then many hypotheses have been put for-ward to explain MTrP pain referral, but despiteconsiderable progress having been made in ourunderstanding of the neurophysiology of pain, the reason for it happening is still not certain. Thetheories that have been advanced include conver-gence–facilitation, convergence–projection andcentral sensitisation.

Convergence–facilitation and convergence–projection theories

These two theories, the first put forward byMackenzie (1909) and the second by Ruch (1949) toexplain the referral of visceral pain, may also applyto the referral of muscle pain. This is because of theextensive convergence of sensory afferent inputs tothe dorsal horn, with neurons to which muscleafferents project, also processing noxious informa-tion generated in nociceptors in other tissues,including viscera.

The assumption underlying these two theorieswith respect to the referral of MTrP pain is that thistakes place because information transmitted cen-tripetally from these dorsal horn-situated conver-gent neurons is not sufficiently specific for thebrain to be able to distinguish between inputs tothe spinal cord from various sources. The validity

of this supposition, however, has to be questionedin view of people usually having little or no diffi-culty in determining whether a pain is arisingfrom either skin, muscle or a viscus.

Central sensitisation

Animal experiments carried out by Mense (1990,1994) have shown that dorsal horn neurons withsensory afferent inputs from nociceptors in a muscle are capable of changing both the size andnumber of their receptive fields in response to theapplication of a noxious stimulus to the muscle.Mense (2001), therefore, suggests that the referralof MTrP pain may be due to the neuroplasticchanges that develop in dorsal horn neurons in thephenomenon known as central sensitisation with,as part of this process, enlargement and increasedsensitivity of dormant nociceptive neurons’ recep-tive fields and a concomitant opening up of previ-ously silent synaptic connections.

Specific patterns of MTrP pain referral

It has for long been known that pain referred fromMTrPs does not follow a segmental or nerve rootdistribution pattern (Travell & Bigelow 1946). It isno doubt because of this that the majority of clin-icians, when presented with pain of MTrP origin,fail to recognize it as being of organic origin (Bonica1957). Yet, as discussed in Chapter 5, it was at least50 years ago that Good in Britain, Kelly in Australiaand Travell & her colleagues in America, all showedin numerous profusely illustrated reports, that eachindividual muscle in the body has its own specificpattern of TrP pain referral.

Admittedly, the clinical picture becomes some-what confused when, as so often happens, there isa composite pain pattern due to more than onemuscle being affected. However, knowledge of all the various individual patterns, each of whichhas to be learnt separately, reduces the chances ofoverlooking the myofascial origin of such painand gives much needed guidance as to whichmuscles in particular should be examined in orderto find the TrPs responsible for it.

With respect to this, it should be noted that,although MTrPs are exquisitely tender to touch,somewhat surprisingly, patients themselves are


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nearly always totally unaware of their presenceand, therefore, cannot be of any assistance when asearch for them is being made. It also has to beremembered that pain from any one TrP is oftenfelt a considerable distance away from it. Forexample, TrP activity in the levator scapulae musclegives rise to pain that is felt not only at the base ofthe neck and down along the inner border of thescapula but it may also extend upwards towardsthe occiput, downwards along the inner side of thearm and occasionally around the chest wall. It isbecause a knowledge of the various specific pat-terns of MTrP pain referral is therefore so essentialthat, during the course of this book, each one willbe described in detail.

Directions in which MTrP pain is referred

Simons (1993) has estimated that in 48% of musclesMTrP pain is referred in a downwards direction; in17% it is referred both locally and downwards; in10% it is confined to the region around the MTrP; in 20% it is in an upwards and downwards direction;and in only 5% is it in an upwards direction alone.

MTrP pain pathways and their relationship tothose taken by Chinese acu-tracts When, duringthe 17th century, news reached the Western worldthat the Chinese believed in the existence of struc-tures now known in the West as acu-tracts, chan-nels or meridians and had precisely defined thevarious courses taken by them, they were immedi-ately dismissed as figments of their imagination, asit was impossible to demonstrate their presenceanatomically. However, when one comes to studythe paths taken by pain referred from MTrPs it isremarkable how often these coincide with those ofChinese acu-tracts.

Macdonald (1982) describes how he persuaded52 consecutive patients with chronic musculoskel-etal pain seen in his practice, to draw maps of theirpain on diagrams of the human body. Somewhat tohis surprise, he found that 85% of them drew thinlines linking one area of pain with another. Andeven more surprisingly he found that 96% of thesethin lines corresponded with that of the coursetaken by one or another of the acu-tracts (merid-ians) described by the ancient Chinese.

One of his patient’s response to needle stimu-lation was particularly remarkable insomuch as

that whenever a needle was inserted into him hehad a feeling of ‘warm water’ flowing from it; and,although the patient had no previous knowledgeof Chinese acupuncture, when needles wereinserted into various parts of his body, the pathstaken by this ‘water’ coincided with those takenby meridians. Figure 7.4 shows the drawing thepatient made of the path taken by it flowing up hisleg and back from a needle inserted into the heeland by comparing it with Figure 7. 5 it will be seenthat this is identical with that taken by the tradi-tional Chinese ‘urinary bladder’ meridian.

Needle-evoked sensations

As will also be discussed in Chapter 10, from the time that the Chinese first began to practiseacupuncture they have described various sensa-tions that may be elicited as a result of inserting a needle into an acupuncture point. These are


Figure 7.4 The pattern of sensation drawn by a patienton an outline of the body following the insertion of aneedle into his heel. Reproduced with permission fromAlexander Macdonald’s Acupuncture from Ancient Art toModern Medicine, 1982.

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collectively known as tê-chhi (sometimes in Westernliterature spelt de-qi). They include numbness,distension, aching, heaviness and soreness. In mostcases a sensation of this type remains confined tothe site where the needle is inserted, but occasion-ally it radiates some distance from it and in rareinstances it travels along the entire course taken bya traditional Chinese acu-tract. When this happensit is known as propagated sensation along a channel (PSC).

The Cooperative Group of Investigation of PSC(1980) in China studied the distribution of theseneedle sensations in 64 228 patients and foundthat these were localized in the majority of them.However, about 20% of the patients described sensations that radiated for short distances andabout 0.4% of them had sensations propagatedalong a channel.

The Research Group of Acupuncture Anaes-thesia at the Institute of Medicine and Pharma-cology in the Fujian Province of China reported

in 1986 that mechanically compressing, cooling, orlocally anaesthetizing the soft tissues at some sitealong the course of a PSC blocked its spread. Suchan observation is somewhat surprising for it tendsto support what is now generally accepted to bethe untenable belief that acupuncture tracts orwhat in the West have come to be known as merid-ians are anatomical structures.

It would seem far more likely, as Becker et al(1976) have pointed out, that such channels andthe propagated sensations along them owe theirexistence to some as yet unidentified electricalactivity in the central nervous system.

In support of this are observations made by Xue(1986), which led him to believe that PSC occurs asa result of activity in the parietal cortex. He cameto this conclusion from descriptions of pain refer-ral given to him by patients with a variety of dif-ferent neurosurgical disorders. One of the moststriking of these was that of a below-knee amputeewho described propagation of sensation from apoint on his stump not only upwards along thesurface of it but also downwards into his phantomlimb. It is, possible therefore, that the ancientChinese evolved their ideas concerning acu-tractsor channels from similarly observing the pathwaystaken by pain arising both spontaneously and inresponse to needle stimulation.

Diagnosis of MTrP pain syndromeAs there are no laboratory tests or routine imagingtechniques currently available to assist with con-firming the presence of this syndrome its diagno-sis can only be made by means of a carefully takencase history and the skilled elicitation of a numberof characteristic physical signs.

Symptoms

Pain The nociceptive type of pain which arises asa result of MTrP activity in the MtrP pain syn-drome typically takes the form of a widespreaddull ache exacerbated by the carrying out of cer-tain movements. This is in contrast to the burningor electric shock-like sensations experienced bypatients with neuropathic pain.

The syndrome is usually confined to one regionof the body but in some cases it affects several


Figure 7.5 Composite drawing of the urinary bladdermeridians taken from several traditional Chinese sources. It will be seen that the course taken is much the same as the pattern of sensation drawn by the patient in Figure 7.1. Reproduced with permission from AlexanderMacdonald’s Acupuncture from Ancient Art to ModernMedicine, 1982.

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regions concomitantly with the pain then beinggeneralized in the same way as it invariably is inpatients with fibromyalgia.

Restricted movements A muscle containing oneor more active MTrPs becomes shortened andbecause of both this and the nociceptive pain,movements are liable to be restricted. This restric-tion may either be a symptom complained of by thepatient, or a physical sign elicited on examination.

Muscle weakness TrP activity in muscles isliable to weaken them with, as a consequence, dif-ficulty in the carrying out of certain movements.

Sleep disturbance Sleep is liable to be disturbedwhen the posture adopted for this causes pressureto be applied to active MTrPs with, as a conse-quence, exacerbation of the pain. This sleep disturb-ance, however, is never as severe or as disabling asthat experienced by patients with fibromyalgia.

Sympathetically-mediated symptoms As thereare sympathetic fibres at a MTrP site (see Fig. 7.1), it is hardly surprising that MTrP activity is notinfrequently associated with the development ofsympathetically-mediated symptoms. These includethe pilomotor changes of goose flesh and localizedsweating, with each of these appearing either spon-taneously or when pressure is applied to the tissuesoverlying an active MTrP. The one, however, whichoften proves to be the most troublesome is intensecoldness of the distal part of a limb as is shown bythe following case.

A female (35 years of age), who had been complainingof persistent intense coldness of the right foot for 3 years, was referred to a vascular surgeon for anopinion as to whether a sympathectomy might behelpful. No operation was advised but shortly after, asshe had been complaining of pain around the right hipfor the same period of time, she informed her doctorthat she would like to try the effects of acupunctureand so was sent to see me.

On examination, she had exquisitely tender TrPs atthe insertion of muscles into the greater trochanterand also along the tensor fasciae latae. And once thesehad been deactivated by means of the carrying out ofsuperficial dry needling (see Ch. 10) on a few occasionsshe not only lost her pain but in addition the right foot,subjectively, became as warm as the left one.

Physical signs

The search for MTrPs The locating of activeMTrPs is clearly the most important part of theclinical examination. The technique required forcarrying this out, however, requires much skilland practice. It is therefore unfortunate that medical students are still not being taught how to do this because as discussed in Chapter 4, it was before World War II that John Kellgren, bycarefully designed experiments and shrewd clinicalobservations, made fundamental contributions toour understanding of the importance of TrPs as acommon source of pain. The failure of most clinical teachers to recognize this is shown bythere still being little or no mention of the MTrPpain syndrome in any of the standard undergrad-uate textbooks.

One reason why so little attention is paid to thisdisorder is because muscle pain in general is stillall too frequently erroneously considered to be no more than a self-limiting minor disability of noparticular importance. The result of this attitude isthat whenever persistent and severe pain affectsthe musculoskeletal system, the muscles them-selves are given no more than a perfunctory exam-ination, whilst skeletal structures such as the joints,bones and intervertebral discs are subjected to closescrutiny with particular attention paid to changesdetected either radiographically or in some casesby magnetic resonance imaging.

The potential danger of this is that should someirrelevant abnormality be discovered during thecourse of carrying out investigations such as theseit may be accorded undue significance. Alterna-tively, should none be found then the pain is liableto be considered to be of little or no consequence.Furthermore, if, in spite of reassurance that noth-ing serious has been found, the patient has thetemerity to continue to complain about the pain,there is always the risk that it will be assumed tobe of psychological origin without the possibilityof its emanation from MTrPs ever having evenbeen considered. The following case history exem-plifies this.

A secretary (42 years of age), who had complained ofpersistent low-back pain for 2 years, was referred toan orthopaedic surgeon who, in view of radiographs ofthe lumbar spine and sacro-iliac joints showing no


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significant abnormality, informed her that there wasnothing serious to worry about and gave no specifictherapeutic advice. As the pain continued to bedisabling she was next referred to a gynaecologist who decided to carry out a dilatation and curettage.No abnormality was found but 10 days post-operativelyshe had a pulmonary infarct!

Her general practitioner then finding that she had marital problems decided that the low-back painmust be associated with these and referred her to apsychiatrist. The latter, however, to his credit came tothe conclusion that her disability was physical inorigin. This led the patient to ask whether acupuncturemight be of help and she was referred to me for anopinion about this.

On examination of the back several MTrPs were located, and after these had been deactivated bymeans of the superficial dry needling techniquedescribed in Chapter 10 on five occasions at weeklyintervals she lost her long-standing pain.

Another mistake often made is to assume thatpain that radiates down a limb must be due tonerve root entrapment even when there are noobjective neurological signs to support this diag-nosis and when the possibility that it might havebeen referred from MTrPs has not even been takeninto consideration.

It therefore cannot be stressed too strongly thatin the investigation of pain of uncertain origin a search for MTrPs is mandatory. Guidance as to which muscles are likely to contain these isobtained by paying careful attention to the distri-bution of the pain and by observing which move-ments of the body are restricted. Each muscleunder suspicion should then be placed slightly onthe stretch and systematically palpated with thetips of the fingers drawn firmly across it in a manner similar to that employed when kneadingdough. The necessity for employing firm pressurehas to be emphasized because, otherwise, TrPs areliable to be overlooked. When this type of flat palpation is carried out over a normal muscle it causes no discomfort. In the vicinity of a TrP it is slightly uncomfortable. And over a TrP itself,because this is a site where nociceptors are in astate of activation and sensitisation, the tendernessis so great as to cause the patient to carry out aninvoluntary flexion withdrawal reflex (the ‘jump’

sign) and in some cases to utter an expletive (the‘shout’ sign).

It is my personal preference when searching forTrPs, which by definition are points of maximumtenderness, to employ the flat palpation techniquejust described for all muscles. Some authoritiesadvocate the use of pincer palpation for thosemuscles that can readily be squeezed between thethumb and fingers. However, this, in my view,cannot be recommended, as even a healthy muscleis extremely tender when compressed in this manner (Lewis 1942).

Pain reproduction The application of pressureto an active MTrP for about 10–15 seconds resultsin the patient’s spontaneously occurring painbeing reproduced. As Gerwin (1999), however, haspointed out the reliability of this test depends onwhether or not the patient is able to provide rele-vant information concerning what is felt. Anotherdifficulty, as Hong et al (1996) have said, is thatpain may be referred from a latent MTrP should itbe subjected to particularly strong pressure.

Palpable taut bands A MTrP that is no morethan a few millimetres in diameter is often to befound at the centre of a palpable taut band severalcentimetres in length.

There is much controversy as to what causesbands of this type to develop, particularly as theyhave been found to be present not only in musclesof patients with the MTrP pain syndrome, but alsoin muscles of seemingly healthy people (Wolfe et al 1992, Njoo &Van der Does 1994).

With respect to all this, it has to be remembered,as explained earlier, that a MTrP contains a num-ber of dysfunctional motor endplates and themuscle fibres to which these are attached becomemarkedly contracted with the development of sev-eral knots. It is possible, therefore, that MTrP-related bands develop because of the increasedtension that develops both in these contractionknots and in the elongated sarcomeres on eitherside of them (Simons et al 1999).

As bands of this type may be found in other-wise healthy people and because it is only possibleto palpate them in superficially placed muscles, itnecessarily follows that the eliciting of them can-not be made one of the essential criteria requiredfor the diagnosis of the MTrP pain syndrome.


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Local twitch response If a finger is drawnsharply across a palpable band in a manner similarto that employed when plucking a violin string it is possible to evoke a transient contraction of the muscle fibres. This local twitch response (LTR)may either be visible or detected under the exam-ining finger. In some cases it is both seen and felt.

A LTR may also be elicited when, during thecourse of carrying out the therapeutic procedureknown as deep dry needling (see Ch. 10), a needleis rapidly thrust into a MTrP. The reason for this isthought to be because of needle-induced stimula-tion of the MTrP’s nociceptors giving rise to a sensory afferent barrage which, on reaching thespinal cord, sets up reflex motor efferent activity.

Gerwin & Duranleau (1997) have shown that itis possible to visualize LTRs by means of the use ofultrasound imaging.

Tender nodules Tender nodules that are mainlyfound in muscles in the lower part of the back and,to a lesser extent, in muscles in the neck and shoul-der region, have over the years given rise to suchconsiderable controversy concerning both theirmorphology and their ability to cause pain, that it will be necessary to discuss these structures atsome length.

The first to examine them microscopically wasRalph Stockman at the University of Glasgowwho, in 1904, as discussed in Chapter 5, reportedthat on histological examination he had foundtheir connective tissue to show patches of inflam-matory hyperplasia. This led him to conclude thatthe pain from them arises as a result of sensorynerves becoming stretched or compressed both byfibrous tissue proliferation and by inflamed con-nective tissue infiltrating the walls of nerves.

It has to be said, however, that the inflamma-tory type of reaction described by him has neversubsequently been confirmed.

The next to investigate these nodules was Schade(1919) who carried out his studies in a German fieldhospital during World War I. He located thesestructures in the muscles of a number of soldiersand observed that they continued to be palpable inthose of them who, for one reason or another, had tobe anaesthetized. He also noted that they were palp-able in those who died up to the time of the settingin of rigor mortis. Furthermore, when this group

were subjected to post-mortem examinations, themuscles containing them were found to be other-wise normal.

As a result of observing that the nodules con-tinued to be palpable both under deep anaesthesiaand after death he concluded that they could nothave developed as a result of muscle having goneinto spasm. Moreover, he considered that the discovery of normal muscle tissue on histologicalexamination ruled out any possibility that nodulesof this type might have developed as a result ofstructural changes in its connective tissue. He, there-fore, suggested that they may have done so as aresult of a change in the colloidal state of musclecytoplasm from sol to gel. And in view of this coinedthe term myogelose (muscle gelling or myogelosis).

The first extensive well-documented study ofcarefully selected material designed to demonstratethe histological changes associated with myogelo-sis was carried out by Glogowski & Wallraff (1951)in Germany. They examined 24 biopsies of whatthey called muscle hardening (muskelharten), but,despite the use of no less than nine tissue stainswere unable to demonstrate any significant abnor-malities; they, therefore, concluded that myogelosismust occur at the sarcoplasmic level beyond reachof the light microscope.

In the meantime, in Britain, Copeman &Ackerman (1944) added to the confusion by erro-neously concluding that nodules felt in the musclesof patients with low-back pain are nothing morethan herniated fat lobules.

It was Brendstrup et al (1957) who carried out the first controlled biopsy and biochemicalexamination of these nodules. In their study themicroscopic appearances of biopsies of paraspinalmuscles containing palpable tender nodules werecompared with those of biopsies taken from nor-mal contralateral paraspinal muscles in patientsundergoing operations for prolapsed interverte-bral discs. They stressed that, as the subjects werefully anaesthetized and the muscle relaxed withcurare, neither painfulness nor muscle spasmcould have been factors in choosing the areas forbiopsy and that the selection was done entirely bypalpating the nodules.

They found a striking difference between themicroscopic appearances of the control biopsymaterial and of the tissue in which these nodules


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was present. By staining sections of these noduleswith toluidine blue they were able to demonstratethe presence in them of much interstitial oedemacontaining acid mucopolysaccharides and an accu-mulation of mast cells. In addition, biochemicalanalysis showed there to be a much higher concen-tration of hexosamine and hyaluronic acid in themthan in the controls. Hyaluronic acid has a strongwater-binding capacity and it was believed it wasbecause of this that the extra-cellular content of thenodules was considerably more than that found inthe control material.

Wegelius & Absoe-Hansen (1956) suggested that it may be this oedematous change in a nodulethat, by distorting the peripheral nerve endings,contributes to the development of the pain produced by it.

The next person to study nodules of this typewas Awad (1973), who took biopsies of muscle inwhich nodules could be felt from 10 patients andexamined them with the electron microscope.Firstly, the skin overlying each nodule to be biop-sied was carefully marked with an indelible pen,and then muscle fasicles, approximately 1 cm wideand 2 cm long, were dissected out after the tissuesinvolved had been firmly grasped between theopposing jaws of a modified chalazion clamp. The reason for doing that was partly to prevent thedevelopment of muscle contraction artefacts butalso to ensure that the fluid content of the muscleremained trapped within the biopsy material.

When examined under the light microscope themuscle fibres appeared normal, except that in everycase there seemed to be an increase of interstitialnuclei. However, of much greater significance wasthe discovery in 8 of the 10 cases of a large amountof amorphous material in between the muscle fasi-cles which, when stained with toluidine blue, wasshown to consist of acid mucopolysaccharides. Thissubstance that is known to have enormous water-binding properties is, under normal conditions,only present in small amounts in muscle extra-cellular tissue.

On electron microscopic examination, it wasnoted that this amorphous material distended thespaces between muscle fibres that were themselvesof normal appearance. In addition, large clusters of platelets were observed and mast cells were seento be discharging mucopolysaccharide-containing

granules into the intercellular space. The next most common finding of any significance was anincreased amount of connective tissue in some ofthe cases.

They concluded that it is this water-retainingmucopolysaccharide amorphous substance in thesenodules that causes them to be space-occupinglesions. That it is the accumulation of this substancein their extracellular tissues that impairs the oxygenflow to muscle fibres and increases their acidity.And that it is this increased acidity that sensitizesmuscle sensory nociceptors and converts theminto pain-producing TrPs.

Awad (1990) some years later came to the con-clusion that several questions still remained to beanswered, including: does the mucopolysacchar-ide in these nodules accumulate as a result of anincreased production of this normally occurringsubstance, or a decrease in its degradation, or achange in its quality?

Nerve root entrapment caused by TrP-inducedmuscle shortening Trp activity in a musclecauses it to become shortened and at certain sitesthis gives rise to nerve root entrapment.

The following are three common examples ofthis: (1) TrP-induced shortening of either the sca-lenus anterior or pectoralis minor is liable to causecompression of the lower trunk of the brachialplexus; (2) TrP-induced shortening of the pirifor-mis muscle is liable to give rise to compression ofthe sciatic nerve; and (3) Trp-induced shorteningof the peroneus longus is liable to be responsiblefor entrapment of the peroneal nerve with, as aconsequence, the development of a foot drop.

Degree of interexaminer concordance in elicititing the physical signs of the MTrP pain syndrome In recent years there have been severalstudies carried out for the purpose of assessing thedegree of concordance among examiners whenattempting to elicit physical signs appertaining tothe diagnosis of the MTrP pain syndrome.

In the study reported by Wolfe et al (1992), fourphysicians experienced in locating MTrPs exam-ined eight patients with MTrP pain syndrome,seven patients with fibromyalgia and eight con-trols for focal tenderness, pressure-induced repro-duction of the pain, pain referral, palpable bands


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and local twitch responses. Agreement with regardto the elicitation of these signs was poor and it wasconsidered by Simons (1996) that the most likelyexplanation for this was that differing examinationtechniques were employed by the participants.

In a study reported by Nice et al (1992), 12 physiotherapists examined the thoracolumbarmuscles of 50 patients with low-back pain. They didhave a uniformly agreed method of examination forit was laid down that a MTrP could only be consid-ered to be present if the application of firm pressurefor 10 seconds to a point of maximum tendernesscaused the patient to report the onset of pain at adistance or an increase in the intensity of the painalready present at the point. Agreement among thetherapists, however, proved to be poor and one pos-sible reason advanced for this by Simons (1996) wasthat they had not been adequately trained.

In a study reported by Njoo & Van der Does(1994), a general practitioner in Holland experi-enced in searching for MTrPs, and four final yearmedical students trained by him in this skill exam-ined muscles in 61 patients with low-back pain andin 63 controls. Their endeavour was to elicit thesame physical signs as those sought in Wolfe et al’sstudy. Out of all those various signs, only localizedtenderness with its associated ‘jump’ sign and painrecognition were generally agreed to be reliableones. Furthermore, it was considered that the highlevel of concordance among those taking part in thisstudy was a reflection of the satisfactory amount oftraining each of them had received.

That inter-examiner agreement can be improvedby training has been shown by two studies carriedout by Gerwin et al (1995). In the first of these, fourclinicians examined 25 people for muscle tender-ness, palpable bands, local twitch responses, andreferred pain. Agreement among them concerningthe elicitation of these signs was poor. Twenty-onemonths later, however, after the same physicianshad been given intensive training, a very satis-factory amount of agreement among them wasachieved.

Criteria for the diagnosis of the MTrP pain syndromeThere are currently no generally accepted criteriafor the diagnosis of the MTrP pain syndrome, but

what is certain is that there is much to be said forkeeping these as simple and as non-controversialas possible.

As previously stated, the palpation of a tautband at a TrP site and the elicitation of a localtwitch response by ‘plucking’ it cannot be includedamongst them, as it is only possible to demonstratethese two physical signs when the muscle contain-ing the TrP is a superficially placed one.

The only widely agreed essential one is thepresence of one or more points of maximum tender-ness detected by the evocation of ‘jump’ and ‘shout’reactions in response to the application of firm pres-sure. This, however, by itself does not allow a dis-tinction to be made between active and latent TrPs.A further prerequisite, therefore, insisted upon bysome authorities is the reproduction of the spontan-eously occurring pain by means of the applicationof sustained pressure to each of the TrPs. However,in my opinion such a procedure subjects the patientto much unnecessary discomfort. My grounds forsaying this are because, when in the absence of anyother obvious pain-producing disorder, TrPs arefound to be present in a region of the body affectedby a persistent dull aching type of pain, it is reason-able to assume that this must be emanating fromthem. And any relief of it obtained by the carryingout of a MTrP-deactivating procedure further helpsto confirm the diagnosis.

It must have been considerations such as thesethat led Yunus (1993) to cogently comment ‘whyshould all patients with regional musculoskeletalpain not be classified as having the myofascial painsyndrome on the basis of pain and tender pointsalone?’ A difficulty arises, however, with respectto this when the pain is generalized for then it isnecessary to decide whether the patient is sufferingfrom fibromyalgia or the MTrP pain syndromeaffecting several regions of the body simultan-eously. Clearly, in order to make this distinctionother considerations have to be taken into accountincluding whether or not the various other charac-teristic clinical manifestations of fibromyalgia arepresent.

Regional MTrP pain syndromesBefore concluding this discussion concerning various aspects of the MTrP pain syndrome it is


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necessary to make clear that this is a term that isemployed collectively to include a number of indi-vidual regional syndromes that will be consideredin turn in Part 3 of this book.

Investigatory procedures

Algometry

As, by definition, a MTrP is a point of maximumtenderness, its presence may be determined semi-objectively by measuring the pressure thresholdover it and comparing this with that obtained overa corresponding contralateral non-tender point. Thepressure threshold is the minimum pressure orforce that induces discomfort. The instrument formeasuring this, known as an algometer, or pressurethreshold meter (Fig. 7.6), is a force gauge fittedwith a disc-shaped rubber tip which has a surfacearea of 1 cm2. The gauge is calibrated in kg/cm2

with a range of measurements up to 11 kg.Before carrying out pressure threshold measure-

ments on patients with MTrP pain, it is essential for them to be in a relaxed state and to have beengiven a detailed explanation of the procedure. Thisinvolves locating a MTrP by means of manual palpation, and then, whilst the instrument is held

against it at an angle of 90°, applying steady pres-sure until the patient reports the onset of discom-fort. This should be done before and after thedeactivation of a MTrP. For once the latter has beencarried out the pressure threshold over a MTrPincreases by about 4 kg. (Fischer 1988a).

Although there is little or nothing to be gainedby measuring the pressure threshold at a MTrPsite in everyday clinical practice, this semi-objectivemeasurement should potentially be of consider-able help to those doctors and lawyers involved inmaking decisions concerning compensation in casesof persistent post-accident MTrP pain. In addition,in clinical trials, its measurement before and afterthe carrying out of a MTrP deactivation procedureis of much value in assessing the efficacy of this(Fischer 1988b).

Fischer (1998c) and Hong (1998) have providedcomprehensive reviews of current knowledgeconcerning the use of this instrument both foridentifying the presence of MTrPs and for assess-ing the therapeutic effectiveness of various MTrPdeactivating procedures.

Thermography

Thermography may be carried out by one or other of three methods. These are infrared radiometry, amethod employing films of liquid crystals and acomputer-analysis controlled electronic infraredradiation technique.

This method of investigation is used to studytemperature changes in the skin overlying a MTrPand its zone of pain referral.

Temperature changes in skin at a MTrP site

The typical thermographic finding in the skinimmediately overlying a MTrP is a discoid hotspot 5–10 cm in diameter. This is produced as aresult of the skin at that site being 0.5–1.0°Cwarmer than the adjacent skin (Fischer 1986, 1998,Fischer & Chang 1986, Kruse & Christiansen 1992).

A thermographic recorded temperature changeof this type, however, is not confined to the skinoverlying a MTrP for, as Simons (2001, p. 221) haspointed out, it is equally liable to be found in thepresence of a radiculopathy, articular dysfunction,enthesopathy and local subcutaneous inflammation.


Figure 7.6 Pressure threshold meter. Reproduced with the permission of Mr R. J. D’Souza.

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It, therefore, follows that this investigation cannot beused specifically for the identification of MTrPs.

Pressure-induced temperature changes at aMTrP’s zone of pain referral

In a controlled study carried out by Kruse &Christiansen (1992), an algometer was used to applysufficient pressure to MTrPs to produce referredpain. This pressure was maintained for 1 minutesand during this time thermographs were recordedboth over the MTrPs and their zones of pain refer-ral every 15 s.

They found a significant lowering of the tem-perature not only in the zones of pain referral butalso well beyond these.

TrPs in skin, ligaments and periosteum

Although TrPs are most commonly present inmuscle they are also liable to be found in the skin,ligaments and periosteum.

Skin TrPs may become activated in seeminglynormal skin and cause pain of a moderately severesharp stinging type to be referred either locally orat a distance (Sinclair 1949, Trommer & Gellman1952). In my experience these are most commonlyto be found in skin scars where they give rise to aburning, pricking or electric-shock type of pain. Itis particularly important to remember this possi-bility when investigating the cause of persistentpost-operative pain.

With respect to the treatment of this latter typeof pain, it should be noted that, although it isimpossible to push a needle into a tough fibrousscar, a TrP in such tissue may readily be deacti-vated by inserting the needle into the healthy sub-cutaneous tissue immediately lateral to the scar atthe appropriate level. The treatment of the follow-ing case exemplifies this.

A female (46 year of age) had a very badly infectedappendix removed. Five months after this, because ofchronic pelvic sepsis, she had to have the right ovaryand fallopian tube taken away, and 1 year later sheunderwent a hysterectomy. Soon after this she startedto complain of intermittent but severe jabs of pain inthe right lower part of the abdomen. As this continuedfor several months, she was extensively investigated,

but when no visceral cause for it was found, she wasreferred to me to assess whether or not acupuncturemight be of help.

On examination, there were exquisitely tender TrPsin the midline scar. And as a result of deactivatingthese by the needling technique described above onthree occasions the pain disappeared.

Ligaments TrPs in the ligaments of joints are alsoa frequent cause of pain and yet are frequentlyoverlooked despite Leriche in 1930 having drawnattention to the manner in which they develop inthese structures following fractures and sprains.Gorrell (1976) has also discussed the diagnosis andtreatment of pain emanating from TrPs in ligamentsaround the ankle. In addition, de Valera & Raftery(1976) have shown that pain emanating from TrPsin strained pelvic ligaments may be relieved byinjecting these points with a local anaesthetic.

It has subsequently become evident that TrPs ina structure of this type can equally well be deacti-vated by means of the far simpler superficial dryneedling technique to be described in Chapter 10.

Periosteum Kellgren (1939), by experimentallyinjecting hypertonic saline into periosteum artificially created TrPs in it and observed that painfrom these was referred either locally or to a distantsite. Inman & Saunders (1944) confirmed this anddrew attention to the importance of periosteal TrPsas a source of pain in various musculoskeletal dis-orders. And Mann (1974) since then has devised atechnique he calls periosteal pecking for the allevi-ation of musculoskeletal pain.

FIBROMYALGIA SYNDROME

There have been several recently published com-prehensive reviews of this commonly occurringsyndrome that affects women some 10–20 timesmore than men. Included amongst these are onesby Bennett (1999), Chaitow (2003), Russell (2001),and Yunus & Inanici (2001).

Symptoms

Pain

The pain is most often described as being of a dif-fuse deep aching in the muscles. In addition, there


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is sometimes discomfort around the joints in theabsence of any objective evidence of these beingswollen (Reilly & Littlejohn 1992).

There is also much early morning stiffness withboth this and the pain being typically worstbetween 11 am and 3 pm (Moldofsky 1994).

The intensity of the pain is liable to fluctuatewith exacerbations of it being brought on by suchfactors as excessive exertion, trauma, stress and colddamp weather.

Unlike the MTrP pain syndrome, in which thepain is confined to one region of the body exceptwhen several regions are affected concurrently,fibromyalgia syndrome (FS) pain is invariablywidespread. The only exception to this is the veryoccasional case where, at an early stage of the dis-ease, it is localized to one particular site. An exampleis when it is initially confined to the chest wall(Pellegrino 1990). When this happens, other dis-orders such as costochondritis, Tietzes’s disease andcoronary heart disease clearly need to be includedin the differential diagnosis.

There is, in addition generalized hyperalgesia(i.e. increased responsiveness to a noxious stimu-lus such as a pin prick) and widespread allodynia(i.e. pain brought on by some innocuous stimulussuch as touch).

Non-restorative sleepIt is common for there to be a persistent feeling of tiredness due to non-restorative sleep. This sleepdisturbance was first investigated electroencephalo-graphically by Moldofsky et al (1975) and againmore recently by Hyyppa & Kronholm (1995).

These studies have shown that there is an intru-sion of stage 1 rapid eye movement light sleepwith fast alpha waves into stage 1V deep restora-tive sleep with slow delta waves.

Carette et al (1995), however, have only foundthese electroencephalographic changes to be pre-sent in one-third of patients with FS. Moreover, theyare not confined to patients with this particular syn-drome; Moldofsky et al (1983) have recorded themin a group of patients with rheumatoid arthritis.

Reactive depressionThere are conflicting findings concerning the incidence of reactive depression in patients with

FS but overall there are grounds for believing that about 30–40% of them suffer from it. This is amuch higher incidence than that found in the general population, but one that is comparable tothat present in patients with rheumatoid arthritis(Ahles et al 1991). However, this is as might beexpected considering that these two disorders havesimilar pain severity, morning stiffness and physi-cal function limitation (Cathey et al 1988), the fac-tors that would seem to be mainly responsible forthe development of this particular psychologicaldisturbance.

Dizziness and light headednessThese symptoms are frequently complained of bypeople with FS. They tend to be particularly notice-able on getting up from a seated or recumbent pos-ition and following long-term immobility. There isoften, in addition, a feeling of impending syncopebut an overt vasovagal attack is uncommon.

There is now reason to believe that an autonomicnervous system dysfunction present in patientswith FS (see p. 95) is most often responsible. OtherFS-related causes for it that have to be consideredinclude proprioceptive dysfunction due to MTrPactivity in a sternocleidomastoid muscle (see Ch. 16)and drug-induced hypotension. Disorders unre-lated to FS, such as brainstem ischaemia and dropattacks of uncertain origin, also have to be includedin the differential diagnosis.

Other complaintsTension headaches, a subjective feeling of swellingin the small joints and paraesthesiae are also com-monly present. In addition, some patients developa poor memory for recent events and a lack of con-centration (Landro et al 1997). It seems likely thatboth of these are due to the distracting effect ofchronic pain and the psychological distress thataccompanies this (Kurtze et al 1998, Sletvold et al1995).

Associated disorders

Irritable bowel syndrome

This commonly occurring disorder that affectsabout one-fifth of the general population has been


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found to be present in approximately two-thirdsof patients with FS (Sivri et al 1996).

Female urethral syndrome

This disorder, in which there is suprapubic dis-comfort, frequency, dysuria and urgency is liableto affect about 50% of women with FS (Clauw et al1997).

Restless leg syndrome

This syndrome, which was first described byEkbom (1960) in otherwise fit people, has beenfound to be present in about one-third of patientswith FS (Yunus & Aldag 1996).

In this disorder the patient suffers from numb-ness and tingling in the legs that is relieved bystretching or walking. It usually comes on when theperson is sitting down to relax of an evening and istemporarily relieved by walking around. It thenbecomes worse again when the patient goes to bedand interferes with any attempt to get off to sleep.

Raynaud’s phenomenon

This is liable to develop in about 40% of patientswith FS (Dinerman et al 1986, Vaeroy et al 1988).

Factors that predispose to the development of FSWhen discussing these it has to be said at the out-set that despite much extensive research in recentyears the aetiology of the disorder remains farfrom certain.

Genetic predisposition

There is a strong family prevalence of FS (Buskilaet al 1996, Pellegrino et al 1989) suggesting that itmay well be genetically determined.

Trauma

An appreciable number of FS sufferers state thattheir illness has developed following their subjec-tion to trauma (Aaron et al 1997, Greenfield et al1992, Waylonis & Perkins 1994).

The strongest evidence to support an associ-ation between trauma and FS is that provided by

Buskila et al (1997) who observed a high preva-lence of FS (22%) in patients who had been sub-jected to a cervical spine whiplash injury.

It has to be said, however, that in contrast to thishe only found that a small number (1% preva-lence) of those who had accidents causing them tofracture legs developed it.

Evidence that trauma, in some as yet unex-plained way, would seem to be one of the causesfor FS developing clearly has important medico-legal implications (Buskila & Neumann 2002).

Bennett (1999) has suggested that one possiblereason why patients with whiplash injuries areparticularly liable to develop FS is because traumato the neck muscles may be a particularly potentevoker of central sensitisation which, as discussedlater, is known to be a major pathophysiologicalfeature of this disorder.

Clauw (2002) has pointed out that variousregional pain syndromes including the MTrP painsyndrome, temporomandibular joint dysfunction,costochondritis and vulvodynia (dyspareunia andvulvar sensitivity) may eventually be followed by the development of FS. He is of the opinion thatthe most likely reason for this happening is thedevelopment of central sensitisation.

Concomitant inflammatory diseases

FS not infrequently develops in conjunction withrheumatoid arthritis (Urrows et al 1994), systemiclupus erythematosus (Middleton et al 1994) andSjogren’s syndrome (Bonafede et al 1995).

One possible reason for this is that any one ofthese chronic inflammatory diseases is liable to beresponsible for the development of a nociceptor-activity-induced sensory afferent barrage that givesrise to central sensitisation with, as a consequence,the amplification of pain and the development ofFS. A genetic predisposition may well be an add-itional factor.

Systemic syndromes with similarsymptomatologyDisorders with symptoms that are liable to simu-late those of FS include chronic fatigue syndrome,somatization disorder (Briquet’s syndrome) andconversion disorder. In addition, various exposure


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disorders have similar symptoms, such as sickbuilding syndrome, Gulf War syndrome and post-silicone breast implant syndrome (Clauw 2002).Also, polymyalgia rheumatica, medication withthe cholesterol-lowering statin group of drugs andadult growth hormone deficiency can all causesymptoms seen in FS.

Diagnostic criteriaThe American College of Rheumatology 1990Criteria for the classification of fibromyalgia (Wolfeet al 1990) include a history of widespread spontan-eously occurring pain, and pain that is evoked ondigital palpation at 11 of 18 specifically definedtender point sites.

Widespread pain

Pain is considered to be widespread when it affectsboth sides of the body both above and below thewaist. In addition, axial skeletal pain (cervical spine,anterior chest, thoracic spine or low back) must be present. Low-back pain is categorized as lowersegment pain.

Tender points

Pain on digital palpation must be present in atleast 11 of the following nine bilateral tender point(TP) sites (Fig. 7. 7):

Occiput: bilateral, at the suboccipital muscleinsertions.

Low cervical: bilateral, at the anterior aspects ofthe intertransverse spaces at C5–C7.

Trapezius: bilateral, at the midpoint of the upperborder.

Supraspinatus: bilateral, at origins above thescapula spine near the medial border.

Second rib: bilateral, at the second costochondraljunctions.

Lateral epicondyle: bilateral, 2 cm distal to theepicondyles.

Gluteal: bilateral, in upper outer quadrant ofbuttock in anterior fold of muscle.

Greater trochanter: bilateral, posterior to thetrochanteric prominence.

Knee: bilateral, at the medial fat pad proximal tothe joint line.

These classification criteria have proved to beextremely useful when employed for the purposeof standardizing research protocols. However, aspointed out in the consensus document onfibromyalgia – The Copenhagen Declaration (WHO1993) and again by Wolfe et al (1995) many patientswith otherwise typical manifestations of FS haveless than 11 tender points (TPs). Furthermore,although the maximum number of these in theabove classification is 18, as Bennett (1999) states,this only accounts for about 3% of potential TP loca-tions. Modification of these classification criteria istherefore permissible when diagnosing the disor-der in everyday clinical practice.


Anterior Posterior

2

5

6

8

9

1

3

4

7

Figure 7.7 Locations of 9 bilateral tender point sites tobe palpated for testing American College of Rheumatologycriteria for classification of FMS. 1, occiput; 2, lowcervical; 3, trapezius; 4, supraspinatus; 5, second rib; 6, lateral epicondyle; 7, gluteal; 8, greater trochanter; 9, knee. Reproduced from Yunus (1992), with permission.

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The difference between tender points and TrPs

A TrP, as defined in the above criteria, is a point ofmaximum tenderness with the application to it offirm pressure (i.e. 4 kg or approximately the pres-sure required to blanch the nail of the palpatingfinger), giving rise to pain confined to that site.This, therefore, is in contrast to the referral of painto a distant site as happens when pressure is appliedto an active TrP as was discussed earlier when con-sidering the MTrP pain syndrome.

Conjoint presence of tender points and TrPs

Although those who formulated the currentlyaccepted criteria for the classification of FS drewspecial attention to the pathognomonic importanceof TPs it is evident that TrPs may also be present.

Bengtsson et al (1986) were among the first toreport that patients with FS may have both TPsand TrPs having found one or more of the latter tobe present in 83.6% of 55 people with this disorder.

Others who have observed this includeGranges & Littlejohn (1993) who found that out ofa group of 60 patients with FS, 41(68.3%) had TrPs.And Gerwin (1995), who in a study of 25 patientswith FS found that 18 (72%) of them had TrPs.

Pathophysiology of FSThree important pathophysiological features arecentral sensitisation, abnormal levels of neuro-transmitters and sympathetic hyperactivity.

Central sensitisation

As discussed in Chapter 6, central sensitisationwith hyperexcitability of dorsal-horn-situatednociceptive neurons develops whenever these cellsare subjected to a sustained sensory afferent barrageas a result of C-polymodal or Group IV nociceptoractivity developing, either because of an inflamma-tory lesion or a nerve injury (Coderre et al 1993,Devor 1988, Doubell et al 1999, Dubner & Basbaum1994).

The effects of this central sensitisation includean increased response to a noxious stimulus (hyper-algesia) and the development of pain in responseto an innocuous stimulus such as that producedby massaging or touching the skin (allodynia). As

both of these phenomena are invariably present inpatients with FS, it is clear that this dorsal hornpathophysiological change is an essential featureof this disorder.

In many cases there is an obvious reason for thishappening. Trauma is the commonest but otherpossible causes include either an infection (viral or bacterial) or some inflammatory process such asthat brought about by rheumatoid arthritis or sys-temic lupus erythematosus.

It has to be remembered, with respect to all this,that central sensitisation continues long after itsinitial peripheral causative stimulus has ceased tobe operative (Coderre et al 1993).

Yunus & Inanici (2001) believe that certain sus-ceptible individuals with FS may develop centralsensitisation spontaneously in the absence of anyperipheral nociceptive stimulation because of‘either a defective inhibitory system or a hyper-stimulated facilitatory pathway’.

Altered serotonin (5-hydroxytryptamine, 5-HT) levels in vascular system

Russell & Vipraio (1994) have shown that there is an abnormally low level of serotonin in theplatelets and, consequently, also in the serum ofpatients with FS.

Wolfe et al (1997) have shown that the serumlevels of this neurotransmitter correlate with thenumber of TPs present in individuals fulfilling theclassification criteria for FS.

Klein et al (1992) reported finding high titres of anti 5-HT and immunoglobulin (IgG, IgM) antibodies in the serum of patients with FS. Thisraised the possibility that an autoimmune processmight be responsible for the low levels of 5-HT in the sera and platelets of patients with FS. Sub-sequent studies, however, have so far failed toshow that these serum antibodies are increased inthis disorder (Russell et al 1995, Vedder & Bennett1995).

Altered serotonin level in central nervous system

When dietary protein is digested in the gut the resultant amino acid tryptophan is absorbedthrough the intestinal mucosa and conveyed to thenucleus raphe magnus (NRM) in the midbrain.


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Neurons in the NRM convert it to serotonin andthis then acts as the neurotransmitter in the paininhibitory system that descends from it.

Although the level of serotonin (5-HT) in the cerebrospinal fluid (CSF) of patients with FShas not been measured, the levels of its precursor,5-hydroxy-tryptophan, and its metabolic product,5-hydroxyindole acetic acid, have. And both ofthem have been found to be significantly lowered(Russell et al 1992, Russell et al 1993). Thus indica-ting that there must be a deficiency of this neuro-transmitter in the central nervous system where itspresence is so essential for the regulation of thenociceptive control process.

Altered substance P level in the central nervous system

This neuropeptide that is released from A-delta, C-polymodal and Group IV sensory afferent ter-minals in the dorsal horn’s Laminae I, II, and V isbelieved to facilitate the nociceptive processes thattake place at these three intra-spinal sites. Fromthese it diffuses out into the CSF and, therefore,measuring the amount of it there provides infor-mation concerning the quantity of it present in thedorsal horn.

Vaeroy et al (1988) were the first to report a sig-nificant increase in the amount of SP in the CSF ofpatients with FS in comparison to that found inhealthy normal controls. Since then three otherstudies have confirmed this finding (Bradley et al1996, Russell et al 1994, Welin et al 1995).

In each of these studies only one test was carriedout on each subject and because this provided noindication as to whether SP elevation in the CSFremains constant or fluctuates in accordance withchanges in a patient’s pain intensity, Russell et al(1998) decided to carry out a study in which CSFsamples were collected from FS patients at monthlyintervals over the course of 1 year. Their findingsled them to conclude that the SP level changesappeared to be integrally related to changes in theseverity of the pain experienced by patients with FS.

Dysfunction of the autonomic nervous system

There is now much evidence to show that dys-function of the autonomic nervous system has a

considerable role in the development of many of the clinical manifestations of FS. Knowledgeconcerning this has been greatly advanced by theintroduction of the technique known as heart ratevariability analysis (Martinez-Lavin 2002).

Because the heart rate normally varies fre-quently and randomly due to the opposing effectsof the sympathetic and parasympathetic nervoussystems on the sinoatrial node, Martinez-Lavin et al (1998) studied the heart rate variability of 30 patients with FS and 30 age/sex matched con-trols over 24 hour periods using a Holter monitor.The outstanding advantage of this particularstudy over previous ones was that the techniqueallowed the monitoring to be carried out duringboth normal daytime activities and sleeping.

The results showed that patients with FS hadless heart rate variability over 24 hours than didthose in the control group. It was considered thatthis was due to decreased parasympathetic influxand conversely increased sympathetic influx on thesinus node.

These FS patients also had an altered circadianvariation of the sympathetic–parasympathetic balance with changes consistent with nocturnalsympathetic hyperactivity.

This circadian variation in the sympathetic–parasympathetic balance with dominant sympa-thetic hyperactivity, particularly nocturnally, hasbeen confirmed by others (Cohen et al 2000, Cohenet al 2001, Raj et al 2000).

Martinez-Lavin (2002) believes that this sympa-thetic hyperactivity both day and night, particu-larly nocturnally, may well offer an explanationfor the development of many of FS’s clinical man-ifestations. At night, for example, it would accountfor the interference with deep sleep. And its unceas-ing presence both day and night may, he believes,induce pain through the mechanism known as‘sympathetically maintained pain’. An hypothesisthat has led him (Martinez-Lavin 2001) to ask ‘isFS a generalised reflex sympathetic dystrophy?’.

His reason (Martinez-Lavin 2002) for postu-lating this is that the pain in FS and in reflex sympathetic dystrophy (complex regional painsyndrome- type 1) has several features in common.He states that these features include: ‘post-traumaticonset, relentless pain disproportionate to the underlying tissue damage and unresponsive to


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analgesic/anti-inflammatory drugs, the presenceof allodynia (in FS tender points reflect a gener-alised state of allodynia), paresthesiae (a typicalfeature of neuropathic pain) and lastly, in both clinical syndromes, pain improves after sympatheticblockade’.

He concludes that ‘Sympathetic nervous systemdysfunction is frequent in FS and may explain itsmultisystem manifestations. It remains to be estab-lished if this dysautonomia plays a major role inthe pathogenesis of FS. We surmise that it does. If so, new types of non-pharmacological and phar-macological therapeutic interventions intended torestore autonomic nervous system homeostasismay be developed.’

Origin of the pain in fibromyalgia syndromeIn conclusion, it has to be said that the primarysource from which FS’s pain arises remains uncer-tain. Histological studies of the muscles have failed

to reveal any evidence that it originates in these.There is, however, much to suggest that the princi-pal pathological changes are in the central nervoussystem. That most patients with the disorder com-plain of persistent fatigue and non-restorativesleep is in accord with this. Also in favour of it isthe discovery that there are significant abnormalitiesin the blood and CSF levels of the neuropeptidesinvolved in central pain-modulating mechanisms.All this leads to the belief that progress in thetreatment of this disorder will be dependant onthe introduction of more effective and less toxicdrugs to combat changes in the nervous system,such as those responsible for the development ofcentral sensitisation. In the meantime, muchworthwhile symptomatic pain relief may beobtained by suppressing nociceptor activity at TrPand TP sites by one means or another, includingthe frequent carrying out of superficially directedneedle-evoked nerve stimulation at these pointson a long-term basis.


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INTRODUCTION

The main purpose of this chapter is to draw atten-tion to the still not sufficiently well recognizedclinical observation that myofascial trigger point(MTrP) pain syndrome and the disorder currentlyknown as complex regional pain syndrome (CRPS)type 1, or what formerly was called reflex sympa-thetic dystrophy (RSD), not infrequently developconcurrently.

It is particularly regrettable that many otherwisecomprehensive current accounts of CRPS type 1(RSD) make no reference to this association consider-ing that it was as long ago as 1943 that Livingston,in his classical monograph Pain Mechanisms, drewattention to the presence of MTrPs in some of hispatients suffering from the disorder and stated thatdeactivation of these points by injecting a localanaesthetic into them provides a significant amountof pain relief.

It is to be hoped that this fundamentally import-ant discovery made by Livingston during WorldWar II will no longer continue to be ignored nowthat at least five recent studies have confirmed itsveracity.

Filner (1989), after looking specifically for MTrPsin 40 patients with this syndrome, then known asRSD, found active pain-producing ones to be pre-sent in 36 of them.

Veldman et al (1993 ) discovered MTrPs to bepresent in 45% of 377 patients with this disorder.Lin et al (1995) searched for MTrPs in 84 patientswith CRPS (RSD) and identified pain-producingones in 82%. Inamura et al (1997) reported the

101

Chapter 8

Concurrent complex regional and myofascial trigger point pain syndromes

CHAPTER CONTENTS

Introduction 101Causalgia 102Reflex sympathetic dystrophy 102Terminological revision 102Clinical manifestations of CRPS type 1 (RSD) 103Aetiological factors common to CRPS type 1 (RSD)

and MTrP pain syndrome 104The pathophysiology of CRPS type 1 (RSD) and

type 2 (causalgia) 104The predisposition of individuals to developing

CRPS 105Treatment of CRPS type 1 (RSD) 105

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At the beginning of World War II his furtherexperience of treating nerve injuries (Leriche 1939)led him to modify this view, once he realized that not all patients with these injuries developcausalgia. This led him to conclude that this dis-order must be a ‘vasomotor and trophic syndromebrought about by the sympathetic reactions per-sonal to the individual in the presence of an externalinjury’.

Leriche’s belief that causalgia must, nevertheless,be essentially sympathetically mediated becamewidely accepted and was influential in persuadingsurgeons both in World War II and in wars in vari-ous parts of the world since then to perform asympathectomy on affected patients.

The results of carrying out this procedure provedto be widely variable but it was a long time beforethe possibility was considered that the reason forthis might be because the pathophysiology of thedisorder is more complex than was at first thought.

REFLEX SYMPATHETIC DYSTROPHY

As the years passed it became clear that a disorderwith very similar clinical manifestations could bebrought about by injury to tissues other than nerves.This led Evans (1946) to introduce the term reflexsympathetic dystrophy, in line with the then prevailing view concerning the pathophysiologi-cal changes responsible for both causalgia and thisparticular disorder, which some referred to asminor causalgia.

TERMINOLOGICAL REVISION

For the relief of this latter disorder various pro-cedures designed to suppress sympathetic efferentactivity have over the years been employed but,as will be discussed when considering currentapproaches to its treatment, their efficacy in generalhas proved to be very disappointing and frequentlyno better than a placebo.

For this and other reasons the aptness of theterm reflex sympathetic dystrophy has in recentyears been questioned. As Stanton Hicks et al (1995)have pointed out, dystrophic changes in the tissuesare not invariably present, and even when they are,it is only at a late stage. In addition, there is no con-vincing evidence that these or any of the disorder’s

presence of the MTrP pain syndrome in 82% of aseries of cases with CRPS (RSD). And Allen et al(1999), in a retrospective study of 134 patients withCRPS (RSD), found that ‘56% had a myofascial com-ponent present at evaluation’.

The following topics will also be discussed:early observations concerning the two closely related disorders originally known as causalgiaand reflex sympathetic dystrophy; the reasons whyit was considered necessary to revise the termin-ology and to introduce the terms CRPS type 1 (RSD)and CRPS type 2 (causalgia); the clinical manifest-ations of CRPS type 1 (RSD); present-day viewsconcerning the pathophysiology of CRPS type 1(RSD); and, finally, the various methods of treatingthe syndrome, including deactivating any MTrPsthat may be found to be present.

CAUSALGIA

Pain of a characteristically burning type thataffected soldiers with nerve injuries from gun shotwounds sustained during the American Civil Warwas described by Mitchell et al in 1864. They statedthat the pain was ‘mustard red hot’, that it wasmade worse by the application of pressure to theskin or the exposure of it to cold air, and that thesite affected, usually a hand or a foot, developedvasomotor, sudomotor and trophic changes.

Three years later Mitchell (1867) called this dis-order causalgia (from the Greek kausis [burning]and algos [pain]).

During World War I there was a resurgence ofinterest in nerve injury-evoked causalgia when in1916 Leriche described the case of a soldier whodeveloped the characteristic burning pain, excessivesweating and skin colour changes of it as a resultof a cannon-ball damaging the left clavicle andadjacent nerves and blood vessels. During thecourse of the operation for this condition Lerichehad to resect 12 cm of the adventitia of the brachialartery and as postoperatively all the symptomswere much improved, he concluded that this musthave been because this resection had led to theremoval of the periarterial sympathetic fibres. He,therefore, carried out a periarterial sympathectomyon other soldiers with similar clinical manifestationsof this disorder in the belief that it is a neuritis ofthe sympathetic nerves (névrite du sympathique).

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other manifestations develop as a result of reflexsympathetic activity.

It was in the light of considerations such as thesethat prompted the International Association forthe Study of Pain (IASP) to arrange for a consensusworkshop, to be held at Orlando, Florida in 1993,for the purpose of reviewing and, if necessary, revis-ing the terminology. The terms hitherto employedfor the two disorders had included a bewilderinglylarge number of names, not only causalgia and RSD(minor causalgia), but also algodystrophy, traumaticangiospasm, shoulder-hand syndrome, reflex neu-rovascular dystrophy, post-traumatic osteoporosisand Sudeck’s atrophy.

Those participating at this workshop realizingthat the pathophysiology of both causalgia andRSD remained far from certain, decided to replacethese terms by the strictly non-committal one ofcomplex regional pain syndrome (CRPS) and todivide this into two separate entities, CRPS type 1(RSD) and CRPS type 2 (causalgia).

This revised terminology has now been officiallyincluded in the IASP’s classification of chronic pain(Merskey & Bogduk 1994) .

CLINICAL MANIFESTATIONS OF CRPS TYPE 1 (RSD)

As CRPS type 1 (RSD) and MTrP pain syndromeare liable to develop concomitantly, it follows thatthose who frequently have to diagnose and treatthe latter need to be familiar with the clinical man-ifestations of the first. For this reason a detailedaccount of them will be given. They include pain,autonomic disturbances, dystrophic changes, muscle weakness and emotional disorders.

PainSomewhat confusingly, in view of the currentlyemployed name for this syndrome, it has nowbeen shown that pain is not a constant feature.

Blumberg & Janig (1994), from a detailed analysisof 190 patients diagnosed as having this disorder,stated that it was not present in 25% of them. Inaddition, Veldman et al (1993), who studied 829patients with this syndrome, found it to be absentin 7% of them.

The spontaneously occurring pain takes theform of a constant or paroxysmal burning, throb-bing or aching sensation. In addition, there may bea mechanically evoked hyperalgesia, hyperaesthe-sia and allodynia. The latter, which develops as aresult of central sensitisation (see Ch. 6 ), is liableto cause considerable suffering. However, some-what surprisingly, considering the intensity of thenociceptive sensory afferent barrage to which dorsalhorn transmission neurons must be subjected to inthis disorder, Blumberg & Janig (1994) only foundit to be present in about 8% of the patients studiedby them.

The severity of the spontaneous and evokedtypes of pain is liable to lead to prolonged immobil-ization and this, in turn, causes muscles to waste,joints to stiffen and in some cases contractures todevelop.

Autonomic disturbancesAbnormalities of the temperature and colour ofthe skin are common. These vasomotor changes arevariable with the affected part being either undulywarm or unduly cold. Veldman et al (1993) foundthat the longer the interval between the onset ofthe disorder and the first examination the morelikely it was for the affected limb to be cold.

Sudomotor changes may also be present but thesetoo are variable so that with some patients there ishyperhydrosis but with others hypohydrosis.

In addition, oedema is frequently present from anearly stage of the disease. Scadding (1999) is of theopinion that these autonomic changes may, in part,be brought about by prolonged immobilization.

Dystrophic changes in skin nails and boneTissue dystrophy, according to Veldman et al (1993),is mainly a late finding and was only present in a small percentage of the 829 patients studied by them.

The skin may become either thin and shinyor thickened. The nails also may become thickened.In addition, osteoporosis may eventually develop.Initially, the diagnosis of this latter disorderdepends on the use of technetium isotope scintigra-phy, but at a later stage a plain radiograph is all thatis required.

Concurrent complex regional and myofascial trigger point pain syndromes 103

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Muscle weaknessIt is common for muscles in the affected limbto become weakened and wasted. Veldman et al(1993), in a prospective study of 829 patients suffer-ing from what at that time they called RSD, foundthat 95% of them had weakening and wasting ofthe muscles in the affected limb. Muscles in thisstate are clearly liable to become overloaded with,as a consequence, the activation of any TrPs theymay happen to contain (see Ch. 7). In addition, thisloss of muscle strength is not infrequently accom-panied by the development of a tremor, especiallyin cases where it is the upper limb that is affected.

Emotional disordersThe severity of any pain that may be present, thedifficulty in alleviating this, and the sufferingcaused by other manifestations of the disorder fre-quently lead to the development of superimposedanxiety and depression.

AETIOLOGICAL FACTORS COMMON TOCRPS TYPE 1 (RSD) AND MTrP PAINSYNDROME

TraumaIt is hardly surprising that these two syndromes mayat times be present concurrently considering thatthe commonest reason for either of them develop-ing is trauma. In addition, as previously stated, theMTrP pain syndrome is liable to develop as a sec-ondary event when muscles in a limb affected byCRPS-type 1 become weakened, wasted and over-loaded with, as a consequence, the activation ofany TrPs that may be present in them.

Livingston (1943), when discussing the type oftrauma responsible for causing what is now calledCRPS type 1 (RSD) stated:

The onset of symptoms may follow the most com-monplace of injuries. A bruise, a superficial cut,the prick of a thorn or a broken chicken bone, astrain or even a post-operative scar may act asthe causative lesion. The event which precipitatesthe syndrome may appear both to the physicianand the patient as of minor consequence, andboth have every reason to anticipate the same

prompt recovery that follows similar injuries.This anticipation is not realised and the symptomstend to become progressively worse.

Vascular disordersEach of these two syndromes may occasionallydevelop following either a myocardial infarct or acerebrovascular accident.

THE PATHOPHYSIOLOGY OF CRPS TYPE 1(RSD) AND TYPE 2 (CAUSALGIA)

It has to be said that, despite much research havingbeen carried out over the years into the patho-physiology of both types of CRPS, the mechanismsresponsible for their clinical manifestations continueto remain highly contentious.

The traditional view that the pathologicalchanges in these two disorders are essentially sym-pathetically mediated ones has recently been chal-lenged, particularly by Schott (1994, 1995, 1998).He has done this because those symptoms andsigns so often encountered in causalgia and relatedconditions, that have traditionally been assumedto be due to sympathetic dysfunction, can insteadbe accounted for by the effects of neuropeptideswith vasoactive and perhaps trophic propertiesthat are released from C-afferent fibres, as recog-nized by Ochoa (1986) and Cline et al (1989).

The sensory afferents that are considered bySchott to be the particular ones involved in thesedisorders, are those that have been found to travelwithin autonomic nerve fibres. These two sets offibres have the conjoint function of innervating anumber of different structures, including those inthe peripheral vascular system.

Schott (1995), persuasively argues that the painand accompanying features in a disorder such asCRPS type 1 (RSD) develop as a result of trauma-evoked activation and sensitisation of these sensoryafferents causing the release of neuropeptides suchas Substance P (SP) and calcitonin gene-relatedpeptide, which then give rise to an inflammatorytype response.

Oyen et al (1993) have provided support for this view by carrying out scintigraphy withindium-111-labelled human non-specific polyclonalimmunoglobulin G, as this demonstrated that


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patients suffering from what they called RSD haveincreased vascular permeability for macromol-ecules, an important characteristic of inflammation.

Veldman et al (1993), during the course of dis-cussing this important finding made by Oyen andhis co-workers, pertinently comments ‘we hopethis observation incites physicians to develop newforms of treatment for this disabling disease’.

All this notwithstanding, that there may be asympathetic efferent component, in addition to thisinflammatory one, is suggested by the findings ofother studies. It has been found, in animal studiescarried out by Gold et al (1994) and by Levine (1986),that noradrenaline released from sympatheticpostganglionic neurons brings about the release of neuron-sensitizing prostaglandins. In additionSanjue & Juu (1989) found that, whereas the effect of noradrenaline on non-sensitized nociceptors isweak, it has considerably enhanced activity whenthese are in a sensitized state as a result of inflam-mation evoked by the release of neuropeptides.

THE PREDISPOSITION OF INDIVIDUALSTO DEVELOPING CRPS

Despite recent advances in knowledge concerningthe inflammatory nature of CRPS, it remains diffi-cult to understand why, as Poplawski et al (1983)have pointed out, type 1 (RSD), develops in lessthan 1% of patients with tissue damage and type 2in less than 5% of those with peripheral nerveinjuries. It has been suggested that this may bebecause only a small number of people are predis-posed to developing a sufficiently exaggeratedinflammatory response. At the same time it has tobe admitted that it is possible for an individual tohave two similar injuries but only to develop a disorder of this type with one of them.

TREATMENT OF CRPS TYPE 1 (RSD)

Uncertainty concerning the pathophysiology of this disorder has led to difficulties in formulating arational approach to its treatment.

PharmacotherapyWhen it became widely accepted that the dis-order was essentially due to aberrant sympathetic

efferent activity, the technique of intravenousregional guanethidine block (IVRGB), introducedby Hannington-Kiff (1974), was for a long timecommonly employed. However, when over theyears those using it found that with many of theirpatients the response to it was only transient andthat a number of them either did not respond atall, or even had a transient exacerbation of pain, itsefficacy was questioned and this then led to thecarrying out of controlled trials.

Jadad et al (1995) have reviewed four such trialsand found that the results in the treatment groupswere no better than those in the control groups.They then conducted a study on patients who hadreported obtaining an analgesic effect from IVRGBand found no significant difference between theeffect of guanethidine and saline.

Ramamurthy & Hoffman (1995), in a randomizedcontrolled trial, also found no significant differencewith respect to pain relief between a guanethidine-injected treated group and a control group. Remark-ably, however, both those in the treatment groupand the control group showed a reduction in trophicand vasomotor changes together with a diminutionin the amount of oedema!

Vanos et al (1992) have found an intravenousblock using ketorolac, a non-steroidal anti-inflammatory drug that reduces prostaglandinrelease, to be effective in improving symptoms in asmall group of patients with CRPS type 1 (RSD).This is particularly interesting in view of currentviews concerning the role of inflammatory-evokingchemical substances in the production of this dis-order’s clinical manifestations and its use, there-fore, deserves to be further explored.

There is no doubt, however, that a simple analgesic such as codeine or a non-steroidal anti-inflammatory orally administered drug should be tried first, as one or other of these is often allthat is required to relieve the pain.

Mellick & Mellick (1997) have found the admin-istration of gabapentin, a drug more usuallyemployed as an anticonvulsant, to be of value inthe treatment of this disorder.

Muizelaar et al (1997) have reported benefitfrom the use of the calcium channel blocking agentnifedipine; also, from the employment of the alpha-adrenergic blocking agent phenoxybenzamine.They found the latter, however, not infrequently


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gives rise to various side-effects including dizzi-ness, ortostatic hypotension and diarrhoea with22% of their patients forced to stop using it becauseof these.

Unfortunately, both Muizelaar et al (1997) andPaice (1995) have found it necessary to draw atten-tion to the difficulty in assessing the relative valueof these different types of drugs due to the regret-table paucity up to now of large scale multicentrecomparative trials.

PhysiotherapyIt is generally agreed that early mobilization of theaffected limb is essential.

PsychotherapyIt is also widely accepted (Scadding 1999) that treat-ment for anxiety and depression is often necessaryin view of the considerable disablement broughtabout by this disorder and the all too frequent fail-ure of various forms of therapy to ameliorate itsphysical manifestations.

Deactivation of myofascial MTrPsThe importance of searching for, and when foundto be present, deactivating MTrPs by one means oranother (see Ch. 11) has been stressed by Filner(1989), Lin et al (1995) and Sola (1999).


ReferencesAllen G, Guler B S, Schwartz L 1999 Epidemiology of

complex regional pain syndrome: a retrospective chartreview of 134 patients. Pain 80(3): 539–544

Blumberg H, Janig W 1994 Clinical manifestations of reflexsympathetic dystrophy and sympathetically maintainedpain. In: Wall P D, Melzac R (eds) Textbook of pain, 3rdedn. Churchill Livingstone, Edinburgh, pp. 685–698

Cline M A, Ochoa J, Torebjörk H E 1989 Chronichyperalgesia and skin warming caused by sensitised Cnociceptors. Brain 112: 621–647

Evans J A 1946 Reflex sympathetic dystrophy. SurgicalClinics of North America 26: 780–790

Filner B E 1989 Role of myofascial pain syndrome treatmentin the management of reflex sympathetic dystrophysyndrome. Communication to the 1st internationalsymposium on myofascial pain and fibromyalgia,Minneapolis

Gold M S, White D M, Ahlgeru S C, Guo M , Levine J D1994 Catecholamine-induced mechanical sensitisationof cutaneous nociceptors in the rat. Neuroscience Letters175: 166–170

Hannington-Kiff J G 1974 Intravenous regional sympatheticblock with guanethidine. Lancet 1: 1019–1020

Inamura S T , Lin T Y, Teitaria M J, Fischer A A et al 1997The importance of myofascial pain syndrome in reflexsympathetic dystrophy. Physical Medicine andRehabilitation Clinics of North America 8: 207–211

Jadad A R, Carroll D, Glynn C J, McQuay H J 1995Intravenous regional sympathetic blockade for painrelief in reflex sympathetic dystrophy: a systematicreview and a randomised double-blind crossover study.Journal of Pain Symptom Management 10: 13–20

Leriche R 1916 De la causalgie envisagée comme unenévrite du sympathique et de son traitement par ladénudation et l’excision des plexus nerveuxpéri-arteriels. Presse Medicin 24: 177–180

Leriche R 1939 The surgery of pain. (Translated by A Young)Baillière, Tindall and Cox, London

Levine J D, Taiwo Y O, Collins S D, Tam J K 1986Noradrenaline hyperalgesia is mediated throughinteraction with sympathetic postganglionic neuroneterminals rather than activation of primary afferentnociceptors. Nature 323: 158–160

Lin T Y, Teixeira M J, Kaziyama H H S, Pai H J et al 1995Myofascial pain syndrome (MPS) asasociated withreflex sympathetic dystrophy (RSD). Journal ofMusculoskeletal Pain 3 (suppl 1): 150

Livingston W K 1943 Pain mechanisms: a physiologicalinterpretation of causalgia. Macmillan, New York

Mellick G A, Mellick L B 1997 Reflex sympathetic dystrophytreated with gabapentin. Archives of Physical Medicineand Rehabilitation 78: 98–105

Merskey H, Bogduk N (eds) 1994 Classification of chronicpain. Description of chronic pain syndromes anddefinitions of pain terms, 2nd edn. IASP Press, Seattle

Mitchell S W 1867 On the diseases of nerves resulting frominjuries. In: Flint A (ed) Contributions relating tocausation and prevention of disease and to campdiseases. US Sanitary Commission Memoirs, New York

Mitchell S W, Morehouse G R, Keen W W, 1864 Injuries ofnerves and their consequences. J B Lippincott, Philadelphia

Muizelaar J P, Kleyer M, Hertogs I A M, De Lange D C 1997Complex regional pain syndrome (reflex sympatheticdystrophy and causalgia): management with the calciumchannel blocker nifedipine and/or the alpha-sympathetic blocker phenoxybenzamine in 59 patients.Clinical Neurology and Neurosurgery 99: 26–30

Ochoa J 1986 The newly recognised painful ABC syndrome:thermographic aspects. Thermology 2: 65–66; 101–107

Oyen W J M, Arntz J E, Claessens R A M J, Van der Meer J V Met al 1993 Reflex sympathetic dystrophy of the hand: anexcessive inflammatory response? Pain 55: 151–157

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Paice E 1995 Reflex sympathetic dystrophy. British MedicalJournal 310: 1645–1648

Poplawski Z L, Wiley A M, Murray J F 1983 Post-traumaticdystrophy of the extremities. Journal of Bone and JointSurgery 65 A; 642–655

Ramamurthy S, Hoffman J 1995 The guanethidine studygroup. Intravenous regional guanethidine in thetreatment of reflex sympathetic dystrophy/causalgia: arandomised double-blind study. Anaesthesia andAnalgesia 81: 718–723

Sanjue H , Juu Z 1989 Sympathetic facilitation of sustaineddischarges of polymodal nociceptors. Pain 38: 85–90

Scadding J W 1999 Complex regional pain syndrome. In: Wall P D, Melzack R (eds) Textbook of pain, 4th edn,Ch. 36. Churchill Livingstone, Edinburgh

Schott G D 1994 Visceral afferents: their contribution to‘sympathetic dependent‘ pain. Brain 117: 397–413

Schott G D 1995 An unsympathetic view of pain. Lancet345: 634–636

Schott G D 1998 Interrupting the sympathetic outflow incausalgia and reflex sympathetic dystrophy. BritishMedical Journal 316: 792–793.

Sola A E 1999 Upper extremity pain. In: Wall P D, Melzack R(eds ) Textbook of pain, 4th edn, Ch. 24. ChurchillLivingstone, Edinburgh

Stanton-Hicks M, Janig W, Hassenbuch S, Haddox J D et al1995 Reflex sympathetic dystrophy: changing conceptsand taxonomy. Pain 63: 127–133

Tilman P B J, Stadhouders A M, Jap P H K, Goris R J A 1990Histopathological findings in skeletal muscle tissue ofpatients suffering from reflex sympathetic dystrophy.Micron Microscop Acta 21: 271–272

Vanos D N, Ramamurthy S, Hoffman J 1992 Intravenousregional block using ketorolac: preliminary results inthe treatment of reflex sympathetic dystrophy.Anaesthesia and Analgesia 74: 139–141

Veldman P H J M, Reynen H M, Arntz I E, Goris R J A 1993Signs and symptoms of reflex sympathetic dystrophy:prospective study of 82 patients. Lancet 342: 1012–1016


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INTRODUCTION

Firstly in this chapter brief mention will be made of various pain-suppressing types of treatmentemployed by primitive man, whose analgesic effects,in retrospect, would seem to have been dependenton bringing into action similar neurophysiologicalmechanisms to those now believed to be involvedin acupuncture.

Following this, current views concerning themechanisms in the peripheral and central nervoussystems considered to be brought into action whenelectroacupuncture and transcutaneous electricalnerve stimulation are used for pain relief will bediscussed.

Then, because in the next chapter the manuallyapplied acupuncture technique known as super-ficial dry needling (SDN) will be advocated for the routine deactivation of primarily activated myo-fascial trigger points (MTrPs), and the techniqueknown as deep dry needling (DDN) for the occa-sional case where the MTrP activity has arisen sec-ondarily to the development of a radiculopathy, itwill be necessary to give a detailed account of thepain-relieving mechanisms believed to be broughtinto action by these two procedures.

Finally, reasons will be given as to why some of the current concepts concerning the manner in which manually applied needle-evoked nervestimulation techniques bring about their pain-suppressing effects have recently had to be challenged.

109

Chapter 9

Neurophysiologicalpain-suppressing effects ofacupuncture and transcutaneouselectrical nerve stimulation

CHAPTER CONTENTS

Introduction 109Primitive pain-suppressing procedures 110The early use of electricity for the combating of

pain 110–111Electroacupuncture for the suppression of

surgically-evoked pain (acupunctureanalgesia) 111–116

Transcutaneous electrical nerve stimulation(TENS) 116–118

Therapeutic acupuncture 118–122Conventional views concerning pain-suppressing

mechanisms involved in manually appliedsuperficial and deep dry needling at MTrPsites 119–121

Challenge to conventional views concerningpain-relieving mechanisms brought into action by therapeutic manual acupuncture 121–122

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A form of treatment closely allied to this andone which has been used in the Far East for at least3000 years, is the application to the body surface ofa substance obtained from the leaves of the mug-wort plant called moxa. A cone of this is placed onthe skin, then set alight and allowed to burn downto its base. This procedure which must, as a resultof damaging the tissues, be extremely painful is yetanother example of a noxious stimulus being usedto combat pain of a more chronic type.

Acupuncture, which has been used in the Easternworld for much the same period of time, is also aform of treatment in which a noxious stimulus isemployed to bring about the alleviation of pain.

All these traditional therapeutic methods, whichover the centuries have employed acute pain todrive out more protracted and severe pain, are now referred to collectively as counter-irritants.As Wand-Tetley (1956), in an extensive historicalreview of their clinical application, has pointed out,they have always mainly been used for the allevi-ation of musculoskeletal pain.

Originally, it was thought that they owed theirefficacy to their ability to cast out evil spirits, butthen it was considered that the effects might be dueto either the power of suggestion or distraction ofattention. It is only since the neurophysiology ofpain has become better understood that it is nowapparent that their analgesic effect lies in theirability to impart a noxious stimulus to the centralnervous system and by so doing to evoke activityin complex endogenous pain-modulating mecha-nisms. An effect which Melzack (1973) has termedhyperstimulation analgesia.

THE EARLY USE OF ELECTRICITY FOR THE COMBATING OF PAIN

The application of an electrical stimulus in orderto alleviate pain also has its origins in antiquity. AsThompson (1998) pointed out, stone carvings thatdate from the Egyptian Fifth Dynasty (circa 2500BC) show the electric fish (Malapterurus electri-cus) being employed for the treatment of painfuldisorders. And more than 2000 years later theancient Greeks made use of the electrical dischargethat emanates from the skate-like torpedo fish toalleviate headaches and arthralgias.

PRIMITIVE PAIN-SUPPRESSINGPROCEDURES

There is no doubt that man has always instinctivelyrealized that by applying a painful stimulus to thebody it is possible to dispel from it pain of a morepersistent nature. As Melzack & Wall (1982) havepointed out, every culture throughout the ageswould seem to have come to realize that brief mod-erate pain tends to abolish severe prolonged pain.

Cupping, a procedure in which a glass cup isheated and then held with its rim against the skin;and scarification, a procedure in which the skin iscut, often in several places, by a sharp instrumentsuch as, originally, a flint, thorn or fish bone, andthen eventually a knife, have from time immemor-ial been employed to induce bleeding in the beliefthat this would release from the body the devil orevil spirit responsible for some particular malady.In addition, however, because both these proced-ures happen to be acutely painful, they have alsobeen used to combat pain of a more persistent typesuch as that which may arise, for example, fromjoints, viscera and muscles.

Cauterization, a procedure in which intense heatis applied to an affected part of the body, has alsobeen employed since the dawn of civilization for avariety of reasons, including the control of haem-orrhage and the alleviation of pain. With respect to the latter it is interesting to find that in Tibet itwas at one time used to alleviate lumbago. Whenemployed for this purpose the treatment involvedproducing several blisters on the back by means ofapplying a red-hot branding iron to it. Next, conespacked with a mixture of sulphur and saltpetrewere placed on the blisters and then lit with a flam-ing torch. As Graham (1939) has commented, theresult must have been a girdle of burns deep enoughto banish any thought of afflictions as mild as lumbago!

A less horrific method of blistering the skin fortherapeutic purposes is the application of someirritant substance such as cantharides. This wascertainly employed by Hippocrates, and used exten-sively since his time, with, for example, WilliamWells, a physician at St Thomas’s Hospital in theearly part of the 19th century, applying it to theskin of the chest wall for the relief of pericardialpain (Baldry 1971).

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THE INTRODUCTION OFELECTROACUPUNCTURE FOR PAIN RELIEF

When in the middle of the 18th century Pieter vanMusschenbroek showed that it is possible to storeelectricity in what have come to be known asLeyden jars, the possibility of using electricity inthe treatment of disease was once again explored.It also happened to be about that time that Jesuitmissionaries, on returning from the Far East,brought news concerning the Chinese practice ofacupuncture to France, and Salandière (1825), whohad been taught how to use this form of treatmentby the physician son of the composer Berlioz,decided that rather than applying a noxious stimu-lus by means of manually manipulating needleshe would do so by passing a direct Galvanic cur-rent through them. It may be seen from his writ-ings on the subject that he employed this electricalform of acupuncture for the treatment of ‘la goutte,les rheumatismes, et les affections nerveuses’.

It was soon found, however, that this galvanicdirect type of current is liable to have undesirableelectrolytic effects leading, in some cases, to tissuenecrosis. It was because of this that Duchenne (1849),18 years after Faraday had introduced the use ofalternating currents, began to use a faradic type ofstimulus when employing electricity for therapeuticpurposes (Macdonald 1998).

Physicians during the 19th century, however,viewed electroacupuncture with considerable sus-picion, due to there being little or no understandingas to how it might work and also because by thattime all forms of electrical treatment had beenbrought into disrepute by charlatans using theminappropriately (Kane & Taub 1975).

Interest in its use was, nevertheless, eventuallyrekindled in the West once the Chinese, in themiddle of the 20th century, began to use what hascome to be known as acupuncture analgesia forthe purpose of suppressing surgically evoked pain.

ACUPUNCTURE ANALGESIA

In 1958 doctors at the First Shanghai Peoples’Hospital decided to try to alleviate severe post-tonsillectomy throat pain in one of their patientsby vigorously manipulating, by hand, a needleinserted into the first dorsal interosseous muscle.

They chose this point, known in the traditionalsystem of Chinese acupuncture as Hoku (some-times spelt Hegu) and also known as Large Intestine4 (see Fig. 15.11), as needle stimulation of it hadbeen used by the Chinese for centuries in the treat-ment of various painful disorders around the face.This was, however, the first time that any attempthad been made to suppress severe postoperativepain in this manner.

The procedure proved to be so effective thatthey next decided to use it on a patient immediatelyprior to the carrying out of a tonsillectomy in anattempt to suppress the pain caused by the oper-ation. This proved to be equally successful and oncea report of it was published acupuncture anaesthe-sia as it was initially called was soon being usedthroughout China (Macdonald 1982).

However, in order to suppress surgically evokedpain, peripheral nerve endings have to be stimu-lated very strongly for at least 20 min; it thereforesoon became apparent that to do this by means ofmanually manipulating needles is a very labori-ous process. Therefore, the Chinese decided toemploy electroacupuncture instead.

Although this procedure was initially referredto as acupuncture anaesthesia, it soon becameapparent that this was not a particularly appropri-ate term as it only suppresses pain and has noeffect on other sensations such as touch and tem-perature. For this reason it is now called acupunc-ture analgesia (AA).

How news about acupuncture analgesiareached the Western worldPeople in the West came to learn about the use ofAA for the suppression of surgically evoked painin China when people, principally from America,went there during the early 1970s.

Dimond in 1971 reported how during the courseof a visit to Beijing, he witnessed the techniquebeing used on a regular basis for the suppressionof pain evoked by a variety of operations, includ-ing dental extractions, thoracotomies and Caesar-ian sections. He also reported how he becameparticularly impressed by the seeming advantagesof this procedure when, on one occasion, he wit-nessed it being used whilst a thoracic surgeon

Neurophysiological pain-suppressing effects of acupuncture and TENS 111

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himself had a lobe of his lung removed. For notonly was the patient so unconcerned about theoperation that throughout it he talked animatedly,but at one stage he ate some fruit and at the endentered into a detailed discussion with those pre-sent concerning the pathological features of theresected lobe!

In 1972, no less a person than President Nixonvisited China on a goodwill mission and both heand his entourage were also shown the techniquebeing used to suppress surgically evoked pain.The President’s personal physician, Walter Tkach(1972), became so enthusiastic about what he sawthat on his return to America he immediately wrotea somewhat emotive six-page article entitled I HaveSeen Acupuncture Work in a widely read magazine.

It was not long after this that various leadingmembers of the medical profession in the Westernworld including Bonica (1974) from America andSmithers et al (1974) from Britain visited China tosee for themselves the technique being used.

Any initial enthusiasm such people in the Westmay have had for it must, however, have beenseverely strained when an article appeared in theDaily Telegraph in 1980 under the title China BurstsAcupuncture Bubble. In this Earnshaw (1980) regret-tably had to draw attention to a report that hadrecently appeared in the Shangai newspaper WenHui Bao revealing that during China’s cultural revo-lution doctors had been forced to use and patientshad been cajoled into receiving acupuncture priorto undergoing major surgery as a matter of politicalexpedience, regardless as to whether or not it waslikely to be effective. Furthermore, that when theprocedure, as so often happened, failed to provideadequate pain relief the patient was ordered not toscream but instead to shout out political slogans! Italso stated that any doctor who deliberately defiedofficial policy by employing some alternative formof anaesthesia took the risk of being denounced as acounter-revolutionary and punished. This depress-ing state of affairs according to Earnshaw was fur-ther compounded by those who wielded politicalpower publishing misleading reports concerningthe efficacy of the procedure.

It is only right to stress, however, that subse-quent to the revolution, doctors in China have doneeverything in their power to make amends for theshortcomings of their former masters by conducting

research into the various aspects of acupuncturewith the highest possible standards of integrityand, as will be seen, so far as the relief of pain isconcerned, have helped to place acupuncture on asound scientific basis.

Among the first to do this were Chiang and hisco-workers, who in 1973 provided scientific evi-dence that acupuncture has an analgesic effect byusing electrical dolorimetry to measure the painthreshold in normal adults before and after theinsertion of acupuncture needles. By this meansthey were able to show that treatment of this typecauses a significant elevation of the pain thresholdall over the body, but with this tending to be great-est in the segments into which needles had beeninserted. They also proved that the widespreadanalgesia produced by an acupuncture stimulus isnot due to some chemical agent being releasedlocally and then transported around the bodythrough the cardiovascular system, by showingthat its production is not interfered with byoccluding the blood supply to a limb above thesite to which the stimulus has been applied.

Evidence that acupuncture’s analgesic effect isdependant on an intact nervous system came fromthe Peking Medical College’s Research Group ofAcupuncture Anaesthesia (1973), who showed inexperiments on humans that the pain threshold isnot elevated should needles be inserted into tissuesaffected by a loss of sensation. Also, from Chang(1973) who showed that the pain threshold remainsunaffected should acupuncture be carried out at asite where a local anaesthetic has been injected.And demonstrated in experimental animals thatsectioning of the anterolateral tract of the spinalcord abolishes acupuncture’s analgesic effect.

It was also in 1973 that Chang reported havingcarried out even more sophisticated experimentson rats and rabbits. In these he recorded impulsesfrom single neurons in thalamic nuclei that hadbeen produced as a result of the application of apainful stimulus to an extremity. He showed thatinhibition of these impulses could be obtained bysqueezing the tendo Achilles and by electricallystimulating cutaneous nerves. Also, by insertingacupuncture needles into the body and that themost effective inhibition was obtained when thelatter was carried out in the same segment as the painful stimulus had been applied.


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One year later the Research Group of Acupunc-ture Anaesthesia at Peking Medical College (1974)produced crucially important evidence to showthat acupuncture analgesia (AA) may be associ-ated with the release of chemical substances intothe central nervous system by showing that the painthreshold in rabbits could be increased by infusinginto their brains cerebrospinal fluid obtained fromother rabbits who had been subjected to acupunc-ture stimulation.

Pioneer research into the neurophysiologyof acupuncture analgesiaIt was certainly extremely propitious that the evi-dence just referred to suggesting the possibility thatAA may be brought about by the release of chem-ical substances was published contemporaneouslywith the discovery firstly of opioid receptors andthen of opioid peptides in the body (see Ch. 6). Forit quickly occurred to many working in this particu-lar field of research that these peptides might bethe ones involved in its production.

Research into this possibility from the 1970sonwards was principally carried out by ProfessorHan and his colleagues at Beijing Medical Univer-sity in China, by Professor Pomeranz and his team at the University of Toronto in Canada andby Professors Besser & Rees, together with theirco-workers, at St Bartholomews Hospital inLondon, UK.

It was incidentally the studies carried out at thislatter hospital that did so much at that time to per-suade various members of the medical professionin Britain to look at acupuncture in a less suspi-cious manner than formerly and to start investi-gating the possibility of employing it clinically forthe alleviation of pain.

Included among these was myself, who, havingjust retired from my post as a hospital-basedphysician in the early 1980s, was so motivated bothby this research being carried out at my almamater and by the work on TrP acupuncture thatwas being conducted at that time by Dr AlexMacdonald at Charing Cross Hospital in Londonfor the alleviation of myofascial pain, as to lead me to spend the years that have since passed fur-ther investigating the use of acupuncture for anal-gesic purposes.

Studies involving the use of naloxone, an opioid peptide antagonist

When in 1974 Pomeranz and his team in Torontobegan to study the neural mechanisms involved in the development of AA, they induced it inawake mice by means of a 20-minutes application ofa low-frequency (4 Hz)/high-intensity electricallyapplied stimulus delivered through needles insertedinto the 1st dorsal interosseous muscle – the trad-itional Chinese Large Intestine 4 (Ho-Ku) point(Fig. 15.11). The AA was tested by measuring thelatency to squeak after applying heat to the nosesof these animals. Then, in order to establish whetheror not AA induced by this means is endogenousopioid peptide (EOP) mediated, Pomeranz & Chiu(1976) observed the effect of administering nalox-one, a specific opioid peptide antagonist. And it was as a result of this experiment that they had the distinction of being the first to confirmthat it is.

This was clearly a very significant discovery,but what was even more exciting was when Mayer et al (1977) confirmed 1 year later that whatPomeranz and his team had found in mice alsoapplied to humans. They did this by means of anexperiment showing that the analgesic effect ofacupuncture on electrically induced tooth pulppain in man is similarly reversed by naloxone.

Two years after this, the first clue as to whetheror not AA is invariably EOP-mediated was pro-vided by Sjölund & Eriksson (1979) when theyshowed that whilst both high-frequency (�100 Hz)low-intensity and low-frequency (�10 Hz) high-intensity electrical nerve stimulation alleviate pain,it is only the analgesia provided by the latter typeof stimulus that is reversed by naloxone.

The situation then became temporarily confusedwhen the following year Chapman et al (1980)reported their inability to reverse with naloxoneAA induced in healthy volunteers subjected toexperimentally inflicted dental pain. And when, 3 years later, by which time (see Ch. 6) it was knownthat stress alone is capable of bringing about therelease of EOPs, Chapman et al (1983) concludedthat any rise in either the cerebrospinal fluid orplasma EOP levels observed when EA is used ineither animal or human experiments, does notoccur as a direct result of the acupuncture itself


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but rather as a result of the stress associated withthe carrying out of these experiments.

Peets & Pomeranz (1987), however, were able torefute this by showing that AA induced both inanaesthetized and awake animals is similar.

When Han et al (1984), carried out experimentson rats given EA at stimulation frequencies of either2, 15 or 100 Hz through needles inserted bilaterallyinto traditional acupuncture points Stomach 36(Fig. 19.1) and Spleen 6 (Fig. 16.1), they found thatnaloxone (1 mg/kg) completely abolished theanalgesic effect of 2 Hz EA, partially reversed thatof 15 Hz EA and had no effect on that of 100 HzEA. They discovered that the reason for this is thatthe type of EOP released into the central nervoussystem (CNS) is dependant on the EA frequencyemployed, and that metenkephalin is liberated at2 Hz, dynorphin A at 100 Hz and a mixture ofenkephalins and dynorphins at 15 Hz. They alsocame to the conclusion that the dose of naloxoneneeded to block EA-induced AA varies accordingto the type of EOP released and therefore on thefrequency of the EA employed.

The basic reason for this variable ability ofnaloxone to block analgesia produced either bymorphine or EOPs is that all three of these sub-stances have different binding affinities for the mu,delta and kappa opioid receptors in the CNS. Bothmorphine and naloxone attach themselves princi-pally to mu receptors, met- and leu- enkephalins todelta receptors and dynorphins to kappa receptors(Bowsher 1987).

The lesson to be learnt from all this, as Han (1985)has pointed out, is that when attempting to showwhether or not the development of EA-induced AAis EOP-mediated, by means of observing whetheror not naloxone blocks the analgesia, it is essentialto take into consideration both the parameters ofthe EA stimulus employed and the dose of naloxoneadministered.

There have been at least 28 reports confirmingnaloxone blockade of AA and seven reports failingto observe this effect (Stux & Pomeranz 1987).

In view of the results of the experiments carriedout by Han et al (1984), it has become easier tounderstand the reasons for this disparity with it now being generally accepted that the EOP-mediated mechanism responsible for AA, both inhumans and animal studies, is best brought into

action with low-frequency/high-intensity stimu-lation. This accounts for four of the failed experi-ments, as the one carried out by Chapman et al(1983) involved the use of a low-frequency/low-intensity EA stimulus and the other three involvedthe employment of a high-frequency/low-inten-sity stimulus. And the reason why the other threefailed may be because naloxone appears to workbest when given before the treatment begins and isunable to reverse analgesia once it has alreadydeveloped (Pomeranz 1989). The implication ofthis is that EOP-mediated AA is not naloxonereversible as is so often stated but rather naloxonepreventable.

It has been shown that a microinjection ofnaloxone into sites in the spinal cord (Peets &Pomeranz 1985) and brain (Zhou et al 1981), whichcontain an abundance of opioid peptides and theirreceptors blocks the development of AA.

With reference to this, Zhou et al (1981, 1982,1984), in experiments on rabbits, have demon-strated that to block the effect of AA by more than70%, it only requires an injection of 1 �g of nalox-one into one or other of the following structures:the periaqueductal grey area of the midbrain, thenucleus accumbens, the amygdala in the limbicsystem and the habenular nucleus situated in thedorsomedial aspect of the thalamus. And that alsoit only requires a microinjection (5–10 �g) of mor-phine into any one of these four sites to producemarked analgesia.

These particular sites, therefore, are of consider-able importance with respect to EOP-mediated AAand will be referred to again when the long-termanalgesic effect of manual acupuncture carried outfor the alleviation of chronic pain is discussedbecause Han (1987) has put forward the sugges-tion it might be sustained activity in the so-calledmeso-limbic neural loop formed by them and thearcuate nucleus in the hypothalamus that may beone of the reasons for bringing this about.

Changes in endogenous opioid peptidecerebrospinal fluid levels in response to electroacupuncture

Evidence in support of EOPs having a role in theproduction of AA has also come from studies of


Chap-09.qxd 11*10*04 10:19 Page 114

EOP levels in the cerebrospinal fluid (CSF) ofpatients before and after EA.

In the first such study, Sjölund et al (1977) col-lected CSF from patients with chronic pain treatedwith EA-like transcutaneous nerve stimulationand measured CSF EOP levels before and aftertreatment. When they applied electrodes to thelumbar region of patients with low-back pain theyobserved that the CSF levels of these peptides haddoubled after 30 minutes of treatment. And that, incontrast to this, when they treated patients withface pain by stimulating in a similar manner theLarge Intestine 4 (Ho-Ku) traditional Chineseacupuncture point in the first dorsal interosseousmuscle of the hand (Fig. 15.11), no changes in thelumbar CSF EOP levels were observed. Thisclearly was because the stimulation was being carried out at a cervical segmental level ratherthan at a lumbar segmental one. It was unfortu-nate that in this particular study the CSF EOP lev-els were measured by receptor-binding assays, asthis did not reveal which EOPs in particular wereinvolved.

In contrast to this, Clement-Jones et al (1980), inthe studies carried out at St Bartholomews Hospital,London, specifically measured CSF concentrationsof beta-endorphin and metenkephalin by radioim-muneassay in a group of patients with recurrentpain before and after a 30 minutes application of low-frequency EA. And found that, although the concentrations of metenkephalin remainedunchanged, the beta-endorphin levels rose after thisparticular type of stimulation had been applied.

Morley (1985), however, has issued a warningthat care has to be taken in drawing conclusionsfrom measurements of CSF levels of EOPs, becausethe presence of these substances in the CSF is mostlikely to arise from overspill of neuronal activityand may, therefore, not necessarily reflect theirdegree of activity in neurons themselves.

This not withstanding, such measurementsbefore and after 20–30 minutes of low-frequency/high-intensity EA stimulation, and the results ofmost of the naloxone studies already discussed,make it reasonable to postulate that the analgesiceffect of this particular type of acupuncture isassociated with the activation of EOP-mediatedpain-modulating mechanisms in the central nerv-ous system.

Development of opioid peptide activity at three sites

It has been shown that low-frequency/high-intensity EA brings about its analgesic effect by therelease of EOPs at three sites, the dorsal horn, themidbrain and the hypothalamus/pituitary complex.

The dorsal horn An EA stimulus of this typeapplied to A-delta skin and Groups II & III musclesensory afferents causes enkephalin and dynor-phin to be released into the dorsal horn with, as aconsequence, the blocking of any nociceptive-generated information transmitted to it via C-polymodal skin and Group IV muscle sensoryafferents.

The midbrain In the midbrain it leads to therelease of enkephalin and this then activates theserotoninergic-mediated pain inhibitory systemthat descends from its periaqueductal grey areadown the dorsolateral funiculus to dorsal horns.

The hypothalamus/pituitary complex Here itcauses adrenocorticotrophic hormone (ACTH) tobe released from the anterior pituitary into the cir-culation. It is presumably because of the liberationof cortisol from the adrenal cortex as a conse-quence of a stimulus of this type that explains whyit would seem to have an anti-inflammatory effecton tissues in general and to act as a bronchodilator.

It also causes beta-endorphin to be released intothe hypothalamus and because the latter projectsto the midbrain the effect of this is to cause activityto develop in the pain inhibitory system thatdescends from there.

Augmentation of acupuncture analgesia (AA) by prevention of EOP degradation

It should be noted that the development of AAmay be enhanced by preventing EOPs from becom-ing degraded by the action of various enzymes forCheng & Pomeranz (1980) have observed that theadministration of the enzyme blockers D-leucineand D-phenylalamine augments the developmentof AAand that a combination of these D-aminoacidsand EA produces a greater amount of analgesiathan the latter alone.


Chap-09.qxd 11*10*04 10:19 Page 115

Comprehensive reviews

Space does not permit for all of the evidence insupport of EOP involvement in AA to be discussedhere and therefore those who wish to know moreabout this subject should consult recently pub-lished comprehensive reviews such as those pro-vided by Han (2001), Pomeranz (2001) and White(1998, 1999).

The role of serotonin (5-hydroxytryptamine) in the development of acupuncture analgesiaWhen acupuncture needles are inserted into musclesfor the purpose of bringing about the developmentof AA, the consequent needle-induced stimulationof A-delta skin and Groups II & III muscle sensoryafferents has several effects, including the creationof activity in the serotonin-mediated descendingpain inhibitory system situated in the dorsolateralfuniculus (see Ch. 6). And, therefore, in view ofthis, it is hardly surprising that the developmentof AA is now known to be influenced by alterationsin the central nervous system’s serotonin levels.

Han & Terenius (1982) state that those initiallyengaged in research into the various aspects of AAat the Peking Medical College, reported in 1975that para-chlorphenylalanine, a serotonin synthe-sis inhibitor, when injected into the lateral ventricleof the rabbit, inhibits its development. Followingthis McLennan et al (1977) found that cyprohepta-dine, a serotonin receptor antagonist also does this.Later, in 1979, Kin et al demonstrated that cianserin,another serotonin receptor blocker, has a similareffect in the cat.

Conversely, Han et al (1979) found that the intra-ventricular administration of 5-hydroxytryptophan,a serotonin precursor, enhances the production ofAA in the rat.

With respect to humans, Han & Terenius (1982)found that the administration of either clomi-pramine which blocks the re-uptake of serotonin,or pargyline, which blocks its degradation, aug-mented the effect of AA in patients who wereundergoing the removal of impacted molar teeth.

It should be noted in view of what has alreadybeen said with regard to the apparent importanceof the nucleus accumbens, the amygdala, the

habenula and the periaqueductal grey in the devel-opment of AA, that during the 1980s Han and hisco-workers published several papers showing thatanalgesia of this type is significantly attenuatedwhen cianserin, the serotonin receptor blocker ismicroinjected into any one of these four brainnuclei (Han 1989).

Zhang & Han (1985) have also shown that therelease of serotonin and its effect on the produc-tion of AA is the same no matter whether the EAis carried out employing either a high- or low-frequency current, and regardless as to whetherthe stimulus is of high or low intensity.

Finally, in view of all that has been discussed, itis hardly surprising to find (Han et al 1980, Zhouet al 1982) that the simultaneous interference withboth serotonin and EOP levels results in a dra-matic decrease or even complete abolition of anyanalgesia induced by EA.

TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION (TENS)

Although transcutaneous electrical nerve stimula-tion (TENS) has proved to be of considerable helpin relieving the pain present in a number of disor-ders, its place in the alleviation of musculoskeletalpain in general and of myofascial TrP pain in particular would seem to be strictly limited.Nevertheless, in view of this type of treatment’sclose relationship to electroacupuncture, its modeof action and the main indications for its use willbe briefly discussed.

Melzack & Wall (1965), as explained in Chapter 6,based their gate-control theory on the suppositionthat the stimulation of large diameter A-beta sen-sory afferents has the effect of blocking the trans-mission of noxious information generated in skinC-polymodal and muscle Group IV nociceptorswhen it reaches the dorsal horn via small diameternon-myelinated sensory afferents.

It was this hypothesis that led Wall & Sweet(1967) to conclude that because large diameter A-beta fibres have a lower electrical resistancethan small diameter C and Group IV do, it shouldbe possible to suppress the transmission alongthese latter fibres by electrically stimulating thelarger diameter ones – a deduction that led themto discover the pain-suppressing use of TENS.


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A form of therapy that over the years has come to be divided into two types: conventional andacupuncture-like.

Conventional TENS (Fig. 9.1)With this type A-beta sensory afferents are stimu-lated by passing a high-frequency (40–150 Hz),

low-intensity current between electrodes attachedto the skin overlying a nerve.

It is believed that a stimulus of this type releasesgamma-aminobutyric acid and that this inhibitoryneurotransmitter blocks the intra-dorsal transmis-sion of noxious information generated in C skinand Group IV muscle nociceptors (Thompson1989, 1998).


TNS

ACU

DCSA-beta

A-beta

A-delta

A-delta

C

C

I

IIIII

IVV

VI

VII

VIII

IXIX

XCC

I

II

IIIIV

VVI

Enlargementof Lamina II

TNSDC

DCS

ACU

Enk

GSG

Figure 9.1 Entry of primary afferentsinto the dorsal horn of the spinal cord,and circuits involved in TENS andacupuncture. Roman numerals refer tolaminae numbers. SG � Substantiagelatinosa cell. G � GABAergicinterneuron, presynaptically inhibitingprimary afferent C fibre terminal.Enk � Enkephalinergic interneuron,postsynaptically inhibiting substantiagelatinosa neuron. The enkephalinergicinterneuron is not only activated, asshown, by A-delta primary afferentterminals, but also by serotoninergicfibres descending from the brainstem(see Fig. 9.2). CC � Central canal.DC � Dorsal column. DCS � Dorsalcolumn stimulation. TNS � Low-threshold, high frequency stimulation.ACU � High-threshold, low frequencystimulation. Dr David Bowsher’sdiagram in Journal of British MedicalAcupuncture Society 1990. Reproducedwith permission.

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Acupuncture-like TENSWith this form of TENS a low-frequency (1–5 Hz),high-intensity current is employed, and becausethe analgesia produced by it is abolished by theopioid peptide antagonist naloxone, it is believedthat a current of this type, like acupuncture, muststimulate A-delta sensory afferents with the result-ant development of opioid peptide-mediated pain suppression. Unfortunately, a strongly appliedstimulus of this type is not well tolerated becauseof it giving rise to strong muscle contractions(Andersson et al 1976, Melzack 1975) and in orderto avoid this Eriksson et al (1979) have introducedan apparatus that allows trains of high- and low-frequency stimulation to be applied alternately.

Johnson et al (1991) have shown that it is onlypossible to decide which of these two forms of TENSbest alleviate any particular type of pain by tryingeach one in turn.

Indications for the use of conventional andacupuncture-like TENS

Well-conducted clinical trials carried out over theyears have provided support for TENS beingemployed for the suppression of a number of dif-ferent types of pain.

Orofacial pain The use of either high-frequencyor acupuncture-like TENS applied to the painfularea has been shown to have a pain-relieving effectin patients with a variety of different acute dentaldisorders such as pulpitis and apical periodontitis(Hansson & Ekblom 1983).

Angina pectoris Borjesson et al (1997), Chauhanet al (1994) and Mannheimer et al (1985) have alldemonstrated the usefulness of high-frequencyTENS in the alleviation of anginal pain.

Dysmenorrhoea There is good evidence to showthat high-frequency TENS is of value in suppress-ing painful menstruation (Dawood & Ramos 1990,Lundeberg et al 1985, Milson et al 1994).

Peripheral neuropathic pain Several studies havedemonstrated that TENS has an important placein helping to alleviate the pain in some but not allpatients suffering from a peripheral neuropathy(Fishbain et al 1996, Meyler & De Jongste 1994).

The presence of tactile allodynia complicates itsemployment for this purpose due to the pressureof the pads inducing pain when they are firstapplied (Hansson & Lundeberg 1999). It shouldalso be noted that with any disorder, such as post-herpetic neuralgia, where there is damage to A-betafibres, it is essential for the electrodes to be placedabove the affected site.

Postoperative and labour pain It was for longthought that TENS had a place in the alleviation ofpostoperative pain, but a systematic review ofcontrolled trials refutes this (Carroll et al 1996).

Similarly it has been widely used for the sup-pression of labour pain, but again an extensivereview of controlled trials has failed to provide sup-port for this (Carroll et al 1997).

Musculoskeletal pain The results of trials todetermine the usefulness of TENS in the treatmentof chronic low-back pain (Deyo et al 1990) and ofacute low-back pain (Herman et al 1994) suggestthat it may have a place in the suppression of mus-culoskeletal pain but the non-specificity of thediagnoses in these two studies makes it difficult tocome to any firm conclusion about this.

Graff-Radford et al (1989), on the other hand,have shown that treatment of this type is capableof alleviating pain that emanates from MTrPs and,therefore, there is a place for using it for that specificpurpose when, as occasionally happens, repeateddry needling carried out at MTrP sites fails to affordany long-term relief.

TENS – analgesia toleranceA serious disadvantage of TENS is that any painrelief obtained with it invariably disappears within30 minutes of the stimulus being discontinued, sothat the treatment has to be applied for severalhours a day. And, even worse, over the course oftime, there is liable to be a declining response to it,a phenomenon Johnson et al (1991) have calledTENS analgesia tolerance.

Comprehensive reviews of all aspects of thisform of treatment have been provided by Thompson(1986, 1994, 1998).

THERAPEUTIC ACUPUNCTURE

Felix Mann (1974), during the course of discussingacupuncture analgesia, a procedure in which a


Chap-09.qxd 11*10*04 10:19 Page 118

very strong needle-evoked nerve stimulus isapplied, usually electrically, for up to 20 minutes inorder to obtain immediate short-term suppressionof surgically induced acute pain, was the first todraw attention to the marked differences betweenthe carrying out of that and of acupunctureemployed therapeutically for the relief of symp-toms of one type or another. Because, as he saidtherapeutic acupuncture is one in which a verymuch lighter needle-evoked nerve stimulus isbriefly applied, usually manually, at approximately7-day intervals, and one that with respect to chronicpain is capable, following successive treatments,of providing gradually increasing long periods ofrelief.

The difference in the state of nerveendings at traditional Chinese acupuncture points and at MTrPsAlthough Melzack et al (1977) showed that tradi-tional Chinese acupuncture points (TCAPs) andmyofascial trigger points (MTrPs) have a veryclose spatial relationship, the important differenceis that a TCAP is only slightly tender due to thenerve endings at such a site being in a quiescentstate, but a MTrP is exquisitely tender because ofthe nerve endings there having become activatedand sensitized for one reason or another, with thecommonest being the subjection of the musclecontaining it to trauma (Ch. 7). This differenceconcerning the state of the nerve endings at thesetwo types of points is of considerable importancebecause, when employing manual acupuncture at a TCAP site for the purpose of suppressingchronic pain, the stimulus applied invariably hasto be a relatively strong one. In contrast to this,when employing MA at a MTrP site for the specificpurpose of alleviating myofascial pain, it is usu-ally only necessary to apply a light one.

Superficial and deep dry needling for thedeactivation of MTrPsWhen treating the MTrP pain syndrome there aregrounds for believing, as discussed in the nextchapter, that manually applied superficial dry

needling (SDN) with needles inserted to a depth of 5–10 mm at MTrP sites should mainly be usedand that deep dry needling (DDN) should bereserved for the minority of cases where MTrPactivity develops as a secondary event such as, forexample, because of an underlying radiculopathy.The neurophysiological mechanisms involvedduring the carrying out of SDN will, therefore,first be considered.

Superficial dry needling’s pain-suppressingmechanisms (Figs 9.1, 9.2)

When SDN is carried out at a MTrP site it is usu-ally only the A-delta sensory afferents that arestimulated for the C-polymodal ones would onlybe recruited should the stimulus applied happento be an exceptionally vigorous and prolongedone. Attention will, therefore, be focussed on whatis known to happen when A-delta fibres are sub-jected to needle-evoked stimulation.

Bowsher (1998), in an extremely comprehensiveand authoritative review of the mechanisms ofacupuncture when employed for the alleviation ofchronic pain, has given a detailed account of theeffects of stimulating A-delta nerve fibres.

As he states, Kumazawa & Perl (1978) haveshown that A-delta nerve fibres in the primateproject principally to Waldeyer cells situated in themost superficial zone (Lamina I) of the spinalcord’s dorsal horn.

Between Lamina I and II there are very small‘stalked’ cells whose presence in the cat was firstdemonstrated by Bennett et al (1982) and in manby Abdel-Maguid & Bowsher (1984). Stalked cellsreceive a direct input from A-delta fibres (Gobel et al 1980) and the effect of stimulating sensoryafferents of this type with a needle is to cause these cells to release the inhibitory opioid peptideenkephalin (Ruda et al 1984). This in turn theninhibits activity in the substantia gelatinosa cellsto which small unmyelinated sensory afferent fibres,such as those connected to MTrP’s Group IV noci-ceptors project. And as a consequence, the input to the dorsal horn of noxious information gener-ated in a MTrP’s Group IV nociceptors becomesblocked.

The intra-dorsal-horn flow of this information isalso interrupted as a result of manual acupuncture-evoked stimulation of A-delta fibres also having


Chap-09.qxd 11*10*04 10:19 Page 119

an inhibitory effect on wide dynamic range trans-mission neurons (Hashimoto & Aikawa 1993).

Indirect development of pain-suppressingactivity in the serotonergic, noradrenergic anddiffuse noxious inhibitory systems

Stimulation of A-delta nerve fibres such as whenSDN is carried out brings about pain suppressionbecause of it causing local activity to develop inand around Waldeyer cells in the dorsal horn’sLamina I, where these sensory afferents princi-pally terminate. In addition, pain suppressionoccurs because cells in this lamina, as discussed atsome length in Chapter 6, have projections to theperiaqueductal grey area in the midbrain at theupper end of the serotonergic-mediated descend-ing pain inhibitory system, to the locus coeruleusin the pons at the upper end of the noradrenergic-mediated descending pain inhibitory system and

to the subnucleus reticularis dorsalis in themedulla at the upper end of the diffuse noxiousinhibitory control system.

Segmental versus non-segmental acupuncture

Should a needle be inserted anywhere in the bodythe above three descending pain-suppressing sys-tems will be brought into action. It is clearly, how-ever, far better to carry out acupuncture at thesame segmental level as any noxiously generatedinformation enters the spinal cord, as this activatesnot only these three systems, but also the powerfuldorsal horn-situated opioid peptide-mediated one.

It is for this reason, as will again be discussed inChapter 10, that when carrying out SDN for thealleviation of MTrP pain, it is necessary to care-fully identify the exact position of each MTrP andthen to take care to insert a needle into the tissuesat that specific site.


To thalamus

Collateral

DISin

DLF

NST

C

A-delta

CT

II

II

III

I

IV

V

Figure 9.2 Diagram of dorsal horn to show the local intraspinal connection between A-delta nerve fibres and enkepha-linergic inhibitory interneuron (II), whose function it is to inhibit activity in C afferent terminal cell (CT). Also, to show theindirect A-delta link with inhibitory interneuron via the collateral connecting the A-delta afferent’s ascending pathway –the neospinothalamic tract (NST) with the descending inhibitory system in the dorsolateral funiculus (DIS in DLF).

Chap-09.qxd 11*10*04 10:19 Page 120

Deep dry needling’s pain-suppressingmechanismsAs will be explained in the next chapter, should astronger stimulus be required, such as, for example,may happen when MTrP activity arises secondaryto the development of a radiculopathy, DDN shouldbe employed.

During the carrying out of this procedure A-delta nerve stimulation must take place as aresult of the needle passing through the skin andsubcutaneous tissues with, as a consequence, all of the pain-suppressing mechanisms just dis-cussed being brought into action. Then, once theneedle enters the substance of the muscle not only are Group II and III afferents stimulated, but also, should the needle be rapidly inserted into a MTrP itself, a local twitch response (LTR) is evoked.

Chu (1995) has postulated that the productionof this response and the consequent changes in thelengths of muscle fibres brought about by it leadsto the setting up of a large diameter sensory affer-ent proprioceptive input to the spinal cord which,by virtue of this having a ‘gate- controlling’ effect,causes blocking of the intra-dorsal horn passage of noxious information generated in the MTrP’snociceptors.

Although this may be one of the mechanismsinvolved, it would seem that there must also be anEOP-mediated one because Fine et al (1988) haveshown that when a needle (together with a smallamount of bupivacaine to suppress the discomfortof this procedure – see Ch. 10) is inserted into aMTrP, any alleviation of myofascial pain that maybe brought about by this procedure is reversed bythe opioid antagonist naloxone.

CHALLENGE TO CONVENTIONAL VIEWSCONCERNING PAIN-RELIEVINGMECHANISMS BROUGHT INTO ACTION BYTHERAPEUTIC MANUAL ACUPUNCTURE

Carlsson (2000, 2002 a, b) has compellingly chal-lenged the currently held views concerning thera-peutic acupuncture’s pain relieving mechanisms.

His grounds for doing so are because the widelyaccepted modus operandi is only capable of offeringan explanation for very short-term pain relief by

virtue of it relying on gate-control mechanisms,which only exert their effect during the time thestimulation is being applied and on descendinginhibitory systems, which, he suggests, are unlikelyto function for more than about 8 hours.

As he explains, because the gate-control anddescending inhibitory mechanisms are so ephe-meral, the conventional model cannot account forthe following widely recognized clinical observa-tions: (1) that the pain relief often lasts for daysafter a single treatment, (2) that the pain relief issometimes delayed for 1–2 days, (3) that the pain is sometimes worse for some days following


A

HNA

PAG

NRM

DLF

DH

Figure 9.3 Han’s proposed mesolimbic loop of analgesia –A neuronal circuit involving the nucleus accumbens (NA),the amygdala (A), the habenula (H) and the upper parts ofthe descending inhibitory system, the periaqueductal grey(PAG) and nucleus raphe magnus (NRM), which areconnected to the dorsal horn (DH) by the dorsolateralfuniculus (DLF).

Chap-09.qxd 11*10*04 10:19 Page 121

treatment and then starts to improve, and (4) thatthere is often a cumulative pain-relieving effectwith increasingly long periods of pain relief beingobtained in response to successive treatments.

In the light of all this he concludes that the cur-rently accepted neurophysiological model is onlycapable of providing an explanation for short-termacupuncture analgesia but not for the long-termpain relief afforded by therapeutic acupuncture.

An alternative mechanism put forward by himto explain the latter is the induction of peripheralevents that might improve tissue function andinduce local pain relief. These include the anti-inflammatory action of neuropeptides like calcitoningene-related peptide; the local release of endorphins;the induction of segmental mechanisms including

long-term depression of A-delta fibre-evoked exci-tatory potentials in the dorsal horn (Sandkuhler2000, Sandkuhler & Randic 1997). Also, the bring-ing into action of central mechanisms includingsympathetic inhibition with a consequent decreasein levels of plasma epinephrine (adrenaline) andcortisone; and possibly the release of oxytocin asthis is believed to induce long-term pain thresholdelevations and to have effects of an anti-stressnature (Uvnäs-Moberg 2002).

Other mechanisms to account for the sustainedanalgesic effect of therapeutic acupuncture dis-cussed by White (1999) include Han et al’s pro-posed mesolimbic loop (Fig. 9.3) and the inductionof mRNA for opioid peptide expression (Guo et al1996).


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127

Chapter 10

Treatment of myofascial triggerpoint pain and fibromyalgiasyndromes

CHAPTER CONTENTS

Introduction 127‘Wet’ needling MTrP deactivating

techniques 128–130Systematic review of ‘wet’ and ‘dry’ needling

clinical trials 131Deep dry needling MTrP deactivating

techniques 131–132Superficially applied MTrP deactivating

techniques including:Vapocoolant spray to skin 132Intradermal and subcutaneous injections of

water and saline 132Superficial dry needling at MTrP sites 132–134Japanese shallow needling 135

Complications of acupunture 135–136Physiological reactions to needling 136–137Post-needling measures to prevent MTrP

reactivation 137–142Treatment of fibromyalgia syndrome 141–146Training required to carry out dry needling

techniques at TrP and TP sites 145

INTRODUCTION

In the first part of this chapter the various methodsavailable for the deactivation of myofascial triggerpoints (MTrPs) will be reviewed.

These include injection either into MTrPs themselves or into the tissues around them of such disparate substances as local anaesthetics, corti-costeroids, non-steroidal anti-inflammatory drugs,botulinum toxin, physiological saline and evenwater alone!

Evidence will be provided to show that all ofthese forms of treatment, which are now often col-lectively referred to as ‘wet’ needling procedures,owe their MTrP pain-relieving effect to one factor,namely the stimulation of nerve endings by theneedle employed to inject them.

Reasons will be given for concluding that these‘wet’ needling procedures have no advantages over,and many disadvantages compared to the employ-ment of ‘dry’ needling ones. In view of this, attentionwill be focussed in particular on the two acupunc-ture (acus (L)-needle) procedures, called superficialdry needling (SDN) and deep dry needling (DDN)that are now widely used for the deactivation ofMTrPs. The measures that sometimes have to betaken to prevent the reactivation of these pointswill also be outlined.

In the second part of this chapter, the variousforms of therapy that are currently being employedin the management of fibromyalgia will be dis-cussed, including the carrying out of needling attender and TrP sites.

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area, pepper region by moving it in and out ofmuscle, injecting 1–2 cc continuously.

Use 0.25 to 0.5% procaine hydrochloride inphysiological saline (unless history of procaineallergy).

Use a sharp 22–24 gauge needle, 1–3 in long,depending on site of trigger area.

Apply haemostasis promptly.Check success of injection. If trigger area is

still tender, reinfiltrate at different depths andangles.

Hong’s modification of Travell’s technique

Travell’s procedure just described has in recentyears been modified by Hong (1994a) as a result ofhim finding that when a needle is rapidly insertedinto different parts of a MTrP it is possible to evokea succession of local twitch responses. He concludedfrom this that a MTrP must be made up of a num-ber of separate loci and that, in order for it to besatisfactorily deactivated, each locus has to be pene-trated in turn.

In order to avoid damaging the muscle whilstdoing this, Hong advises pushing the needle in and out of the MTrP at the very fast speed of100–200 mm/s. A manoeuvre of this type clearlydemands much manual dexterity. Furthermore, itinevitably causes much bleeding into the tissueswith, because of this, an appreciable amount ofpost-treatment soreness.

Hong (1994b) has carried out a trial to comparethe MTrP pain-relieving effectiveness of either usinga needle alone or of injecting a local anaestheticthrough it and from the results of this concludedthat the latter is preferable.

Hong’s method of deactivating MTrPs is nowmuch used (Simons et al 1999), but despite the useof a local anaesthetic the repeated insertion of aneedle into each TrP causes a considerable amountof pain; also, much bleeding with, as a conse-quence, the development of post-treatment sore-ness. Furthermore, there is at present no evidenceto show that the results obtained with it in allevi-ating pain arising as a result of the primary acti-vation of MTrPs are any better than those obtainedwith the far simpler and very much less painfulsuperficial dry needling technique advocated laterin this chapter.

‘WET’ NEEDLING MTrP DEACTIVATINGTECHNIQUES

Injection of a local anaesthetic into MTrPsAs already discussed in Chapter 4, when duringthe 1930s John Kellgren found that pain in the dis-order he called myalgia emanates from points thathave since come to be called MTrPs, he alleviatedit by injecting a 1% solution of procaine (novocain)into each of them in turn.

He presumably employed a local anaestheticbecause of its nerve blocking effect. Yet, althoughthe latter only lasts for some hours he found it waspossible to obtain pain suppression for at least 24hours and often for even longer. Such prolongedperiods of relief, therefore, could not have beendue to the action of the local anaesthetic but, withhindsight, must have been due to the bringing intoaction of the various needle-evoked pain suppress-ing mechanisms discussed at some length in thelast chapter. Thus, although Kellgren did not realizeit at the time, his observations in retrospect servedto re-affirm what physicians like Churchill and SirWilliam Osler in the latter part of the 19th centuryand Sun Ssu-mo in the 6th century had discoveredconcerning the pain-alleviating effect of insertingneedles into points of maximal tenderness.

With respect to all this it has to be said that JanetTravell, the American physician, who from the1940s onwards, took over the study of MTrP painfrom where Kellgren left off, was quick to realizethat the prolonged analgesia produced by inject-ing a local anaesthetic into a MTrP could equallywell be attained by simply inserting a needle intoit (Travell & Rinzler 1952). On finding, however,that a needle on entering a MTrP gives rise to anunacceptable amount of acute pain, she decided tocontinue to inject a small amount of procaine(0.25%) through it in order to suppress this treat-ment evoked discomfort.

Her method of carrying out the procedure wassuccinctly described in a classic paper entitled ‘TheMyofascial Genesis of Pain’ (Travell & Rinzler 1952)as follows:

By pressing on trigger area, demonstrate painreference to patient.

Ask patient to announce when pain radiation isfelt during infiltration. When needle hits trigger

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Injection of normal saline into MTrPsBecause a local anaesthetic may at times give riseto undesirable side-effects the American physicianAnders Sola decided during the 1950s to seewhether it is possible to deactivate a MTrP byinjecting normal saline into it.

From a trial on 100 consecutive patients withneck and shoulder MTrP pain Sola & Kuitert (1955)came to the conclusion that ‘the use of normalsaline has none of the disadvantages often associ-ated with the use of a local anaesthetic but appearsto have the same therapeutic value’.

One year later Sola & Williams (1956) reportedsimilarly good results from treatment in the sameway of 1000 patients with MTrP pain in variousparts of the body.

Interestingly enough, it does not seem to haveoccurred to them that the effectiveness of this typeof treatment might have been due to the effect of theneedle itself rather than to that of injecting isotonicsaline.

Unlike them Frost et al (1980) clearly thought thatphysiological saline was unlikely to have any spe-cific pain relieving effect because, when carryingout a trial to assess the efficacy of injecting the long-acting local anaesthetic mepivacaine into MTrPspresent in 28 patients in an active treatment group,they injected normal saline into the MTrPs of 25patients in a control group. They were therefore atfirst somewhat surprised to find that 76% in the‘control’ group and only 57% in the ‘treatment’group had pain relief. A result, however, which onrefection led them to conclude:

… the more favourable effect of physiologicalsaline may be due to the longer duration of irri-tation since nerve impulses are not blocked bysaline … the study therefore raises questionsabout the mechanism by which local injectionsinto muscles relieve pain, since there is a possibil-ity that a similar effect might also be achieved bymerely inserting a needle into a trigger point. …

Support for this belief has come from three fur-ther trials comparing the pain-relieving effect ofsaline with that of a local anaesthetic.

Tfelt-Hansen et al (1981), injected either lidocaine(lignocaine) or normal saline into tender points oftwo groups of patients with migraine and showed,

according to the patients’ assessments using visualanalogue scales, that both were equally effective.

Tschopp & Gysin (1996), in patients with MTrPspain in the head and neck regions, compared thepain-relieving effectiveness of injecting lidocaine(lignocaine) into MTrPs in one group of patients,the longer-acting local anaesthetic bupivicaine intothem in a second group and saline into them in athird group. Subjective assessments by the patientsled to the conclusion that all three substances are ofequal efficacy.

McMillan et al (1997) divided patients withcraniofacial MTrP pain into three groups. One groupwas treated by having both procaine injected intotheir MTrPs, plus the carrying out of superficialdry needling at these sites. A second group had dryneedling of their MTrPs plus injection of salineinto the superficial tissues at these sites. And athird group had a superficial injection of saline andsuperficial dry needling at their MTrP sites. Allthree groups had similarly significant pain relief asjudged by a variety of tests including the use ofvisual analogue scales and algometers.

Injections of steroidal and non-steroidalanti-inflammatory drugs into MTrPsAlthough histological examination of tissues atMTrP sites have never shown any evidence of aninflammatory lesion, trials have, nevertheless, beencarried out to assess the value of injecting either anon-steroidal anti-inflammatory drug (NSAID) ora steroid into MTrPs. This having been said, it hasto be admitted that NSAIDs have an inhibitoryeffect on cyclooxygenase and as a result depressthe production of prostaglandins that assist in sen-sitizing MTrPs’ nociceptors.

Frost (1986), in patients with myofascial pain inthe neck, shoulder or lower back, compared theeffect of injecting the NSAID diclofenac into MTrPsin one group of patients with that of injecting lido-caine (lignocaine) into points of this type in anothergroup. From an assessment employing visual ana-logue scales the pain relief in both groups wasequally good.

Drewes et al (1993) have carried out a study tocompare the effectiveness of relieving myofascialpain from injecting either diclofenac or pred-nisolone into MTrPs. Both forms of treatment

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proved to be equally effective with 84% of patientsin the two groups being significantly improved asjudged by verbal pain questionnaires and a phys-ician’s evaluation.

The possibility, however, cannot be excludedthat the pain relief in both groups was due to theone factor common to both namely the effect ofinserting a needle into the MTrPs. Moreover, aswas pointed out by those carrying out the trial, theuse of these drugs is not without risks. Diclofenac,particularly if injected into the superficial tissues,is liable to cause necrosis of the skin. And therepeated injection of a steroid drug into a muscle is liable to result in its fibres becoming damaged.Also, when given more superficially it is liable tocause the skin to become pitted and depigmented.For these reasons alone the injection into MTrPs ofeither a non-steroidal anti-inflammatory drug or acorticosteroid as advocated by Bourne (1979, 1984)cannot be recommended.

Despite this there have been two other cortico-steroid trials.

Frost et al (1984), divided patients with chronicmyofascial pain into three groups and over a periodof 6–12 days treated them on three occasions asfollows. One group was given injections of isotonicsaline (8 ml) into MTrPs, a second group, injectionsof isotonic saline (2 ml) into MTrPs, and a thirdgroup injections of isotonic saline (1 ml) plus pred-nisolone (1 ml) into points of this type. As judgedby visual analogue scales all three groups didequally well with overall 84% of the patients stillobtaining some relief 2 months after the treatmentshad finished.

Garvey et al (1989) divided patients with myofas-cial low back pain into three groups. They injected1.5 ml of 1% lidocaine (lignocaine) into MTrPs inone group; 0.75 ml of 1% lidocaine (lignocaine)plus a corticosteroid (Aristospan) into MTrPs in asecond group; and inserted needles into MTrPs ina third group. From information obtained withpain scales they concluded that there was no sig-nificant difference in the pain-alleviating effect ofthese three forms of treatment.

The results of these two trials, therefore, con-firmed what had already been established, thatthere is no advantage to be obtained from the use ofa corticosteroid drug when deactivating MTrPs. AsTravell & Simons (1983) have pointed out, the only justification for the employment of a steroid

injection so far as the management of musculo-skeletal pain disorders is concerned is in the treat-ment of an inflammatory lesion such as a rotatorcuff tendinitis or lateral epicondylitis.

Injection of botulinum A toxin into MTrPsTsui et al (1986), because of botulinum A toxin’sability to relax muscle when injected into it, suc-cessfully used this toxin for the treatment of spas-modic torticollis.

Cheshire et al (1994) then decided in view ofthis to see whether it had any place in the treatmentof MTrP pain. And on comparing the effect of nor-mal saline with that of this toxin in six patients withmyofascial pain found that four of them obtainedbenefit from the toxin.

Following this, Yue (1995) carried out a retro-spective study of 112 patients who had had thissubstance injected into MTrPs and found that 86%of them reported having been helped, with an aver-age pain reduction of 36.5%. Seventeen per cent ofthe patients, however, complained of moderate tosevere side-effects, with the commonest of thesebeing muscle weakness sufficient to impair motorfunctions and the eventual onset of muscle atrophy.

Since then Wheeler et al (1988) have dividedpatients with refractory cervicothoracic paraspinalmyofascial pain into three groups and injected intotheir MTrPs either botulinum toxin (50 units in 2 mlof normal saline); botulinum toxin (100 units in 2 mlof normal saline): or 2 ml of normal saline alone.The effectiveness of the three treatments as judgedby subjective assessments made by the patientswas equally good and thus showed that the painalleviation in all three groups was primarily due tothe one factor they had in common, namely theapplication of a needle-evoked nerve stimulus.

In view of this and because of the side-effects ofthis toxin, contrary to what Lang (2002) has had tosay on the matter, there would seem to be no placefor its use in the routine treatment of MTrP pain.

It is, nevertheless, extremely interesting to findthat this substance, which is know to block therelease of acetycholine from motor nerve termin-als at neuromuscular junctions, has the ability todeactivates MTrP for, as Simons (1996) has said,this is a ‘strong indicator that the MTrP mechanismis intimately associated with the neuromuscularjunction’.


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SYSTEMATIC REVIEW OF ‘WET’ AND ‘DRY’ NEEDLING CLINICAL TRIALS

Cummings & White (2001) have carried out anextremely valuable systematic review of all therandomized controlled trials in which the treatmentof myofascial pain has involved the use of either‘wet’ needling or ‘dry’ needling. Some of these trialsare referred to in this chapter and others will be discussed in Chapter 11 when the evaluation ofacupuncture’s ability to relieve nociceptive pain ingeneral will be considered.

Their search led them to state: ‘The principalfindings of this review are that, when treating myo-fascial pain with TrP injections, the nature of theinjected substance makes no difference to the out-come, and that wet needling is not therapeuticallysuperior to dry needling.

Thus they, as a result of meticulously analysingthe results of clinical trials carried out during thelatter part of the 20th century, have now confirmedwhat Sir William Osler (1909) at the beginning of itintuitively concluded from his own clinical obser-vations, that in order to alleviate what is currentlycalled myofascial pain it is necessary to do no morethan simply stimulate nerve endings at points ofmaximum tenderness with a needle!

Deep dry needling MTrP deactivatingtechniquesThe person who during the latter part of the 20thcentury pioneered the use of deep dry needling(DDN) at MTrP sites was the Czech physician KarelLewit. He, unlike Travell & Rinzler (1952), was not deterred by it being a painful procedure, on thecontrary, in his paper on the subject (Lewit 1979)entitled ‘The Needle Effect in the Relief of Pain’ hestated that ‘the effectiveness of the treatment isrelated to the intensity of pain produced at the trig-ger zone and to the precision with which the site ofmaximum tenderness is located by the needle’.

In this paper he reported the results of treating241 patients with pain emanating from what hevariously called trigger zones, pain spots and sitesof maximal tenderness by means of inserting dryneedles into these points. He called the immediateanalgesia produced by this procedure ‘the needleeffect’. He also reported having obtained it in 86.8%of the patients. A finding that led him to state that

‘the pain relieving effect previously ascribed tolocal anaesthetics may in fact be due to needling’.He thus had come to the same conclusion as hadbeen reached by Travell & Rinzler 30 years earlier.

Chen Gunn (1989, 1996, 1998), a physician work-ing in Vancouver, has since then written extensivelyin support of the use of DDN. He calls his particu-lar technique ‘intramuscular stimulation’ (IMS).When employing it he inserts a needle deep into thebelly of a muscle, but unlike Lewit, does not believeit is necessary to penetrate the MTrPs themselves.

His method is widely used, but one of its maindisadvantages is that it is a very painful procedure,with he himself (Gunn 1989) stating that when aneedle is inserted into a tightly contracted band ofmuscle the ‘patient experiences a peculiar cramp-like sensation as the needle is grasped … the inten-sity of the cramp parallels that of the spasm: it canbe excruciatingly painful, but gradually resolvesas the spasm eases’. He also points out that thespasm is frequently so prolonged and the needle,because of this, so firmly grasped that it is often10–30 minutes before it can be released.

This notwithstanding he employs this particu-lar type of DDN routinely in all patients sufferingfrom MTrP pain.

Jennifer Chu, on the other hand, uses a form of DDN specifically for the alleviation of MTrPpain that arises as a secondary event following the development of either a cervical (Chu 1997) orlumbar (Chu 1999) radiculopathy.

Chu, like Hong (see p. 128), is of the opinion,that for the best results, the needle should berepeatedly inserted into various parts of an MTrPfor the purpose of evoking a succession of localtwitch responses. A procedure she calls twitch-obtaining intramuscular stimulation (TOIMS).

DisadvantagesDDN is not only extremely painful but is also liableto cause damage to nerves, blood vessels and otherstructures.

For these reasons and because experience has ledme to believe that for the purpose of deactivatinga primarily activated MTrP superficial dry needling(SDN) is not only just as effective, but far simpler tocarry out and much less likely to cause tissue dam-age, my personal preference (Baldry 2002b) is to


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employ SDN for the vast majority of my patientswith MTrP pain and to reserve DDN for the smallnumber of them in which MTrP actively arises sec-ondary to the development of a radiculopathy.

SUPERFICIALLY APPLIED MTrPDEACTIVATING TECHNIQUES

The application of a vapocoolant spray to the skinTravell & Rinzler (1952) found that they coulddeactivate MTrPs by spraying the local anaestheticethyl chloride across the skin overlying them whilstat the same time stretching the affected muscle.This substance, however, is potentially explosiveand, therefore, Travell (1968) eventually employedinstead the safer alternative fluori-methane, a mix-ture of two fluorocarbons.

Those who have since given detailed accountsof the indications for and the manner of carryingout this muscle stretch and spray technique includeRachlin (1994) and Travell & Simons (1983).

The present position however is that, whilststretching the muscles after deactivating TrPs inthem is still considered to be of considerableimportance, the application of a vapocoolant is notany longer widely employed.

THE INJECTION OF WATERINTRADERMALLY AT MTrP SITES

Byrn et al (1991), in a preliminary uncontrolled trialcarried out in Gothenburg, Sweden, found thatinjecting sterile water into the skin overlying activeMTrPs in the necks of patients suffering fromwhiplash injuries relieved the pain emanatingfrom them for appreciable periods of time.

Subcutaneous injections of either water or normal saline at MTrP sitesUnfortunately water injected into the skin givesrise to an intense and extremely distressing burningsensation. Therefore, Byrn et al (1993), in a muchlarger trial, decided to compare the effectivenessof injecting either sterile water or isotonic saline(0.3–0.5 ml) into the subcutaneous tissues over-lying active TrPs present in the neck muscles ofpatients with whiplash injuries.

Their conclusion was that of the two, waterinjected into the subcutaneous tissues at MTrPssites gives most pain relief and for this reason havesince continued to use it extensively.

The one considerable disadvantage, however, is that water, when injected into the subcutaneoustissues, like when injected into the skin, gives rise to an intense burning sensation similar to thatcaused by a wasp sting.

Wreje & Brorsson (1995) found this when carry-ing out a multicentre randomized controlled trialto compare the effectiveness of combined subcuta-neous and intracutaneous injections of either ster-ile water or physiological saline at MTrP sites forchronic myofascial pain. For this reason its use forthis particular purpose is unlikely to be widelyadopted.

SUPERFICIAL DRY NEEDLING AT MTrP SITES

Initially it was my practice to use DDN for thedeactivation of MTrPs until the early 1980s when apatient was referred to me with pain down the armfrom a TrP in the scalenus anterior muscle. In viewof the proximity of the lung it was considered wisernot to push the needle into the MTrP itself butrather to insert it more superficially into the tissuesimmediately overlying it. This proved to be allthat was required for after leaving the needle insitu for a short time and then withdrawing it theexquisite tenderness at the MTrP site was found tohave been abolished and the spontaneous occur-ring pain alleviated.

This superficial dry needling (SDN) techniquewas then used to deactivate TrPs elsewhere in thebody where it proved to be equally effective evenwhen the muscles containing them were deep lying.Another interesting observation was that any pal-pable bands found to be present at the MTrP sitesbefore such treatment disappeared after it.

At about the same time Macdonald et al (1983)confirmed the efficacy of SDN in alleviating painarising from MTrPs in the lumbar region by meansof a trial carried out at Charing Cross Hospital,London, UK. In this study 17 consecutive patientswith chronic lumbar MTrP were divided into twogroups. One group was treated by means of SDN,with the needles inserted to a depth of 4 mm at


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MTrP sites. And a control group was treated byhaving electrodes applied to the skin overlyingMTrPs connected by non-current carrying wires toa purposely impressive TENS machine repletewith dials, flashing lights and cooling system thatmade a ‘whirring’ sound. The results of this trialwere such as to allow unbiased ‘blinded’ observersto conclude that the effectiveness of SDN is signi-ficantly superior to that of a placebo.

DETERMINATION OF THE OPTIMUMSTRENGTH OF NEEDLE-EVOKED NERVE STIMULATION

The responsiveness of people to the needle-evokednerve stimulation procedure known as acupunc-ture is widely variable (Mann 1992). Whilst mostare average responders there are some who arestrong reactors and others who are weak ones.Thus when carrying out SDN at MTrP sites it isessential to establish the optimum strength ofstimulation for each individual patient, as a stimu-lus that is not sufficiently powerful to alleviate aweak reactor’s MTrP pain may be enough to causea strong responder to experience a distressing albeittemporary exacerbation of it.

The reason for this variability amongst peopleis not certain but there are grounds for believingthat weak reactivity may be genetically determined.

In support of this is that Peets & Pomeranz(1978) have identified a strain of mice (CXBX) who,because they are genetically deficient in endo-genous opioid peptide receptors, respond poorly to needle-evoked nerve stimulation. And thatMurai & Takeshige (1986) had difficulty in pro-ducing analgesia by this means in a strain of ratsdeficient in endorphins.

Another possibility that has to be consideredwhen attempting to explain why some people areweak responders to needle-evoked nerve stimula-tion is that they may have excessive amounts ofendogenous opioid peptide antagonists in theirnervous systems. Subsequent to the ancient Chineseputting forward their belief in a yin-yang balancein the body it has been confirmed that every typeof physiological activity is regulated by an oppos-ing one. Examples of these include the counterbal-ancing effects of insulin and glucagon; of calcitoninand parathyroid hormone; and generally speaking

of the sympathetic and parasympathetic nervoussystems (Han 2001). It was in view of this that thediscovery of endogenous opioid peptides in the1970s (see Ch. 6) prompted a search for substancesin the body possessing antiopioid activity. Severalhave since been found including orphanin FQ(Yuan et al 1999), nocistatin (Okuda-Ashitaka et al1998), and angiotensin 11 (Kaneko et al 1985), butas already discussed in Chapter 6, the most power-ful one is cholecystokinin-8 (CCK-8).

With respect to this, Han (1995) has shown thatan electroacupuncture stimulus accelerates therelease of endogenous opioid peptides and thatthese then stimulate neurons to release CCK-8 as anegative feedback mechanism.

There are therefore grounds for believing thatthe reason why some people are weak responders to needle-evoked nerve stimulation is because ofvarious genetically determined factors includingan inherent tendency to secrete excessive amountsof opioid antagonists.

TECHNIQUE RECOMMENDED FOR THECARRYING OUT OF SDN IN THETREATMENT OF A PRIMARILY ACTIVATED MTrP POINT

A MTrP is of such exquisite tenderness (see Ch. 7)that the application of firm pressure to it gives riseto a flexion withdrawal (the ‘jump’ sign) and often,in addition to this, the utterance of an expletive(the ‘shout’ sign).

Clinical experience has led me to believe that theoptimum strength of needle stimulation requiredto alleviate an individual patient’s MTrP pain is theminimum amount necessary to abolish these tworeactions.

In view of this it is my practice (Baldry 1995,1998, 2001, 2002 a, b) on first treating someone, toinsert an acupuncture needle (0.3 mm � 30 mm)into the tissues overlying each MTrP to a depth ofabout 5–10 mm (i.e. sufficient to allow it to be self-standing). The needle is then left in situ for 30 sec-onds. And on withdrawing it pressure equal tothat exerted before treatment is reapplied to theMTrP site to see whether the ‘jump’ and ‘shout’reactions have been abolished. This usually provesto be so but if not the needle is reinserted and leftin situ for 2–3 minutes. In a small minority of cases


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re-testing for the above two reactions shows it isnecessary to increase the stimulation still more bymeans of yet once again re-inserting the needle andnot only leaving it in situ for some time but alsointermittently twirling it.

The purpose of adopting this step-by-stepapproach when determining each individualpatient’s responsiveness to SDN at a MTrP site isto reduce the risk of causing a temporary but, never-theless, distressing exacerbation of pain as a resultof exceeding that person’s optimum needle stimu-lation requirement. Nevertheless, it has to be admit-ted that there is a small group of patients who aresuch very strong reactors that even a needle left insitu for 30 seconds proves to be more than neces-sary. For these people all that is required is for theneedle to be inserted into the superficial tissuesand then immediately withdrawn.

During subsequent treatments the optimumamount of stimulation found initially to be neededfor each patient should be strictly adhered to.

THE NUMBER OF TREATMENT SESSIONS

There would seem to be general agreementamongst those health professionals in the Westernworld who use needle-evoked nerve stimulationfor the relief of chronic pain that treatment shouldnot be carried out more often than once a week.This is because the full effect of such treatmentoften does not become apparent for several daysand it may, therefore, be misleading to try to assesshow much response there has been to it before theend of that time.

INFORMATION TO BE GIVEN TO APATIENT AT THE END OF THE FIRSTTREATMENT WITH SDN

The patient should be told that any pain reliefobtained from the first treatment may only last for 1–2 days; and that occasionally there is a delayof 12–14 hours before this is obtained or con-versely but rarely, in view of the particular tech-nique employed, there may be a temporaryexacerbation of it. And that should the latter happen the amount of stimulation given on sub-sequent occasions may have to be reduced.

The patient should also be informed that treat-ment will initially be given at weekly intervals andthe length of time for which relief is obtained aftereach session should hopefully increase to the extentthat after the third one it may well last for 7 daysor more and that following this a decision will bemade as to whether further treatment is requiredand if so for how long.

It should be explained that in general the num-ber of sessions required and the interval betweenthem varies according to a person’s individualresponsiveness and, in particular, to how long thepain has been present prior to starting treatment.That because of this people with chronic pain mayhave to have SDN repeated every 4 weeks for anindefinite period and conversely, those who haveonly had pain for a relatively short duration mayonly require two to three treatments at weeklyintervals.

It should also be made clear that should progressnot appear to be satisfactory after the third sessionboth the diagnosis and the method of treatmentmay need to be reviewed.

SYSTEMATIC SEARCH FOR MTrPs

It is important for needling to be carried out atevery active MTrP site. The failure of primary MTrPpain to respond to SDN is often because one ormore points have been overlooked. Prior to startingtreatment therefore it is essential for the search forthem to have been carried out in a systematic man-ner. Then once all the obviously active MTrPs havebeen deactivated it is important to check that nonehave been overlooked. This should be done byascertaining the range of movements now possibleand by systematically palpating the muscles in theaffected region again.

THE SEPARATE OR SIMULTANEOUSDEACTIVATION OF MTrPS

It is my practice when first treating a patient, andon all occasions with strong reactors, to deactivateeach MTrP in turn so that the time for whichthe needle is left in situ can be accurately deter-mined. Then on subsequent occasions, in thosecases where the response to the initial treatmenthas shown that needles can be left in situ for an


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appreciable period of time without fear of exacer-bating the pain, all of the MTrPs are deactivatedsimultaneously.

JAPANESE SHALLOW NEEDLING

The SDN method just described needs to be dis-tinguished from the shallow needling one cur-rently used in the traditional Japanese channel typeof therapy known as keiraku chiryo. During the carry-ing out of this very thin needles (0.12–0.14 mm) areinserted into the skin to a depth of not more than1–2 mm at traditional Chinese acupuncture pointsites (TCAPs). And in some cases this lightlyapplied stimulus is augmented by pairs of needlesbeing linked together by an ion pumping cord.This device, according to Birch & Felt (1999), ‘con-nects one shallowly inserted needle into another,allowing for a tiny electrical current to flow betweenthe two needles’.

Trials employing this shallow needling proced-ure for the alleviation of myofascial pain includeone by Birch & Jamison (1998) and another byCeccherelli et al (2002).

Birch & Jamison divided 46 patients with chronicmyofascial neck pain into two groups. Group I hadneedles (connected by IP Cords) inserted to a depthof 2–3 mm (shallow needling) at what were deemedto be relevant TCAPs. Group II had needles insertedto the same depth at what were deemed to be irrel-evant TCAPs. And Groups III was a medication-only control one.

Their conclusion was that ‘the results of thisstudy suggest that combined treatment with rele-vant acupuncture, heat and IP cords is more help-ful in relieving myofascial neck pain than irrelevantacupuncture or medication alone’.

Ceccherelli and his co-workers divided 42patients with lumbar myofascial pain into twogroups. Group I had needles inserted to a depth of2 mm (shallow needling) and Group II had needlesinserted into muscle. In both groups the needlingwas carried out at five predetermined TCAPs andfour arbitrarily chosen MTrP sites. They con-cluded that their clinical results showed that theirdeep stimulation technique had a better analgesiceffect than their shallow needling one.

It may therefore be seen that the shallowneedling techniques employed in these two trials

were very different from the one called SDN byme, in that needles are not only inserted to a sig-nificantly greater depth (5–10 mm) but also, this is done at all active MTrP sites found to be presentin any particular patient.

COMPLICATIONS OF ACUPUNCTURE

A prospective survey carried out by White et al(2001) showed that when acupuncture is carriedout by doctors and physiotherapists the incidenceof side-effects is minimal and that the ones that dooccur are far less harmful than those produced bymany of the drugs currently being prescribed forcombating pain.

The various adverse effects of acupuncturehave also been extensively and comprehensivelyreviewed by Rampes (1998) and by Rampes &Peuker (1999).

Vaso-vagal attacksSome people faint at the sight of a needle let alonewhen it is inserted into them. People who areapprehensive about being needled or have a pasthistory of passing out when being inoculatedshould not be persuaded against their will to haveany form of acupuncture. Moreover, as a liabilityto fainting is often unpredictable, it is importantthat everyone on the first occasion should betreated lying down. Having said this, it has to beadmitted that the incidence of this complicationwould seem to be low, as Chen et al (1990) havereported it only occurring 55 times during thecourse of carrying out 28,285 acupuncture treat-ments (0.19%).

ConvulsionsVery occasionally a person who has fainted inresponse to needle stimulation may proceed tohave an epileptic fit. Over the past 20 years thiscomplication has only arisen in one of my patients,a known epileptic. Hayhoe & Pitt (1987), howeverhave reported two cases.

Post-treatment drowsinessIt is not uncommon for a patient to feel sleepyfollowing dry needling. The greater the amount of


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stimulation given the more likely is this to occur,but with a strong reactor it may happen with onlya lightly applied stimulus.

As such a reaction is impossible to predict it iswise for a patient when first treated to be accom-panied by a friend who can, if necessary, drive the car on the journey home. A study carried outby Brattberg (1986) on 122 patients treated withacupuncture in a hospital in Sweden revealed that56% of them were deemed to be so drowsy as to beunsafe to drive themselves home after it.

Damage to visceraVisceral damage has been reported to occur duringthe carrying out of DDN, but is most unlikely tohappen when SDN is employed. Nevertheless, caremust be taken in both the chest wall and lower neckregions to always insert the needle at an obliqueangle in order to avoid inducing a pneumothoraxfor, as Rampes & Peuker (1999) have pointed out,post-mortem examinations have shown that a punc-ture depth of as little as 10 mm either parasternallyor in the region of the midclavicular line can reachthe lung.

In the popliteal region care must be taken not torupture a Baker’s cyst. When this happened to oneof my patients during the course of inserting nee-dles into periarticular tender points in the poplitealspace for the treatment of osteoarthritis of the kneethe considerable pain, tenderness and swelling ofthe calf that took place simulated that which ariseswith a deep vein thrombosis. Gray (1996) has alsoreported a similar case where this happened.

HaemorrhageWith SDN bleeding into the tissues is uncommonand when it does occur may readily be controlled bythe application of firm pressure. Occasionally, how-ever, a haematoma may develop. This is particu-larly liable to happen with elderly people and withpatients on steroids as a result of capillary fragility.

People on anticoagulants should not be treatedwith dry needling. Smith et al (1989) reported howa man taking warfarin, on being needled, bled somuch that pain and swelling in the leg developed tosuch an extent as to require the carrying out of ananterior compartment decompression fasciotomy.

Needles lost or forgottenIt is easy to overlook a needle, especially when ithas been inserted into a part of the body coveredby hair such as the upper part of the neck or scalpof a woman. Therefore, in all cases needles shouldbe counted when being inserted and again whenbeing taken out.

Transmission of infectionDue to the now universal usage of disposable nee-dles by doctors and physiotherapists when carry-ing out acupuncture there is no longer any risk ofthis procedure causing hepatitis B to be transmit-ted. In the past, however, there were some seriousoutbreaks of this mainly due to poor hygienictechniques employed by non-medically qualifiedpractitioners. The first to be documented in theUK was reported by the Communicable DiseaseSurveillance Centre of the Public Health LaboratoryService in 1977. And up until the end of the 1980sthere were several other outbreaks in various partsof the world including ones reported by Kent et al(1988) and by Slater et al (1988).

The transfer of AIDS by acupuncture needleshas not proved to be a problem. One possible casereported by Vittecoq et al (1989) was not subse-quently substantiated.

Skin disinfectionRoutine disinfection of the skin before the carryingout of needling is not considered to be necessary asbacteria resident in it are not liable to cause infectionprovided host immunity is not seriously impaired.However, as Hoffman (2001) has stated, in anycase where the skin is manifestly dirty it should bewashed and if there is overt evidence of infectionit should be disinfected with alcohol. Laurence &Bennett (1987) recommended using 70% ethyl orisopropyl alcohol for this purpose.

PHYSIOLOGICAL REACTIONS TONEEDLING

Wheal and flareSir Thomas Lewis (1942) observed that following asuperficial injury to the skin there is often an intense


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vasodilation at the site of injury followed by thedevelopment of oedema (wheal) and a spreadingredness (flare). As Fields (1987) has said, this isprobably due to Substance P (SP) causing hista-mine to be released from mast cells. This reaction,which is commonly observed when a needle isinserted into or through the skin, often providesthe patient with a pleasant warm feeling but occa-sionally it is so excessive as to cause a protractedburning sensation.

Needle-evoked sensationsThe Chinese from the earliest days have describedvarious sensations that arise in response to needlestimulation. In the Western literature they are oftenreferred to as de qi, although the sinology scholarsLu & Needham (1980) have stated that the Chinesetraditionally called them tê chhi (obtaining the chhi)or chen kan (responding to the needle).

These sensations include first of all ma (a feel-ing of numbness), then chang (a feeling of disten-sion), followed by chung (a feeling of heaviness)and after this suan (a feeling of soreness).

Wang et al (1985), from studies in which directmicroelectrode recordings were made from singlefibres in the median nerve during the time thatneedling was being carried out distally, confirmedthat stimulation of Group II muscle afferents pro-duces numbness, stimulation of Group III onesgives rise to sensations of distension and heaviness,and stimulation of unmyelinated Group IV onescauses soreness to develop. De qi may also be pro-duced in response to needle-evoked stimulation ofA-delta nerves in the skin (see Ch. 11).

These subjective responses are not only felt atthe needle site but may on occasions travel slowlyup or down a limb. Lu & Needham (1980) duringthe course of discussing this drew attention to astatement concerning the cure of headache whichappeared in a book entitled Chi Sheng Pa Sui, pub-lished in 1315. It said, … Ask the subject to cough,then insert the needle at Ho-Ku (Large intestine 4 –see Fig. 15.11) on both sides to a depth of 5 fen(1.53 cm) and turn it counter-clockwise while thepatient inhales three times. Then clockwise againfor three deep breaths. Repeat the counter-clockwiseturning only this time for five inhalations and thecontrary ones again in the same way. The patient

will then feel the sensation (suan) rising slowlyfrom the hands right up to the shoulders like athread. Finally ask the patient to take one morebreath and withdraw the needle. …

As Lu & Needham (1980) commented:

This strongly suggests that the conception of theacu-tracts may have arisen, at least in part, fromthe subjective sensations of those who wereundergoing acupuncture. It would have beennatural enough to envisage thread-like lines ofcommunication after such experiences and whatmore reasonable than to suppose that the almostindefinable chhi flowed along them.

PREVENTION OF MTrP REACTIVATION

Identification of causative factorsIn every case it is essential to take a detailed his-tory aimed at identifying the factors responsiblefor causing the MTrPs to become active in order toascertain whether any of them can be avoided inthe future.

Muscle stretching exercisesExercises to stretch muscles that have becomeshortened as a result of MTrP activity should invari-ably be taught and carried out by the patient on aregular basis. For the effect of these is to activateA-beta nerve fibres with, as a consequence, theevocation of pain-suppressing activity in largediameter nerve fibres, similar to that broughtabout by conventional TENS (see Ch. 9).

Exercises designed to strengthen muscles should,however, be avoided as these are liable to causethem to become overloaded with, as a consequence,the risk of reactivating any TrPs that may be present.

Correction of postural and structural disordersIt is particularly important to correct any posturalor structural disorder that may be present espe-cially in cases where there is TrP activity in eitherthe neck or lower back muscles.

Following the deactivation of TrPs in the cer-vical muscles the patient should be advised toavoid situations where the neck is liable to become


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persistently hyper-extended, kinked (Fig. 10.1) orflexed (Fig. 10.2). And the patient should be toldthat when using a computer for any length of timeto check that the position of the screen is such asnot to cause the shoulders to be kept in a persist-ently elevated position.

Attention should also be drawn to the import-ance of avoiding kinking of the neck during sleep

as a result of resting the head on either too manyor too few pillows (Fig. 10.3).

Should the initial physical examination of thepatient have revealed that one of the shoulders islower than the other, then the length of the two


Figure 10.1 Overloading of the right sternocleidomastoidmuscle as a result of prolonged kinking of the neck.

Figure 10.2 Overloading of the posterior cervical groupof muscles as a result of sitting crouched over a desk.

A

B

C

Figure 10.3 Pillow arrangement. A patient with TrPs inmuscles of the neck must ensure that the pillowarrangement is such as to avoid it becoming kinkedduring sleep. A, Correct pillow arrangement. B and C,Incorrect pillow arrangement.

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legs should be compared as this deformity may bedue to a scoliosis brought about as a result of alower-limb length inequality (Fig. 10.4) which, ifleft uncorrected (see below) will cause the over-loading of the neck muscles to persist.

The length of the upper arms should also bechecked because if these in a relaxed standingposition do not reach the level of the iliac crest(Fig. 10.4), then on sitting, it may not be possible toplace the elbows on the arm rest of a chair (Fig. 10.5)with, as a consequence, strain being imposed on themuscles of the neck and the reactivation of anyTrPs that may be present in them. Therefore, shouldthey be found to be abnormally short the height ofthe arm rest should be suitably adjusted.

Following the deactivation of TrPs in muscles ofthe lower back an examination should be carriedout to exclude a lower limb length inequality, asmall hemipelvis, short upper arms and a Morton’sfoot deformity.

Lower-limb length inequalityLower-limb length inequality (LLLI) may be a con-genital deformity. In such a case one side of the bodytends to be smaller than the other. Also, there isliable to be upper arm length inequality, asymmetryof the two halves of the pelvis and a slight but dis-cernible asymmetry of the face. Alternatively, itmay be acquired as a result of an injury or a badlyfitting hip prosthesis.

A LLLI tends to cause the patient to stand withthe weight of the body shifted to the side of theshorter limb and the knee on the contralateral sideslightly flexed. On walking there is also tilting ofthe torso.

It also leads to the development of a scoliosis.This tends to be C-shaped when the leg length dif-ference is 6 mm (1/4 inch) or less and causes sag-ging of the shoulder on the side opposite to that ofthe short leg (Fig. 10.6). Conversely, should the leglength difference be 1.3 cm (1/2 inch) or more thescoliosis which develops is S-shaped and thiscauses sagging of the shoulder on the same side asthe short leg (Fig. 10.7).


A B

Figure 10.4 A: Person whose arms are of sufficientlength in relation to the height of the torso for theelbows to reach the iliac crest. B: Person with abnormallyshort arms so that in the relaxed standing position theelbows do not reach the level of the iliac crest.

Figure 10.5 A person with abnormally short upper arms may be unable to place elbows on the arm rest of a chair.

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Inequality of the two halves of the pelvisIn some patients with a LLLI one side of the pelvisis smaller than the other. This leads to the devel-opment of a compensatory scoliosis and a corres-ponding sagging of the shoulder on that side. Thescoliosis may be corrected by the person con-cerned sitting on a cushion placed under theischial tuberosity on the affected side (Fig. 10.8).

Short upper armsThis abnormality not only puts a strain on the muscles in the neck and shoulder girdle, but isalso liable to cause the development and perpe-tuation of TrP activity in the quadratus lumborummuscle. Therefore, whenever such activity is foundto be present in this muscle an examination toestablish whether or not this particular structuraldisorder may be contributing to it should be carried out.


A B

Figure 10.6 A: Diagram to show C-shaped scoliosis andsagging of the left shoulder produced by right leg being6 mm (1/4 inch) or less shorter than the left one. B: Correction of scoliosis by raising the right heel.

A B

Figure 10.7 A: Diagram to show S-shaped scoliosis andsagging of the right shoulder produced by right leg being 1.3 cm (1/2 inch) or more longer than the left one.B: Correction of scoliosis by raising the right heel.

When assessing whether or not there is a LLLIthe patient should stand with the legs straight andthe feet together in order that the relative heightsof both the iliac crests and the greater trochantersmay be compared.

Travell & Simons (1992) have described how toassess LLLI by means of the carrying out of a radio-logical examination, but, although this is a moreaccurate procedure, it is not one which need beemployed routinely.

Should a LLLI be found to be present it has to bedecided whether this is a true inequality thatrequires the heel on the short side to be raised, oran apparent one due to the leg-raising effect ofTrP-induced shortening of the quadratus lumbo-rum muscle, as in the latter case it is correctable bydeactivating TrPs in this muscle. Whenever itproves to be a true inequality, then it should becorrected by placing filing cards or pages of a jour-nal under the foot on the shorter side so that a cob-bler can increase the thickness of the heel of theshoe accordingly.

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Morton’s foot deformityThis disorder, which was described by Morton in1935, is one in which there is a short first metatarsalbone and a relatively long second one. Harris &Beath (1949) found it to be present in about 40% ofpeople. The deformity causes medio-lateral rockingof the foot with a consequent strain being imposedon a number of muscles including the gluteusmedius maximus in the buttock and the peronealmuscles vastus medialis in the lower limb. Its cor-rection requires the placing of a pad under the firstmetatarsal head.

ALLEVIATION OF STRESS

There is now good evidence to show that stressmay not only cause MTrP activity to develop butmay also cause it to persist (McNulty 1994).

As Gerwin & Dommerholt (2002) have pointedout ‘trigger point EMG activity has been shown toincrease dramatically in response to mental andemotional stress, whereas adjacent non-trigger pointmuscle activity remains normal’.

Treatment directed towards reducing stress following the deactivation of MTrPs is therefore incertain cases essential.

Banks et al (1998) showed that autogenic relax-ation training significantly and dramaticallyreduced the needle-evoked EMG activity in TrPs

in the upper trapezius muscles of 21 chronic painpatients.

My preferred method is to employ hypno-therapy and to teach the patient to practice auto-hypnosis once or twice a day on a regular basis(Hilgard & Hilgard 1994).

CORRECTION OF BIOCHEMICALDISORDERS

Gerwin (1992) has stressed the importance of rec-ognizing the presence of certain biochemical dis-orders as, in his experience, a failure to correct anyone of these may cause MTrP activity to persist.These include sub-clinical hypothyroidism, irondeficiency, vitamin B12 insufficiency and a lowserum folic acid level.

Gerwin (1995), during the course of examining96 subjects for both fibromyalgia and myofascialpain found that 16% of those with MTrP pain syn-drome had a vitamin B12 deficiency and 10% hadbiochemical evidence of hypothyroidism.

Gerwin & Dommerholt (2002), with reference toiron deficiency, have stated that ‘of women with achronic sense of coldness and chronic myofascialpain, 65% have a low normal or below normalserum ferritin, largely from an iron intake insuffi-cient to replace menstrual iron loss. Other causesof low serum ferritin include blood loss associatedwith chronic intake of mixed cyclooxygenase 1 & 2non-steroidal anti-inflammatory drugs’.

TREATMENT OF FIBROMYALGIASYNDROME

The management of the fibromyalgia syndrome(FS) involves the use of a large number of differenttypes of treatment. Each of these will be brieflydiscussed.

More comprehensive reviews of this subjectinclude amongst others those published by Bennett(1999), Inanici & Yunus (2001), Russell (2001) andSimms (1994). Because FS at the present timeremains a very disabling one with no known cureit requires long-term skilled management thatincludes patient education, the prescribing ofsymptom-relieving drugs, psychotherapy and theemployment of various physical modalities.


BA C

Figure 10.8 A: Hemipelvis on the right side smallerthan on the left side causing S-shaped scoliosis. B:Scoliosis corrected by raising right buttock. C: Scoliosismade worse by raising left buttock.

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Education of the patientWhen FS is first diagnosed it is essential to reassurethe patient that, although it is a chronic disorder, it is not one that reduces life expectancy and thatthe various forms of treatment currently availableenable its symptoms to be kept under sufficientcontrol as to allow a reasonably active life to be ledboth in the home and at the work place.

It is also essential to explain to the patient thatsuccessful management of it cannot only dependon physician-based therapeutic regimes but mustalso include patient-orientated self-help program-mes (Burckhardt & Bjelle 1994).

Symptom-relieving drugsDrugs are mainly required for the relief of sleepdisturbances, pain and affective disorders.

Sleep disturbances

Non-restorative sleep Non-restorative sleepwhich not only contributes so much to FS patients’feelings of persistent tiredness but also exacer-bates their pain should be treated with a tricyclicantidepressant. The one most widely used is amit-ryptyline given 1–3 hours before going to bed. Thisinitial recommended dose is 10 mg and it can gradually be increased to 50–75 mg if necessary, butoften, especially in older people, 20 mg proves tobe sufficient.

The commonest side-effect, as with all drugs inthis group, is a dry mouth.

Contraindications to it being prescribed includea history of urinary retention, prostatic hyper-trophy, narrow angle glaucoma, impaired liverfunction and epilepsy.

Its main disadvantage is that tolerance buildsup after 3–4 months use but discontinuing it for a 2–4 week period usually allows sufficient CNS re-adaptation to take place for its use to be resumed.During the break from it Russell (2001) recom-mends the use of aprazolam.

The possibility of using the pineal hormonemelatonin in FS because of its sleep-promotingproperty has been explored by Citera et al (2000)in a 4 week open study of 25 patients with this dis-order. They found that this hormone given in a doseof 3 mg at night lowered the tender point countand significantly improved the quality of sleep.

Further studies are therefore clearly indicated toconfirm the value of this drug.

Sleep apnoea It has been estimated that about25% of males and 15% of females with FS havesleep apnoea (Bennett 1999), which requires treat-ment with positive airway pressure or surgery.

Restless leg syndrome In this disorder firstdescribed by Ekbom in 1960 there is an intolerablediscomfort in the legs which first comes on whensitting down at the end of a day and the involun-tary movements of them then prevent the personconcerned from getting off to sleep. Yunus & Aldag(1996) have reported an appreciable incidence ofthis syndrome in patients with FS.

Its treatment includes the use of either L-dopa(Montplaisir et al 1986) or clonazepam (Boghen et al1986).

Pain

Amitryptyline at night not only helps to providerestorative sleep but also by so doing helps toameliorate the pain in patients with FS.

The analgesic most widely prescribed is para-cetamol (acetaminophen), but there is no convin-cing evidence of its efficacy in this disorder (Wolfeet al 2000).

It is also generally agreed that most patients donot derive much benefit from a non-steroidal anti-inflammatory drug such as ibuprofen and there isno case for prescribing a corticosteroid one likeprednisolone (Clark et al 1985).

Tramadol, a weak opioid agonist and a nor-adrenaline uptake inhibitor, is, however, proving tobe moderately effective (Biasi et al 1998), althoughunfortunately it is poorly tolerated by about 20%of patients with this disorder (Russell 2001).

In view of the marked hyperalgesia and allody-nia present in patients with FS as a result of centralsensitisation there are grounds for believing that aN-methyl-D-aspartate (NMDA) antagonist shouldbe helpful. Support for this comes from a double-blind train carried out by Sorensen et al (1995) inwhich the pain suppressing effects of intravenousinfusions of isotonic saline and ketamine werecompared, and the latter was shown to provide asignificantly greater reduction of pain intensity.

Unfortunately ketamine not only has to be givenintravenously but is also liable to give rise to a


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number of particularly undesirable adverse effects.The routine use of a NMDA antagonist for treat-ment in FS and other pain disorders will, therefore,have to await the discovery of a far less toxic one.

Affective disorders

As with patients suffering from chronic pain dis-orders those with FS are liable to become anxiousand depressed.

Anxiety As with any other chronic disorder theuse of a benzodiazepine drug is not recommendedbecause of the risks of dependence and withdrawalseizures (Leventhal 1999).

In view of this, it has been my practice for someyears, as previously stated, to employ hypnother-apy in patients with this and similar chronic paindisorders and to teach them how to practice auto-hypnosis for 10 minutes once or twice a day on aregular basis. It is, therefore, gratifying to find thatHaanen et al (1991), in a randomized controlledtrial carried out for the purpose of comparingphysical therapy with hypnotherapy in patientswith FS, have provided objective evidence of theability of the latter form of treatment to lower theintensity of pain, improve sleep and lessen morn-ing fatigue.

Depression When depression is a prominent fea-ture in patients with this disorder, fluoxetine, aselective serotonin reuptake inhibitor has beenshown in controlled studies to both relieve it andto improve sleep (Wolfe et al 1994).

With respect to this it should be noted thatGoldenberg et al (1996) have provided evidence tosuggest that a combination of amitryptyline andfluoxetine may be better than either drug alone.

Physical modalities

Muscle stretching and aerobic exercises

It is important for patients with FS to be taughthow to carry out on a regular daily basis bothmuscle stretching and aerobic exercises. The lattershould initially be for 10 minutes periods threetimes a day and should include regular walkingand the use of a stationary exercise bicycle.

Some hospitals provide group exercise program-mes for patients with this disorder. An interestingalternative recently reported by Richards & Scott

(2002) is the carrying out of such a programme inthe ‘healthy living centres’ recently set up with thehelp of grants from the UK’s National LotteryFund. A randomized controlled trial conducted bythem led to the conclusion that ‘the carrying out ofgraded aerobic exercise is a simple, cheap, effective,and potentially widely available treatment forfibromyalgia’.

Electroacupuncture

Deluze et al (1992) carried out a randomized con-trolled trial of this particular type of acupuncturein 54 women and 16 men with FS.

In the ‘treatment’ group (36 patients), electro-acupuncture with a variable high-/low-frequencyand an intensity sufficient to induce visible mus-cular contractions was applied to needles insertedto a depth of 10–25 mm into the first dorsalinterosseous muscle (i.e. Hegu or Large Intestine 4)bilaterally, into a point in the anterior tibial muscleknow as Stomach 36 (Zusanli) bilaterally and intovarious other points which they said ‘dependedon the patient’s symptoms and pain pattern andaccording to the empirical efficacy of the sites inthe treatment of pain’. This is a somewhat imprecisedescription which in my opinion makes it difficultto be certain which points in particular were used!

The ‘control’ groups had the same number ofneedles inserted but only to a depth of 3–4 mmand 20 mm away from the points chosen for the‘treatment’ group. They stated that ‘the currentused was similar to but weaker than that used inthe real procedure … (so that) … there was no muscular contraction’.

They found that the ‘pain threshold which wasconsidered to be the main parameter improved by70% in the treatment group and 4% in the controlgroup’.

As Lewis (1993) has pointed out, this is a verysurprising result not because the treatment groupdid so well, but because the ‘control’ group did sobadly. The reason for him saying this is becausethe points into which needles were inserted in thislatter group of patients were only 20 mm awayfrom those used in the treatment group anddespite the stimulus being weaker, from what isknow concerning the pain-alleviating neurophysi-ological mechanisms of acupuncture, it is veryunlikely that it did not have some therapeutic


Chap-10.qxd 11*10*04 10:25 Page 143

effect. Furthermore, that four patients in this ‘con-trol’ group had to withdraw from the trial becauseof an exacerbation of their pain is an added reasonfor believing that the electrical stimulus employedin their ‘treatment’ had more than a placebo effect.

Although the result of this trial clearly showsthat electroacupuncture with needles inserted intotraditional Chinese points is capable of alleviatingthe pain of FS, there are in my opinion three reasonsfor not using it. One is that the stimulus providedby this particular type of acupuncture is liable tobe more powerful than the optimum required byFS patients who, as a group are widely recognizedto be strong reactors to needle-evoked nerve stimu-lation procedures. The second is that it requiresthe use of a machine not normally available to, andspecial training not usually undertaken by thosewho treat this disorder. And the third reason isbecause manually applied dry needling carried outeither at traditional Chinese acupuncture pointsites or at tender point sites are far simpler proce-dures and seemingly equally effective ones.

Manual acupuncture at traditional Chinese acupuncture point sitesSandberg et al (1999) chose manual acupuncturewhen carrying out a cross-over designed pilot studyin 10 patients with FS because as they stated ‘thisis a milder form of sensory stimulation than elec-troacupuncture and our clinical experience has ledus to believe that FS pain is liable to be aggravatedby too strong a stimulus’.

The first five referred patients, group I, receivedacupuncture treatment over a period of 2–3 months.The subsequent five patients, group II, acted ascontrols for 2–3 months, after which treatment wasgiven as in group I. Six months after the end of thetreatment, group I crossed over to form a controlgroup.

The traditional Chinese acupuncture pointsemployed were Large Intestine 4 (Hegu) in the firstdorsal interosseous muscle of the hand, Stomach36 in the tibialis anterior muscle and what theydescribed as ‘points in the upper part of the body …within the most painful area’. Also they said, ‘foradditional stimulation from the lower part of thebody one or two more points in the lower extrem-ities were used’. Yet another imprecise statement,

similar to that employed in the trial just previouslydiscussed, which makes it extremely difficult todetermine which points in particular were used.They furthermore stated that ‘the strength of theneedle stimulation was enough to elicit the sensa-tion of ‘de Qi’ but … noxious painful stimulation …was avoided’. Avery important feature of the studywas that the treatment parameters were variedaccording to the optimum amount of stimulationrequired by each individual patient; this is a consid-eration not sufficiently often included in the proto-cols of acupuncture trials. A very interesting andencouraging finding in this pilot study was thatnot only did 78% of the patients report consider-able pain relief immediately after completion of thetreatment, but 56% continued to experience this 1month later and 33% after 2–3 months.

Their particular method of treatment, therefore,even when the shortcomings of a crossover studyare taken into account, shows considerable prom-ise. Its only disadvantage is that it relies on insert-ing needles into traditional Chinese acupuncturepoints and, therefore, cannot be used by the major-ity of health professionals who treat FS as theyhave no knowledge as to where these points aresituated!

Sprott et al (1998) also confirmed the value ofmanually applied traditional Chinese type acupunc-ture in the alleviation of FS pain when they used itto treat 29 patients (25 women, 4 men) sufferingfrom this disorder over a 6-week period (six singletreatments once a week), according they said ‘toan individually adapted therapy strategy follow-ing acupuncture rules’.

They found that the treatment ‘… was associatedwith decreased pain levels and fewer positive ten-der points as measured by VAS and dolorimetry…’And in addition confirmed that, ‘… this was accom-panied by decreased serotonin and substance Plevels in serum, suggesting that acupuncture ther-apy is associated with changes in the concentrationsof pain-modulating substances in serum …’

Tender point injectionsAnother approach to the treatment of FS pain andone which is proving to be helpful is to inject alocal anaesthetic into tender points (Yunus et al1998).


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In an open study carried out by Reddy et al(2000) 41 patients with FS had a mixture of 1%lidocaine (lignocaine) (1/2 cc) and triamcinolonediacetate (1/4 cc) injected into tender points. Theyadmitted that the inclusion of a corticosteroid wasmore because of the continuation of a ‘tradition’than because it had any scientific basis for, as hasbeen shown by Yunus et al (1989), there is no evidence of an inflammatory lesion in the musclesof FS patients in electron microscopic studies.

A tender point injection of this type gratifyinglyled on average to a 12-week-long period of painrelief at each injected site.

A serious disadvantage though was that thestimulus was so strong that in order to combat any resultant post-injection soreness the treatedareas had to be rested for 48 hours and ice had tobe applied to them for 20–30 minutes/hour for 4–8 hours. Because of this the treatment had to berestricted to no more than five sites or, in patientswith particularly bad pain, to no more than eightsites.

Figuerola et al (1998) have studied plasma met-enkephalin (ME) levels in 15 women with FS beforeand after the following different forms of treatmentto tender points – 5 patients had lidocaine (ligno-caine) hydrochloride injected into them, 5 hadinjections of saline into them and 5 had dry nee-dles inserted into them.

Significant increases in plasma ME concentra-tions were observed in all groups 10 minutes afterfinishing each treatment session irrespective of theprocedure employed. A finding strongly suggest-ing that this biochemical change was brought aboutby the effect of the needle was that this was theone stimulus common to all of the three groups.

Superficial dry needling at tender and TrP sitesIn view of it having been found that an injection of a local anaesthetic/corticosteroid mixture intotender points is liable to give rise to such a con-siderable amount of soreness at that site that thenumber of them treated has to be strictly limited,there is clearly a case for either injecting a localanaesthetic alone, as Inanici & Yunus (2001) nowdo, or for simply inserting a needle into the super-ficial tissues overlying it.

The main advantage of carrying out SDN is that the strength of the stimulus applied, ratherthan being the same for everyone, can readily beadjusted to suit each individual patient’s optimumrequirement. This is particularly important whentreating patients with FS because in general theytend to be strong reactors to needle-evoked nervestimulation. And because, due to the lack of treatment-induced tenderness, providing the stim-ulus applied is a light one the needling can be car-ried out at all the tender and TrPs present in turn.

It is, therefore, my practice to insert a needle toa depth of about 5 mm at a tender/TrP site and toleave it in situ for from 10–30 seconds according towhat is found by trial and error to be the time nec-essary to abolish the exquisite tenderness at thepoint being treated.

With SDN carried out in this way it is usually nec-essary to repeat it once a week for 3–4 weeks, then at2-week intervals, and finally at 4–6 week intervalson a long-term basis. Although due to the nature ofthe underlying disorder, the treatment has perforceto be protracted, most patients find it to be worth-while as the pain relief afforded by it appreciablyimproves the quality of their lives (Baldry 2000).

Training required in order to carry out superficial and deep dry needling

In concluding this chapter it is felt necessary to saythat whilst SDN carried out at either tender pointsor TrP sites, and DDN carried out at these lattersites are forms of acupuncture, the employment ofthese two needle-evoked nerve stimulation tech-niques does not require knowing where traditionalChinese acupuncture points are situated, or for thatmatter any particular training in the carrying out oftraditional Chinese acupuncture in general. All thata physician or physiotherapist who wishes to makeuse of them has to have is the skill required to locateTrPs and tender points, and the ability to insert needles into the tissues at these particular sites.

Having said this, it behoves all health profession-als who employ these two techniques to familiarizethemselves with the principles and practice of trad-itional Chinese acupuncture (TCA). This is because,as has already been shown in this book, much ofwhat is known concerning the neurophysiologicalmechanisms involved in the pain-alleviating effects


Chap-10.qxd 11*10*04 10:25 Page 145

of needle-evoked nerve stimulation techniques ingeneral has come from experiments involving theinsertion of needles into TCA points. And becausewithout having knowledge of TCA in general it is

impossible to be able to fully comprehend and eval-uate clinical trials carried out to ascertain whatplace if any it may have in the treatment of a musclepain disorder such as fibromyalgia.


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INTRODUCTION

The future of acupuncture for the relief of nocicep-tive pain and the decision as to whether or not thisparticular type of treatment will eventually becomereadily incorporated within the framework of ortho-dox Western medical practice for this purpose willlargely depend on clinical trials showing its abilityto do this is significantly greater than that of apowerful placebo.

This, however, presents a considerable chal-lenge because, as Belgrade (1994) has cogentlycommented:

… The complexity of testing a therapeutic modal-ity like acupuncture is an order of a magnitudegreater than for testing drugs. Look at the vari-ables involved: definition of acupuncture, choiceof points, type of stimulation, technique of theacupuncturist, frequency and duration of treat-ment and the problems of choosing an appropri-ate placebo that is similar enough to acupuncturebut would not be expected to have a significantacupuncture effect. These variables create over-whelming problems for research design andimplementation …

Such difficulties have been extensively reviewedby many reflective clinicians well skilled in theprinciples and practice of this needle-evokednerve stimulation type of therapy. These include,amongst others Ernst (1999a, 1999b), Ernst &White (1997, 1999), Filshie & Cummings (1999),Han (1994), Lewith & Machin (1983), Lewith &Vincent (1995, 1998), Richardson & Vincent (1986),

149

Chapter 11

Scientific evaluation ofacupuncture’s ability to relieve nociceptive pain

CHAPTER CONTENTS

Introduction 149Is traditional Chinese acupuncture-evoked pain

relief dependent on inserting needles atspecifically designated sites? 150

Individuals’ varying responsiveness to placebos 150–151

Credible placebos 151–153Opioid peptide-mediated placebo-evoked

analgesia 153–154The designing of future acupuncture clinical

trials 154–158Possible future therapeutic advances relevant to

the use of acupuncture for pain relief 158

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groups showed significant improvement in ten-derness and subjective report of pain as evaluatedby two independent observers, as well as in activ-ity of the joint. Because there was no differencebetween the two groups the improvement wasattributed to a placebo effect. It is more likely, how-ever, that it is stimulation within a large area andnot merely at a point that has an effect. Similarconclusions can be drawn from an excellent studyof acupuncture control over pain in patients withsickle-cell anaemia (Co et al 1979). In fact, intensestimulation at many sites of the body may beeffective. It is the intense stimulation rather thanthe precise site that appears to be the crucial fac-tor… . That the pain relief produced by acupunc-ture cannot be attributed simply to a placebo effectis also indicated by the fact that analgesia can beproduced in animals such as monkeys and mice(Vierck et al 1974, Pomeranz et al 1977, Sandrew et al 1978) …

All this leads to the posing of two further ques-tions. What is a placebo? And what placebo in par-ticular is best for use in trials to assess thepain-relieving efficacy of acupuncture?

PLACEBOS

Before discussing placebo-controlled trials for theevaluation of the pain-relieving properties ofacupuncture, it is first necessary to say somethingabout them in general. The term placebo, which isderived from the Latin word placere (to please), hasan established ecclesiastical usage in the phrasePlacebo Domino (I shall please the Lord) thatappears in the opening antiphon of the vespers forthe dead. According to the Shorter Oxford Diction-ary it has, in addition, been used by the medicalprofession since 1811 to describe some medical sub-stance given more to please than benefit a patient.However, it has always seemed to me that it wouldhave been more apposite for the word in the med-ical sense to have been derived from the Latinplacare (to placate) because therapeutically it isgiven more to pacify or appease than it is to givepleasure to a patient!

Wall (1994, p. 1301) has commented, ‘the mythis widely quoted in papers and textbooks that afixed fraction of patients respond to placebos, with

Vincent (1989), Vincent & Lewith (1995), Vincent &Richardson (1986).

The purpose of this chapter is to provide anoverview of this complex subject.

POINT SPECIFICITY

The first question that has to be asked whenattempting to assess the pain-relieving efficacy oftraditional Chinese acupuncture is – does its effec-tiveness with respect to this depend on needlingbeing carried out at specifically designated sites?

My main reason for advocating this when deacti-vating trigger points (TrPs) is that experience hastaught me that it only requires one such point to beleft in an active state for a certain amount of painto persist.

What, however, has to be considered is whetherthis precision is also required when needling trad-itional Chinese acupuncture points, now that bothMann (1992) and Campbell (1999, 2001) have astu-tely observed that needling carried out anywherewithin a sizeable area provides as good analgesiaas does needling at specifically nominated sites.

This it has to be said is not some new discoveryfor Melzack as long ago as 1984 wrote with con-siderable perspicacity on the subject as follows:

… An impressive number of studies show thatacupuncture stimulation need not be applied atthe precise points indicated on acupuncturecharts. It is possible, for example, to achieve asmuch control over dental pain by stimulating anarea between the fourth and fifth fingers, whichis not designated on acupuncture charts as relatedto facial pain, as by stimulating the Hoku pointbetween the thumb and index finger which is sodesignated (Taub et al 1977). The decreases in painobtained by stimulation at either site are so largeand occur in so many patients that it is unlikelythat the pain relief is due to placebo effects.Rather, the results suggest that the site that canbe stimulated is not a discrete point but a largearea, possibly the whole hand.

The same conclusion can be drawn from anotherstudy – a double-blind experiment on the efficacyof acupuncture on osteoarthritic pain – in whichthe control patients received ‘placebo’ acupunc-ture stimulation at sites just adjacent to the ‘real’acupuncture sites (Gaw et al 1975). Patients in both

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the figure of 33% being commonly quoted’. He alsopointed out that:

… Where these sources quote the origin of themyth, they refer to Beecher (1955) who indeedgives the figure of 35.2%. However, had theybothered to read the paper, they would havefound that this figure is an average of Beecher’sown 11 studies, each of which varied widely fromthe average. Scanning a large number of double-blind studies shows the fraction of placeboresponders varying from close to 0% (Tyler 1946)to near 100% (Liberman 1964) depending on thecircumstances of the trial. Clinical pains are asso-ciated with a larger number of placebo respondersthan experimental pains are (Beecher 1959)…There is no fixed fraction of the population whorespond to placebos …

Wall (1994, p. 1034) also stated:

… By far the commonest proposal is that theplacebo effect depends on the expectation of thesubject. There is nothing subtle about this. Placeboreactors can be identified before the trial by sim-ply asking the subject what they expect to be theoutcome of the therapy. Those who doubt do notrespond to the placebo while those with highexpectations do. The very extensive literature onthis is reviewed by Bootzin (1985). Lasagna et al(1954) investigated many aspects of postoperativepatients who responded to placebos and to anal-gesic drugs and concluded that ‘a positive placeboresponse indicated a psychological set predispos-ing to anticipation of pain relief‘ …

… Expectation is a learned state and thereforeyoung children do not respond to placebos asadults do since they have had neither the timenor the experience to learn. Similarly in adults,the learning of expected effects will depend onculture, background, experience and personality.A desire to believe, please and obey the doctorwill increase the effect while hostility decreasesit. Obviously, part of the expectation of the patientwill depend on the expectation, enthusiasm andcharisma of the therapist, and therefore there aremany reports on this doctor–patient interaction.Expectation in a laboratory experiment may bemore limited than in a clinical setting; this mayexplain why rates and intensities of placebo effects

tend to be less in the laboratory than in the clinic(Beecher 1959) …

Credible placebosControlled trials may entail comparing a grouptreated with acupuncture with either a waiting-listgroup, a group given an alternative treatment, or a group given a placebo. As Vincent (1989) haspointed out when discussing the methodology ofcontrolled trials of acupuncture, the main problemis to select a credible placebo. It is, therefore, neces-sary to discuss this subject at some length.

In the past it was common for patients in theplacebo control group to be treated by means ofneedling carried out at sites some distance awayfrom traditional Chinese acupuncture points. Theuse of these so-called sham points should, how-ever, be discontinued (Richardson & Vincent 1986)because, as previously discussed, it is now knownthat needling anywhere in the body has an anal-gesic effect mainly because of the bringing intoaction of the diffuse noxious inhibitory controlsystem identified by Le Bars et al (1979, 1991).

It was because of this that Ezzo et al (2000), afterhaving carried out an extensive review of 51 ran-domized controlled trials carried out between 1980and 1999, concluded that ‘there is limited evidencethat acupuncture is more effective than no treat-ment for chronic pain; and inconclusive evidencethat it is more effective than placebo, sham acupunc-ture or standard care’.

In recent years, therefore, much effort has beenput into trying to find a credible placebo. Borkovec& Nau (1972) were the first to study the credibilityof analogue therapy rationales in the treatment ofpsychological disorders. As Lewith & Vincent (1998)have pointed out, the main questions identified byBorkovec & Nau in their ‘Credibility treatmentrating scale’ were:

1. How confident do you feel that this treatmentcan alleviate your complaint?

2. How confident would you be in recommendingthis treatment to a friend who suffered fromsimilar complaints?

3. How logical does this treatment seem to you?4. How successful do you think this treatment

would be in alleviating other complaints?

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Placebos currently employed

Inactivated transcutaneous electrical nervestimulation machine

Macdonald et al (1983) were the first to use aninactivated transcutaneous electrical nerve stimu-lation (TENS) machine especially fitted with a num-ber of flashing lights in an attempt to increase anyexpectation of its efficacy. Petrie & Langley (1983)also used this device in a pilot study carried out toassess the value of acupuncture in the treatment ofchronic cervical pain.

Petrie & Hazleman (1985), however, were thefirst to employ Borkovec & Nau’s credibility scalewhen comparing the relative plausibility of acu-puncture and sham TENS in patients suffering fromchronic neck pain. As they stated:

… the potent analgesic effect of placebo is wellrecognised (Evans 1974). Such an effect, however,is variable (Doongaji et al (1978), and is influ-enced by a number of factors, not least of whichare the physical appearance of the placebo andthe manner in which it is presented (Buckalew &Ross 1981) …

They concluded that ‘the present study showsby means of a questionnaire designed to measurepatient expectation of effectiveness that a placeboTENS treatment offers equal suggestibility to thatof acupuncture’.

Inactivated laser

Irnich et al (2001, 2002), in trials carried out onpatients with chronic neck pain, used a laser penthat had been purposely deactivated by the manu-facturer. And in order to ensure double ‘blinding’(see p. 154) neither the patients nor therapist wereinformed about this.

Non-invasive needling techniques

Placebos of this type have been used in the pastbut which in no way could be considered by a patient to be credible. They include rubbing nee-dles against the skin (Borglum-Jensen et al (1979)and gluing needles to the skin (Gallacchi et al 1981).

More credible ones have included the employ-ment of a pencil-like probe (Molsberger & Hille

1994), the tapping of a needle’s guide tube againstthe skin (Lao et al 1995), and the insertion of ablunted cocktail skin through such a tube (Whiteet al 1996).

Recently, two even more credible but unfortu-nately slightly more invasive needling techniqueshave been invented.

Stretberger & Kleinhenz (1998), working at the Clinic of Anesthesiology in Heidleberg, havedesigned a needle with a blunt tip which, by mov-ing inside its handle, gives rise to a pricking sensa-tion on touching the skin similar to that felt whena needle penetrates the skin. In a study whichinvolved 60 volunteers divided into a ‘needle’group and a ‘placebo needle’ group none of themin either group suspected that the instrumentemployed had not penetrated the skin. The onlydifficulty, as will be discussed again later, was thatthe needle-evoked sensation known as de qi wasfelt by some of these volunteers both with placeboneedling and real acupuncture. A finding that ledthem to comment, ‘De qi in placebo needlingcould be caused by the pressure of the ring andplastic cover, by psychological influences, or bypain produced by direct pressure on a pain recep-tor in the skin.’

Park et al (1999) at the University of Exeter, UK,have invented a sham needle (Park Sham Device(PSD) that, by telescoping on making impact withthe skin, avoids penetration of it (Fig. 11.1).

This PSD has now been subjected to two ran-domized controlled trials (Park et al 2002). In thefirst study carried out in a district general hospital,58 patients were enrolled in a clinical trial ofacupuncture for acute stroke. Not one of thesepatients realized they had not been subjected topenetrative needling but as Park and his co-workersstated, ‘this finding may be limited by the factsthat these patients may have had abnormal sensa-tions because of their recent stroke and were pos-sibly disorientated from hospital admission …Experience in other clinical settings will berequired for further validation of the device.’

In the second study carried out in a universitylaboratory, 40 healthy acupuncture-naive adultvolunteers were tested. In this trial the surrogatemeasure of activity adopted was experience of thespecific needle sensation known as de qi. And asjudged by that none of the participants realized


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they had not been subjected to acupuncture. Thesefindings led them to conclude ‘that the newlydeveloped PSD is valid as a control procedure fortrials of the efficacy of acupuncture, or morespecifically, the needle penetration aspect of treat-ment’. They also, however commented, ‘furtherinvestigation of this device will be required toestablish its performance in the hands of differentclinicians, in different acupuncture points particu-larly with a different anatomical configuration(e.g. in more curved skin or in hairy regions), andwith sham needles made to match different manu-facturers’ styles’.

All this notwithstanding, that these two types ofnon-penetrative needling employed in both the trialcarried out in Germany and the one in Englandcaused a significant number of participants to exper-ience the needle-evoked sensation of de qi showsthat they cannot be considered to be entirelyinactive forms of treatment because presumably thissensory effect must have been brought about as a

result of pressure applied to the skin causingA-delta nerves to be stimulated which, as discussedin Chapter 10, is a sine qua non for the evoking ofneedle-induced analgesia.

Placebo analgesiaThe greatest hindrance to proving or disprovingwhether or not the analgesic effect produced byacupuncture is no more than a placebo effect is thata placebo itself is now known to afford pain reliefin response to cues that suggest it is an effectivetreatment. Furthermore, it has recently been con-firmed that this placebo-evoked analgesia, likeacupuncture-evoked analgesia, is opioid peptide-mediated (ter Reit 1998) and because of this, aswas shown some years ago, is naloxone reversible(Levine et al 1978, Levine & Gordon 1984).

As Fields & Basbaum ( 1999) have pointed out, itis possible in experiments using tourniquet-inducedischaemic pain as a model, to demonstrate a


1

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10 11

Figure 11.1 Park’s sham needle unit: 1. Needle handle, 2. Guide tube, 3. Guide o-ring, 4. Park tube, 5. Flange,6. Double-sided tape, 7. Skin, 8. Dermis, 9. Muscle, 10. Dull tip of sham needle, 11. Sharp tip of needle. (Reproducedwith permission of Park J. et al (1999) Development of a new sham needle. Acupuncture in Medicine 17(2): 111)

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significant placebo analgesic effect. And that, whilstnaloxone does not affect pain in subjects who havenot been given a placebo, it has been shown to significantly reduce placebo analgesia (Amanzio &Benedetti 1999).

The weight of current evidence, therefore, sup-ports a role for endogenous opioids in the produc-tion of placebo analgesia particularly now thatLipman et al (1990) have reported finding endogen-ous opioid-like material in the cerebral spinalfluid (CSF) of chronic pain patients after their painlevels had dropped following placebo administra-tion. And now that Benedetti (1996) has demon-strated not only a reduction of placebo analgesiaby naloxone but an enhancement of it by the chole-cystokinin antagonist proglumide.

In the light of all this, it is perhaps possible thatthe prevailing preoccupation with trying to find asuitable placebo for the purpose of comparing itsanalgesic effect with that produced by acupunc-ture might be misconceived and it may be betterinstead to test acupuncture against other anal-gesics as Loh et al (1984) did in a trial to determinethe place of this needle-evoked nerve stimulationtherapy in the prevention of migraine.

In that study patients were randomly assignedeither to Group A, who received acupuncture for3 months followed by drug therapy for the next3 months, or to Group B, who were given drug ther-apy first followed by acupuncture treatment forthe same periods of time. The two groups wereswitched at the end of each 3-month period after a2-week interval to allow for the effects of acupunc-ture to have worn off and for the excretion of anyresidual drugs.

The outcome of all this was that the frequencyand duration of migraine was found to be signifi-cantly less during the period of acupuncture treat-ment and that most patients much preferredhaving that particular form of therapy.

OTHER ACUPUNCTURE TRIAL-RELATEDFACTORS REQUIRED TO BE TAKEN INTOCONSIDERATION

BlindingIn drug trials it has for long been accepted thatboth the patient and therapist should not be able

to distinguish between the active substance beingtested and the inert one, as the expectations ofeither of them are liable to strongly influence theresults, as Noseworthy et al (1994) showed in arandomised placebo-controlled multiple sclerosisdrug trial.

In acupuncture trials such double-blinding is notpossible for whilst the patient can readily be‘blinded’ it is clearly not possible to ‘blind’ the ther-apist who by word or action may unwittingly com-municate bias. Hansen & Hansen (1983) sought toovercome this difficulty by the employment ofso-called ‘standardised minimal interaction’, butin general, the best that can be achieved is to havea ‘blinded’ independent evaluator.

RandomizationThe random placing of patients into a treatmentgroup and a control group is a well-established prac-tice in all clinical trials since its first successful useby the UK’s Medical Research Council in a trial car-ried out in 1948 to ascertain the efficacy of strepto-mycin in the treatment of pulmonary tuberculosis.

In that trial, because only one disease wasinvolved the employment of this procedure wasrelatively straightforward. With many acupuncturetrials, however, as Hansson & Lundeberg (1999)have pointed out, difficulties in ensuring thatpatients with exactly the same type of pain areevenly distributed between an active and a controlgroup have arisen when attempts have been madeto assess the efficacy of this type of treatment inpatients with conditions such as dental, neck orlow-back pain that lack diagnostic precision. This isbecause they are liable to be suffering from eithermyofascial TrP nociceptive pain, nociceptive painfrom some other cause, radiculopathic pain, neuro-pathic pain or a combination of these making theassessment of results, even when randomization isemployed, virtually impossible due to the respon-siveness of these different types of pain to acupunc-ture almost certainly being very different.

There is therefore a pressing need when attempt-ing to assess the value of acupuncture in patientswith any regional pain disorder to ensure that thepain suffered by those randomized to either anactive treatment group or a control group is of thesame type.


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Needle stimulation strengthFor the purpose of conducting acupuncture trialsit might seem essential for the strength of the dryneedle-evoked stimulus applied to each patient inthe treatment group to be kept constant. In trialswhere manual acupuncture is employed, this wouldmean keeping the needles in situ for the same lengthof time in everyone; also, either not twirling themor twirling them, and in the case of the latter, thisbeing carried out in exactly the same manner andto the same extent. It is, however, apparent fromeveryday clinical practice that, so far as manualacupuncture is concerned, the optimum amountsof stimulation required for individual patients arewidely different and can only be found for eachperson by a process of trial and error.

Therefore, the insistence on a fixed amount ofstimulation for every patient is liable to result insome patients being overstimulated, with as a con-sequence, exacerbation of their pain and othersbeing understimulated with, as a result, the treat-ment not given a chance to exert its maximum effect.

Macdonald et al (1983) are therefore in my opin-ion to be commended, for in their study on patientswith low-back pain, they made provisions in their trial protocol for the strength of stimulus to be varied according to individual patients’requirements.

Number of treatment sessionsWith acupuncture treatment it is rare for there tobe any appreciable benefit after only one treat-ment and, therefore, in my opinion, it is not appro-priate to attempt to evaluate the effectiveness of this type of therapy in a trial in which it is onlygiven on one occasion as has been the case in anumber of trials, such as the ones carried out byIrnich et al (2002), Jensen et al (1979) and Moore &Berk (1976).

It usually requires 3–4 sessions before a deci-sion can be made as to whether a patient’s pain islikely to respond to acupuncture (Lewith 1985) andoften more than these before any long-term reliefis obtained. This, however, it has to be admittedvaries according to both the type of pain disorderbeing treated and the person’s individual respon-siveness to acupuncture.

In acupuncture trials, therefore, it would notseem prudent to allow only a fixed number of sessions to be given to every patient for fear thatwith some individuals this may not be sufficient toallow them to achieve their maximum response. Amore realistic approach might be to allow eachpatient to receive up to a maximum of 10 treatmentsdepending on their individual requirements, aswas done in the traditional Chinese acupuncturetrial carried out by Coan et al (1980) and the TrPone carried out by Macdonald et al (1983).

Design of acupuncture trialsOf the various trials so far completed in which theeffect of acupuncture has been compared eitherwith that of some other type of treatment in cur-rent use such as physiotherapy or with that of aplacebo treatment, the design of most of them hasbeen one in which the comparison has been madebetween two groups, one receiving acupunctureand the other serving as a control.

A few trials, however, have been of the cross-over type in which the treatments being comparedhave been given sequentially in random order toeach patient in turn. A trial of this type though hascertain disadvantages when the effect of acupunc-ture is being assessed because the speed of responseto such treatment and the immediate duration ofrelief from it varies widely from person to person,with in some cases there being a considerabledelay before its full effect manifests itself. For thisreason acupuncture and then some other form oftreatment should be given with only a short interval in between, any delayed response from theacupuncture may cause confusion when attemptingto assess the effectiveness of the second treatment.Such a problem is not confined to acupuncture tri-als alone but applies to any trial in which sometype of physical treatment is being evaluated. It is,therefore, apparent that if a cross-over design isused in trials of this kind it is essential for there tobe a long interval of up to several months inbetween each type of treatment (Lewith & Machin1983).

A further problem with a cross-over trial is thata person who seems to be doing well with the ini-tial treatment may be reluctant or even unwillingto change from this to some other form of treatment.


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On balance, therefore, with acupuncture trials,group comparison is preferable.

Numbers required in trials for theevaluation of acupunctureThe number of patients required in order to makean acupuncture trial statistically valid depends onseveral factors including the anticipatory clinicaldifferences between the treatments being com-pared, the level of statistical significance con-sidered appropriate and what are considered to bethe chances of detecting such differences. Advicetherefore should always be taken from a statisti-cian with special training in this particular type ofwork ( Lewith & Machin 1983).

The assessment of resultsAssessments of the results of an acupuncture trialshould be made immediately at the end of a laiddown course of treatment and then at varyingintervals after this, depending on the disorder beingtreated and in particular on its natural history.

Whilst agreeing with Richardson & Vincent(1986) in their reference to trials already completedthat ‘the relative paucity of long-term follow-updata is especially disappointing with chronic painpatients where the need to demonstrate lastingbenefits from a new treatment is of paramountimportance’, exception has to be taken to theirview that ‘temporary relief of pain in such a groupmay be of theoretical interest but will have littlesignificance‘ for it has to be remembered that evenwhen the relief from chronic pain with acupunc-ture or for that matter any form of treatment isfound to be only short lasting, this is not necessar-ily a failure so far as the patient is concerned as the quality of life is often improved by repeating thetreatment at frequent intervals. And within thiscontext, it has to be borne in mind that, whilst itmay be possible to demonstrate that acupuncture,so far as the alleviation of chronic pain is concerned,is a valuable symptomatic form of treatment, thevery nature of the condition makes it unlikely thatit will often be shown to be a ‘cure’.

Methods of measuring pain reliefUnfortunately there are no objective means ofmeasuring changes in the character and intensity

of pain because, as Scott & Huskisson (1976) pointedout over 20 years ago, ‘measurement of pain mustalways be subjective since pain is a subjectivephenomenon – only the patient can therefore meas-ure its severity.’

The pain-measuring devices that have proved tobe of value include the visual analogue scale, thegraphic rating scale (Huskisson 1974a, b) and theMcGill Pain Questionnaire (Melzack 1975).

As patients find it extremely difficult to remem-ber any changes that may occur in their perceptionof pain over a period of time, it is very helpful forthem to be issued with diaries so that they can recorddetails concerning pain levels, medication intakeand sleep on a daily basis (Lewith et al 1983). Inaddition to information provided by the patient, theassessor should take into account such factors aschanges in mobility and time off work. Finally, withcertain disorders such as, for example, shoulder-cuff lesions, use should be made of a goniometer formeasuring joint movements (Fernandes et al 1980).

These subjective and objective methods of assess-ment clearly apply to pain trials in general and asthere is nothing particular about them in relationto acupuncture trials they will not be discussedfurther, but anyone who requires more detailedinformation should consult an extensive review ofmeasuring and assessing pain in general providedby Melzack & Katz (1999) and an account of howmethods of measuring pain should be employedin the assessment of acupuncture treatment in par-ticular provided by Vincent & Chapman (1989).

FUTURE ACUPUNCTURE CLINICAL TRIALS

Trial protocolsFrom what has already been said in this chapter it isobvious that the carrying out of acupuncture clini-cal trials in the future will demand the employing ofmethodology of a higher standard than heretoforewith, as an essential component of this, the drawingup of well-designed protocols (White & Park 1999).

Recommended standards for the reporting ofacupuncture trials

In an attempt to improve the quality of acupunc-ture trials an international group of experienced


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acupuncturists have devised a set of recommenda-tions called Standards for Reporting Interventionsin Controlled Trials of Acupuncture (STRICTA),which all those engaged in investigating the effi-cacy of this type of therapy are urged to adopt(Macpherson et al 2002).

These recommendations are meant to beemployed in conjunction with the ConsolidatedStandards for Reporting Trials (CONSORT) state-ment. This statement, which was originally drawnup by Begg et al (1996) and then subsequentlyshown by Moher et al (2001a) to have a positiveinfluence on the quality of trial reporting, was notonly revised by Moher et al (2001b), but also ultim-ately further explained and elaborated by Altmanet al (2001).

These STRICTA recommendations are con-sidered to be of such fundamental importance that ithas been decided to publish them concurrently inall the principal journals devoted to the study ofacupuncture. The hope is that the implementation

of these will so improve the reporting of acupunc-ture trials as to make both their critical appraisaland the interpretation of their results far easierthan when, for example, ter Reit et al in 1990 car-ried out a criteria-based meta-analysis of them.

They are therefore reproduced here (Table 11.1)to serve as a benchmark for all those wishing toparticipate in the carrying out of future trials.

It should be emphasized that these STRICTAguidelines are not immutable for the intention is tore-draft them as and when subsequent experienceand debate dictates.

My only comment concerning this matter is thatthe giving of multiple types of acupuncture tothose in the ‘treatment’ group, as Irnich et al (2002)recently did when they needled not only triggerand traditional Chinese acupuncture points butalso auricular ones in a study of patients withchronic neck pain, is best avoided as it makes therelative contribution of each of them to the overallresults of such a trial difficult to assess.


Table 11.1

Intervention Description

Acupuncture rationale 1 Style of acupunctureRationale for treatment (e.g. syndrome patterns, segmental levels, trigger points) andindividualization if used. And literature sources to justify rationale

Needling details 2 Points used (uni/bilateral)Numbers of needles insertedDepths of insertion (tissue level, mm or cun)Responses elicited (e.g. de qi or twitch response)Needle stimulation (manual or electrical)Needle retention timeNeedle type (gauge, length, and manufacturer )

Treatment regime 3 Number of treatment sessions Frequency of treatment

Co-interventions 4 Other interventions (e.g. moxibustion, cupping, herbs, exercises, lifestyle advice)

Practitioner background 5 Duration of relevant trainingLength of clinical experienceExpertise in specific condition

Control interventions 6 Intended effect of control intervention and its appropriateness to research question and,if appropriate, blinding of participants (e.g. active comparison, minimally active penetrating or non-penetrating sham, inert)Explanations given to patient of treatment and control interventionsDetails of control intervention (precise description, as for Item 2 above, and other items if different)Sources that justify choice of control

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Prospective participants in acupuncture clinical trialsThe time has passed when acupuncture clinical tri-als can continue to be carried out by practitionersin private practice with inadequate numbers, diffi-culty in finding suitable controls and little or nostatistical advice. For as Filshie & Cummings (1999)have so rightly said ‘too much time has been spentby lone enthusiasts and inexperienced researchteams who may have repeated previous errorsmade by academics unfamiliar with the subject’.

The carrying out of clinical trials requires con-siderable expertise and can only in the future beadequately conducted by university-based researchteams with money for it provided either by thegovernment or charitable research trusts. However,as Ernst & White (1997) have commented, ‘researchincluding that appertaining to acupuncture isexpensive, there are no sponsors from industryand official funding bodies do not view acupunc-ture as a priority’.

Regrettably, we are currently in the unfortunateposition that hospital-based physicians will notuse acupuncture without clinical-trial-based evi-dence to support this but at the same time such trials cannot be carried out by them without themfirst becoming experienced in the practice of it!

There is however light on the horizon for asHayhoe (1998) has pointed out, several British uni-versities now provide lectures on acupuncture fortheir medical students and one, Exeter, has a chairin Complementary Medicine. In addition, therehas recently been a strong move to integrate com-plementary medicine within the UK’s NationalHealth Service (Foundation for Integrated Medicine1997). And in the USAa conference organized by theNational Institute of Health (1997) has published aconsensus statement concluding that there is nowsufficient evidence of acupuncture’s value to justifyits incorporation within the framework of conven-tional medicine.

Moreover, in the UK the numbers of doctorspractising acupuncture is steadily rising, with themembership of the British Medical AcupunctureSociety now being over 1400 medical practition-ers. Also, acupuncture is now available in 86% ofhospital-based chronic pain services (ClinicalStandards Advisory Group Report 1999) and isused in 37% of hospices (Wilkes 1992).

There are therefore sound grounds for believingthat clinicians with access to research facilities maywell be increasingly persuaded to enter into thedifficult domain of assessing acupuncture’s pain-relieving capability including, so far as the myofas-cial trigger point pain and fibromyalgia syndromesare concerned, the conducting of large scale trialsto provide evidence-based data concerning the rel-ative efficacy of and indications for superficial anddeep dry needling at trigger and tender point sites.

Possible future therapeutic advancesrelevant to the practice of acupunctureBefore closing this chapter it should be pointedout that over the course of time the practice ofacupuncture for the relief of pain may becomegreatly changed by future pharmaceutical innova-tions that then, in turn, will themselves have to besubjected to the rigours of carefully conductedclinical trials.

There are at least two possibilities. One is theintroduction into clinical practice of a cholecys-tokinin octapeptide receptor antagonist as thiswould have the effect of tilting the opioid and antio-pioid balance in the central nervous system (CNS)and, by so doing, would considerably assist with thetreatment of chronic pain with acupuncture (Han1994). The other is the introduction of a ketamine-like non-toxic N-methyl-D-aspartate receptor antag-onist, which would significantly decrease dorsalhorn central sensitisation and thus reduce the chron-icity of such disorders as the myofascial trigger pointpain and fibromyalgia syndromes.


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165

Chapter 12

Chest pain

CHAPTER CONTENTS

Introduction 165Anterior chest wall MTrP pain syndrome 166Similarities between the referral patterns

of anterior chest wall TrP pain and cardiacpain 167

Anterior chest wall MTrP pain and cardiac pain –the differential diagnosis 175

The use of traditional Chinese and TrPacupuncture in the treatment of coronaryheart disease 178

Anterior chest wall MTrP pain syndrome andother musculoskeletal pain disorders – thedifferential diagnosis 178

The development of MTrP pain in associationwith mitral valve prolapse 179

Posterior chest wall myofascial TrP activity 179Intercostal pain 183Post-thoracotomy pain 183Thoracotomy scar pain 183Section of an intercostal nerve 184

INTRODUCTION

In discussing the practical applications of triggerpoint (TrP) acupuncture in Part Three of this book,the indications for its use in the alleviation of certain types of chest pain will firstly be con-sidered because, historically, some of the earliest clinical observations concerning the referral ofpain from TrPs were made just before World War IIon patients with these in the muscles of the chestwall.

Attention will mainly be directed to cardiacpain and to musculoskeletal pain in this chapterbecause, so far as chest pain is concerned, it is inthe alleviation of these two types of pain thatacupuncture has its main application.

At the outset it has to be made clear that clin-ically there is often difficulty in distinguishingbetween cardiac and TrP pain because their pat-terns of distribution are often identical. Further-more, the added difficulty is that both may bepresent together.

Attention was fist drawn to the phenomenon of secondary TrP activation in the muscles of thechest wall in patients with coronary heart diseaseby two University of Pennsylvania physicians,Joseph Edeiken and Charles Wolferth, when in1936 they reviewed some cases of coronary throm-bosis in which pain in the shoulder had developedduring the course of strict bed rest.

Edeiken & Wolferth reported that on examin-ation of the muscles around the scapula in two oftheir patients, they found focal areas of exquisitetenderness, or what they called trigger zones in

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in this manner, she was prompted to read the vari-ous other important contributions to the subjectpublished over the next few years including thoseof Kellgren (1938), Steindler & Luck (1938) andSteindler (1940). From these she learnt that suchpain may be alleviated by injecting procaine into‘tender spots’ (trigger zones) in the muscles.

As a result of reading these reports Travelldecided in 1940 to persuade Dr Myron Herman,the medical resident at Sea View Hospital, to injectprocaine into trigger areas in the chest walls ofpatients with painful shoulders at that hospital(Travell et al 1942). It was because the results of this treatment were so impressive that Travelland her cardiologist colleague, Seymour Rinzler,decided to investigate a number of other patientsunder their care in the general medical wards atthe Beth Israel Hospital. The outcome of this wasthat in 1948 they published two outstanding papers.In one they drew attention to the fact that TrPsmay develop in the muscles of the chest wall as asecondary event in patients with cardiac pain andreported that it is possible to relieve the latter byinjecting procaine into these points, or by sprayingthe skin overlying them with ethyl chloride(Rinzler & Travell 1948). In the other they showedhow closely the pattern of pain, occurring as aresult of the primary activation of chest wall TrPs,may simulate that of ischaemic heart disease(Travell & Rinzler 1948). They were not, however,the first to recognize this, as Gutstein (1938), Kelly(1944) and Mendlowitz (1945) had previouslydescribed how pain from ‘tender spots’ in the muscles of the chest wall may have a similar patternof distribution to that of cardiac pain.

ANTERIOR CHEST WALL MTrP PAIN SYNDROME

This syndrome (Baldry 1997, 2001) mainly arisesas a result of either trauma-induced or stress-induced activation of TrPs in muscles of the anter-ior chest wall. It may also develop as a secondaryevent in patients with coronary artery disease as aresult of TrPs in muscles present in the zone of car-diac pain referral becoming activated as a result ofcardiac pain-evoked muscle spasm. In addition, itis liable to arise, for some as yet unexplained reason,in patients with mitral valve prolapse (see p. 179).

view of the fact that by applying pressure to thesezones they were able to reproduce the spontan-eously occurring pain in the shoulder. They fur-ther stated that one of their patients had noticedfor himself that pressure over one of these so-called trigger zones caused pain to be referred tothe left shoulder, up the left side of the neck anddown the left arm.

The significance of such observations mightreadily have been overlooked had it not been thatthis report came to the attention of Janet Travell,the American physician who has since contributedso much to the subject of referred pain from TrPs,at a time when she herself was suffering from a painful shoulder, not following a coronarythrombosis, but after having strained some musclesduring the course of her work. As she said in herautobiography, Office Hours: Day and Night (1968):

Poking around at night on the muscles over myshoulder blade, trying to give some ‘do-it-yourself’massage, I was astonished to touch some spotsthat intensified, or reproduced my pain, as thoughI had turned on an electric switch. It was my firstintroduction to the enigmatic trigger area. Nonerve existed, I knew, to connect those firingspots directly with my arm. I was baffled, but Idid not discard the observation on the groundsthat I could not explain it.

It was because Travell found that she couldreproduce pain in herself in exactly the same man-ner as Edeiken & Wolferth had done in patientswith myocardial infarction that prompted her tostudy the subject further. The opportunity to dothis arose almost immediately when, in 1936, shewas appointed to work under Dr Harry Gold in theCardiac Consultation Clinic at Sea View Hospitalon Staten Island, New York. At this hospital, whichspecialized in the treatment of tuberculosis, a largenumber of patients, having been kept in bed forlong periods, suffered severe pain in their shoul-ders and arms. As she says in her autobiography:

When I examined them by systematic palpationof the scapula and chest muscles, I easily uncov-ered the presence of trigger areas. I knew what tolook for . . .

Her interest in the referral of pain from what arenow called myofascial TrPs having been aroused

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SIMILARITIES BETWEEN THE REFERRALPATTERNS OF ANTERIOR CHEST WALL TrP PAIN AND CARDIAC PAIN

Pain from TrPs in muscles on the left side of theneck and chest wall and cardiac pain may havesimilar referral patterns.

Primary TrP pain referral may simulate that ofcardiac pain referral when there is TrP activity inonly one muscle. More often, however, such activ-ity develops in several muscles simultaneously, orspreads from one muscle to another until ultim-ately several are involved.

As pointed out by Travell (1976), a good exampleof such a chain reaction is when TrP activity arisesin the sternal division of the sternocleidomastoidmuscle causing pain to be referred down thelength of the sternum. Pain in this distributionmay then lead to the development of TrP activityin the sternalis muscle, with, as a result of this, painbeing referred to the pectoral region and the devel-opment of secondary TrP activity in the pectoralismajor muscle. These TrPs may then be responsiblefor pain being referred to the left shoulder anddown the left arm. This, therefore, is a good exam-ple as to how doing nothing more serious thanstraining a muscle in the neck may lead to thedevelopment of pain with a referral pattern exactlysimilar to that of coronary heart disease pain.

As it cannot be stressed too strongly it will be reit-erated that what makes the differential diagnosisdifficult is that not only may primary TrP pain havea similar pattern of referral to that of ischaemic heartdisease pain, but secondary TrP activity may alsodevelop in muscles that happen to lie within an areaaffected by the pain of this cardiac disorder.

The various muscles liable to be involvedinclude those in the neck, the sternal division of thesternocleidomastoid and the scaleni; in the chest, the sternalis, the subclavius, the pectoralis major,the pectoralis minor and the serratus anterior; andin the abdomen, the rectus abdominis and the exter-nal oblique muscles. The clinical manifestationsand treatment of TrP activity in each of these mus-cles will therefore be considered in turn.

Sternocleidomastoid muscleTrP activity in the lower end of the sternal divisionof the muscle may cause pain to be referred over

the upper part of the sternum (Fig. 16.6). TrPs else-where in this muscle refer pain to the face andscalp. Therefore, any discussion concerning theactivation and deactivation of them will be deferreduntil Chapter 16.

Scalene muscles

Activation of TrPs

TrP activity in any of the three scalene musclesmay develop as a primary event by straining theneck such as when pulling with the hands againsta strongly resistant force, or when lifting or carry-ing awkwardly some heavy object. Also, TrP activ-ity may develop as a result of the muscle strainbrought about by severe bouts of coughing, or byholding the neck in some awkward position eitherwhen lying or standing; and as a secondary eventwhen there is TrP activity in the sternocleidomas-toid muscle.

Specific pattern of pain referral

Pain from TrPs in either the scalenus anterior,medius, or posterior (Fig. 12.1) is liable to be referredanteriorly over the pectoral region; posteriorlyalong the medial border of the scapula; and later-ally across the front of the shoulder and down thearm. When the latter occurs, it is felt both in the frontand back of the arm, and extends to the thumb andindex finger (Fig. 12.2).

Pain from TrP activity in one or other of thesemuscles on the left side because of its distributionand because it sometimes only comes on withexertion may closely simulate coronary heart dis-ease pain.

In differentiating between the two it is helpfulto remember that referred pain from the scalenusanterior muscle is relieved when both the arm andclavicle are elevated by placing the forearm on theaffected side across the forehead (Ochsner et al1935); and it is aggravated by contracting the muscle by rotating the head as far as possible to theside of the pain whilst pulling the chin down intothe supraclavicular fossa.

With regard to the effect the position of the armhas on this type of pain, it is of interest to note thata man under my care, with pain in the chest and

Chest pain 167

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Figure 12.1 Muscles of the front of the neck. On the right the sternocleidomastoid has been removed.

Styloglossus Digastric

Stylohyoid

Mylohyoid

Sternocleidomastoid

Levator glandulae thyroideae

Sternohyoid

Cricothyroid

Sternothyroid

Transverse process of atlas

Splenius capitis

Hyoglossus

Fascial loop round digastric tendon

Longus capitis

Levator scapulae

Omohyoid

Trapezius

Scalenus medius

Scalenus posterior

Scalenus anterior

Figure 12.2 The pattern of pain referral from a trigger point or points (▲) in a scalene muscle.

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down the right arm from TrP activity in the rightscalenus anterior muscle, found that, although thepain was always aggravated by carrying heavyloads with the arm hanging down at the side of thebody, it was never present when, with the armheld high, he carried the British Legion banner atex-Servicemen’s parades.

TrP examination

TrPs in the scalenus anterior are found by palpatingthe muscle where it lies behind the posterior borderof the sternocleidomastoid muscle. It is useful todistend the external jugular vein by putting pres-sure on it at the base of the neck, as the vein crossesthe scalenus anterior muscle usually just about thelevel where TrP activity in this muscle occurs.

The scalenus medius lies lateral to the scalenusanterior and at a much deeper level against thetransverse processes of the vertebrae. TrPs in it mayreadily be identified by pressing against these struc-tures. The scalenus posterior is far more difficult topalpate, but, fortunately, TrP activity in it seems tobe much less common than in the other two.

TrP activity often develops in the scalenus anter-ior and medius concomitantly.

Associated TrPs

Satellite TrPs may develop in the various musclessituated in the regions to which pain from TrP activ-ity in the scalene muscles is referred. Anteriorlyreferred pain may cause TrPs in the pectoralismajor to become activated. Pain referred to theback of the arm may cause TrPs to become acti-vated in the triceps, and pain referred down thefront of the arm may cause similar activity todevelop in the brachioradialis and the extensorcarpi radialis. TrP activity in the scalene musclesmay also occur in association with it developing inthe levator scapulae muscle (see Ch. 14).

Deactivation of TrPs

Deactivation of TrPs in the scalenus anterior andmedius should be carried out with the patient inthe supine position, with the head supported by apillow and turned towards the opposite side. Indeactivating TrPs in the scalenus anterior, care has

to be taken not to puncture the external jugularvein, or to damage the cervical spinal nerve rootsand part of the brachial plexus where they emergein the groove between the scalenus anterior andmedius. It must, however, be remembered thatneedling a scalene TrP itself may cause momen-tary intense pain to shoot down the arm and thattherefore this alone does not necessarily implythat a nerve root has been irritated.

Thoracic outlet entrapment syndromeCompression of the brachial plexus and subclavianvessels as a result of TrP-evoked shortening of thescalene muscles will be discussed in Chapter 15.

Sternalis muscle

Activation of TrPs

TrP activity arises in this muscle as a primaryevent usually as a result of trauma to the front ofthe chest. And as a secondary event when pain isreferred to the region of the sternum as a result ofcoronary heart disease or the development of TrPactivity in either the lower end of the sternocleido-mastoid muscle or a scalene muscle.


This muscle is only present in about one in 20 people, but when it does exist, the development ofTrP activity in it is liable to give rise to deep sub-sternal pain with, at times, radiation of this acrossthe left or right pectoral region and down the innerside of the arm to the elbow (Fig. 12.3).

TrP examination

TrPs occur anywhere along the length of this mus-cle and are found by systematically palpating itagainst both borders of the underlying sternum.Firm pressure on a TrP causes considerable localtenderness and at times the referral of pain in a lat-eral direction.

Associated TrPs

TrP activity in this muscle is rarely an isolatedevent. It usually occurs in conjunction with similar

Chest pain 169

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activity in the pectoralis major muscle. And, asstated earlier, pain from TrP activity in the sternaldivision of the sternocleidomastoid muscle maybe referred downwards over the sternum andcause TrPs in it to become activated.

TrP deactivation

A TrP in this muscle is readily located by flat pal-pation. A needle is then inserted into the tissuesoverlying it after it has first been trapped betweentwo fingers.

Subclavius muscle

Activation of TrPs

TrPs in this muscle are liable to become activatedfor the same reasons as, and often in conjunctionwith, points in the pectoralis major muscle.


TrP activity in this muscle causes pain to be referredacross the front of the shoulder, down the front ofthe arm in the midline, the front of the forearm on the radial side, and the radial side of the palmarsurface of the hand and fingers. As Travell & Simons(1983) have pointed out, pain for some curiousreason is not felt at either the elbow or the wrist(Fig. 12.4).

TrP examination

TrPs in this muscle are usually to be found at itsmedial end around the site of its insertion into the1st rib (Fig. 12.4).

Associated TrPs

TrP activity in this muscle invariably occurs inassociation with similar activity in the pectoralismajor muscle.


A needle should be inserted superficially at anypoints of maximum tenderness found to be pre-sent just below the clavicle.

Pectoralis major

Activation of TrPs

The factors which may cause primary TrP activityto develop in this muscle include lifting a heavyweight or holding it for a sustained period; anytask that involves either repeated adduction of thearm, such as when cutting a hedge with manuallyoperated shears, or sustained adduction of it, suchas when the arm is placed in a sling for any lengthof time. Also, exposure of the muscle to draughtsor damp; persistent contraction of the muscle as aresult of chronic anxiety; and, in particular, theadoption of a faulty slouching posture when read-ing, writing or the carrying out of some task at awork bench.

Secondary TrP activity may develop in thismuscle when pain from coronary heart disease isreferred to the left side of the chest anteriorly.


Figure 12.3 The pattern of pain referral from a triggerpoint or points (▲) in the sternalis muscle.

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Specific patterns of pain referral

This muscle is divided according to its variousattachments into a clavicular section, a sternal sec-tion, and a costo-abdominal section. These mergetogether to be inserted by means of a tendon into thelateral lip of the bicipital groove of the humerus(Fig. 12.5). The specific patterns of TrP pain referralvary according to the particular section affected.

TrP activity in the clavicular section of the muscle causes pain to be referred both locally and,even more markedly, over the shoulder as far asthe anterior part of the deltoid muscle (Fig. 12.6).

TrP activity in the sternal section is foundmainly along the parasternal and mid-clavicularlines, with TrPs along the parasternal line referringpain locally and over the sternum. TrPs in the mid-clavicular line give rise to severe pain overthe anterior part of the chest and thus, on the leftside, over the praecordium. From there it oftenspreads down the inner aspect of the arm and is

felt particularly strongly over the medial epi-condyle. It then terminates in the ring and littlefingers (Fig. 12.7).

TrP activity along the lateral free margin of themuscle, where it forms the anterior axillary fold,gives rise to pain and tenderness in the breast, aswell as tenderness of the nipple. In women this notinfrequently leads to an erroneous diagnosis ofmastitis, even when the texture of the breast is nor-mal (Fig. 12.8).

TrP examination

TrPs in all sections of this muscle should be locatedby flat palpation with the patient lying down.

Associated TrP activity

TrP activity in the pectoralis major may occur inconjunction with similar activity in the sternalis,sternocleidomastoid, and scalene muscles. Satellite

Chest pain 171

Figure 12.4 The pattern of pain referral from a trigger point or points (▲) in the subclavius muscle.

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Figure 12.5 Superficial muscles of the front of the chest and upper arm. Left side.

Sternocostal part of pectoralis major

Clavicular part of pectoralis major

Deltoid

Costo-abdominal part of pectoralis major

Latissimus dorsi

Serratus anteriorCoracobrachialisBiceps

BrachialisTriceps (long head)Triceps

Triceps (medial head)Triceps

Brachioradialis

Brachialis

Bicipital aponeurosis

Figure 12.6 The pattern of pain referral from a triggerpoint or points (▲) in the clavicular section of thepectoralis major muscle.

Figure 12.7 The pattern of pain referral from a triggerpoint or points (▲) in the sternal section of the pectoralismajor muscle.

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Chest pain 173

TrPs may also be found in the anterior deltoidmuscle due to it lying within the pectoralis major’spain referral zone.


When deactivating TrPs in the pectoralis major orany other muscle covering the chest wall, needlesshould never be inserted vertically for fear of pene-trating the pleura and producing a pneumothorax,but should always be inserted in an oblique direction.

Bilateral TrP activity

When TrP activity occurs in both the right and leftpectoralis major muscles simultaneously the painmay be said by the patient to be ‘across the chest’,a description that immediately raises the possi-bility of it being due to coronary heart disease.However, the circumstances prevailing prior tothe development of the pain may be of diagnostichelp as shown by the following case history.

A maintenance fitter (47 years of age) sent for hisgeneral practitioner in the middle of the night becauseof pain across the chest and shortness of breath. Apain-relieving injection was given. Blood specimenswere taken that night and the next 2 days for cardiac

enzyme studies. These proved to be normal as did asubsequent ECG both at rest and after exercise.

However, as he continued to get episodes of painacross his chest most days he was at first givennifedipine (Adalat), but when it became obvious hewas not suffering from angina, he was put on tonaproxen (Naprosyn). And when this did not proveparticularly helpful, he was given clomipramine(Anafranil) as it was thought the persistence of thepain might be associated with nervous tension anddepression. After 7 months he was referred to me forfurther assessment. On going back over the history itbecame apparent that the initial attack of nocturnalpain had started after lifting a particularly heavy pieceof machinery. Also, that the subsequent episodes ofpain that he described as stabbing in character werenot brought on by walking, but usually came on afterhaving exerted himself carrying out some heavy taskat work. They were also particularly troublesome onadopting certain positions in bed.

From the history, therefore, it was most likely thatthe pain was of muscular origin. And on examination,TrPs were found to be present in the sternal section ofthe pectoralis major, along the parasternal line on theright side and mid-clavicular line on the left side, alsoalong the free edge of the costo-abdominal section ofthe muscle on the left side.

Once these TrPs had been deactivated by means of the carrying out of superficial dry needling on three occasions at weekly intervals and one furthertime 2 weeks later lasting relief from the pain wasobtained.

Pectoralis minor

Activation of TrPs

The factors responsible for the development of TrP activity in this muscle (Fig. 12.9) are similar to those responsible for this happening in the pectoralis major and therefore it often developssimultaneously in both of these muscles.


Pain from TrP activity in this muscle is referredwidely over the front of the chest so that on the leftside it is felt over the praecordium, over the frontof the shoulder, and at times down the ulnar side

Figure 12.8 The pattern of pain referral from a triggerpoint or points (▲) in the lateral free margin of thepectoralis major muscle.

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Figure 12.9 The deep muscles of the front of the chest and arm. Left side.

Pectoralis minor

Subclavius

Subscapularis

Long head of biceps

Short head of biceps

Coracobrachialis

Latissimus dorsi

Teres majorSerratus anterior

Biceps

Brachialis

of the arm to the hand, where it is felt in the mid-dle, ring and little fingers (Fig. 12.10).

TrP examination

When locating TrPs in this muscle the patient may either be seated or lying in the supine position.In either case the pectoralis major should be slack-ened by having the patient’s arm lying comfort-ably to the side with the forearm across theabdomen. The pectoralis minor is then put on thestretch by getting the patient to brace the shoulderbackwards. TrPs are usually to be found in thelower part of the muscle where it is attached to theribs, or in the upper part close to its attachment tothe coracoid process.


This is the same as for the pectoralis major muscle.

Serratus anterior muscle

Activation of TrPs

TrP activity may develop in this muscle (Fig. 12.9)when it is strained either as a result of the carrying

Figure 12.10 The pattern of pain referral from a trigger point or points (▲) in the pectoralis minor muscle.

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out of some athletic pursuit or during the courseof severe coughing. Anxiety, with the muscles ofthe chest wall held in a persistently contractedstate, is another cause.


Pain from TrP activity in this muscle which wrapsitself closely around the rib cage is referred to theside and back of the chest, and, at times, down theulnar aspect of the arm (Fig. 12.11). The patientmay also complain that it is painful to take a deepbreath – the so-called stitch in the side.

TrP examination

With the patient lying down and turned so that theaffected side is uppermost, the muscle is put onthe stretch by pulling the arm backwards. TrPs init are usually located in the mid-axillary line atabout the level of the 5th and 6th ribs in line withthe nipple (Fig. 12.11).

Associated TrPs

TrP activity in this muscle is often an isolatedevent. After a time, however, TrPs in its mainantagonist the latissimus dorsi may also becomeactivated.


The TrPs are deactivated by superficial dryneedling carried out with the patient lying with theaffected side uppermost. The needle should bedirected at a shallow angle almost parallel to thechest wall towards an underlying rib so as to avoidentering the pleural space.

Rectus abdominis and external obliquemusclesThe effects of TrP activity developing in these twomuscles will be discussed in detail when consider-ing abdominal pain in Chapter 20. It is necessaryto state here, however, that TrP activity in theupper part of the rectus abdominis muscle and inthe upper part of the external oblique muscle may

cause pain to be referred upwards over the lowerpart of the chest anteriorly. When this occurs,either on the left or right side, it is liable to be mis-diagnosed as being pleural in origin in spite of theabsence of either a pleural rub or any signs ofintrapulmonary disease. And on the left side it mayclosely mimic the pain of coronary heart disease(Kelly 1944).

Activation of TrPs

This commonly occurs either as a result of acutetrauma or chronic overloading with the latter oftenhaving an occupational basis.

TrP examination

The patient should be placed in the supine posi-tion and instructed to stretch the muscles by hold-ing the breath in deep inspiration. TrPs in theupper part of the rectus abdominis are usually tobe found in the angle between the costal marginand the xiphisternum. In the upper part of theexternal oblique muscles they are either along orunder the lower border of the rib cage (Figs 20.3and 20.4).


Each TrP should be trapped between two fin-gers prior to inserting a needle into the tissuesoverlying it.

ANTERIOR CHEST WALL MTrP PAIN ANDCARDIAC PAIN – THE DIFFERENTIALDIAGNOSIS

As has already been stated, muscles in the chestwall when subjected to trauma of one kind oranother may develop TrP activity with the patternof pain referral resulting from this being identicalwith that seen in coronary heart disease. Also, thesame chest wall muscles may develop satellite TrPactivity as a result of being within the area affectedby pain from coronary heart disease.

It is, therefore, easy to see that diagnostic confu-sion may readily occur and, whilst it is obviouslyimportant not to overlook angina when present, it

Chest pain 175

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Figure 12.11 A, B and C The pattern of pain referral from a trigger point or points (▲) in the serratus anterior muscle.

BA

C

TP

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is equally essential not to diagnose chest pain asbeing anginal when it is only muscular in origin.This is a mistake as frequently made today as itwas when Allison (1950) wrote in reference to non-cardiac chest pain:

… the frequency with which such patients areseen in routine out-patient work emphasizes theneed for a reorientation towards pain in the chest,and suggests that in clinical teaching pride ofplace is too often given to angina pectoris inexplanation of the pain, and too little regard ispaid to local structural causes.

One particular circumstance when primaryanterior chest wall TrP pain may be overlooked iswhen it occurs in someone known to have a his-tory of coronary heart disease. Chest pain arisingsoon after recovery from a myocardial infarction,if accompanied by fever and a pericardial rub, isreadily recognized to be part of the post-infarctionsyndrome (Dressler 1959). If, however, it occurs by itself, there is a tendency to assume it must be anginal, and to overlook the possibility that itmay have arisen as a result of the activation ofTrPs. Similarly, anterior chest wall TrP pain mayerroneously be assumed to be anginal when itoccurs at some time following coronary by-passsurgery.

The relevance of all this to the practice of TrPacupuncture is that, whilst pain arising as a resultof the primary activation of TrPs is readily allevi-ated by means of superficial dry needling carriedout at these points, and whilst, as will be explainedlater, treatment of this type may have a limitedplace in the overall management of coronary heartdisease, clearly before using it for the alleviation ofany type of chest pain, it is essential to have madean exact diagnosis as to its cause. For this reasonthe various problems that arise in differentiatingbetween cardiac pain and TrP pain will now be discussed.

When attempting to distinguish between thesetwo types of pain careful history-taking is clearly ofprime importance, but this by itself may be incon-clusive. This is because, whilst with ischaemic heartdisease there is substernal tightness and frequentlyradiation of pain up into the neck, across the chestto the shoulder and down the left arm, what is less

well known is that pain emanating from TrPs inanterior chest wall muscles may have a referral pattern exactly the same as this. And, moreover,although angina is characteristically brought on byexertion, chest wall TrP pain may also be aggra-vated by this. The difference is that whereas withangina the amount of effort required to produce thepain is fairly constant, with TrP pain it is liable tovary widely from day to day. Also, pain of this typeis often aggravated by stretching and twistingmovements of the chest wall muscles.

Furthermore, angina may on occasion come onat rest. When this is due to the heart rate increas-ing in response to some emotional upset, it usuallyonly lasts for a relatively brief period, whereas, incontrast to this, when TrP pain develops at rest it isliable to persist for a long time. Also, both types ofpain may disturb sleep. With ischaemic heart dis-ease this is sometimes because of a tachycardiabrought on by dreaming, and with non-cardiacTrP pain, it is due to the adoption of some posturethat puts the muscles on the stretch.

The finding of TrPs on clinical examination isclearly only of limited value as it does not help todistinguish between cardiac pain with superim-posed TrP pain and primary myofascial TrP pain.

The response to a therapeutic trial of sublingualglyceryl trinitrate may also be misleading sincethe placebo effect of this ensures that up to 30% ofpatients with chest pain from any cause may beimproved.

Electrocardiography, too, has its limitations, as it is not uncommon for a patient with wide-spread coronary heart disease to have a normaltracing. Conversely, any abnormal changes seenmay only be a reflection of what has happened inthe past and have no relevance to the pain underinvestigation. An ECG taken after exercise testingmay also occasionally be misleading.

It therefore follows that there are times when in order to distinguish between coronary arterydisease pain and a non-cardiac chest wall painsuch as that which emanates from primarily activated TrPs either a coronary arteriogram, orassessment of left-ventricular function by themore recently introduced technique of radionu-clide technetium angiography performed at restand during exercise (Borer et al 1977, Petch 1986)may be necessary.

Chest pain 177

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THE USE OF TRADITIONAL CHINESE AND TrP ACUPUNCTURE IN THE TREATMENTOF CORONARY HEART DISEASE

AnginaThe use of traditional Chinese acupuncture for the treatment of angina has, over the years, beenextensively investigated by Ballegaard and his co-workers (Ballegaard 1998). Nevertheless, in viewof the various highly effective anti-anginal agentsnow available, the place for this in its routine man-agement must be strictly limited.

If, however, superimposed upon episodes ofanginal pain, a more persistent type of pain devel-ops with tenderness of the chest wall, then TrPsshould be sought and, if found, should be deacti-vated by means of the carrying out of superficialdry needling at these TrP sites.

Myocardial infarctionThe pain of myocardial infarction, although severe,is generally of relatively limited duration and usually satisfactorily controlled by analgesics. How-ever, at times, in spite of a patient’s general condi-tion improving, the pain persists for an unusuallylong time. One reason for this is the secondarydevelopment of TrP activity in the muscles of thechest wall (Rinzler & Travell 1948, Kennard &Haugen 1955). And when this is so, it may readilybe alleviated by means of dry needle stimulationof nerve endings in the tissues immediately over-lying these points.

Coronary by-pass surgeryWhen chest pain recurs soon after a coronary by-pass operation, there is an instinctive tendency,particularly on the part of the patient, to assume itmust be anginal and that the operation has been afailure. It has to be remembered, however, thattrauma to the chest wall muscles whenever a tho-racotomy is performed for any purpose is veryliable to activate TrPs in these muscles and for thisto be the cause of the pain. In such circumstances,therefore, a search for TrPs should always be madeand, if found, deactivated by the carrying out ofsuperficial dry needling.

ANTERIOR CHEST WALL MTrP PAINSYNDROME AND OTHERMUSCULOSKELETAL PAIN DISORDERS –THE DIFFERENTIAL DIAGNOSIS

There are several anterior chest wall muscu-loskeletal disorders which, because of the distribu-tion of their pain and the presence of focal areas of exquisite tenderness, have to be distinguishedfrom the MTrP pain syndrome (Baldry 1997, 2001).

These include, amongst others, pathological frac-tures of the ribs, costochondritis, Tietze’s diseaseand fibromyalgia.

Pathological rib fracturesMultiple pathological fractures of the ribs withfocal areas of pain and tenderness may be due tometastases from carcinoma of the breast, kidney,lung, prostate or thyroid; also to osteomalachia,osteoporosis or Pagets disease of bone.

Costochondritis (syns: costosternalchondrodynia, costosternal syndrome,chest wall syndrome)The pathogenesis of this disorder is uncertain butpossibly trauma is a contributory factor. With it anumber of costal cartilages, usually the second to the fifth become painful and extremely tender.The pain may remain localized, but frequently it radiates across the chest towards the shoulder,down the arm and, in some cases, up into the neck (Bonica & Sola 1990). On either side of thechest, therefore, its pain referral pattern may simu-late pain from anterior chest wall TrPs, and on the left side that of coronary heart disease.Furthermore, at times it may develop in conjunc-tion with this latter disorder (Wolf & Stern 1976,Epstein et al 1979).

Tietze’s syndromeThis much rarer syndrome, first described by theGerman physician Tietze in 1921, is one where,unlike with costochondritis, the pain is confined toone or more of the upper four costal cartilages. Italso differs from that disorder in so much that the


Chap-12.qxd 11*10*04 10:26 Page 178

affected cartilages are not only tender but swollen(Kayser 1956).

With both costochondritis and Tietze’s syn-drome, pecking the costal cartilage with a dry nee-dle often provides temporary pain relief and theadvantage of it over the alternative of injecting acorticosteroid is that it can be repeated as often asis found to be necessary.

FibromyalgiaPatients with fibromyalgia are liable to have tender points at their second costochondal junc-tions. This rarely causes any diagnostic difficultyas there are usually, in addition to pain in manyregions of the body, various other characteristicmanifestations of this disorder. However, as dis-cussed in Chapter 10, very occasionally the pain atan early stage of this disease may be confined tothe chest wall (Pellegrino 1990).

THE DEVELOPMENT OF MTrP PAIN INASSOCIATION WITH MITRAL VALVEPROLAPSE

When Maresca et al (1989) examined 30 patientswith mitral valve prolapse, they found that 30 ofthem had TrPs in muscles of the chest wall andthat 12 of them had pain emanating from thesepoints. The reason for TrP activity developing inthis disorder is not known.

POSTERIOR CHEST WALL MYOFASCIALTrP ACTIVITY

TrP activity in certain muscles of the posteriorchest wall such as the supraspinatus and infra-spinatus cause pain to be referred mainly to theshoulder region and down the arm. These muscleswill, therefore, be discussed in Chapter 13. AndTrP activity in others, such as the levator scapulae,trapezius, and rhomboids causes pain to be feltpredominantly in the neck, shoulder girdle anddown the arm; a detailed account of these muscleswill, therefore, be given in Chapter 14.

The two muscles in the posterior part of thechest in which TrP activity causes pain to be felt in

the upper part of the back itself as well as downthe arm are the serratus posterior superior and thelatissimus dorsi. It is to these two muscles, there-fore, that attention will now be directed.

Serratus posterior superior

Activation of TrPs

Primary activation of TrPs in this muscle may occuras a result of protracted bouts of coughing. Thismay also happen when the scapula is pressed hardagainst it by the shoulders being persistently ele-vated and rotated forwards such as may occurwhen sitting for long periods at a desk or workingsurface that is too high. Also, satellite TrPs maydevelop in this muscle when TrP activity in the sca-lene muscles causes pain to be referred to the poste-rior chest wall around the inner part of the scapula(Fig. 12.2).


This thin quadrilateral muscle, situated beneaththe trapezius and the rhomboids, and attachedmedially to the spines of the 7th cervical vertebraand the first three dorsal vertebrae, and inferolat-erally by four fleshy digitations to the 2nd, 3rd, 4thand 5th ribs near to their angles behind the upperpart of the scapula, is liable to develop TrP activityat various sites near to this inferolateral insertion(Fig. 12.12). When this occurs, pain is felt as a dull

Chest pain 179

Figure 12.12 With the arm to the side, a trigger point inthe inferolateral part of the serratus posterior superiorcannot be palpated as it lies behind the upper inner part ofthe scapula. To palpate a trigger point at this site,therefore, the scapula has to be pulled forwards as shown.

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ache around the insertion of the muscle into theribs behind the scapula. From there it radiates tothe back of the shoulder and down the back of thearm to be felt particularly around the medial epi-condyle. Occasionally, it is felt down the inner sideof the forearm and hand as far as the little finger(Fig. 12.13). This pain pattern is similar to that pro-duced by compression of the 8th cervical nerveroot (Reynolds 1981). It is distinguished from thisby there being no objective neurological signs andby pressure on these TrPs reproducing the charac-teristic pain pattern.

TrP examination

The patient sits forwards with the arm stretchedacross the front of the chest in order to bring thescapula out of the way so that the muscle can bepalpated where it lies behind the upper part of thisbone deep to the trapezius and rhomboid muscles.The muscle is then examined by rolling a finger

over it against an underlying rib. Associated TrPsmay also be found in the rhomboids and in someof the nearby paraspinal muscles.

Associated TrPs

TrPs in this muscle are often associated with TrPactivity in the synergistic inspiratory scalene musclesin the neck, the nearby erector spinae muscles, andoverlying rhomboids.


With the patient lying on the opposite side andwith the scapula brought well forwards, a needleis inserted at an angle of 45° into the tissues overlying the TrP whilst fixing this between twofingers over a rib. Care must be taken not to insertthe needle perpendicularly into an intercostalspace as this may result in the pleura being penetrated.


Figure 12.13 The pattern of pain referral from a trigger point or points (▲) in the serratus posterior superior muscle.

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Latissimus dorsi muscleLatissimus dorsi, which translated from the Latinmeans ‘widest of the back’, is an appropriate name for this muscle with its extensive fan-shapedattachment to the trunk that stretches from thespinous processes of the lower six thoracic, and allthe lumbar vertebrae and sacrum in the midline tothe crest of the ilium and to the last four ribs. Andwhich then sweeps upwards into the axilla to formwith the teres major muscle the posterior axillaryfold prior to the tendons of these two muscles thenjoining together to be inserted into the bicipitalgroove of the humerus (Fig. 12.14). For some rea-son, despite this muscle covering such a large areaof the back, TrPs usually only become activated inthe part of it that is situated in the posterior axil-lary fold.

Activation of TrPs

These TrPs in the posterior axillary fold becomeactivated when the upper part of the muscle at itsinsertion into the humerus is subjected to strain.

Examples of when this may occur include reach-ing forwards and upwards with the arm whilstcarrying some heavy object; stretching the armsuch as when hanging on to a rope; or strainingthe arm whilst engaging in some unusually heavytask such as digging or weeding.


From TrPs in the posterior axillary fold, pain of adull aching type is referred to the inferior angle ofthe scapula and the part of the back immediatelyaround this; it may also extend to the posterioraspect of the shoulder, and down the inner side ofthe arm, forearm and hand, to terminate in thering and little fingers (Fig. 12.15).

The pain is persistent and is neither aggravatednor relieved by any type of movements. It is becauseof this lack of relationship to movements andbecause the TrPs responsible for it are tucked awayin the posterior axillary fold that probably accountsfor its myofascial origin being both easily and com-monly overlooked.

Chest pain 181

Figure 12.14 Superficial muscles of the back of the neck and upper part of the trunk. On the left, the skin, superficialand deep fasciae have been removed. On the right, the sternocleidomastoid, trapezius, latissimus dorsi and deltoid have been dissected away.

Semispinalis capitisSternocleidomastoid

Trapezius

Deltoid

Latissimus dorsi

Splenius capitisRhomboideus minor

Rhomboideus majorLevator scapulae

Supraspinatus

Infraspinatus

Teres minor

Teres major

Serratus anterior

Serratus posterior inferior

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TrP examination

TrPs in this muscle are most readily found by pla-cing the patient in the supine position and puttingit on the stretch by means of abducting the armand placing the hand behind the head.

Both the superficial and deep parts of the musclein the posterior axillary fold should be examined,because when Simons & Travell (1976) inserted7.5% saline into the muscle at this site, an injectioninto the deep fibres referred pain to the back aroundthe lower part of the scapula, whilst an injection intothe superficial ones referred pain down the arm.

Associated TrPs

TrP activity is likely to develop at the same time inthe anatomically closely related teres major andthe long head of the triceps.


Once a TrP is located it is held between the thumband fingers whilst a needle is inserted into the tis-sues overlying it. As TrPs in this muscle tend to begrouped together, both in its superficial and deepparts, this procedure may have to be repeated sev-eral times.

Paraspinal musclesMyofascial pain in the posterior chest wall may alsoarise from TrP activity in superficial paraspinalmuscles (erector spinae) such as the iliocostalis tho-racis and in deep paraspinal muscles such as themultifidius.

The pain from TrP activity in the iliocostalisthoracis muscle at the mid-thoracic level is con-centrated around the inferior angle of the scapula,but it also spreads upwards and downwards (Fig.12.16).

The pain that emanates from a TrP in the multi-fidus at the mid-thoracic level remains localizedaround it deep in the paravertebral region (Fig.12.17).

Rectus abdominis muscleMyofascial pain in the lower part of the posteriorchest wall may, at times, be referred there from


Figure 12.16 The pattern of pain referral from a trigger point (▲) in the iliocostalis thoracis muscle.

Figure 12.15 The pattern of pain referral from a triggerpoint or points (▲) in the latissimus dorsi muscle wherethis muscle together with the teres major muscle formsthe posterior axillary fold.

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TrPs in the upper part of the rectus abdominis at the site where the muscle becomes inserted intothe rib cage at the junction of the costal margin andxiphisternum (Fig. 20.3).

INTERCOSTAL PAIN

Pain that radiaties from the back to the front of thechest in a direction parallel with the ribs and fromthe lower part of the chest to the anterior abdom-inal wall may be due to a vertebral disorder caus-ing irritation of an intercostal nerve root. In allsuch cases, therefore, radiographs of the dorsalspine are mandatory. It should be remembered,however, that in the early stages of metastaticinvolvement of vertebrae, the radiographic appear-ances may remain normal.

The possibility that the pain is the precursor ofa herpes zoster rash also has to be considered.

Alternatively, and what for long has been known,but somehow lost sight of, is that pain in this dis-tribution may be due to the development of TrPactivity in an intercostal muscle. Kellgren in 1938produced it experimentally by injecting hypertonicsaline into intercostal muscles. And Kelly in 1944reported that pain around the chest in several

patients under his care emanated from foci ofexquisite tenderness in these particular muscles.

The following case illustrates how TrP activityin an intercostal muscle may be overlooked unlessspecifically looked for.

A farmer (36 years of age) developed severe painradiating from the back to the front of the right sideof the chest in the 5th intercostal space. When after 2 years he continued to complain of this in spite ofhaving been given analgesics for most of this time, hisgeneral practitioner referred him to a pain clinic in order to exclude the possibility of nerve rootentrapment. There were no objective neurologicalsigns; also, chest and spine X-rays were normal. Inspite of this an intercostal nerve block was carried out but with no significant improvement. Whensubsequently he was seen by me there were two fociof exquisite tenderness to be found, one in themultifidus muscle at the level of the 5th thoracicvertebra, and one in an intercostal muscle in theposterior axillary line. Deactivation of these two TrPsby dry needle stimulation resulted in temporary relieffor a few days and after repeating this on twosubsequent occasions at weekly intervals permanentrelief was obtained.

POST-THORACOTOMY PAIN

Pain around the chest that develops following athoracotomy may be due to the development oftrauma-evoked TrP activity either in the surgicalscar itself or in the muscles of the chest wall.Alternatively, it may develop as a result of thedivision of an intercostal nerve.

THORACOTOMY SCAR PAIN

It is not uncommon for persistent pain to developin and around a thoracotomy scar. One and anoften overlooked reason for this happening is thedevelopment of TrP activity in the scar tissue.

It often requires deactivation of these TrPs bymeans of needles inserted into the tissues immedi-ately lateral to the scar (see Ch. 10) to be repeatedseveral times before such pain is brought undercontrol as shown by the following case.

Chest pain 183

Figure 12.17 The pattern of pain referral from a triggerpoint (▲) situated deep in the paravertebral gutter in themultifidus muscle at the mid-thoracic level.

Chap-12.qxd 11*10*04 10:26 Page 183

A man (56 years of age), discovered to have an opacity in the right lung on a routine chest radiograph,was submitted to a thoracotomy. Histologicalexamination of the lesion proved it to be benign. One month later he began to complain of pain alongthe scar. He was reassured that there was no evidenceof a stitch abscess but was offered no specifictreatment. The pain persisted and eventually he wasgiven Distalgesic to take as and when required. In spiteof this, the pain gradually became worse and by thetime he was referred to me 12 months later, inaddition to the chest pain, he was getting severeattacks of cramp-like pain in the upper part of theanterior abdominal wall.

On examination, four TrPs were found in the scar. Itrequired deactivation of these to be carried out on sixoccasions at weekly intervals before any lasting painrelief was obtained.

SECTION OF AN INTERCOSTAL NERVE

Persistent post-thoracotomy pain may also occuras a result of the division of an intercostal nerve.This is often associated with a severe burning andmarked hyperaesthesia of the chest wall. This doesnot, in my experience, respond to acupuncture.Transcutaneous electrical nerve stimulation (TENS),however, is sometimes helpful.


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Rinzler S, Travell J 1948 Therapy directed at the somaticcomponent of cardiac pain. American Heart Journal 35:248–268

Simons D G, Travell J 1976 The latissimus dorsi syndrome. A source of mid-back pain. Archives of Physical Medicine and Rehabilitation 57: 561

Steindler A 1940 The interpretation of sciatic radiation andthe syndrome of low-back pain. Journal of the AmericanMedical Association 110: 106–113

Steindler A, Luck J V 1938 Differential diagnosis of pain lowin the back. Journal of the American Medical Association110: 106–113

Travell J 1968 Office hours: day and night. World PublishingCompany, New York

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Travell J 1976 Myofascial trigger points: clinical view. In:Bonica J J, Albe-Fessard D (eds) Advances in painresearch and therapy, Vol. 1. Raven Press, New York

Travell J, Rinzler S 1948 Pain syndromes of the chestmuscles. Resemblance to effort angina and myocardialinfarction, and relief by local block. Canadian MedicalAssociation Journal 59: 333–338

Travell J, Rinzler S, Herman M 1942 Pain and disability ofthe shoulder and arm: treatment by intramuscular

infiltration with procaine hydrochloride. Journal of theAmerican Medical Association 120: 417–422

Travell J, Simons D 1983 Pectoralis major muscle (subclavius muscle) in myofascial pain and dysfunction.The trigger point manual. Williams & Wilkins, Baltimore, p. 577

Wolf E, Stern S 1976 Costosternal syndrome. Its frequencyand importance in differential diagnosis of coronaryheart disease. Archives of Internal Medicine 136: 189–191

Chest pain 185

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INTRODUCTION

When presented with a case of persistent pain inthe shoulder region, rheumatoid arthritis, otherinflammatory arthritides, crystal arthropathy andhaemarthrosis of the glenohumeral joint, osteo-arthritis of the acromioclavicular joint and, occa-sionally, of the glenohumeral joint, and diseases ofthe bone all have to be included in the differentialdiagnosis. Far more often, however, such painoccurs either as a result of a soft-tissue disorder inthe vicinity of the glenohumeral joint, or because it is referred to the shoulder region from triggerpoints (TrPs) in nearby muscles.

The purpose of this chapter is to discuss the clin-ical manifestations and treatment of these lattermore commonly occuring causes of shoulder pain.

SOFT-TISSUE DISORDERS

The soft-tissue disorders in and around the gleno-humeral joint that will be considered are rotator cufftendinitis, subacromial bursitis, bicipital tendinitisand capsulitis.

Rotator cuff tendinitisThe rotator cuff

The musculotendinous cuff muscles, the supras-pinatus, the infraspinatus, the teres minor, and thesubscapularis have a conjoined tendinous inser-tion into the humerus. The supraspinatus tendonis attached to the laterally placed greater tuberos-ity; the infraspinatus and teres minor tendons are

187

Chapter 13

The painful shoulder

CHAPTER CONTENTS

Introduction 187Shoulder pain due to:

Rotator cuff tendinitis 187–189Bicipital tendinitis 189Capsulitis (frozen shoulder) 189–192

Shoulder pain due to:Nerve root entrapment 192Primary MTrP activity 192–203

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the pain is also localized around the greatertuberosity, but it is resisted external rotation thatmakes it worse. Pain from subscapularis tendinitisis experienced over the lesser tuberosity and isaggravated by resisted medial rotation.

Natural history of the disorder

When attempting to assess the effectiveness of any form of treatment, including acupuncture, inrelieving the pain of this disorder, it is importantto realize that its natural history is usually that of amild ache at rest and pain brought on by certainmovements which persists for weeks or monthsand then eventually undergoes spontaneous reso-lution. On occasions, however, the pain may sud-denly become more intense due to the developmentof an acute inflammatory reaction in the tendonand the tissues adjacent to it, including those inthe wall of the subacromial bursa. Calcium isliable to become deposited in a degenerative ten-don and when, in the case of the supraspinatustendon, this suddenly bursts into the subacromialbursa, there is very severe pain and marked restric-tion of movements, with abduction and externalrotation in particular aggravating the pain.

Subacromial bursitisSubacromial (subdeltoid) bursitis used to beincluded amongst the primary causes of shoulderpain, but it is now generally recognized that inflam-matory changes in the bursa do not occur as a primary event but are always secondary to aninflammatory lesion in an adjacent tendon. AsCailliet (1981) says, ‘any adjacent inflammation ofthe tendon causes inflammation of the bursa. It isinconceivable that bursitis could exist without ten-dinitis and vice versa’.

Cuff tears

It is generally agreed that cuff tears are far com-moner than previously supposed. It is now recog-nized that it only requires some minor injury tocause partial or complete tear of a tendon that hasalready been weakened by degenerative changes.The patient who is often in the 40–70 age rangeexperiences a tearing sensation in the shoulder

attached immediately below this, and the sub-scapularis tendon is attached to the medially placedlesser tuberosity. As a result of their attachments tothe humerus these tendons act as rotators of thejoint and in addition, by combining with the del-toid muscle, abduct the arm.

Inflammation is liable to develop in any of theserotator cuff muscles’ tendons but the supraspinatustendon is the one that is most commonly affected.

Pathogenesis

In young adults this disorder is liable to developsuddenly when oedematous and haemorrhagicchanges take place in these tendons as a result ofthe sudden overloading of the cuff muscles with thearm in the elevated position such as, for example,when throwing a cricket ball.

In older people the disorder develops moreinsidiously with slowly progressive degenerativeand ischaemic changes eventually causing the cuffto become so weakened that the acromion, cos-toacromial ligament and acromioclavicular jointimpinge on it (Matsen et al 1990). This impinge-ment is liable to be made worse should degenera-tive changes take place in the acromion andhumeral head. Eventually, attrition of the cuff maycause it to rupture.

Symptoms and signs

With tendinitis affecting any part of the cuff, thereis a nagging ache at rest and an increase in the painon the carrying out of certain movements. The onesaffected depend on which tendon or tendons inparticular are involved. In addition, sudden severepain may develop should the cuff become torn.

With supraspinatus tendinitis, active abductionof the arm is painful through the intermediate range(60–120°). The painful arc is probably due to theinflamed tendon rubbing against the acromionbecause it is abolished by externally rotating thearm, thus placing the greater tuberosity behind theacromion, before carrying out abduction. The pain isalso aggravated by resisted abduction. Tendernessis maximal over the tendon where it blends with theanterior part of the capsule of the shoulder joint.

The clinical presentation with infraspinatus andteres minor tendinitis is similar. In both conditions

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followed immediately by severe pain that oftenincreases in intensity until it reaches a peak about2 days later. It then remains very acutely painful fora further 4–7 days. On examination there is usuallyexquisite tenderness on palpation over the greatertuberosity. There is marked aggravation of pain onresisted abduction, and most significant of all, oncethe patient has raised the arm, there is an inabilityto control the lowering of it to the side. This, how-ever, does not occur exclusively with a rotator cufftear but may also be observed with a 5th cervicalnerve root lesion.

It is essential to confirm the diagnosis andassess the extent of a tear by contrast radiography.Minor tears usually heal spontaneously within 2months and require only symptomatic treatment.Extensive tears may need to be repaired surgically.

Bicipital tendinitisThe tendon of the long head of the biceps, attachedabove to the superior rim of the glenoid fossa,passes downwards enclosed in a sheath of syn-ovium through the glenohumeral joint to emergefrom it through an opening in the capsule close tothe latter’s humeral attachment. The tendon thendescends in the bicipital groove situated betweenthe greater and lesser tuberosities (Fig. 12.9). Thisstructure is liable to develop a degenerative tendin-itis that clinically presents with pain and tendernessto pressure over the bicipital groove. Moreover, thepain is characteristically aggravated by attemptingto supinate the arm against resistance.

Acromioclavicular joint strain

When the acromioclavicular joint becomes mechan-ically strained, the pain that develops is limited to the tip of the shoulder and aggravated by fullpassive adduction of the arm across the chest.

Treatment of a tendinitis in the glenohumeral joint regionThe principal object of treatment both for acute andchronic tendinitis in the vicinity of the glenohumeraljoint is to symptomatically relieve pain and to ensurethat full movements of the joint are restored asquickly as possible, for the longer they remain

restricted, the more likely it is that a disabling cap-sulitis or so-called frozen shoulder may develop.

Anti-inflammatory drug therapy

A widely adopted regime (Barry & Jenner 1996,Dalton 1995) is firstly to employ an orally adminis-tered non-steroidal anti-inflammatory drug. Andthen, if necessary, to inject a corticosteroid/localanaesthetic mixture into the subacromial bursa.Such treatment may have to be repeated at inter-vals. Therefore, rather than using a long-actingsteroid such as methylprednisolone, which is liableto cause tissue atrophy, it is better to employ shorteracting hydrocortisone acetate (Hazleman 1990).

Unfortunately, a steroid injection not infre-quently gives rise to appreciable post-treatmentpain. In addition, repeated injections are liable todamage the soft tissues and when injected into ajoint may destroy it (Bentley & Goodfellow 1969).Repeated injections may also have systemic effects;Koehler et al (1974) have shown that the hypothal-amic/pituitary/adrenal axis is affected 48 hoursafter an injection of 80 mg of methyl prednisoloneacetate into a knee with plasma cortisol levelsbeing suppressed for 3–6 days. In addition, there isalways the small but definite risk of infectiondeveloping at the site of a steroid injection.

TrP acupuncture

The examination of a patient with rotator cuff ten-dinitis should include a search for TrPs in both thevicinity of the cuff itself and in the muscles of theneck, shoulder girdle, upper arm and anterior chestwall, as deactivation of these by means of the carry-ing out of superficial dry needling at regular inter-vals is often sufficient by itself to alleviate the pain.

Capsulitis (frozen shoulder)Frozen shoulder is one of the great enigmas ofmedicine with there being no general agreementas to its nature, diagnosis or treatment, and withthe situation still further confounded by a confus-ing terminology.

Duplay (1896) first termed the condition peri-arthrite scapulohumerale. It has also been knownas periarthritis and pericapsulitis. Then in 1945Neviaser coined the term adhesive capsulitis

The painful shoulder 189

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because of appearances he found at operation on10 cases. These included thickening and contractionof the capsule; also adhesions between opposedsynovial surfaces were observed, particularly inthe inferior part of the joint. It was not, however,because adhesions were a striking feature that hedescribed the capsulitis as being adhesive, butrather because he noted that during manipulationof the shoulder after an incision through the ante-rior capsule, the capsule separated from the headof the humerus in the same manner as adhesivestrapping peels from the skin.

There is undoubtedly a widespread acute inflam-matory reaction involving the capsule and the rota-tor cuff, with the latter being reported at operationto be extremely friable (Bunker 1985). It is not sur-prising, therefore, that radioisotope scans showgleaming hot spots in the shoulder region (Binderet al 1984).

Pathogenesis

The disorder is liable to develop whenever move-ments at the shoulder joint are restricted. It may,therefore, occur either following some injury tothe shoulder including repeated episodes of minortrauma (Wright & Haq 1976), or as a complicationof a tendinitis, or when the arm remains immobilefor some appreciable period of time such as with ahemiplegia.

It is particularly liable to develop in patientswith diabetes mellitus and when it does so is oftenpresent bilaterally (Satter & Luqman 1985). Why itis prone to develop as a complication of this dis-order is not known. Possible reasons suggestedinclude the predilection of diabetics to infection or because of the development of a vasculitis(Nash & Hazleman 1989). Patients with hyper andhypothyroidism are also susceptible to developingit (Bowman 1988, Wolgethan 1987).

Clinical diagnosis

Capsulitis is a condition in which there is consid-erable pain and stiffness around the shoulder withmarked restriction of all glenohumeral joint move-ments, both passive and active. External rotation ismore severely affected than abduction or internalrotation. An important characteristic of the pain isthat it is particularly liable to disturb sleep.

It was because of this marked restriction of allmovements that Codman (1934) introduced theterm ‘frozen shoulder’, and, although that has sincehad much popular appeal, as Bunker (1985) pointedout, the acute inflammatory nature of the conditionmakes it somewhat of a misnomer.

The clinical diagnosis may be confirmed byarthrography, which shows a marked reduction inthe volume of the glenohumeral joint so that itonly accommodates a few millilitres of contrastmedium instead of the normal 10–15 ml (Bruckner1982).

Natural history of the disorder

It is important when considering the influence ofvarious forms of treatment on this disorder,including the possible place of acupuncture in itsmanagement, to have a clear knowledge of its nat-ural history for, as Lloyd-Roberts & French (1959)when writing about this said:

A knowledge of the average time between onsetand recovery is of outstanding importance if theeffects of treatment are to be assessed in a diseasewhich usually resolves spontaneously.

The pain usually remains severe for about 3 months, after which it begins to abate, but therestriction of movements continues for much longer.The condition is usually eventually self-limiting,burning itself out within 2 years in the absence ofany treatment (Grey 1977). A minority of cases,however, have some permanent disability.

Treatment

A variety of different treatments have been advo-cated, including local steroids, oral steroids, ultra-sound, radiotherapy and sympathetic ganglionblock, but the reports concerning these have beenconfusingly inconclusive and conflicting, and asthe condition is a naturally resolving one, onlythose studies that have included controls will beconsidered.

Lloyd-Roberts & French (1959), in studying aseries of patients suffering from what they termedperiarthritis or capsulitis of the shoulder, treatedone group with an intra-articular injection of hydro-cortisone combined with forcible manipulation


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under anaesthesia followed by active supervisedmovements; and another group with oral corti-sone for 1 month plus active supervised move-ments. They concluded that the group treatedwith manipulation and local hydrocortisone didbetter than the group treated with oral cortisone.

Kessel et al (1981) from a carefully controlledtrial concluded that manipulation in combinationwith systemic steroids is of value. As Bruckner(1982) has pointed out, however, manipulationtogether with steroids is generally reserved forthose patients who have made no improvement9–12 months from the onset, and, therefore, afterthe acute phase of the disease is over. As he says ‘itwould be very helpful if a simple treatment couldbe shown to cut short this common and oftenextremely painful condition’.

The administration of corticosteroids, eitherlocally or systemically, has been popular in thetreatment of frozen shoulder ever since they firstbecame available for therapeutic use. Cyriax &Troisier (1953), in treating what they termed ‘freez-ing arthritis’, recommended giving an intra-articular injection of hydrocortisone, but the resultsof this were poor. Subsequently, Cyriax (1980) advo-cated the use of multiple intra-articular injectionsof hydrocortisone at weekly or biweekly intervals.The dangers inherent in this, however, have alreadybeen alluded to when discussing the managementof tendinitis.

Lee et al (1974) compared the effects of threeforms of treatment (heat plus exercises; intra-articular hydrocortisone plus exercises; hydrocor-tisone around the biceps tendon plus exercises)with the effect of treatment with analgesics alone.All three groups in which exercise was usedobtained a significantly improved range of move-ments to a similar degree. The analgesic group’sresponse was not as good.

Richardson (1975) showed no difference inrelief of pain in one group treated with steroidinjections and in another treated with a placebo.And finally, Bulgen et al (1984) have shown thatthere is no long-term advantage of steroid injec-tion over mobilization, ice, or no treatment in themanagement of the frozen shoulder.

It is in the light of these conflicting reports thatBruckner (1982) concludes that in the majority ofcases, reassuring the patient that it is a self-limiting

condition, advising the use of simple ‘pendulum’mobilizing exercises, and, in the early stages of thecondition, controlling the pain by some simplemeans, is as much as can be hoped for.

Acupuncture also has a place in alleviating thepain present at the early stage of this disorder.Camp (1986), one of the few British rheumatolo-gists with experience in the use of it, has foundthis form of therapy to be certainly as helpful ascorticosteroid injections in the treatment of thefrozen shoulder. She advocates ‘acupuncture asthe treatment of choice in preference to the verypainful cortico-steroid injections and the largelyuseless physiotherapy’, but makes it clear that, inher opinion, acupuncture, like local steroids, isonly of symptomatic benefit and does not alter thenatural history of the condition.

There is no doubt, as Bruckner (1982) has said indiscussing the shortcomings of numerous reportson the treatment of the ‘frozen shoulder’, that ‘it isessential to design prospective trials that will givedefinite answers, by carefully defining the condi-tion under study (excluding shoulder pain with-out passive limitation of movement), treatingpatients only in the acute stage (first 6 months) andincluding a proper control group’. It would alsoseem reasonable, in view of Camp’s observations,to include in any such trial one group treated withacupuncture. Firstly, however, it is necessary toestablish which particular acupuncture technique ismost suitable for the alleviation of this type of pain.My reason for saying this is because, in my experi-ence, the pain of frozen shoulder can be aggravatedby carrying out superficial dry needling at TrP sitestoo vigorously. Gentle brief stimulation of nerveendings in the tissues overlying these points is oftenall that is necessary. This is similar to what Camp(1986) has found, as she states: ‘sometimes attemptsat needling trigger points simply produces morepain and a violent reaction to acupuncture. Movingthe needle away from the trigger points and treat-ing more peripheral points, results almost in com-plete loss of symptoms in these cases’.

The matter, however, is far from straightfor-wards for undoubtedly there are some patientswho only respond to strong stimulation and it isfor this reason that Mann (1974) has found that onoccasions patients with a persistently painfulshoulder require the powerful stimulus provided


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by ‘pecking’ the periosteum over the coracoidprocess.

There is no doubt, as stressed throughout thisbook, that patients’ individual responsiveness toneedle-evoked nerve stimulation varies widelyand it is essential to take account of this, not onlyin everyday clinical practice, but also when draw-ing up clinical trial protocols.

Secondary activation of myofascial TrPs in tendinitis and capsulitisIt is common for the persistent pain and restrictedmovements associated with tendinitis and, in par-ticular, with capsulitis to lead to the secondaryactivation of TrPs in muscles in the anterior andposterior axillary folds, the upper arm, the shoul-der girdle and neck.

REFERRAL OF PAIN TO THE SHOULDERREGION

Pain in the shoulder region may occur in theabsence of any lesion in or around the glenohumeraljoint and be due to it being referred there, eitherbecause of nerve root entrapment, or because of theprimary activation of TrPs in muscles in the neckand shoulder girdle, or because of a lesion aroundthe diaphragm irritating the phrenic nerve.

Nerve root entrapment pain referralPain in the shoulder and upper extremity canoccur as a result of pressure on a cervical nerveroot such as may occur with cervical disc hernia-tion or cervical spondylosis. For reasons to begiven in Chapter 14, there are grounds for believ-ing that these disorders are not responsible for thisas often as is commonly supposed. Certainly cer-vical spondylosis cannot be assumed to be thecause just because the characteristic appearancesof this degenerative condition are demonstrableradiographically. The only circumstances in whichthe diagnosis of a nerve root lesion can be madewith any confidence is when there are objectiveneurological signs and when in particular the elec-tromyogram (EMG) is abnormal.

On clinical examination, movements of theshoulder are free and do not aggravate the pain,

whereas neck movements with, in particular, forcedextension and sideways rotation commonly do.

With a C6 nerve root lesion there is usually painand stiffness in the neck as well as pain in theouter part of the shoulder. Pain may also radiatedown the arm to the thumb and first finger. Inaddition, there is weakness and wasting of thebiceps muscle and depression of the biceps jerk.

A C7 nerve root lesion is associated with pain inthe upper scapular region and the outer side of theshoulder. It may also radiate down the arm to themiddle and index fingers. In addition, there is weak-ness and wasting of the triceps muscle and depres-sion of the triceps jerk. A C8 nerve root lesion causespain to be felt in the outer part of the shoulder andmid-scapular regions.

Muscles in the areas affected by radiculopathicpain are often found to contain secondarily activatedTrPs and these need to be deactivated by means ofthe carrying out of superficial dry needling.

Primary myofascial TrP pain referralIt is well known that pain may be referred to theshoulder region from some disorder around thediaphragm irritating the phrenic nerve. In add-ition, it may be referred to this site from TrPs thathave become primarily activated when muscles in the upper part of the chest wall and neck have become acutely strained or chronically over-loaded. For some reason, this is still not generallyrecognized, in spite of attention having first beendrawn to it by Edeiken & Wolferth as long ago as1936. Also, Kellgren described cases of it 2 yearslater, and since then it has been the subject of several detailed reports.

These include one by Kelly (1942), which hewrote whilst serving in the Australian Army Med-ical Corps and another by Travell et al (1942). Inaddition, Sola et al (1955) and Sola & Kuitert (1955)gave descriptons of it based on observations madeby them whilst serving as medical officers in theUnited States Air Force.

Unfortunately when these reports were firstpublished they were for some reason largelyignored, but in recent years the importance of this particular cause of shoulder pain has onceagain been stressed, so that, hopefully, it may nowbegin to receive the recognition it deserves (Baldry


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1998, 2001, Bonica & Sola 1990, Simons et al 1999,Sola 1999).

The muscles most frequently involved includethe supraspinatus, infraspinatus, levator scapulae,trapezius, deltoid, long head of triceps, latissimusdorsi, teres major, biceps and subscapularis. TrPsin these muscles can only be found by systemati-cally examining each muscle in turn. The searchfor these, however, is greatly assisted by everymuscle having its own specific pattern of TrP painreferral.

Supraspinatus muscle (see Fig. 12.14)Activation of TrPs TrP activity may develop in the supraspinatus muscle when it is subjected tostrain, as for example, by the carrying of a heavyload such as a suitcase with the arm hanging bythe side. Alternatively, by pulling a heavy object orlifting it to, or above, the shoulder level with thearm outstretched. In addition, the repeated over-loading of the muscle by such means is liable toconvert an acute condition into a chronic one.

Specific pattern of pain referral TrP activity inthis muscle causes pain to be referred to the regionof the deltoid muscle. Because of its distributionthis pain is often erroneously diagnosed as beingdue to subdeltoid (subacromial) bursitis, which, asexplained earlier, is a condition that rarely, if ever, occurs as a primary event. The pain fre-quently extends down the arm and forearm and, asTravell & Simons (1983, p. 368) stated, it is oftenfelt particularly strongly over the lateral epicondyle(Fig. 13.1).

Movements aggravating the pain This referredpain is usually a dull ache at rest that is made worseby abducting the arm, and by passively stretchingthe muscle by adducting the arm behind the back.

Some of the commoner types of movementslikely to aggravate the pain include reachingupwards either to brush the hair, shave, or cleanthe teeth.

TrP examination The patient should sit comfort-ably, or lie with the affected side uppermost. Asthe TrPs have to be palpated through the trapezius


Figure 13.1 The pattern of pain referral from a trigger point or points (�) in the supraspinatus muscle.

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muscle they are often found more readily if themuscle is put on the stretch by placing the forearmof the patient behind the back at waist level. Theirlocation is either at the medial or lateral parts ofthe muscle, or in both places (Fig. 13.1). In add-ition, there may be one in the tendon of the musclenear to its insertion (Fig. 13.2).

Associated TrPs TrP activity may develop in thesupraspinatus muscle alone, but more often itdevelops in the infraspinatus at the same time, andalso quite often in the trapezius, levator scapulaeand deltoid muscles.

Similarity to radiculopathic pain distributionReferred pain from supraspinatus TrPs is similarin distribution to that from a C5 nerve root lesion(Reynolds 1981). There is, however, an absence ofobjective neurological signs, and electromyographyshows no abnormality.

Deactivation of TrPs The deactivation of TrPs inthis muscle presents no problem despite it lyingbehind the trapezius muscle.

Infraspinatus muscle (see Fig. 12.14)Activation of TrPs This is usually brought about bythe muscle being subjected to some sudden strainsuch as, for instance, when reaching backwardsfor support when falling; or when it is repeatedlyput on the stretch, such as when reaching back-wards to pick up objects from the back of a carwhen sitting in the front of it.

Specific pattern of pain referral Referred painfrom TrPs in this muscle is felt deep inside thefront of the shoulder joint and for this reason issometimes erroneously thought to be due to anarthritis of the glenohumeral joint which, as statedearlier, is rare. It may also radiate down the antero-lateral aspect of the arm and forearm to the radialaspect of the hand, sometimes reaching the thumband first two fingers (Fig. 13.3) (Travell et al 1942,Travell 1952, Sola & Williams 1956, Pace 1975,Rubin 1981).

This particular type of shoulder pain is particu-larly disturbing at night because it not only prevents


Figure 13.2 The pattern of pain referral from a trigger point or points (�) in the supraspinatus tendon.

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the patient from lying on the affected side, but is alsotroublesome when lying on the unaffected side.

Characteristic disorder of movements There isan inability to internally rotate and adduct the armat the shoulder. The hand-to-shoulder blade test inwhich a normal individual’s finger tips can reachthe spine of the scapula reveals this typical restric-tion of movement (Fig. 13.4). A sufferer from thishas difficulty in doing up buttons, manipulating azip fastener, or putting a hand into a back trouserpocket.

TrP examination With the patient sitting in achair, the muscle should be stretched by bringingthe hand and arm across the front of the chest tograsp the contralateral arm rest of the chair.

Flat palpation of the infraspinatus fossa shouldthen be carried out systematically. One or moreTrPs are usually to be found somewhere along aline immediately beneath the spine of the scapula.

Differential diagnosis Referred pain to the shoul-der from TrP activity in the infraspinatus muscle

may closely simulate that arising from gleno-humeral joint disease. Also, as it causes pain toradiate down the arm in a similar distribution tothat occurring with irritation of the 5th, 6th and7th cervical nerve roots, a full neurological exam-ination is essential and, at times, an EMG may benecessary to distinguish between them. Confusionis particularly likely to occur in patients who alsohave neck pain (see Ch. 14).

Deactivation of TrPs This should be done withthe patient lying on the opposite side, with thearm resting on a pillow placed against the chest.The needle is inserted into the tissues overlying aTrP whilst fixing the latter between two fingerspressed against the scapula. Care must be takennot to push the needle too hard against the scapulaas penetration of the infraspinatus fossa with theproduction of a pneumothorax has been reported(Travell & Simons 1983, p. 385).

Teres minor (Fig. 13.4) This muscle with itsattachments immediately adjacent to and just below


Figure 13.3 The pattern of pain referral from a trigger point or points (�) in the infraspinatus muscle.

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those of the infraspinatus, and having actions thatare almost identical to the latter, has TrP activitybrought about by exactly similar stresses, i.e.stretching and reaching behind the shoulder.

However, unlike the infraspinatus, it is one of theless commonly involved muscles. Sola & Kuitert(1955) found only about 7% of their patients withshoulder pain had TrPs in this muscle.

Teres minor is rarely involved without simul-taneous involvement of the infraspinatus, and usu-ally notice is drawn to it by the patient continuingto complain of pain in the posterior part of theshoulder, once pain deep in the front of the shoulderhas been satisfactorily alleviated by deactivatingTrPs in the infraspinatus.

Levator scapulae and trapezius muscles Thesemuscles are discussed in detail in Chapter 14 asTrP activity in them is mainly responsible for pain

and limitation of movement of the neck. It is, how-ever, also liable to cause pain to be referred to theposterior part of the shoulder (see Figs 14.1 & 16.6).

Deltoid muscle (see Fig. 12.14) The deltoid mus-cle, so-called because being triangular in shape itresembles the Greek letter � (delta), is made up ofthree parts: the anterior, middle and posterior.

Activation of TrPs This occurs mainly in theanterior and posterior parts of the muscle, either asa secondary or a primary event. It often occurs as asecondary phenomenon, both in the anterior andposterior parts simultaneously, when pain isreferred to that area from TrPs in the supraspina-tus and infraspinatus muscles. The pain that arisesas a result of TrP activity in this muscle remainslocalized to that area, and is not projected to somedistant site.

In the case of primary activity, the clinical pic-ture differs according to whether the anterior orposterior part is involved and so each will be con-sidered separately.

ANTERIOR PART Primary TrP activity may bebrought about by direct trauma to the upper partof the arm such as may occur with a fall, or whenit is damaged by the impact of a ball, or the recoilof a gun. Also, when the muscle is subjected tosudden overload such as when grasping a rail tobreak a fall, or when the muscle is recurrently over-loaded such as may occur when some heavy objectsuch as a tool or instrument is repeatedly held atshoulder level.

Symptoms The patient complains of pain atrest over the anterior part of the deltoid muscle(Fig. 13.5). This is made worse by movement, and,in particular, there is difficulty in raising the armto the horizontal so that drinking becomes trou-blesome.

Signs Pain is aggravated by asking the patientto abduct the arm with the elbow straight and thepalm to the front. The patient also has difficulty inpassing the hand across the small of the back.Normally, it is possible to rest the hand on the backof the opposite arm. With anterior deltoid TrPactivity, it may only be possible to reach the mid-line (Fig. 13.6).

Differential diagnosis Pain arising as a result ofTrP activity in the deltoid muscle has be distin-guished from that arising because of a sprain of


Figure 13.4 To illustrate how a normal person, on placingan arm behind the back, is able to reach the spine of thecontralateral scapula with the finger tips. With trigger pointactivity in either the supraspinatus or infraspinatus or both,this is not possible.

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Figure 13.5 The pattern of pain referral from a trigger point (�) in the anterior part of the deltoid muscle.

the acromioclavicular joint that lies underneaththe proximal attachment of the anterior part of thismuscle. This injury, common in rugby players, ischaracterized by pain and tenderness localized tothe shoulder tip and there are of course no TrPs tobe found in the deltoid muscle itself.

POSTERIOR PART Primary TrP activity may occuras a result of injecting some irritant substancessuch as an antibiotic, vitamin or vaccine into thispart of the muscle, or when it is subjected to exces-sive strain during sporting activities.

Symptoms The patient complains of pain at theback of the shoulder at rest, and this is made worseby movement (Fig. 13.7). External rotation is alsolimited so that whilst the hand can be brought upto the head it cannot be wrapped around the backof the head.

Signs Pain is aggravated by asking the patientto abduct the arm with the elbow straight and thepalm facing backwards.

TrP examination This is carried out by flat pal-pation preferably with the muscle under moderate

tension by slightly abducting the arm. Because the muscle is superficially situated taut bands atTrP sites are often felt and local twitch responsesreadily elicited.

TrPs present in the front of this muscle are usu-ally to be found in its upper part. This is in con-trast to those present at the back of it which areusually situated in its lower part (Fig. 13.8).

TrP deactivation This should be done with thepatient lying on the opposite side.

Associated TrPs TrP activity is rarely confinedto the deltoid alone. In addition to the musclesalready mentioned, anterior deltoid TrP activitymay be associated with similar activity in thebiceps brachii, the clavicular section of the pec-toralis major, and the coracobrachialis. Posteriordeltoid TrP activity is often associated with thedevelopment of similar activity in TrPs in the longhead of the triceps, and in the two muscles thatform the posterior axillary fold – the latissimusdorsi and the teres major. Each of these muscleswill, therefore, be discussed in turn.

Chap-13.qxd 11*10*04 10:27 Page 197

BICEPS BRACHII MUSCLE (see Fig. 12.9) TrPs are tobe found in the lower part of this muscle justabove the elbow (Fig. 13.9).

Activation of TrPs These TrPs are liable tobecome activated when the muscle is strained bylifting a heavy object with the arm outstretched.By carrying out some task with the elbow flexedfor a long time such as occurs when cutting ahedge. When supinating against resistance such aswhen using a screwdriver. And, as with the infra-spinatus muscle, when suddenly reaching back-wards for support to prevent a fall.

Specific pattern of pain referral TrP activity in thedistal part of the muscle near to the elbow causespain to be referred upwards to the anterior surfaceof the shoulder joint, and sometimes to a lesserextent to the suprascapular region (Fig. 13.10). Thereis no restriction of movement at the shoulder joint

but pain is aggravated by raising the hand abovethe head.

TrP examination The examination is carried outwith the patient seated and with the elbow restingon a table. With the hand supinated, the elbow isslightly flexed to slacken the biceps muscle. TrPsin elongated tense bands are usually found in thedistal part of the muscle (Winter 1944) and may,therefore, be located by sliding the examining fin-ger across the lower part of both heads.

Deactivation of TrPs Once a TrP has been locatedin this part of the muscle it should be trappedbetween two fingers whilst a needle is insertedinto the tissues overlying it. Care should be takento avoid penetrating either the median or radialnerves; the one lying along the medial and theother along the lateral border of the lower part ofthis muscle.

CLAVICULAR SECTION OF THE PECTORALIS MAJOR MUSCLEA detailed discussion concerning the activation ofTrPs in this muscle is given in Chapter 12, butattention must be drawn here to the fact that anyin the clavicular section of this muscle may beresponsible for pain in the front of the shoulder,and may also cause abduction of the arm at theshoulder joint to be restricted (see Fig. 12.6).

CORACOBRACHIALIS (see Fig. 12.9) This muscle,together with the pectoralis minor and the shorthead of the biceps, is attached at its upper end tothe coracoid process, and at its lower end to themiddle of the humerus.

TrP activity in it usually does not become evi-dent until TrPs in other shoulder muscles, particu-larly the anterior deltoid, have first been successfully deactivated. As Travell & Simons (1983, p. 440)have pointed out, TrP activity in this muscleshould be suspected when despite deactivatingTrPs in neighbouring muscles the patient continuesto complain of pain over the anterior deltoidregion, and down the back of the arm to the dor-sum of the hand, but sparing for some reason theelbow and wrist (Fig. 13.11). TrPs in this muscleare usually to be found in in the upper part of itdeep to the anterior deltoid (Fig. 13.11).

In order to deactivate TrPs in this muscle thepatient should be placed in the supine positionwith the arm externally rotated.

TRICEPS (LONG HEAD) A detailed account of thevarious parts of the triceps muscle and their patterns


Figure 13.6 To illustrate how a normal person onputting the arm behind the back can reach across to restthe back of the hand on the opposite arm. With triggerpoints in either the anterior deltoid or coracobrachialismuscle it is usually not possible to reach past the midline.

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Figure 13.7 The pattern of pain referral from a trigger point in the posterior part of the deltoid muscle.

Figure 13.8 To illustrate the usual location of triggerpoints in the upper anterior part and lower posterior partof the deltoid muscle.

Figure 13.9 To show the usual location of triggerpoints in the lower part of the biceps muscle just abovethe elbow.

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of TrP pain referral will be given when discussingpain around the elbow joint in Chapter 15.Reference, however, must be made here to thelong head of this muscle (Fig. 13.12) because whenTrP activity develops in the posterior part of thedeltoid it may also arise in this and in the latis-simus dorsi and the teres major. TrPs in the longhead cause pain to be referred upwards over theback of the arm to the posterior part of the shoul-der and sometimes downwards along the back ofthe forearm (Fig. 13.13).

A person with TrP activity in this muscle, wheninstructed to raise both arms above the head withthe elbows straight and palms to the front, finds itimpossible to hold the arm on the affected sidetight against the side of the head (Fig. 13.14).

TrP examination TrPs when present are usuallyto be found in the mid third of the long head (Fig 13.13).

TrP deactivation A detailed discussion of thiswill be given in Chapter 15.

LATISSIMUS DORSI AND TERES MAJOR (see Fig. 12.14)These muscles, which together form the posterioraxillary fold, often have TrP activity in them at thesame time.


Figure 13.11 The pattern of pain referral from a trigger point or points (�) in the coracobrachialis muscle.

Figure 13.10 The pattern of pain referral from triggerpoints (�) in the lower part of the biceps muscle.

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TrP activity in the latissimus dorsi muscle has already been discussed in Chapter 12 as itmainly causes pain to be felt in the chest wallaround the inferior angle of the scapula. The pain,however, may also be referred to the back of theshoulder and down the inner side of the arm (see Fig. 12.15).

Teres major is attached medially to the lowerpart of the scapula; and laterally converges withthe latissimus dorsi muscle to form the posterioraxillary fold before being inserted into thetuberosity close to the latissimus dorsi in the bicip-ital groove (see Fig. 12.14). TrP activity in it causespain to be felt in the posterior part of the shoulderwhen reaching forwards and upwards and occa-sionally along the back of the forearm (Fig. 13.15).

A person with TrP activity in this muscle hasdifficulty in pressing the raised outstretched armtightly against the side of the head in the sameway as someone with TrP activity in the long headof the triceps does. (Fig. 13.14).

TrP examination TrPs are liable to be foundboth at the inner and outer ends of the muscle (Fig.13.16). Those present medially at the insertion ofthe muscle into the lower lateral border of the


Greater tuberosity

Teres minor

Humerus

Long head of triceps

Lateral head of triceps

Latissimus dorsi

Olecranon

Teres major

Infraspinatus

Triangular space

Quadrangular space

Deltoid

Spine of scapula

Supraspinatus

Figure 13.12 The dorsal scapular muscles and triceps. Left side. The spine of the scapula has been divided near itslateral end and the acromion has been removed together with a large part of the deltoid.

Figure 13.13 The pattern of pain referral from a triggerpoint or points (�) in the long head of the triceps muscle.

Chap-13.qxd 11*10*04 10:27 Page 201

scapula may be located by applying pressureagainst the underlying scapula. Those occurringlaterally in the posterior axillary fold may belocated by gripping the fold between the thumband fingers but my preference is to use flat palpa-tion (see Ch. 7). This may be done with the patientsitting but is easier to do with the patient lyingsupine and the arm abducted to 90°.

Deactivation of TrPs TrPs in the vicinity ofwhere this muscle inserts into the scapula are mostreadily deactivated with the patient lying on thecontralateral side. TrPs in the posterior axillaryfold should be deactivated with the patient lyingin the supine position and the arm abducted at aright angle.

SUBSCAPULARIS MUSCLE It is important not tooverlook TrPs hidden away in the subscapularismuscle in anyone with persistent pain in theshoulder (Fig. 13.17).

Activation of TrPs TrPs are liable to becomeactive in this muscle when repeated movementsinvolving a considerable amount of internal rota-tion are carried out. Also, as a result of direct


Figure 13.14 To illustrate the difficulty experienced inbringing the ipsilateral arm up against the ear whenthere is trigger point activity in either the long head ofthe triceps or the teres major muscle.

Figure 13.15 The pattern of pain referral from a triggerpoint at the inner end of the teres major muscle.

Figure 13.16 To show sites at which trigger points areliable to become activated in the teres major muscle.

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trauma to the shoulder. And when the shoulderjoint is immobilized for any length of time in theadducted and internally rotated position.

Specific pattern of TrP pain referral Pain eman-ating from TrPs in this muscle is very severe evenat rest and is made worse by movement. It is pre-dominantly felt over the back of the shoulder butalso extends up towards the scapula and down theback of the arm to the elbow. There may also besome pain around the back of the wrist (Fig. 13.18).

Characteristic disturbance of movements TrPactivity in this muscle gives rise to progressivelypainful restriction of abduction and external rota-tion of the shoulder joint.

Associated TrPs When TrPs become active inthis muscle similar activity is liable to develop inthe pectoralis major, latissimus dorsi, teres major,long head of the triceps, and the anterior and pos-terior part of the deltoid muscles.

TrP examination TrPs in this muscle are usuallyto be found along the axillary border of the sub-scapular fossa. These are difficult to palpate unlessthe arm is well abducted and traction is put on it for the purpose of abducting the scapula.Unfortunately, however, severe pain and limita-tion of movement often makes this difficult.

Deactivation of TrPs The patient should beplaced in the supine position with the armabducted if possible to 90°, with the hand placedbehind the head and anchored beneath the pillow.When a TrP is located it should be fixed betweentwo fingers and a needle inserted parallel to therib cage into the tissues overlying it.


Figure 13.18 The pattern of pain referral from a trigger point or points (�) in the axillary part of the subscapularis muscle.

Figure 13.17 The subscapularis muscle with a triggerpoint (�) near to the insertion of this muscle into thehumerus.

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Baldry P E 1998 Pain in and around the shoulder’sglenohumeral joint. In: Filshie J, White A (eds) Medicalacupuncture, a Western scientific approach. ChurchillLivingstone, Edinburgh, pp. 44–48

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Neviaser J S 1945 Adhesive capsulitis of the shoulder.Journal of Bone and Joint Surgery 27: 211–222

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Sola A E, Rodenberger M L, Gettys B B 1955 Incidence of hypersensitive areas in posterior shoulder muscles. American Journal of Physical Medicine 34:585–590

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infiltration with procaine hydrochloride. Journal of theAmerican Medical Association 120: 417–422

Travell J G, Simons D G 1983 Myofascial pain and dysfunction.The trigger point manual. Williams & Wilkins, Baltimore

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INTRODUCTION

Persistent pain in the neck with restriction of itsmovements, with or without referral of the paindown the arm, is a commonly occurring disorder,and before deciding on whether or not to useacupuncture in an attempt to relieve it, it is obvi-ously essential to first of all establish its cause.

Some of the less common causes and ones thatrequire other forms of treatment include primaryor secondary malignant disease infiltrating nerveroots or vertebral bodies; a variety of other dis-orders affecting the vertebrae such as fractures,infective lesions and rheumatoid arthritis; andsome disorders of the muscle such as polymyalgiarheumatica. The exclusion of these clearly requiresthe taking of a detailed history, a carefully conducted clinical examination, and some basicinvestigations including an erythrocyte sedimen-tation rate (ESR) and cervical radiographs.

It is hardly necessary to cite cases illustratingthe importance of making an accurate diagnosisbefore embarking upon treatment of any type butthe following one, although it occurred a long timeago, is worth quoting as it is firmly imprinted onmy mind for reasons that will become obvious.

A man (56 years of age) developed persistent pain inthe neck with restricted movements. He was treatedfor several months symptomatically but when, in spiteof this, the pain became progressively worse, he wasreferred to my outpatient clinic for assessment. Onexamination there were no abnormal neurologicalsigns, but whilst he was having X-rays of his neck andchest, he suddenly collapsed due to the development

207

Chapter 14

Pain in the neck

CHAPTER CONTENTS

Introduction 207Acute rupture of the annulus fibrosus with

herniation of the nucleus pulposus 208Cervical spondylosis 208–209Cervical myofascial TrP point pain

syndrome 209–214Factors responsible for the primary activation of

MTrPs in the neck 214–218Treatment of persistent neck pain including

the identification and deactivation of MTrPs 218–219Acupuncture clinical trials 219–221

Chap-14.qxd 13*10*04 14:38 Page 207


It therefore follows that, although in adultsunder the age of 40 years, the sudden onset ofsevere pain in the neck and arm is often consideredto be due to the entrapment of a nerve from a rup-tured intervertebral disc, except in the minority ofcases where there are definite physical signs ofthis, such as weakness of muscles, sensory changesand the loss of a tendon jerk, together with evi-dence of disc protrusion on magnetic resonanceimaging (MRI) at a level corresponding with thatshown by the physical signs, such an assumptionis unjustified.

The commonest cause for acute neck painwould seem to be the primary development of TrPactivity in the muscles in that region. In support ofthis belief are the observations that pain of thistype usually develops when these muscles havebeen subjected to some acute strain, and that insuch circumstances careful examination of variousneck muscles, including the levator scapulae, sple-nius cervicis and trapezius reveals the presence ofTrPs with pressure on them aggravating the spon-taneously occurring pain. In addition, should acuteneck pain be associated with considerable musclespasm causing the neck to be pulled to one side(acute wry neck) TrPs are likely to be found in thesternocleidomastoid muscle.

TrP activity may also develop as a secondaryevent in muscles to which pain has been referred asa result of nerve root entrapment caused by eithera cervical disc prolapse or cervical spondylosis.

Cervical spondylosisCervical spondylosis is liable to develop from theage of 40 years upwards. It is a very commonlyoccurring degenerative condition affecting thediscs and facet joints of the 5th, 6th and 7th cer-vical vertebrae. A striking feature of the conditionis the development of osteophytes, both anteriorlyand posteriorly. It is the posterior osteophytes thatare of particular importance because, if sufficientlybig, they may cause narrowing of the spinal canalwith the gradual onset of a spastic paraplegia, orthe narrowing of one or other of the intervertebralforamina with the development of nerve rootentrapment, giving rise to pain in the neck andarm and the eventual appearance of neurologicalsigns in the arm. In contrast to this, anterior

of a quadriplegia! The appearances on the radiographsof the neck at first sight seemed to be normal until itwas realized that only six cervical vertebrae werevisible, one having collapsed so completely as a result of metastatic infiltration as to have virtuallydisappeared. The chest radiograph revealed the site ofthe primary growth.

This having been said it is now necessary to dis-cuss some of the common causes of persistent neckpain as it is in the treatment of these that acupunc-ture has much to offer.

It is now evident that persistent neck pain withor without referral of this down the arm is oftendue to the primary activation of trigger points(TrPs) in muscles in the neck and shoulder region(Michele et al 1950, Sola & Kuitert 1955, Long 1956,Sola & Williams 1956, Michele & Eisenberg 1968,Travell & Simons 1983). Neurologists, however,continue to put most emphasis on nerve rootentrapment as being the principal cause of thistype of pain. With patients under the age of 40years, pain is ascribed to acute rupture of an inter-vertebral disc, and with those older than this, it isconsidered to be due to cervical spondylosis(Posner 1982, Matthews 1983). These two condi-tions will, therefore, be considered first.

ACUTE RUPTURE OF THE ANNULUSFIBROSUS OF AN INTERVERTEBRAL DISC WITH HERNIATION OF THE NUCLEUS PULPOSUS

From early adult life to middle age the interverte-bral disc undergoes a degenerative process.Among the various biochemical changes whichtake place in the nucleus pulposus is a gradualdecrease of its water content with a consequentprogressive loss of its fluidity (Urban & Maroudas1980).

Eventually as a result of this degenerativeprocess the annulus fibrosus may rupture. Whenthis happens the nucleus pulposus, provided it isstill in a sufficiently fluid state, herniates throughit and impinges on a nerve root. This, however, isrelatively rare (Waddell 1982) as by the time an annulus fibrosus is liable to tear the nucleuspulposus tends to be too inspissated to flowthrough it.

Chap-14.qxd 13*10*04 14:38 Page 208

osteophytes and also narrowing of the interverte-bral spaces, although often seen on lateral radi-ographs in this condition, are not a cause of eithersymptoms or signs.

It needs to be stressed that radiographic appear-ances of cervical spondylosis are frequently seenin asymptomatic elderly people (Pallis et al 1954,Friedenberg & Miller 1963, Heller et al 1983).

Pallis et al (1954) carried out a detailed clinicaland radiographic study of asymptomatic cervicalspondylosis in a random group of 50 inpatientsover the age of 50 years suffering from a variety ofother medical and surgical disorders. A number ofthese patients, despite having no neurologicalsymptoms were found to have pyramidal tract andposterior column signs, together with radiographicevidence of moderate or severe narrowing of theirspinal canals from posterior osteophytic, kyphotic,and subluxation changes of cervical spondylosis.What, however, was of particular relevance, whenconsidering neck pain and the part that cervicalspondylosis may play in producing this, was thatthey found that a number of patients with no painin the neck or arm had severe osteophytic narrow-ing of one or another intervertebral foramen. And that approximately one-third of these hadneurological evidence of nerve root involvement inan arm.

Heller et al (1983) compared the cervical radio-graphs of two groups of patients. One groupincluded all patients over the age of 60 yearsreferred to their department of radiology duringthe course of one particular year specifically for X-ray examinations of the neck. The other groupconsisted of all of the patients, also over the age of 60 years, referred to the department that yearfor barium studies. They not only found that 85%of those specifically referred for neck X-rays hadradiographic evidence of cervical spondylosis, butalso that there was no significant difference in theprevalence and extent of the radiographic changesin the two groups. Furthermore, there was no con-sistent relationship between symptoms and X-rayappearances.

There are therefore certain enigmas associatedwith this commonly occurring condition. Foremostamongst these is that whilst the condition causespain in the neck and arm to develop in some people,others with equally severe radiographic changes

remain symptomless. Furthermore, as a corollary tothis, the presence of radiographic changes of cervi-cal spondylosis in a person suffering from pain inthe neck does not necessarily imply that the latteris due to this disorder as these X-ray appearancesof it are often no more than a fortuitous finding insomeone whose pain is due to some other causeincluding in particular the primary developmentof TrP activity in muscles of the neck.

Nerve root entrapment from cervical spondy-losis is of course the most likely cause of persistentpain in the neck and arm when the latter occurs inassociation with objective neurological signs of it such asmuscle wasting, sensory loss, and depression of oneor other of the tendon jerks in an arm (biceps jerk –C5 root; supinator jerk – C6 root; triceps jerk – C7root) together with, in particular, an electromyo-graphic abnormality. In such circumstances thepresence of posterior osteophytes on the lateralview of a cervical radiograph helps to confirm thediagnosis. It, nevertheless, has to be rememberedthat osteophytes are not the only cause of nerveentrapment in cervical spondylosis as this mayalso develop as a result of fibrosis in a dorsal rootsleeve, a tissue reaction that requires a myelogramfor its detection (Frykholm 1951).

Unlike what one might expect with nerve rootentrapment, either from well-developed posteriorosteophytes or peri-radicular fibrosis in cevicalspondylosis, the pain arising as a result of it is notpersistent but episodic, with each bout lastingfrom a few weeks to a few months, with the aver-age being about 6 weeks. As pointed out byHopkins (1993) it is not known why pain suddenlyarises from a root or roots that must have beencompressed for some considerable time or why, asis usually the case, it spontaneously disappears.One possible explanation he suggests is thattrauma to the nerve leads to the development ofinflammatory oedema of the tissues around theroot or roots that over the course of time sponta-neously subsides.

CERVICAL MYOFASCIAL TrP PAINSYNDROME

A far commoner and frequently overlooked causeof persistent neck and shoulder girdle pain, withor without pain down the arm, is the primary

Pain in the neck 209

Chap-14.qxd 13*10*04 14:38 Page 209

development of TrP activity in muscles in the neckand shoulder girdle.

Muscles in which this TrP activity is liable tocause neck and shoulder girdle pain to developare the levator scapulae, the splenius cervicis,other posterior cervical muscles, the trapezius andrhomboids. The ones in which TrPs are liable tocause pain to be referred down the arm include thelevator scapulae, the scalene muscles (Ch. 12), the supraspinatus and the infraspinatus (Ch. 13).The sternocleidomastoid muscle, although situ-ated in the neck, will be discussed in Chapter 16 as its TrP pain referral is to the head and face.

Each of these muscles, other than those dealtwith elsewhere, will be considered in turn withregard to the sites at which TrPs arise in them andtheir specific patterns of pain referral. This will befollowed by a discussion concerning the factorsresponsible for causing this TrP activity to developand its treatment.

Levator scapulae muscleWhen persistent pain in the neck with restrictionof its movements is due to TrP activity, this usuallydevelops in several muscles at the same time,either on one side or, as is often the case, on bothsides of the neck. It is, however, this muscle that isthe one most frequently involved (Fig. 12.14).


The pain from TrP activity in this muscle is mainlyfelt at the base of the neck, but it may also extendupwards towards the occiput, outwards to the backof the shoulder and downwards along the innerborder of the scapula (Fig. 14.1).

The pain may also radiate anteriorly around thechest wall along the course of the 4th and 5th inter-costal nerves when it may erroneously be diagnosedas being either anginal or pleural, or even morefrequently, as being due to intercostal nerve-rootentrapment. In addition, it quite commonly extendsdown the arm along the posteromedial aspect ofthe upper arm and the ulnar border of the forearmand hand to terminate in the ring and little fingers.A pattern of referral that coincides with the

cutaneous areas of distribution of spinal segmentsC8, T1 and T2 (Fig. 14.2).

Of those patients in whom levator scapulae TrPpain is referred to these distant parts of the bodysome only experience it down the arm, some onlyfeel it around the chest wall, whilst others areaware of it at both sites simultaneously.


Figure 14.1 The pattern of pain referral to the neck,shoulder and inner border of the scapula from a triggerpoint or points (�) in the levator scapulae muscle. Pain inthis distribution occurs as a result of activity in either atrigger point at the angle of the neck or one near to theinsertion of this muscle into the superior angle of thescapula, or in both.

Chap-14.qxd 13*10*04 14:38 Page 210

Scapulocostal and scapulohumeral syndromesMichele et al (1950), Russek (1952) and Michele &Eisenberg (1968), in describing the condition inwhich pain is referred down the arm and around thechest wall as a result of TrP activity in the levatorscapulae muscle, call it the scapulocostal syndrome.Long (1956) more appropriately divides it into thescapulocostal and scapulohumeral syndromes,because, as he states, ‘trigger point pain around thechest wall and down the arm, although commonlyoccurring in consort, does not always do so’.

TrP examination

TrPs may be found at two separate sites in thismuscle. One is at the angle of the neck where themuscle emerges from beneath the anterior borderof the trapezius muscle. The other is situated lowerdown the back at the attachment of the muscle tothe superior angle of the scapula (Fig. 14.1).

The point at the angle of the neck where theupper TrP is situated is best palpated with thepatient sitting comfortably with the elbows sup-ported on arm rests. This helps to relax both thelevator scapulae and trapezius, and allows the clinician to pull the trapezius out of the way. Oncethe levator scapulae muscle has been identified,the TrP is most readily located by gently turning the

head to the opposite side as this puts the muscle onthe stretch. The lower placed TrP may also belocated with the patient in the sitting position and is best identified by rolling the fingers acrossthe muscle fibres just above the superior angle ofthe scapula.

Splenius cervicis


TrP activity may be found in the upper part of themuscle and in the lower part. The TrP in the upperpart refers pain to the head and will, therefore, beconsidered in greater detail in Chapter 16.

It is the TrP in the lower part of the muscle thatcauses pain to be felt locally around the base of theneck.

TrP examination

This TrP may be located at the angle of the neckwhere the muscle lies between the trapezius medi-ally and the levator scapulae laterally. It is advis-able to rotate the head and neck to the oppositeside in order to put the muscle on the stretch whenattempting to identify it (Fig. 14.3).


Figure 14.2 Some other patterns of painreferral from a trigger point (�) in the levatorscapulae near to its insertion into the superiorangle of the scapula. These include referraldown the inner side of the arm to the ring andlittle fingers. And referral around the chest wallalong the course of the 4th and 5th intercostalnerves.

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Posterior cervical muscles halfway downthe back of the neckThe paravertebrally situated posterior cervicalmuscles are arranged in four layers. In descendingorder of depth, these layers consist of the upperpart of the trapezius; the splenius capitis and cervicis; the semispinalis capitis and cervicis; andthe multifidi and rotatores. With a painful stiffneck there is frequently an exquisitely tender TrPclose to the spine in one or other of these posteriorcervical muscles at about the level of the 4th or 5thcervical vertebra (Fig. 14.4). The depth at whichthe TrP lies and therefore the muscle involvedvaries from person to person.


Pain from a TrP in one of these posterior cervicalmuscles at this level is referred upwards towardsthe base of the skull and downwards over theshoulder girdle towards the upper part of thescapula (Fig. 14.5).

Trapezius muscleTrP activity in this muscle is very common. There areseveral sites where this may develop and therefore

reference will first be made to some anatomicalfeatures of the muscle. It will be remembered thatthe two trapezius muscles together take the shapeof a diamond. They extend in the midline from the occiput above, to the 12th thoracic vertebrabelow, and fan out on both sides to be attached tothe clavicle in front and the spine of the scapulabehind.

For descriptive purposes the muscle may there-fore be conveniently divided into an upper partextending from the occiput down to the 5th cer-vical spine, a middle part extending from the 6thcervical spine to the 3rd dorsal vertebra, and a


Figure 14.3 The pattern of pain referral from a triggerpoint (�) at the base of the neck in the lower part of thesplenius cervicis muscle.

1

23

45

6 7

Figure 14.4 To show the positions of some commonlyoccurring trigger points at the back of the neck andshoulder girdle.1. Trigger point in a depression between the upper endsof the trapezius and sternocleidomastoid muscles close tothe mastoid process and coinciding in position with thetraditional Chinese acupuncture point Gall Bladder 20(see Ch. 16).2. Trigger point in a posterior cervical muscle at the levelof the 4th cervical vertebra. The particular muscleinvolved depending on the depth at which the triggerpoint lies – see text.3. Trigger point in the ligamentum nuchae.4. Trigger point in the splenius cervicis muscle at theangle of the neck.5. and 6. Trigger points in the levator scapulae muscle.7. Trigger point in the upper free border of the trapeziusmuscle halfway between the spine and acromion andcorresponding in position with the traditional Chineseacupuncture point Gall Bladder 21.

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lower part extending from the 4th to the 12th dor-sal vertebra (Fig. 12.14).

Upper part of the muscle

The most frequently occurring TrP in the trapeziusmuscle is to be found along the upper border of the shoulder girdle about half way between the spine and the tip of the shoulder. This point,therefore, coincides in position with the well-known traditional Chinese one known as GallBladder 21.

TrP activity at this site is the cause of pain beingreferred up the side of the neck to the base of theskull, and on occasions around the side of the headto reach the temple and back of the eye (TP1 Figs14.6 & 16.6D).

Sometimes there is a further TrP in this upperpart of the muscle situated just below the onealready described (TP2 Fig. 14.6). This also causespain to be referred up the side of the neck.

Middle part of the muscle

A TrP near to the acromion may be responsible forpain being referred to the posterior part of theshoulder (TP3 Fig. 14.6).

Lower part of the muscle

A TrP (TP4 Fig. 14.6) may be found in the outerborder of the lower part just above the level of theinferior angle of the scapula. Also another one mayoccur just below the inner end of the scapularspine (TP5 Fig. 14.6). These two TrPs are not ofteninvolved but when they are, they may cause pain tobe referred to the upper scapular and neck region.They are, therefore, always worth looking for ifneck pain persists after activity in the other TrPsalready described has been adequately suppressed.

Rhomboids (major and minor) (see Fig. 12.14)

Activation of TrPs

This occurs less frequently than in the other shoul-der girdle muscles, but factors that cause it includeprolonged working in a round-shouldered pos-ition; also strain on the muscles from an upper thor-acic scoliosis, such as may occur idiopathically, orfollowing chest surgery.

It may also occur when these muscles, togetherwith the trapezius, become overloaded by havingto counteract tension in the pectoralis major andminor brought about by TrP activity developing inthese latter two muscles.


Figure 14.5 The pattern of pain referral from a triggerpoint (�) in a posterior cervical muscle at the level of the4th cervical vertebra.

1

23

4

5

Figure 14.6 Trigger points (�) in the trapezius muscle.

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Pain from TrPs in these muscles (Fig. 14.7) is con-fined mainly to an area immediately medial to theinner border of the scapula (Fig. 14.8).

TrP examination

With the patient seated and the arms wrappedtightly around the front of the chest in order to bringthe scapulae forwards the TrPs are located by meansof deep palpation through the trapezius muscle.

ACTIVATION OF MID-LINE TrPS IN THE LIGAMENTUM NUCHAE

Pain on extending or flexing the neck is often asso-ciated with the presence of one or more TrPs in theligamentum nuchae connecting the apices of thecervical vertebral spines (Fig. 14.4). In all suchcases therefore it is important to palpate along thelength of this ligament from the occiput above tothe spine of the 7th cervical vertebra below.

FACTORS RESPONSIBLE FOR THEPRIMARY ACTIVATION OF TrPS IN THE NECK

These include trauma to the neck such as that sus-tained as a result of a whiplash injury; posturaldisorders; sagging of, tilting of and persistent pres-sure applied to the shoulder girdle; strain transmit-ted to the neck as a result of a lower limb disorder;and anxiety-evoked contraction of muscles. Eachof these will be considered in turn.

Whiplash injuryTrPs in the muscles of the neck may become acti-vated as a result of various forms of trauma suchas that incurred when falling from a horse or trip-ping whilst going downstairs, but one of the com-monest nowadays is the whiplash injury liable toaffect the occupants of a stationary car when this ishit from behind by another car.

As previously discussed by me (Baldry 1996,2001), all the various aspects of this particular typeof injury have over the years given rise to consid-erable controversy.

Extensive reviews of the literature concerning ithave been provided by Barnsley et al (1994); by the Quebec Task Force on Whiplash AssociatedDisorders (Spitzer et al 1995); by The World Con-gress on Whiplash Associated Disorders held inVancouver during February 1999 (Anton 2000); byRyan (2000) and by Galasko et al (2000).

Factors responsible for the development of pain

Activation of myofascial TrPs It is still not suffi-ciently well recognized that the commonest reasonfor pain in this disorder developing is trauma-induced activation of TrPs in the muscles of theneck (Baldry 1996, 2001, Byrn et al 1991, 1993,Evans 1992, Fricton 1993, Mailis et al 1995, Simons


Figure 14.7 Trigger points (�) along the medial borderof the scapula in the rhomboid muscles.

Figure 14.8 The pattern of pain referral from a triggerpoint or points in the rhomboid muscles.

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et al 1999) and in muscles of the upper anteriorchest wall including, in particular, the pectoralisminor (Hong & Simons 1993).

It therefore follows that in all cases of whiplashinjury a systematic search for TrPs in these musclesis mandatory.

Facet joint damage The reason why pain mayarise from facet joints following a whiplash injuryis still not certain (Gibson et al 2000). Some of thepossible causes include occult fractures, capsularruptures and intra-articular haemorrhages (Taylor &Twomey 1993).

Bogduk & Simons (1993) have shown thatbecause an individual facet joint and the musclearound it share the same nerve supply, the patternof pain referral from TrPs in that muscle and fromthe joint is the same. In view of this any TrP foundto be present should first be deactivated. If despitedoing this the pain persists, then the possibility thatit may also be arising from the facet joint has to beconsidered and a diagnostic block of the nervessupplying it carried out (Bogduk & Marsland 1988).

Intervertebral disc damage There are grounds forbelieving that persistent localized pain in the neckfollowing a whiplash injury may develop as a resultof tears in the richly innervated outer third of adisc’s annulus fibrosus, as these have been shown tobe present in patients with this disorder by means ofthe carrying out of cineradiograms (Buonocore et al1996) and MRI scans (Davis et al 1991). The latterhave shown that avulsion of the disc from the verte-bral endplate may be yet another cause.

RADIOGRAPHIC AND MRI FINDINGS The carrying outof radiography and MRI are widely employed foridentifying the above skeletal causes of pain in thisdisorder but interpreting the significance of abnor-malities found by this means demands considerablecaution. This is because, as Ryan (2000) has pointedout, the Quebec Task Force (Spitzer et al 1995)reported that MRI and radiographic examinationsare confounded by age-related changes in bony andsoft tissues. And because Boden et al (1990), fromthe carrying out of MRI on 63 asymptomatic volun-teers, observed an abnormality such as a herniateddisc, bulging disc or foraminal stenosis in 19% ofthese people and found that the frequency of abnor-malities in those aged 40 years or more was 28%.

Conversely, it has to be said that an all too fre-quent cardinal error is to conclude that because aradiographic or MRI examination fails to show any

significant abnormality that any persistent pain thatmay be present in someone with this disorder mustbe due to either neuroticism or compensation-seeking avarice without considering the possibil-ity that the pain may be emanating from TrPs inthe muscles.

Pain in the head The commonest reason for thisdeveloping in someone with a whiplash injury isTrP activity in one or more of the following muscles.The posterior cervical muscles, the upper part ofthe trapezius and the sternocleidomastoid.

Paraesthesiae in the fingers There are three rea-sons why paraesthesiae in the fingers may arise inthis disorder. One is because of the development ofa thoracic outlet syndrome as a result of TrP-evokedshortening of the pectoralis minor muscle and thescalenus anterior muscle causing compression ofunderlying vessels and the brachial plexus; a secondis the development of a cervical radiculopathy; anda third is the development of a carpal tunnel syn-drome. This latter disorder may be brought aboutas a result of perineural oedema of the mediannerve occuring either because of vascular com-pression at the thoracic outlet, because of a hyper-extension injury to the wrist caused by excessivegripping of the steering wheel, or because of brac-ing the hands on the dashboard during the collision(Evans 1992).

Spatial disorientation The type of spatial dis-orientation that most often affects patients with awhiplash injury is dizziness and light-headednesswith a sudden loss of balance and a tendency toveer to one side when walking. This may on occa-sions be due to vertebrobasilar insufficiency(Schneider & Schemm 1961) but far more often(see Ch. 16) it is due to a change in the tension andshortening of the clavicular part of the sternocleido-mastoid muscle brought about as a result oftrauma-induced TrP activity (Travell 1967, Weeks &Travell 1955).

Cognitive impairment Psychometric assessmentof patients with whiplash injuries have shown thatsome of them have impaired attention, concentra-tion and memory (Kischka et al 1991, Radanov et al1991). Possible reasons for these cognitive disordersinclude the distracting influence of persistent neck and head pain, together with the anxiety anddepression produced by this and the effects ofdrugs given to combat these symptoms (Shapiro et al 1993).


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Emotional disturbances Persistent whiplashinjury-evoked pain, like any other chronic pain,may lead to the development of anxiety anddepression. These two disorders of the affect, fur-thermore, are liable to be made worse by any jobinsecurity, marital disharmony or social disrup-tion that may be brought about by the physicaldisability.

Late whiplash syndrome It has been estimatedthat approximately 75% of patients with whiplashinjuries recover within 3–6 months and that theremaining may develop what is known as the latewhiplash syndrome – a condition in which symp-toms, including in particular pain, persist for longerthan 6 months.

Factors that Radanov et al (1991) have identi-fied as being predictive of this developing includethe severity of the initial neck pain, the presence ofcognitive disorders, and the effects of ageing.

Pettersson et al (1995), from MRI studies, haveshown that the syndrome is particularly likely todevelop in those who have an antecedent narrow-ing of the cervical canal.

This syndrome is also more liable to developwhen the trauma to the neck is so severe that paincomes on immediately after it rather than beingdelayed for 24–48 hours, as is more usually thecase. This notwithstanding, it has to be said thatpatients who have been subjected to no more thanmild or moderate injury may also develop it.Possible reasons for this include undiagnosed andtherefore untreated causes of the pain such as TrPactivity, facet joint injury or disc damage. Anotheris the central sensitisation of dorsal horn-situatednociceptive neurons that develops as a result ofthe sensory afferent barrage set up when there ispersistent activation and sensitisation of nocicep-tors in either TrPs or other structures.

A clear understanding of these various causativefactors is of considerable importance because theprolongation of symptoms in a patient with awhiplash injury has for all too long been attrib-uted to either neuroticism or a subconscious oreven conscious exaggeration of them for the pur-pose of obtaining financial compensation (Pearce1989). The following case typefies this.

A builder (46 years of age), as a result of a caraccident, was admitted to hospital unconscious and

with severe bruising of the right side of the neck, rightshoulder and right elbow.

He recovered consciousness within a matter ofhours, the bruising disappeared over the next fewweeks, but he was left with much pain in andrestricted movements of the right side of the neck andin spite of physiotherapy, neck traction and thewearing of a collar he still had this pain when seen byan orthopaedic specialist 3 months after the accident.The patient was told at this stage that no furthertreatment was likely to be helpful but that the painwould disappear spontaneously with time.

When, at follow-up 6 months later, he still hadconsiderable pain and limitation of movements of the neck, and had also by then developed headaches and unsteadiness on sudden movements,the same specialist told him that with patience itwould all settle down and that certainly he wasunlikely to have trouble once a compensation claimhad been settled! The patient felt the implications ofsuch a remark to be totally unjustified particularly asbeing a self-employed person he was desperatelyanxious to get back to work. His general practitionerwondered if he might be helped by acupuncture andwhen seen by me 12 months after the accident he was obviously having much genuine pain in the neckcausing him to take large amounts of analgesics.

On examination, there were many exquisitelytender TrPs to be found in several muscles of the neck,and after these had been deactivated by means of thecarrying out of superficial dry needling at weeklyintervals on six occasions, his pain was sufficientlywell controlled to allow him to return to work, andafter two further treatments over the next month itdisappeared.

This response to acupuncture was gratifying but of course it would have been possible to haverelieved his pain much more quickly if only thedevelopment of TrP activity had been recognized at amuch earlier stage.

Postural disordersTrP activity may arise in the neck muscles whensome faulty posture is persistently adopted. Thisnot infrequently occurs occupationally as a resultof a desk or workbench not being adjusted to anindividual’s body build. Machine operators andtypists are some of those particularly at risk.


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A draughtsman (29 years of age) had two attacks ofsevere rightsided neck pain with restricted movements.Each time he was told he must have ‘slipped a disc’and was treated by having his neck intermittentlystretched and immobilized in a collar.

On each occasion he obtained little or no benefit from these measures, had to take much timeoff work, and the pain persisted for about 6–8 weeks.In view of this experience, when 1 year later itrecurred a third time, he asked his general practitionerabout the possibility of acupuncture and was referredto me. I saw him within a week of the pain developing,and found TrPs to be present in the right levatorscapulae muscle at the angle of the neck; in the free border of the trapezius half-way between theangle of the neck and the tip of the shoulder; and athird half-way down the side of the neck in a posterior cervical muscle.

When these were deactivated by means of thecarrying out of superficial dry needling the painimmediately abated and full movement of the neckwas restored. It was only necessary to repeat theprocedure once again a week later before lastingimprovement was obtained. However, what was ofparticular importance to him was that he did not haveto take any time off work. It is not sufficient tocontent oneself with effectively alleviating pain,without at the same time seeing whether there isanything that has to be done in order to prevent arecurrence. In this case it was found that each attackhad occurred at a time when pressure of workdemanded that he sat at his drawing board for aparticularly long period on a chair that was too lowwith, because of this, his shoulder girdle abnormallyelevated.

TrP activity in neck muscles may develop toowhen the neck has to be turned to one side for longperiods such as when a secretary has to read short-hand notes whilst typing, or when the neck is keptfixed in one position for a long time, such as whenwatching a play or driving a car, also when it isrepeatedly rotated such as watching a tennis match.

It also may occur during sleep when the neckbecomes kinked at an acute angle either due to thepillow being too high or too low.

A girl (14 years of age) suffered from severe neck pain that much affected her schooling for


3 years because the significance of too high a pillowwas not recognized. During that 3 years she was givenseveral courses of physiotherapy, had had her neckstretched and from time to time had worn a collar.When eventually she was seen by me it only requiredthe deactivation of TrPs on three occasions to bring thepain under control. On investigating the cause of thepain it became apparent that the child for many yearshad insisted on sleeping with the head resting onthree pillows. Since this habit has been changed, shehas had no recurrence of pain.

Sagging of the shoulder girdleThe activation of TrPs commonly occurs in those,who because of occupational strains, obesity, oreven laziness, have become round shoulderedwith drooping of the shoulder girdle – the so-calledsyndrome of the sagging shoulders.

Tilting of the shoulder girdleThis is not an uncommon reason for TrP activity todevelop. It occurs either secondary to a pelvic tilt insomeone who because of a congenital or acquireddefect has one leg longer than the other, or becauseof the habitual use of a walking stick which is too long.

Transmitted strain to the neckAny painful disorder affecting the lower limbmay, by putting a strain on all parts of the spine,cause not only the development of TrP activity inthe muscles of the lower back but also in the musclesof the neck.

Persistent pressure on the shoulder girdleTrP activity may develop in the neck muscles whenthey are subjected to persistent strain from thewearing of unsuitable clothing, such as an over-coat that is too heavy, or shoulder straps that aretoo tight.

Environmental factorsThese include exposure either to draughts or todamp.

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AnxietyA common cause of TrPs developing in neck muscles is when these are persistently held in acontracted state because of nervous tension. Whenthis is the predominant cause the patient often alsocomplains of headaches.

PREVENTATIVE MEASURES

It must be stressed that, although pain from any ofthe above causes may readily be alleviated bymeans of the carrying out of superficial dry needlingat TrP sites, such pain will recur unless the reasonsfor it developing are identified and measures aretaken to avoid the re-activation of the TrPs.

TREATMENT OF PERSISTENT NECK PAIN

Because of the traditional belief that persistent painand stiffness of the neck are mainly due to nerve-root entrapment, either from an acute prolapse of an intervertebral disc, or from cervical spondy-losis, treatment usually includes continuous ormore often intermittent traction; the wearing of a specially designed collar; and the use of variousforms of physiotherapy.

Pain of this type may persist for many monthsor years but often it subsides spontaneously afterabout 6–8 weeks, and it is now generally agreedthat none of the standard forms of treatment, suchas neck traction (Steinberg & Mason 1959, BritishAssociation of Physical Medicine Trial 1966), thewearing of a collar (Matthews 1983), or differenttypes of physiotherapy including diathermy andultrasound (Rogers & Williams 1981), significantlyinfluence its course.

There is, therefore, much need for a differentapproach to the treatment of persistent neck painand now that it is realized that often it is associ-ated with the development of TrP activity in themuscles, we have in superficial dry needling at TrP sites one of considerable promise. This firstbecame apparent to me some years ago now,when, as it so happened, one of the first patients tobe treated by me with this particular form of ther-apy had pain of this type.

A housewife (61 years of age) was referred to myoutpatient clinic with angina, but what troubled her

even more was that for the past 6 months, since sheand her husband had been in a car accident, she hadhad persistent pain in the neck with marked restrictionof its movements. She further informed me that shehad not mentioned this to her general practitioner asshe could not face having to wear a collar! An X-ray ofthe cervical spine showed, as might be expected atthat age, the characteristic appearances of cervicalspondylosis. In addition, however, examination of herneck muscles revealed the presence of TrPs and shewas, therefore, asked to attend my outpatient clinicagain for me to attempt to relieve her pain by meansof deactivating these.

It must have been with a certain amount oftrepidation that she kept her appointment for this asshe brought her husband with her for moral support!TrPs were found at three similar sites on both sides ofher neck and deactivated by means of needles beinginserted into the tissues immediately overlying them fora short period. Much to her surprise (and to a certainextent mine also!) on withdrawing the needles shefound that her neck was very much more comfortableand that she could move it through a full range ofmovements. She said that her husband would neverbelieve this and so asked if he could come into thetreatment room to witness it!

After expressing pleasure at his wife’s response totreatment, he revealed that he too, since the caraccident, had had persistent pain in his neck and hadexperienced severe limitation of its movements.Further, he said that he had had two courses ofintensive treatment for what he had been told wassevere arthritis of the neck, and wondered whether asan act of desperation he also might be allowed to trythe effects of acupuncture.

Examination showed him to have several TrPs inboth sides of his neck and once these had beendeactivated in a similar manner the immediate resultswere as gratifying as in the case of his wife.

Ultimately the wife had to have treatment on fouroccasions and the husband on six in order to obtainlasting relief from their pain. My memory, however, ofthose two walking down the hospital corridor aftertheir first treatment both joyfully moving their headsfrom side to side in evident amazement at their new-found freedom of neck movements will forever beindelibly imprinted on my mind, and at the time thesight of it did much to strengthen my resolve to studyacupuncture further!


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There can be no doubt that in both these cases theneck pain was due to TrP activity developing in musclesthat had become strained as a result of the car accidentand that the radiographic appearances of degenerativeskeletal changes observed in both of them werechance findings. It is interesting to note that thehusband had been told that the reason for his failure to respond to physiotherapy was becausethe arthritis in his neck was so bad!

Identification and deactivation of TrPsThe two cases just quoted once again serve to illus-trate how important it is in all cases of persistentneck pain to examine the muscles of the neck forTrPs. Moreover, such an examination has to be car-ried out in a systematic manner as it is essential toavoid overlooking any of them that may be con-tributing to the pain.

The patient should therefore be seated comfort-ably in a chair but with the head and arms suitablypositioned to put the muscles on the stretch. Eachmuscle should then be examined in turn in orderto ensure that no TrPs are overlooked and thateach in turn has a needle inserted into the tissuesoverlying it. Particular care, however, must betaken when putting needles into muscles aroundthe base of the neck and chest wall, never to insertthem in a vertical direction but always at an angleso as to avoid penetrating the pleura.

As previously stated (see Ch. 8), when treatingmyofascial pain by the carrying out of superficialdry needling at TrP sites this needle-evoked nervestimulation procedure should never be carried outso energetically as to cause a temporary exacerba-tion of the pain. For some reason it would seem thatthis is especially likely to happen when deactivatingTrPs in muscles around the head and neck. There-fore, in carrying out such treatment in this particu-lar part of the body, it is advisable to be especiallycareful not to keep needles in situ for longer thanis necessary and to keep any manipulation of themdown to a minimum (see Ch. 10).

Results of employing acupuncture for the treatment of neck painEveryday clinical experience would appear to sug-gest that the treatment of persistent neck pain with

acupuncture is very rewarding. It would seem thatapproximately 70% of patients obtain long-termrelief from repeating this type of treatment on sev-eral occasions but the number of times this has tobe carried out is largely dependent on the length oftime the pain has been present before it is started. Aminority of cases only obtain relief for short periodsand the treatment, therefore, has to be repeated on a regular basis at fairly frequent intervals. Suchpatients however find this a small price to pay forhaving their pain kept under control. A small groupof patients obtain no benefit from it. These are usually people who have not only had pain ofmuscular origin for many years but also have someother underlying chronic skeletal pain disorder.

When considering results, however, it is diffi-cult to generalize, for in the treatment of persistentneck pain with acupuncture the effectiveness ofthis not only depends on the underlying path-ology, but also on a person’s individual degree ofresponsiveness to needle-evoked nerve stimula-tion (see Chs 9 & 10).

Clinical trials

White & Ernst (1999) have carried out a systematicsearch of randomized controlled trials of acupunc-ture for neck pain. During the course of discussingthis, Ernst (1999) stated that ‘twenty-four studiesmet our predefined inclusion and exclusion cri-teria. The trials were highly heterogenous and fewwere of acceptable quality as estimated by theJadad score (Jadad et al 1996) … Of the five sham-controlled studies, one was positive and four werenegative. On the basis of these findings, we con-cluded that data are insufficient to state with cer-tainty that acupuncture is more effective thansham acupuncture or other controlled interven-tions in the treatment of neck pain’.

A major criticism of all the trials reviewed bythem is that they had been carried out on patientswith non-specific chronic neck pain so that the treat-ment and control groups studied could well havecontained people suffering from pain that may havebeen either of muscular origin, skeletal origin or acombination of these and which also may have beeneither nociceptive, neuropathic or a mixture of both.The response to acupuncture of pain of such dis-parate types is likely to be very different so as to


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make the interpretation of results when trials arecarried out on patients with ill-defined heterog-eneous chronic neck pain virtually impossible.

It is clearly essential when carrying out anacupuncture clinical trial to do so on patients witha single well-defined disorder. At first sight itmight be thought, for example, that Loy (1983) ful-filled this criterion in a trial in which the relativepain-relieving efficacy of electroacupuncture andphysiotherapy was compared in patients diag-nosed as having pain due to cervical spondylosis,mainly on the grounds of there being evidence ofthis radiographically. However, as stated earlier in this chapter, pain in the neck cannot be assumedto be due to this degenerative disorder without evi-dence of nerve root entrapment because, in mostcases, without this the changes of it seen on an X-ray are usually no more than a chance findingand the pain due to some other cause, the com-monest being TrP activity in the neck muscles.Thus, chronic neck pain diagnosed as being due tocervical spondylosis on radiographic evidencealone, as in Loy’s trial, may well be due to any oneof a variety of disorders making randomizationinto homogenous ‘treatment’ and ‘control’ groupsimpossible.

There have been up to now few trials to assess theefficacy of TrP acupuncture alone in the treatmentof the cervical myofascial TrP pain syndrome.

As previously discussed in Chapter 10, Hong(1994) carried out a well-planned trial to comparethe effectiveness of lidocaine (lignocaine) injec-tions with that of deep dry needling at myofascialTrP sites in the upper trapezius muscle. And Chu(1997) compared the effects of deep dry needlingat TrP sites and at non-specific sites in patientswho had cervical nerve root irritation pain and thesecondary development of myofascial TrP pain.

Most other acupuncture trials carried out onpatients with this TrP syndrome have had needlesinserted either at traditional Chinese acupuncturesites alone or at a combination of both these andTrP sites.The following are examples of this.

Birch & Jamison in 1998 reported the results of acontrolled trial carried out to assess the value ofJapanese acupuncture in the treatment of chronicmyofascial neck pain. The treatment, however, wasnot carried out at myofascial TrP sites but insteadneedles connected together by ion pumping cords

(see Ch. 10) were inserted very shal-lowly at whatwere deemed to be either ‘relevant’ or ‘irrelevant’traditional Chinese acupuncture points. Their con-clusion was that ‘relevant traditional Chineseacupuncture … contributes to modest pain reduc-tion in persons with myofascial neck pain.’

Irnich et al in 2001 reported the results of a ran-domized trial of acupuncture in patients withchronic neck pain that was considered to haveeither emanated from TrPs or to have arisen as aresult of a whiplash injury. No mention is made inthe report as to how many with this latter disorderhad active TrPs.

Three procedures were employed in the ‘treat-ment’ group. These were dry needling carried outat some of the TrP sites, acupuncture carried out‘according to the rules of traditional Chinese medi-cine’ and ear acupuncture. There were two ‘con-trol’ groups. One of them had an inactivated laserpen applied to similar points and the other wastreated with massage.

The conclusion was that ‘acupuncture is aneffective short term treatment for patients withchronic neck pain.’

It may be seen therefore that despite there hav-ing been a large number of patients in this trial withpain emanating from myofascial TrPs, the designof it precluded any information being obtained con-cerning the value of dry needling carried out onthese points alone.

Irnich et al in 2002 reported the results of a ran-domized double-blind sham-controlled trial inpatients with chronic neck pain that had ariseneither as a result of TrP activity or what they called‘the cervical irritation syndrome’.

The aim of the trial was to compare the imme-diate effects on motion-related pain and cervicalspine mobility of three types of treatment given toeach patient on single occasions. These treatmentswere: (1) needles inserted into traditional acupunc-ture points and one or two ear points; (2) dryneedling carried out at myofascial TrP sites; and(3) sham laser carried out at traditional Chineseacupuncture points. There was a 1 week wash-outperiod between the carrying out of each of theseprocedures.

The results showed that ‘acupuncture is supe-rior to sham in improving motion-related pain andrange of movements following a single session of


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treatment in chronic neck pain patients’. Unfortu-nately, once again the design of the trial was suchthat they had to admit that ‘it is not possible toconclude from our data whether needling classicalacupuncture points is more effective than needlingother sites’.

It may therefore be seen that there remains apressing need for suitably designed trials to be

carried out to assess the relative efficacy, advantagesand disadvantages of, Japanese shallow needling,superficial dry needling and deep dry needlingcarried out at TrP sites for the alleviation of cervi-cal myofascial pain.


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223

Chapter 15

Pain in the arm

CHAPTER CONTENTS

Introduction 223Neck and arm pain from cervical spondylosis,

cervical disc prolapse or myofascial TrPactivation 223–224

Paraesthesiae as a result of nerve rootcompression or TrP activity 224

Referral of pain down the arm from TrPs in theneck and shoulder-girdle muscles 224–225

Cervical radiculopathic brachial pain followed by the development of MTrP brachial pain 225–226

Pain referral down the arm from the heart andfrom TrPs in the chest wall muscles 226

Triceps muscle 226Brachial plexus injuries 227

Brachial plexus compression (thoracic outletsyndrome) 227–228

Lateral epicondylalgia (syns: lateral epicondylitis,tennis elbow) 228–235

Medical epicondylalgia (syns: medialepicondylitis, golfer’s elbow) 235

Pain in the wrist and hand from TrPs in theforearm muscles 235–242

Cubital tunnel syndrome 240–241Pain in the wrist and hand from local

TrPs 242–247Carpal tunnel syndrome 243Neuralgic amyotrophy 247Shoulder–hand syndrome 248Repetitive strain injury 248

INTRODUCTION

In this chapter brachial pain occurring as a resultof the primary activation of trigger points (TrPs) inneck, shoulder girdle, chest wall, upper arm, fore-arm and hand muscles will be discussed. Also, thenecessity for carefully distinguishing between TrPpain and radiculopathic pain in those cases wheretheir referral patterns happen to be similar andwhen TrP pain arises as a secondary event followingthe development of radiculopathic pain.

In addition, attention will be drawn to a num-ber of disorders including lateral and medial epi-condylalgia, neuralgic amyotrophy, shoulder–handsyndrome, and repetitive strain injury where thepathogenesis of the brachial pain is complex andTrP activity is only one of the factors responsiblefor its development.

NECK AND ARM PAIN FROM CERVICALSPONDYLOSIS, CERVICAL DISC PROLAPSEOR MYOFASCIAL TrP ACTIVATION

As already stated in Chapter 14, and repeated now,as it cannot be too strongly emphasized, there isno justification for assuming that pain in the neckand down the arm, in the absence of objective evidence of nerve root involvement, is necessarilydue to either cervical disc prolapse or spondylosis.The commonest cause for its development is primary myofascial TrP (MTrP) activity.

Furthermore, even if there should be evidenceof nerve root entrapment both clinically, elec-tromyographically and from the carrying out of

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magnetic resonance imaging (MRI), it has to beremembered that TrP activity not uncommonlydevelops as a secondary event in a region affectedby radiculopathic pain.

PARAESTHESIAE AS A RESULT OF NERVEROOT COMPRESSION OR TrP ACTIVITY

A diagnostic pitfall is to assume that because paindown a limb is accompanied by various paraesthe-siae such as numbness, burning, and pins and needles, such symptoms must inevitably be due tonerve root entrapment. That this is not necessarilyso and they at times are complained of by patientswith primary MTrP pain was first pointed out bySola & Kuitert (1955) and again more recently bySimons et al (1999, p. 20). The following case exem-plifies this.

A publican’s wife (56 years of age) with a 12-yearhistory of intermittent neck pain for which she hadfrequently worn a collar, once again developed pain inthe neck and down the left arm. However, whatdisturbed her most this time was a feeling of ‘pins and needles’ spreading down both sides of that arm onmoving it. She was informed by her doctor that thiswas because she had a trapped nerve and was givensome physiotherapy and told to wear a collar onceagain, but when after 5 months her symptoms had not improved, she herself asked for someacupuncture.

The most striking feature in this case was thatwhenever pressure was applied to a TrP in thesupraspinatus muscle, it invariably brought on thesensation of pins and needles in the outer arm, andwhen pressure was applied to a TrP in the levatorscapulae muscle a similar sensation travelled down theinner side of the arm to the ring and little fingers.There were no abnormal neurological signs. Afterdeactivation of these TrPs by means of superficial dryneedling carried out on four occasions at weeklyintervals both the pain and paraesthesiae disappeared.

REFERRAL OF PAIN DOWN THE ARMFROM TrPs IN THE NECK ANDSHOULDER-GIRDLE MUSCLES

Michele et al (1950), Russek (1952), Long (1956),and Michele & Eisenberg (1968) were amongst

some of the first to draw attention to how com-monly TrP activity in muscles in the neck andshoulder girdle is the cause of pain being referreddown the arm. Then in 1971, Aronson et al pub-lished a report on 16 patients seen by them over an8-month period with brachial pain emanatingfrom TrPs that had been misdiagnosed as beingdue to a radiculopathy. They stated that theyreported these because they felt it was still not suf-ficiently well recognized that brachial pain ofmyofascial origin may readily be mistaken forpain of cervical nerve root origin in those caseswhere their patterns of referral down the arm aresimilar. They also stated that prior to these patientsbeing seen by them, because their pain had a cer-vical nerve root distribution, they had been mis-diagnosed by orthopaedic and neurosurgeons assuffering from nerve root entrapment and subjectedto prolonged periods of neck traction and the wear-ing of cervical collars.

They pointed out that what led them to the cor-rect diagnosis was the absence of objective neuro-logical signs and the discovery on careful palpationof exquisitely tender trigger areas with pressureon these causing the pain to be reproduced.

Muscles in the neck and shoulder girdle with TrPpain referral similar to that of radiculopathic painreferral are the supraspinatus, the infraspinatus, thescalenus anterior and the levator scapulae.

TrP activity in the supraspinatusAs stated in Chapter 13, pain from TrPs in thismuscle is referred to the outer side of the shoulderover the area of the deltoid muscle and down theouter side of the upper arm to the lateral epi-condyle, where it is often felt particularly strongly.Its pattern of referral, therefore, coincides with thecutaneous area of distribution of the C5 nerve root,and for this reason its clinical presentation is simi-lar to that of pain from entrapment of this nerve(Reynolds 1981).

TrP activity in the infraspinatusAs stated in Chapter 13, pain from TrPs in thismuscle is referred to the front of the shoulder, theanterolateral border of the arm and forearm, andsometimes it extends as far as the radial aspect of


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the hand. Its pattern of referral, therefore, coin-cides with the cutaneous area of distribution of theC5, C6 and C7 nerve roots and for this reason itsclinical presentation is similar to that of pain fromentrapment of these nerve roots (Reynolds 1981).

TrP activity in the scalenus anteriorAs stated in Chapter 12, pain from TrPs in thismuscle is referred down both the anterior and pos-terior aspects of the upper arm, the radial borderof the forearm, and terminates in the thumb andindex finger, and, therefore, may also simulate aC5–C7 nerve root lesion (Reynolds 1981). Such painis likely to persist for months or years as TrPs inthis muscle, because of its anatomical position, areparticularly liable to be overlooked.

A man (52 years of age) was referred to me with an11-year history of pain down the outer side of theright arm extending from the shoulder to the indexfinger and thumb. The pain had been intermittent with episodes of it being brought on by bouts of heavy lifting at work. He had had numerous courses of physiotherapy directed to the neck for what he was told was a ‘trapped nerve’. Having received nobenefit from these he decided to try acupuncture as a last resort!

On examination of the neck there were twoexquisitely tender TrPs in the right scalenus anteriormuscle, with pressure on one of these causing pain toshoot down the arm to the thumb in the samedistribution as the spontaneously occurring pain. Thedeactivation of these by means of superficial dryneedling carried out at these two points quicklybrought the pain under control.

TrP activity in the levator scapulaeAs stated in the previous chapter, TrP activity inthe levator scapulae muscle is a common cause ofpain being referred down the arm. Michele &Eisenberg (1968) estimated that it is responsiblefor more than 90% of all cases of cervicobrachialpain. The pain from TrPs in this muscle is referreddown the inner side of the arm to the ring and lit-tle fingers in a similar manner to that of C8 T1nerve root entrapment pain.

Electromyography may be required to distin-guish MTrP pain from cervical nerve root entrap-ment pain, but in practice this is rarely necessarybecause when TrP activity is responsible for the pain,pressure on the relevant TrP almost always, in myexperience, causes pain to shoot down the arm in thedistribution of the spontaneously occurring pain.

A prison officer (54 years of age), 2 years beforepresentation, developed pain in his neck as a result offalling off his motor bike. At that time he was toldthat his neck X-ray showed quite marked arthriticchanges, but in spite of this, the pain only lasted for 3 weeks. He was then symptom-free until 9 monthsbefore being referred to me after suffering a carcollision-evoked whiplash injury to his neck. At firstthe neck felt persistently stiff with pain on turning itto the left side. After some weeks, he also began to getpain down the inner side of the left arm, with pins andneedles in the ring and little fingers.

He was given a variety of different forms oftreatment in the physiotherapy department, includingneck traction, and was told to wear a collar. Whenafter 9 months the pain in the neck and arm had notimproved, and he had lost much time off work, he informed his doctor he would like to tryacupuncture.

On examination there was quite marked limitation ofneck movements on the left side and, in addition, therewere several TrPs to be found in the muscles of the neckand shoulder girdle. In the levator scapulae musclethere were two: one at the angle of the neck, and oneat the site where the muscle is inserted into thesuperior angle of the scapula. These were of particularinterest because pressure on either of them caused painto radiate down the medial side of the arm to the ringand little fingers in exactly the same distribution as thatof pain from a C8 T1 nerve root lesion.

Following deactivation of these TrPs by the carryingout of superficial dry needling on two occasions the painwas brought sufficiently under control for him to beable to return to work.

CERVICAL RADICULOPATHIC BRACHIALPAIN FOLLOWED BY THE DEVELOPMENTOF MTrP BRACHIAL PAIN

From what has already been said, it may be seenthat the patterns of pain referral down the arm

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from either compression of a cervical nerve root orTrP activity in a neck or shoulder girdle musclemay in certain cases be identical. To add to theconfusion it has to be remembered that a muscle,such as for example the pectoralis minor or sca-lene anterior, when shortened as a result of TrPactivity, may compress roots of the underlyingbrachial plexus with, as a consequence, radiculo-pathic and TrP pain radiating down the arm con-comitantly. It should also be remembered that, asSimons et al (1999, p. 81) have pointed out, TrPactivity is liable to develop as a secondary event inmuscles innervated by an entrapped nerve rootdue to the effect nerve root compression has on aTrP’s dysfunctional motor endplates.

PAIN REFERRAL DOWN THE ARM FROMTHE HEART AND FROM TrPs IN THECHEST WALL MUSCLES

Pain that radiates down the arm does not of coursenecessarily stem from either a cervical nerve rootlesion or from TrPs in the muscles of the neck orshoulder girdle. It may also, as already stated inChapter 12, be referred down the arm from TrPs in the muscles of the chest wall or from the heart incoronary artery disease.

Pain down the arm from TrP activity in musclesof the chest wall is usually readily distinguishedfrom pain emanating from the muscles of the neck,because the pain is almost always felt in the chestitself as well as in the arm, as may be seen from thediagrams of the TrP pain patterns of such musclesas the pectoralis major (Fig. 12.7), pectoralis minor(Fig. 12.10), serratus anterior (Fig. 12.11), serratusposterior superior (Fig. 12.13) and the latissimusdorsi (Fig. 12.15).

It is important to remember, however, thatwhilst anginal pain is usually felt across the frontof the chest, as well as at other sites such as theneck and arm, at times it may be predominantlyfelt in the neck and arm, and occasionally it maybe confined entirely to the arm. The latter may besomewhat misleading and is not sufficiently wellrecognized, despite it having been well known toWilliam Heberden (1818) nearly 200 years ago, asmay be seen from reading Chapter 70 entitled‘Pectoris Dolor’ in his famous Commentaries on theHistory and Cure of Diseases.

TRICEPS MUSCLE

This is the only muscle in the upper arm in whichTrP activity is likely to give rise to widespreadpain affecting both the neck and arm.

Activation of TrPsTrPs may become activated in the long, medial orlateral heads of the muscle as a result of it becom-ing overloaded during the carrying out of sportssuch as tennis and golf or doing ‘press ups’. Also,when this happens as a result of sitting for anylength of time with the arm held forwards withoutthe elbow being adequately supported, such aswhen driving a car for a long distance.

TrPs in the medial and lateral heads give rise to localized pain around the epicondyles of thehumerus and will therefore be referred to later inthe chapter when discussing lateral and medialepicondylalgia.

LONG HEAD OF THE TRICEPS

It is TrP activity in the long head of the triceps thatcause pain to radiate over a wide area of the neckand arm.

Specific pattern of pain referralPain from these TrPs is referred upwards over theposterior part of the shoulder, occasionally to thebase of the neck and sometimes down the back ofthe forearm to the wrist (Fig. 13.13). It is because ofthis pattern that the pain is sometimes confusedwith that of a C7 radiculopathy.

TrP examination TrPs in this head are usually to be found deep inthe belly of the muscle just below the level of theposterior axillary fold (Fig. 13.13). They are pre-sent in taut bands which, when plucked, give localtwitch responses.

When TrPs in the long head are the cause of painit is not possible to press the upraised arm hardagainst the ear when the elbow is kept straight(Fig. 13.14).


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Deactivation of TrPsWhen deactivating TrPs in the triceps muscle by means of the carrying out of superficial dryneedling, the patient should lie in the semi-proneposition with the affected arm uppermost.

BRACHIAL PLEXUS INJURIES

The brachial plexus may be damaged by stabwounds, bullets, or iatrogenically by surgical oper-ations on the neck. The nerves in such cases, how-ever, usually remain in continuity and, with presentday neurosurgical techniques, repair operationsusually result in good functional recovery withoutany serious residual pain.

When, however, this plexus is damaged duringthe course of irradiating neoplastic glands in theneck, this may lead many years later to gradualwasting of the muscles of the hand and the devel-opment of severe pain. This neuropathic type ofpain is not readily controlled by drugs or acupunc-ture, but transcutaneous electrical nerve stimula-tion (TENS) sometimes proves helpful.

Avulsion of brachial plexus cervical nerve rootsBy far the commonest type of brachial plexusinjury at the present time is the tearing away of itsnerve roots from the spinal cord during the courseof a motorcycle accident. This type of tractionlesion, unfortunately usually affects an otherwise fityoung man leaving him with an irreversibly para-lyzed and totally anaesthetic arm, and one in which,in almost 90% of cases, there is severe intractablepain that takes the form of a persistent severeburning as if the arm is on fire (causalgia), andsuperimposed upon this are episodic paroxysms ofintense momentary shooting pain through the arm.

As Wynn Parry (1980, 1984) pointed out, thesingle most helpful method of gaining some relieffrom the pain is for the patient to distract his mindfrom it by concentrating on work or hobbies. By thismeans it is often possible for him to get through aworking day quite comfortably but, as soon as hesits down to relax in the evening, the pain buildsup and at times becomes almost unbearable.

Analgesic drugs have little effect on it, but WynnParry (1984) has found TENS to be helpful.

With respect to this, just as acupuncture doesnot work if needles, whether they be stimulatedmanually or electrically, are inserted into a part ofthe body deprived of feeling, so TENS does notwork if the electrodes are applied to skin that isanaesthetic. It is therefore essential in combatingthe pain of a nerve root avulsion lesion firstly tomap out the area of anaesthesia and then to placethe electrodes on skin above the upper level of this.

Compression of the brachial plexus(thoracic outlet syndrome)Until about 30 years ago, it was widely taught thata common cause of generalized pain spreadingdown the arm from the neck, with pins and needlesin the fingers, was compression of the lower trunkof the brachial plexus, either by it being stretched asit passed over a cervical rib, or compressed as itpassed between the scalenus anterior and a normalfirst rib (the scalenus anterior syndrome).

It is now realized that, although a cervical rib isfrequently seen on routine X-rays of the neck, onlyin about 10% of cases does it cause symptoms, and also that entrapment of the brachial plexus bythe scalenus anterior muscle with its very similarclinical picture is also uncommon. Nevertheless,when a patient presents with pain in the arm in thedistribution of the C8 T1 nerve roots, such causesof what collectively is known as the thoracic outletsyndrome have to be considered.

In this syndrome there is pain down the innerside of the arm, often from the elbow downwards,associated with paraesthesiae such as numbnessor pins and needles affecting the ulnar side of thehand; also some sensory loss on the ulnar side ofthe hand and forearm, and wasting of the smallmuscles of the hand supplied by the ulnar nerve,such as the interossei and adductor pollicis.

When these neurological symptoms and signsare due to stretching of the brachial plexus over acervical rib, there may also be evidence of com-pression of the subclavian artery, including a bruitto be heard in the neck on auscultation and circu-latory changes to be found in the fingers.

The stretching of the brachial plexus over a cer-vical rib most commonly gives rise to symptoms

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and signs in middle-aged women when loss oftone in the muscles of the shoulder girdle causesthis to droop. Relief from pain may, therefore,often be obtained by exercises designed tostrengthen these muscles. However, when vascu-lar changes predominate, or there is progressivewasting of the muscles of the hand, then the ribshould be removed. Before embarking upon this,care should be taken to exclude an ulnar nervelesion at the elbow as this may cause similar neuro-logical signs in the forearm and hand.

When the underlying cause of the syndrome is a taut shortened scalenus anterior, then the neuro-logical changes may be associated with symptomsfrom pressure on the subclavian vein, and onlyrarely with those associated with pressure on theartery.

Scalenotomy for the relief of pain in thescalenus anterior syndrome proved to be disap-pointing and is no longer performed. If the condi-tion occurs because of myofascial TrPs in thescalenus anterior then these should be deactivatedby the carrying out of superficial dry needling.

With respect to all this it has to be rememberedthat when pain arises as a result of the develop-ment of TrP activity in this muscle, without short-enening of it due to this giving rise to pressure onthe brachial plexus, then the referral of pain isdown the radial side of the forearm and hand (Ch. 12).

Finally, it cannot be stressed too strongly that inall cases where there is pain down the inner side ofthe arm from the neck with pins and needles in thering and little fingers, in the absence of objectiveneurological signs and of signs of vascular com-pression, an active search for TrPs in the levatorscapulae should always be made, as this is fre-quently a cause of pain in this distribution (Ch. 14).

LATERAL EPICONDYLALGIA (SYNS:LATERAL EPICONDYLITIS, TENNISELBOW)

TerminologyThe disorder in which in response to repeatedmicrotrauma severe pain develops in the lateralepicondylar region, with pressure on the lateral

epicondyle and resisted dorsiflexion at the wristmaking it worse, is best called lateral epicondylalgia.This is because tennis elbow is a misnomer, as theplaying of tennis is an aetiological factor in its pro-duction in less than 5% of the people affected by it(Coonrad & Hooper 1973), and because epi-condylitis is an inappropriate term as there is noinflammation of the epicondyle itself.

Pathophysiology

Enthesopathy

This disorder is an enthesopathy affecting thecommon extensor tendon at its attachment to thelateral epicondyle. Chard & Hazleman (1989),from studying biopsy material taken prior to thecarrying out of surgery for this disorder, foundthat initially there is an inflammatory reaction inand later degenerative tissue damage of this tendon.Potter et al (1995) have since reached the same con-clusion as a result of correlating MRI, histopatho-logical and surgical findings.

Inflammatory reaction and TrP activityDoubt concerning the type of inflammatory lesionpresent in this disorder has recently been raised asa result of Ljung et al (1999) investigating it bymeans of employing immunohistochemistry andantibodies to the neuropeptides Substance P (SP)and calcitonin gene-related peptide. It was shownby this means that nerve fibres distributed in association with a subpopulation of small blood vessels showed SP-like and calcitonin gene-relatedpeptide-like immunoreactivity. Furthermore, con-trary to what is generally believed, there were noinflammatory-cell infiltrates and only a few solitarymast cells.

This study therefore provided evidence in sup-port of suggestions previously made that theinflammatory reaction in this disorder is of a neuro-genic type with the release of these neuropeptidesfrom sensory afferent nerve endings causing micro-vascular leakage and local oedema formation. A finding that clearly has important implicationswith respect to the rationale for the use of corticos-teroids in its treatment.


Chap-15.qxd 13*10*04 14:39 Page 228

Another important discovery made in recentyears is that the pain in this disorder is not onlydue to the development of an enthesopathy butalso to the development of TrP activity in variousmuscles in the vicinity of the elbow. These includethe supinator, brachioradialis, extensor carpi radi-alis longus and brevis, extensor digitorum and thelower end of the lateral margin of the medial headof the triceps (Simons et al 1999, pp. 734–742).

Clinical featuresIn this disorder there is a persistent dull ache with,at times, bouts of acute pain on the outer side ofthe elbow. The pain is aggravated by putting thewrist extensors on the stretch, such as when thepronated wrist is passively flexed. It is also madeworse by any action that causes these muscles tocontract, such as when the wrist is extendedagainst resistance. It is possible therefore to lift achair comfortably when it is gripped with thehand, palm upwards, but there is considerableaggravation of the pain when this is done with thehand palm downwards.

There is, in addition, some weakness of the gripwith a tendency to drop objects. Also, any attemptto sustain a grip such as when shaking handsaggravates the pain.

The lateral epicondyle is invariably extremelytender. Also, in some cases the surrounding tissuesfeel warm and appear to be swollen.

Differential diagnosisOther causes for pain in the lateral epicondylarregion include arthritis of the elbow joint, andreferral of it there either as a result of cervicalnerve root entrapment or because of the develop-ment of TrP activity in a muscle of the neck, particu-larly the supraspinatus.

Factors responsible for development of TrP activityTrP activity in muscles in the vicinity of the epi-condyle develops as a result of trauma. This activ-ity may arise when there is direct injury to theelbow or when the muscles and their attachments at

or near to the elbow become suddenly wrenched. Itmore often arises, however, when the muscles aretraumatized as a result of repeated strenuous exten-sor movements at the wrist.

The supinator, as its name implies, is the princi-pal muscle responsible for supinating the handand forearm at the radioulnar joint, but the bicepsassists with the movement providing the elbow isflexed slightly. It therefore follows that wheneverthe muscle is liable to be subjected to undue strain,such as when hitting a tennis ball backhanded,both the elbow and wrist should be held in aslightly flexed position. It is when tennis playersfail to do this and take backhand shots with the armstraight that the supinator becomes overloaded.This then causes TrP activity to develop in it with,as a consequence, the referral of pain to the lateralepicondyle.

It is not, however, only tennis players who areliable to develop the disorder, but anybody whohas to hold the arm straight with the forearm in aposition of supination for any length of time, or hasto carry a load with the elbows flexed and thehands held in the pronated position. Heavy objectsin fact should always be carried with the hand palmupwards, as then much of the strain is taken by thebiceps.

Other common activities liable to put an abnor-mal strain on this muscle include the repeated turn-ing of a stiff door knob, the unscrewing of a tight jarlid, the controlling of a heavy dog straining at theleash, and the raking of leaves.

Similar activities may also sometimes lead tothe activation of TrPs in the brachioradialis and theextensor carpi radialis longus. In addition, TrPsmay become activated in the extensor digitorum asa result of forceful repetitive movements of the fingers by such people as musicians, craftsmen andgardeners.

TrP examination at the elbowTrPs in the supinator are usually to be found at itsdistal attachment to the anterior surface of theradius just below the insertion of the tendon of thebiceps into the radial tuberosity. When searchingfor them the hand should be fully supinated. Alsothe brachioradialis should be pushed out of theway in a lateral direction. This is most readily done

Pain in the arm 229

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if the elbow is slightly flexed. Any TrPs presentwill then be found to lie just under the skinbetween the biceps tendon medially and the bra-chioradialis laterally (Fig. 15.1).

The finding of TrPs in the brachioradialis andextensor carpi radialis longus should be carried outwith the elbow slightly flexed and with the foreamresting comfortably on a pillow in the prone pos-ition (Fig. 15.2). They are located about 3 cm distalto the lateral epicondyle (Figs 15.3 & 15.4).

The locating of TrPs in the extensor digitorumshould be carried out with the arm in the same position as for the brachioradialis and extensorcarpi radialis longus. TrPs in this muscle lie about6 cm below the lateral epicondyle (Fig. 15.5).

The anatomical arrangement of the triceps muscle is such that the medial head just above theelbow extends from one side of the arm to theother beneath the muscle’s common tendon ofattachment to the olecranon process of the ulna.


Extensor carpi radialis brevis

Flexor pollicis longus

Pronator quadratus

Flexor retinaculum

Abductor pollicis brevis

Flexor pollicis brevis

Abductor digiti minimi

Lumbricals

Flexor digitorum superficialis tendon

Deep transverse metacarpal ligaments

Flex. dig. min. brevis

Opponens digiti minimi

Flexor carpi ulnaris

Flexor digitorum profundus

First dorsal interosseous

Adductor pollicis, transverse part

Adductor pollicis, oblique part

Abductor pollicis longus

Flexor carpi radialis (cut tendon)

Brachioradialis tendon

Extensor carpi radialis longus

Supinator

Brachioradialis

Figure 15.1 The deep flexor muscles of the right forearm.

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Pain in the arm 231

Extensor carpi ulnaris

Extensor digiti minimi

Ulna

Extensor indicis

Abductor digiti minimi

Intertendinous connexions

Extensores carpi radialeslongus et brevis


Radius

Extensor pollicis longus

Extensor pollicis brevis

Extensor digitorum

Brachioradialis

Brachialis

Extensor carpi radialis longus

Extensor carpi radialis brevis

First dorsal interosseus

Extensor digiti minimi

Extensor carpi ulnaris


Olecranon

Fascia from tricepscovering anconeus

Triceps

Figure 15.2 Muscles of the extensor aspect of the right forearm, superficial layer.

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The lower part of the lateral border of the medialhead is, therefore, just above the lateral epi-condyle, and the lower part of the medial borderof this head is just above the medial epicondyle(Fig. 15.6).

A TrP in the medial border refers pain to themedial epicondyle and sometimes down the armto the ring and little fingers and will be discussedagain when considering medial epicondylalgia

and when considering the differential diagnosis ofulnar nerve entrapment (p. 240).

It is a TrP in the lateral border of the medialhead just above the elbow which commonly refers


Figure 15.3 Pattern of pain referral from a trigger point(�) in the brachioradialis muscle.

Figure 15.4 Pattern of pain referral from a trigger point(�) in the extensor carpi radialis longus muscle.

Figure 15.5 The pattern of pain referral from a triggerpoint (�) in the extensor digitorum muscle (ring fingerextensor).

Medial head Medial head

Lateral head Long head

Figure 15.6 The medial, lateral and long heads of thetriceps muscle. It should be noted that the lower part ofthe medial head just above the elbow extends from oneside of the arm to the other beneath the muscle’scommon tendon of attachment to the olecranon processof the ulna.

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pain to the lateral epicondyle in ‘tennis elbow’. Itis found about 4 cm or approximately 1.5 in abovethe lateral epicondyle near to the attachments ofthe extensor carpi radialis longus and the brachio-radialis (Figs 15.7A & B).

Treatment

Non-steroidal anti-inflammatory drugadministration

Hay et al (1999), in a randomized controlled trialcarried out to compare the relative efficacy of alocal corticosteroid and the NSAID naproxen forthe treatment of this disorder, concluded that a 2-week course of this NSAID gave no better painrelief than that provided by a placebo.

Local injection of a corticosteroid

It is a long established practice to inject a steroid atthe enthesopathy site. Methods of doing this varybut a widely employed one (Chard 1995) is to injectat the site of maximum tenderness on the lateral epi-condyle a hydrocortisone (10–25 mgs)/local anaes-thetic mixture with the needle inserted far enoughfor it to impinge upon the periosteum. A fan-shaped injection procedure is then carried out thatinvolves frequent partial withdrawals and reinser-tions of the needle. The main disadvantage of thistechnique is that it is liable to give rise to muchpain during the time it is being carried out.

Reviews of steroid injection clinical trials

A review carried out by Assendelft et al (1996) of12 clinical trials led them to conclude that the painrelief following a corticosteroid injection in thisdisorder is usually relatively short-lasting and oftenhas to be repeated after 4–6 weeks.

A sytematic review of randomized controlledtrials identified by a search of six databases carriedout by Smidt et al (2002) led them to conclude that it is not possible to draw firm conclusions as to the long-term effectiveness of steroid injectionsin this disorder due to the lack of high-qualitystudies; therefore, more better designed, conductedand reported randomized controlled trials withintermediate and long-term follow up are needed.

Altay et al (2002), employing the pepperingtechnique already described have compared thepain-relieving effectiveness of injecting a corticos-teroid (triamcinolone)/local anaesthetic mixturewith that of injecting a local anaesthetic alone intothe lateral epicondyle. That they obtained equally

Pain in the arm 233

A

B

Figure 15.7 (A) Trigger point in the lateral border of themedial head of the triceps muscle. (B) Pattern of painreferral from this trigger point.

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good results raises the possibility that with bothtypes of treatment the pain relief was due to theeffect of the one factor common to both – the pep-pering of the periosteum with a needle (i.e. to thecarrying out of acupuncture).

Acupuncture carried out at traditional Chineseacupuncture points

Haker & Lundeberg (1990) carried out a study in 82patients with lateral epicondylalgia to compare thepain-alleviating effect of inserting needles deeplyinto five traditional Chinese acupuncture points(Large intestine 10, 11, 12 [Fig. 15.8], Lung 5 [Fig. 15.9] and Sanjiao 5, a point immediately abovethe transverse crease of the wrist on its dorsal side)with that of inserting them superficially at thosesites. In each of the two groups the needles were leftin situ for 20 minutes, 2–3 times a week, for a total of10 treatments.

The results of this trial showed that deepneedling is superior to superficial needling whencarried out at these traditional Chinese acupunc-ture points.

Acupuncture carried out concomitantly at thelateral epicondyle’s point of maximumtenderness, traditional Chinese acupuncturepoints and TrP sites

In view of differences of opinion concerning theoptimum method of employing acupuncture forthe treatment of lateral epicondylalgia, Webster-Harrison et al (2002) have carried out an e-mail-collated consensus study. Those taking part in thiswere 14 medical practitioners who teach on theBritish Medical Acupuncture Society’s trainingcourses.

The consensus of opinion was that the optimumacupuncture treatment and the one that should beused in any future randomized controlled trial isas follows.

At the initial treatment needles should be inserteddeeply into the following traditional Chineseacupuncture points – Large intestine 4 (situated infirst dorsal interosseous muscle) and Large intes-tine 11 (situated in the depression at the lateral endof the transverse cubital crease). A needle shouldalso be inserted at the lateral epicondyle’s point ofmaximum tenderness far enough for it to reach theperiosteum. In addition, needles should be inserted


Large intestine 10

Large intestine 11Large intestine 12

Small intestine 8Triple warmer 11

Figure 15.8 Traditional Chinese acupuncture points atthe back of the elbow.

Heart 3

Lung 5

Figure 15.9 Traditional Chinese acupuncture points onthe inner and outer sides of the front of the elbow.

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at three TrP sites. The duration of needling at thetraditional Chinese points should be 5 minutes,and at the periosteum site and TrP sites it shouldbe limited to no more than 3 minutes.

On subsequent occasions the strength of stimula-tion at these sites should be increased or decreasedaccording to an individual patient’s responsive-ness to the initial treatment.

It was recommended that acupuncture shouldbe carried out weekly for a minimum of 2 weeksand that up to eight treatments should be given ifevidence of improvement warrants this.

The main purpose of formulating this standardacupuncture treatment regime is for it to be usedin any future large-scale randomized controlledtrial. There is certainly a great need for one asGreen et al (2002), from a very extensive computersearch for trials carried out between 1966 and 2001,found that during that time there had only beenfour small randomized controlled trials worth con-sidering. And from the results of those they wereled to conclude: ‘There is insufficient evidence toeither support or refute the use of acupuncture(either needle or laser) in the treatment of lateralelbow pain … . Further trials, utilising appropriatemethods and adequate sample sizes, are neededbefore conclusions can be drawn regarding theeffect of acupuncture on tennis elbow.’

My personal current practice is to carry out bothpecking of the periosteum at the lateral epicondyle’spoint of maximum tenderness and superficial dryneedling at all the TrP sites found to be present inthe nearby muscles.

MEDICAL EPICONDYLALGIA (SYNS:MEDIAL EPICONDYLITIS, GOLFER’SELBOW)

This is a similar condition to that which affects thelateral epicondyle, but one that occurs far less com-monly. It arises when, as a result of the flexor muscles of the wrist and hand becoming strained,TrPs become activated in these muscles near totheir common tendon attachment to the medialepicondyle.

It is characteristic of this disorder that resistedflexion of the wrist, when the elbow is extended,aggravates the pain.

The advantages and disadvantages of a localcorticosteroid in this condition are similar to those

when using this form of treatment in lateral epi-condylalgia so they will not be further discussed.

Acupuncture carried out in a similar manner tothat used in the treatment of lateral epicondylalgiais a worthwhile alternative, and, with respect toTrPs, there are two of these that usually have to bedeactivated. One is to be found in the commonflexor tendon near to its attachment to the medialepicondyle not far from the traditional Chineseacupuncture point Heart 3 (Fig. 15.9); the other isto be found along the medial border of the medialhead of the triceps immediately above the medialepicondyle (Fig. 15.10), and therefore in the regionof the Chinese acupuncture point Small Intestine 8(Fig. 15.8).

PAIN IN THE WRIST AND HAND FROMTrPs IN THE FOREARM MUSCLES

Persistent pain confined to the wrist and handregion may occur as a direct result of some local

Pain in the arm 235

Figure 15.10 Pattern of pain referral from a triggerpoint in the medial border of the medial head of thetriceps muscle.

Chap-15.qxd 13*10*04 14:39 Page 235

disorder, or it may arise indirectly as a result of itbeing referred there from TrPs some distance awayin the muscles of the forearm. It is particularlyessential to bear the possibility of the latter inmind as, otherwise, with there being nothingabnormal to find at the site where the pain is felt,there is always the risk that any patient sufferingfrom this may be considered to be either neuroticor a malingerer.

Although it is now over 40 years since Kelly(1944) first drew attention to the clinical import-ance of this particular cause of pain in the wristand hand, too little attention is still being paid to itin current medical teaching, and, therefore, it willbe dealt with at some length.

Forearm extensor musclesThe forearm extensor muscles in which TrP activ-ity is liable to cause pain to be referred to the wristand hand include the extensor carpi radialis longus,the extensor carpi radialis brevis, the extensor

carpi ulnaris, and the extensor digitorum. TrPactivity in the anatomically closely related bra-chioradialis and supinator muscles may also beresponsible for this (Fig. 15.2).

Activation of TrPs in these muscles

TrPs in these muscles are liable to become acti-vated as a result of carrying out forceful twistingmovements with some tool such as a screwdriveror trowel whilst holding it with a very firm grip.

Specific TrP pain patterns

Supinator muscle TrPs in the supinator musclerefer pain primarily to the lateral epicondyle, butat times they may also cause it to be felt in the regionof the first dorsal interosseous muscle (Fig. 15.11).

Brachioradialis muscle TrPs in the brachioradi-alis muscle, in contradistinction to those in thesupinator muscle, refer pain primarily to the region


Figure 15.11 Pattern of pain referral from a trigger point (�) in the supinator muscle.

Chap-15.qxd 13*10*04 14:39 Page 236

of the 1st dorsal interosseous muscle, and onlyoccasionally to the lateral epicondyle (Fig. 15.3).

Extensor carpi radialis longus TrPs in the exten-sor carpi radialis longus refer pain to the lateralepicondyle and down the forearm to be felt pre-dominantly on the dorsum of the hand in theregion of the anatomical ‘snuff box’ – the hollowon the outer side of the wrist between the tendonsof the extensor pollicis radialis longus and brevis(Fig. 15.4).

It has to be remembered that when TrPs in theabove muscles refer pain to the region of the 1stdorsal interosseous muscle or the anatomical‘snuff box’, satellite TrPs may develop at thesesites, and have to be distinguished from primarilyactivated ones that, as will be discussed later, mayalso develop at these sites as a result of trauma tothe wrist.

It is also of interest to note in passing that theChinese in their traditional system of acupuncturehave a well-known point, Large Intestine 4 (Ho-Kuor Hegu), in the first dorsal interosseous muscle

(Fig. 15.12), and another point, Large Intestine 5(Yang Xi in the anatomical ‘snuff box’, Fig. 15.13).

Extensor digitorum TrPs in the extensor digito-rum cause pain to be referred down the back of theforearm, back of the hand and into individual fin-gers, depending on which muscle fibres areinvolved. The middle finger extensor probably isthe one most often involved (Fig. 15.14).

TrPs in the ring and little finger extensors arealso liable to cause pain to be referred upwards tothe lateral epicondyle (Fig. 15.5).

Extensor carpi radialis brevis TrPs in the exten-sor carpi radialis brevis are found below the levelof those occurring in the extensor carpi radialislongus at about 6 cm (or approximately 2 in) belowthe elbow crease. Pain from these TrPs is referredto the back of the hand and wrist (Fig. 15.15).

Extensor carpi ulnaris TrPs in this muscle occurat about the same level in the forearm as those inthe extensor carpi radialis brevis, and as Gutstein(1938) showed, refer pain to a localized area aroundthe ulnar side of the back of the wrist (Fig. 15.16).

The following case illustrates how TrPs in several extensor forearm muscles may be respon-sible for the development of a composite pain pattern.

Pain in the arm 237

Large intestine 4

Figure 15.12 The traditional Chinese acupuncture pointLarge Intestine 4 (Hoku or Hegu) in the 1st dorsalinterosseous muscle.

Large intestine 5

Figure 15.13 The traditional Chinese acupunture point Large Intestine 5 (Yang Xi) in the anatomical snuffbox – the hollow on the outer side of the wrist betweenthe tendons of the extensor pollicis radialis longus andbrevis muscles.

Figure 15.14 The pattern of pain referral from a triggerpoint (�) in the extensor digitorum muscle (middle fingerextensor).

Chap-15.qxd 13*10*04 14:39 Page 237

Deactivation of these TrPs by means of the carryingout of superficial dry needling on four occasions atweekly intervals relieved her of the pain, but on goingback to gardening she again developed pain in thehand as a result of the reactivation of TrPs in theforearm and eventually she decided it was better toemploy someone to do the weeding!

Forearm flexor musclesThe forearm flexor muscles in which TrP activity isliable to cause pain to be referred to the front of thewrist and hand include the flexor carpi radialis, theflexor carpi ulnaris, and the flexor digitorum (super-ficialis and profundus), all of which are attachedproximally to the medial epicondyle by means of acommon tendon; also the flexor pollicis longuswhich is attached proximally to the radius.

Anatomical relationships of the muscles

In order to be able to identify in which of thesevarious muscles a particular TrP is located, it ishelpful to remember that they are arranged inthree layers with the superficial layer consistingof the flexor carpi radialis, and the flexor carpiulnaris, separated by the palmaris longus; theintermediate layer consists of the flexor digitorum


Figure 15.15 The pattern of pain referral from a triggerpoint (�) in the extensor carpi radialis brevis muscle.

Figure 15.16 The pattern of pain referral from a triggerpoint (�) in the extensor carpi ulnaris muscle.

A housewife (60 years of age), who was also a keengardener, and who frequently gripped the handle of a trowel tightly whilst weeding, presented with a 9-month history of pain at the back of the wrist, atthe base of the thumb, and in the fingers, togetherwith some discomfort in the outer part of the elbow.

She complained that the fingers felt bloated and asif they were going to burst. She also complained thatthe grip of her hand was becoming increasingly weak,and that this, together with the pain and swelling ofher fingers, and the consequent difficulty with bendingthem, had led her to become concerned that she mightbe developing arthritis.

The patient was examined sitting comfortably on achair with the forearm resting on a pillow, and theelbow slightly bent.

The weak grip was confirmed by getting the patientto squeeze two of my fingers. This action also increasedthe pain both at the elbow and in the hand.

Flat palpation of the extensor muscles just belowthe lateral epicondyle revealed TrPs to be present inthe extensor carpi radialis longus, and these must havebeen partly responsible for the lateral epicondyle pain,and pain at the base of the thumb. There were alsoTrPs in the extensor carpi radialis brevis, which musthave been responsible for the pain at the back of thewrist and TrPs in the extensor digitorum that musthave been partly responsible for the pain at the elbow,and also in the fingers.

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superficialis (Fig. 15.17); and the deep layer con-sists of the flexor digitorum profundus, and theflexor pollicis longus (Fig. 15.1).

Activation of TrPs

TrPs situated in the hand and finger flexor musclesin the forearm are liable to be activated by pro-longed gripping. It commonly occurs, for example,when the steering wheel of a car is gripped tightlyduring a long journey, particularly when the handsare placed on the top of the steering wheel in theflexed position.

TrPs in the flexor pollicis longus become activatedas a result of gripping tightly with the thumb whilstcarrying out any twisting pulling movement suchas may occur when weeding.

Specific pain patterns and TrP locations

Flexor carpi radialis and flexor carpi ulnarisTrPs in these two muscles cause pain to be referredeither to the radial aspect or the ulnar aspect of thepalmar surface of the wrist according to which oneis involved (Fig. 15.18). The TrPs in either of thesemuscles are to be found high up the forearm just

Pain in the arm 239

Medial intermuscular septum of arm

Palmaris longus

Flexor carpi radialis

Flexor digitorum superficialis

Palmar aponeurosis, central portion

Adductor pollicis, transverse head

Flexor digitorum superficialis, radial head

Bicipital aponeurosis

Pronator teres

Brachioradialis




First dorsal interosseous

Fibrous flexor sheath

Second lumbrical

Deep transverse metacarpal ligaments

Palmaris brevis

Flexor retinaculum

Pisiform

Tendon to ring finger


Figure 15.17 The superficial flexor muscles of the left forearm, the palmar aponeurosis and the digital fibrous flexorsheaths.

Chap-15.qxd 13*10*04 14:39 Page 239

below where each muscle is attached to the medialepicondyle (Fig. 15.18). As both muscles are in thesuperficial layer, the TrPs in each of them are eas-ily recognized by their exquisite tenderness tolight touch and by the fact that pressure on themcauses a readily visible local twitch response, andthe evoking of the specific pain pattern of the par-ticular muscle involved.

Flexor digitorum superficialis and profundusTrPs in various parts of these two muscles referpain to individual fingers. Such points are to befound at almost the same level in the forearm as those in the flexor carpi radialis and ulnaris(Fig. 15.19). However, as the digital flexors liedeep to the hand flexors, any TrPs in them aremore difficult to locate, and require firm pressureto elicit the deep seated tenderness associatedwith their presence, and even with this, neither alocal twitch response nor any of the various spe-cific pain patterns can be evoked.

Flexor pollicis longus TrPs in this muscle causepain to be felt in the thumb. As this muscle is deeplying, firm pressure is required to elicit any TrPtenderness in it. Such points are usually to befound on the radial side of the forearm about one-quarter way up from the wrist crease (Fig. 15.20).

Ulnar nerve entrapment at the elbow(cubital tunnel syndrome)The ulnar nerve at the elbow is held in a groovebehind the medial epicondyle by a fibrous expan-sion of the common flexor tendon. It then enters theforearm beneath an arch formed by the humeral


BA

Figure 15.18 The patterns of pain referral from triggerpoints (�) in (A) the flexor carpi radialis muscle and (B)the flexor carpi ulnaris muscle.

BA

Figure 15.19 The patterns of pain referral from triggerpoints (�) in the flexor digitorum superficialis (A) radialhead (B) humeral head.

Figure 15.20 The pattern of pain referral from a triggerpoint (�) in the flexor pollicis longus muscle.

Chap-15.qxd 13*10*04 14:39 Page 240

and ulnar heads of the flexor carpi ulnaris muscleto occupy a space bounded by the flexor carpiulnaris superficially and medially, the flexor digi-torum superficialis superficially and laterally, andthe flexor digitorum profundus behind it.

The ulnar nerve is at risk of being damaged eitherby external pressure being applied to it where itlies behind the medial epicondyle, or by it becom-ing constricted in the cubital tunnel by arthritic or other structural changes affecting the elbowjoint. Not infrequently, however, this entrapmentmay occur in the absence of structural pathologicalchanges. In some of these cases there is evidence ofTrP activity in the forearm flexor muscles, butexactly how this leads to pressure being exertedon the nerve is far from clear.

The symptoms of ulnar nerve entrapment aregradual in onset with numbness and tingling affect-ing the fifth finger and the ulnar half of the ringfinger, followed at a later stage by weakness andwasting of the small muscles of the hand. If theulnar nerve becomes damaged where it lies behindthe medial epicondyle, then pressure on the nerveat that site will reproduce the symptoms. The onlyeffective treatment when the nerve is bound downby fibrous tissue is a surgical operation to release itfrom the groove and transpose it to the front of theelbow. If, on the other hand, TrPs are found to bepresent just below the medial epicondyle in theflexor muscles, then deactivating them may insome cases, presumably by reducing tension in themuscles, be sufficient to relieve the pressure on thenerve.

It should be noted that pain is not an outstand-ing feature with ulnar nerve entrapment and,therefore, in all cases when pain affects the medialside of the forearm and hand, an alternative diag-nosis should be sought. The differential diagnosisincluding cervical nerve root entrapment (C8 T1nerve roots), TrP activity in the levator scapulaemuscle (Ch. 14) and TrP activity in the medial border of the medial head of the triceps.

TrP in the medial distal border of the medialhead of the triceps

A TrP may be found in the medial border of themedial head of triceps just above the medialmalleolus.


It refers pain to the medial epicondyle (p. 210) anddown the inner side of the anterior forearm to ter-minate in the ring and little fingers (Fig. 15.10).

TrP location

It is best located and then deactivated with a dryneedle, with the patient lying down in the supineposition with the arm externally rotated, the forearmsupinated, the elbow slightly flexed, and the wholeof the arm supported comfortably on a pillow.

The following case illustrates how failure to rec-ognize TrP activity in muscles around the medialepicondyle could have resulted in an unnecessaryoperation.

A ward sister (36 years of age) complained that for 1year she had had pain around the left elbow radiatingdown the inner side of the arm with some discomfortin the little and ring fingers. An orthopaedic surgeonthought it was due to ulnar nerve root entrapment and recommended that the nerve should be transposedfrom behind the medial epicondyle to the front of thejoint. The patient, not liking the thought of having anoperation, asked to be referred to me to see whetheracupuncture had anything to offer.

On examination there were two exquisitely tenderTrPs, one in the medial border of the medial head of thetriceps just above the medial epicondyle and anotherjust below it. After deactivating these by means of thecarrying out of superficial dry needling on threeoccasions, she was relieved of her symptoms.

Palmaris longus and pronator teres musclesTrP activity in these two forearm muscles may alsocause pain to be referred to the hand.

Palmaris longus

This vestigial muscle is not always present, butwhen it is, it also is attached proximally to themedial epicondyle and distally to the palmar fascia,and has as its main action the cupping of the hand.It also assists flexion of the hand at the wrist.

It lies, as previously stated, in the superficial layerof the flexor forearm muscles, between the flexorcarpi ulnaris and the flexor carpi radialis (Fig. 15.17).

Pain in the arm 241

Chap-15.qxd 13*10*04 14:39 Page 241

Location of TrPs TrPs in this muscle are foundhigh up in the forearm just below the medial epi-condyle (Fig. 15.21).

Activation of TrPs These TrPs may become acti-vated as a result of repeatedly gripping someobject such as a tennis racquet or tool excessivelytightly. They may also become activated as a sec-ondary event whenever pain is referred to the upperpart of the forearm from similar points just abovethe medial epicondyle in the medial head of the tri-ceps muscle. In addition, Simons et al (1999, p. 746)have observed that patients with Dupuytren’scontracture invariably have one or more activeTrP(s) in this forearm muscle.

Specific pattern of pain referral There is a per-sistent unpleasant tingling sensation in the palmof the hand, and the patient complains of discom-fort on applying pressure to any object held in thepalm. This, therefore, makes the handling of toolsdifficult.

Deactivation of TrPs Deactivation of these TrPsjust below the elbow is carried out with the fore-arm extended and well supported.

Pronator teres

This forearm muscle, whilst not a flexor of thehand or fingers, is conveniently dealt with here in

view of its anatomical relationship in the flexorforearm muscles. This muscle is attached above bytwo heads, the humeral head being attached to themedial epicondyle, and the ulnar head to the coro-noid process of the ulna. The median nerve entersthe forearm between these two heads. The muscledistally is attached to the lateral surface of theradius (Fig. 15.17).

Location of the TrP A TrP in this muscle may be found just below the crease of the elbow, in theproximal part of the muscle, to the medial side ofthe biceps tendon (Fig. 15.22). Activity in it is liableto develop as a result of a fracture at either theelbow or wrist.

Specific pattern of pain referral Pain from aTrP in this muscle is referred down the anterior sur-face on the radial side to be felt in particular aroundthe radial side of the wrist, in much the same areaas pain from TrP activity in the flexor carpi radialis(Fig. 15.22).

A patient with an active TrP in this muscle findsit difficult to turn the hand into the fully supinatedposition and usually is not able to turn it beyondthe mid position.

Pain in the wrist and hand from local TrPsAny activity that puts a strain on the muscles inthe region of the wrist or hand, including the thumb


Figure 15.21 The pattern of pain referral from a triggerpoint (�) in the palmaris longus muscle.

Figure 15.22 The pattern of pain referral from a triggerpoint (�) in the pronator teres muscle.

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and fingers, may lead to the development of per-sistent pain at these sites as a result of the devel-opment of TrP activity in them. However, what isnot so well known is that pain in exactly the samedistribution may also occur because of TrP activitydeveloping some distance away in the muscles ofthe forearm.

It, therefore, follows that in every case wherepain in the hand develops as a result of TrP activ-ity, it is essential to ascertain whether this is occur-ring locally in the hand, or high up in the forearm,or both, before any decision can be made as towhere acupuncture needles should be inserted.

It is because this is of such fundamental import-ance that a somewhat lengthy account of myofas-cial TrPs in the forearm has just been given, and itis hoped that this will help to clarify any confusionconcerning the subject prior to turning to the morestraightforward concept of wrist and hand painoccurring as a result of local TrP activity.

However, before doing this, consideration mustbe given to pain at the wrist occurring as a result of median nerve compression in the carpal tun-nel, and also as a result of tenosynovitis aroundthe wrist joint.

Carpal tunnel syndrome

Although this syndrome became recognized as aclinical entity soon after World War II (Brain et al1947), and there are now good descriptions of it instandard textbooks, a brief account of it must begiven here as the pain at the wrist, which oftenradiates up the arm, sometimes as far as the shoul-der, has to be distinguished from other causes ofpain in the arm, and particularly from pain ascend-ing up the arm as a result of myofascial TrP activity.

It occurs principally in middle-aged women,but may occur in younger women and is occasion-ally seen in men. The cause of compression of themedian nerve in the carpal tunnel is usually notknown but it is sometimes due to a tenosynovitis inrheumatoid arthritis, fluid retention during preg-nancy, and soft tissue swelling in either myxoedemaor acromegaly.

The essential symptoms are pain in the arm andparaesthesiae in the fingers. The pain is character-istically nocturnal, awaking the patient in theearly hours of the morning. It is felt at the wrist,

but often ascends up the arm, at times as high asthe shoulder. The paraesthesiae usually affect theindex, middle and radial side of the ring finger, butsurprisingly on occasions may involve the littlefinger.

These nocturnal symptoms are often relievedby hanging the arm over the side of the bed. Onwaking in the morning, the hand often feels stiffand swollen.

During the day, the arm is not troublesome butthe paraesthesiae persist and are made worse byany activity such as knitting or holding a book.

The condition, as might be expected, most oftenaffects the dominant side but eventually it maybecome bilateral. The nocturnal pain, and the noc-turnal and diurnal paraesthesiae may persist formany months without any objective neurologicalsigns developing, but eventually weakness andwasting of two of the thenar muscles (abductorpollicis brevis and opponens pollicis) cause flat-tening of the outer half of the thenar eminence.

On examination, the pain and tingling can oftenbe provoked by applying pressure to a point ofexquisite tenderness over the anterior carpal liga-ment. If any doubt as to the diagnosis remains, anelectrical conduction test may be carried out, but ithas to be remembered that this test may be mis-leadingly normal in cases with a short history.

Treatment Initially conservative measures shouldbe used including the avoidance of activities thataggravate the symptoms and the wearing of asplint at night. Should symptoms persist, and par-ticularly when there is evidence of muscle wasting,decompression of the median nerve by division ofthe flexor retinaculum is essential.

Tenosynovitis in the wrist region

This is a common cause of pain in the region of thewrist. Inflammation of the synovial sheaths sur-rounding the tendons around the wrist joint isliable to occur whenever the forearm muscles areused excessively or the fingers are worked bothhard and rapidly. The condition may thereforeoccur as a result of recreational pursuits or occu-pational tasks.

Pain, which can be quite severe, is felt along theline of one or more tendons at the wrist. It is usually

Pain in the arm 243

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associated with swelling, and characteristicallycrepitus will be detected on moving the tendon.The tenosynovitis affecting the conjoined tendonsof the extensor pollicis brevis and abductor pollicislongus as they pass over the styloid process of theradius (de Quervain’s disease) is liable to occur asa result of any activity associated with strenuousrepetitive movement of the thumb. In this condi-tion there is pain and tenderness over the styloidprocess and, in particular, crepitus may be elicitedon extending the thumb.

Treatment For this disorder, rest of the affectedpart on a splint or in plaster is helpful. Cases that do not respond to this should have an injection of a corticosteroid into the tendon sheath. Extreme care,however, has to be taken not to inject the materialinto the tendon itself as this may cause it to rupture.

Pain in the thumb

Pain in the thumb may occur as a result of it beingreferred there from TrPs in the muscles of the forearm or from TrPs locally in the muscles aroundthe thumb. The muscles around the thumb liableto contain these include the adductor pollicis, anda muscle mass consisting of the opponens polliciscovered by the abductor and flexor pollicis brevis.In practice, it is difficult to differentiate betweenthese three muscles when attempting to locate TrPsin them but it would seem to be the opponens pol-licis in which TrP activity most commonly occur.

When TrP activity develops in these muscles italso often takes place in the 1st dorsal interosseousmuscle with a point of exquisite tenderness to befound in the anatomical snuff box.

The relative anatomical relationship of theadductor and opponens pollicis, and the approxi-mate position of their TrPs and patterns of painreferral from them are shown in Figures 15.23, 15.24and 15.25. The action of the adductor pollicis is tobring the thumb adjacent to and parallel with theindex finger. The action of the opponens pollicis isto bring the thumb across the palm to touch thepads of the ring and little fingers. TrP activity isliable to arise in these muscles whenever the thumbis strained by some form of sustained grippingaction. Writing or sewing therefore may do thiswhen continued for long periods, but perhaps the

commonest activity to cause it is weeding whenthe ground is dry.

Gardening is therefore a good example of whereTrP activity developing locally in the musclesaround the thumb or in the forearm is liable to causepain to arise in it. TrPs some distance above thewrist in the flexor pollicis longus may be activatedby twisting and pulling movements associated withpulling out weeds. And TrPs just below the lateralepicondyle, in either the extensor carpi radialislongus or the brachioradialis, are likely to be acti-vated by tightly gripping the handle of a trowelwhilst shifting heavy soil.

Post-traumatic pain in the thumb When pain fol-lowing trauma to the thumb persists long after anyovert evidence of tissue damage has disappeared,it is usually due to the development of TrP activity.The following case is a good example of this.

A housewife (50 years of age) fractured her left wrist.Soon after the plaster was removed she noticed painat the base of the left thumb that persisted for about2 months. It then recurred intermittently, two to threetimes a year, for about 3–4 weeks at a time. After thishad gone on for about 4 years, she was referred to mefor assessment.

On getting her to analyze in detail any particularcircumstances associated with the onset of the pain, itsoon became apparent that this always started whenshe cooked for more than two people, and usedespecially large and heavy saucepans, which for someinexplicable reason, considering she was right-handed,she was always in the habit of lifting them off thestove with the left hand.

On examination, the appearances of the thumbwere normal, but there were exquisitely tender TrPs in the adductor pollicis, the opponens pollicis, and the 1st dorsal interosseous muscle. Deactivationof these by means of the carrying out of superficial dry needling on two occasions relieved the pain.Following this she made a determined effort to lift the saucepans with her right hand and has had nofurther trouble.

When post-traumatic pain in a peripheral struc-ture such as the thumb has persisted continuouslyfor some time, it may eventually start to spread upthe limb. It would seem that Leriche (1939) musthave observed this in what he called ‘posttraumatic


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Pain in the arm 245

Pronator quadratus

Slip to abductor pollicis brevis

Opponens pollicis


InterosseiCruciform fibres in digital sheath

Opponens digiti minimi


Flexor digitorum superficialis


Palmaris longus

Pisiform boneFlexor retinaculam

Abductor digiti minimiFlexor digiti minimi brevis

Fourth lumbrical

Third lumbrical

Second lumbrical

Interossei

Cruciform fibres in digital sheath

First lumbrical

Adductor pollicis



BrachioradialisFlexor carpi radialis

Figure 15.23 Superficial dissection of muscles of the palm of the right hand.

Figure 15.24 The pattern of pain referral from a triggerpoint (�) in the adductor pollicis muscle.

Figure 15.25 The pattern of pain referral from a triggerpoint (�) in the opponens pollicis muscle.

spreading neuralgia’ and also Taylor (1938) inwhat he called ‘ascending neuritis’.

As this type of antidromic referral of pain is notwell recognized, other than with median nerveentrapment, two examples of it occurring follow-ing trauma will be described.

A 16-year-old schoolgirl tripped and, in falling,wrenched her right thumb backwards by catching it onthe edge of a desk.

There was much immediate pain with, according toher, considerable swelling and bruising of the tissues atthe base of the thumb. When, after 6 weeks, the latter

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disappeared but the pain persisted, she was referred toan orthopaedic specialist. An X-ray of the hand showedno abnormality and in particular no evidence of afractured scaphoid. However, in view of the persistentpain, he immobilized the thumb and wrist in a plaster,but on removing this 6 weeks later, the pain was as badas ever, and, in addition, the thumb felt stiff and weak.Physiotherapy was, therefore, given and a month latershe was discharged from his care. The pain persistedmaking gripping a pen difficult and interfering with herschool work. As the appearances of the thumb andwrist were normal, her doctor began to wonderwhether anxiety about forthcoming exams was a factorin the prolongation of her symptoms, but he becameconcerned when the pain started to spread up theouter side of her arm, at first as far as the elbow, buteventually up to the shoulder.

Eight months after the accident she was referred tome for assessment as to whether acupuncture mightbe helpful. On examination there was nothing abnormalto be seen but there was some generalized tendernessof the thumb with restriction of its movements, andalso there were TrPs to be found on the outer, innerand dorsal aspects of the base of the thumb and in theanatomical ‘snuff box’. Three needles were thereforeinserted around the base of the thumb and one intothe anatomical ‘snuff box’. When a needle was put intothe latter site, pain immediately shot up the outer sideof the arm towards the elbow along the line ofdistribution of the spontaneously occurring pain.

When seen 1 week later, she reported she hadexperienced relief from pain but only for 3 days. On re-examining her, it became obvious that satellite TrPs inthe extensor muscles just below the lateral epicondyle,in the deltoid, and in the supraspinatus had beenoverlooked on the first occasion. Needles were, therefore,inserted into the tissues overlying these points as well asthe ones around the base of the thumb. Treatment atregular intervals had to be given for another 2 monthsbefore lasting relief from the pain was obtained.

The second case is that of a 40-year-old womanwhose son, who suffered from a learning disability,attacked her and caught hold of her right thumb,wrenching it backwards. Bruising and swelling aroundthe joint fairly quickly subsided, but it left her withpersistent pain, which was not only felt around thethumb but after a time gradually spread up the outerside of the arm.

When seen by me 1 year after the injury, the pain inher thumb at rest and, in particular, on using it, wasseriously affecting her life. TrPs were found around thebase of the thumb, and satellite ones at the elbow andin the shoulder girdle. These had to be deactivatednine times over the course of the next 3 monthsbefore permanent control of the pain was finallyobtained.

Pain in the palm of the hand

It will be remembered from what was said earlierthat a persistent prickling type of discomfort in thepalm of the hand may develop when TrPs becomeactivated just below the elbow in the palmarislongus muscle. This sometimes occurs in patientswith contracture of, and tender nodules in thepalm from the development of Dupuytren’s con-tracture. In addition, localized pain in the palm,also in association with the presence of a tendernodule, may occur in the disorder known as trig-ger finger.

Trigger finger Repeated trauma to the handmay lead to the development of a reaction in thesheath of one of the digital flexor tendons in thepalm and when this occurs the finger when flexedbecomes locked.

In this condition, usually referred to as a triggerfinger, there is an exquisitely tender point at thesite of a nodule in the palm just proximal to thehead of the metacarpal bone.

Traditionally, it is taught that a corticosteroidshould be injected locally into the synovial sheath,but this is not necessary and, of course, if by a mis-take it should happen to be put into the tendon, itcan cause this to rupture. However, there is noneed to use this form of treatment as the conditioncan be relieved equally well simply by inserting aneedle into the point of maximum tenderness, andstimulating the nerve endings at that site by rotat-ing the needle a few times.

There are three aspects concerning this thatnever cease to surprise me. Firstly, that the needleonly has to be inserted a short distance into theskin. Secondly, that the response to needle stimu-lation in this condition is good, with it usuallyonly being necessary to carry it out on one or twooccasions, even when the disorder has been pre-sent for some considerable time. Thirdly, that with


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this technique not only is the pain readily con-trolled, but the finger movement is also quicklyrestored to normal. The following case is quoted asa typical example.

A 62-year-old company director had had a triggerfinger (ring finger on the right hand) for 6 months. Itwas not so much the locking of the finger on flexionthat worried him as the discomfort in the palm whentrying to grip a golf club! His doctor, somewhatsurprisingly, did not inject hydrocortisone into thetendon sheath, but contented himself with telling thepatient that the condition was not bad enough towarrant an operation! Eventually the patientpersuaded the doctor to let him try the effects ofacupuncture and so he was referred to me.

On examination, there was the usual exquisitelytender point in the palm. A needle was inserted into theskin overlying this and then subjected to a rotarymovement until the immediate pain induced by theneedle penetrating the skin had been replaced by afeeling of numbness. This occurred after about 20rotary movements of the needle. On withdrawing theneedle, there was no residual tenderness at the site,and not only could he move the finger freely, but,more important, from this particular patient’s point ofview, he could grip a golf club comfortably! Sincehaving treatment on two occasions he has had nofurther trouble.

Pain in the fingers

As has already been said, pain and swelling of thefingers may occur as a result of the activation ofTrPs high up in the forearm in either the flexor digi-torum (p. 240) or the extensor digitorum (p. 237).

Pain in the fingers with stiffness of their move-ments may also occur because of the activation ofTrPs in the interosseous muscles of the hand. TrPsin these may be activated as a primary event wheneven a small object has to be held firmly for a longtime, such as a needle by a seamstress, or a paint-brush by an artist.

Heberden’s nodes

A Heberden’s node is a small nodule that developson the dorsolateral or dorsomedial aspect of a ter-minal phalanx at its joint. At first it may be painfuland tender but eventually it is symptomless.

The significance of Heberden’s nodes is still nomore certain than when (Simons et al 1999, p. 788)asked ‘What are these little hard knobs, about thesize of a small pea, which are frequently seen uponthe finger, particularly a little below the top, nearthe joint?’

In more recent years it has become customary toassociate these with the development of osteoarthri-tis of the finger joints, but (Simons et al 1999, p. 788) state that in addition they are frequentlyassociated with the primary activation of TrPs inthe interossei.

Tender points around arthritic small joints of the hand

Exquisitely tender points are often to be found onpalpating the tissues around osteoarthritic smalljoints of the hands. There are no absolute rules asto their distribution and one has to palpate care-fully around a painful joint in order to find them.Deactivation of them with a needle often has amarkedly pain-relieving effect.

SOME MULTIFACTORIAL BRACHIAL PAIN DISORDERS

As stated in the introduction to this chapter theseinclude lateral and medial epicondylalgia, neuralgicamyotrophy, the shoulder–hand syndrome andrepetitive strain injury. The elbow pain disordershaving already been discussed it now only remainsnecessary to consider the other three.

Neuralgic amyotrophyThis disorder, also called cryptogenic brachialplexus neuropathy, is one where for some reason,possibly a viral infection, there is a sudden onset ofsevere pain in the shoulder and upper arm followedeventually by the development of weakness andwasting of muscles such as the serratus anterior, deltoid, supraspinatus, infraspinatus and trapezius.This initial pain usually spontaneously subsideswithin a relatively short time but overloading of thewasted muscles eventually causes TrP activity todevelop in them with, as a consequence, the pro-duction of myofascial TrP pain that requires the car-rying out of superficial dry needling for its relief.

Pain in the arm 247

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Shoulder–hand syndromeThis sympathetically mediated brachial pain dis-order is one that arises secondary to the develop-ment of a frozen shoulder (see Ch. 13).

It usually has a gradual onset, with initiallythere being a severe burning pain in the shoulderregion accompanied by vasomotor changes in thehand. Then, after a time, despite the shoulder painusually starting to become less intense, trophicchanges begin to take place with atrophy of brachialmuscles, thickening of the palmar fascia and atro-phy of the nails. In addition, TrP activity is liable todevelop in the atrophied muscles.

The treatment of this disorder, as Sola (1999) haspointed out, is difficult and includes the giving ofnarcotics for the relief of the very severe pain, sym-pathetic blocks, the deactivation of TrPs and thecarrying out of exercises to maintain function.

Repetitive strain injuryThis injury, which over the years has been knownby a number of different names including, occupa-tional cervicobrachial disorder, occupational over-use syndrome, chronic upper limb pain syndrome,refractory cervicobrachial syndrome, localizedfibromyalgia and cumulative trauma disorder, firstcame to be recognized as being a clinical entity whenkeyboard operators in Australia began to complainof work-related brachial pain in the early 1980s.

In Britain there started to be a dramatic rise inits reported incidence in the 1990s (Reilly 1995).with keyboard operators employed in clearingbanks, the newspaper industry and various otherlarge organizations such as the Inland Revenue, thePost Office and British Broadcasting Corporationbeing amongst those suffering from it.

As the various factors contributing to its devel-opment, pathophysiology and clinical manifest-ations have been discussed by me at some lengthelsewhere (Baldry 2001), it is only necessary hereto reiterate that it is now becoming increasinglywidely recognized that much of the pain at anearly stage in this disorder emanates from myofas-cial TrPs (Grange & Littlejohn 1993, Headley 1997,Lin et al 1997).

There is reason to believe that it is the sensoryafferent barrage set up as a result of persistentnociceptor activity in these structures that is one ofthe main causes for nociceptive neurons in thedorsal horn undergoing neuroplastic changes withthe development of central sensitisation. This cen-tral sensitisation then, in turn, is not only respon-sible for the persistence of the nociceptive TrP pain,but also for the spread of it. In addition, A-beta-mediated pain starts to develop as a result of thesesensitised dorsal horn neurons responding to light-touch-induced stimulation of mechanoreceptors inthe skin.

The persistent sensory afferent input to the dorsal horn from peripheral nociceptive painsources including TrPs also has a stimulating effecton spinal-cord-situated sympathetic preganglionicneurons with, as a consequence, the developmentof sympathetically maintained pain of a burningcharacter and the production of allodynia. Also, insome cases, this sympathetic overactivity is respon-sible for coldness of the affected limb and swellingof its tissues.

Deactivation of the myofascial TrPs should becarried out and measures taken to prevent theirreactivation as early in the course of the disorderas possible in order to help avoid the developmentof cental sensitisation and the various pain disorders that arise as a result of this.


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251

Chapter 16

Pain in the head and face

CHAPTER CONTENTS

Introduction 251Migraine 251Tension-type headaches 259Migraine and tension type headaches – a

continuum 260Cluster headaches (migrainous neuralgia) 261Pain in and around the temperomandibular

joint 261Trigeminal neuralgia 265Atypical facial pain 265Trauma-induced myofascial TrP cephalalgia 266Post-traumatic headache 268Torticollis 268Temporalis muscle 269TrP Activity in skin muscles: orbicularis oculi,

zygomaticus and occipitofrontalis 270

INTRODUCTION

In this chapter attention will first be drawn to thepathogenesis, pathophysiology, clinical manifest-ations and management of migraine and tension-type headaches. Following this, the diagnosis andtreatment of myofascial trigger point (MTrP) painreferred to the temperomandibular region, theface and the head will be discussed.

MIGRAINE

Migraine may conveniently be divided into theclassical and common types.

Classical migraine usually takes the form of self-limiting episodes of severe throbbing pain affect-ing one side of the head, often in association withnausea, vomiting, photophobia and facial pallor.An attack is generally preceded by one or anotherprodromal symptom including, most commonly, adisturbance of vision, but also at times tingling andnumbness down one side of the body, and occa-sionally a disturbance of speech.

Common migraine, as its name implies, occursfar more often. It is less likely to be unilateral andalthough it may be associated with nausea andvomiting, there are no prodromal symptoms.

AetiologyA striking feature of migraine and one that is ofconsiderable relevance when considering its aeti-ology is that it is three times commoner in womenthan men. This female preponderance would seemto be associated with vascular changes that occur

Chap-16.qxd 11*10*04 10:30 Page 251


trigeminal brain stem’s sensory nuclear complexknown as the subnucleus caudalis.

The subnucleus caudalis, which because of itsmorphological and physiological similarities tospinal dorsal horns is also known as the medullarydorsal horn, not only receives this vascular-mediated input, but also, as will later be discussed,myofascial and emotionally evoked (supraspinal)ones.

Following integration of these three inputs atthis site, migraine-evoking activity is transmittedup the quinto-thalamic tract to the thalamus. Onreaching the latter, this migraine-evoking activityis influenced by a serotenergic input from the midbrain’s dorsal raphe nucleus and by a cate-cholaminergic one from the pontine-situated locuscoeruleus before being transmitted to the cerebralcortex.

Myofascial component

When palpation of the head and neck muscles ofpatients subject to migraine is carried out, bothduring and in between attacks of this disorder, it isevident that there is not only widespread tender-ness of these muscles, but also small discrete focalpoints of maximum tenderness.

That these intramuscularly situated points areimportant sources of pain in this disorder was firstconfirmed by Hay (1976) when he showed that aninjection of a local anaesthetic into them during anattack aborted it and in between attacks reducedthe frequency with which they developed. Simi-larly, when Tfelt-Hansen et al (1981) systematic-ally examined the muscles of the neck and scalp in 50 patients during typical common migraineattacks, they found tender points to be present inthese muscles in all cases. Moreover, an injectioninto these tender points during an attack of eithera local anaesthetic or saline, both proving to beequally effective, caused 24 out of 48 of thesepatients to become symptom-free within 70 min. This was a much shorter time than the averagenatural duration of an attack.

As the results with saline were found to be asgood as those obtained with a local anaesthetic, it isreasonable to conclude that the effectiveness of thelatter when injected into tender points in migraineis not, as Hay (1976) suggests, because it blocks

as a result of fluctuations in oestrogen and proges-terone levels, and there is a tendency for the dis-order to occur in association with menstruation,early pregnancy, the menopause and the taking ofthe contraceptive pill.

An attack may also be brought on in some people by the intake of certain foodstuffs such aschocolate, citrus fruits, tyramine-containing cheesesand alcohol, especially red wine. Alcohol is a non-specific vasodilator, whereas tyramine leads to therelease of noradrenaline in migrainous patients thatcauses a cerebral vasoconstriction followed by arebound vasodilation.

Attack may also be associated with a fall in thelevel of blood sugar, either from fasting or as areactive hypoglycaemia following the ingestion ofan excessive amount of carbohydrate. As will bediscussed later, when attempting to prevent therecurrence of migraine it is essential to exclude, as far as possible, these various causative factorsbefore turning to the use of acupuncture.

PathophysiologyThe three factors responsible for its developmentare vascular, myofascial and emotional.

Vascular component

Although the ingenious blood flow studies inmigraine with the radioisotope xenon, carried outby Olesen & Lauritzen (1982), have shown that thecirculatory changes in this condition are not asstraightforward as previously thought, it is stillgenerally agreed that in classical migraine the pro-dromal phase is associated with cerebral vasocon-striction, and that in both common and classicalmigraine the painful stage is characterized by asignificant dilation of extracranial and intracranialblood vessels.

When in this disorder, for some as yet unknownreason, trigeminal unmyelinated C-sensory afferentnociceptors in the walls of blood vessels in thebrain, meninges and venous sinuses become acti-vated, vasoactive neuropeptides such as Substance P(SP), calcitonin gene-related peptide and neurokininA are released with the setting up of a neurogenicinflammatory reaction (Moskowitz & Cutrer 1993).The consequence of this is for noxiously generatedinformation to be conveyed to that part of the

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the flow of nerve impulses from these points, butbecause both this and a saline injection bring abouta needle-evoked stimulation of nerve endings simi-lar to that obtained by the employment of theacupuncture technique of dry needling.

When Loh et al (1984) compared the effects ofacupuncture and drug therapy in patients withmigraine and muscle tension headaches, theyfound tender points in the neck and scalp musclesin 34 out of 41 cases examined in between attacksand, not surprisingly, considering what has justbeen said, found acupuncture to be a worthwhileprophylactic when these points were present butnot when they were absent. As the stimulation ofperipheral nerve endings at tender points in themuscles of the neck and scalp, either by injecting a chemical into them or by inserting a dry needleinto them during the migraine, is sometimes cap-able of foreshortening its duration, and consideringthat if this is carried out between incidences itoften prevents recurrence, it seems reasonable toconclude that these tender points must be TrPs.Also in favour of this is the clinical observationthat the overzealous stimulation of these pointswith dry needles in a migrainous subject is liableto bring on an attack of migraine.

These TrPs in the muscles of the neck and scalpwill be referred to again when discussing the treat-ment of migraine with acupuncture, but beforeturning to this, it is necessary to draw attention tosome of the changes observed in the plasma andCSF levels of endogenous opioid substances insimple and migrainous headaches, as these mayhave some relevance when considering the ration-ale for using this form of therapy.

Sicuteri et al (1978) found low concentrations of amorphine-like substance in the cerebrospinal fluidof chronic headache patients. Anselmi et al (1980) ina study of idiopathic headache sufferers found simi-larly low levels both in the cerebrospinal fluid (CSF) and plasma. It also has been shown that dur-ing a migraine attack the plasma beta-endorphinlevels are significantly lower than in betweenattacks. It would seem possible, therefore, that theperiodicity of migraine may, in part, be related tofluctuations in the levels of these naturally occur-ring pain suppressors. The discovery by Facchinettiet al (1981) that a group of patients with chronicheadache, who reacted poorly to acupuncture, had

low levels of plasma beta-endorphin may also be of much significance when one considers the man-ner in which acupuncture is thought to achieve itsanalgesic effect (Ch. 10).

Emotional (supraspinal) component

Henryk-Gutt & Rees (1973) found that up to about70% of migraineurs consider that emotional upsetsplay an important part in the development of theirheadaches. And it is now generally recognizedthat measures to help reduce stress are an essentialpart of the prophylactic management of the disorder.

Vascular-myofascial-supraspinal (emotional)paradigm

Olesen (1991), in the light of what is known con-cerning the vascular, myofascial and supraspinal(emotional) contributions to migraine has for-mulated a vascular-supraspinal-myogenic (VSM)model to account for its varying manifestations.

According to this model it is the varyingstrengths of these three inputs to the trigeminalsubnucleus caudalis that determines the characterof an attack. Thus, when all three inputs are equallystrong migraine with aura develops. When the myo-fascial and supraspinal components are strongerthan the vascular one, migraine without auradevelops. And when the vascular input is strongbut the other two are weak, only a migraine auradevelops.

Biochemical changesIt has been shown that changes in the serotonin,noradrenaline and oestrogen levels in the bodycontribute to the development of migraine.

Serotonin (5-hydroxytryptamine)

As Marcus (1995) has pointed out, support for thebelief that alterations in blood and brain serotoninlevels influence the development of migraine comesfrom a number of recently carried out studies.

Goadsby & Lance (1990), showed that migrainemay be relieved by increasing the level of sero-tonin in the blood by means of giving an intra-venous infusion of a 0.1% solution of it. Marcus

Pain in the head and face 253

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(1995) has suggested that a possible reason whyincreasing the peripheral serotonin level by thismeans may relieve migraine is that it has an auto-inhibitory effect on the brain’s serotonin-producingcentre in the dorsal raphe nucleus.

Conversely, Bank (1991) has shown that as aresult of increasing the production of serotonin inthe brain by means of administering the serotonin-releasing agent reserpine, it is possible to precipi-tate an attack of migraine. And that the effect ofgiving the serotonin receptor antagonist methy-sergide is to block this reserpine-induced effect.

Noradrenaline (norepinephrine)

Curran et al (1965) have shown that during attacksof migraine plasma noradrenaline levels decreaseand their metabolites increase. The significance ofthis finding, however, is not certain. It could bebecause this catecholamine is primarily involvedin the pathogenesis of migraine or, alternatively, itmay simply be due to a pain-evoked stress reaction.

Oestrogen

Marcus (1995), during the course of studying theinterrelationship between oestrogen levels andrecurring migraine, found that 60% of females whosuffer from this type of headache have an increasedincidence of it around the time of menstruation, andthat 14% of women with this disorder only have itthen. There is evidence to show that the onset ofmenstrual-related migraine coincides with the timethat there is an oestrogen deficiency and that inorder to counteract this it is necessary for oestro-gen to be administered premenstrually (Somerville1975).

Use of acupuncture in the treatment of migraineAs already indicated, acupuncture is capable ofaborting an attack of migraine, but its main use is in the prevention of attacks. It is, of course,remarkable that it is possible to prevent migrainedeveloping by stimulating nerve endings in betweenheadaches. The only other painful disorder thatcomes to mind in which acupuncture is used pro-phylactically in this manner is dysmenorrhoea

when, according to traditional Chinese teaching itis helpful, premenstrually, to stimulate the so-calledSpleen 6 point situated in the lower part of the leg about a hand’s breadth above the medialmalleolus (Fig. 16.1).

When considering the place of acupuncture rela-tive to other forms of therapy in the prophylaxis of migraine, it has to be remembered that it is atime-consuming procedure. Each treatment ses-sion lasts for about 20–30 minutes, and in thosecases in which the technique proves to be helpful,treatment has to be repeated on a number of occa-sions at frequent intervals. There is, moreover, noway of predicting which patients will benefit fromit, and, for this reason, every patient has to begiven a preliminary trial of three treatments atweekly intervals before a decision can be made asto whether or not to continue with it.

My policy, therefore, when presented with apatient whose attacks of migraine are sufficientlyfrequent as to require prophylactic treatment, isfirstly to ascertain whether or not food substances,alcohol, the contraceptive pill or psychogenic


Kidney channel

Liver channel

Spleen channel

Spleen 10

Spleen 9

Spleen 6

Figure 16.1 The traditional Chinese acupuncture points Spleen 6, 9 & 10.

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factors are contributing to the situation. It has to beadmitted that the exercise of excluding a suspectfood substance or a particular type of alcoholic drinkdoes not usually seem to be particularly reward-ing. The reduction of nervous tension, however, bymeans of hypnotherapy, and teaching the patientto practise autohypnosis on a daily basis, is, in my experience, often very helpful. Most cases alsorequire prophylactic drug therapy. Some patientsfind the beta-adrenoceptor blocking drug propra-nolol effective, others obtain greater benefit from theanti-serotonin agent pizotifen, whilst others preferthe alpha-2 receptor agonist drug clonidine. Plum(1982), however, finds the most effective and thesafest agent in migraine prophylaxis to be amitrip-tyline, thus confirming Lance & Curran’s (1964)carefully conducted cross-over trial, which showedthis drug to be the best of a number of drugs in thetreatment of chronic tension headache. That trialwas particularly noteworthy as it showed that theresponse to amitriptyline could not be correlatedwith the presence or absence of depressive symp-toms. Since then, others have shown that this drugmay be an even more effective migraine prophy-lactic in non-depressed patients than in those overtlydepressed (Couch et al 1976, Couch & Hassanein1976).

It is now recognized that the tricyclic group ofdrugs have both an antidepressant effect and anentirely separate analgesic effect. The analgesiceffect not only comes on more rapidly than anymood change, but is also obtained with a rela-tively low dosage (average 75 mg each evening).This is mentioned not only because of its import-ance so far as the treatment of migraine and othertypes of chronic pain are concerned, but also, inparticular, because it is now known that both theanalgesic and the antidepressant effects of tricyclicdrugs are brought about by their action on the cen-tral serotoninergic system. Because of this, theyhelp to potentiate the effectiveness of acupuncture,a technique that, it will be remembered (Ch. 10),depends largely for its action on evoking activityin the serotonin-mediated descending inhibitorysystem in the central nervous system.

The implications of all this, so far as migraine is concerned, are that this disorder is sometimesresponsive to amitriptyline and sometimes to acu-puncture, and that there are good grounds for

believing that a combination of the two might beeven more effective, but statistically controlled trials to confirm this have yet to be carried out.

The situation may therefore be summarized bysaying that the place for acupuncture is when forone reason or another the various drugs alreadymentioned are contraindicated, or when side-effectsfrom them leads to them being discontinued, orwhen they fail to reduce the frequency and sever-ity of the headaches.

Location of points to be stimulated

Acupuncture is usually only of value in the treat-ment of migraine when there are tender points inthe muscles of the neck and scalp. For reasons pre-viously given, there are good grounds for refer-ring to these as TrPs, and some people, includingmyself, believe that the most logical means of carry-ing out acupuncture in this condition is to insertneedles into the tissues overlying them. The iden-tification of these points, therefore, necessitates asystematic search of the muscles down the back ofthe neck, across the top of the shoulders, and overthe scalp, each time a person is treated. However,as will be seen from some of the clinical trials to bediscussed later, many physicians with consider-able experience in the use of needle stimulationtherapy, prefer to use the same set of predeterminedtraditional Chinese acupuncture points in everycase. These include one just medial to the mastoidprocess (Gall Bladder 20), one over the middle ofthe upper border of the trapezius (Gall Bladder 21)and points in the temporal region also on the GallBladder meridian (Fig. 16.2) together with a pointin the first dorsal interosseous muscle of the hand(Large Intestine 4) (Fig. 15.11) and one in the firstdorsal interosseous muscle of the foot (Liver 3)(Fig. 16.3).

The muscles in which activated TrPs are to befound in migraine and tension headaches includethe paravertebrally situated posterior cervical muscles, the trapezius muscle at the highest point ofthe shoulder girdle, the sternocleidomastoid muscleand the temporalis muscle. These latter two muscleswill be further discussed later in the chapter.

Posterior cervical muscles Sites at which TrPsmay become activated in the four layers of the


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posterior cervical muscles (in descending order ofdepth – the trapezius, the splenii, the semispinalismuscles, and multifidi together with the rotatores)are shown in Figure 16.4. The referral of pain fromthese TrPs varies somewhat according to the par-ticular point or points involved and the muscle ormuscles in which they are situated, but in generalit is to the occiput, and from there along the side ofthe head to the temporal region, and in somecases, to the eye (Fig. 16.5).

When palpating a TrP in the posterior cervicalgroup of muscles, it is not usually possible to becertain in which particular muscle it lies but thisdoes not matter as the deactivation of any of thesepoints, as with TrPs in general, is best carried outby means of light manual stimulation of a needle

inserted superficially to a depth of approximately5 mm. This is particularly important when treatingmigraine as any form of vigorous stimulation maycause an attack of pain to develop.

Trapezius muscle There is almost invariably anexquisitely tender TrP in the upper free border ofthe trapezius muscle about midway between thespine and the acromium, corresponding in positionwith the traditional Chinese acupuncture point GallBladder 21. The referral of pain from this TrP is upthe side of the neck, and when particularly severe, itis also referred along the side of the head to the tem-ple and eye (Fig. 16.6D). The deactivation of thispoint should be carried out in a similar manner.


Liver 3

Figure 16.3 The traditional Chinese acupuncture point Liver 3.

Figure 16.4 Trigger points (s) in the posterior cervicalmuscles at the upper part of the back of the neck.

Figure 16.5 A commonly occurring pattern of painreferral from the posterior cervical muscle trigger points shown in Figure 14.4.

Gall bladder 14

Gall bladder 20

Gall bladder 21

Gall bladder 1Gall bladder 3

Figure 16.2 The upper part of the traditional ChineseGall Bladder meridian. The lower part, not shown, extends down the outside of the trunk, leg and foot to terminate at the base of the 4th toe.

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A

SternocleidomastoidClavicularSternalTemporalis

B

Lateral pterygoid UpperTrapezius

Lower

C D

Medial pterygoid

Pain pattern

MasseterSuperficial Deep

Trigger point

E F

Figure 16.6 Patterns of pain referral from trigger points in masticatory muscles and two neck muscles. (Reproducedwith permission of D G Simons and J G Travell from Wall P D and Melzack R (eds) 1984 Textbook of Pain.)

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There is such a close spatial correlation betweenWestern style TrPs and traditional Chinese acupunc-ture points around the head and neck involved inthe treatment of migraine that it probably makeslittle difference to the outcome as to which are used.But what does require to be carefully investigatedis whether in the treatment of this disorder there isanything to be gained by following the traditionalChinese practice of inserting needles into pointssome distance away in the hand and foot.

Distant points It will be remembered fromChapter 1 that according to the traditional Chineseapproach to acupuncture various parts of the bodyare said to be linked by channels known as acu-tracts or meridians so that pain in one part of thebody can be treated either by inserting needleslocally at that site, or by inserting them into pointssome distance away from the area of pain, provid-ing that both the latter and the distant points liealong the same meridian. As discussed in Chapter2, ever since the Western world first heard aboutacupuncture 300 years ago, it has always been verysceptical about acu-tracts or meridians, knowingthat contrary to the teaching of the ancient Chinese,they are anatomically not demonstrable. It is, there-fore, extremely interesting that in recent yearsneuroanatomical research has shown that certainparts of the body are linked in a manner hitherto notthought possible. For example, studies by Rossi &Brodal (1956) and those by Torvik (1956) show thatthere are direct projections from the spinal cord to the trigeminal nucleus. Micro-electrode studiescarried out in cats by Sessle et al (1981) also demon-strated that the responsiveness evoked in individ-ual neurons in the trigeminal subnucleus caudalisas a result of stimulating the tooth pulp is consid-erably inhibited by stimulation of the forepaws.

Such observations have considerable relevanceto the practice of acupuncture. For example, Mannet al (1973), in discussing some cases of chronicpain treated with acupuncture, stated: ‘In the caseof pain in the distribution of the trigeminal nerve,acupuncture was applied to the ipsilateral extrem-ities.’ And they went on to explain that this wasdone because ‘there is a projection from the spinalcord to the spinal trigeminal nucleus of both sides,and stimulation of limb nerves can bring aboutprimary afferent depolarisation in the spinaltrigeminal nucleus’.

Neuroanatomical studies carried out in theWestern world during recent years therefore givecredence to the ancient belief of the Chinese thatby stimulating a point called by them Hoku (TheJoining of the Valleys) or Large Intestine 4, in thefirst dorsal interosseous muscle of the hand (Fig.15.11), it is possible to control pain occurring in theface and scalp.

It will be remembered, however, from Chapter 9,that several investigators, including Andersson &Holmgren (1975), Jeans (1979), and also Chapmanet al (1980), who have compared the relative effectiveness of near and distant points, have concluded that stimulating points near to the siteof pain is more effective than stimulating distantones.

Certainly, when attempting to alleviate musculo-skeletal pain by Western-style TrP acupuncture, it is only considered necessary to stimulate theTrPs believed to be the source of pain. It is there-fore interesting to note that when it comes to alle-viating the pain of migraine, or to preventing itfrom recurring, many physicians in the Westernworld with considerable experience in the use ofacupuncture employ both proximal and distalpoints. Loh et al (1984), for example, in their statis-tically controlled trial of acupuncture versus drugtherapy, in cases of migraine and muscle tensionheadaches of such severity as to warrant referral tothe National Hospital for Nervous Diseases inLondon, used local traditional acupuncture pointsaround the neck and scalp (Gall bladder 20 and 21in the neck; Gall bladder 3 in the temple and 14 inthe forehead [Fig. 16.2]) together with two distantpoints – one in the first dorsal interosseous musclein the hand (Large intestine 4 [Fig. 15.11]), and theother in the first dorsal interosseous muscle in thefoot (Liver 3 [Fig. 16.3]). And by using this combi-nation of points, they were able to conclude ‘thatacupuncture is a beneficial treatment for headacheand migraine for some patients, and that its morewidespread use is justified’.

Vincent (1989) also stimulated local and distanttraditional Chinese acupuncture points in a well-designed, carefully conducted, randomized con-trolled trial in which he was able to show that ‘trueacupuncture was significantly more effective thanthe control procedure (see Ch. 11) in reducing thepain of migraine’.


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It has to be said, however, that the situation is far from straightforward as Jensen et al (1979), in their placebo versus acupuncture trial usinguniversity students in Denmark suffering fromrepeated headaches, used only the distal pointLiver 3 in the foot but, nevertheless, in spite ofemploying this point alone concluded ‘that acupunc-ture is a relevant therapy for headache with a def-inite symptomatic effect’.

Felix Mann (1996) has also for many years beenrecommending the needle-evoked stimulation ofnerve endings at the Liver 3 point in patients withmigraine. And Campbell (2001) during the courseof discussing this states:

… One should always look for trigger points inthe head and neck and these should generally betreated if they are present. However, Liver 3alone can also work and if it does it has certainadvantages: it is quicker to perform and is some-thing that patients can do for themselves if neces-sary. Features that suggest trying Liver 3 first are a convincing history of headaches being pre-cipitated by particular foods (chocolate, cheese)or by alcohol and the occurence of a visual orother type of aura before the headaches. In otherwords I think that Liver 3 is probably the firsttreatment to try for classic migraine and migrainetriggered by food sensitivities. …

In view of these diverse, but seemingly success-ful methods of using acupuncture in the preven-tion of primary headaches, there is, in my opinion,a pressing need for controlled trials to be set up inorder to compare the relative efficacy in migraineof stimulating:

1. local and distant points2. local points only3. distant points only.

Unfortunately, one of the difficulties in assess-ing the value of any type of treatment in migraineis that it is a type of disorder that is liable to bereadily responsive to a placebo. Matthews (1983)in discussing this matter states:

… the placebo effect in migraine is so markedthat virtually any form of treatment adminis-tered with sufficient aplomb, as for example,acupuncture, will produce a remission in a highproportion of patients.

The results of Dowson et al’s trial (1985), inwhich the effect of traditional Chinese acupunc-ture and that of a placebo in the treatment of sim-ple and migrainous headache were compared,tend to confirm this view. This was an extremelywell conducted, single blind, randomized studywith certain particularly commendable features,including the use of pain diaries in which patientsconscientiously recorded their treatment responsesfor 4 weeks prior to treatment, during 6 weeks oftreatment and for 24 weeks follow-up; and, theemployment of an extremely well-thought-out typeof placebo treatment that involved the placing oftwo electrodes on the skin over the mastoid processconnected to a TENS stimulator, the circuitry ofwhich was so adjusted as to allow the red light onthe machine to flash whilst preventing any currentfrom reaching the patient. The authors admit that:

… the numbers entered into the study are smalland we have analysed those suffering from sim-ple headache and migrainous headaches together.It is possible that a larger study with a separateanalysis for specific types of headache might revealthat acupuncture is successful in some instances,but not in others.

And they conclude:

… it appears that the complaint of headache isvery sensitive to placebo therapy, but it is pos-sible that acupuncture has a real therapeutic effectof approximately 20% over placebo. We would,therefore, recommend that future studies shouldbe planned with more patients and on the basisof this assumption.

TENSION-TYPE HEADACHES

The Headache Classification Committee of theInternational Headache Society (1988) introducedthe term tension-type headache (T-TH) to includea number of other hitherto commonly employedones. These were tension headaches, muscle con-traction headaches, psychogenic headache andstress headache.

Clinical manifestationsA T-TH characteristically takes the form of a dullaching sensation or vice-like constriction that


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usually affects the whole of the head, but may insome cases be localized to one or other region of it.

On clinical examination a number of pericranialmuscles are found to be tender. Lous & Olesen(1982) found that the muscles most commonlyaffected in this way were the sternocleidomastoidand masseter (92%), the temporalis (76%), and thelateral pterygoid (70%). Furthermore, systematicpalpation of each muscle in turn reveals the pres-ence of well-defined points of maximum tender-ness that, as Simons (2001) has persuasivelyargued, have all the characteristics of activeMTrPs.

The activation of MTrPsOriginally it was thought that compression of smallblood vessels in the muscles, brought about as aresult of the latter undergoing psychogenic-evokedcontraction leads to ischaemia-induced activationof nociceptors at MTrP sites.

This theory, however, had to be discarded oncePeterson et al (1995) and Schoenen et al (1991) failedto confirm increased electromyographic (EMG)activity of the head and neck muscles in T-TH. Andbecause, as Olesen & Bonica (1990) have pointedout, any muscle contraction that may be present in this disorder is never of sufficient degree to constrict blood vessels.

EMG studies carried out at MTrP sites by Lewis(1994) and by McNulty et al (1994) have, however,shown that psychological stress is capable of acti-vating MTrPs seemingly as a result of it causingautonomic nervous system hyperactivity. Banks et al (1998), have provided confirmation of this byshowing that localized EMG activity found to bepresent within MTrPs is significantly and dramat-ically increased by a psychological stressor such asmental arithmetic and decreased by autogenousrelaxation training.

Measures to reduce the frequency andseverity of tension-type headachesProphylactic measures should be employed when-ever the frequency of the headaches is more thantwo a week and the duration of each episode is formore than 3–4 hours.

Pharmacotherapy

Amitryptyline is widely employed with a dose of10–20 mg/day often being all that is required toreduce the frequency of the attacks. Alternatively,a serotonin-specific reuptake inhibitor such as flu-oxetine may be employed. Saper et al (1994), haveshown in a controlled trial that this is more effect-ive than a placebo.

Acupuncture

Needle-evoked nerve stimulation at traditionalChinese acupuncture points cannot be recom-mended on present evidence. Vincent (1990), in astudy involving 14 patients, found that it wassuperior to sham acupuncture in only four of them.And Tavola et al (1992) found it to be no more effect-ive than a placebo.

TrP acupuncture, however, clearly has a soundphysiological basis in view of it having been shownthat a nociceptive input to the subnucleus caudalisfrom TrPs in the neck muscles is a primary reasonfor the disorder developing. Patients with T-TH,like those with migraine, are in general strongreactors and so short duration (approximately30 seconds) superficial dry needling carried out atMTrP sites is usually all that is required.

MIGRAINE AND TENSION TYPEHEADACHES – A CONTINUUM

It is now generally recognized that migraine andT-TH are so closely related as to form a continuum(Baldry 2001).

Hopkins (1993) during the course of discussingthis has stated:

… A consensus has developed that patients withchronic recurrent headaches have at differenttimes varying amounts of the features that have,in the past, been called migrainous ... and at othertimes features of headaches that have in the past been called tension headaches or muscle-contraction headaches …

It was for this reason that Loh et al (1984), whencomparing the relative effectiveness of acupunc-ture and standard medical management in thetreatment of chronic recurrent headache, stated


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that they had to include these two types of cepha-lalgia in the same trial because ‘patients commonlyhave both kinds of headache and frequently do notdifferentiate them when they report their progress.Although there are clear-cut examples of migraineand of muscle-tension headaches, there are manyheadaches where it is artificial to assign them toone or other of these two categories.’

Olesen (1991) is of the opinion that what deter-mines whether a patient at any particular timedevelops a tension-type headache or migraine isthe relative strengths of three inputs – vascular,myofascial and emotional (supraspinal). Withmigraine there are, in descending order of strengths,vascular, supraspinal and myofascial inputs to thesubnucleus caudalis. In contrast to this, with T-THthey are myofascial, supraspinal, and vascular ones.

CLUSTER HEADACHES (MIGRAINOUSNEURALGIA)

This is a relatively rare disorder, but one that hasto be distinguished from migraine, particularly asboth may occur in the same patient. Also becausethe management is different and because, so far asmy limited experience is concerned in attemptingto treat it with acupuncture, it is not relieved bythis form of treatment. It is a condition that pre-dominantly affects men in the 40–60 years agegroup. It is characterized by an excruciating painaround the eye, spreading to the face and temple,with profuse watering and redness of the eye andstuffiness of the nose. Each attack lasts from about20–120 min once or several times every day in a‘cluster’ lasting 3–8 weeks. The symptom-freeintervals between the clusters are widely variable.

The patient usually knows what time of day ornight to expect an attack and an ergotamine sup-pository inserted some hours before will oftenabort it. Other prophylactic agents currently being used are lithium carbonate and nifedipine(Silberstein et al 1998).

PAIN IN AND AROUND THETEMPEROMANDIBULAR JOINT

It must be emphasized at the outset that pain inand around this joint is rarely due to arthritis.Admittedly, patients with rheumatoid arthritis

sometimes have radiographic evidence of this in thejoint, but pain from it is uncommon (Chalmers &Blair 1973). Similarly, osteoarthritic changes shownon an X-ray of this joint are usually no more than afortuitous radiological finding (Cawson 1984). Inthe later years of adolescence, pain in the region of this joint is very commonly due to caries in apartially erupted wisdom tooth.

Another important cause of pain in this regionis the development of MTrP activity. A disorderthat Schwartz (1956) called the temperomandi-bular joint pain-dysfunction syndrome and othershave termed the myofascial pain dysfunction syn-drome (Laskin 1969, Mikhail & Rosen 1980). Sharav(1999), when recently discussing it at some length,simply called it temperomandibular myofascialpain. My personal preference, however, is to call itthe temperomandibular MTrP pain syndrome asthis has the merit of drawing attention to the allimportant source of the pain.

The temperomandibular MTrP pain syndromeThis disorder, which mainly affects women, maydevelop at any age. The patient experiences a dull,continuous, poorly localized ache mostly aroundthe ear, the angle of the mandible and the tem-poral area but also often in the jaws, teeth and sideof the face. The continuous ache is punctuated bymomentary jabs of sharp pain (Bell 1977). Thepatient may also complain of various clicking orpopping noises in the joint on opening the mouth,and also of limited mouth opening and dizziness(Sharav et al 1978).

On examination, the limited mouth opening andthe abnormal sounds in the joint that sometimes areproduced on attempting this may be confirmed.The muscles around the joint are tender and sys-tematic palpation of these reveals the presence offocal points of exquisite tenderness, or TrPs, particu-larly in the lateral pterygoid, the masseter, and themedial pterygoid muscles (Travell & Simons 1983,pp. 168–182). The exact location of these TrPs willbe described later, but first it is necessary to saysomething about the aetiology of the syndrome andits management in general, for it is certainly nogood directing treatment at these points alone with-out at the same time correcting other disorders.


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Aetiology of the syndrome and its management

There would seem to be a triad of factors respon-sible for the condition including occlusal distur-bances, psychological disorders, and perhapsbecause of one or other or both of these, the acti-vation of TrPs in the masticatory muscles.

Occlusal disturbances

There is much controversy concerning the partplayed by occlusal disturbances in the aetiology ofthis syndrome. Some authorities, such as Clarke(1982), believe there is no significant differencebetween those occurring in patients with this syn-drome and those found in asymptomatic controls.Others, such as Sharav (1999), consider that suchdisturbances are a prerequisite for the develop-ment of dysfunction and pain. And it should benoted in relationship to this that the AmericanDental Association (Ayer 1983) has lent its sup-port to the view that the use of dental appliancesdesigned to temporarily modify the occlusion arehelpful in the treatment of this condition.

Psychological disorders

Since Schwartz (1956) first drew attention to theimportance of psychological disorders in the aeti-ology of this condition, it is generally agreed thatanxiety, depression, frustration, and resentmentmay singly or collectively contribute to this syn-drome with bruxism – a purposeless grinding orgnashing of the teeth – being an outward manifest-ation of such disorders of mood.

Treatment must therefore include the prescrib-ing of an antidepressant or tranquillizer accordingto whichever is most appropriate, or the use ofvarious relaxation techniques such as biofeedback(Stem et al 1979) or hypnotherapy. My preferenceis for the latter and to teach the patient to practiseautohypnosis on a regular basis each day.

MTrPs

The masticatory muscles in which activated TrPsare likely to be found include the lateral pterygoid,the masseter, the medial pterygoid, and the tem-poralis muscles. Greene et al (1969) in a study of

277 patients with temperomandibular joint paindysfunction found that, of those in pain, 84% hadtenderness of the lateral pterygoid and 70% hadtenderness of the masseter muscle.

Sharav et al (1978) observed much the same in a series of 42 patients, with active TrPs occurringin the lateral pterygoid in 83% and in the masseterin 69%.

As in practice, it is better to deactivate TrPs in the masseter muscle before dealing with those inthe more deeply lying lateral pterygoid muscle; themasseter muscle will be considered first.

Masseter muscle The masseter muscle consistsof a superficial and deep part. The superficial part,which is the larger of the two, arises from thezygomatic process of the maxilla, and the zygo-matic arch. Its fibres pass downwards and back-wards to be inserted into the angle and lower halfof the ramus of the mandible. The deep part, muchof which is concealed by the superficial part arisesfrom the zygomatic arch, and its fibres pass verti-cally downwards to be inserted into the lateralsurface of the coronoid process and upper half ofthe ramus of the mandible (Fig. 16.7).

Activation of TrPs TrPs in this muscle maybecome activated as part of the myofascial painsyndrome, but additionally when there is pro-longed overstretching of the muscle as sometimesoccurs during a dental operation or as a result ofthe direct trauma of an accident, and secondarily,when pain is referred to the region of this musclefrom TrP activity in the sternocleidomastoid muscle. The TrP activity is the cause of referred pain,restriction of jaw opening and, somewhat surpris-ingly, tinnitus (Travell 1960).


Figure 16.7 The masseter muscle.

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Specific pattern of pain referral TrPs in thesuperficial layer of the muscle are responsible forpain being referred along both the maxilla andmandible, around the molar teeth, and in andaround the temperomandibular joint (Fig. 16.6F).

Those in the deep layer refer to the region of thetemperomandibular joint and ear (Fig. 16.6F). Theymay also be responsible for the development oftinnitus. Deafness or giddiness, however, neveroccur.

TrP examination In locating TrPs, it is necessaryto put the muscle on the stretch by propping openthe mouth. A cylindrical cardboard air-tube usedfor respiratory function measurements is very use-ful for this purpose.

TrPs in the superficial part of the muscle usuallyoccur near to either the upper or lower attach-ments, where they are best located by flat palpa-tion. On occasions they may be found in its bellyand are then best located by gripping the musclebetween a finger inserted into the mouth and thethumb pressed against the cheek. TrPs in the deeppart are located by palpating it where it overliesthe posterior part of the ramus of the mandible,just in front of the external auditory meatus.

Deactivation of TrPs When deactivating a TrPwith a dry needle, the point should be either fixed

between two fingers placed side by side extra-orally,or it should be held in a pincer grip, between a fin-ger inside the mouth, and the thumb on the out-side pressing against the cheek.

Lateral (external) pterygoid muscle The lateralpterygoid muscle lies deep to, and mainly behind,the coronoid process and zygomatic arch. It is madeup of two divisions – the superior and inferior.

Attachments The superior division is attachedin front to the sphenoid bone and behind to thecapsule of the temperomandibular joint. The infer-ior division is attached in front to the lateral pterygoid plate and behind to the neck of themandible (Fig. 16.8).

Activation of TrPs This occurs with malocclu-sion of the teeth or with overuse of the muscle as aresult of anxiety-induced bruxism, or both.

Specific pattern of pain referral TrPs in thismuscle are responsible for pain being referred to thetemperomandibular joint and around the region ofthe maxillary sinus (Fig. 16.6C).

TrP examination The locating of TrPs at theanterior attachment of the inferior division is bestcarried out by intraoral palpation. With the mouthopen and the lower jaw drawn towards the side to be examined, a finger is squeezed between themaxilla and the coronoid process of the mandible,


Temporalis

Lateral pterygoid upper head

Lateral pterygoid lower head

Medial pterygoid deep head

Medial pterygoid superficial head

Buccinator

Figure 16.8 The leftptyerygoid muscles. Thezygomatic arch and part ofthe ramus of the mandiblehave been removed.

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along the roots of the upper molar teeth. If thespace is too narrow to admit a finger, some instru-ment such as the handle of a dental mirror should beemployed. The finger is slid as far along the lengthof the coronoid process as possible, a manoeuvrefacilitated by having the mouth partially closed.Pressure is then applied in an inwards directiontowards the lateral pterygoid plate to test for theexquisite tenderness of TrP activation. Similar ten-derness from a TrP in the temporalis muscle at itsattachment to the coronoid process may be elicitedby pressing with the finger, at exactly the same sitebut in an outwards direction.

TrPs in other parts of the muscle are best locatedby extraoral examination. It must be remembered,however, that it is impossible to palpate the musclefrom the outside with the mouth closed because thesuperior division is then behind the zygomatic arch,and the inferior division behind the ramus of themandible. The examination, therefore, must alwaysbe carried out with the mouth open. It is then pos-sible to palpate the mid parts of both the superior and inferior division through the bony aperture,bounded above by the zygomatic arch, and belowby the coronoid process anteriorly and the con-dyloid process posteriorly (the mandibular notch). In order to palpate the mid part of the superior division, pressure should be exerted in an upwardsand forwards direction, and for the inferior div-ision it should be applied in a downwards and forwards direction. It is only possible to elicit tenderness at these sites, however, if TrPs in theoverlying masseter muscle have previously beendeactivated.

Deactivation of TrPsINTRAORAL APPROACH It is possible to deactivate

TrPs in the anterior part of the inferior division byinserting a needle intraorally, but this should onlybe attempted by someone skilled in manipulatingneedles within the mouth. Otherwise it is better touse an external approach.

EXTRAORAL APPROACH In order to deactivate TrPsin the lateral pterygoid muscle extraorally, thepatient should be placed in the supine positionand the mouth propped open.

For TrPs in the anterior part of the inferior div-ision, the needle is inserted through the massetermuscle, and then through the mandibular notch inthe direction of the upper molar teeth.

For TrPs in the anterior part of the superior divi-sion, the needle is passed under the zygomaticarch just anterior to the temperomandibular jointin an upwards and forwards direction towards theorbit.

For TrPs further back, in either division of themuscle, the needle is inserted through the mandibu-lar notch perpendicular to the surface and slightlyposteriorly. To reach the superior division, the nee-dle is directed upwards beneath the zygomatic arch,and to reach the inferior division the needle isdirected downwards towards the angle of themandible.

Medial pterygoid muscle If, after deactivatingTrPs in the masseter and lateral pterygoid muscles,opening the mouth is still painful and restrictedwith, in addition, some difficulty in swallowing,then it is possible that there are active TrPs in themedial pterygoid muscle.

Attachments The medial pterygoid muscle isattached below to the angle of the jaw and aboveto the lateral pterygoid plate (Fig. 16.8).

TrP examination The patient should be placedin the supine position, with the mouth proppedopen. The muscle is first palpated from the outsideby pressing a finger against the inner surface of themandible at its angle. At this site the lower end ofthe muscle is just within reach of the finger. Anintraoral examination is then carried out in order toreach parts of the muscle higher up. With the padof the finger facing outwards, it is inserted into the mouth and slid behind the lower molar teethuntil it encounters the bony edge of the ramus of the mandible, and just behind this, it comes upagainst the muscle running in a vertical direction(Fig. 16.6E).

Deactivation of TrPs Deactivation of TrPs in thismuscle is technically difficult but fortunately asTravell & Simons (1983, p. 254) point out, it is usu-ally possible to control the pain by stretching themuscle, and then applying a vapocoolant spray to it. The patient is placed in the supine positionand encouraged to stretch the muscle by placingtwo fingers behind the lower incisor teeth, and the thumb under the chin, and then pulling themandible forwards and downwards to open thejaws fully. Whilst this is being done, the vapoc-oolant spray is swept from the neck below upwards


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towards the temperomandibular joint. It is import-ant to ensure that the spray does not go into the eyeby placing a pad over it.

Temporalis muscle The temporalis muscle is thethird most commonly involved of the masticatorymuscles after the masseter and lateral pterygoid inthis myofascial TrP pain syndrome (Greene et al1969) but as the activation of TrPs in this musclemay also occur for many other reasons, all of thevarious causes will be considered together later inthe chapter.

TRIGEMINAL NEURALGIA

Trigeminal neuralgia clearly has to be included inthe differential diagnosis of pain in and around theface, but as this book is primarily concerned withmusculoskeletal pain, only brief reference will bemade to its clinical features in order that it may bedistinguished from other causes of facial pain. Thiscondition of unknown aetiology may develop atany age, but it is most commonly seen from the ageof 50 years onwards. In young people, it occasion-ally heralds the onset of multiple sclerosis.

The pain usually involves the 2nd or 3rd div-isions of the nerve. It commonly takes the form of unilateral, brief, very severe electric-shock likestabs repeated at frequent intervals in short-lastingbouts with intervals of freedom from pain varyingin duration from minutes to hours. After severalweeks, the pain spontaneously remits but recurssome time later. Unfortunately, there is a tendencyover the course of time for the remission periods to get shorter whilst the bouts of pain in an attackget progressively more severe, and the attacks lastlonger.

Each bout of pain is usually precipitated bysome non-noxious stimulus such as shaving, wash-ing, or even just touching or moving the face. Also,in some people, eating, drinking or brushing theteeth may bring on an attack.

It is important to note that with idiopathictrigeminal neuralgia there are no abnormal phys-ical signs including no sensory loss.

TreatmentCarbamazepine is the drug of choice in the treat-ment of this condition, but unfortunately, in about

25% of patients it is ineffective and in about 25% of patients it cannot be tolerated. Therefore, onlyabout 50% can be successfully treated with it(Loeser 1984).

Other anticonvulsants currently being used inthe treatment of this disorder include lamotrigineand tizanidine (Zakrzewska 1999). A systematicreview of the use of them in the treatment of neuro-pathic pain, including trigeminal neuralgia, hasbeen carried out by McQuay et al (1995). The alter-native, when medical management proves to beineffective, is to carry out one or other of the vari-ous surgical procedures now available (Zakrzewska1999).

ATYPICAL FACIAL PAIN

Pain in the face, which from its character is clearlynot due to trigeminal neuralgia, and which, follow-ing careful investigation, is not found to be due todisease of the teeth, bones or sinuses, is often diag-nosed as atypical facial pain. The very term signi-fies how ill-defined the condition is, and regrettablyall too often the possibility of the pain beingreferred from TrPs in muscles in this region is notconsidered. It must be admitted, however, thatthere is a group of patients who have pain in theface, which, unlike that of trigeminal neuralgia, ispersistent in character, is often associated with anarea of sensory loss, and not infrequently is bilat-eral. Also, on examination, in addition to there beingno evidence of disease of any of the structures ofthe face, there is also no evidence of TrP activity in the neighbouring muscles, and, therefore, by aprocess of exclusion, the only diagnosis possible isone of atypical facial pain (Weddington & Blazer1979).

As patients with atypical facial pain often showsome evidence of emotional instability, treatmentusually consists of giving an antidepressant, some-times in combination with a phenothiazine. Suchdrugs, however, are only occasionally helpful in thiscondition. The anticonvulsants, carbamazepine anddiphenylhydantoin, are also sometimes recom-mended, but there seems to be no scientific basisfor this and only a small number of patients arelikely to be helped. Side effects from any of thesedrugs are common and such treatment should neverbe embarked upon until, by careful examination,


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the possibility that the pain may be coming frommyofascial TrPs has been carefully excluded.

TRAUMA-INDUCED MYOFASCIAL TrPCEPHALALGIA

This particular type of cephalalgia does not appearas a separate entity in the International HeadacheSociety’s Classification (Headache ClassificationCommittee of the International Headache Society1988), but those who include a search for TrPs aspart of their routine physical examination in allcases of persistent head pain have come to realizethat it is an extremely common, but poorly recog-nized disorder. The TrP activity may develop(Baldry 1999) as a result of sudden severe trauma,such as that brought about by a whiplash injury orbecause of muscle overloading from, for example,the adoption of a faulty posture. This TrP activityis liable to develop in one or more of the follow-ing muscles – the trapezius and posterior cervicalgroup (see Ch. 14), the sternocleidomastoid, thetemporalis and the occipito-frontalis.

Sternocleidomastoid muscleMany errors in diagnosis and, consequently, muchinappropriate treatment are due to a lack ofawareness that the activation of TrPs in the stern-ocleidomastoid muscle is an important cause ofpersistent pain in the head and face, and also, incertain cases, is the cause of a distressing type ofpostural dizziness.

Activation of TrPs

TrPs frequently become activated in the upperpart of this muscle on one side of the neck inpatients with tension headaches, in those withmigraine, and in those with both. They may alsobecome activated in any part of this muscle whenthe neck is kept turned to one side for any lengthof time, such as, for example, when typing a longreport from shorthand notes.

They may become activated in the muscles on both sides of the neck as a result of the headbeing tilted backwards for some time such as, forexample, when painting a ceiling or sitting at thefront of the theatre watching a play being performedon a high stage. However, one of the commonest

causes of bilateral activation of TrPs in this muscleis when the muscles on both sides of the neckbecome strained as a result of a whiplash injuryoccurring as a result of one car running into theback of another. When this happens, TrPs in thelevator scapulae, posterior cervical, and the trapez-ius muscles also become activated with the devel-opment of a painful stiff neck (Ch. 14); whilst TrPsin the sternocleidomastoid muscle are liable to giverise to a variety of symptoms including pain in thehead and face, and postural dizziness.

Symptoms from TrP activation in the sternocleidomastoid muscle

TrPs at the upper part of the sternal division of themuscle near to its insertion into the mastoid processare responsible for pain being referred to the occipi-tal region and to the top of the head, often withmarked tenderness of the area of the scalp affected(Fig. 16.6B). Those in the mid-part of this divisionrefer pain along the supraorbital ridge, around theeye, and into the cheek (Fig. 16.6B). The activationof TrPs in this part of the muscle sometimes occursin association with TrP activity in other musclessuch as the temporalis, the masseter, the externalpterygoid, the orbicularis oculi and the zygomati-cus, and unless the presence of TrPs in these muscles is recognized, the composite pain pattern isliable to be misdiagnosed as that of atypical facialneuralgia.

Travell (1981) reported a very interesting case ofTrP activity in muscles such as those just men-tioned that had been the cause of intractable painin the face for 13 years before the true cause of thepain was finally established. It is perhaps unfortu-nate that she referred to this as a case of atypicalfacial neuralgia for, in my view, such a diagnosisshould be reserved for that group of cases in whichmyofascial TrP activity is not present, and thatcases in which pain is due to this are better referredto as examples of the chronic facial myofascial TrPpain syndrome.

TrPs at the lower end of this division near to itsattachment to the sternum refer pain in a down-wards direction over the upper part of the ster-num. The pattern of this is such that it is liable tobe mistaken for pain that is myocardial in origin(Fig. 16.6B).


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TrPs in the deeper clavicular part of the muscleare likely to refer pain either into the ear andpostauricular region, or across the front of the forehead (Fig. 16.6B).

TrP activity in the sternal division also affectsthe autonomic nervous system and may be thecause of conjunctival redness and watering of theeye and nose similar to that seen with migrainousneuralgia (Travell 1960, 1981). This is liable to bevery confusing when this TrP activity is respon-sible for pain developing around the eye, except of course that in migrainous neuralgia an attack of pain, although very intense, usually only lastsfor less than 1 hour. TrP activity in this muscle may also cause disturbed proprioception with thedevelopment of postural dizziness.

Disturbances of proprioception brought aboutby TrP activity in the sternocleidomastoidmuscle

Cohen’s investigations (1959, 1961) into body orien-tation carried out in monkeys have shown that,whilst it is the function of the labyrinths to giveinformation concerning the position of the head inspace, information concerning the position of thehead in relationship to the body comes from pro-prioceptive mechanisms in the neck. In humans,the main muscle concerned with this would seemto be the sternocleidomastoid and it is because ofthis that unilateral TrP activation in it is often thecause of postural dizziness developing.

In my experience, it never takes the form of gid-diness or vertigo if, by these terms, one means asudden disturbance of balance associated with asensation of rotation either of the person concernedor of their surroundings, but rather it is a sensationof unsteadiness and loss of balance with a tendencyto veer to one side when attempting to walk in a certain direction. This disorientation and loss of co-ordination is mainly postural and occurs whenmovements of the body or head involve a change intension in the affected sternocleidomastoid muscle.Such symptoms may be associated with nausea, butnever with vomiting, tinnitus or nystagmus. In thedifferential diagnosis, an anxiety state, and also in the elderly, vertebrobasilar ischaemia have to beconsidered. Postural dizziness due to sternocleido-mastoid TrP activity may occur at any age, with

Weeks & Travell (1955) reporting a case of it occur-ring in an 11-year-old girl.

Travell, who was one of the first to recognizethis condition, and who in 1955 published a reportof 31 adults suffering from it, maintains that theTrPs responsible for this phenomenon are alwayssituated in the clavicular part of this muscle, andthat, therefore, it is associated with frontal head-ache with either the one or the other dominatingthe clinical picture (Travell 1967).

Most of the cases of this type of postural imbal-ance that have come under my care have been inpatients who, in addition to having TrP activity inthis muscle, also have had painful stiff necks due tosimilar activity occurring in other muscles of theneck as a result of whiplash injuries. It is alwaysinteresting to observe how often in the referral letter this unsteadiness is assumed to be due to‘nerves’ brought on by the shock of the accident. Itis also remarkable how often the disorder disap-pears once the appropriate TrPs have been deacti-vated by inserting dry needles into them.

In considering the mechanism by which posturaldizziness occurs as a result of TrP activity in thesternocleidomastoid muscle, it has to be remem-bered that the sensory innervation of this musclecomes from the anterior primary rami of the 2ndand 3rd cervical nerves, and that Cohen (1961) inexperiments on monkeys and baboons producedan exactly similar type of unsteadiness and loss ofbalance in these animals by artificially cutting offthe sensory input from these two nerves.

Furthermore, the clinical implications of this arethat when pain in the head, superficial tendernessof the scalp, postural dizziness and nausea occuras a result of some injury in which there has beenmarked hyperextension of the neck, the two possi-bilities that have to be considered are that thesymptoms may be due either to TrP activation inthe sternocleidomastoid muscle, or to direct injuryto an upper cervical spinal nerve.

Behrmann (1983) reviewed 17 cases in whichthese symptoms were due to a traumatic neur-opathy of the 2nd cervical spinal nerve, and in 12of them the injury to the nerve was caused byexactly the same type of acceleration-decelerationroad-traffic accident, with a wrenching movementof the head, as that which is liable to cause TrPactivation in the sternocleidomastoid muscle.


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The main distinguishing feature would seem to bethat with the TrP syndrome there is no sensory loss,but with trauma to the second cervical spinal nerve,there is diminished sensation to pin prick over one side of the head or localized to the periorbital,temporal, or suboccipital areas.

POST-TRAUMATIC HEADACHE

The post-concussional syndrome of headaches,persistent tenderness of the scalp, postural dizzi-ness, irritability, and failure of concentration is awell-recognized entity but one about which thereis considerable diversity of opinion concerning itsaetiology. Many experienced clinicians, such asMatthews & Miller (1972) incline to the belief thatit is psychogenic in origin. In support of this view,Matthews & Miller point out that the condition iscommoner after minor head injuries than it is aftermajor ones, and that it rarely occurs in head injuriessustained in the house or during sport. Indeed, itarises most often from trauma incurred during atraffic accident, and even more frequently fromtrauma associated with an industrial accident, andparticularly in those circumstances when there is a claim for compensation – and to quote theseauthors ‘ “treatment” is fruitless’. From the fewcases of post-traumatic headache, either with orwithout a history of concussion that have comeunder my care, it is my belief that TrP activation inthe muscles of the neck, such as the splenii, trape-zius and sternocleidomastoid muscles, is an import-ant cause not only of persistent headache, but alsoof persistent scalp tenderness and postural diz-ziness. It is also my belief that in all such cases asystematic search for TrPs is mandatory because,when present, deactivation by means of dry needle stimulation is likely to prove helpful. Thisis a view also supported by the observations ofRubin (1981). There is, therefore, a pressing needfor a large-scale survey of cases of post-traumaticheadache and dizziness in order to establish thetrue incidence of myofascial TrP activity in thiscondition.

Certainly the post-traumatic headache syn-drome not only occurs as a result of head injuries,but may also develop whenever the muscles of theneck are subjected to the trauma of being held persistently in a state of hyperextension, as, for

example, in the following case, when this occurredas a result of a meningitis.

A female business executive (41 years of age)developed severe retraction of her neck during thecourse of what was said to be a viral meningitis. Theillness was sufficiently bad for her to be kept inhospital for 6 weeks. Shortly after getting over theacute stage of the illness, she began to develop severebilateral temporal headaches, a painful stiff neck, anda feeling of unsteadiness on walking. Eighteen monthslater, because of these symptoms persisting, she wasadmitted to a neurological unit for investigationsincluding a brain scan. No abnormality was found butshe continued to have these symptoms and, by thetime she was referred to me 3 years later, she wasfrequently off work because of the severity of theheadaches and was taking 8 Ponstans a day. Onexamination, there were exquisitely tender TrPs in theposterior cervical muscles, the levator scapulae, thetrapezius, and the sternocleidomastoid muscles.Deactivation of these by means of the carrying out ofsuperficial dry needling gradually caused her symptomsto abate but the procedure had to be repeated atregular intervals over the course of the next 3 monthsbefore the headaches and postural dizziness werefinally brought under control.

TORTICOLLIS

Torticollis (Latin, tortus – twisted; collum – neck) isof two distinct types. The one is a spasmodic con-traction of the neck muscles due to a lesion in thebasal ganglia, and the other a constant pullingover of the neck muscles due to the activation ofTrPs in them.

The clinical picture of spasmodic torticollis isone in which there is paroxysmal contraction ofthe neck muscles causing the head to be frequentlyand involuntarily turned forcibly to one side. Thisis a very distressing condition and one in whicheventually the head may become permanentlyturned to one side. On examination, there is anobvious severe and painful contraction of the ster-nocleidomastoid muscle but, on closer inspection,it becomes obvious that all of the muscles of theneck are involved.

Treatment is far from easy, but selective block-ing of the muscles identified as being responsible


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for the abnormal movements using repeated injec-tions of botulinum toxin is sometimes helpful.

The other type of wry neck, and one that it isessential to distinguish from the spasmodic typeas it is so far more readily treatable, is the one inwhich there is persistent contraction of the neckmuscles causing the neck to be constantly pulledover to that side, and occurring as a result of the activation of TrPs in various muscles of theneck, including the posterior cervical muscles, thelevator scapulae, the trapezius and the sternocleido-mastoid muscle.

A man (30 years of age) had, in his early teens, beenaccidentally shot in the head causing him to have adepressed fracture of the skull and a hemiplegia. Since that time he had had much pain in the neckwith restriction of neck movements and recurrentheadaches. He was referred to me, because during theprevious 18 months he had developed a constant andpainful spasm of his neck muscles causing the neck tobecome increasingly pulled over to the affected side.On examination, there were numerous, obviously veryactive, TrPs in the muscles of the neck. These weredeactivated by means of the carrying out of superficialdry needling initially once a week and after a time atless frequent intervals.

After 4 weeks, the pain in the neck becameappreciably less, but treatment had to be continuedfor another 4 weeks before he could begin to keep hisneck upright without discomfort. Eventually, however,with further treatment spread over several months, hislong-standing headaches and pain in the neckdisappeared. Also, he entirely lost any evidence of atorticollis and regained full movements of the neck.Another interesting aspect of the case that is worthnoting is that on the initial examination there wasexquisite tenderness of the scalp around thecraniotomy scar and, on closer examination, it became apparent that there was one focal point ofmaximum tenderness in the scar itself. It wasconsidered, therefore, that this must be a TrP, and,although needling it was difficult due to the scarbeing tough, and also because it was a very painfulprocedure, the treatment, nevertheless, very quicklybrought about a dramatic lessening of the generalizedtenderness around the scar; and as a result ofrepeating it a few further times, the tendernessdisappeared altogether.

TEMPORALIS MUSCLE (Fig. 16.9)

This muscle, which is attached to the temporalbone above and the coronoid process of themandible below, quite commonly develops TrPactivity in it. This may occur in people who aretense, in migrainous subjects, and in those withthe temperomandibular myofascial TrP pain syn-drome. It is also liable to occur when the muscle issuddenly cooled by being exposed to a draught, orwhen it is subjected to direct trauma such as mayoccur with a fall on the head or being hit by a golfball. In addition, it may develop as a secondaryevent when pain is referred to the temporal regionfrom TrPs in either the sternocleidomastoid orupper trapezius muscle.

Location of TrPs and their specific pain patternsThe sites at which TrPs are likely to be foundinclude:

1. the anterior part of the temple at the lateral endof the supraorbital ridge

2. midway between this point and the ear alongthe line of the zygomatic arch

3. on the same line just in front of the ear4. just above the ear.

The referral of pain from a TrP at site 1 is alongthe supraorbital ridge and, on occasions, towardsthe upper incisors; that from a TrP at sites 2 and 3 islocally in the region of the temple and sometimes


Inferior temporal line

Temporalis

Lateral ligament oftemporomandibularjointLateral pterygoid

Figure 16.9 Left temporalis. The zygomatic arch andmasseter have been removed.

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downwards into the teeth of the upper jaw; andthat from a TrP at site 4 is in a backwards andupwards direction from it (Fig. 16.6A).

Locating TrPs When examining the temporalismuscle for TrPs, they are more readily found if themuscle is put slightly on the stretch by having themouth propped partially open.

TrP deactivation It is relatively easy to deactivateTrPs in this muscle by means of the carrying out ofsuperficial dry needling but even with this caremust be taken not to puncture the temporal artery.

Differential diagnosis It has to be said that,although persistent pain in the temporal region iscommonly due to TrP activation, when it occurs inthe middle-aged and elderly, the possibility that itmay be due to giant cell arteritis must always beconsidered. In this disorder the pain may be in anypart of the head but is commonest in the temporalregion, and when this is so it is often made worseby mastication – a state of affairs sometimes some-what ineptly referred to as jaw claudication con-sidering that the jaw is incapable of limping! Onexamination, the temporal artery is characteristicallythickened and pulseless, there is much surround-ing tenderness, and, in some cases, the overlyingskin is reddened. The physical signs, however, areoften by no means obvious and in any case ofdoubt it is essential to have the ESR measured as

with this condition it is invariably appreciably elevated.

This disorder has been discussed at some lengthbecause, unless the possibility of it occurring istaken into consideration, the pain and tendernessassociated with it may all too readily be assumedto be due to TrP activation. This is a mistake thatcould have far-reaching consequences, because,whilst time is being wasted treating the conditionwith acupuncture rather than with a corticosteroid,there is always the risk of blindness developing.

TrP ACTIVITY IN SKIN MUSCLES:ORBICULARIS OCULI, ZYGOMATICUS AND OCCIPITOFRONTALIS (Fig. 16.10)

Orbicularis oculiTrPs may become activated in this muscle as a pri-mary event in someone who persistently frowns,or as a secondary event when pain is referred tothe orbit from TrPs in the sternomastoid muscle.

The TrP lies above the eyelid just beneath theeyebrow against the bone of the orbit. The referralof pain from this is down the side of the nose (Fig. 16.11).

In deactivating this point with a dry needle,superficial needling is particularly necessary


Frontal belly of occipitofrontalis

Orbicularis oculiOrbital part

Palpebral part

Procerus

Levator labii superioris alaeque nasi

Transverse part of nasalis

Levator labii superioris

Zygomaticus minor

Orbicularis oris

Levator anguli oris

Zygomaticus major

Buccinator

Depressor labii inferioris

Depressor anguli oris

Platysma

Figure 16.10 Muscles ofthe scalp and face. Rightlateral aspect.

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because due to the laxity of the tissues at this sitethere is a risk of a haematoma developing.

Zygomaticus majorThis muscle, which assists in controlling facialexpression by drawing the angle of the mouthupwards and backwards, attaches above to thezygomatic bone, and below to the angle of themouth.

A TrP in it may become activated either as aresult of direct trauma to the face or secondary toTrP activation in the masticatory muscles. Thispoint is usually situated just above the corner ofthe mouth and is best located with the mouthpropped wide open and the muscle held in a pin-cer grip with one digit intraorally and the otherextraorally. Pain from it is referred upwards alongthe side of the nose to the forehead (Fig. 16.12).The TrP is generally to be found in a palpable bandof muscle and to deactivate it, a needle should beinserted into the superficial tissues overlying it.


Figure 16.11 The pattern of pain referral from a triggerpoint in the orbicularis oculi muscle.

Figure 16.12 The pattern of pain referral from a triggerpoint in the zygomaticus muscle.

Occipitofrontalis muscleThis cutaneous muscle of the scalp is in two parts –the frontalis situated anteriorly, and the occipitalissituated posteriorly. The action of both of themacting together is to wrinkle the forehead.

A TrP in the frontalis is liable to become acti-vated in someone who persistently frowns, andalso, when TrPs in the sternomastoid muscle referpain to the frontal region of the head.

The TrP is usually situated above the inner endof the eyebrow. Pain from this is referred locallyaround the TrP site. In order to deactivate it, a nee-dle should be inserted superficially and obliquelyinto the skin (Fig. 16.13). A TrP in the occipitalis partof the muscle often becomes activated as a result ofTrPs in the posterior cervical muscles referring painto the occipital region. It refers pain over the side ofthe head from the occiput to the orbit (Fig. 16.14). Itis readily identified by palpating gently over theback of the head and this point also should be deactivated by inserting a needle superficially andobliquely into the skin.

Figure 16.14 The pattern of pain referral from a triggerpoint in the occipitalis belly of the occipitofrontalis muscle.

Figure 16.13 The pattern of pain referral from a triggerpoint in the frontalis belly of the occipitofrontalis muscle.

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INTRODUCTION

The main indication for acupuncture in the alle-viation of low-back pain is when such pain ismechanical in its relationship to activity, and inparticular when it emanates from myofascial trig-ger points (MTrPs). These may have become activated as a primary event when the musclescontaining them have become either overloadedor subjected to direct trauma. Alternatively, butless commonly as a secondary event following thedevelopment of nerve root entrapment from, forexample, disc prolapse or spondylitic changes inthe spine.

It therefore follows that before contemplatingthe use of such treatment it is necessary to excludeother causes of low-back pain of a non-mechanicalnature including inflammatory, metabolic, and neo-plastic disorders of the spine; also referred painfrom abdominal or pelvic organs; and the pain ofperipheral vascular disease.

It is only possible to do this by taking a carefulhistory, by carrying out a detailed physical exam-ination including in particular a systematic searchof the musculature of the lower back for triggerpoints, and by carrying out certain investigations.With respect to the latter, it is essential in all casesto measure the erythrocyte sedimentation rate(ESR) and to have radiographs (PA, oblique andlateral views) of the spine. In certain circumstancesit may also be necessary to carry out more highlyspecialized investigations such as magnetic res-onance imaging (MRI) and, on occasions, certainspecific biochemical blood tests.

275

Chapter 17

Low-back pain

CHAPTER CONTENTS

Introduction 275Mechanical and non-mechanical low-back pain

276–277Clinical examination and investigation of patient

with low-back pain 277–281Intervertebral disc prolapse 281–287Pain arising from degenerative changes

in the intervertebral discs and facet joints 287–289

Chronic lumbar myofascial TrP pain syndrome 289–294

Spondylolisthesis 294Central and lateral canal stenosis 295–297

Management of chronic low-back pain 297–307Acupuncture clinical trials 307–311

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why history-taking must be supplemented with acareful physical examination including palpationof the femoral pulses.

Further, when a patient with low-back paincomplains that the legs become painful, weak, andaffected by paraesthesiae on walking, and that thisis relieved by resting, and, in particular, by adopt-ing a squatting position, the possibility of stenosisof the spinal canal, either congenital or acquired,has to be considered (Porter 1987). This should beinvestigated accordingly by tomography, or byultrasonic measurements (Porter et al 1978), or,preferably, by computerized axial tomography(Schumaker et al 1978).

Non-mechanical low-back painNon-mechanical low-back pain occurs far lesscommonly than that of the mechanical type. Itoccurs as a result of neoplastic, infective, inflam-matory, or metabolic disease of the spine, and forseveral reasons, including the fact that its intensitybears no relationship to physical activity, the his-tory tends to be different.

The onset is usually insidious, with the paingradually increasing in intensity, and being assevere when resting at night as it is during the day.It may, in fact, seem to be worse at night becausethere is nothing to distract the mind from it, andunlike mechanical type pain, it cannot be eased bya change of position.

Ankylosing spondylitis, the principal inflam-matory disease affecting the lower back, will besingled out for special mention because of certaindistinctive features in the history (Calin et al 1977),and because it is the one non-mechanical disorderin which acupuncture may be of much help inrelieving pain. The disease, which affects men fivetimes more commonly than women, declares itselfin early adult life by the insidious onset of painaffecting both sides of the lower back and spread-ing to the buttocks. This pain characteristicallycauses early morning waking and on rising thereis considerable stiffness, but this is relieved byactivity. In addition, there may be a history of iritis,and a family history of the disease. Careful atten-tion to the history is essential because, althoughonce the disease has become established the ESR

DIFFERENTIAL DIAGNOSIS BETWEENMECHANICAL AND NON-MECHANICALLOW-BACK PAIN

Although it would clearly be inappropriate in abook of this type to enter into a detailed discussionof all the various diagnostic features that help toseparate mechanical from non-mechanical low-backpain; it, nevertheless, may help to ensure thatacupuncture is not used inappropriately if brief ref-erence is made to a few of the more important ones.

Mechanical low-back painThe history given by a patient with low-back painof mechanical type is quite different from that whenthe pain is due to some non-mechanical cause, andtherefore simply by listening to the patient care-fully one can often obtain considerable help in dis-tinguishing between these two fundamentallydifferent types of pain.

The commonest form of low-back pain is thatwhich occurs as a result of some structural dys-function and, because of the direct relationship ithas with activity, it may be said to be of the mechan-ical type. It tends to be more noticeable in carryingout movements after sitting or lying down forsome time. Also, twisting, lifting, bending, andcoughing often make it worse. It is relieved byresting and, therefore, as might be expected, thereis often a history of it being most troublesome dur-ing the course of daytime activities. It may, never-theless, come on in bed at night as a result ofturning or lying awkwardly, but when this occursit is quickly eased once a comfortable position isfound.

There is sometimes a complaint that the painbecomes worse on sitting down. This may seemsurprising, but the reason for this will be explainedlater when discussing the location of TrPs.

It has to be remembered that a history of pain inthe buttocks and thighs, brought on by walkingand relieved by resting, may be vascular in origin,and develop as a result of aorto-iliac occlusion(Leriche’s syndrome). In addition, it is possible forsciatica to occur as a result of atheromatous obstruc-tion in the internal iliac artery causing ischaemiaof the sciatic nerve (Lamerton et al 1983). This is

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is elevated and there are diagnostic radiographicchanges in the sacroiliac joints and lumbar spine,in the early stages both the ESR and the X-rayappearances may be normal. In such circumstancesit may sometimes be necessary to carry out tech-netium scanning of the sacroiliac joints in order todemonstrate the presence of sacroiliitis. When theclinical picture is not straightforward, the HLA-B27 test may also be helpful, as a positive test isstrongly suggestive of this disease being the causeof the pain. At the same time, it has to be remem-bered that it may only be a reflection of a carrierstate, with the pain being due to some other cause.

PAIN REFERRED TO THE BACK FROMABDOMINAL AND PELVIC ORGANS

When pain in the lower part of the back occurs asa result of it being referred to that site from someabdominal or pelvic disorder, it is usually accom-panied by other symptoms that direct attention tothe organ involved. This, however, is not invari-able, particularly in the initial stages, and one hasto be particularly wary when there is a history ofrecent trauma to the back as this may be diagnos-tically misleading.

A woman (54 years of age) developed persistent painacross the lower back shortly after being involved in acar accident. The pain was unremitting and in spite of it being present day and night, and not relieved byrest, the trauma was assumed to be responsible, and in view of this she spent several months havingphysiotherapy. By the time she was referred to me foran opinion as to whether acupuncture might behelpful, the character of the pain together with thefact that she was losing weight and feeling generallyunwell, led to further investigations that ultimatelyrevealed the presence of a carcinoma of the body ofthe pancreas.

DUAL PATHOLOGY

When taking the history it has to be rememberedthat in spite of the philosophical maxim of the14th-century Franciscan, William of Occam, that‘Entities are not to be multiplied without necessity’

(Occam’s razor), symptoms indicative of abdom-inal or pelvic disease, and low-back pain may notnecessarily be due to the same cause.

Several cases have been referred to me by a gas-troenterological colleague for acupuncture because,although there have been symptoms of an abdom-inal disorder, such as the irritable bowel syn-drome, or diverticulitis, there has in addition beenlow-back pain that, from its relationship to pos-ture and movement, has clearly been of a mechan-ical type and, therefore, eminently suitable for thisform of treatment.

CLINICAL EXAMINATION

As a detailed account of the proper manner inwhich to examine the back is to be found in anystandard textbook, only some of the more salientfeatures will be mentioned here with special refer-ence to those of particular importance in comingto a decision as to whether or not acupuncturemight be helpful in the symptomatic relief of lumbosacral pain.

The examination really begins as soon as thepatient enters the room, and particularly whilsttaking the history, as observations at that stageconcerning the patient’s appearance, expression,and manner of describing symptoms often give agood indication as to whether or not there is likelyto be an underlying debilitating disease. In thisway an idea as to the degree to which the pain isaffecting the patient and the psychological make-up of the individual can also be obtained. As willbe explained later, there is often a complex inter-relationship between psyche and soma in the patho-genesis of mechanical type low-back pain, whichoften influences the response to any form of treat-ment, including acupuncture, and which oftenmakes it necessary to treat both the mind and the body.

The first part of the formal examination of theback should be carried out with the patient stand-ing and with sufficient clothes removed to give anuninterrupted view of the whole length of the spineand legs.

On inspection, the trained eye will readily note the café-au-lait patch possibly indicative of a

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neurofibroma, the midline dimple or tufts of hairover a spina bifida occulta, the patch of erythemaab igne from prolonged usage of a hot water bot-tle, and the lower lumbar hump characteristics ofspondylolisthesis. However, from an everydaypractical point of view, and particularly whenacupunture is likely to be used, the most import-ant observations at this stage are those concerningwhether or not there is inequality of the length ofthe two legs.

Short-leg syndromeA short leg, either when this is of congenital ori-gin, or when it is acquired, usually as a result of afracture, puts a considerable strain on the musclesof the lower back, so that when TrPs in these muscles become activated for one reason or another,the effect of this strain is to nullify any attempt todeactivate these points. It is therefore a waste oftime employing any technique such as acupunc-ture for this purpose without at the same time correcting the deformity.

The physical findings associated with relativeshortness of one leg include the pelvis being seento be titled in association with a compensatoryscoliosis; also, on the side of the short leg, theshoulder is held lower, the hip is less prominent,there is a loss of the hollow of the flank, and thegluteal fold is lower than the one on the oppositeside (Nichols 1960).

Travell & Simons (1983, pp. 105–109) considerthat a discrepancy in leg length of 1.3 cm (1/2”)may cause no symptoms throughout a lifetime ifMTrPs do not become activated, but if, for one rea-son or another, this occurs, then it only needs adiscrepancy of 0.5 cm (3/16”) to perpetuate thisTrP activity.

Travell (1976) believes that the quadratus lum-borum is the one muscle in particular in which TrPactivity is most likely to persist in the presence of a short leg.

It is important to realize that an uncorrected shortleg has far-ranging consequences because it may notonly cause low-back pain to become chronic, but it may also, by putting a strain on the ipsilateralmuscles of the neck, cause TrPs to become acti-vated in those mucles with the consequent devel-opment of persistent neck pain and headaches.

Two commonly used techniques for assessingdifferences in leg length, carried out with the patientlying down, are unreliable because the patient isnon-weight bearing. These include one where atape measurement is made from the anterior super-ior iliac spine to the tip of the medial malleolus;and the other where, with the knees straight, thedistance is measured between comparable pointson the medial malleoli. A better method is to havethe undressed patient in the standing positionwith the feet together. An approximate estimate of the comparative length of two legs can then be made by palpating the iliac crests, or posteriorsuperior iliac spines. Pages of a journal shouldthen be placed under the foot of the short leg, andthe number of these gradually increased until thepelvis and shoulder are level. This gives a measureas to how much the shoe on the affected sideshould be raised, a task that in my experience isbest done by a cobbler with a special interest inand experience of this type of work.

Curves of the lumbar spineOn inspection of the back with the patient stand-ing, the curves of the lumbar spine should also beobserved. Loss of its normal lordosis may occurwith certain inflammatory conditions but it mayalso result from pregnancy and obesity. Any scoli-osis also should be noted. This may develop inpainful conditions as a result of muscle spasm, oras discussed above, it may occur together with apelvic tilt, when the legs are of unequal length.When due to the former, it is sometimes only seenon forward flexion, whereas with the latter thismovement usually causes it to disappear.

Wasting of the musclesIt should also be noted whether there is any wast-ing of the muscles. Wasting of the paraspinal muscles, for example, often occurs with chronic inflammatory conditions of the spine.

Movement of the spineThe movements of the spine should next be tested,including forward flexion, lateral flexion, extension


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and rotation. In the case of non-mechanical paindue to inflammatory or neoplastic conditionsthere is often a generalized restriction of all lum-bar movements. When pain is of a mechanicaltype and, therefore, likely to be suitable for treat-ment with acupuncture, only certain movementsare likely to be limited, and observing which theseare gives helpful guidance as to where TrPs arelikely to be found. TrPs are also often more readilypalpable when muscles are put on the stretch. Andfollowing treatment with acupuncture, it is wise tore-test the spine’s range of movements as in thisway attention may be drawn to TrPs that havebeen overlooked.

Examination of the patient lying downFor the second part of the examination the patientlies face upwards on the examination couch inorder that the abdomen may be examined for evi-dence of visceral disease. The femoral pulses shouldalso be palpated at this stage.

This should be followed by an assessment ofhip and knee movements, a neurological examin-ation, and the carrying out of the straight-leg raising test (Lasègue’s sign). A vaginal or rectalexamination should then be performed when indicated.

Search for TrPsThe final part of the examination and one thatshould be carried out especially carefully is asearch for TrPs. This is of particular importancewhen the pain is found to be of the mechanicaltype and due to some relatively benign structuraldisorder because it would seem that it is from acti-vated TrPs that much of this pain emanates. Thereason for saying this is that pressure applied tothese points aggravates the pain and relief from it may often be obtained simply by deactivatingthese points by means of the acupuncture tech-nique of inserting dry needles into the tissuesoverlying them. This search has to be conducted inan unhurried and systematic manner because,unlike the TrPs responsible for similar pain in theneck, which tend to be found at identical sites ineveryone, the distribution of TrPs in the lower

back has no fixed pattern and is in fact widelyvariable from person to person.

The patient should first be placed in the proneposition, and the muscles of the back from thelower thoracic region downwards should be palpated by placing the examining hand flat onthe back and rolling the skin and subcutaneous tissue over the underlying muscle by means offlexing fingers in a manner similar to that used inkneading dough.

TrPs in the lower back occur as focal areas ofexquisite tenderness either in muscle which other-wise feels normal, or in elongated fibrous bands ofmuscle (palpable bands) or in so-called ‘fibrositic’nodules.

It is a good rule to start the search by palpatingalong the length of the spine in the midline fromthe level of the 10th dorsal vertebra above, to thecoccyx below, and then systematically to examineevery part of the musculature on each side of theback in turn, by palpating along lines about 1 cmapart and parallel to the spine, from a similar levelabove, to the upper border of the buttocks below.The muscles of the buttocks should next be pal-pated, first using light pressure, and then deeppressure, and this should be followed by palpationof the muscles along the back of the leg.

The patient should then roll on to each side inturn so that the muscles of the flank can be pal-pated from the iliac crest above to the greatertrochanter below, with special attention being paidto the area around the latter structure as it is surpris-ing how often there is a crop of TrPs in musclesnear to their sites of attachment to it. The outerside of the thigh should then be palpated becauseit is common to find TrPs along the length of thetensor fasciae latae and iliotibial tract.

The examination should be completed by get-ting the patient to lie in the supine position andthe search for TrPs continued by palpating themuscles of the anterior abdominal wall and theinner side of the thigh, with special attention beingpaid to sites where the adductor muscles of the legbecome attached to the pelvis and the iliopsoasmuscle attaches to the lesser trochanter.

Back pain referred from TrPs in the abdominalwall musculature is discussed in Chapter 20. It isimportant to remember that TrPs in and aroundthe pubic region and the upper inner part of

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the thigh, at or near to the site of the attachment of the adductor muscles to the pelvis, may not onlybe associated with low-back pain, but on occasionsare responsible for pain being referred to the hipregion, to the scrotum, or to the vagina. It shouldalso be noted that it is activation of these TrPs thatsometimes makes a person with low-back paincomplain that the pain is worse on sitting down.The following case is a typical example.

A housewife (62 years of age) was referred to me withpersistent pain in the lower back and buttocks thatwas made worse both by certain movements and onsitting down. Dry-needle deactivation of many TrPs inthe lower back relieved her of much of the pain butthe pain on sitting persisted. There was no TrP in theregion of the ischial tuberosity to account for this butthere were some exquisitely tender ones at the sites ofinsertion of the adductor muscles into the pubis, andonce these were deactivated the sitting positionbecame comfortable.

An account of some of the commoner sites whereTrPs are to be found in the muscles of the lowerback, and their specific patterns of pain referral,will be given towards the end of this chapter. It is remarkable how often they coincide in positionwith traditional Chinese acupuncture points (seeFig. 17.1).

INVESTIGATIONS OF ASSISTANCE INDISTINGUISHING BETWEEN THEMECHANICAL AND NON-MECHANICALTYPES OF LOW-BACK PAIN

Erythrocyte sedimentation rate (ESR)The erythrocyte sedimentation rate, using thestandard Westergren technique, is one of the mostreliable means of distinguishing between these twotypes of low-back pain in view of the fact that withmechanical type low-back pain the rate is usuallynot above the upper limit of normal of 25 mm inthe first hour, whereas with disorders responsiblefor non-mechanical type pain the rate is in generalwell above this. One important exception is earlyankylosing spondylitis when the rate in about 20% of cases may for a time remain normal.

Plain radiographsAs will be seen when chronic low-back pain is con-sidered in detail later, there is no clearly definedrelationship between its development and theradiographic changes of disc or facet joint degen-eration. Also, with acute disc prolapse, the plain X-ray appearances are normal. In the assessmentof low-back pain of the mechanical type, therefore,there is little to be learnt from plain radiographs of the spine. The main importance of having themis to exclude non-mechanical causes of low-backpain including infective, inflammatory, and neo-plastic lesions. It is essential to bear in mind, how-ever, that in the early stages of such disorders theradiographic appearances may be normal, and,therefore, at times it is wise to have a technetiumscan. It is believed that an increased uptake of thisradioisotope is dependent on an increased boneblood flow and metabolism, and as this is commonto all these various diseases, it necessarily followsthat a positive result does not distinguish betweenthem, but does serve to rule out the possibility of


a

ab

Figure 17.1 The traditional Chinese (a) Urinary bladderand (b) Du acu-tracts.

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the pain being only mechanical in type (McKillop &McDougal 1980).

Magnetic resonance imagingMRI, which was introduced in 1982 has proved tobe of considerable help in the investigation of low-back pain disorders (Kleefield & O’Reilly 1992).

SOME CAUSES OF MECHANICAL TYPELOW-BACK PAIN AND THEIRMANAGEMENT

There are many potential causes of low-back painof the mechanical type, both psychological andphysical, and frequently, several of them con-tribute to the condition simultaneously. The situ-ation is further complicated by the fact that theexact manner in which some of the factors operateremains obscure. There can be no doubt that it is because of such difficulties that the managementof this type of pain remains far from satisfactory,and why the effects of most forms of treatment for it, including acupuncture, are notoriouslyunpredictable.

It was because of this that Nachemson (1979)was prompted to say:

Having been engaged in research in this field for nearly 25 years and having been clinicallyengaged in back problems for nearly the sameperiod of time and as a member and scientificadviser to several international back associations,I can only state that for the majority of our patients,the true cause of low-back pain is unknown …since the cause is unknown there is only symptom-atic treatment available.

This undoubtedly is true, so the remainder ofthis chapter will be devoted to reviewing the clin-ical characteristics of the various structural dis-orders in the lower back considered to be capableof giving rise to pain of the mechanical type, andexamining the various neurological mechanismsthought to be responsible for this. An attempt willalso be made to evaluate the various forms ofsymptomatic treatment available, in order to assesswhich of them in the light of our present knowledgeseem to be based on sound physiological principles.

The purpose of this is to show that acupuncturemay be included amongst these, and that there ismuch to be gained by using it, either in conjunc-tion with, or at times instead of, some of theseother so-called more orthodox forms of treatment.

During the course of this review it will beobserved how often with many of these structuraldisorders, MTrPs are an important source of pain.The activation of points is sometimes a primaryevent and at other times a secondary one. There isa need for wider recognition of this phenomenonnow that it has been shown that deactivation ofthese points by the acupuncture technique of dryneedle stimulation is not only frequently effectivein alleviating low-back pain, but also is both sim-ple to apply and safe to use, this being more thancan be said for some of the more complex forms oftreatment in current use.

ACUTE LOW-BACK PAIN

The description of Mixter & Barr in 1934 of thesymptoms and signs of a prolapsed intervertebraldisc (PID) and how the pain from this conditioncan often be relieved by a laminectomy wasundoubtedly of considerable importance. However,since the chemistry of the intervertebral disc hasbecome better understood (Urban & Maroudas1980), it is now recognized that PID as a cause ofacute low-back pain must be a comparatively rareevent. The reason for this is that the central nucleuspulposus of a disc, over the years, becomesincreasingly inspissated, and it is only possible forit to bulge through a ruptured annulus fibrosusand impinge on a nerve root, whilst it still remainsin a relatively fluid state. This is approximately upto the age of 50 years, and during this earlier partof adult life rupture of an annulus fibrosus isuncommon because the degenerative changes arestill at an early stage.

As Dixon (1980) rightly points out, disc pro-lapse is probably the most overdiagnosed cause oflow-back pain, and goes on to state that ‘indeedthe whole myth of the “slipped disc” is one of thedeep rooted weeds that have sprung up in thisarea. Discs do not “slip” in the way in which lay-men and not a few doctors imagine’. He believesthat this over-diagnosis may be due to the fact thatmost patients with proved prolapse give a history

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of past episodes of acute low-back pain withoutnerve root compression, and that the diagnosis isoften one of convenience. Wyke (1980) in supportof this view estimates that ‘contrary to popularimpression … less than 5% of patients with back-ache have prolapsed intervertebral discs’, but atthe same time agrees that 70% of those with PIDhave backache as the initial symptom.

It is now generally accepted that acute mechan-ical type low-back pain is most commonly due tosome primary disorder of muscle, for example,such as when the tendinous attachments of musclesbecome avulsed, or muscle fibres and their fascialsheaths become torn as a result of the lower backmuscles being suddenly overloaded as a result of aheavy object being lifted in the stooping position or,for example, when the muscles become strained bybeing overloaded for some considerable time.Alternatively, it may occur when the back isexposed to draughts or damp, or, at times, for noobvious reason. Formerly, its development undersuch circumstances led to a diagnosis of fibrositis ormyositis, or more recently to one of myofasciitis. Aspreviously explained (Ch. 5) all such terms are nolonger acceptable as inflammatory changes in themuscle have never been demonstrated.

Acute low-back pain also commonly occurswhen the nociceptive receptor systems in eitherthe fibrous capsules of the facet joints or the lum-bosacral ligaments become stimulated as a resultof the spine being subjected to persistent posturalstress. The clinical picture, irrespective of thestructure or structures involved, is one of acutelocalized pain with reflex spasm of the paraverte-bral muscles, and the presence of exquisitely ten-der TrPs. This picture is identical to that seen withthe much rarer acute disc prolapse at a stagebefore pain extends down the leg. With regard tothe activation of TrPs, the only difference is thatwith disorders of the muscle or ligaments the acti-vation is a primary event, but with facet jointstrain or disc prolapse it is a secondary one.

It therefore follows that with the developmentof acute low-back pain, because of the difficulty in distinguishing clinically between these variouscauses, it is impossible to make a precise diagno-sis, and it is better, in my opinion, to refer to allsuch cases as being examples of the acute lumbarmyofascial TrP pain syndrome. This at least helps

to guard against the all too frequent error ofassuming that acute low-back pain must be due toa ‘slipped disc’, and for this reason alone, auto-matically subjecting the person concerned to aperiod of strict bed rest without first of all carryingout a detailed examination. Admittedly acute low-back pain may require bed rest, but it is essentiallythe severity of the pain that dictates when this is necessary. Bed rest should certainly never beprescribed without there first being a systematicsearch for TrPs, because, when present, the deacti-vation of these by acupuncture by alleviating thepain may obviate the need for bed rest, or it mayshorten the period for which it is required, as isillustrated by the following case.

A housewife (38 years of age) suddenly developedsevere pain in the left lower back after bending forsome time doing some strenous gardening. Shetherefore took to her bed and called the doctor. Afterlistening to the story, he told her she must have‘slipped a disc’, and that she would have to lie flat onher back for 2–3 weeks. This immediately created adomestic crisis as she and her family had planned todrive to Switzerland 2 days later. The husbandtherefore persuaded the general practitioner to let me see her.

On examination she was lying very still andreluctant to move because of the pain it caused.When, after a certain amount of persuasion, she rolledover sufficiently for her back to be examined, onefocal area of exquisite tenderness in the left flank wasfound, with pressure on this considerably aggravatingthe pain. After deactivating this TrP with a dry needle,the patient was more comfortable. When seen thenext day, she reported that the pain relief had onlylasted for about 2 hours, and on re-examination theTrP was as tender as before. It was, therefore, onceagain deactivated with a dry needle, and this time thepain relief was longer lasting, so that 24 hours latershe was able to set off on the journey to Europewithout any discomfort.

Spontaneous resolution of acute low-back painIt could be argued that in the case just quoted thepain might have resolved spontaneously within afew days, but from its severity and the degree of


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muscle spasm present, this would seem to havebeen unlikely.

Nevertheless, it is important to remember inassessing the effects of any form of treatment foracute low-back pain that most of those who sufferfrom it become symptom-free in 4–6 weeks irre-spective of treatment (White 1966, Rowe 1969) andas Waddell (1982) says in discussing the subject‘frequently treatment simply takes the credit fornatural history and the passage of time’.

This no doubt is true but acute low-back painthat persists for 4–6 weeks can often seriouslyinterfere with a person’s ability to work or to carryout sporting activities, and if it can be shown, asmy everyday clinical experience would lead me tobelieve, that acupuncture by its direct action onTrPs is capable of alleviating the pain more quicklythan might be expected if left to resolve spontan-eously, then such treatment is obviously wellworth using. The difficulties of proving this statis-tically, however, are formidable as with a condi-tion with such a relatively short natural history,the numbers of cases required both for the treat-ment and control groups would be extremely large,and in order that such a trial could be completedin a reasonable time, many centres would have toparticipate.

ACUTE SCIATICA

Following Mixter & Barr’s important contributionto the subject of acute disc prolapse in 1934, itbecame generally assumed that the diagnosis ofthis condition, and that of acute sciatica were synonymous and, moreover, it was also widelybelieved that the sciatic pain was invariably due tothe disc exerting pressure on a nerve root.

In recent years it has been found necessary tomodify these concepts because, although it isundoubtedly true that acute sciatica may occurwhen a disc is sufficiently badly prolapsed as toexert pressure on a nerve root, it is now realizedthat acute pain along the course of the sciatic nerveis more often due to it being referred down theback of the leg from TrPs in the muscles of thelower back. These TrPs become activated either asa result of a partially prolapsed disc causing the back muscles to go into spasm, but even more

frequently as a result of the muscles being sub-jected to strain during the course of some physicalactivity.

Firstly, therefore, a description will be given ofthe clinical picture that arises when acute sciaticais caused by a badly prolapsed disc pressing on anerve root, and following this, acute sciatica of thereferred type will be discussed.

Acute prolapse of a disc with ‘sciatica’ due to pressure on a nerve rootThere is often a history of recurrent episodes oflow-back pain before the eventual sudden onset ofsciatica with a severe shooting type of pain thatradiates from the lower back, down the leg to the foot.

The discs most likely to prolapse include theone between the 4th and 5th lumbar vertebraewith involvement of the 5th lumbar nerve root,and the one between the 5th lumbar vertebra andthe sacrum with involvement of the 1st sacralnerve root. Much less commonly, the disc betweenthe 3rd and 4th vertebrae prolapses with involve-ment of the 4th lumbar nerve root.

With involvement of the 5th lumbar nerve root,pain is felt in the buttock, down the posterolateralaspect of the thigh and leg, and over the inner halfof the foot; dorsi flexion of the toes is weak; andthe tendon reflexes are normal.

With involvement of the 1st sacral nerve root,pain is felt in the buttock, down the back of thethigh and leg and along the outer side of the foot;plantar flexion of the foot is weak and the anklejerk diminished.

With the less common involvement of the 4thlumbar nerve root there is pain down the outerside of the thigh, and the inner side of the leg.There is weakness of knee extension and a dimin-ished knee jerk. The pain in the buttock and thigh,no matter which root is involved, is associatedwith widespread muscle tenderness and the spasmof paravertebral muscles leads to the spine becom-ing rigid with a loss of the normal lumbar lordosisand the development of a scoliosis.

In addition to nerve root pain, there is at anearly stage of the disorder pain in the back broughtabout as a result of an inflammatory reactioncaused by the liberation of phospholipase A-2 and

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other enzymes from the nucleus pulposus followingits extrusion (Saal et al 1990). This particular typeof pain is always worst during the first 3 weeksdue to the extruded disc absorbing water and,because of this, temporarily increasing in size.

Eventually, the prolapsed disc becomes smallerpartly because of a gradual decrease in its fluidcontent, but also because of enzymatic resorptionand phagocytosis together with resolution of theinflammatory process. It is because of all this that,after a period of time, discogenic pain tends to disappear spontaneously, and this is also why con-servative treatment in some cases is all that isrequired.

Factors that aggravate the pain

Disc pain is aggravated by sitting, lifting andmovements that twist the torso. Relief is usuallyobtained by lying down. It is also invariably madeworse by coughing, sneezing and straining to openthe bowels.

Influence of the vertebral canal‘s size on the pain

Porter (1993), from carrying out MRI studies, hasfound that the factor that determines whether ornot pain is felt with a disc lesion is the size andshape of the vertebral canal. He compared the ver-tebral canal measurements in 173 patients withdisc protrusion with 671 healthy controls, and foundthat it is those with disc lesions who have particu-larly small canal measurements and, therefore whoare particularly likely to suffer pain. However, it isnot only the size of the canal, but also its shapethat matters, with a small trefoil-shaped canalbeing particularly disadvantageous.

Straight leg-raising test (Lasègue’s sign)

This test involves the passive flexion of the leg atthe hip with the knee straight. The test is said to bepositive when there is a restriction of movement to45º or less.

This test is positive with compression of the 5th lumbar or 1st sacral nerve roots, and for manyyears subsequent to Mixter & Barr’s original paperin 1934 it was thought that limitation of straight

leg-raising only occurs when there is pressure on a nerve root by a prolapsed intervertebral disc.Therefore, nobody was surprised when Edgar &Park (1974) found the straight leg-raising test to bepositive in 94% of patients with a surgically con-firmed prolapse pressing on a nerve root, or that in95% of such cases, pain could be induced in theaffected leg by raising the opposite leg (the wellleg-raising test). Such teaching, however, has hadto be revised since King & Lagger (1976) haveshown that a positive Lasègue’s sign also occurswith acute sciatica of the referred type, and that insuch cases it can be reversed by interrupting thearc between the posterior primary division, thecord, and the anterior primary division of a rootsegment. This no doubt explains why Spangfort(1972), in a computer-aided analysis of 2504 oper-ations, found that of those patients with acute sciatica shown not to have a prolapsed disc atoperation, 88.8% of them had a positive Lasègue’ssign pre-operatively.

It therefore now has to be accepted that therestricted straight leg-raising that occurs withacute sciatica is not necessarily indicative of nerveroot entrapment as it also occurs when the pain isof the referred type.

TrPs

Activation of TrPs in the muscles of the back andleg is a prominent feature in all cases of acute discprolapse. Chu (1995), during the course of carry-ing out electromyographic studies, has shown thatTrPs in the paraspinal muscles commonly becomeactivated as a secondary event following thedevelopment of nerve root entrapment. Simons etal (1999) attribute this to compression of motornerves activating and perpetuating primary TrPdysfunction at the motor endplate.

Radiographic examination

A plain X-ray of the spine is never of help in thediagnosis of acute disc prolapse because, asexplained earlier, it always takes place at a time oflife when disc degeneration is at an early stageand, therefore, before there has been time for nar-rowing of the intervertebral space to take place.

The best means of confirming the presence of adisc prolapse is by the carrying out of MRI. With


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respect to this, however, it has to be rememberedthat it is not uncommon for disc protrusion todevelop without it giving rise to nerve root entrap-ment. Jensen et al (1994) showed this when theycarried out a MRI study of the lumbar spine inpeople without back pain and found an appre-ciable incidence of disc prolapse.

It, therefore, follows that evidence of such a lesionon MRI cannot be assumed to be the cause of anypain that may be present unless there are clinicalsigns of nerve root entrapment at the same seg-mental level as that indicated on the scan.

Acute sciatica of the referred type

From what has been said it is clear that a confidentdiagnosis of disc prolapse with acute sciatica dueto the entrapment of a nerve root can only be madewith any degree of confidence when there areobjective neurological signs, including motorweakness followed later by muscle wasting, sens-ory impairment, suppression of tendon reflexes,and, particularly, if it is possible to obtain con-firmatory evidence of nerve root compression bythe carrying out of MRI.

With most cases of acute sciatica, however,there is no neurological deficit and the pain isreferred from TrPs in the muscles and ligaments of the lower back. King & Lagger (1976) believethat this occurs when a partially prolapsed discimpinges on the sinu-vertebral nerve causing theparavertebral muscles and adjacent ligamentsinnervated by posterior rami to go into acute spasm,with this, in turn, causing TrPs in these structuresto become activated. The consequence of this, toquote King & Lagger, is that ‘pain impulses initi-ated in these posterior rami areas are referred toareas innervated by the anterior rami of the sameand juxtaposed spinal roots’. In support of theirhypothesis is their ability to alleviate this type ofpain and, at the same time, to render negative theLasègue’s sign by interrupting this arc betweenthe posterior rami, the cord, and the anterior rami,by deactivating these TrPs. It is only a pity that the methods they chose to use in order to achievethis were somewhat unnecessarily complicated andincluded radio-frequency percutaneous rhizotomy(Shealy et al 1974) and multiple bilateral percuta-neous rhizolysis (Rees & Slade 1974).

The concept, however, that radiation of paindown the leg, in patients with low-back pain, is not necessarily due to nerve root entrapment and thatsometimes it may occur as a result of it beingreferred down the leg from TrPs in the musclesand ligaments of the back, is not a recent one. Itwas first put forward by Steindler & Luck (1938),when they showed that it is possible to alleviatenot only the pain in the back, but also the paindown the leg simply by injecting procaine into aTrP in the lumbar region. It was their observationsconcerning this that led them to develop their pro-caine hydrochloride test for use in patients withboth low-back and leg pain. The test consists ofinjecting procaine into a TrP situated in a lumbarmuscle or ligament in order to prove whether ornot it is from that point that both the low-back and leg pain emanates. Such proof, according tothem, required the following five postulates to befulfilled:

1. The insertion of the needle into the TrP mustaggravate the local pain in the back.

2. The insertion of the needle into the TrP mustelicit or aggravate the pain referred down theleg.

3. The injection must suppress the referred pain.4. The injection must suppress local tenderness.5. Limited lumbar flexion or straight leg-raising

must return to normal following the injection.

It is of course now recognized that with referredleg pain from TrPs in the back it is possible to ful-fil these criteria of Steindler & Luck even moresimply just by inserting an acupuncture needle intothe tissues overlying them. This, however, in noway detracts from the importance of their work,and it is only very much to be regretted that untilrecent years such little attention has been paid tothe basic principles propounded by them.

It is clear from what Steindler & Luck had to sayon the subject that they believed that with mostcases of sciatica of the referred type, the painstemmed from TrPs activated by what they termeddeep ligamentous injuries and myofasciitis.However, the possibility, as suggested by King &Lagger, that such activation may also develop as aresult of partial prolapse of a disc does not seem tohave occurred to them.

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There is no doubt that this type of referred painmay be produced by either of these means but,because, for reasons already given, a prolapseddisc is somewhat of a rarity, the commonest causewould seem to be an acute primary strain of themuscles and ligaments.

Management of disc prolapse

Surveys, such as those carried out by Friedenberger& Shoemaker in 1954 and by Weber in 1983 haveshown that immediate surgery is only required forthose with a midline disc rupture causing dys-function of the bowel or bladder. All other patientswith this disorder should initially be treated conservatively, as only a minority of them willultimately be shown to need surgery.

Conservative treatmentShort-term bed rest followed by mobilization

Complete bed rest may be required for the first 1–2weeks. This should be followed by increasingmobilization and the eventual carrying out of aprogressive exercise programme (Manniche et al1991, Saal & Saal (1989), Wynn Parry 1994).

Analgesics and corticosteroids Pain controlrequires the use of analgesics. In addition, because itis now recognized that much of the initial pain isdue to an inflammatory reaction brought about by enzyme release and the consequent liberation ofprostaglandins and leukotrienes, corticosteroids arebeing increasingly used. A drug of this type may be administered either orally (Johnson & Fletcher1981), or intramuscularly (Green 1975), or, evenmore commonly, intrathecially. Bogduk (1995), how-ever, during the course of questioning the value of using the latter route has stated, ‘there is no compelling data from double-blind trials that vindi-cate the use of lumbar or caudal epidural steroids’.Despite this, an injection of this type continues to be widely used for the suppression of nerve rootinflammation. Currently it is invariably givenunder fluoroscopic control (Dreyfuss 1993).

Indications for surgical intervention The gen-eral consensus of opinion is that a discetomyshould be carried out in those cases where there isa worsening of the symptoms over the months,together with a progressively increased restrictionof straight leg raising and deviation of the lumbar

spine to one side. Other indications include painevoked by contralateral straight-leg raising and aloss of diurnal changes in straight leg raising onthe affected side. With a partial disc rupture thediurnal change with this test may be as much as30°, but once the rupture is complete this is nolonger observed and the prognosis without sur-gery is poor (Porter & Trailescu 1990).

Post-laminectomy pain One of the commonestreasons for the persistence of pain following alaminectomy is overlooked TrP activity in the lum-bar muscles (Gerwin 1991). These TrPs may havebecome active either pre-operatively or as a resultof the traumatisation of muscles during the oper-ation. They may also develop in incisional scars. Ittherefore follows that in all cases where pain per-sists following a laminectomy a search for TrPs isessential and when found to be present deacti-vated by means of the carrying out of superficialdry needling. The one exception to this is whenTrPs in the paravertebral musles have become acti-vated as a secondary event following the develop-ment of nerve root compression pain when deepdry needling should be employed (Chu 1995).

There are two other much less common reasonsfor the pesistence of pain post-operatively. Theseare: (1) infection in the disc space (Fouquet et al1992), and (2) the development of arachnoiditis(Ransford & Harries 1972, Symposium 1978).

With respect to all this, it has to be said that,even when strict criteria for surgery are adheredto, there is no certainty that removal of the discwill alleviate the pain. Spangfort (1972), in a reviewof the results of 2504 laminectomies selected forsurgery because of clear-cut neurological signs ofnerve root entrapment, found that complete reliefof both leg and back pain occurred in only 60% ofcases.

Failure to relieve pain in those with nerve rootentrapment is usually attributed to one or other ofthe following causes:

● The exploration being carried out at the wrongsite.

● A second disc prolapse being overlooked.● The nerve root continuing to be compressed by

the posterior intervertebral joints.● Spinal stenosis causing pressure on the nerve

root.


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● An extraforaminal lateral disc herniation,though this is rare (Nelson 1980).

It may also be due to chronic irreversible nervedamage having developed prior to the operationbeing carried out (Wynn Parry 1989).

Spinal fusion When pain due to a prolapseddisc is not relieved by laminectomy it is notuncommon to attempt to provide structural sup-port for the spine by means of fusing together sev-eral vertebrae. The results of this operation in suchcircumstances have, however, been very disap-pointing leading Loeser (1980), somewhat tersely,to remark:

… the greatest folly of all in the management oflow-back pain is the use of fusion of the verte-brae in the absence of demonstrated instabilitydue to a congenital or acquired lesion. There sim-ply is no good evidence that fusion is ever bene-ficial to the patient with only a herniated lumbardisc; there is considerable evidence that it maybe deleterious. Why patients are subjected to amajor operative procedure with no evidence ofefficacy is beyond my comprehension.

There can be no doubt that one of the major disadvantages of the operation is that by render-ing the spine rigid it seriously interferes with the low-threshold mechanoreceptor pain-inhibitingmechanism (Ch. 6), as the action of the latter isentirely dependent on an ability to carry out nor-mal movements. Also, the rigidity of the backseems to put an abnormal strain on the paraverte-bral muscles, and this in itself must encourage theactivation of MTrPs. In addition, it is not uncom-mon to find iatrogenically induced TrPs in themidline surgical scar.

Patients who have come under my care withpersistent pain in spite of having had a spinalfusion following failed laminectomy have, notunnaturally, been very depressed, particularly asmost of them have been told that, other than thelong-term use of analgesics, there is nothing morethat can be done. Each one without exception,however, has been found on examination to havereadily demonstrable TrPs and it has been possibleto improve the quality of life by repeatedly deacti-vating these points with a dry needle. Unfortunately,and probably mainly because of the mechanical

disadvantage to which the operation puts thespine, the pain relief from acupuncture is seldomlong-lasting and the necessity of having to con-tinue with treatment on a long-term basis has to be explained to the patient at the outset in order to avoid any undue disappointment.

In conclusion, it has to be said that when painpersists following a laminectomy, it is firstlyessential to ascertain that it is not due to residualnerve root compression, but once this has beenexcluded, it is better to attempt to alleviate thepain by the acupuncture technique of deactivatingTrPs rather than to embark on a spinal fusion thatleaves the spine permanently rigid and rarelyrelieves the pain.

CHRONIC MECHANICAL TYPE LOW-BACK PAIN

The pathogenesis of chronic mechanical type low-back pain is poorly understood, and as a con-sequence of this both the manner in which thecondition is investigated, and its treatment are farfrom satisfactory (Flor & Turk 1984, Turk & Flor1984). The greatest obstacle to the rational treat-ment of chronic low-back pain is the difficulty ofdeciding in any particular case the primary sourceof the pain. The main possibilities are that the paincomes either from degenerative changes in the inter-vertebral discs and facet joints, or from MTrPs.

Pain arising from degenerative changes in the intervertebral discs andfacet jointsThere can be no doubt that degenerative changesin the spine are potentially capable of causing low-back pain for, as Wyke (1987, p. 59) has pointedout, the structures in the vicinity of the spine inwhich nociceptive receptor systems are presentinclude the spinal ligaments, the periosteum, theduramater, the walls of the blood vessels, and alsothe fibrous capsules of the facet joints.

It is generally believed that the degenerativechanges in the spine start first in the discs, and thatit is the reduction in the vertical height of the lumbarspine occurring as a result of this that encouragesthe development of arthritic changes in the facetjoints (Vernon-Roberts & Pirie 1977).

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Hirsch et al (1963) were among the first to showthat the facet joint is a potential source of chronicback pain by showing that pain in the back and legcan be artifically induced by injecting 11% hyper-tonic saline around it.

Mooney & Robertson (1975) studied the mattermore specifically by injecting 5% hypertonic salineinto a facet joint in five normal individuals and 15patients with chronic pain in the back and leg.They first ensured that the needle was directly inthe joint by means of inserting it under fluoro-scopic control and then injected sufficient contrastmedium into the joint to outline its capsule. Ineach case, within about 5 s of injecting the hyper-tonic saline, pain was felt in the lower back, andwithin 20 s, this had increased in intensity and hadspread to the greater trochanter and down the pos-terolateral part of the thigh. Such pain patterns,however, are in no way specific. Similar ones havebeen produced, as discussed in Chapter 4, byKellgren, and also by Inman & Saunders, by inject-ing hypertonic saline into muscles and ligaments,and the possibility cannot be excluded thatMooney & Robertson’s hypertonic saline did notremain confined to the facet joints, and, by dif-fusing into the tissues, it may have also stimulatedother structures in the vicinity.

Fairbank et al (1981) have also studied theeffects of injecting a local anaesthetic into facetjoints for the purpose of ascertaining whether ornot this procedure might act as a diagnostic aid. Intheir study, 25 adults suffering for the first timefrom severe low-back pain, were given an injec-tion into a facet joint under X-ray control. The facetjoints selected for injection were situated at pointsof maximum tenderness. Their results were that 14obtained immediate relief (the responders) and 11did not (the non-responders). They concluded thatthis might suggest that the responders had pain ofmechanical origin possibly arising in the facetjoint, and that the non-responders’ pain may haveoriginated from one of the many other possiblesources in the back.

The reason for their conclusions being so tenta-tive was that they were aware that the anaestheticmay not have remained confined to the facet joint,but may have diffused out into the tissues toinvolve the nerve root or the posterior primaryramus, and that this, in turn, may have affected

other structures with a common innervation. It isof course possible that by using points of max-imum tenderness for their injection that the anaes-thetic was acting on nerve endings at TrPs because,as they admitted, Lewit (1979) had alleviated painof this type simply by inserting dry needles intosuch points.

It may therefore be seen that various experi-mental studies aimed at showing whether or notfacet joints are an important source of low-backpain have been somewhat inconclusive, and cer-tainly observations by pathologists and above allby radiologists, would seem to suggest that thewidely-held view that chronic mechanical typelow-back pain, from middle age onwards, is mainlydue to degenerative changes in the lumbar discsand facet joints, is almost certainly erroneous.

It was in 1932 that Schmorl & Junghanns, fromtheir classic autopsy studies of over 4000 spines,established that degenerative changes in the lum-bar spine are present in 50% of the population bythe end of the 4th decade, in 70% at the end of the5th decade, and in 90% at the age of 70. And sincethen, numerous comparative studies by radio-logists have shown that the radiographic features of disc degeneration, including the narrowing ofintervertebral spaces, osteophyte formation, disccalcification, and Schmorl’s nodes, as well as thoseof facet joint arthrosis, are found as commonly inasymptomatic controls as they are in those withlow-back pain (Splithoff 1952, Hult 1954, Hussar &Guller 1956, Horal 1969, Magora & Schwartz 1976).

Furthermore, there is also no evidence to sug-gest that the intensity of lumbar pain is in directproportion to the amount of degenerative changesseen on a radiograph. It is not uncommon for aperson with only slight changes to have severepain, and conversely, for a person with advancedchanges to be symptomless.

It would therefore seem that, whilst degenera-tive changes in the spine may make some con-tribution towards the development of chroniclow-back pain, there is no direct correlationbetween the two, and in everyday clinical practiceit would seem important not to assume justbecause there is radiographic evidence of disc andfacet joint degeneration that this is necessarily thecause of the pain, as often this is not more than achance investigatory finding in someone whose


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pain can be shown to be primarily muscular in ori-gin. Waddell (1982), with considerable wisdom,comments:

… the case for degenerative disc disease as theexplanation of backache must still be regarded asnot proven. It is important to treat patients andnot X-rays of spines.

Lumbar facet joint syndrome

All this not withstanding the lumbar facet jointsyndrome is still currently considered by many tobe a clinical entity, despite it having no generallyaccepted pathognomonic symptoms or physicalsigns (Jackson et al 1988, Schwarzer et al 1994a). Itis for this reason that the diagnosis has to be madeby determining whether or not the pain is allevi-ated by injecting, under fluoroscopic control, alocal anaesthetic into any joint that on deep palpa-tion is found to be markedly tender or one that,when put through movements, is found to bepainful.

Diagnostic facet joint block procedure Originallyonly one local anaesthetic was employed but thisgave such an unacceptably high false-positiveresponder rate that it is now recommended thatthe test should be carried out using firstly a short-acting one (lidocaine [lignocaine]) and followingthis a longer acting one (bupivacaine). Analgesiahas to be obtained with both for a patient to beconsidered a true responder. Unfortunately, how-ever, even with this Schwarzer et al (1994a) had afalse-positive rate of 38% and they also found(Schwarzer et al 1994b) that the prevalence ofchronic low-back facet joint pain was only 15%.

Treatment The treatment of this disorder is toinject a cortocosteroid/local anaesthetic into thesuspected painful joint. There have been two con-trolled trials to assess the efficacy of this. In thefirst carried out by Lillius et al (1989) patientsjudged from a facet joint diagnostic block to havefacet joint pain were randomly divided into threegroups. Two of these were given either an intra-articular injection of a steroid/local anaestheticmixture or a pericapsular injection of it. The thirdgroup was given an injection of saline into theaffected joint. It was found that these three types

of treatment gave similar results with only 36% ofthe patients overall achieving pain relief lastingfor 3 months.

The second trial was carried out by Carette et al(1991), in which the treatment group received anintraarticular injection of prednisolone and thecontrol group an intraarticular injection of saline.Only 42% in the treatment group and 33% in thecontrol group had significant pain relief lasting 3 months.

It may therefore be seen from the results ofthese two trials that any pain relief provided by asteroid injection was only obtained in a disap-pointingly small number of patients, and that asaline injection proved to be equally pain reliev-ing. One possibility is that any pain relief obtainedwith either of these was simply due to the one fac-tor common to both, i.e. the stimulating effect ofthe needle used for the injection on nerve endings.

Deyo (1991), during the course of commentingon what was found in both these trials, offeredanother explanation when he said:

The poor results of these two studies may haveoccured because, despite careful diagnosticefforts, many patients had a source of pain otherthan the facet joints, or because a corticosteroidinjection is inefficacious even when a facet jointis the source of the pain. In either event, the formof treatment appears to be over-used and min-imally effective.

Jackson (1992), 1 year later, with commendableperspicacity posed the question: ‘the facet syn-drome, myth or reality?’ and concluded that hisprovocative question could only be answered bythe carrying out of further clinical trials.

Chronic lumbar myofascial TrP pain syndromeThose currently responsible for teaching medicine,when considering the causes of mechanical-typelow-back pain, tend to dismiss pain of muscularorigin as being of little or no consequence, andhardly worthy of their attention. This is no doubt,in part, not only because the pathology of theunderlying condition continues to remain so sin-gularly elusive, but also because it is now generally

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agreed that the condition is not of an inflamma-tory nature and, therefore, diagnoses such asfibrositis and myofasciitis are no longer acceptable,so there is even difficulty in knowing what to callthe condition!

Everyday clinical experience, however, leadsme to agree with Wyke (1987, p. 74) that irritationof the nociceptive receptor system in the lumbarmuscles, their fascial sheaths, their tendinousinsertions, and in the ligaments of the spine is acommon cause of chronic low-back pain. Thisoccurs either directly as a result of various factorsto be discussed acting locally on the muscle or liga-ments, or indirectly, as a result of anxiety causingthem to be held in a state of persistent tension.There can be no doubt that mechanical type low-back pain that is primarily muscular in origin isfrequently both severe and incapacitating; and itmay affect not only adults, but also children (Bates &Grunwald 1958, Grantham 1977).

Careful examination of the lumbar muscles andthe supraspinous ligament in someone withchronic mechanical type low-back pain frequentlyreveals the presence of focal points of exquisitetenderness. In the lower back these points may befound in muscle that otherwise feels normal, butoften they are present in palpable bands orfibrositic nodules that develop in the substance ofthe muscles. Of particular significance is the factthat pressure applied to these points exacerbatesany pain felt locally in the back, and at timescauses pain to radiate down the leg in the samedistribution as that occurring spontaneously. Thisof course is no recent observation for, as explainedin Chapter 4, Kellgren first drew attention to thesignificance of ‘tender spots’ in muscles as progeni-tors of musculoskeletal pain nearly half a centuryago, and once Janet Travell shortly after this, forobvious reasons, called them TrPs, she and othershave written extensively about them.

Unfortunately, when the idea that TrPs might be an important source of low-back pain was firstput forward, the climate of opinion was against it due to the medical profession in the Westernworld at that time being firmly wedded to thebelief that acute ‘lumbago’ and sciatica are princi-pally caused by the prolapse of an intervertebraldisc, and that chronic ‘lumbago’ and sciatica occur

as a result of degenerative changes in the discs andfacet joints.

This for many years was to remain one of thedeeply entrenched beliefs of medical orthodoxy. Itis, therefore, very much to the credit of St ClaireStrange, that in his Presidential address to the section of orthopaedics of the Royal Society ofMedicine, London, in 1966, he had the boldness toquestion the validity of this view by stating that,whilst he had no doubt that such lesions may attimes be the cause of low-back pain, he was certainfrom his everyday clinical experience that theywere not the only ones, and that, in investigatingsuch pain, more attention should be paid to exam-ining the muscles for points of maximum tender-ness in what he termed ‘muscle bundles in spasm’that are, ‘sometimes “as slender as the shaft of apin” and at other times “as thick as a pencil” ’, orin other words to look for what today would becalled TrPs in palpable bands. His insistence onthe importance of such an examination stemmedfrom his belief that it is from these structures thatmuch of the pain emanates, for, as he said, whenyou press on one of these tender spots ‘the patientknows you have “found the spot”, found the siteof the pain from which he is complaining. Andyou can see it in his face’.

Since the 1930s, therefore, a succession of peoplehave drawn attention to the importance of TrPs inthe aetiology of musculoskeletal pain, includingthat which affects the lower back, and yet thosecurrently engaged in research into the problems oflow-back pain still pay scant attention to them.

However, now that such leading authorities onthe neurophysiology of pain as Melzack & Wall(1982) have come to recognize the importance ofTrPs in the genesis of musculoskeletal pain in gen-eral, those engaged in investigating and managingchronic mechanical type low-back pain can nolonger afford to ignore the part played by thesestructures in its development.

There is, as yet, no adequate explanation as towhy some people more than others are prone toactivate TrPs in their lumbar muscles, and for thisreason to be particularly liable to suffer from chroniclow-back pain. Certainly there is no definite evi-dence that structural disorders of the spine makeany significant contribution to this. Admittedly, it


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is theoretically possible for MTrPs to become acti-vated as a result of structural disorders of the spinecausing the lumbar muscles to go into spasm, but,as has already been discussed, so far as degenera-tive changes are concerned, a number of well-controlled studies have failed to show any directrelationship between the presence of radiograph-ically observable degenerative changes in the discsand facet joints, and the development of inter-mittently recurrent low-back pain.

There is, in addition, no definite evidence thatother structural disorders such as sacralization ofthe spine, spondylolisthesis, or various abnormalcurvatures of the spine are associated with theactivation of TrPs. It has, for example, been gener-ally assumed that the abnormal fusion that some-times occurs between the 5th lumbar vertebra andthe sacrum – so-called sacralization of the spine –is a cause of chronic low-back pain, but Magora &Schwartz (1978), from their extensive survey, wereunable to confirm this.

Similarly, although the forward shift of one vertebra or another – so-called spondylolisthesis –has been said to contribute to the development ofchronic low-back pain, the evidence for this is con-flicting with some observers such as Hult (1954),Horal (1969), and Torgerson & Dotter (1976) sup-porting this belief, but with others, includingSplithoff (1952) and Rowe (1965), being unable todemonstrate such a relationship.

Furthermore, although congenital or acquiredabnormalities such as scoliosis, kyphosis, exagger-ated lordosis, and spina bifida occulta have allbeen assumed to cause chronic low-back pain, sev-eral studies including those of Hult (1954), Horal(1969), Torgerson & Dotter (1976), and Magora &Schwartz (1978) have failed to confirm this.

Before leaving the subject of the possible activ-ation of TrPs in response to structural disorders inthe spine, the following observations will be madeconcerning the most common of these, namelydegenerative changes in the discs and facet joints.

Although myofascial TrPs are frequently foundto be present in cases of mechanical type low-backpain, where degenerative changes are demonstrableradiographically, there is no correlation betweenthe number of TrPs present and the amount ofdegenerative change in the spine; furthermore,

distribution of the TrPs in the back often bears norelationship to the part of the spine affected bydegenerative changes, and when one comes toconsider the treatment of low-back pain by theacupuncture technique of dry needling TrPs, experi-ence shows that it is wrong to assume that thechances of a good response diminish in proportionto the amount of degenerative disease present. Onthe contrary, a patient with little or no degenerativechanges in the spine may, for reasons to be dis-cussed later, have a poor response to this type oftreatment, whereas, conversely, a patient withadvanced degenerative disease may respond well.

A woman (89 years of age), who had had episodes oflow-back pain since the age of 35 years, and hadexperienced severe pain in the left buttock for 1 year,asked her doctor if she might try acupuncture, only tobe told that this would be a waste of time as the X-rayof her lumbar spine showed that the pain was due tosevere arthritis. However, she finally got her own way!And, on examination, there were only two TrPs to be found, which were in muscles situated in thepostero-inferior part of the chest wall at the level ofthe 10th and 11th ribs. The pain in the buttock mustclearly have been referred from these (Fig. 15.3) as itdisappeared after deactivating them with a dry needleon only two occasions. Following this she remainedfree from pain for 18 months in spite of the advanced‘arthritic changes’ in the spine.

It is from having had a similarly good responseto acupuncture in a large number of cases of chroniclow-back pain with equally advanced degenera-tive changes on X-rays of the spine, that leads meto believe that such changes in the discs and facetjoints are often no more than a chance radiographicfinding in someone whose pain is primarily due tothe activation of TrPs by factors acting directly onthe muscles themselves.

Those who treat chronic low-back pain bymanipulating the spine might not agree with thisbut, nevertheless, it would seem reasonable topostulate that any success they may have with thisform of treatment may be due more to theirmanipulative procedures exerting traction onmuscles than to any effect these procedures mayhave on the spine itself. This would certainly be in

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keeping with Travell’s observation (1968) that it ispossible to inactivate myofascial TrPs by passivelystretching affected muscles.

Physical and psychological factors capable of activating myofascial TrPs

Some of the physical factors capable of activatingmyofascial TrPs in the lumbar muscles include, asTravell & Simons (1983, p. 644) point out, the sud-den overloading of the muscles as when liftingobjects whilst in an awkward position such aswith the back twisted and flexed; or when they aresubjected to sustained overloading, as may occurduring the pursuit of athletic activities, or at work,particularly when this involves much heavy lift-ing, stooping, or the adoption of awkward stand-ing or sitting postures.

Surgeons should also note that the putting ofpatients into unusual postures such as theTrendelenburg or lithotomy positions for pro-longed periods, particularly when the muscles areparticularly relaxed due to the effects of a generalanaesthetic, is liable to cause the activation ofMTrPs with the development of chronic postoper-ative low-back pain.

Magora (1970), who has extensively investi-gated the relationship between low-back pain andoccupational factors has found that this type ofpain is more frequent in those whose work forcesthem to sit for prolonged periods, than in thosewho constantly move about. And that heavy lift-ing, particularly when this is only occasional, is afrequent cause of this type of pain. He also foundthat low-back pain occurs with about the same fre-quency in those with sedentary occupations as in those doing heavy labour, but the sedentaryworker’s symptoms come on more after weekendathletic activities.

It is interesting to note, too, that, although hefound a high incidence of absence from workamongst manual workers because of the pain pre-venting them from carrying out their duties, theincidence of back pain correlated best with howphysically demanding workers perceived theirwork to be, rather than how objectively demand-ing it was. As he pointed out, its incidence is also more closely related to whether there are psychological problems at the workplace or at

home rather than to objective physical factors.When Westrin (1973) studied low-back pain, heconcluded that its incidence is especially high inthose not happy with their job situation, thosewho are divorced, or those who have problemswith alcohol.

This therefore leads to a consideration of psy-chological factors that so far as chronic low-backpain is concerned, seem to be of particular import-ance as TrP activators. Turk & Flor (1984) state that ‘chronic back pain is increasingly viewed as apsychophysiological and psychosocial problemstemming from the interaction of physical, psy-chological and social factors’. It has, in fact, to beaccepted that the condition is often multifactorialand this reflects itself in its treatment, which notinfrequently has to include therapeutic proced-ures directed both to the mind and the body.

There is a large group of patients who hold themuscles of their scalp, neck, or lower back in astate of persistent tension in response to nervousstrain, and as already discussed in Chapter 7 thisleads to the activation of TrPs in these muscles with,as a result, of this, the development of either per-sistent headaches, or chronic pain in the neck, orchronic low-back pain, or a combination of these.

Some people come to recognize that their attacksof pain coincide with times of particular stress.One young executive, for example, told me thatpublic speaking terrified him, and that his low-back pain always came on about 2 weeks beforehaving to address a business conference. Others candate the onset of recurrent low-back pain to somespecific time when they were subjected to someparticularly distressing experience. One house-wife, for example, told me that her attacks of neckand low-back pain started the year that both herhusband and only daughter died within 6 monthsof each other.

It obviously cannot be assumed that either ananxiety state or an agitated depressive one (reactivedepression), occurring in association with chroniclow-back pain, has necessarily contributed to thedevelopment of this, because often such moodchanges develop some months after the onset ofthe pain, and in such circumstances have to beconsidered to have arisen as a result of it.

It is important to realize that so-called psycho-logical low-back pain is, in reality, psychosomatic


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because, as has already been explained, there arealmost invariably TrPs to be found in the musclesusually in the form of foci of maximum tendernessin palpable bands or ‘fibrositic’ nodules. This hasconsiderable diagnostic and therapuetic implica-tions because when an overtly anxious personwith low-back pain is found to have no abnormal-ity of the spine on X-rays, no evidence of disease in the pelvis, and as all too often happens, the TrPsin the muscles are overlooked, there is a tendency for it to be assumed that the pain must be entirelypsychological in origin, and for the patient con-cerned to be referred to a psychiatrist. This, in myexperience, is rarely helpful, not because of anylack of expertise on the part of the latter, butbecause in such a case it does not matter howmuch psychotherapy is given, it will in no wayinfluence the course of the pain unless at the sametime the TrPs are deactivated. The converse, how-ever, is also true, that when psychological factorscontribute to low-back pain no amount of TrPdeactivation by acupuncture or by any other meanswill give any lasting relief from the pain, unless atthe same time some form of therapy is given toreduce the nervous tension.

It is my belief that, whenever possible, it ispreferable for the patient to receive both theseforms of treatment from the same physician, and it is for this reason that the patients with psy-chosomatic low-back pain under my care receivefrom me a combination of hypnotherapy andacupuncture.

An even more serious error, and one which notinfrequently occurs because of a general lack ofunderstanding concerning the significance of TrPs,and, therefore, a failure to look for them, is to con-clude that a patient with normal X-ray appear-ances of the lumbar spine is in need of psychologicalhelp, or, even, is frankly malingering, when in factthe pain is entirely of organic origin. An exampleof this is given here.

A housewife, at the age of 35 years was referred to anorthopaedic surgeon because of persistent low-backpain, only to be told that the pain could not be comingfrom her back because the X-ray of her spine wasnormal. She was then referred to a gynaecologist, whofinding no abnormality on physical examination,carried out a dilatation and curettage. This operation

was complicated 10 days later by a near-fatalpulmonary infarct. The patient then continued to bequite markedly incapacitated by persistent pain foranother 2–3 years, and, as during this time certainmarital difficulties had arisen, it was assumed that thepain must be of psychological origin and she wasreferred to a psychiatrist. It was very much to hiscredit that he frankly admitted he could find nopsychiatric cause for the pain, and the patient indesperation then asked her doctor whether she couldtry acupuncture.

On examination, there were some TrPs in quiteenormous, exquisitely tender fibrositic nodules andpalpable bands. Once these TrPs had been deactivatedwith a dry needle at weekly intervals on fouroccasions, she obtained lasting relief from pain for thefirst time for many years.

It has to be admitted that some people whoselow-back pain has occurred as a result of injury atwork or in a traffic accident, and who are claimingcompensation for this, do exaggerate their symp-toms. Unfortunately, however, a litigant is some-times unjustifiably assumed to be doing this, oftenfor no better reason than that the X-ray of the spineis normal, when a careful examination of the backwould show a sound physical basis for the pain inthe form of activated TrPs in the muscles.

A self-employed heating engineer, very anxious tokeep his business going but unable to do so because of persistent low-back pain following a car accident,very much resented being told by an orthopaedicsurgeon that his symptoms would not improve untilhis claim for compensation had been settled,particularly as when he eventually decided to tryacupuncture, it only required dry needle stimulation ofTrPs to be carried out on three occasions before hispain was sufficiently alleviated for him to return toquite hard physical work.

Finally, before leaving the subject of the influenceof psychological factors on chronic low-back pain, ithas to be said that, in my experience, acupunctureoften fails to relieve this type of pain in those who,because of long-standing neuroticism, persistentlyhold their lumbar muscles in a state of tension, andsimilarly is rarely helpful in those who developlow-back pain as a manifestation of conversion

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hysteria in order to escape from seemingly intolera-ble domestic, marital or occupational obligations.

A prison officer, who had complained of low-back painfor many years, was finally persuaded by his generalpractitioner to come to me for treatment withacupuncture. During the course of taking the history itseemed obvious that for some time he had found thepain to be extremely useful to him in so much that itenabled him to avoid some of the more arduous dutiesassociated with his job. It, therefore, came as nosurprise to me when, after two sessions, he failed toattend for any further treatment. He told his doctorthat this was because the treatment had made himworse, but almost certainly it was because, perhapsunknowingly, he was afraid it might eventually makehim better!

IMPORTANCE OF DISTINGUISHINGBETWEEN NOCICEPTIVE ANDRADICULOPATHIC CHRONIC LOW-BACKAND LEG PAIN

It is important to realize that the insidious devel-opment of combined low-back and ‘sciatic-type’leg pain may be either nociceptive, radiculopathic,or a mixture of both. For all too long there has been a belief that pain in this distribution, particu-larly when it is accompanied by restricted straightleg raising, must be due to nerve root entrapment.However, from what has already been said, and aswill be seen when TrP pain referral patterns fromindividual muscles in the lower back are considered,it is evident that chronic ‘sciatica’, even when it isassociated with restricted straight leg raising, maybe entirely due to the primary activation of MTrPs.At the same time, it has to be clearly understoodthat MTrPs may become activated as a secondaryevent in areas affected by pain from nerve rootentrapment.

It therefore follows that in all cases a systematicsearch for TrPs is essential. Also, in those caseswhere the history or physical signs suggest thatthe pain might be radiculopathic, further investi-gations, such as computerized axial tomography(CAT scanning) or MRI should be carried out.

Pain in this distribution occurring as the resultof the primary activation of MTrPs is readilyrelieved by acupuncture. If, however, there is any

suggestion that the pain might be due to nerveroot entrapment, then it is better not to embarkupon acupuncture until this has been fully investi-gated. The reasons for this are that, should nerveroot entrapment be present, not only will the deac-tivation of TrPs with dry needles do no more thantemporarily alleviate the pain, but also the longerthe nerve root remains compressed, the morelikely it is to become irreversibly damaged, so that,even if surgical decompression is eventually car-ried out, the operation may not relieve the pain.

Wynn Parry (1989), from reviewing experimen-tal studies carried out by various people over the past years has concluded that compression of a nerve ultimately leads to the development ofirreversible pain-producing degenerative changesboth in the nerve itself and in the central nervoussystem. As he points out, it is this peripheral andcentral damage that is the main reason for surgeryfailing to relieve symptoms from nerve root com-pression and why, when this happens, further opera-tions are also doomed to failure.

As therefore it is essential to be able to recognizethe clinical manifestations of the various causes ofchronic nerve root entrapment in the lower backthese will now be considered.

SpondylolisthesisSpondylolisthesis, the forward displacement of avertebra relative to the one below it, may either be congenital or acquired. Nelson (1987) reviewedthe diagnosis and management of five separatetypes, but only the degenerative type that affectsadults from the age of 40 years onwards will bediscussed.

Symptoms and signs

Degenerative spondylolisthesis affects mainlyfemales and occurs predominately at the L 4/5 level.The back pain is aggravated by activity, relievedby resting and is commonly made worse by stand-ing. The pain in the leg is in the distribution of anerve root with physical examination revealingthe presence of a motor and sensory deficit. In add-ition, bilateral paraesthesiae and muscle weaknessmay be present in those cases in which degenera-tive changes have led to the development of spinalstenosis.


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Investigations

Plain radiography, and either CAT scanning or MRIare necessary in order to confirm the diagnosis.

Treatment

Conservative treatment may be all that is neces-sary in mild cases, but surgery is required for therelief of severe pain with evidence of nerve rootcompression.

Spinal stenosisEisenstein (1977), from a comparison of Africanand Caucasoid skeletons, showed that it is when acongenitally narrowed spinal canal becomes fur-ther narrowed as a result of the development ofdegenerative changes in the posterior facet jointsthat symptoms develop. The clinical manifest-ations depend on whether the stenosis is of thecentral canal, or of the lateral root canal.

Central canal stenosis (neurogenicclaudication)The patient, usually a middle-aged male, gives along history of low-back pain and a more recentone of a vice-like claudication type pain with feel-ings of numbness, tingling and heaviness affectingone or both legs. The pain, as when due to vascu-lar disease, is brought on by walking and relievedby resting. Characteristically, relief from the painis obtained by bending forwards. It is for this rea-son that patients with this disorder adopt an ape-like posture with both hips and knees flexed – theso-called simian stance (Simkin 1982). It is alsobecause bending forwards relieves the pain thatpatients have less pain walking up a hill thandown a hill and continue to be able to cycle longdistances even when it is too painful to walk morethan short distances on the flat (Figs 17.2 & 17.3).

Clinical examination

Physical signs are widely variable. In some casesthere is some limitation of straight leg raising andevidence of a lower motor neurone lesion, but withothers their straight leg raising is normal and thereare no abnormal neurological signs.

Peripheral pulses may or may not be palpabledepending on whether arterial occlusion is or isnot also present. The provisional diagnosis there-fore mainly comes from the history.

Investigations

Plain radiographs of the lumbar spine frequentlyshow diffuse degenerative changes; a myelogramshows segmental filling defects or a total block andultrasound measurements confirm the reduced dia-meter of the vertebral canal.

Treatment

When symptoms are relatively mild, conservativemeasures may be helpful, but in those cases wherethere is severe pain and walking is restricted to

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Figure 17.2 The simian stance – a classic postureadopted by patients with neurogenic claudication, withflexed hips and knees. Reproduced with Professor Porter’spermission from The Lumbar Spine and Back Pain,Churchill Livingstone 1987.

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short distances in association with a progressiveneurological deficit, it is essential to carry outsome form of surgical decompression.

Lateral root canal stenosisIn this condition pain in the back with radiationdown one leg occurs as a result of stenosis at thissite causing entrapment of a nerve root – usuallythe 5th lumbar or 1st sacral. The stenosis may occuras the result of bony encroachment from osteo-phytes or ossified spinal ligaments, or from softtissue changes including facet joint capsule hyper-trophy, posterior longitudinal ligament thickeningand scar tissue developing around a rupturedannulus fibrosus or extruded nucleus pulposus.

Symptoms

The sciatic pain is in the same distribution as witha disc lesion but, unlike the latter, it is not relievedby lying down and remains severe and unremit-ting both day and night. Fortunately, however,unlike with disc pain, coughing and sneezing doesnot make it worse. In a series of 78 cases reportedby Getty et al (1981), 58% also had numbness andparaesthesiae in the leg and 17% had claudication.

Physical signs

These are widely variable. In the series of patientsreported by Getty et al (1981), only 49% showedevidence of a motor deficit and only 38% hadimpairment of sensation to light touch and pin-prick. Perhaps most surprising of all, most had anormal straight leg raising test.

It is probably because patients with lateral canalstenosis are liable to have bizarre sensory symp-toms together with a paucity of physical signs,and frequently have unrestricted straight leg rais-ing despite complaining of severe sciatica that thediagnosis in the past was frequently overlookedand patients suffering from it ran the risk of beingconsidered to be neurotic.

Investigations

Plain radiographs may show a reduction of theL5/S1 disc space. A CAT scan will usually reveal


(a)

(b)

Figure 17.3 The cycle test. The cycling distance is thesame in vascular intermittent claudication whether thespine is flexed (a) or upright (b). The extended spine in (b) limits the cycling distance in neurogenic claudication.Reproduced with Professor Porter’s permission from TheLumbar Spine and Back Pain, Churchill Livingstone 1987.

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the presence of degenerative changes in the facetjoints, but similar changes may also be evident inpatients who do not suffer from back pain.

It is not possible to demonstrate the presence ofnerve root entrapment in a stenosed lateral canalon a myelogram. Leyshon et al (1981), however,have shown that the diagnosis may be confirmedby electromyographic studies.

Management

Porter et al (1984) have shown that the root painnot infrequently gradually subsides spontaneously.However, as Wynn Parry (1989) points out, the dif-ficulty is that whilst waiting for this to happen aproportion of patients develop irreversible pain-producing changes both in the entrapped nerveand in the central nervous system. It is obvious,therefore, that any decision concerning if andwhen surgical decompression should be carriedout requires considerable clinical experience.

Indications for acupuncture and TENS

There is an important place for acupuncture andTENS as part of the conservative treatment of lumbar chronic nerve-root entrapment pain andalso post-operatively in those cases where surgeryhas failed to relieve this.

Acupuncture is of particular value in thosecases where the nerve root is not severely com-pressed and much of the pain is coming from sec-ondarily activated MTrPs.

TENS is likely to be more helpful in cases wherethe pain is predominately neurogenic, but it mustbe remembered that the electrodes should neverbe placed on anaesthetic skin, but always on skinwhere the sensation is normal in order that thehigh-frequency low-intensity stimulus providedby this form of therapy may be enabled to recruitA-beta nerve fibres.

MANAGEMENT OF CHRONIC LOW-BACK PAIN

It is a measure of the general public’s disillusion-ment with all the various conventional methods of treating chronic low-back pain that it is everincreasingly turning to alternative forms of ther-apy including acupuncture.

It is not possible, however, to come to any con-clusions concerning the possible place of acupunc-ture in the treatment of chronic low-back painwithout first of all critically appraising some of theother more widely used forms of treatment,including drugs, physiotherapy, spinal supports,and steroid injections.

Drugs

Analgesics

Various non-narcotic pain-killing drugs such asaspirin, phenacetin, paracetomol and pentazocine,together with a number of non-steroidal antiinflam-matory drugs, and even, at times, narcotic onessuch as pethidine, are prescribed for chronic backpain. Although they are all capable of relieving painfor short periods, this is more than offset by the dis-advantages of using them on a long-term basisincluding tolerance, habituation and side effects,many of which are liable to be of a serious nature.

Antidepressants

Patients with chronic low-back pain are sometimessufficiently depressed as to require a tricyclic antidepressant, but in addition a drug of this typemay also be used for its analgesic effect.

The evidence that tricyclic antidepressants havean analgesic action independent of their antide-pressive properties includes Monks’ (1981) havingfound that the onset of analgesia in chronic painconditions with this group of drugs is more rapid(3–7 days) than that of their antidepressant effect(14–21 days). Couch & Hassanein (1976) havingshown that they are capable of producing chronicpain relief in the absence of an antidepressantresponse, and Couch et al (1976) having reportedthat this may also occur in patients in whom thereis no detectable evidence of depression.

It would seem that the analgesic and antide-pressant effects of this group of drugs are due totheir ability to increase the concentration in thebrain and spinal cord of amine transmitters suchas serotonin (Sternbach et al 1976). Controlled tri-als comparing a tricyclic antidepressant with aplacebo in chronic low-back pain have givensomewhat equivocal results with Sternbach et al(1976) showing that amitriptyline, and Jenkins

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et al (1976) showing that imipramine, are no betterthan a placebo, but with Sternbach et al (1976)showing that clomipramine (Anafranil) is moreeffective than a placebo.

Muscle relaxants

As nervously holding muscles tense aggravatesmusculoskeletal pain, it might be thought thatdiazepam would be helpful in the management ofchronic low-back pain, but Hingorani (1966), fromthe results of a double-blind controlled trial, wasunable to confirm this.

Physiotherapy

Ultrasound

Sclapbach (1991) has pointed out that despite thefact that ultrasound is probably one of the mostfrequently used physiotherapeutic modalities forthe relief of musculoskeletal pain, there have beenremarkably few controlled studies to assess itseffectiveness for this purpose.

During the past 35 years there have only beennine such trials and, of these, only one has been inpatients with low-back pain. This was a study car-ried out by Nwuga (1983) who compared bed restand ultrasound, bed rest and sham ultrasound,and bed rest alone for the relief of acute low-backpain from intervertebral disc prolapse. Unfortu-nately, as bed rest was used in all three groups andis known to be effective itself in relieving acutelow-back pain (Deyo et al 1986, Wiesel et al 1980),the results of the trial are difficult to interpret.

Sclapbach (1991), from a review of these ninestudies, is of the opinion that, ‘based on the resultsof the few available controlled trials, it must beconcluded that we are far from being able to judgeeither the efficacy or inefficacy of therapeuticultrasound’.

Exercises

Exercises are sometimes advocated, but there is nogood evidence that increasing the strength of thelumbar muscles reduces the frequency with whichlow-back pain recurs, and, indeed, Nachemson

(1980) warns against them in view of the fact thatthey may increase the load on the lumbar spine tounacceptable levels.

Manipulation

This highly specialized form of physical therapyhas many advocates and is widely practised bydoctors and others but, having no personal experi-ence of its use, it would be wrong for me to expressany opinion concerning its efficacy, other than tosay that, from a study of the literature it wouldseem that, whilst it is of undoubted value in the treatment of acute low-back pain (Berquist-Ullman & Larsson 1977), its place in the manage-ment of chronic low-back pain is far less certain(Doran & Newell 1975, Glover et al 1974, Evans et al 1978, Sims-Williams et al 1982).

Spinal supports

Corsets are widely prescribed, but in spite of thefact that, at times, they are incredibly elaboratethere is little or no evidence that they are of anybenefit. A corset may, in fact, do harm, because bylimiting the movements of the back it may lead towasting of the muscles and, in addition, it is liable tosuppress the action of the low-threshold mechanore-ceptor large diameter fibre pain-modulating mech-anism (Ch. 6). Furthermore, a corset sometimesaggravates low-back pain by exerting pressure onTrPs. Quinet & Hadler (1979) in referring to thesedevices remark:

The widespread use of these gimmicks ought tobe curtailed until we have data suggesting thatour patients are more likely to profit from theircontinued use than are orthopaedic supplyhouses.

Injections of a corticosteroid and/or localanaesthetic into points of maximumtendernessSince Kellgren, nearly 50 years ago, started inject-ing novocain into ‘tender spots’ in order to allevi-ate musculoskeletal pain, this type of treatmenthas been commonly employed in the treatment oflow-back pain. Then once corticosteroids became


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available, the injection of a steroid/local anaes-thetic mixture has been used (Bourne 1979). Andin order to decide whether there was any advan-tage in using a steroid, Bourne (1984) decided tocompare the effects of injecting, on repeated occa-sions, either, a corticosteroid/lidocaine (lignocaine)mixture, or lidocaine (lignocaine) by itself, intopoints of maximum tenderness in the lower back,in the treatment of chronic back pain. He con-cluded that the mixture gave better results.

It should be noted that the injection was some-times given under the deep fascia but at othertimes into the periosteum, and, also, that amongstthe transient side effects were menstrual irregular-ities, flushing of the face and glycosuria. Bourneascribed the good results obtained with a steroidto certain softening and stretching effects on thecollagen, together with the growing of new fibro-cytes, and a consequent reduction in tissue tensiondescribed by Ketchum et al (1968) and Ketchum(1971). If, indeed, this type of tissue reaction doescontribute to pain relief, it is bound to take timeand hardly accounts for the immediate relief frompain so often observed when tender ‘spots’ areneedled.

The alternative explanation is that a cortico-steroid, when introduced into the tissues, and particularly when injected around the periosteum,has a powerful irritant effect on peripheral nerveendings, and in a similar manner to stimulatingnerve endings with a dry needle, evokes activityin pain-modulating mechanisms in the centralnervous system.

TrP acupunctureFrom what has just been said in reviewing some ofthe present methods of treating chronic low-backpain, it is clear that none of them are particularlyeffective, some are associated with undesirable sideeffects, and some can only be carried out in spe-cially equipped centres. Few would disagree withWaddell (1982) when he says:

Future improvements in treatment for backacheand the creation of a truly scientific basis fortreatment depend on better biochemical under-standing, more accurate identification and local-ization of the source of pain, recognition ofspecific clinical syndromes within mechanical

backache, and critical evaluation of the effective-ness of treatment. While awaiting such develop-ments it is best to use the simplest, safest, andcheapest treatment possible.

Acupuncture certainly fulfils these criteria, andthere is therefore much to be said for exploring itsuse in everyday clinical practice and, above all, bythe setting up of statistically controlled clinical tri-als. In my view, because of its simplicity, it is bestto employ it as a first line of treatment, and then to turn to other more complex therapeutic proce-dures in those cases not helped by it.

The TrPs from which chronic neck pain is referredare situated in much the same muscles in every-one, but this certainly is not so with the TrPsresponsible for chronic low-back and leg pain, andfor this reason the task of finding them is thatmuch more difficult. However, the task is facili-tated by having a knowledge of specific patternsof pain referral from TrPs in individual muscles.

Paraspinal musculature

TrPs in the paraspinal musculature may occureither in the superficial group of muscles knowncollectively as the erector spinae, or in muscles deepto this such as the multifidus and rotatores.

The two muscles in the superficial group (theerector spinae) most likely to develop TrPs are thelongissimus thoracis and lateral to this, the ilio-costalis lumborum muscle (Fig. 17.4).

Referred pain from TrPs in these muscles ismainly felt locally in areas immediately adjacentto these points, but sometimes it is felt at a dis-tance. As King & Lagger (1976) have shown, TrPsin the erector spinae muscles may cause pain to bereferred down the course of the sciatic nerve. And,as Travell & Simons (1983, p. 637) have stated, TrPsin the iliocostalis lumborum muscle at the upperlumbar level, and in the longissimus thoracis atthe lower thoracic level, cause pain to be referredto the buttock (Figs 17.5 & 17.6). It is because ofthis that, earlier in this chapter, it was stressed thatthe search for TrPs must always start some dis-tance above the 12th rib.

The two muscles in the deep group likely todevelop TrPs are the multifidi and rotatores. Painfrom these TrPs is referred to the midline with thedevelopment of exquisite tenderness on palpating

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Longissimus cervicis

Levatores costarum breves

External intercostal

Multifidus

Spinalis thoracis

Iliocostalisthoracis

Longissimus capitis

Semispinalis capitis

Ligamentum nuchae

Semispinalis cervicisLongissimus cervicis

Iliocostalis cervicis

Longissimus thoracis

Iliocostalis lumborum

Quadratus lumborum

Erector spinae

Lateral intertransverse muscle

Transversus, origin from thoracolumbar fascia

Quadratus lumborum

Inferior obliqueRectus capitis posterior major

Rectus capitis posterior minor

Superior oblique

Figure 17.4 The deep muscles of the back. On the left side the erector spinae and its upward continuations (with theexception of the longissimus cervicis, which has been displaced laterally) and the semispinalis capitis have beenremoved.

Figure 17.5 The pattern of pain referral from a triggerpoint (�) in the ilicostalis lumborum muscle.

Figure 17.6 The pattern of pain referral from a triggerpoint (�) in the longissimus thoracis muscle.

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the spinous processes (Fig. 17.7A). Deep TrPs lowdown in the sacral region may also refer pain in adownwards direction to the coccyx and cause it tobecome very tender (Fig. 17.8).

It should also be noted, as stated by Travell &Simons (1983, p. 637), that TrPs in the iliocostalismuscle in the lower part of the thorax and in themultifidus muscle anywhere along the length ofthe lumbar spine may refer pain anteriorly to the abdomen, and that such pain may readily be misinterpreted as being visceral in origin (Fig. 17.7B).

Examination to locate TrPs in these muscles Theexamination to locate TrPs in the paraspinal muscles should be conducted either with thepatient seated and leaning forwards to flex thespine or with the patient in the semiprone positionwith the painful side uppermost, and the knees

brought up towards the chest. The full prone posi-tion should be avoided because, if the muscles areallowed to become too relaxed, it is difficult toidentify palpable bands.

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A B

Figure 17.7A&B The pattern of painreferral from a trigger point (�) in thedeep group of paraspinal muscles(multifidi and rotatores) in the upperlumbar region.

Figure 17.8 The pattern of pain referral from a triggerpoint (�) in the deep group of paraspinal muscles(multifidi and rotatores) in the sacral region.

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TrPs in the superficial erector spinae musclesare readily felt by palpating down the length of theparavertebral gutter.

In order to identify a TrP in one of the deepermuscles it is necessary to apply firm pressure imme-diately lateral to the spine in a posteromedialdirection towards the body of a vertebra at thelevel of a tender spinous process.

Deactivation of TrPs TrPs in the superficial para-spinal muscles should be deactivated with needlesinserted at right angles to the skin, except in thelower thoracic region where, to avoid any chanceof penetrating the pleura, it is wiser to insert themtangentially.

In deactivating TrPs in the more deeply situatedparaspinal muscles, the needles have to be insertedlateral to the midline and in a diagonal directiontowards the vertebral bodies.

Supraspinous ligament connecting the apices of the lumbar vertebral spines

TrPs in the paraspinal muscles are often accompa-nied by TrPs in the midline supraspinous ligament,and when present these should also be deactivated.

Traditional Chinese acupuncture points As willbe seen from Figure 17.1, traditional Chineseacupuncture points are located down the midlinein the so-called ‘Du’ channel, and in the paraverte-bral region in the so-called ‘Urinary Bladder’ chan-nel. There is, therefore, a close spatial correlationbetween points in the Chinese system and the TrPsjust described.

Quadratus lumborum muscle (Fig. 17.9)

It is relatively common for TrPs to become acti-vated in this muscle but because it lies deep to theparaspinal muscles they tend to get overlooked(Travell 1976). Sola & Williams in 1956 reported itto be a frequent cause of unilateral low-back painamongst young adults in the American Air Force.

Activation of TrPs TrPs in this muscle becomeactivated either when, because of a sudden twist-ing or stooping movement, an acute strain is puton the muscle, or when because of bending for longperiods the muscle is subjected to sustained or

repeated overload. The patient may then complainof pain on walking, but particularly on stooping ortwisting, such as when turning over in the bed,also on rising from a chair, and with sharp respira-tory movements such as coughing or sneezing.

Specific patterns of pain referral The pattern ofpain referral depends on whether the TrPs are inthe superficial lateral part or the deeper medialpart of the muscle. When TrPs are located in thelateral part, the pain is referred down to the outerside of the iliac crest and over the greater trochanter(Fig. 17.10). It may also extend anteriorly towardsthe groin. When they are located in the medialpart, the pain is referred to the region of thesacroiliac joint and buttock (Fig. 17.11). Accordingto Sola & Williams (1956) TrP activity in this muscle is also a frequent cause of anterior abdom-inal pain.

TrP examination TrPs in this muscle, particu-larly in its deeper medial part, are liable to be over-looked unless care is taken to put the muscle on the stretch. The patient whilst lying on theunaffected side, as during the examination of theparaspinal muscles, should separate the 12th ribfrom the iliac crest, by reaching upwards with thefree arm whilst at the same time drawing downthe pelvis by dropping the uppermost thigh back-wards on to the couch. This manoeuvre brings themuscle nearer to the surface whilst at the sametime tensing it.

TrPs in the superficial lateral part of the muscletend to be found, either where it inserts into the12th rib, or into the iliac crest.

TrPs in the medial deeper part of the musclemay be located by exerting firm pressure directed


Figure 17.9 The quadratus lumborum muscle.

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medially towards the transverse processes of thevertebrae. Again TrPs in this part of the muscletend to cluster in the upper part around the 12thrib or in the lower part at the level of the 4th lumbar vertebra.

Glutei muscles (see Fig. 18.6)

TrPs in the gluteus maximus may occur at any of a variety of sites in the belly of this muscle. They become activated as a primary event or secondarily when pain is referred to the buttockfrom TrPs in muscles situated in the postero-inferior part of the chest wall.

Pain from TrPs in this muscle is referred locallyto the buttock itself and the coccyx (Fig. 17.12).

TrPs in the gluteus medius and minimus areoften found near to their insertions into the greatertrochanter. The referral of pain from these is intothe buttock, and also sometimes down the outerside of the thigh along the length of the iliotibialtract, and when this happens it is often associatedwith the secondary activation of TrPs in this struc-ture (Fig. 17.13).

With TrPs situated more posteriorly in one orother of these muscles, the pain is referred downthe back of the thigh when it may be misdiagnosedas sciatica (Fig. 17.14).

Deactivation of TrPs in the glutei and iliotib-ial tract with a dry needle usually presents no difficulties, providing it is carried out systematic-ally and no TrPs are overlooked.

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Figure 17.10 The pattern of pain referral from triggerpoints (�) in the lateral part of the quadratus lumborummuscle.

Figure 17.11 The pattern of pain referral from triggerpoints (�) in the medial part of the quadratus lumborummuscle.

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Piriformis muscle (Fig. 17.15)

TrP activation in the piriformis muscle may alsocause pain to be referred to the buttock, to the hip,and down the back of the leg in the distribution ofthe sciatic nerve (Fig. 17.16).


Figure 17.13 The pattern of pain referral from a triggerpoint (�) in either the gluteus medius or minimus near tothe attachment of these muscles to the greatertrochanter.

Figure 17.14 The pattern of pain referral from a triggerpoint (�) in the posterior part of either the gluteusmedius or minimum muscles.

Figure 17.15 The outer part of the piriformis musclewith its attachment to the greater trochanter. The sciaticnerve is shown in its normal position behind this muscle.

Figure 17.12 The pattern of pain referral from a triggerpoint (�) in the gluteus maximus muscle.

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result of the development of trauma-induced TrPactivity may cause entrapment of the nerve andthe development of ‘sciatica’ – the so-called piri-formis syndrome.

Piriformis syndrome The type of trauma respon-sible for TrP activity developing in this syndromeincludes the overloading of the muscle, such aswhen twisting the trunk sideways during the courseof bending to pick up a heavy object. Also, directtrauma to the muscle such as, for example, in aroad traffic accident. And when the muscle is heldin a shortened position for any length of time suchas may happen when lying with the hips flexedand legs widely abducted during the course of asurgical operation.

The syndrome occurs six times more often inwomen than in men (Cailliet 1977). On examin-ation there is marked tenderness over the sciaticnotch, and the pain is made worse by attemptingto abduct and externally rotate the thigh againstresistance. This test is most readily carried out byapplying resistance to the outside of the thigh whilstthe patient in the sitting position attempts toabduct the leg (Pace & Nagle 1976).

TrP tenderness may be elicited by exerting deeppressure on the lateral part of the muscle throughthe overlying gluteal muscles. Active TrPs near toits medial attachment, however, can only belocated when pressure is applied to the region ofthe greater sciatic notch during the course of car-rying out a rectal or vaginal examination.

Cummings (2000) has recently provided a com-prehensive, well-referenced review concerning thediagnostic features, the clinical examination andthe various procedures available for the treatmentof this syndrome. These include stretching of themuscle with or without the application of a vapoc-oolant spray, the application of external pressure,rectal massage and acupuncture. With respect tothe latter he recommends:

… brief dry needling of TrPs with a 75 mmacupuncture needle in piriformis. The positionadopted for needling is that which puts piriformison stretch. The needle is inserted over the site ofmaximum tenderness and advanced until theincreased resistance of the stretched muscle isreached or the patient recognises their pain …When aiming for the most medial portion of

Low-back pain 305

Figure 17.16 The pattern of pain referral from a triggerpoint (�) in the piriformis muscle.

This muscle, an external rotator of the hip,arises from the internal surface of the sacrum, andthen passes outwards and downwards throughthe sciatic notch to become inserted into thegreater trochanter of the femur (Fig. 18.6).

The sciatic nerve on leaving the pelvis is nor-mally situated behind the muscle (Fig. 17.15) but in more than 10% of people the peroneal part of the nerve passes through the belly of the muscle (Grant 1978), and in less than 1% ofpeople the entire sciatic nerve passes through themuscle (Beaton & Anson 1937). In those patients in whom part or the whole of the sciatic nervetakes this course, shortening of the muscle as a

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piriformis accessible externally an additional nee-dle can be inserted as a guide of depth on to thesacrum at the medial border of the sciatic notch …

Pain in and around the sacroiliac joint

Pain in the region of the sacroiliac joint in a youngman may herald the onset of ankylosing spondylitisand appropriate investigations should be carriedout to exclude this. Pain from sacroiliac strain mayalso occur during the last few months of pregnancyand in the postpartum period, but it is doubtfulwhether it is possible to subject this joint to strainat any other time of life.

During the later stages of pregnancy, hormonally-induced laxity of the ligaments of the joint takesplace, and this is sometimes associated with painboth in the region of this joint and the hip, and, onoccasions, down the front of the thigh. On examin-ation, there is often quite marked tenderness overone or both sacroiliac joints, but the temptation to attempt to relieve this pain by inserting dry needles into points of maximum tenderness should,in my opinion, be resisted. This is because nowthat it has been shown that it is possible to inducelabour at full term by stimulating nerve endings inthe pelvic region, it might be difficult to defendoneself in a court of law if acupuncture carried outnear to term for the treatment of low-back painappeared to be responsible for labour starting prematurely. It was as well that my policy of notcarrying out acupuncture during pregnancy wasadhered to in the case of the 8-months pregnantwoman who was particularly anxious for me toalleviate some persistent sacroiliac pain by meansof this technique, because 2 days after advising heragainst having acupuncture in view of her beingpregnant, she spontaneously went into labour!

Pain in the region of the sacroiliac joint may alsooccur following pregnancy when the joint, havingopened during delivery, fails to close properly.Radiographic investigation may also show evidenceof misalignment of the pubic rami. The sacroiliacpain may be relieved by inserting a dry needle intoa point of maximum tenderness along the line ofthe joint but, in my experience, this usually, evenwhen repeated, only gives temporary relief, and if the pain becomes chronic, there is a case forstrengthening the ligaments by injecting a sclerosingagent into them.

Sacroiliac strain unrelated to pregnancy

Low-back pain occuring without any relationshipto pregnancy is often diagnosed as being due tosacroiliac strain, particularly by osteopaths, butthe joint normally has such little movement, dueto it being held in position by particularly strongligaments, that other than during pregnancy itseems very unlikely to be subjected to strain, andalso it seems equally unlikely that it is amenable to manipulative procedures. However, it has to be admitted that in cases of chronic low-back painthere is often exquisite tenderness on applyingpressure to the ‘dimple’ overlying the joint, andthe insertion of an acupuncture needle into thepoint of maximum tenderness is often very helpful.

Iliopsoas muscle (Fig. 17.17A)

In the investigation of chronic low-back pain noexamination for TrPs is complete without finallyturning the patient into the supine position tocheck for TrPs in the anterior abdominal wall andin the groin.

The activation of a TrP immediately below theinguinal ligament, in the tendon of the iliopsoasmuscle where it lies in close relationship to thefemoral artery, just before it becomes inserted intothe lesser trochanter of the femur, is a cause of painbeing referred up a line immediately lateral to thespine in the paravertebral gutter, and also in somecases down the front of the thigh (Figs 17.17A,B).Deactivation of the TrP with a dry needle is bestcarried out with the thigh abducted and externallyrotated, and with care being taken not to damagethe femoral nerve.

TrP activity in the iliopsoas muscle may be asso-ciated with similar activity in muscles in the lowerback such as the quadratus lumborum, but occa-sionally it is present on its own. It is important to examine the groin routinely for TrPs in all casesof low-back pain as otherwise they can easily beoverlooked.

A physical training instructor (34 years of age), whilstplaying football, twisted his left leg and shortly afterdeveloped pain in the left lower back, and down theback of the leg a far as the calf; any stretchingmovement of the trunk made the pain worse. Anosteopath manipulated his spine on several occasionsbut without any improvement in the pain, and after


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this had persisted for 12 months, he was sent to mefor possible treatment with acupuncture. In view of the history there was no doubt in my mind that TrPs would be readily demonstrable in the muscles of the lower back, and it came as a great surprise tome when this proved not to be so. However, on gettinghim to lie on his back, TrPs were found in the groin, inthe iliopsoas and adductor tendons. It is interesting tonote that, as so often happens, in spite of them beingexquisitely tender, he was quite unaware of theirpresence until pressure was put on them at the time ofthe examination. Also of particular interest was thefact that the insertion of a needle into one of themevoked a transient sensation of pain in the back anddown the leg in exactly the same distribution as thatoccurring spontaneously. Furthermore, the importanceof the part played by these TrPs in provoking the pain

was further confirmed by the latter being alleviatedquite dramatically once they were deactivated withdry needles. The first time that this was done he waspain-free for 3 days, and, although the pain had beenpresent for over a year, it was only necessary to repeatthe procedure on two further occasions at weeklyintervals before he obtained lasting relief.

Clinical trials to assess the effectiveness of acupuncture in the treatment of chronic low-back pain

The general consensus of opinion among thosewith much experience of using acupuncture in thetreatment of chronic low-back pain is that it pro-vides worthwhile symptomatic relief in about 70%of cases. This, however, can be considered to be no

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TP

A B

Figure 17.17A&B Patterns of pain referral from a trigger point (�) in the iliopsoas muscle near to its insertion intothe lesser trochanter.

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more than a clinical impression, as the number ofstatistically controlled trials so far conducted hasbeen small, and of those that have been carriedout, most have been poorly designed and havelacked sufficient numbers of patients in them.

It has to be admitted that the objective assess-ment of the effectiveness of acupuncture, or anyother type of treatment, in relieving chronic low-back pain is particularly difficult because the con-siderable uncertainty concerning the aetiologicalfactors responsible for this type of pain in any par-ticular individual, makes it virtually impossible todivide cases into clearly definable sub-groups. It isbecause of this that the Working Group on BackPain (1979), set up by the Minister of Health, con-sidered that in order to be certain that randomiza-tion ensured that all the various factors likely toinfluence the outcome of treatment are equally dis-tributed amongst the actively treated group andthe control group in any such trial, it might well benecessary to study up to 500 pairs or more. TheWorking Group, however, being well aware of thevery considerable practical problems associatedwith conducting trials of such magnitude, sug-gested that initially it might be more expedient tosettle for less than that which might be consideredto be ideal.

Some of the problems related to statisticallycontrolled trials designed to assess the effective-ness of acupuncture in relieving musculoskeletalpain including that which affects the lower backhave already been considered in Chapter 11, andso at this stage nothing more need to be said otherthan to draw attention to some personal observa-tions made during the course of using this form oftreatment in a large number of cases of chroniclow-back pain that seem to me to be of relevancewhen planning, carrying out, and assessing theresults of such trials.

Firstly, it is my belief that the response toacupuncture seems to bear little or no relationshipto the amount of degenerative changes a personhas in the lumbar discs or facet joints, but it doesseem to be very much influenced by his or her psy-chologcial state. By this it is meant that at one endof the spectrum psychologically stable people withlow-back pain often respond well to acupuncture,in spite of having advanced degenerative changesin their spine, whereas at the other end of the

spectrum, the response to this form of treatment inpeople who hold their lumbar muscles in a state ofpersistent tension because of chronic anxiety is liableto be poor, even when the X-rays of their spinesare normal. The implication of this, with respect toclinical trials, might seem to be that, so far as psy-chosocial factors and degenerative changes in thespine are concerned, that of the two, it is particularlyimportant that randomization ensures that neur-oticism is evenly spread between the treatmentand control groups. It was no doubt consider-ations such as these that led Mendelson et al (1983),in their statistically controlled study of the use of acupuncture in low-back pain, to carry out adetailed pre-trial psychological assessment in alltheir patients. And there are many who now believethat psychosocial factors are of such importanceboth in the aetiology of chronic low-back pain, andin causing it to persist, as to make it essential withsome patients to employ various psychologicalforms of relaxation therapy, such as hypnosis(Crasilneck 1979) or biofeedback (Keefe et al 1981),in addition to physical measures applied locally tothe back, such as acupuncture. Trials in anxiouslow-back pain patients to assess whether or notthe use of acupuncture and a relaxation techniquegive better results than those obtained by the useof one of these treatments on its own have not asyet been carried out.

Before leaving the subject, it must be admittedthat the belief that unrelieved chronic anxiety tendsto nullify the effects of acupuncture is not held byeveryone, with, for example, Levine et al (1976)finding that a high score on psychometric indica-tors of anxiety and depression is a significant pre-dictor of successful needle puncture analgesia inpatients with chronic pain. It is clear, therefore,that with such diversity of views on this subjectthere is much scope for clinical trials specificallydesigned to resolve this issue.

The other matter that has to be considered whendiscussing the design of clinical trials to assess theefficacy of acupuncture in relieving chronic low-back pain, and, for that matter, all other forms ofmusculoskeletal pain, is that responders to acupunc-ture may be divided into a group consisting ofthose who obtain long-lasting relief from chronicpain after a comparatively few treatment sessions,and another group consisting of those who benefit


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from acupuncture but require ongoing treatmentover a long period in order to keep chronic painadequately suppressed.

These differences in people’s reaction to acupunc-ture so far as low-back pain is concerned, again seemto bear little or no relationship to the type or extentof any pathological changes that may happen to bepresent in their spines, but, as with musculo-skeletal pain anywhere in the body, it does seem to depend on the varying manner in which indi-viduals’ endogenous pain-modulating mechanismrespond to peripheral nociceptive stimulation.

The ability of acupuncture in some people attimes not only to give symptomatic relief, but tocut short a long-standing episode of pain is wellrecognized, and a possible explanation for thisphenomenon is given in Chapter 10. However, ithas to be realized that such a response may, onoccasions, be more apparent than real and be dueto the acupuncture treatment being given coinci-dentally with the onset of a natural remission. Ifby chance this should happen to occur with anumber of patients in a clinical trial, then of courseit might seriously interfere with the results. And itwas in an attempt to safeguard against this asmuch as is possible that Macdonald et al (1983), intheir statistically controlled trial of acupuncture inthe relief of chronic low-back pain, only includedpatients whose pain had persisted for at least 1year. Their reasoning behind this was, of course,that the longer chronic pain persists, the less likelyit is to undergo a spontaneous remission.

Many chronic low-back pain sufferers onlyobtain relatively short periods of symptomaticrelief from acupuncture and because of this haveto be given it at fairly frequent intervals on a long-term basis. Such relief, however, is clearly of greatbenefit to them, and repeated treatment with aprocedure so free of side effects as acupuncture is,of course, a small price to pay for it. Fox & Melzack(1976) clearly had this in mind when, during thecourse of commenting on the results of their com-parative trial of transcutaneous electrical stimula-tion and acupuncture in the treatment of chroniclow-back pain, they stated:

… transcutaneous stimulation and acupuncture,however, are not ‘cures’ and repeated treatmentsare usually necessary to provide continuing

periods of relief. When it is recalled that many ofthe patients in this study had suffered pain foryears, and several had undergone major surgerywithout relief, the value of a technique whichbrings partial relief for a few hours or days at a time is especially evident. It makes the differencebetween unbearable and bearable pain, betweena sedentary, sometimes bed-ridden life and onethat, for at least several hours or days a week,allows a normal social, family, or business life.Even a few hours or days of pain at tolerable levels permits some of these patients to live withmore dignity and self-assurance, so that life ingeneral becomes more bearable.

These differing effects of acupuncture on chroniclow-back pain, with at times it being capable ofgiving long-lasting relief, and at other times givingshort-term, but nevertheless much appreciated,relief, have to be taken into account when evaluatingthe results of clinical trials.

Furthermore, when planning such trials it hasto be remembered that individuals vary widely asto how much peripheral nerve stimulation theyrequire in order to obtain optimum response, andalso as to how many times treatment has to be givenin order to bring the pain under control. It wouldtherefore seem expedient, when drawing up proto-cols for these trials, to allow for these varyingtreatment requirements, by permitting the rulesgoverning the administration of the acupunctureand the control type of therapy to be more flexiblethan those governing the prescribing of pharma-cological substances in drug trials.

Such considerations of course apply to acupunc-ture trials in general and have already beenreferred to in Chapter 11, but it is appropriate todraw attention to them again here because itwould seem that up to now only Macdonald et al(1983) have realistically taken them into accountwhen drawing up the protocol for their trial inpatients with chronic low-back pain. In that trialthe effect of inserting needles superficially throughthe skin to an approximate depth of 4 mm at TrPsites was compared with that obtained by aplacebo treatment consisting of the placing of elec-trodes on the skin at similar points and then attach-ing them to a non-functioning TENS machine. Theprotocol for this trial laid down that treatment

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both in the acupuncture group and in the placebocontrol group should be given once a week. Forthe acupuncture group, it was decided that eachtreatment should take the form of needles beingleft in situ, without any form of rotation, for 5 min,and that if, on any occasion, such treatment failedto produce beneficial results, then at the next treat-ment the needle insertion time had to be doubled,and if necessary on a further occasion doubledagain up to a maximum of 20 min. If there was stillno response, electroacupuncture had to be used. Itwas laid down that, initially, impulses of 700 �sduration should be obtained at a frequency of2 Hz, with the amplitude being increased approxi-mately every 2 min to maintain the stimulationjust above the pain threshold. Again if 5 min of thistreatment produced no effect, the duration had tobe doubled at each treatment up to a maximum of20 min. The number of treatments given could bevaried according to an individual’s response withan arbitrarily defined upper limit of 10. The num-ber of treatments was reduced, however, if furtherimprovement failed to occur, or, indeed, if the paincontinued to progress.

The rules governing the application of electrodesto the skin over the TrPs in the control group wereexactly similar, including that if the patient reporteda worsening of the pain immediately following‘treatment’, as happened in three cases, then inexactly the same way as with the needle insertiontime in the acupuncture group, the electrode appli-cation time was reduced.

The trial was small, but nevertheless, largelydue to its design, it was possible to show a statis-tically significant superiority of superficial dryneedling over placebo in the alleviation of chroniclow-back pain.

Ernst & White (1998), have recently carried outa meta-analysis of all the various randomized con-trolled trials conducted to date to assess the valueof acupuncture in the treatment of back pain.During the course of discussing their findingsErnst (1999) has concluded that reasonably goodevidence supports the use of acupuncture in thetreatment of this disorder but goes on to say that‘unfortunately numerous caveats prevent firmerconclusions’.

One of my criticisms is that in the majority of trials the effects of needling carried out at traditional

Chinese acupuncture points and sham points havebeen compared. This is of dubious value because,as emphasized by van Tulder et al (1999), in theirsystematic review of the effectiveness of acupunc-ture in the management of acute and chronic low-back pain, the needling of so-called shampoints must invariably afford a certain amount ofpain relief for reasons discussed at some length inChapter 11, so as to make it difficult to compare therelative effectiveness of the two types of treatment.

Another shortcoming is that low-back pain is asymptom not a specific entity, so that patientsadmitted to such trials are likely to be sufferingfrom a variety of different disorders with the painin some of them being nociceptive and in othersneuropathic. This makes the interpretation of resultsvirtually impossible as the responsiveness toacupuncture of these two types of pain is likely tobe very different. It is for this reason that Thomas &Lundberg (1994) are to be commended for specif-ically discussing the importance of modes ofacupuncture in the treatment of chronic nocicep-tive low-back pain.

Two recent trials are worthy of special mention,as in both, care was taken to include only patientssuffering from the MTrP pain syndrome.

Kovacs et al (1997) carried out a randomized,double-blind, multi-centre trial to assess the valueof treatment called by them neuroreflexotherapydirected at TrPs in low-back muscles. This form oftherapy consisted of the implantation of staplesinserted 2 mm below the surface of the skin at TrPsites in the lumbar muscles for up to 90 days andepidermal burins (metal studs) inserted into ten-der points in the ear for up to 20 days. A controlgroup was treated in a similar manner, but withthe devices implanted 5 cm away from the TrPs inthe back and the tender areas in the ear. From theresults they concluded that:

… neuroreflexotherapy intervention seems to bea simple and effective treatment for rapid ameli-oration of pain episodes in patients with chroniclow back pain …but further studies are essentialto confirm the present results on a larger sample.

Ceccherelli et al (2002) carried out a double-blind, randomized controlled study in patientswith lumbar myofascial pain to compare shallowneedling (insertion of the needle to a depth of 2 mm)


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in one group and deep needling (insertion of theneedle to a depth of 1.5 cm) in another group carried out at eight traditional Chinese acupunc-ture sites and four TrP sites. From their results theyconcluded that deeply applied stimulation has abetter therapeutic effect than shallow needling.

As most people who treat the myofascial painsyndrome do so by directing treatment at all of

the TrPs present in each individual case, there isclearly a need for large scale trials to be carried outto compare the effectiveness of doing this in threegroups of patients. One group treated with shal-low needling (2 mm insertion at the TrP sites), asecond treated with superficial needling (5–10 mminsertion at the TrP sites) and a third with needlesinserted deeply into the TrPs themselves.

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INTRODUCTION

As pain in the leg from entrapment of lumbar nerveroots and from trigger points (TrPs) in the musclesof the lower back and buttocks has been dealt within the previous chapter, and as pain in and aroundthe hip, knee, and ankle joints will be discussed inChapter 19, this chapter will be restricted to a con-sideration of pain in the lower limb occurring as aresult of the activation of TrPs in muscles of thelower limb itself.

Investigations to ascertain the cause of persistentpain in the leg are usually directed at excludingdiseases of the bones or joints, circulatory disorders,and neuropathies, but the possibility that such painmight occur as a result of the activation of TrPs inthe muscles is all too frequently passed over, withthe result that it is often allowed to continue formuch longer than it need.

A man (75 years of age) began to get pain in thecalves, ankles, and the soles of the feet on climbingstairs, together with troublesome cramps in the calvesat night disturbing his sleep. After the symptoms hadbeen present for 4 weeks, he sought medical advice. Asinvestigations at that time showed no evidence ofarthritis, no circulatory disturbance, and no evidenceof a diabetic neuropathy, he was treatedsymptomatically with paracetamol for the pain onexertion, and quinine sulphate for the nocturnalcramps. These, however, had little or no effect andafter a further 3 months he was referred to me as acase of persistent pain in the legs of unknown cause.

On taking this history, it became apparent that thepatient spent much time cruising on the river. This

315

Chapter 18

Pain in the lower limb

CHAPTER CONTENTS

Introduction 315Adductor longus muscles 316Quadriceps femoris group of muscles 316Hamstrings 318Tibialis anterior muscle 318Gastrocnemius muscle 319Soleus muscle 319Painful heel 320Metatarsalgia 322Pain in a toe 323

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it suddenly to give way. This often occurs beforethis TrP activity is a cause of pain. It therefore follows that a history of painless buckling of theknee is an indication for examining this muscle fora TrP and, if present, for it to be deactivated bymeans of inserting a dry needle into the tissuesoverlying it.

For those interested in comparing positions ofTrPs with those of traditional Chinese acupuncturepoints, it should be noted that the TrP in the vastusmedialis just above the knee is in close relationshipto the traditional Chinese point Spleen 10 (Fig. 16.1)and one in the vastus lateralis, just above the knee,occurs close to the Chinese point Gall bladder 33(Fig. 18.2).

Pain from a TrP just above the knee in the vastusmedialis, is felt around the inner side of the knee(Fig. 18.3).

involved frequently opening heavy lock gates, and toassist with this he was in the habit of pressing hardwith his legs against concrete blocks. It would seemthat this must have strained the muscles of his calvesfor, on examination, there were numerous exquisitelytender TrPs in the gastrocnemius and soleus muscles.Deactivation of these with dry needles on only oneoccasion gave him relief from the symptoms for 3days, and after repeating the procedure a further threetimes at weekly intervals they disappeared altogether. Astate of affairs of course that could have beenachieved both more quickly and at an earlier stage ifonly the diagnosis had been made more promptly.

The muscles in the leg which, in my experience,most often develop active TrPs are the adductorlongus, the quadriceps femoris group of muscles,the hamstrings, the tibialis anterior, the gastrocne-mius, the soleus, the peronei and the dorsalinterossei.

ADDUCTOR LONGUS MUSCLES (Fig. 18.1)

TrPs in the adductor longus commonly developnear to its insertion into the pubis, and as referralof pain from these is predominantly into the groin,as well as down the inner side of the thigh, consid-eration will be given to pain from TrPs in this muscle when discussing pelvic pain in Chapter 20.

QUADRICEPS FEMORIS GROUP OFMUSCLES (Fig. 18.1)

TrPs may become activated in any of the quadricepsgroup of muscles (the rectus femoris, the vastusmedialis, the vastus intermedius and the vastuslateralis), when these muscles become strainedeither as a primary event, or secondarily to walkingbadly because of some painful disorder in the foot,ankle or knee.

With arthritis of the knee it is the vastus medialisthat most commonly develops TrPs. The vastusmedialis is the main muscular support of the knee,and as pointed out by Travell (1952), the develop-ment of TrP activity in it, whether this be due to aprimary muscle strain, or to arthritis in the knee, isliable to cause the knee to become unstable and for

IlliacusTensorfasciae latae

Psoas major

Sartorius

Rectusfemoris

Vastuslateralis

Ligamentumpatellae

Tendon ofsartorius

Vastusmedialis

Adductormagnus

Gracilis

Adductorlongus

Pectineus

Iliotibial tract

Figure 18.1 Superficial muscles of the thigh. Extensoraspect.

Chap-18.qxd 11*10*04 10:31 Page 316

Pain from a TrP just above the knee, in the vastuslateralis, is referred up the side of the thigh, fromthe TrP below, up as far as the greater trochanterabove (Fig. 18.4).

TrPs in the vastus intermedius and rectus femorisare usually to be found in the upper third of thethigh, and pain from these is referred down theanterior surface of the thigh (Fig. 18.5).

Pain in the lower limb 317

Gall bladder 32

Gall bladder 33

Gall bladder 34

Figure 18.2 Some traditional Chinese acupuncturepoints along the Gall Bladder meridian in the region ofthe knee joint.

Figure 18.3 The pattern of pain referral from a triggerpoint (�) in the vastus medialis muscle.

Figure 18.4 The pattern of pain referral from a triggerpoint (�) in the vastus lateralis muscle.

Figure 18.5 The pattern of pain referral from a triggerpoint (�) in the rectus femoris muscle.

Chap-18.qxd 11*10*04 10:31 Page 317

Pain from TrPsWhen TrPs are widespread throughout the bellies ofthe hamstrings, they cause these muscles to becomeshortened with, as a consequence of this, restrictedflexion of the hip and a positive straight-leg raisingtest (Simons & Travell 1984).

TIBIALIS ANTERIOR MUSCLE (Fig. 18.9)

The tibialis anterior muscle, which arises mainlyfrom the upper two-thirds of the lateral surface ofthe tibia, is a thick fleshy muscle that ends in a tendon attached on the medial side of the foot tothe medial cuneiform bone and the first meta-tarsal bone.

Active TrPs usually occur in the belly of the muscle, with pain from this being referred downthe front of the shin, the medial side of the ankle


Piriformis

Gemellus superior

Sacrotuberous ligament

Obturator internus tendon

Gemellus inferior

Quadratus femoris

Adductor magnus

Gracilis

Semitendinosus

Semimembranosus

Popliteus

Biceps femoris, short head

Vastus lateralis

Biceps femoris, long head

Gluteus maximus

Gluteus minimus

Gluteus medius

Figure 18.6 The muscles of the gluteal region and flexor aspect of the right thigh. Posterior aspect.

HAMSTRINGS (Fig. 18.6)

TrPs in the hamstring muscles – the biceps femoris,the semimembranosus and the semitendinosus –are liable to become activated either in the bellies ofthese muscles high up on the posterior surface ofthe thigh or in their tendons at their sites of attach-ment just below the knee. It will be rememberedthat the lower attachment of the biceps femoris, thelateral hamstring, is by a tendon inserted into the fibula; the semimembranosus is inserted intothe medial condyle of the tibia; and the semitendi-nosus, together with the gracilis and sartorius muscles, are inserted by a conjoined tendon – thepes anserinus (the goose’s foot) – into the upperpart of the medial surface of the tibia (Fig. 18.7).

Pain from TrPs in the bellies of these muscles isreferred mainly to the region of the popliteal fossa(Fig. 18.8).

Chap-18.qxd 11*10*04 10:31 Page 318

pointed out, in members of the armed services whodo much marching. The pain is quickly broughtunder control by deactivating the TrP with a dryneedle, but is liable to recur if any activity respon-sible for the TrP activation is persisted with.

GASTROCNEMIUS MUSCLE (Fig. 18.11)

TrPs become activated in the belly of the musclein the centre of the calf as a result of the musclebecoming strained either, as a primary event, orwhen a limp develops as a result of a painful dis-order occurring in the heel or foot, and also when,because of a circulatory disorder, the musclebecomes ischaemic (Fig. 18.12).

The pain from TrPs in this muscle is felt in thecalf and the sole of the foot. It is often worse onwalking uphill, and may be associated with thedevelopment of nocturnal cramps. As may be seenfrom the case quoted at the beginning of the chapter,nocturnal cramps should not be treated with quin-ine sulphate until a search for TrPs in this musclehas been carried out, because, if these are present,the cramps will not be brought under control untilthey have been deactivated.

SOLEUS MUSCLE (Figs 18.9 & 18.11)

The soleus, a broad flat muscle situated immedi-ately anterior to the gastrocnemius, and which,together with the latter, is inserted into the calcaneusby means of the Achilles tendon, is liable to developTrPs in its distal third for the same reasons as theydo in the gastrocnemius.

Pain from these TrPs is referred distally alongthe Achilles tendon to the heel (Fig. 18.13). Simons &Travell (1983) state that the pain may also bereferred upwards to the sacroiliac joint. No casewith this particular pattern of referral has, as yet,come under my care. They also point out that theankle jerk may be decreased or absent in patientswith TrP activity in the soleus. And that the deacti-vation of the TrPs restores this reflex to normal.

Activation of TrPs in the gastrocnemiusand soleus as a consequence of lower leg ischaemiaIntermittent claudication (L. claudicatio, limping orlameness), a condition characterized by calf pain


Vastus medialis

Sartorius

Gracilis

Pes anserinus(Goose’s foot)

Tibia

Tibialis anteriorExtensor

retinacula

Flexorretinaculum

Abductorhallucis

Calcaneus

Tendo calcaneusFlexor hallucis longus

Flexor digitorum longus

Tibialis posterior

Soleus

Gastrocnemius,medial head

Semimembranosus

Semitendinosus

Figure 18.7 The muscles of the right leg, medial aspect.

Figure 18.8 The pattern of pain referral from a triggerpoint (�) in the belly of the biceps femoris muscle.

and foot, and sometimes extending as far as thebig toe (Fig. 18.10).

TrP activity in this muscle is liable to develop inathletes and, as Sola & Williams (1956) have

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brought on by exertion and relieved by resting(angina cruris), is primarily due to femoropoplitealartery occulusion. However, Dorigo et al (1979)have shown that another factor contributing to thepain is the activation of TrPs in the gastrocnemiusand soleus when these muscles become ischaemicas a result of an impaired arterial blood supply tothe leg. They further showed that deactivatingthese TrPs, by injecting procaine into them, increasesthe exercise capacity of the limb in spite of the bloodflow to the limb remaining the same. Deactivationof TrPs in these two muscles is therefore a worth-while symptomatic therapeutic procedure in thiscondition and one that can be carried out even

more readily and just as effectively by insertingdry needles into the tissues overlying these TrPs.

PAINFUL HEEL

Persistent pain may develop in the heel, either bybeing referred from TrPs in the soleus muscle, orfrom an inflammatory reaction occurring in eitherthe Achilles tendon, or the plantar fascia. Thisinflammatory reaction in both Achilles tendinitisand plantar fasciitis may develop as a result of someunderlying disease such as ankylosing spondylitis,psoriatic arthropathy, or Reiter’s disease. More com-monly, however, it occurs as a result of an injury to


Patellar ligament(quadriceps tendon)

Tibialis anterior

Peroneus longus

Extensor digitorum longus

Extensor hallucis longus

Upper extensor retinaculum

Lateral malleolus

Lower extensor retinaculum

Extensor digitorum brevis

Peroneus tertius

Medial malleolus

Tibialis anterior

Extensor digitorum longus

Extensor hallucis brevis

Extensor hallucis longus

Soleus

Gastrocnemius

Insertion of sartorius

Figure 18.9 Muscles on the extensor aspect of the right leg.

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the heel or pressure from an ill-fitting shoe. At timesit seems to occur for no apparent cause.

Achilles tendinitisIt is particularly important to distinguish betweenpain developing in the base of the heel as a resultof an inflammatory lesion in the tendon and pain


Figure 18.10 The pattern of pain referral from a triggerpoint (�) in the tibialis anterior muscle.

Semimembranosus

SemitendinosusGracilis

Gastrocnemiusmedial head

Flexor digitorumlongus

Calcanean tendon

Calcaneus

Peroneus longus

Peroneus brevis

Soleus

Gastrocnemiuslateral head

Plantaris

Biceps femoris

Figure 18.11 Muscles of the right calf; superficiallayer.

Figure 18.12 The pattern of pain referral from atrigger point (�) in the gastrocnemius muscle.

Figure 18.13 The pattern of pain referral from atrigger point (�) in the soleus muscle.

Chap-18.qxd 11*10*04 10:31 Page 321

referred to that site from TrPs in the soleus muscle.In Achilles tendinitis, the tendon is liable to beslightly swollen and there may be crepitus over itwhen the foot is moved. Also, on examination,exquisitely tender TrPs are to be found in the tissuesaround the tendon.

The pain may be relieved by inserting dry needles into the tissues overlying these TrPs.Admittedly, this usually has to be repeated three ormore times at weekly intervals in order to obtain anylasting benefit but it is certainly preferable to inject-ing hydrocortisone into them. Not only is hydro-cortisone associated with the development of muchpost-injection pain, but also, should it inadvertentlybe injected into the tendon itself, this structure mayrupture and then need to be repaired surgically.

Plantar fasciitisThe plantar fascia is attached by a tendon insertedinto the periosteum of the calcaneus. Trauma, withtearing or stretching of the plantar tendon fibres,causes the periosteum to become detached from thecalcaneus, with, as a consequence of this, the devel-opment of subperiosteal inflammation, the layingdown of fibrous tissue, the deposition of calciumand the formation of a calcaneal spur. It is thoughtthat the initial pain and discomfort is probably dueto the soft-tissue inflammation and that at a laterstage it is due to the spur (Cailliet 1977). However,not infrequently, there is radiographic evidence of acalcaneal spur in people who are asymptomatic.Furthermore, plantar fasciitis may occur withoutthe development of a spur. Radiographically a cal-caneal spur in traumatic fasciitis has smooth bordersin contrast to one occurring in association with aseronegative arthropathy when they are fuzzy.

Plantar fasciitis leads to the development ofsevere pain under the heel, and also, in some cases,in the sole of the foot. It is a condition that mostoften occurs in those whose work requires muchstanding. On examination, there is a point of max-imum tenderness close to where the plantar tendonattaches to the calcaneus. It is standard practice toinject hydrocortisone plus a local anaesthetic intothis point. It is often necessary to carry out this pro-cedure more than once. It is also possible to controlthe pain simply by inserting into the point of maximum tenderness a dry needle and then leaving

it in situ for 3–5 minutes. There is no need to carryout any twirling movements, particularly as at thisparticular site, it is liable to cause considerable pain.If the needle is left in place for a sufficient length oftime, with this varying according to the needs of the individual patient, it will be found on with-drawing it, that the original exquisite tendernesshas disappeared, and that weight bearing can becarried out far more comfortably. For long-termpain relief, however, it is usually necessary torepeat this procedure on several occasions. In addi-tion, strain should be taken off the plantar fascia by the wearing of a sorbo rubber heel pad with thecentre cut out.

METATARSALGIA

Metatarsalgia, a condition characterized by thedevelopment of pain and tenderness in the regionof the metatarsal heads, may be either congenitalor acquired.

Congenital metatarsalgia (Morton’s syndrome)The underlying abnormality consists of a congeni-tally short first metatarsal bone and a relatively longsecond one (Morton 1952, 1955). This makes thefoot unstable with a tendency for the ankle to rockinwards on standing. It is because of this that theankle often becomes recurrently sprained. Callusesare liable to form under the prominent secondmetatarsal head. Also, on examination, the secondtoe is seen to protrude. The diagnosis is readily con-firmed by an X-ray of the foot taken with the patientstanding. The structural instability of the foot, andthe pain in the sole occurring as a result, causes thepatient to hobble. This, in turn, puts a strain on muscles throughout the whole of the leg and becauseof this pain, frequently becomes widespread due tothe activation of TrPs in various muscles.

The instability of the foot is liable to result in thehip being held in an adducted and internally rotatedposition, the knee being internally rotated, and the ankle pronated. As a consequence of this, TrPsbecome activated in the glutei muscles, particu-larly the gluteus medius (p. 304), the vastus medi-alis (p. 332), and the peroneus longus and brevis(Travell 1975).


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TrPs in the peroneus longus are to be found onthe lateral surface of the leg about a hand’s breadthbelow the head of the fibula. TrPs in the peroneusbrevis occur lower down the outside of the legabout two hand breadths above the external malle-olus. Pain from TrPs in both these muscles is referreddown the outer side of the leg and foot often as far as the little toe, with it being felt particularlystrongly on the outer side of the ankle (Fig. 18.14).

The pain in the foot is best combated by placing apad in the shoe under the head of the first metatarsalbone. Widespread pain throughout the leg necessi-tates careful examination of the muscles from thehip downwards for TrPs and any that are exquisitelytender should then be deactivated by means ofinserting needles into them.

Acquired metatarsalgiaAn anatomical abnormality such as claw-toes oran equinus deformity of the foot leads to stretchingof the interosseous ligament and depression of thetransverse arch so that instead of, as normally, mostof the weight being placed on the 1st and 5thmetatarsal heads, it is transferred to the 2nd, 3rdand 4th heads causing them to become painful andtender.

Treatment is directed at elevating the arch byinserting a pad inside the shoe under the 2nd and3rd metatarsal bones proximal to the heads. It shouldnot be placed under the heads themselves as thisaggravates the pain.

Another cause for pain developing in the sole ofthe foot is a neuroma on the digital nerve betweenthe 3rd and 4th toes, or, occasionally, between the2nd and 3rd ones (Morton’s neuroma). This condi-tion, for some reason, most often occurs in middle-aged women who characteristically find whenaffected by it that taking off their shoes and massag-ing the soles of their feet gives them comfort.

On examination, the pain is aggravated by press-ing between the metatarsal heads rather than overthem. The pain is relieved by wearing broader shoesand by elevating the transverse arch by suitablypadding the inside of the shoe. It is also sometimesnecessary to attempt to suppress the pain by insert-ing a dry needle into a point of maximum tender-ness. If this fails to give relief, a hydrocortisone-localanaesthetic mixture should be injected into it. Inparticularly stubborn cases the neuroma may haveto be excised. It also has to be remembered thatmetatarsalgia may also herald the onset of rheuma-toid arthritis, long before the disease manifests itselfby the development of a polyarthritis.

Finally, it is important to bear in mind thatmetatarsalgia, no matter how it is caused, may, byplacing a strain on the muscles of the leg, lead toTrPs becoming activated in them, with, as a resultof this, pain developing over a wide area. Suchwidespread pain is best brought under control bydeactivating these TrPs by means of the acupunc-ture technique of inserting dry needles into the tis-sues overlying them.

PAIN IN A TOE

Pain in a toe is clearly most often due to someobvious local pathology, but occasionally the painpersists in spite of the tissues in and around thetoe having a normal appearance. In such a case itis likely that the pain is being referred to that sitefrom a TrP some distance away.

Trauma may cause TrPs to become activated ina dorsal interosseous muscle. When this occurs,pain is referred to the side of the toe to which the muscle is attached. In relation to this it will beremembered that the 1st dorsal interosseous muscle is attached to the medial side of the 2ndtoe. The 2nd, 3rd and 4th dorsal interosseous muscles are attached to the lateral side of the 2nd,3rd and 4th toes.


a

b

Figure 18.14 The pattern of pain referral from atrigger point (�) in (a) the peroneus longus muscle(b) the peroneus brevis muscle.

Chap-18.qxd 11*10*04 10:31 Page 323

Pain in the big toe may be referred from a TrPhigh up on the outer aspect of the leg in the tibialisanterior muscle, or from a TrP in the region of themedial malleolus (Fig. 18.15).

A schoolgirl (14 years of age) complained bitterly ofpain in the big toe. Her doctor was at a loss to accountfor this as the appearances of the toe were normal andan X-ray of the foot showed no abnormality.

When, 6 months later, she was seen by me, the onlyabnormality to be found was an exquisitely tenderpoint on the inside of the foot just in front of themedial malleolus. Long-term relief from the pain wasobtained by deactivating this TrP with a dry needle ontwo occasions. On going back over the history it seemslikely that she had activated the TrP some monthspreviously at a time when she wrenched her ankle inthe gymnasium.


Figure 18.15 The referral of pain to the big toe from atrigger point near to the medial malleolus.

ReferencesCailliet R 1977 Soft tissue pain and disability. F A Davis,

Philadelphia, p. 288–290Dorigo B, Bartoli V, Gristillo D, Beconi D 1979 Fibrositic

myofascial pain in intermittent claudication. Effect ofanaesthetic block of trigger points on exercise tolerance.Pain 6: 183–190

Morton D J 1952 Human locomotion and body form. Astudy of gravity and man. Williams & Wilkins, Baltimore

Morton D J 1955 Foot disorders in women. Journal of theAmerican Medical Women’s Association Feb 10: 41–46

Simons D G, Travell J G 1983 Myofascial origins of low backpain. Postgraduate Medicine 73: 66–108

Simons D G, Travell J G 1984 Myofascial pain syndromes.In: Wall P D, Melzack R (eds) Textbook of Pain. ChurchillLivingstone, Edinburgh, p. 271


Travell J 1952 Pain mechanisms in connective tissue. In:Ragan C (ed) Connective Tissues, Transactions of theSecond Conference, 1951, Josiah Macy Jnr Foundation,New York, p. 86–125

Travell J 1975 Pain and the Dudley J Morton foot (longsecond toe). Archives of Physical Medicine andRehabilitation 56: 566

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INTRODUCTION

In this chapter pain in and around various jointsthat have not already been considered in previouschapters will be discussed. A detailed account willbe given as to how acupuncture may be used toalleviate the pain of osteoarthritis, and also thepain in and around a non-arthritic joint that occursas a result of its referral there from distant myofas-cial trigger points (MTrPs). Brief reference will alsobe made to its limited application in the treatmentof rheumatoid arthritis.

OSTEOARTHRITIS

In order to be able to give a rational explanation asto how acupuncture may be used, either alone, or inconjunction with other forms of treatment, in thealleviation of osteoarthritic pain, it is first necessaryto give a short summary of present-day knowledgeconcerning the aetiology and pathology of the dis-order. In particular it is important to consider thevarious mechanisms thought to be responsible forthe development of its characteristic type of pain.

Modes of presentationThe manner in which this condition presents andthe course it takes are widely variable depending onwhether it affects one joint alone or many, and inthe case of the latter, depending on which joints inparticular are involved. Its presentation and naturalhistory are also influenced by whether it occurs asa separate entity or as part of some systemic disease.

325

Chapter 19

Pain in and around joints

CHAPTER CONTENTS

Introduction 325Osteoarthritis:

Overview of pathophysiology andmanagement 326–330

Knee joint 331–335Hip joint 335–337Small joints of the hands and feet, elbow joint

and ankle joint 337–338Referral of pain to non-arthritic joints from

distant MTrPs 331, 334, 336Clinical trials to assess the value of acupuncture

in relieving osteoarthritic pain 338–339Rheumatoid arthritis 339

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Other predisposing factors include age, gender,obesity and race (Creamer 1999).

Monarticular hip diseaseOsteoarthritis of the hip joint sometimes occursalone, and would then seem to be a separate entityif for no other reason than, unlike generalizedosteoarthritis, it is commoner in men (Wood 1976).The clinical course is also different. Pain in general-ized osteoarthritis tends to be episodic but the painin monarticular hip disease is usually persistentwith a slow or, at times, rapid increase in intensity.This is a distinction of some importance consider-ing how essential it is to take into account the natural history of pain from any particular jointwhen attempting to assess the effectiveness of sometreatment, such as acupuncture, in relieving it.

Primary and secondary osteoarthritisOsteoarthritis is traditionally divided into twogroups, a primary one, and one in which it occurssecondary to some underlying disorder. This, how-ever, is far from satisfactory because although,admittedly, examples of the latter include congen-ital, traumatic and inflammatory conditions actinglocally and various metabolic diseases such as alka-ptonuria and haemochromatosis affecting the bodyin general, it is often by no means clear why so-called secondary osteoarthritis should developas a result of, for example, some relatively minorcongenital disorder of a joint. The term primary isalso somewhat of a misnomer. Idiopathic or cryp-togenic would be far more appropriate, for there isno doubt that the more that becomes known aboutthe condition, the smaller this group will become.

Biochemical and mechanical factors in the aetiology of the diseaseAs stated earlier, the long-held concept that pri-mary osteoarthritis is entirely mechanical in originand due to ‘wear and tear’ of the cartilage is nolonger tenable. It is true that a mechanical factorplays a part in its development, but there are nowgood reasons for believing that biochemical factors,yet to be identified, must also contribute.

Joints involvedThe joints most commonly affected by this disorderare the knee, hip and small joints of the hands andfeet, including the carpo-metacarpal joint of thethumb, the terminal interphalangeal joints of thefingers (sometimes in association with Heberden’snodes), the proximal interphalangeal joints (some-times in association with Bouchard’s nodes), andthe metatarsophalangeal joint of the big toe.

The disorder may be monarticular but it is notuncommon, particularly in women, for it to begeneralized and affect the knees and small joints ofthe hands and feet concomitantly (Huskisson et al1979).

Other joints that may occasionally becomeosteoarthritic are the shoulder and elbow. The cer-vical and lumbar facet joints are also usuallyincluded amongst those liable to be affected but,as already discussed in Chapters 14 and 17, degen-erative changes both in these joints and the inter-vertebral discs in the disorder known as spondyli-tis only cause chronic cervical and lumbar painto develop when they give rise to nerve rootentrapment.

Predisposing factorsIt is generally agreed that genetic factors play amajor role in the development of osteoarthritis(Stecher 1955, Kellgren et al 1963) but, as Harper &Nuki (1980) have pointed out, there is still much tobe learnt about these.

This genetic predisposition is of particularimportance because for a long time the disorderwas considered to be more likely to occur in jointsrepeatedly subjected to trauma. It was said, forexample, to be more common in miners workingunderground, particularly in confined spaces.Huskisson (1985), however, points out that thisapparent, somewhat simplistic link betweenosteoarthritis and trauma is not confirmed byrecent studies that show, for example, thatosteoarthritis of the knee is no commoner in para-chute jumpers or footballers, except in those whohave had a menisectomy, and then there wouldseem to be some genetically determined under-lying biochemical predilection in addition to themechanical insult to the joint.

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Inflammation of the synoviumIn recent years it has become apparent that chronicinflammation of the synovium is an important fea-ture in the pathology of the disease. This is a find-ing of considerable significance as it has led to abetter understanding of the mechanisms respon-sible for the pain, and as a direct result of this to amore rational approach to methods of alleviating it.

The disease in fact was originally known asosteoarthritis, but in order to emphasize what wasconsidered to be its mechanistic nature, it becamefashionable, not so long ago, to call it osteoarthro-sis. However, with recent recognition (Dieppe 1978)that inflammation of the synovium is an importantpart of the pathological process, it is clearly prefer-able to revert to the original terminology. The tis-sue first to be affected and ultimately destroyed inosteoarthritis is cartilage, and fragments of thisfloating in the joint space are known to cause aninflammatory reaction in the synovium (George &Chrisman 1968). In addition, various chemical sub-stances, such as pyrophosphates (McCarty 1976)and hydroxyapatite (Dieppe et al 1976, Schumacheret al 1977), found on occasions in crystal form inosteoarthritic joints, may also contribute to thisinflammatory response in some patients.

The realization that an inflammation of the syn-ovium similar to that seen in rheumatoid arthritisoccurs in osteoarthritis has come from observa-tions made both by clinicians and pathologists.

Clinically, it has now become widely recognizedthat an osteoarthritic joint may not only be painfulbut may also show evidence of warmth, swelling,redness, and stiffness on waking and after pro-longed sitting. These are, as Ehrlich (1975) haspointed out, all classical symptoms and signs ofinflammation. It is interesting to note with respectto this that Huskisson et al (1979), in comparing andcontrasting the clinical features of 100 consecutivecases of rheumatoid arthritis and 100 consecutivecases of osteoarthritis, frequently found evidenceof inflammation in those with osteoarthritis. Suchevidence included morning stiffness, redness ofdistal interphalangeal joints, warmth, and effusionin the knees. And as they said:

… the absence of morning stiffness has oftenbeen suggested as a helpful diagnostic feature ofosteoarthritis, but it was noted by almost as

many of our patients with osteoarthritis as thosewith rheumatoid arthritis. Synovial fluid alsoprovided evidence for a low-grade inflammationwith greater than normal number of cells.

Evidence for an inflammatory reaction beingpresent has also been obtained by thermographyconfirming that osteoarthritic joints are warm(Collins et al 1976), although not to the same degreeas in rheumatoid arthritis, thus confirming the clin-ical impression that the reaction is less severe.

Pathological evidence of an inflammatory reac-tion in the synovium includes Cooper et al’s (1981)finding of this to be present in synovial tissuetaken from patients with osteoarthritis as com-monly as in tissue taken from patients with rheuma-toid arthritis. Schumacher et al (1981) observedsynovial inflammation to be present in a large pro-portion of osteoarthritic knees examined at autopsy,and Goldenberg et al (1982) noted its presence in the majority of synovial specimens taken fromosteoarthritic patients during the course of surgicaloperations.

Much space has been devoted to discussing thisinflammatory change, because, as Fassbender (1975)has said, and as will be seen from the following dis-cussion, it is in general only when synovitis occursin an osteoarthritic joint that it becomes painful.

Pathological changes in an osteoarthriticjoint, and the relationship of these to the production of painAs has already been stated, the primary change inosteoarthritis is the destruction of the articular car-tilage, and with the narrowing of the joint spacethat occurs as a result of this, changes take placefairly quickly in the underlying bone (Radin et al1976). These include microfractures, sclerosis, andremodelling of the bone with the formation ofosteophytes and the development of cysts.

When attempting to understand how pain mayarise in an osteoarthritic joint, it is important toappreciate that there are no receptor nerve end-ings in the articular cartilage, synovium, or themenisci (Wyke 1981). Pain therefore cannot arisedirectly from the cartilage itself.

Subchondral bone, however, is well sup-plied with nerves and therefore it would not be

Pain in and around joints 327

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unreasonable to assume that the various changesjust described that take place in it and that start todevelop at an early stage in the disease, are likelyto generate pain. It is therefore somewhat surpris-ing to find that there is no good evidence for this.For example, Lawrence et al (1966), in studyingthe relationship between symptoms and X-raychanges in an extensive population survey, foundthat bone cysts in the metacarpophalangeal jointsand hip joints were seen no more frequently inthose with pain than in those without pain. AndDanielsson’s (1964) 10 years’ prospective study ofpatients with osteophytes in the region of the hipshowed that they contributed little to the evolu-tion of the osteoarthritic process or to the develop-ment of pain.

This therefore explains the seeming paradoxthat it is possible to have extensive osteoarthriticchanges in a joint, including a well-marked loss ofjoint space, sclerosis, cysts and osteophytes demon-strable radiographically, and yet for the joint not tobe painful. And, as a corollary to this, it can neverbe assumed just because an X-ray shows changesof the disease in a joint that any pain from which aperson may be suffering necessarily comes fromthis source. It is only possible to make a decisionabout this following a careful clinical examination.

Although it is true that at rest pain in the kneeor hip may occur as a result of intramedullaryvenous stasis and hypertension both in patientswith osteoarthritis of these joints and in those with-out (Arnoldi et al 1980), most of the various formsof pain that often occur episodically in osteoarth-ritis, including the morning stiffness and the achingtype of discomfort that initially comes on withmovements but subsequently occurs at rest andalso at night, would seem to develop only if andwhen there is inflammation of the synovium.

The synovium itself, as stated earlier, is devoidof nociceptive receptors but when it becomesinflamed, and because of the effect this has onother tissues, pain occurs as a result of stimulationof nerve endings in the synovial blood vessels, thejoint capsule, the fat pads, the collateral ligaments,and the adjacent muscles. There are various waysin which this occurs.

Firstly, there are nociceptive receptors in theadventitial sheaths of the vessels in the wall of thesynovial sac, and when the latter becomes inflamed,

stretching of these receptors leads to the productionof pain.

Secondly, pain occurs because chemical sub-stances such as 5-hydroxytryptamine, prosta-glandins, histamine, and polypeptide kininsreleased from inflamed synovial cells get carried inthe synovial fluid to the adjacent articular fat padsand joint capsule, where they have an irritant effecton the nociceptive receptors in these structures.

Thirdly, the fibrosis that ultimately develops inthe capsule, and even at times in the adjacent muscles, in cases in which the inflammatory pro-cess becomes chronic, causes the tissues to contract,and this again leads to stimulation of their sensoryreceptors, particularly with movements of the joint.

Fourthly, pain develops because the changes that take place in an osteoarthritic joint lead tostrain developing in various periarticular struc-tures including the adjacent collateral ligaments, themuscle tendons, particularly at their sites of attach-ment to bone, the muscles around the joint, and incases where a faulty posture develops, in musclessome distance from it. As a result exquisitely tender‘spots’ (points of maximum tenderness) developin periarticular structures.The exquisite tendernessof these points is due to them being sites wherenociceptive nerve endings are in an activated andsensitized state, and it is because of this that theyare particularly important sources of osteoarthriticpain so that, as will later be discussed, treatmentdirected at conteracting this increased nociceptiveactivity by means of the carrying out of superficialdry needling is often all that is necessary to abolishthe arthralgia.These points of maximum tender-ness when present in muscles and ligaments in thevicinity of the joint have the characteristics of TrPs,with pressure applied to them causing pain to bereferred to the joint region. Others, however, suchas those to be found in the tissues around arthriticsmall joints of the hand and in articular fat pads ofknees have the characteristics of tender points,with pressure applied to them causing pain to befelt locally at these sites.

Pain and its correlation with X-ray changesIt can therefore be seen from what has just beensaid that the reason for pain developing in anosteoarthritic joint is not because of cartilage


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damage, or of structural alterations in the subchon-drial bone’s architecture, but mainly because ofchanges in the soft tissues of the joint and periar-ticular structures causing nociceptive nerve endingactivity to develop at trigger and tender point sites.As previously mentioned, this explains why pain inosteoarthritis does not necessarily correlate with theextent of the radiological changes. The one excep-tion to this is osteoarthritis of the hip where gener-ally the pain is proportional to the extent of thejoint damage seen on a radiograph (Kellgren 1961).

Management of osteoarthritisAs there is, as yet, no means of arresting osteoarth-ritis, its management in the main is directed towardsthe symptomatic relief of pain up to the time whenreplacement of the joint proves to be necessary.

It is my belief that a TrP approach to acupunc-ture has an important place in this but it shouldnot be looked upon as a technique necessarily tobe used on its own but rather one that at timesshould be used in conjunction with other forms oftherapy. It is therefore necessary to say somethingabout the advantages and disadvantages of thesein order that their place relative to that of acupunc-ture can be seen in a proper perspective.

Dieting

Many studies have shown a relationship betweenobesity and osteoarthritis, particularly when thisaffects the knee joint in women (Felson et al 1988,Schouten et al 1992).

Martin et al (1996), in a study of post-menopausalobese women with knee osteoarthritis have shownthat dieting and exercise carried out over a 6-month period led to the alleviation of the painand improved function.

Analgesics

Simple analgesics may be helpful, but the discoverythat the occurrence of pain in this disorder is closelyassociated with the development of an inflamma-tory process has led to an increased use of non-steroidal anti-inflammatory drugs (NSAIDs).

When considering the use of an analgesic or aNSAID, it is as well to remember that aspirin hasthe properties of both.

Non-steroidal anti-inflammatory drugs It hasto be kept in mind when contemplating the use ofNSAIDs in osteoarthritis that most of the patientssuffering from this are elderly, and that because ofthis their metabolism and excretion of drugs areoften impaired. Moreover, because those in laterlife frequently need a variety of drugs for manydifferent complaints, there is always the risk ofdrugs interacting. NSAIDs, for example, oftenincrease the effects of anticoagulants, and decreasethose of diuretics.

NSAIDs, too, by inhibiting the synthesis ofprostaglandins, are liable to aggravate late-onsetasthma, and in conditions such as the nephroticsyndrome, hepatocellular failure, and cardiac fail-ure, in which glomerural filtration is prostaglandin-dependent, their use is liable to precipitate uraemiaand increase oedema. Also, because of their effecton prostaglandins they are liable to cause gas-trointestinal bleeding, either from an erosive gas-tritis or peptic ulcer, which is a particularly seriousevent in an elderly arteriosclerotic person.

Although it is generally agreed that all NSAIDshave potentially dangerous side effects, their advan-tages must be weighed against their disadvantages,and there is no doubt that when used judiciouslythis group of drugs often gives dramatic relief.

It is important to bear in mind that they shouldnever be prescribed on a long-term basis, butalways intermittently and even then in the lowestpossible dosage. Also, there are times when thepresence of other conditions or individual intoler-ance precludes their use, and since adverse reportsconcerning them have reached the popular press,an increasing number of the public are refusing totake them. Furthermore, as Creamer (1999) has said‘evidence for the superiority of NSAIDS over para-cetamol is largely lacking and, at least under trialconditions, many patients on chronic NSAID ther-apy for knee osteoarthritis can cease medicationwithout apparent deterioration in symptoms’.

Physiotherapy

Controlled trials of different forms of physiother-apy including immersing the hands in warm wax,short-wave diathermy, infra-red irradiation, andfaradism show that all of them give a certainamount of temporary relief, but none are of any


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lasting value (Hamilton et al 1959). There are cer-tain physical measures, however, that are of con-siderable help. For those with osteoarthritis of thehip or knee, it is useful to carry a walking stick heldin the contralateral hand. Warm baths and swim-ming are of benefit for those with hip disease. It hasalso been shown (Fisher et al 1993) that quadricepsstrengthening exercises reduce pain and improvefunction in patients with knee osteoarthritis.

Intra-articular injections of corticosteroids

As the pain in osteoarthritis would seem to bedirectly related to the development of an inflamma-tory reaction in the synovium it might be thoughtthat it would be helpful to inject a corticosteroidinto the joint. In general, however, the results havebeen disappointing. Miller et al (1958) and Wrightet al (1960) showed that such injections give no better results than can be obtained from injectionsof a placebo. Admittedly, Dieppe et al (1980), usinga long-acting preparation, triamcinolone hexace-tonide, found that the relief from pain with this wasgreater than with a placebo, but even so the bene-fit was so slight and short lasting as to lead them toconclude that this form of treatment could not berecommended for use in everyday clinical practice.

This notwithstanding, controlled trials of theuse of intra-articular steroids in the treatment ofknee osteoarthritis provide some evidence of theirefficacy, but only for up to 4 weeks (Creamer 1997).

Aspiration of a synovial effusion

The effusion developing as a result of synovitis issometimes so large that the volume of fluid itselfcauses pain. In such a case simply aspirating itoften affords considerable relief.

Treatment directed at periarticular points ofmaximum tenderness

There is no doubt that when attempting to allevi-ate osteoarthritic pain by some method appliedlocally to the joint, by far the best is to employsome technique directed specifically at the TrPsand tender points that, as stated earlier, are to befound in various structures in and around the joint.There are essentially three ways of doing this: either

to inject hydrocortisone or a local anaesthetic intothem as advocated by Dixon (1965) for the relief of osteoarthritic knee joint pain, or to deactivatethem by means of the acupuncture technique ofstimulating A-delta nerve fibres in the overlyingtissues with dry needles.

When deciding which of these methods to adopt,it has to be remembered that a local anaesthetic,when injected into either a TrP or a tender point,does not depend for its pain-suppressing effect onits ability to anaesthetize nerve endings. In the sameway a corticosteroid does not achieve this effectsolely because of its local anti-inflammatory action.What these methods have in common, as with theinjection of many other substances, including saline,is that of having a non-specific irritant effect on A-delta nerve fibres that in turn activates centrallyplaced pain-modulating mechanisms, in exactly thesame manner as the carrying out of superficial dryneedling at such points achieves this. Furthermore,there is reason to believe that this latter form oftreatment increases plasma cortisol levels. Roth et al(1997), in experiments on 20 healthy male students,showed that manual stimulation of acupuncturepoints brings about a significant increase in cortisollevels 5, 25 and 45 min after cessation of the stimu-lation. It is findings such as this that may explain, asPomeranz (2001) has said, why acupuncture is help-ful in suppressing the inflammation of arthritis.

The clinical observation that not infrequently following manual acupuncture for the relief of painin an osteoarthritic small joint of the hand there is asignificant decrease in the periarticular soft-tissueswelling may presumably be because of this. Thefollowing case is a particularly striking example:

A housewife (62 years of age) was referred to me witha 6-month history of severe pain from an osteoarthriticfirst carpometacarpal joint. On examination, the tissuesaround the joint were noted to be considerably swollen.Nevertheless, within 3 days of deactivating TrPs withdry needles for the first time, the swelling totallydisappeared, and after a further three treatment sessionsthere was long-term relief from pain.

PAIN FROM A SPRAINED JOINT

When a joint becomes sprained much of the pain islikely to arise as a result of TrPs in the soft tissues


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around it becoming activated and may, conse-quently, be alleviated by the carrying out of super-ficial dry needling at these points.

KNEE JOINT

Pain in and around a normal knee jointPain in and around a normal knee joint may bereferred there from an arthritic hip joint. Also fromTrPs in one or more muscles some distance fromthe joint. These include (Baldry 2001) the anter-iorly situated adductor longus, rectus femoris,vastus medialis, vastus lateralis and the poster-iorly situated semimembranosus, semitendinosus,biceps femoris and popliteus.

Osteoarthritis of the knee jointOsteoarthritis commonly involves the knee jointand when it does so it affects either the patello-femoral compartment, or the medial or lateraltibiofemoral compartments, or any combination of these.

Patellofemoral compartment

Involvement of the patellofemoral compartment is occasionally the predominant feature and has to be distinguished from chondromalacia patellae,a disorder of adolescents and young adults. Thisparticular disorder often starts between the ages of15 and 30 years, and usually begins on the medialaspect of the patella. The reason for this, as Wiberg(1941) has shown, is that whereas contact betweenthe lateral facet of the patella and the femur isgood at all stages of flexion, contact between themedial facet and its corresponding condyle on thefemur is poor at about 90° of flexion with, as a consequence of this, undue wear of the cartilagetaking place at this site. The condition, somewhatsurprisingly, sometimes gradually remits, but atother times slowly progresses over the years andbecomes indistinguishable from osteoarthritis.

The symptoms of the condition are pain behindthe patella on walking and, in particular, ondescending stairs. On examination of the joint,there is patella crepitation. A good diagnostic test is

the eliciting of pain by getting the patient to con-tract the quadriceps whilst the patella is held firmlyagainst the femoral condyles. Also, in favour ofthe diagnosis is the eliciting of pain by sliding the patella to one side or the other, with the legextended. On palpation of the soft tissues TrPs areto be found along the sides of the patella. The com-monest site for these is its upper lateral edge(Dixon 1965).

The pain in this condition, which typically isintermittent in nature, is readily alleviated bydeactivating these TrPs by means of inserting dryneedles into the tissues overlying them. It is a pro-cedure, however, because of the nature of the dis-ease, that usually has to be repeated from time totime. Occasionally the pain is so persistent as tonecessitate some form of surgery being carried out.

Tibiofemoral compartments

With osteoarthritis of the tibiofemoral compart-ments, changes usually occur in both the medial andlateral ones but they are commonly most markedon the medial side.

Pain arises as a result of TrP activity developingin the collateral ligaments, in tendons adjacent tothem, in the articular fat pads, and in muscles nearto and, at times, some distance from the joint. Also,in muscles in and around the popliteal fossa.

TrPs in the collateral ligaments TrPs are usuallyto be found in these ligaments at their upper andlower attachments (Fig. 19.1). One of the common-est sites is the anteromedial aspect of the upper partof the tibia in the area somewhat fancifully knownas the pes anserinus or goose’s foot (Fig. 18.7). Thepes anserinus is where the lower part of the medialcollateral ligament, and superficial to this, the ten-dons of the sartorius, gracilis, and semitendinosusmuscles become attached to the tibia. A bursa ispresent between the ligament and tendons.

Careful inspection will often reveal several TrPsin this area, and for the best results, it is necessary todeactivate each one of them with a dry needle. It isinteresting to note, however, that in the traditionalChinese system, there is only one acupuncturepoint in this area – the so-called Spleen 9 (Fig. 16.3).

Tender points in the medial and lateral articularfat pads The fat pads are extrasynovial, but


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intracapsular, and change their shape with everymovement of the knee. Tender points in thesestructures are to be found on either side of thequadriceps tendon. The medial fat pad is the onemost commonly affected (Fig. 19.1).

TrPs in the vastus medialis muscle TrPs areoften found in the vastus medialis muscle justabove the knee (Fig. 19.1). In conjunction with TrPsat other sites they may be a source of pain, but on

occasions without pain developing, they are thecause of the knee suddenly buckling. As Travell(1951) has pointed out, this structure is the mainmuscular support of the knee and when, as some-times happens, TrP activity in it occurs in isolation,the contraction of the muscle is in some way inhib-ited before pain develops, with, in consequence, theknee suddenly giving way without warning, andcausing what is tantamount to a ‘drop’ attack.

TrPs in the iliotibial tract The strain imposedon the lower limb by an osteoarthritic knee jointsometimes leads to TrPs developing along theouter side of the thigh in the iliotibial tract, andbelow the knee between the tibia and fibula, withone often coinciding in position with the well-known Chinese acupuncture point, Stomach 36(Fig. 19.1).

TrPs in the popliteal fossa The main sites whereTrPs are sometimes to be found in the poplitealfossa are in the midline and along its outer borders(Fig. 19.2). The point, at the centre of the fossa inthe midline, situated in the popliteus muscle, cor-responds in position with the traditional Chineseacupuncture point, Urinary Bladder 40. On theouter side points may be found, above, in the bicepsfemoris, and below, in the lateral head of the gas-trocnemius. And, on the inner side, points may befound, above, in the vicinity of the semimembra-nosus and semitendinosus tendons, and below, inthe medial head of the gastrocnemius. It is inter-esting to note that there are two Chinese acupunc-ture points on the outer sides of the popliteal fossanamely, Urinary Bladder 39 on the lateral side, andKidney 10 on the medial side (Fig. 19.2).

Factors influencing response to treatment

Whilst bearing in mind that osteoarthritic pain inthe knee, certainly in the earlier stages of the dis-ease, tends to be episodic with natural remissions,it would seem that with treatment directed at TrPsin and around the joint, it is possible to obtain,often in a quite dramatic manner, long-lasting relieffrom pain of many months’ duration.

Factors, however, that may influence the responseinclude joint instability, obesity and unequal leglength.


TP1

TP2

TP3

TP4

TP2TP3

TP4TP5

A

Extra 32

Spleen 10

Spleen 9

Stomach 34

Stomach 35& Extra 32

Stomach 36

B

Figure 19.1A and B (A) Trigger points (�) on theanterior aspect of the knee. (1) in the vastus medialismuscle. (2) & (4) at the upper and lower insertions of thecollateral ligaments. (3) in fat pads (Both these triggerpoints corresponding in position with traditional Chineseacupuncture points Extra 32 and, on the lateral side alsowith Stomach 35). (5) Trigger point corresponding inposition with traditional Chinese acupuncture pointStomach 36. (B) Traditional Chinese acupuncture points (•).

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Joint instability

Progressive degenerative changes in the cartilageand subchondrial bone may ultimately lead todevelopment of considerable joint instability. Whenthis occurs, the strain imposed upon the surround-ing ligaments and muscles causes TrPs in thesestructures to remain in a state of persistent activity.It is because of this that any relief from painobtained by deactivating these TrPs with dry nee-dles tends to be only short lived. However, in spiteof this, it is often possible by repeating treatmentat frequent intervals to considerably improve thequality of a person’s life.

A housewife (62 years of age) was referred to me foracupuncture with a 5-year history of severe pain inthe right knee, which for the past year had become sobad that she could do nothing more than hobblearound the house with the aid of a stick.

On examination there was evidence of marked jointinstability; also, the scar of a patellectomy carried outfor osteoarthritis of the patellofemoral compartment.The current X-ray showed extensive changes of thisdisease, affecting particularly the medial tibiofemoralcompartment.

Exquisitely tender TrPs were found in and around the medial collateral ligament, with deactivation ofthese by dry needle stimulation giving immediate relieffrom pain. But, in spite of repeating this procedure onseveral occasions, the relief never lasted for more than2–3 weeks. The patient would not contemplateundergoing any further surgery. However, by repeatingacupuncture every 3 weeks for over 4 years now, thepain has been kept under such good control as to allowher to lead a reasonably active life, including doing herown shopping and gardening. The object lesson here isthat with acupuncture, provided a patient has sufficienttenacity of purpose to persevere with treatment, it isoften possible to obtain long-term benefit from thecumulative effects of short-term pain relief.

Obesity

It is not uncommon for a person suffering fromobesity to develop osteoarthritis of the knee joint.The relationship between the two, however, is farfrom clear. The rarity of the disease developing inthe ankle joint, except when it has been subjectedto some form of trauma, shows that excessiveweight bearing is not an important aetiologicalfactor. There is no doubt, however, that obesityaggravates the condition and this is probablybecause of the fact that it impedes the body’s normalmovements. Dixon (1965) considers the ‘Fat lady’sknee’ to be a distinct clinical syndrome that includesmedial ligament strain, excessive tenderness overthe medial ligament, and tender hypertrophy offat pads medial and posterior to the knee. In hisseries of cases with this syndrome, infiltration ofthe medial ligament and tender fat pads with alocal anaesthetic produced no lasting benefit.

He found that the pain was relieved in the minor-ity who could be persuaded to lose weight, but


a

b

c

Figure 19.2 Trigger points (�) and traditional Chineseacupuncture points (•) in the region of the poplitealfossa. The central trigger point corresponds in positionwith the traditional Chinese acupuncture point UrinaryBladder 40(a). Acupuncture points b & c are UrinaryBladder 39 and Kidney 10 respectively.

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concluded that the full syndrome of ‘Fat lady’s knee’is hard to help. This has not always been my experi-ence when treating osteoarthritis of the knee inobese women with acupuncture, although for anylasting benefit to be obtained this has to be repeatedseveral times. Unfortunately, Dixon does not statehow often injections of a local anaesthetic weregiven. If only once, as the report seems to imply, thenit is no wonder that the results were disappointing.Many fat middle-aged females that have been undermy care with this condition have obtained relativelylong remissions from pain that has been present forseveral months or years after deactivating TrPs bymeans of the carrying out of superficial dry needlingfirstly weekly and then, if necessary, depending oneach patient’s individual responsiveness, at gradu-ally increasing intervals. The following case is one ofthe more impressive examples:

A 22 stone (139.7 kg) lady hobbled into my consultingroom on a stick having persuaded her generalpractitioner to let her try acupuncture for severe painof 8 years’ duration in osteoarthritic knees. He told her that in view of her considerable obesity she waswasting her time. This was an opinion that, at thattime, was shared by me, especially as on examinationthere was considerable swelling of the joints with awell-marked genu varus deformity. However, not todisappoint her, needles were inserted into the tissuesoverlying TrPs in the medial ligament and the vastusmedialis muscle. After two treatments the pain wassufficiently alleviated as to allow her to give up using astick, and after two more treatments, i.e. 1 month fromstarting treatment, she became virtually free from pain.In addition, in spite of only managing to lose about 2 stone, she remained like this for 12 months. At thatstage further treatment had to be given, but onceagain her response was similarly gratifying.

Short leg syndrome

It is important in examining the knee joint to takeaccount of the length of the two legs (see Ch. 17),as when there is real or apparent shortening of one leg, the knee on the contralateral side is liableto become osteoarthritic. This occurs because thecompensatory position of flexion and externalrotation in which the ‘longer’ leg is held on walk-ing, causes abnormal stretching of the medial

ligament, and the excessive lateral mobility of the knee joint occurring as a result of this, leads tothe development of destructive changes in thejoint and particularly its lateral femoropatellarcompartment.

Any relief from pain obtained by deactivat-ing TrPs that develop in the soft tissues is liableto be short lived unless the shortness of thecontralateral leg is corrected by the wearing of araised shoe.

Pain referred to the knee from some distant site

As Kellgren pointed out over 40 years ago (Ch. 4),pain in the region of the knee may occur as a resultof being referred there either from the hip joint, orfrom tissues around the lumbar spine, or from themuscles of the thigh. Any examination of a painfulknee should, therefore, always include an examin-ation for TrPs in muscles or tendons at these sites.Radiographic evidence of arthritis in the knee jointis no reason for omitting this search because, asalready stated, no matter how extensive the car-tilage and bone changes from this may be, they arenot in themselves a cause of pain.

A schoolmistress (56 years of age) was sent to me with a 5-month history of severe pain in the knees,due, according to the referral letter, to radiographicallyconfirmed osteoarthritis in these joints.

On examination, the contours and movements of thejoints were normal and, most important of all, therewere no TrPs in the soft tissues around them. Therewere, however, exquisitely tender ones in the region ofboth sacroiliac joints, also down the outer sides of thelegs in the upper parts of the iliotibial tracts, and inmuscles in the upper inner parts of the thighs.

In order to alleviate the knee pain, it was necessary to deactivate all of these TrPs by insertingdry needles into the tissues overlying them and, inorder to obtain lasting benefit, to repeat thisprocedure on five occasions at weekly intervals.

Persistent pain from a ‘strained’ non-osteoarthritic kneeThe activation of TrPs in the soft tissues aroundthe knee joint, in exactly the same sites as in


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osteoarthritis, may occur as a result of trauma. Asanywhere else in the body, failure to recognizetheir presence and to deal with them appropriatelymay lead to many months of unnecessary disability.

A builder’s labourer (43 years of age) fell off somescaffolding, and shortly after this the left knee becameswollen and painful. The swelling quickly subsided butthe pain persisted and 3 months after the accident, hewas seen by an orthopaedic surgeon. He detected noabnormality either on clinical examination or onarthroscopy, and, more to placate the patient than forany other reason, arranged for him to have a course ofphysiotherapy. When, after a further 2 months, the painwas no better, the surgeon concluded that there couldbe no organic cause for it.

After the patient had been off work for 9 months,and in imminent danger of losing his job, his doctorreferred him to me for assessment as to whetheracupuncture might be of help.

The patient, a sensible, placid and, quite obviously,normally a very hard working type of person, told methat he was in a state of despair because, although hehad full movements of the knee, it ached persistentlyand this was so bad at nights as to prevent him fromgetting any sleep.

On examination, there were two exquisitely tenderTrPs immediately adjacent to the upper medial andlateral edges of the patella, and another one on themedial aspect of the tibia just below the knee. Afterdeactivating these TrPs with dry needles on only twooccasions, he lost his pain and within a very short timewas able to get back to work.

Hip osteoarthritisOsteoarthritis of the hip may develop in adultsunder the age of 40 years, if the joint has beendamaged by some inflammatory arthritis, or sub-jected to strain from some congenital or acquireddeformity. Far more commonly, however, it affectspeople from middle age onwards.

The pain in osteoarthritis of this joint takes theform of a severe dull ache that, over the course oftime, gets progressively worse. It is, therefore, unlikethe episodic type of pain that so commonly occurswhen other joints are affected by this disorder. It isfelt especially in the groin, the inguinal region, overthe greater trochanter, and outer side of the buttock.


The pain may also be referred to the knee jointdue to both this and the hip joint being innervatedby the obturator nerve. The strain imposed on themuscles of the back may cause pain to develop inthe lumbar region and it may also radiate downthe thigh, particularly on the outer side.

The pain, which initially is aggravated by walk-ing and relieved by resting, is at a later stage pre-sent the whole time. On clinical examination, thereis pain on movement of the joint, and limitation ofits movements with those particularly affectedbeing internal rotation and extension. Atrophy ofthe gluteal and quadriceps muscles may beobserved. On palpation periarticular TrPs are foundto be present.

The pain, which in the case of this particular hipjoint, is in direct proportion to the extent of jointdamage seen on a radiograph (De Ceulaer &Watson Buchanan 1979) would seem to be due toseveral different causes.

As stated previously, the cartilage does not havea nerve supply and, surprisingly, neither osteo-phytes (Danielsson 1964) nor bone cysts (Lawrenceet al 1966) in themselves would seem to give riseto pain. However, large cysts in the femoral headmay cause the latter to collapse with the produc-tion of sudden intense pain.

Pain in the hip, as in the knee, both whenosteoarthritis is present and when it is not, is occa-sionally due to intraosseous venous stasis andintraosseous hypertension – the so-called ‘intra-osseous engorgement pain syndrome’ (Lemperg &Arnoldi 1978). This pain, which is worse towardsthe end of the day’s activities, and persists at rest,may be alleviated by lowering the intraosseouspressure by some surgical procedure such as anosteotomy (Arnoldi et al 1971).

The pain that acupuncture is able to influence isthat which develops as a result of TrPs that havebecome activated in the periarticular tissues forthe same reasons as those that appear in osteo-arthritis of the knee joint.

Examination for TrPs

No examination to establish the cause of pain in andaround the hip joint is complete without a system-atic search for TrPs. There are three main sites wherethese are usually to be found, irrespective of

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whether the pain is due to osteoarthritis of the hip oris primarily muscular in origin. In distinguishingbetween these two causes of pain in the region itshould be remembered that with osteoarthritis thereis often considerable limitation of movements of thejoint and usually, but not always, by the time thatpain from this condition develops there are charac-teristic abnormalities to be seen on a radiograph.There are occasions, however, in the early stages ofthe disease when the pain of a restrictive capsulitisdevelops before X-ray changes become apparent.

Location of TrPs in arthritis of the hip joint andnon-arthritic painful disorders around it

TrPs are mainly to be found at one or more of thefollowing three sites: the groin, the upper part ofthe thigh close to where the femoral artery passesbehind the inguinal ligament, and in the vicinityof the greater trochanter.

TrPs in the groin usually develop in the adductorlongus muscle near to its insertion into the pubicbone (Travell 1950) (Fig. 18.1).

In addition, there is sometimes a TrP to befound immediately below the inguinal ligament,anterior to the capsule of the joint, in the iliopsoasmuscle (Fig. 17.15).

TrPs also frequently occur in muscles in theregion of the greater trochanter, and in particularin the gluteus medius and minimus close to wherethese muscles become attached to it. In order notto overlook any of the TrPs in this region it is necessary to palpate the tissues overlying andadjacent to the greater trochanter in a systematicmanner, with special attention being paid to thegluteal muscles as they converge towards it frombehind, to the various muscles immediately over-lying it, and as Sola & Williams (1956) pointed out,to that part of the tensor fasciae latae situatedimmediately below it (Fig. 19.3).

It should be noted that a TrP in the gluteusmedius or minimus close to the greater trochantermay not only give rise to pain in the hip region butmay also cause it to be referred down the outerside of the thigh and leg (Fig. 17.13). Also, a TrPimmediately below the iliac crest in one or other ofthese muscles may not only give rise to pain in thehip region, but also cause it to be referred downthe back of the thigh and leg (Fig. 17.14).


Superficial dry needling carried out at TrP sites inmild-to-moderate osteoarthritis of the hip gives acertain amount of relief from pain but the effect isnever as dramatic or as long lasting as it is withosteoarthritis of the knee. There is therefore muchto be said for combining the effects of acupunctureand drug therapy including the use of either aNSAIDs, or a simple analgesic, or both.

Treatment to relieve the pain of an osteoarthritichip usually has to be given over a long period oftime and, therefore, one of the great advantages ofusing both acupuncture and a drug together isthat the pain-relieving effect of the former makes it possible to keep the dose of the latter to a min-imum, and thereby helps to reduce the risks of anypotential side effects from it.

Non-osteoarthritic hip pain

Dry needling carried out at TrP sites when painaround the hip is primarily of muscular origin ison the other hand very rewarding and often, in myexperience, it is possible to bring even quite long-standing pain fairly rapidly under control.

A racehorse breeder (51 years of age) was referred to meby a gastroenterologist because of long-standingepigastric pain emanating from a MTrP just below thexiphisternum (see Ch. 20). The patient, finding that thiswas quite quickly relieved by acupuncture, then enquiredwhether similar treatment might help alleviatepersistent pain in his right hip! It transpired that 18 years


Figure 19.3 Trigger points in and around the greatertrochanter and along the tensor fasciae latae.

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previously he had had a car accident, since when he hadhad considerable pain in the right groin and hip regioncausing him to have a pronounced limp.

After having had this limp for about 10 years it gotso bad that he was referred to an orthopaedicspecialist who encased the lower back and hip inplaster. Apart from making his back muscles weak, thishad had no effect, and he was told that, although theX-ray, as yet, showed only a slight abnormality, hewould eventually require an operation on his hip, butthat, in the meantime, he should keep the pain undercontrol with analgesics.

On examination, there were good movements of thehip joint and the only abnormal finding was thediscovery of two TrPs in the adductor longus muscle:one just below the inguinal ligament and the other atthe insertion of the tendon into the pubic bone. Quiteremarkably, after deactivating these TrPs with dryneedles on only two occasions, the pain of 18-years’standing disappeared, and when seen 2 years later ithad not recurred.

This is yet another striking example of how TrPactivation as a result of trauma may at times causepain to persist virtually indefinitely, but provided thetissues are otherwise healthy, deactivation of the TrPs,no matter how long this is delayed, quickly alleviatesthe pain.

Periosteal pecking

It should be noted that for pain in the hip regionMann (1974) advocates pecking the periosteum ofthe greater trochanter with a dry needle, and forpain in the knee region, pecking the upper medialaspect of the tibia. Stimulating periosteal nerveendings in this manner is undoubtedly a powerfulform of acupuncture, but a somewhat painful one,and in order to assess whether the results obtainedby it are any better than those achieved by system-atic deactivation of MTrPs around the knee andhip as just described, it would be necessary tocarry out a carefully conducted statistically con-trolled clinical trial.

Pain in and around the small joints of the handsThe pain from generalized osteoarthritis of thesmall joints of the hands is usually best controlled


by the use of a NSAID, but occasionally one fingerjoint in particular is especially painful, and in sucha case it is helpful to palpate around the joint inorder to locate tender points and then to carry outsuperficial dry needling at these sites. Pain in thefirst carpometacarpal joint of the thumb is usuallymore troublesome than in the finger joints pre-sumably because of the important part played bythe thumb in grasping objects. For this reasondeactivation of tender points around this joint andof TrPs in nearby muscles when it is affected byosteoarthritis is only helpful in the earlier stages ofthe disease. It is, however, extremely effective inalleviating pain that sometimes persists followinga sprain of the joint. Case histories illustrating thishave already been given in Chapter 15.

Pain in the wristWhen a wrist is sprained, TrPs become activatedin the periarticular tissues, and the deactivation ofthese by means of the carrying out of superficialdry needling is very helpful in relieving the painassociated with this condition.

Pain in the elbowOsteoarthritis of this joint is rare unless the jointhas previously been damaged by trauma or inflam-mation. However, when, occasionally, it does occur,the acupuncture technique of deactivating TrPs inthe periarticular tissue overlying the medial andlateral epicondyles, and in the cubital fossa, is cer-tainly helpful in relieving the pain. Much morecommonly, persistent pain develops in the region ofthe elbow joint due to TrP activation occurring as aresult of trauma to the soft tissues. ‘Tennis’ elbowand ‘golf’ elbow with pain localized to one or othersides of the joint have already been discussed (Ch. 15). At times, however, this post-traumaticpain around the elbow is more generalized andthe movements of the elbow joint, because of this,become restricted.

A man (40 years of age) was ostensibly referred to mebecause of persistent pain in the neck of 6 monthsduration. During the course of examination, however,it was noted that the left elbow was supported in aspecially constructed leather splint. On enquiring about

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this it transpired that he had been fitted with this 10years previously because of persistent pain in theregion of the elbow joint following an injury sustainedwhilst serving in the S.A.S. He said he religiously wore the splint as advised, but it had done little tocontrol the pain and he had learnt to live with itbelieving that nothing further could be done. All thesplint seemed to have done was to make the elbowextremely stiff. An X-ray showed no significantabnormality in the joint itself. However, examinationof the surrounding muscles showed there were someexquisitely tender TrPs that clearly had originally beenoverlooked, and after these had been deactivated withdry needles on four occasions at weekly intervals, thepain was brought under control and full movements ofthe joint restored.

Pain in the feetThe only joint in the foot commonly affected byosteoarthritis is the metatarsophalangeal joint ofthe big toe, and when this occurs as part of thegeneralized form of the disease is usually mildand rarely requires any special form of treatment.

Pain in the ankleIt is remarkable that considering that this joint hasto bear all the weight of the body that it is rarelyaffected by osteoarthritis, even when subjected torepeated trauma as, for example, with footballers.When, occasionally, there is persistent pain fromosteoarthritis of this joint, activated TrPs are to befound clustered around the malleoli and on thedorsum of the foot midway between these twostructures. Deactivation of these by dry needlestimulation, provided this is repeated on severaloccasions at weekly intervals, will often cause thepain to remit for an appreciable period of time.

TrPs at these sites also become activated whenthe joint is sprained (Travell & Rinzler 1952, Bonica1953). As Bonica points out, rather than immobil-izing the joint as is standard practice, it is better to get rid of the pain by deactivating the TrPs, andthen encourage active movements. He advocatedinjecting the TrPs with a local anaesthetic, butdeactivating them with a dry needle is simplerand just as effective.

CLINICAL TRIALS TO ASSESS THE VALUEOF ACUPUNCTURE IN RELIEVINGOSTEOARTHRITIC PAIN

It is impossible to assess adequately the value ofacupuncture in a disorder such as osteoarthritis inwhich, somewhat paradoxically, progressive andirreversible damage to a joint is often associatedwith self-limiting episodes of pain, withoutrecourse to carefully conducted large scale clinicaltrials. Unfortunately, up to now there has been adearth of these.

The difficulties associated with the carrying outof acupuncture trials in general, and in particular,the problems posed in attempting to compare itseffectiveness with that of a placebo were discussedin Chapter 11. It is, however, essential to realizethat such difficulties are particulary great whencomparing the effectiveness of acupuncture or, forthat matter, any other form of treatment with thatof a placebo, in alleviating the pain of osteoarth-ritis, due to the placebo treatment response in thiscondition often being much in excess of the nor-mally attained 30% level. Traut & Passarelli (1956),for example, found that 59% of 182 patients withosteoarthritic pain obtained relief from this whengiven lactose tablets!

It is, therefore, not possible to dissent fromEvans’s (1974) opinion that in order to ascertainwhether any form of treatment gives better resultsthan a placebo in the alleviation of osteoarthriticpain, carefully conducted comparative trials aremandatory. This having been said, it is of courseessential when carrying out such trials to ensurethat the procedure used in the control group is atrue placebo!

With respect to this it would, for example,appear to have been unwise for Gaw et al (1975), intheir otherwise carefully conducted trial, to assessthe efficacy of traditional Chinese acupuncture(TCA) in relieving osteoarthritic pain, to have acontrol group in which needles were inserted intosites, ‘outside of, but contiguous to, traditionalacupuncture points’, on the assumption that treat-ment of such a type had only a placebo effect.Patients in both groups responded to their respect-ive treatments equally well, but it would be wrongto conclude from this that acupuncture in the treat-ment of this condition is no better than a placebo


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treatment for, as Mann et al (1973) so rightlyobserved, when discussing the subject of acupunc-ture in general, ‘because of the lack of precise local-ization of acupuncture points it is difficult toconceive of nearby placebo points’. The implicationof this is that the two groups in Gaw et al’s studywere in reality both treated with acupuncture.

It is clearly for this same reason that Takeda &Wessel (1994) found that both TCA and shamacupuncture significantly reduced pain, disabilityand stiffness in patients with osteoarthritis of theknee because, although the needles in the so-called sham group were inserted very superfi-cially into the skin, as discussed in Chapters 10and 11, this is sufficient to stimulate A-delta nervefibres and by so doing to have a significant pain-blocking effect.

Confirmation of the efficacy of TCA in the treat-ment of knee osteoarthritis, however, does comefrom well-planned randomized controlled trialscarried out by Berman et al (1999), Christensen et al(1992) and Petrou et al (1988).

TCA points commonly used for the treatment ofknee osteoarthritis include Spleen 9 and 10, andStomach 34 and 36 ( Fig 19.1).

Tillu et al (2001), in a prospective randomizedtrial to compare the relative efficacy of unilateraland bilateral TCA in the treatment of kneeosteoarthritis, used not only these points, but alsoa distant point – Large intestine 4 in the first dorsalinterosseous muscle of the hand (Fig 15.11). Theyfound that unilateral acupuncture is as effective asbilateral acupuncture in increasing function andreducing pain in the affected joint, but whetheradding this distant point appreciably improved theeffectiveness of the treatment is open to conjecture.

There have been two well-planned trials toassess the efficacy of TCA in alleviating the pain ofhip osteoarthritis. One of these was carried out byMcIndoe et al (1995) and the other by Haslam(2001).

In McIndoe et al’s trial, the relative effectivenessof TCA and intra-articular steroid injections wascompared. In Haslam’s trial, the effect of acupunc-ture in one group was compared with that of thegiving of advice and the carrying out of exercisesin a second group.

Both trials confirmed the efficacy of acupunc-ture, but what is of particular interest with regard

to the one carried out by, Haslam is that six TCApoints (GB 29, 30, 34, 43, St 44 & LI4) and 4 ‘ah shih’points (i.e. TrPs) were needled. The necessity forusing both these two neurophysiologically differenttypes of points concomitantly is open to questionand can only be determined by carrying out a trialto compare the relative effectiveness of employingTCA in one group of patients, and TrP acupuncturein another group. In view of the close spatial rela-tionship between periarticular TCA points and TrPs(see Figs 19.1 & 19.2) it would seem reasonable topredict that both types of acupuncture will proveto be equally efficacious in relieving osteoarthriticpain. If so, then deciding which one to use routinelyin everyday clinical practice will have to dependon each individual therapist’s personal proclivity.

RHEUMATOID ARTHRITIS

In considering whether or not acupuncture has a place in the management of rheumatoid arthritis,it is necessary to bear in mind that the disease goes through two main stages, an early activesevere inflammatory phase and a late destruc-tive one.

Early active acute inflammatory phaseThe disease has either a sudden onset with the rapidinvolvement of many joints or a more insidiousone with a gradual spread of the pathologicalprocess until ultimately many joints are affected ina roughly symmetrical manner.

In the early active phase of the disease, irre-spective of the type of onset, there is an acuteinflammatory reaction affecting the synovium ofthe joints and tendon sheaths. In addition to synovial hypertrophy and effusions, there is alsoconsiderable swelling of soft tissues as a result ofthe development of periarticular inflammatoryoedema.

Treatment at this stage of the disease must, ofnecessity, be directed at combating the acuteinflammatory reaction by means of rest, both gen-eral and local, physiotherapy and the administra-tion of anti-inflammatory drugs. The severity ofthe inflammatory reaction and the large number ofjoints involved precludes considering the use ofacupuncture for pain relief at this stage.


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Late destructive phaseThe later stages of the disease are characterized bydestructive changes in and around the joints withrelatively little inflammatory reaction, althoughwith, at times, some secondary osteoarthriticchanges.

At this phase of the disease one particular jointmay remain persistently painful (Camp 1998) andin such a case superficial dry needling at periartic-ular tender point sites should be carried out.


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INTRODUCTION

The type of abdominal and pelvic pain most likelyto be helped by acupuncture is that which occurs asa result of the activation of trigger points (TrPs) inthe muscles, fasciae, tendons and ligaments of theanterior and lateral abdominal wall, the lower back,the floor of the pelvis, and the upper anterior partof the thigh (Baldry 2001).

Such pain, however, is all too often erroneouslyassumed to be due to some intra-abdominal lesionand, as a consequence of being inappropriatelytreated, is often allowed to persist for much longerthan is necessary. As Renaer (1984) so rightly says:

… when confronted with abdominal pain com-plaints, most doctors will automatically think ofpain originating in the abdominal viscera. Yet itwould appear strange if tissues so abundantlyinnervated as the skin and the fasciae of theabdominal wall hardly ever caused pain.

An important reason why doctors tend to over-look the possibility of abdominal pain arising fromstructures encasing the internal organs is becausethe majority of present-day textbooks on gastro-enterology, together with most sections on the sub-ject in undergraduate textbooks of medicine, whilstgiving detailed descriptions of diseases of the vis-cera and the characteristics of pain associated withthese, make little or no reference to the diagnosisand treatment of pain emanating from the abdom-inal wall itself. This failure on the part of mostauthors of textbooks to emphasize the importance ofdistinguishing between visceral and somatic pain isnot only surprising, but much to be regretted, as

343

Chapter 20

Abdominal and pelvic pain

CHAPTER CONTENTS

Introduction 343–344Abdominal wall MTrP pain 344–350Abdominal pain from lumbar MTrPs 350Lumbar pain from abdominal wall MTrPs 351Pelvic floor MTrP pain 351–354Gynaecological MTrP pain 355–356Referral of MTrP pain to the scrotum 356

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Other physicians who stressed the importance ofdistinguishing abdominal wall pain from visceralpain during the 1930s were Hunter (1933) andTelling (1935). In addition, Lewis & Kellgren (1939)carried out extremely important experimental work,in both human healthy volunteers and animals, onmusculoskeletal pain that arises from the abdominalwall itself, and also that which is referred to theabdomen from muscles in the lower back (see Ch. 4).

From the 1940s onwards, several clinicians havepublished reports concerning the diagnosis andtreatment of abdominal wall MTrP pain based ontheir own personal series of cases, including Kelly(1942), Young (1943), Gutstein (1944), Theobald(1949), Good (1950a, b), Melnick (1954, 1957a),Long (1956), Mehta & Ranger (1971), Applegate(1972) and Bourne (1980). In addition, Simons et al(1999) have provided an extensive review of thewhole subject in their TrP manual.

ABDOMINAL WALL MTrP PAIN

Examination of the patientIn order to diagnose MTrP abdominal wall painand to distinguish it from visceral pain, it is essen-tial to palpate the abdomen with the muscles ofthe anterior wall both in a relaxed and contractedstate, because abdominal wall pain emanates from focal areas of exquisite tenderness, or TrPs,and the tenderness at these points is increasedwhen the muscles are held taut and decreasedwhen they are relaxed.

The procedure and the reason for carrying it outcannot be explained better than by quoting Long(1956) who states:

The painful area is compressed rather firmlybeneath a single finger or thumb, with sufficientpressure barely to pass the threshold of pain. Thepatient is then asked to raise both legs straight,causing both heels to leave the examining surfaceby a distance of a few inches only. The resultantcontraction of the anterior abdominal wall willpush the examining finger away from the visceraand simultaneously increasingly compress theabdominal wall beneath the finger. If, on thismanouver, the pain increases it is of abdominalwall origin; if it decreases it is of visceral origin.

there can be no doubt that pain occurring as the result of activation of TrPs in the abdominalwall is relatively common. One gastroenterologist,who invariably includes this possibility in his dif-ferential diagnosis whenever presented with acase of persistent abdominal pain, regularly refersto me an appreciable number of such patients fortreatment with acupuncture. It, therefore, came asno surprise to me to find that Ranger et al (1971),working in a large district general hospital, wereable to collect a series of 100 patients with abdom-inal wall pain over a period of 2 years.

Despite this paucity of information concerningabdominal wall TrP pain in most current textbooks,there have been many important contributions tothe subject in various journals over the past 50years or more. One of the earliest was contained inan address entitled ‘Myofibrositis as a Simulatorof other Maladies’, delivered by Murray in 1929 tothe Newcastle upon Tyne and Northern CountiesMedical Society.

The fact that, because of the time in whichMurray lived, he attributed the pain to fibrositis inno way detracts from the importance of his observa-tions concerning what clearly today would be calledmyofascial trigger point (MTrP) pain. In the part ofhis address dealing with abdominal wall pain, hesays ‘such pain is of a dull aching character gener-ally felt at one spot from which it tends to radiate’.He then goes on to state that pain of this type is oftenmade worse by stretching and twisting movementsof the trunk, and he stresses the importance of pal-pating the abdomen with the muscles both in a stateof relaxation and of contraction when attempting todistinguish between visceral and somatic pain.

He describes how, by the use of this examinationtechnique, he was able in three cases of persistentabdominal pain to demonstrate that the pain wasarising from circumscribed tender areas in the muscles and that pain in the right iliac fossa previ-ously ascribed to chronic appendicitis, pain in theright hypochondrium said to be due to biliary colic,and pain in the epigastrium attributed to a gastritis,was in each case due to what he called ‘fibrositis’ ofthe abdominal wall. He concludes by reporting thathe was able to relieve this persistent pain, which intwo cases had been present for several months, andin one case for 4 years, by applying an iodine andbelladonna ointment to the areas of tenderness.

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Murray (1929) advocated producing tension inthe abdominal muscles by getting the patient toraise the head and upper part of the body from therecumbent position. De Valera & Raftery (1976) recommend getting the patient to elevate both thefeet and head. Travell & Simons (1983) advise get-ting the supine patient to hold a deep breath. Thereis little to choose between any of these methods and it is my personal practice to adopt whicheverone seems to be the most suitable for a particularindividual.

Muscles involvedThe principal anterior abdominal wall muscles inwhich TrPs are liable to become activated includethe two rectus abdominis muscles on either side ofthe midline, and the external and internal obliquemuscles in the flanks (Figs 20.1 & 20.2).

Location of the TrPsRectus abdominis

Common sites for TrP activation in this muscleinclude the epigastric region near to its insertion into

the lower ribs; in its belly, half-way between thexiphisternum & the umbilicus and half-way bet-ween the umbilicus & the pubis; also at or near toits insertion into the pubic bone (Fig. 20.3).

External and internal obliques

Common sites for TrP activation in these musclesinclude the hypochondrium, the iliac crest and closeto the inguinal ligament. It may also occur any-where along a line joining the tip of the twelfth ribabove and the iliac crest below (Fig. 20.4).

SymptomatologyActivated TrPs in the anterior abdominal wall may,as with TrPs anywhere else in the body, be respon-sible for the development of pain but, in addition,because of a somatovisceral reflex in the abdomen,they are also capable of causing other symptomsincluding anorexia, flatulence, nausea, vomiting,diarrhoea, colic, dysmenorrhoea and dysuria.

Melnick (1954), in a series of 56 patients withabdominal wall TrPs, found the latter to be thecause of flatulence and bloating in 25% of the cases,vomiting in 11%, heartburn in 11% and diarrhoea

Abdominal and pelvic pain 345

Pectoralis major

Sheath of rectus, anterior layer

Tendinous intersections

Inguinal ligament

Spermatic cord

Crest of ilium

Lumbar triangle

Linea semilunaris

Linea alba

External oblique

Latissimus dorsi

Serratus anterior

Figure 20.1 The left external oblique muscle.

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in 4%. Theobald (1949) has reported relieving dys-menorrhoea by deactivating TrPs in the lower partof the rectus abdominis about half-way betweenthe umbilicus and pubis, and Hoyt (1953) hasreported relieving dysuria by deactivating TrPs inthe lower abdominal muscles.

The pain itself often takes the form of a dull ache.Alternatively, it may, as pointed out by Ranger et al(1971) be sharp and burning in character. It tends tobe aggravated by twisting or stretching movementsof the trunk. Patients sometimes complain more ofdiscomfort than of actual pain (Kelly 1942). This isbecause, as Travell & Simons (1983) state, ‘TrPs inthe anterior abdominal wall, and particularly thosein the rectus abdominis, are liable to cause theabdomen to become lax and distended with flatus’.

It is also noticeable how often patients withupper abdominal TrP pain complain of this beingmade worse by the pressure of their clothes.In addition, as pointed out by Murray (1929),epigastric TrP pain may be aggravated by post-prandial distension of the stomach.


Latissimus dorsi

Intercostalis internus of10th intercostal space

Digitations of serratus anterior

Rectus abdominis

Obliquus internus

Figure 20.2 Muscles of the right side of the trunk. The external oblique has been removed to show the internaloblique, but its digitations from the ribs have been preserved. The sheath of the rectus abdominis has been opened andits anterior lamina removed.

A farm labourer (50 years of age) had an 18-monthhistory of epigastric pain that was always worsewhenever his abdomen became distended following ameal. After he had been found to have a normal bariummeal, gastroscopy, and ultrasound scan, he was referredto me as a possible case of abdominal wall TrP pain. On examination, he had two well-defined exquisitelytender TrPs in the linea alba 3 inches below thexiphisternum and after these had been deactivated withdry needles on two occasions, he had no further trouble.

In addition, pain from TrPs in muscles in theupper part of the abdomen may be brought on byflexing the trunk.

A market gardener (62 years of age), whose workinvolved much heavy lifting, suffered from attacks ofsevere pain in the right upper quadrant of theabdomen about 3–4 times a week, with each attacklasting about 15–20 min and coming on whenever his work necessitated him bending over for any lengthof time. At one stage it was thought he might have

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some type of diaphragmatic hernia. However, allinvestigations were negative and after he had hadrecurrent bouts of pain for 4 years, he was referred tome for an opinion as to whether acupuncture mighthelp to relieve it. On examination, a single TrP waslocated in the lateral border of the right rectus musclejust below the ribs that had presumably becomeactivated by the strain of heavy lifting. The point wasso exquisitely tender to touch that the patient visiblyjumped when pressure was applied to it. Somewhat tomy surprise in view of the long history, there were nofurther attacks of pain following deactivation of theTrP with a dry needle on only one occasion.

Differential diagnosisPain and flatulence occurring as a result of TrPs inthe right upper quadrant in either, one of the obliquemuscles, or in the lateral border of the rectus muscle,is liable to be erroneously ascribed to gall bladderdisease, particularly if, by chance, ultrasound scan-ning reveals the presence of gall stones.

Pain and tenderness in the right lower quadrantoccurring as a result of TrP activity in the lateralborder of the rectus muscle is apt to be diagnosed asbeing due to appendicitis, particularly as the TrPfrequently occurs in the region of McBurney’s point,approximately 1–2 inches from the anterior super-ior iliac spine along the line joining this spine andthe umbilicus. Persistent right iliac fossa pain israrely, if ever, due to chronic appendicitis but fre-quently occurs as a result of the activation of a TrP.

Epigastric pain, particularly when accompaniedby dyspeptic symptoms and occurring as a result ofTrP activity in the rectus abdominis, is liable to beattributed to a hiatus hernia if, by chance, the latterhappens to be found on radiographic examination.

Finally, there is a risk of pain in the left lowerquadrant from TrPs in the outer border of the rec-tus or the obliques being considered to be due todiverticulitis if, by chance, a barium enema revealsthe presence of diverticulae in the lower part of thecolon.

Factors responsible for the primaryactivation of anterior abdominal wall TrPsThe various factors responsible for the primaryactivation of abdominal wall MTrPs include: acute


Figure 20.3 Some common trigger point sites (�) inthe rectus abdominis muscle.

Figure 20.4 Some commonly occurring trigger pointsites (�) in the external oblique muscle.

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trauma to the muscles, as a result, for example, of an accident or surgical operation; repeated minortrauma to, or chronic overloading of them, such asmay occur during the course of certain occupa-tional tasks and sporting activities; muscle strainoccurring as a result of a faulty posture; viral infec-tions; chronic anxiety, causing the muscles to beheld persistently tense; and exposure of them to thecold or damp.

The following abstracts of case notes have beenselected from my own series of patients with per-sistent abdominal wall TrP pain in order to illus-trate some of the commoner ways in which TrPs inthe abdominal wall undergo primary activation.

Trauma

A company director (56 years of age) developed severe discomfort and tenderness of the muscles in the right hypochondrium. A cholecystogram was normal. However, the pain persisted and after it had been present for 4 months, he was referred tome. It was significant that the pressure of a tight belt and also flexing his trunk made the pain worse, as on examination there were three well-definedexquisitely tender TrPs in the right external obliquemuscle. These must have been activated as a result of trauma, as it transpired that the onset of thesymptoms coincided with him being knocked over by a dog. It was only necessary to deactivate theseTrPs with dry needles on one occasion to relieve him of his symptoms.

A farrier (37 years of age) suffered bouts of pain in the left upper part of the abdomen. Allinvestigations, including an ultrasound scan of the abdomen, were negative. When seen by me 14 months after the onset of the pain, it had becomeso incapacitating as to prevent him from working.There were several TrPs in the muscles behind the leftlower ribs and these must have become activated by repeated occupational trauma, as he gave a history that the pain always came on after he hadspent 2–3 hours shoeing horses, during which time hepressed the legs of the animals tightly against the leftupper part of his abdomen. He had no further painonce the TrPs had been deactivated with dry needleson two occasions, and he made adjustments to themanner in which he worked.


A farmer (49 years of age) with a 5-year history ofintermittent epigastric pain and with no abnormalityon a barium meal or gastroscopy gave a history thathe was always worse on the days when he strainedhimself closing a particularly stiff tailboard of a lorry.He also observed that his upper abdomen often feltquite sore after cattle had knocked against it onmarket days. Three TrPs were found in the upper partof the rectus muscle and his pain disappearedfollowing the deactivation of these with dry needleson four occasions.

Faulty posture

A schoolboy (15 years of age) was referred to me witha 4-year history of pain in the right upper part of theabdomen. It was particularly troublesome whenever heput any weight on his right leg in the gymnasium orwhile playing rugby. He had been fully investigated ata pain clinic with the only abnormality discoveredbeing a minor defect in the 8th dorsal vertebra.Because of this it was considered that the pain mightbe due to nerve root entrapment but an intercostalnerve block and an epidural injection had proved to bevalueless.

On examination he had several exquisitely tenderTrPs in the external oblique just below the costalmargin and also a number in muscles around thegreater trochanter. With hindsight, there can be nodoubt that the TrPs in the leg were the first to becomeactivated following a fall when aged 11, and that painfrom these caused him to adopt a faulty posture, withthe result that, as a secondary event, the TrPs in theabdominal wall became activated. After deactivatingthese TrPs with dry needles on three occasions, he hadno further trouble.

A laboratory technician (31 years of age) with a 4-monthhistory of pain in the right loin radiating anteriorlytowards the groin, on being found to have noabnormality in the urogenital tract was referred to me asa possible case of musculoskeletal pain. There werenumerous TrPs in muscles both posteriorly and anteriorly.It transpired that the pain always came on after she hadbeen sitting for any length of time at a work bench andshe felt herself that she had strained her muscles bysitting on a stool that was too low. The TrPs were readilydeactivated and she has had no further pain sinceinsisting on being given a higher stool.

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Exposure to cold or damp

Pain in the muscles of the anterior abdominal wallnot infrequently occurs as part of a condition,which, because of the nebulous nature of its under-lying pathology, has over the years come to beknown by a variety of names including fibrositis,myalgia and, in more recent years, myofascitis.Although there can now be no doubt that the con-dition is associated with the activation of TrPs inthe abdominal wall muscles, the reason for thisactivation is far from certain. Exposure to cold ordamp has traditionaly been considered to be animportant aetiological factor but there is of courseno absolute proof of this.

Postoperative pain

Many patients referred to me with abdominal pain that has come on postoperatively have beenfound to have active TrPs either in the muscles of the lower back or the anterior abdominal wallor both. There is no doubt that the activation has occurred as a result of the muscles havingbeen traumatized or strained during the course ofsome surgical procedure. In addition, postopera-tive pain is sometimes due to TrPs developing insurgical scars.

In all such cases the pain continues to be trou-blesome for a long time unless the TrPs are satis-factorily deactivated.

Secondary activation of abdominalwall TrPsTrPs in the anterior abdominal wall can becomeactivated as a secondary event in response to thepain of visceral disease. It is then possible for painfrom the abdominal wall TrPs to continue to betroublesome long after the visceral disease hasbeen successfully treated. Melnick (1957b) describesa patient in whom epigastric pain, originally dueto a duodenal ulcer, persisted for a long time afterthe ulcer had healed as a result of the activation ofTrPs in the rectus muscle.

The reasons for TrP activity occurring in associ-ation with the irritable bowel syndrome wouldseem to be more complex and, therefore, will beconsidered separately.

Irritable bowel syndrome

The irritable bowel syndrome has been defined as,‘syndromes of abdominal pain and disturbance ofbowel action of more than 3 months duration with-out any organic cause’ (Blendis 1984). It is a dis-ease that affects not only adults but also children(Apley & Naish 1958). The pain in children is pre-dominantly periumbilical (Stone & Barbero 1970),whereas in adults it is more often over the colon,with the commonest site being the left iliac fossa(Waller & Misiewiez 1969).

Holdstock et al (1969), from manometric studiesusing radiotelemetering capsules in the small intes-tine and proximal colon, and air-filled balloons inthe sigmoid colon, have shown that attacks of painin various chronic pain syndromes, including theirritable bowel syndrome, seem to be related tochanges in intraluminal pressures in either the smallor large intestine.

On clinical examination, there are areas of localized tenderness over one or other parts of the colon with this most often being over thedescending part, but sometimes over the trans-verse part, and occasionally over the whole colon.On palpating the abdomen with the musclesrelaxed it seems as if it is the colon that is tender,but, on getting the patient to tense the abdominalwall, it becomes obvious that often much of thistenderness is in localized areas of the abdominalwall muscles.

Kendall et al (1986) and also Hall (1986) con-sider that these focal areas of tenderness in themuscle occur as a result of a viscerosomatic reflex(Procacci & Zoppi 1983). This may be true, butnevertheless it has to be remembered that Lewis &Kellgren (1939) showed that an injection of a 6%salt solution into the belly of the rectus muscle justbelow and 1 inch outside the navel gave rise to ‘acontinuous pain lasting 3 to 5 minutes of unpleas-ant severity and having a character not to be dis-tinguished from that of colic’. In other words,Lewis & Kellgren, by artificially creating a triggerzone in an abdominal wall muscle, were able, bymeans of a somatovisceral reflex, to produce apain not dissimilar to that which occurs with theirritable bowel syndrome.

Furthermore, it has to be remembered that such symptoms as dyspepsia (Watson et al 1976),

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dysuria (Fielding 1977), and dysmenorrhoea(Waller & Misiewicz 1969) are frequently presentin irritable bowel syndrome, and that, as discussedearlier, these are all symptoms that anterior abdom-inal wall TrPs, by virtue of a somatovisceral reflex,are capable of producing.

The question, therefore, that has to be asked iswhether the pain and other symptoms in this con-dition are primarily due to a disorder of the gut withthe focal areas of tenderness in the anterior abdom-inal wall musculature developing as a secondaryevent, or whether these tender points are actuallyTrPs and the prime cause of all these various symp-toms? If it is the latter, then it would be reasonableto expect that deactivation of these points by onemeans or another would relieve the symptoms.Kendall et al, however, state that they have notbeen able to alleviate the pain by infiltrating themwith local anaesthetic agents with or without theaddition of steroids. They also have observed thatthese anterior abdominal wall tender points,unlike TrPs, do not seem to be constant in positionbut move from place to place.

These observations notwithstanding, what iscertain is that many cases of irritable bowel syn-drome have been referred to me for treatment with acupuncture because, in addition to havingvisceral pain, they have also had pain made worseby twisting and stretching movements of the trunk,that was clearly muscular in origin. In all thesecases, TrPs have invariably been found to be pre-sent at constant sites in the muscles of either thelower back or the anterior abdominal wall. In someinstances, this particular type of pain appears tohave developed as a result of the skeletal musclesbeing held tense during bouts of intra-abdominalpain. In other cases it seems as if the irritable bowelsyndrome and the TrP pain have arisen independ-ently of each other, which is hardly surprising con-sidering that both this particular disorder of thegut (Esler & Goulston 1973) and musculoskeletalpain disorders (Crown 1978) frequently occur inpeople of an anxious disposition.

MTrP pain occurring either coincidentally with,or developing as a result of irritable bowel syn-drome is well worth treating with acupuncture,because once the TrPs have been deactivated withdry needles any residual visceral pain is so muchmore readily coped with.

Deactivation of abdominal wall TrPsIt is obviously possible to deactivate TrPs in theabdominal wall, as elsewhere in the body, by avariety of different methods. Murray (1929) clearlyachieved this by applying an iodine and belladonnaointment to the skin overlying them. Many clini-cians including Travell & Simons (1983) advocateinjecting a local anaesthetic into them. Bourne (1980)favours the use of a corticosteroid local anaestheticmixture.

Mehta & Ranger (1971), Ranger et al (1971), andalso Applegate (1972), presumably because theyconsidered the pain to be due to the entrapment ofa cutaneous nerve as it passes through an anteriorabdominal wall muscle, felt obliged to inject phe-nol into a point of maximum tenderness.

There can be no doubt that the reason why all of these methods are capable of alleviating this typeof pain is because they all have one property incommon, namely an irritant action on A-delta nervefibres, with this in turn activating pain-modulatingmechanisms in the central nervous system. Thiseffect of course can be achieved far more straight-forwardly simply by deactivat-ing TrPs withacupuncture needles (Ch. 8). In addition, withregard to this, it has been my experience that ante-rior abdominal wall TrPs are particularly easy todeactivate with dry needles, so that even withpain of long duration it is rarely necessary to carryout this procedure more than two to three times.This is in marked contrast to TrP pain in either thecervical or lumbar region, where it is often neces-sary to continue with the treatment for far longer.This may be because during the course of everydaylife a much greater mechanical strain is imposedon muscles in the neck and back.

Pain in the abdomen from TrPs in thelower backLewis & Kellgren (1939) were able to show that aninjection of hypertonic saline into the supra-spinous ligament at the level of the 9th thoracicvertebra gave rise to pain posteriorly in the regionof the first lumbar vertebra, and anteriorly over the9th costal cartilage and down towards the umbili-cus. They also observed rigidity of the upperabdominal muscles on the side of the injection


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when this experimentally induced pain was at itsheight.

The following year, Kellgren (1940) publishedan account of several cases in which somatic painsimulated visceral pain. These included the case ofa housewife who had a 1-year history of epigastricpain and nausea coming on 1 h after meals, togetherwith epigastric tenderness, but with no abnormal-ity demonstrable on a barium meal. Examinationof the back, however, revealed the presence of amid-dorsal kyphosis of the spine and any attemptto straighten the latter caused the epigastric painto be reproduced. In addition, there were focalareas of marked tenderness in the region of the 8th and 9th thoracic vertebrae and an injection ofnovocain into these abolished the epigastric painand tenderness. Also presented was the case ofanother housewife with a 6-month history of con-tinuous pain in the right hypochondrium and lowerangle of the scapula, together with episodes ofmore severe pain, nausea, and flatulence. Therewas tenderness and rigidity of the upper abdominalmuscles, but a cholecystogram was normal. Shealso had a mid-dorsal kyphosis and it was possibleto reproduce her pain by forcibly flexing andextending this part of the spine. There were tenderareas in the region of the 6th and 7th thoracic inter-spinous ligaments and, as in the previous case, aninjection of Novocaine into these abolished theabdominal pain and rigidity.

These cases, reported by Kellgren nearly 50 yearsago, have been quoted in order to show that it hasfor long been known that abdominal pain may, onoccasions, occur as a result of being referred therefrom TrPs in the lower back, and that in all cases ofabdominal pain not obviously due to some visceraldisease, it is important to search for TrPs, not only inthe anterior abdominal wall musculature, but alsoin the muscles and ligaments of the lower back.

Pain in the lower back owing to TrPs inanterior abdominal wall musclesIn my experience whenever a patient with low-back pain finds it is uncomfortable to stand upstraight and also when any attempt passively toextend the spine makes the pain worse, it is oftenbecause of the activity of TrPs in the lower part ofthe rectus muscle at or near to its insertion into the

pubic bone, or in the lower border of the externaloblique muscle along its insertion into the inguinalligament. It is, therefore, important in all such casesnot only to look for TrPs in the lumbar muscles butalso in the anterior abdominal wall.

PELVIC PAIN

The type of pelvic pain most likely to be amenableto treatment with acupuncture is that which occursas a result of the activation of TrPs in muscles andligaments in the pelvic floor and in the adductorlongus tendon near or at its attachment to thepubic bone.

Chronic pelvic floor MTrP pain syndromeTrP activation in this condition occurs in variousmuscles and ligaments in the pelvic floor with theprincipal muscles involved being the levator ani,the coccygeus, the piriformis and the medial fibresof the gluteus maximus (Figs 20.5 & 20.6).

Thiele (1937) was one of the first to draw atten-tion to this condition when he described what hecalled coccygodynia (pain around the coccyx) fromspasm of the levator ani and coccygeus musclesoccurring in conjunction with pain around the buttock and down the back of the thigh from spasmof the piriformis.

During the 1940s and 1950s, Thiele and otherspublished papers on coccygodynia, with one of themost interesting being that of Dittrich (1951), as heappears to have been the first person to recognizethat pain in this condition occurs as a result of itbeing referred from TrPs. In his paper he describedtwo cases of coccygeal pain occurring as a result ofit being referred to the coccyx from TrPs in adiposetissue in the sacral region. His contribution to thesubject is, however, otherwise limited because heseems to have believed that TrPs in this conditiononly occur at this site and makes no mention of thepossibility of them occurring in the muscles of thepelvic floor.

During the course of reviewing the clinical fea-tures of coccygodynia, Thiele (1963) pointed outthat it is only in the 20% of cases in which coccygealpain is due to direct trauma that the coccyx is ten-der, and that in the other 80% of cases not due totrauma this lack of tenderness of the bone means


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CoccyxCoccygeus

Obturator internus

Levator ani

Ischiocavernosus

Bulbospongiosus

Corpus spongiosum penis

Superficial fascia, membranous layer

Transversus perinei superficialis

Piriformis

Figure 20.5 The muscles of the male perineum.

Urethra

Vagina

Anus

Sphincter ani externusGluteus maximus

Levator ani

Transversusperinei superficialis

Bulbospongiosus

Ischiocavernosus

Clitoris

Figure 20.6 The muscles of the female perineum.

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that the pain cannot be due to disease of this struc-ture itself or to arthritis of the sacrococcygeal joint,but rather that it must be referred to the coccyx frompelvic muscles which, for one reason or another,have gone into spasm.

Coccygodynia is not really a particularly aptname for this disorder because, as Thiele himselfrecognized when he first introduced the term inthe 1930s, the pain is rarely confined to the coccyx.On the other hand, as he originally pointed out, itis a condition that is always associated with spasmof the pelvic floor muscles, and for this reason otherphysicians have given it a variety of other namesincluding the levator spasm syndrome (Smith 1959),the levator syndrome (McGivney & Cleveland 1965)and the levator ani spasm syndrome (Lilius &Valtonen 1973).

However, none of these terms are entirely satis-factory, as the levator ani muscle is usually onlyone of the muscles involved and, therefore, muchto be preferred is tension myalgia of the pelvicfloor, a term introduced by Sinaki et al (1977) at the Mayo Clinic. Nevertheless, even this can beimproved upon for there are now good groundsfor believing that the pain is referred over a fairlywide area from points of maximum tenderness orTrPs in muscles of the pelvic floor, and for this rea-son a more appropriate term for it is the chronicpelvic floor MTrP pain syndrome.

Clinical manifestations

The condition occurs predominantly in females. It isnow generally agreed that the commonest and moststriking feature is pain coming on when seated. Itmay also be felt during the acts of sitting downand standing up. There is usually no pain on lyingdown or on walking about, except that sometimessudden twisting movements of the trunk arepainful. One of my patients found sitting in a chairso distressing that he was reduced to watching tel-evision or reading a book kneeling on the floor.Straining at stool may also aggravate the pain, butnot as often as might be thought. Sinaki et al (1977)reported it in 33% of their patients. It is also sur-prising that dyspareunia is rarely a problem. Thepain usually takes the form of a somewhat ill-defined aching or throbbing sensation in either theanterior or posterior parts of the perineum or

throughout that region. In addition, the pain mayspread to the buttocks, hips and backs of the thighs.

It is generally agreed that this condition mainlyoccurs in those of an anxious disposition, and fromwhat some of my patients with this condition havetold me, it clearly tends to occur in those who tenseup the muscles of their pelvic floor at times of stress.There is usually, however, in addition some localcause for the condition developing.

On examination, exquisitely tender TrPs may befound on external examination of the perineum, insome cases, however, they can only be located bythe carrying out of a rectal examination.

Patients with this condition seem to be particu-larly prone to TrP activation and often give a historyof TrP pain in other parts of the body such as theneck or lower part of the back. Unfortunately, thissyndrome is still not as widely recognized as itsimportance deserves, the pain all too frequentlybeing attributed to some mechanical disorder ofthe spine or to some inflammatory condition such asproctitis, prostatitis, cervicitis, urethritis, or vagin-itis and, as a consequence of this, treated inappro-priately. Alternatively, after the patient has beenseen by a series of consultants specializing inorthopaedics, urology, gynaecology and neurol-ogy, and they each in turn having found nothingto account for the pain, it is not uncommon for theopinion of a psychiatrist to be sought.

Aetiology

Many of the physicians who over the years havepublished reports drawing attention to the painbeing due to pelvic floor muscle spasm have consid-ered that in many cases the spasm is secondary tosome inflammatory lesion in the pelvis and haveemphasized that the pain is not directly due to thelatter itself. They have also stated that with manypatients there is no inflammatory lesion present.The situation would seem to be that in all cases thespasm of the pelvic floor muscles is due to the acti-vation of TrPs in them, and that in those patientswhere this is not secondary to some pelvic inflam-matory lesion, it is due to the muscles being sub-jected either to acute trauma or to repeated minortrauma or to chronic strain. The following casesexemplify how one or other of these three factorsmay lead to the development of this syndrome.

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Acute trauma

A housewife (65 years of age) was referred to me with a 6-month history of persistent posteriorlysituated perineal pain. On examination, there was asingle exquisitely tender TrP situated half-waybetween the coccyx and the posterior margin of the anus. The pain quickly subsided once this TrPhad been deactivated with dry needles on twooccasions. There can be little doubt that this TrP hadbeen activated as a result of surgical trauma as theonset of the pain coincided with an operation for arectal prolapse.

Repeated minor trauma

A businessman (58 years of age) with pain in thetesticles that came on as soon as he sat down on achair, and which was relieved by standing or walkingabout, was investigated by a general surgeon, aurologist, a neurologist, and an orthopaedic specialist.When none of these specialists could account for hispain, it was suggested to him that he should be seenby a psychiatrist. This he refused to do and after thecondition had caused him considerable distress for 4years, his general practitioner, as an act ofdesperation, referred him to me to see whetheracupuncture might help.

On examination there were many exquisitely tender TrPs in the anterior perineal muscles andmuscles on the inner side of the thigh near to theirattachment to the pubic bone. Deactivation of theseTrPs with dry needles gave immediate, but verytemporary relief and the procedure had to be repeated12 times over the course of 5 months before the painfinally disappeared. This man had a long history oflow-back pain and it would seem that the reason forhim activating TrPs in the pelvic floor was because hehad traumatized his perineum by sitting on the hardsaddle of a rowing machine for 20 min twice a day for12 years carrying out exercises designed to strengthenthe muscles of his back!

Recurrent muscle strain

A housewife (48 years of age) developed a throbbingpain mainly around the rectum, but spreadingforwards to the anterior perineum and down thethighs. This only came on when she sat down and was

relieved by standing. It was made worse when, onsitting, she crossed her legs but was eased by openingthem. Two gynaecologists and a neurologist failed tofind the cause and after the pain had been present for3 years she was referred to me to see whetheracupuncture might help.

On external examination, there were many TrPsthroughout the muscles of the perineum anddeactivation of these with dry needles was carried outon several occasions. There was, in addition, muchtenderness on rectal examination and she was,therefore, also given rectal massage. These measures,however, only gave her partial relief. She was a verytense person and there is no doubt this aggravated thesituation, as there was still further improvement onceshe had been taught autohypnosis.

The reason for her developing the condition wasthat she had become obsessed about completelyemptying her rectum and for many years had regularly spent up to 20 min each day straining at stool.

Treatment

Some cases, like those quoted above, have TrPs thatcan readily be identified on external examination of the pelvic floor, and it is a relatively straight-forward procedure to deactivate these by means ofinserting dry needles into them. Response to this,however, is generally slow and in order to obtainany long-term relief it usually has to be repeatedmany times.

Most cases also have TrPs that are only dis-cernible on rectal examination and with these, rec-tal massage, similar to that used for massaging theprostate, is said to be helpful (Thiele 1937, 1963).Cummings (2000), however, during the course ofdiscussing this particular form of treatment, hasshrewdly commented that it does not appear tohave become as popular in the UK as possibly insome other European countries.

Deep heat, by means of diathermy, applied eitherper rectum or externally, is also useful in helpingto relax the muscles (Sinaki et al 1977). In addition,because this condition usually develops in highlyanxious people and is aggravated by them nerv-ously holding the pelvic muscles in a state of ten-sion, relaxation techniques such as biofeedback orhypnosis should also be employed.


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Gynaecological MTrP painSlocumb (1984, 1990), an American gynaecologist,must be given the credit for being the first to recognize this syndrome. He specifically looked forMTrPs in 177 women referred to his clinic withchronic pelvic pain, and found this to haveemanated from TrPs in the anterior abdominal wall(89%), in the vaginal fornices (71%) and in the sacralregion (25%). He stressed that when searching forMTrPs in this disorder, the conventional bimanualvaginal examination should not be employed.Instead, he advocated firstly palpating the loweranterior abdominal wall muscles. Then palpatingthe tissues around the vaginal introitus. Followingthis, the tissues high up in the paracervical region.

Pathogenesis

This disorder is due to trauma-evoked MTrP activityoccuring either during childbirth or pelvic surgery.

Character of the pain

The pain is of a diffuse poorly localised achingtype. When emanating from TrPs in the lowerabdominal wall muscles it is exacerbated whenthese are stretched either by a distended bladderor twisting of the torso. Pain from TrPs in the vagi-nal wall is exacerbated by coitus. In addition, TrPactivity higher up in the paracervical region isliable to give rise to dysmenorrhoea.

Treatment

Slocumb deactivated the TrPs by injecting a localanaesthetic into them. However, in view of what isnow known about the subject (Ch. 10), it is clearthat superficial dry needling is not only simpler butequally effective.

Adductor longus syndromePain in the groin and down the inner side of thethigh to the knee is liable to be due to a TrP becom-ing activated in the adductor longus muscle (Travell1950, Long 1956). In my experience the TrP is mostoften located in the tendon of this muscle near toor at its insertion into the pubic bone (Fig. 18.1).

This activation may occur secondary to somechronic painful condition such as osteoarthritis of


the hip or it may develop as the result of the muscle being subjected to trauma.

In the female this may be the cause of seeminglyinexplicable vaginal pain.

A young woman developed a distressing throbbingpain in her vagina and around the urethral orificewhen aged 20 years. It was worse after any physicalactivity such as dancing and sexual intercourseaggravated it. She also noticed that it was morenoticeable whenever she was emotionally upset. Overthe years she saw several gynaecologists but no causefor it was found and eventually she was sent to apsychiatrist. He, however, was unable to help and afterit had been present for 14 years, her generalpractitioner referred her to me in what he described asa faint hope that acupuncture might help!

On examination, there was an exquisitely tender TrPin the right adductor longus tendon near to itsinsertion into the pubis. Pressure on this pointaggravated the pain and on inserting a needle into it,she exclaimed ‘that is my pain’ as an electric shock-like sensation shot up into the vagina and down theinner side of her thigh.

Deactivation of the TrP with a dry needle gavetemporary relief and after the procedure had beenrepeated eight times during the course of 12 weeks,the pain no longer returned.

On seeking a reason for the activation of the TrP, ittranspired that for some months prior to the onset ofthe pain she had been in the habit of frequentlytravelling very long distances seated on the pillion of amotor cycle whilst gripping tightly with her thighs forsupport.

In the male, TrP activation in this muscle maybe the cause of seemingly inexplicable scrotalpain. Several men referred to me with pain in thisregion have been found to have TrPs in this mus-cle; but, at the same time, it has to be rememberedthat TrPs at other sites may also be responsible forthis pattern of pain referral.

Anterior pelvic floor MTrP painMuscles in the anterior half of the pelvic floor in which TrP activity may develop include the bulbospongiosus and the ischiocavernosus (Figs20.5 & 20.6).

Chap-20.qxd 11*10*04 10:33 Page 355

Bulbospongiosus muscle

This muscle is attached posteriorly to the perinealbody situated in the centre of the pelvic floor.From there in the female it divides into two partsthat anteriorly attach to the clitoris. In the malefrom its posterior attachment to the perineal bodyit divides into two parts that wrap around the cor-pus spongiosum on the posterior aspect of thepenis and around the corpus cavernosum on itsanterior aspect.

Ischiocavernosus muscles

These two muscles form the lateral boundaries ofthe perineum. Posteriorly, in both sexes, the mus-cle is attached to the ischial tuberosity. Anteriorly,in the male it inserts into the base of the penis andin the female into the base of the clitoris.

Development of TrP activity in these musclesTrP activity is liable to develop in these muscleswhen they are subjected to direct trauma such aswhen falling astride a hard surface or when strainedduring the course of carrying out some sportingactivity. One of my patients, a keen footballer,damaged them employing a device to strengthenhis upper thigh muscles!

Locating of TrPs in these muscles In the femaleTrPs present in the bulbospongiosus may be foundby applying firm pressure to the lateral wall of theintroitus, and in the ischiocavernosus by applyingfirm pressure in the region of the clitoris.

In the male TrPs in the bulbospongiosus arelocated by palpating over the mid-line bulb at theroot of the penis and TrPs in the ischiocavernosusmuscle by palpating along the lateral aspect of theroot of the penis.

Travell & Simons (1992) recommend deactivatingthese TrPs by injecting a local anaesthetic into them.It is, however, in my experience easier and just aseffective to carry out superficial dry needling.

Scrotal painWhenever scrotal pain develops for no obviousreason, the possibility of it being referred to thescrotum from TrPs elsewhere has to be consid-ered.

These TrPs may be either in the external obliquemuscle just above the inguinal ligament; or in theadductor longus muscle near to its insertion intothe pubic bone; or in the muscles of the pelvicfloor; or, as Kellgren (1940) showed, in musclesand ligaments in the upper lumbar region in thevicinity of the 1st lumbar vertebra. The referral ofpain to the scrotum from such a distant site pre-sumably is associated with the fact that the genitalbranch of the genito-femoral nerve arises from the1st and 2nd lumbar nerves (Yeates 1985).

A man (74 years of age), shortly after havingundergone a prostatectomy, developed scrotal pain,which was made worse by various physical activitiessuch as gardening and was aggravated by sitting forlong periods in his car. There was no obvious cause forthis pain in the testicles or neighbouring pelvic organs.He was, therefore, told that with time it woulddisappear! However, after it had been troubling himfor 3 years he expressed a wish to try the effects ofacupuncture.

On examination, physical signs were confined tothe lower back where there were several TrPs invarious parts of the musculature, including two inexquisitely tender fibrositic nodules immediately tothe right of the 1st lumbar vertebra. For anatomicalreasons just discussed, it would seen likely that it wasfrom these that the pain was being referred to thescrotum.

As so often happens with TrPs, the patient wasunaware of their presence, but on direct questioninghe did admit that for about the same period of time hehad had some aching in the lower back, but had notthought it worth mentioning as the scrotal pain wasso much more distressing.

Deactivation of these TrPs on five occasions overthe course of 7 weeks brought the low-back andscrotal pain under control.

The close temporal relationship between theprostatectomy and the onset of aching in the lowerback and pain in the scrotum would make itreasonable to assume that the activation of the TrPswas due to the low-back muscles having been strainedduring the course of the patient being lifted on or offthe operating table, or to them being traumatized as aresult of the patient lying for some appreciable timeon the table.


Chap-20.qxd 11*10*04 10:33 Page 356


Apley J, Naish N 1958 Recurrent abdominal pains – a fieldsurvey of 1000 school children. Archives of Diseases inChildhood 33: 165–167

Applegate W V 1972 Abdominal cutaneous nerve entrapmentsyndrome. Surgery 71: 118–124


Blendis L M 1984 Abdominal pain. In: Wall P D, Melzack R(eds) Textbook of pain. Churchill Livingstone, Edinburgh,p. 356

Bourne I H J 1980 Treatment of painful conditions of theabdominal wall with local injections. Practitioner 224:921–925

Crown S 1978 Psychological aspects of low backpain. Rheumatology and Rehabilitation 17:114–124

Cummings M 2000 Piriformis syndrome. Acupuncture inMedicine 18(2): 108–121

de Valera E, Raftery H 1976 Lower abdominal and pelvicpain in women. In: Bonica J J, Albe-Fessard D (eds)Advances in pain research and therapy, Vol 1. RavenPress, New York, pp. 933–937

Dittrich R J 1951 Coccygodynia as referred pain. Journal ofBone and Joint Surgery 44A: 715–718

Esler M D, Goulston K 1973 Levels of anxiety in colonicdisorders. New England Journal of Medicine 288: 16–20

Fielding J F 1977 The irritable bowel syndrome. Clinics inGastroenterology 6: 607–622

Good M G 1950a The role of skeletal muscles in thepathogenesis of disease. Acta Medica Scandinavica 138:285–292

Good M G 1950b Pseudo-appendicitis. Acta MedicaScandinavica 138: 348–353

Gutstein R R 1944 The role of abdominal fibrositis in functionalindigestion. Mississipi Valley Medical Journal 66: 114–124

Hall M W 1986 Treatment of functional abdominal pain bytranscutaneous nerve stimulation (correspondence).British Medical Journal 293: 954–955

Holdstock D J, Misiewicz J J, Waller S L 1969 Observationson the mechanism of abdominal pain. Gut 10: 19–31

Hoyt H S 1953 Segmental nerve lesions as a cause of the trigonitis syndrome. Stanford Medical Bulletin 11:61–64

Hunter C 1933 Myalgia of the abdominal wall. CanadianMedical Journal 28: 157–161

Kellgren J H 1940 Somatic simulating visceral pain. ClinicalScience 4: 303–309

Kelly M 1942 Lumbago and abdominal pain. MedicalJournal of Australia 1: 311–317

Kendall G, Sylvester K, Lennard-Jones J E 1986 Treatment offunctional abdominal pain by transcutaneous nervestimulation (correspondence). British Medical Journal293: 954–955

Lewis T, Kellgren J H 1939 Observations relating to referredpain, viscero-motor reflexes and other associatedphenomena. Clinical Science 4: 47–71

Lilius H G, Valtonen E J 1973 The levator ani spasmsyndrome: a clinical analysis of 31 cases. AnnalesChirurgiae et al Gynaecologiae 62: 93–97

Long C 1956 Myofascial pain syndromes. Part III. Somesyndromes of the trunk and thigh. Henry Ford HospitalMedical Bulletin 4: 102–106

McGivney J Q, Cleveland B R 1965 The levator syndromeand its treatment. Southern Medical Journal 58: 505–510

Mehta M, Ranger I 1971 Persistent abdominal pain.Anaesthesia 26(3): 330–333

Melnick J 1954 Treatment of trigger mechanisms ingastrointestinal disease. New York State Journal ofMedicine 54: 1324–1330

Melnick J 1957a Symposium on mechanism andmanagement of pain syndromes. Proceedings of theRudolf Virchow Medical Society, City of New York 16:135–142

Melnick J 1957b Trigger areas and refractory pain in duodenalulcer. New York State Journal of Medicine 57: 1037–1076

Murray G R 1929 Myofibrositis as a simulator of othermaladies. Lancet 1: 113–116

Procacci P, Zoppi M 1983 Pathophysiology and clinicalaspects of visceral and referred pain. In: Bonica J (ed)Advances in pain research and therapy, Vol 5. RavenPress, New York, pp. 643–656

Ranger I, Mehta M, Pennington M 1971 Abdominal wallpain due to nerve entrapment. Practitioner 206: 791–792

Renaer M 1984 Gynaecological pain. In: Wall P D, Melzack R(eds) Textbook of pain. Churchill Livingstone, Edinburgh,p. 373

Simons D, Travell J, Simons L 1998 Myofascial pain anddysfunction. The trigger point manual, Vol 1, Ch. 49.Williams and Wilkins, Baltimore

Slocumb J C 1984 Neurological factors in chronic pelvic pain:trigger points and the abdominal pelvic pain syndrome.American Journal of Obstetrics and Gynaecology 149:536–543

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Sinaki M, Merritt J L, Stillwell G K 1977 Tension myalgia ofthe pelvic floor. Mayo Clinic Proceedings 52: 717–722

Smith W T 1959 Levator spasm syndrome. MinnesotaMedicine 42: 1076–1079

Stone R T, Barbero G J 1970 Recurrent abdominal pain inchildhood. Pediatrics 45: 732–738

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Theobald G H 1949 The relief and prevention of referredpain. Journal of Obstetrics and Gynaecology of the BritishCommonwealth 56: 447–460

Thiele G H 1937 Coccygodynia and pain in the superiorgluteal region and down the back of the thigh: causationby tonic spasm of the levator ani, coccygeus and piriformismuscles and relief by massage of these muscles. Journal ofthe American Medical Association 109: 1271–1275

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Thiele G H 1963 Coccygodynia: cause and treatment.Diseases of the Colon and Rectum 6: 422–436

Travell J 1950 The adductor longus syndrome: a cause ofgroin pain. Bulletin of the New York Academy ofMedicine 26: 284–285

Travell J G, Simons D G 1983 Myofascial pain anddysfunction. The trigger point manual. Williams &Wilkins, Baltimore, pp. 660–683

Travell J G, Simons D G 1992 Myofascial pain anddysfunction. The trigger point manual, Vol. 2. Williamsand Wilkins, Baltimore

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Yeates W K 1985 Pain in the scrotum. British Journal ofHospital Medicine 33(2): 101–104

Young D 1943 The effects of Novocaine injections on simulatedvisceral pain. Annals of Internal Medicine 19: 749–756


Chap-20.qxd 11*10*04 10:33 Page 358

Note: Page references in italics indicateillustrations

19th century, Western world, historicalreview, 21–7

A

A-delta nociceptors, 47, 47, 49AA see acupuncture analgesiaabdominal pain, 343–358

case studies, 346, 346–7, 348differential diagnosis, 347irritable bowel syndrome, 349–50low-back pain, 350–1muscles involved, 345, 346, 347, 345myofascial trigger point (TrP) pain

syndrome, 344–50referred pain, 351symptomatology, 345–7TrPs, 345TrPs activation, 347–50

Achilles tendinitis, 321–2acu-tracts, myofascial trigger point

(TrP) pain syndrome, 82, 82–3, 83acupuncture analgesia (AA)

EOPs, 114–16naloxone studies, 113–14pain-suppression, 110–15research, 113–16serotonin role, 116

adductor longus muscles, lower limbpain, 316, 316

adductor longus syndrome, pelvicpain, 355

aetiological factorsCRPS, 104migraine, 251–2

myofascial trigger point (TrP) painsyndrome, 104

osteoarthritis, 325algometry, myofascial trigger point

(TrP) pain syndrome, 88–9anaesthetics, local, 128, 143–4analgesia

OMAS, 63–4osteoarthritis, 325placebos, 153–4stimulation-produced

analgesia, 61tolerance, TENS, 118see also acupuncture analgesia

angina, chest pain, 178ankle pain, 338–9

see also lower limb painankylosing spondylitis, low-back pain,

276–7annulus fibrosus rupture, neck pain,

208–9anterior chest wall MTrP pain

syndrome, 166–79cf. cardiac pain, 167–75differential diagnosis, 175–9historical review, 3–12

anti-inflammatory drug therapy,bicipital tendinitis, 189

anxietyFS, 143myofascial trigger point (TrP) pain

syndrome, 77neck pain, 218

arm muscles, 230, 231, 232arm pain, 223–49

brachial plexus injuries, 227–8case studies, 224, 225–6cervical spondylosis, 223–4disc prolapse, 223–4

lateral epicondylalgia, 228–35levator scapulae muscle, 224medial epicondylalgia, 235myofascial trigger point (TrP) pain

syndrome, 223–4paraesthesia, 224referred pain, 226, 229–33supraspinatus muscle, 224tennis elbow, 228–35thoracic outlet syndrome, 227–8triceps muscle, 229–30

arthritis see osteoarthritis; rheumatoidarthritis

ascending pathways, nociceptive pain,51, 53

autonomic nervous system,dysfunction

CRPS, 105FS, 95–6

B

Bache, Franklin, 24–5back pain, low- see low-back painBayle, Pierre, 18beta-lipotrophin, 60, 60biceps muscle, shoulder pain, 199, 200bicipital tendinitis

anti-inflammatory drug therapy,189

shoulder pain, 189Bigelow, N H, 35biochemical disorders, correction, 141blood circulation, discovery, 6–7botulinum A toxin, injections, 130Boym, Michael, 18brachial pain disorders, multifactorial,

wrist and hand pain, 247–8

359

Index

Index.qxd 11*10*04 10:34 Page 359

brachial plexus injuries, arm pain,231–2

brainstem’s reticular formation, 54

C

C-polymodal nociceptors, 47–8, 48, 49

capsulitisacupuncture, 191–2clinical diagnosis, 190corticosteroids, 191natural history, 190pathogenesis, 190referred pain, 192–3secondary activation, myofascial

TrPs, 192–203shoulder pain, 189–203steroid injections, 191treatment, 190–2

carcinoma, low-back pain, 277cardiac pain, cf. anterior chest wall

MTrP pain syndrome, 166167–75

carpal tunnel syndrome, wrist andhand pain, 243

case studiesabdominal pain, 346, 347,

347–8arm pain, 224, 225–6chest pain, 183, 184cubital tunnel syndrome, 240–1elbow, 337head and face pain, 266hip, 336knee, 333–4, 335levator scapulae muscle, 217low-back pain, 227, 280, 281–2, 287,

293–4, 307–8lower limb pain, 315–16myofascial trigger point (TrP) pain

syndrome, 78, 80, 84, 85neck pain, 207–8, 215, 217, 219, 224

225–6obesity, 333osteoarthritis, 329pelvic pain, 351–4PID, 281post-traumatic headache, 268scrotal pain, 356thumb pain, 244–6toe pain, 323torticollis, 268trigger finger, 246ulnar nerve entrapment, 240whiplash, 214, 215, 216wrist and hand pain, 238

caudal projections to theperiaqueductal grey, OPMDIS, 62

causalgia, CRPS, 102, 104–5central canal stenosis, low-back pain,

295–6cerebrospinal fluid (CSF), EOPs,

113–15cervical myofascial TrP pain

syndrome, neck pain, 209–13

cervical radiculopathic brachial pain,225–6

cervical spondylosisarm pain, 223–4neck pain, 208–9

chest pain, 165–85angina, 178anterior chest wall MTrP pain

syndrome, 166–79case studies, 183, 184coronary by-pass surgery, 178FS, 179intercostal pain, 183intercostal pain, nerve section,

184mitral valve prolapse, 179myocardial infarction, 178post-thoracotomy pain, 183posterior chest wall myofascial TrP

activity, 179–83rib fracture, 178tender spots, 166thoracotomy scar pain, 183–4Tietze’s syndrome, 178–9

Chhi-Po, 6, 9cholecystokinin octapeptide, OPMDIS,

62Churchill, J M, 22–3Cleyer, Andreas, 17clinical trials

future, 156–8low-back pain, 307–11neck pain, 220–1osteoarthritis, 338–9see also scientific evaluation

cluster headaches, 261cognitive impairment, whiplash,

215complex regional pain syndrome

(CRPS)aetiological factors, 104autonomic nervous system,

dysfunction, 103causalgia, 102, 104–5clinical manifestations, 103–4emotional disorders, 104muscle weakness, 104

myofascial trigger point (TrP) painsyndrome, 101–7

pain, 101pathophysiology, 104–5pharmacotherapy, 105–6physiotherapy, 106predisposing factors, 105psychotherapy, 106terminological revision, 102–3tissue dystrophy, 103treatment, 105–6

complications, acupuncture, 135–6Consolidated Standards for Reporting

Trials (CONSORT), 157convulsions, 135coracobrachialis muscle, shoulder

pain, 198, 198coronary by-pass surgery, chest pain,

178corticosteroids

capsulitis, 189lateral epicondylalgia, 234–5low-back pain, 297

Coxe, Edward, 25CRPS see complex regional pain

syndromeCSF see cerebrospinal fluidcubital tunnel syndrome

case studies, 240wrist and hand pain, 241

cycle test, low-back pain, 296

D

deep dry needling (DDN)disadvantages, 131–2pain-suppression, 120review, 131–2training, 145

deltoid muscle, shoulder pain,196–203, 197, 199, 203

depression, FS, 91, 143descending inhibitory system,

55–6descending systems

diffuse noxious inhibitory controls,65

dorsolateral funiculus, 62nociceptive pain, 61–5non-opioid-peptide-mediated, 64–5noradrenergic, 65OPMDIS, 62–3stimulation-produced analgesia, 61

diagnosisabdominal pain, 346–7anterior chest wall MTrP pain

syndrome, 175–9

INDEX360

Index.qxd 11*10*04 10:34 Page 360

capsulitis, 192FS, 93–4lateral epicondylalgia, 228myofascial trigger point (TrP) pain

syndrome, 83–8diffuse noxious inhibitory controls,

descending systems, 61disc prolapse

arm pain, 223–4low-back pain, 281–2, 282–7management, 286–7neck pain, 223–4surgical intervention, 286–7

dizziness, FS, 91dorsal horn, 50–3

EOPs, 115inhibitory interneurons, 53laminae, 50nerve connections, 120neuroplasticity, 53TENS, 117transmission cells, 50–3

dorsolateral funiculusdescending systems, 61–2OPMDIS, 62

drowsiness, post-treatment, 135–6

E

elbowcase studies, 337golfer’s elbow, 235osteoarthritis, 337tennis elbow, 228–35TrPs, 229–33

electroacupunctureFS, 143–4pain-suppression, 111

electrocardiography, chest pain, 177

Elliotson, John, 23Ellman, P, 41emotional aspects, pain, 66–8emotional disorders, CRPS, 103emotional disturbances, whiplash,

216endogenous opioid peptides (EOPs),

AA, 113–15epicondylalgia

lateral, 228–4medial, 234

erythrocyte sedimentation rate (ESR),low-back pain, 280

extensor carpi radialis brevis muscle,referred pain, 237, 238

extensor digitorum muscle, referredpain, 237, 237

external oblique muscle, anterior chest wall MTrP pain syndrome,175

F

face pain see head and face painfacet joint damage

low-back pain, 287–9whiplash, 215

female urethral syndrome, FS, 92fibromyalgia syndrome (FS), 90–6

aerobic exercise, 143affective disorders, 142–3anxiety, 143associated disorders, 91autonomic nervous system,

dysfunction, 95–6central sensitization, 94chest pain, 179depression, 91, 143diagnosis, 93–4dizziness, 91drugs, symptom-relieving, 142–3education, patients, 141electroacupuncture, 143–4female urethral syndrome, 92inflammatory diseases, 92–3irritable bowel syndrome, 91knowledge evolution, 37–43light headedness, 91muscle stretching, 143nodules, 38–9nosological obfuscation, 37–8pain, 142pain origin, 96palpable bands, 38–42pathophysiology, 94–6physical modalities, 143–4predisposing factors, 92–3Raynaud’s phenomenon, 92restless leg syndrome, 92, 142SDN, 145serotonin levels, 94–5sleep apnoea, 142sleep disturbance, 142sleep, non-restorative, 91substance P, 95symptoms, 90systemic syndromes, 92TCAPs, 144tender point injections, 144–5trauma, 92treatment, 141–5

finger pain, wrist and hand pain, 247Floyer, Sir John, 17foot pain see lower limb pain

forearm extensor muscles, wrist andhand pain, 236–8

forearm flexor muscles, wrist andhand pain, 238–40

forgotten needles, 136frontal cortex, 55frozen shoulder see capsulitisfuture clinical trials, 156–8future therapeutic advances, 158

G

gastrocnemius muscle, lower limbpain, 319, 320, 321

gate-control theoryneurophysiology, 56–8nociceptive pain, 58revision, 57–8substantia gelatinosa, 52, 56–7

glutei muscleslow-back pain, 303–5, 304lower limb pain, 318

golfer’s elbow, 235gynaecological MTrP pain, pelvic pain,

355–6

H

haemorrhage, 136hamstrings, lower limb pain, 318–19,

318hand pain see wrist and hand painHan’s mesolimbic loop, 121, 121–2head and face pain, 251–71

atypical facial pain, 265–6case studies, 269cluster headaches, 261lateral (external) pterygoid muscle,

263–4masseter muscle, 262, 262–3medial pterygoid muscle, 264–5migraine, 251–9occipitofrontalis muscle, 270–1, 271orbicularis oculi muscle, 270post-traumatic headache, 268skin muscles, TrPs activity, 270–1sternocleidomastoid muscle, 267–9temperomandibular joint, 261–5temporalis muscle, 269, 269–70tension-type headaches, 259–61torticollis, 268–9trauma-induced myofascial TrP

cephalagia, 266–8trigeminal neuralgia, 265zygomaticus major muscle, 270–1,

271

Index 361

Index.qxd 11*10*04 10:34 Page 361

head pain, whiplash, 215Heberden’s nodes, wrist and hand

pain, 247heel pain, 320–2herniation, neck pain, 208–9hip, case studies, 336–7hip osteoarthritis, 335–7historical review, 3–27

Japan, 13–20news spread, acupuncture/

moxibustion, 13–20, 111–13traditional Chinese acupuncture,

3–12Western world, 19th century,

21–7Hockaday, J M, 35Hong’s modification, local anaesthetic

injection, 128hypothalamus/pituitary complex,

EOPs, 115

I

iliopsoas muscle, low-back pain,306–7, 307

infection transmission, 136inflammatory diseases, FS, 92infraspinatus muscle

shoulder pain, 194–5, 195, 196TrPs activity, 224–5

injectionsbotulinum A toxin, 130Hong’s modification, 128local anaesthetic, 128, 144–5NSAIDs, 129–30saline, 32–6, 128, 132steroid, 129–30, 191, 233–4, 298,

329water, 132

intercostal pain, chest pain, 183irritable bowel syndrome

abdominal pain, 349–51FS, 91–2

J

Japan, acupuncture/moxibustion,13–20

Japanese shallow needling, cf. SDN,135

joints pain, 325–41ankle, 338hip osteoarthritis, 335–7knee, 331–5osteoarthritis, 325–30sprains, 330–1

K

Kaempfer, Englebert, 18–19keiraku chiryo, 135Kellgren, J H, referred pain, 32–5knee

case studies, 333–4joint instability, 333joint pain, 331–5obesity, 333–4osteoarthritis, 331–5patellofemoral compartment, 331referred pain, 334short-leg syndrome, 334sprains, 334–5TCAPs, 333tibiofemoral compartments, 331–2treatment response, 332–5TrPs, 331, 332

L

laminectomy, low-back pain, 286Lasègue’s sign, low-back pain, 284lateral epicondylalgia, 228–35

clinical features, 229differential diagnosis, 229inflammatory reaction, 228–9pathophysiology, 228steroid injections, 233–4TCAPs, 234–5terminology, 228treatment, 233–5TrPs activity, 229–3

lateral epicondylitis see lateralepicondylalgia

lateral (external) pterygoid muscle,head and face pain, 263–4

lateral root canal stenosis, low-backpain, 296–7

latissimus dorsi muscleposterior chest wall myofascial TrP

activity, 181–2shoulder pain, 200–1

leg pain see lower limb painlevator scapulae muscle

arm pain, 224case studies, 217neck pain, 210, 210–11, 211, 217paraesthesia, 224shoulder pain, 196

Lewis, Sir Thomas, 32ligaments, myofascial trigger point

(TrP) pain syndrome, 90ligamentum nuchae, neck pain, 214light headedness, FS, 91

limbic system, 55Livingston’s vicious circle, myofascial

trigger point (TrP) painsyndrome, 80

LLLI see lower-limb length inequalitylocal anaesthetic injection, 144–5

Hong’s modification, 128MTrPs, 128

lost needles, 136low-back pain, 275–314

abdominal pain, 350–1acupuncture, 299–311acute, 281–2acute sciatica, 283–7ankylosing spondylitis, 276–7carcinoma, 277case studies, 277, 280, 282, 291, 293,

306–7causes, mechanical, 281central canal stenosis, 295–6chronic lumbar myofascial TrP pain

syndrome, 289–94chronic mechanical type, 287–94clinical examination, 277–80clinical trials, 307–11corticosteroids, 298–9curves, lumbar spine, 278cycle test, 296degenerative changes, 287–9disc prolapse, 281–2, 283–7drugs, 297–8dual pathology, 277ESR, 280exercises, 298facet joint damage, 287–9glutei muscles, 303, 304iliopsoas muscle, 306–7, 307laminectomy, 286Lasègue’s sign, 284lateral root canal stenosis, 296–7management, 297–311manipulation, 298mechanical, chronic, 287–94mechanical/non-mechanical,

276–7, 280–1MRI, 281, 284–5MTrPs, 292–4muscle wasting, 278muscles, back, 300neurogenic claudication, 295–6nociceptive pain, 294–7pain syndrome, 289–90physiotherapy, 298PID, 281–2, 283–7piriformis syndrome, 304,

304–6quadratus lumborum muscle, 302,

302–3, 303

INDEX362

Index.qxd 11*10*04 10:34 Page 362

radiculopathic chronic, 294–7radiography, 280–1, 284–5referred pain, 277, 285–6, 291,

300–7, 300–7, 353sacroiliac joint, 306sciatica, acute, 283–7short-leg syndrome, 278spinal fusion, 287spinal stenosis, 295spinal supports, 298spine movement, 278–9spondylolisthesis, 294–5spontaneous resolution, 282–3steroid injections, 298–9TrPs activity, 290TrPs search, 279–80ultrasound, 298vascular origin, 276

lower-limb length inequality (LLLI),139–41

lower limb pain, 315–24Achilles tendinitis, 321–2adductor longus muscles, 316, 316ankle pain, 338case studies, 315–16gastrocnemius muscle, 319,

319–20glutei muscles, 318hamstrings, 318, 318heel pain, 320–2metatarsalgia, 141, 322–3Morton’s syndrome, 141, 322–3plantar fasciitis, 322quadriceps femoris muscles, 316,

316–17short-leg syndrome, 278, 334soleus muscle, 319–20, 320, 321tibialis anterior muscle, 318–19,

320, 321toe pain, 323–4, 324vastus lateralis muscle, 316–17, 317,

318vastus medialis muscle, 316–17, 317

M

magnetic resonance imaging (MRI),low-back pain, 281, 284–5

masseter muscle, head and face pain,262, 262–3

measuring pain-suppression, 156mechanical/non-mechanical low-back

pain, 276–7, 280–1medial epicondylalgia, arm pain,

235medial epicondylitis see medial

epicondylalgia

medial pterygoid muscle, head andface pain, 264–5

mesolimbic loop, Han’s, 121, 121–2metatarsalgia, 143, 326–7midbrain, EOPs, 115migraine, 251–9

acupuncture, 254–9, 256–7aetiology, 251–2biochemical changes, 253–4emotional (supraspinal)

component, 253myofascial component, 252–3noradrenaline (norepinephrine), 254oestrogen, 254pathophysiology, 252–3serotonin role, 253–4vascular component, 252vascular-myofascial-supraspinal

(emotional) paradigm, 253Minnesota Multiphasic Personality

Inventory (MMPI), 66mitral valve prolapse, chest pain, 179MMPI see Minnesota Multiphasic

Personality InventoryMoldofsky, Harvey, 42–3, 43Morton’s syndrome, 141, 322–3moxibustion, 110

described, 4–5news spread, 13–20

MPS see myofascial pain syndromeMRI see magnetic resonance imagingMTrPs see myofascial trigger pointsmuscle ischaemia, myofascial trigger

point (TrP) pain syndrome, 77muscle stretching, MTrPs, 137muscle wasting

low-back pain, 278myofascial trigger point (TrP) pain

syndrome, 77muscle weakness

CRPS, 104myofascial trigger point (TrP) pain

syndrome, 83myocardial infarction, chest pain, 178myofascial pain syndrome (MPS)

knowledge evolution, 37–44nodules, 38–9nosological obfuscation, 37–8palpable bands, 38–42

myofascial trigger point (TrP) painsyndrome, 73–90

abdominal pain, 344–51acu-tracts, 82, 82–3, 83aetiological factors, 104algometry, 89arm pain, 223–4case studies, 78–9, 80–1, 84–5CRPS, 101–7

diagnosis, 83–8electrical activity, 75–6Group IV nociceptors, 76–7incidence, 74investigatory procedures, 89–90latent points, 78ligaments, 90Livingston’s vicious circle, 80local twitch response, 86low-back pain, 290–4mechanisms, 79–81muscle wasting, 77muscle weakness, 84natural history, 78–9neck pain, 223–4nerve root entrapment, 87nociceptor activity, 77–8pain reproduction, 85palpable bands, 185pathophysiology, 74–5pathways, pain, 82–3pelvic pain, 351–4periosteum, 90persistence, 79–81physical factors, 292–4physical signs, 84–8primary points, 78psychological factors, 292–4referred pain, 77–8, 81–3regional, 88–9satellite points, 78secondary points, 78sleep disturbance, 84sympathetically-mediated

symptoms, 84symptoms, 83–4temperature changes, skin, 89–90tender nodules, 86–7thermography, 89

myofascial trigger points (MTrPs)biochemical disorders, 141botulinum A toxin injections, 130deactivating techniques, 132, 134–5,

219local anaesthetic injection, 128muscle stretching, 137NSAIDs injection, 129–30postural disorders correction, 137–9reactivation prevention, 137–41saline injections, 129, 132SDN, 119–20, 132–3searching, systematic, 134steroid injections, 129–30stress, 141structural disorders correction,

137–8cf. TCAPs, 119tension-type headaches, 259–60

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myofascial trigger points (MTrPs)(contd.)

water injection, 132wet needling techniques, 128–30see also trigger points

N

naloxone studies, AA, 113–14Nan Ching, 8neck pain, 207–22

annulus fibrosus rupture, 208–9anxiety, 218case studies, 207–8, 216, 217, 218–19cervical myofascial TrP pain

syndrome, 209–14cervical radiculopathic brachial

pain, 225–6cervical spondylosis, 208–9clinical trials, 219–221disc prolapse, 223–4herniation, 208–9levator scapulae muscle 210,

210–11, 211, 217, 225ligamentum nuchae, 214myofascial trigger point (TrP) pain

syndrome, 223–4paraesthesia, 215, 224persistent, 218–19posterior cervical muscles, 212, 213postural disorders correction, 216preventative measures, 218referred pain, 224results, acupuncture, 219–21rhomboid muscles, 213–14, 214scapulocostal syndrome, 211scapulohumeral syndrome, 211shoulder girdle, 217splenius cervicis, 211, 212spondylosis, 208–9supraspinatus muscle, 224transmitted strain, 217trapezius muscle, 212–13, 213treatment, 218–19whiplash, 214–17

needle-evoked sensations, 137Nei Ching, 4–12neospinothalamic pathways, pain, 51,

54neuralgic amyotrophy, wrist and hand

pain, 247neurogenic claudication, low-back

pain, 295–6neuropathic pain, 47

cf. nociceptive pain, 65–6neurophysiology

descending inhibitory system, 56

gate-control theory, 56–8knowledge advances, 1950s and

1960s, 56knowledge advances, 1970s and

1980s, 58–65opiate receptors, 58–9opioid peptides, 59–61pain, 45–72pain, nature of, 46pain types, 46–55

news spread,acupuncture/moxibustion,13–20, 111–13

nociceptive pain, 47–56ascending pathways, 51, 53–6descending systems, 61–5gate-control theory, 56–8low-back pain, 294–7cf. neuropathic pain, 65–6pain-suppression, scientific

evaluation, 149–61nociceptor activity, myofascial trigger

point (TrP) pain syndrome, 76–8nodules, 38–9non-steroidal anti-inflammatory drugs

(NSAIDs)injections, 129–30osteoarthritis, 329

noradrenergic descending inhibitorysystem, 65

nosological obfuscation, 37–8NSAIDs see non-steroidal anti-

inflammatory drugs

O

obesitycase studies, 334knee, 333–4

occipitofrontalis muscle, head and facepain, 271, 271

Office Hours: Day and Night, 166OMAS see opioid-peptide-mediated

analgesia systemopiate receptors, neurophysiology,

58–9opioid-peptide-mediated analgesia

system (OMAS), 63–4opioid-peptide-mediated descending

inhibitory system (OPMDIS),62–3

opioid peptidesbeta-lipotrophin, 60, 60neurophysiology, 59–61

OPMDIS see opioid-peptide-mediateddescending inhibitory system

orbicularis oculi muscle, head and facepain, 270–1, 271

Osler, Sir William, 25–6osteoarthritis, 325–30

aetiological factors, 326analgesics, 329aspiration, 330biochemical factors, 326case studies, 330clinical trials, 338–9corticosteroids, 330dieting, 329elbow, 337hip, 335–7inflammation of synovium, 327joints involved, 326knee, 331–5management, 329–30mechanical factors, 326monarticular hip disease, 326NSAIDs, 329pathological changes, 327–8physiotherapy, 329–30predisposing factors, 326presentation, 325primary, 326secondary, 326steroid injections, 330wrist and hand pain, 337X-ray changes, 328–9

P

paindescending inhibitory system, 56emotional aspects, 66–8nature of, 46neuropathic, 47neurophysiology, 45–72nociceptive, 47–56pathways, 51, 52, 53–5psychogenic, 46referred pain, early observations,

32–6types, 46–55

pain origin, FS, 96pain-suppression

AA, 111–16challenges, conventional views,

121–2DDN, 121effects, acupuncture, 109–25electricity, 110electroacupuncture, 111measuring, 156placebos, 150–4point specificity, 150

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primitive procedures, 110scientific evaluation, 149–58SDN, 119–20

paleo-spino-reticulo-diencephalicpathways, pain, 51, 53

palmaris longus muscle, wrist andhand pain, 242, 242

palpable bandsFS, 37–41MPS, 37–42myofascial trigger point (TrP) pain

syndrome, 83–4paraesthesia

arm pain, 224levator scapulae muscle, 224neck pain, 213, 224supraspinatus muscle, 224whiplash, 215

paraspinal muscles, posterior chestwall myofascial TrP activity, 182

Park Sham Device (PSD), placebos,152–3, 153

pathways, pain, 48–55, 51, 52ascending, 51, 53descending systems, 61–5neospinothalamic, 51, 54paleo-spino-reticulo-diencephalic,

51, 54pectoralis major muscle, anterior chest

wall MTrP pain syndrome,170–3, 173, 174

pectoralis minor muscle, anterior chestwall MTrP pain syndrome,173–5, 174

pelvic pain, 351–6adductor longus syndrome, 355anterior pelvic floor MTrP pain, 355–6case studies, 354–6chronic pelvic floor MTrP pain

syndrome, 352–4gynaecological MTrP pain, 355–6muscles involved, 345, 346myofascial trigger point (TrP) pain

syndrome, 351–4scrotal pain, 356testicular pain, 354, 355

periaqueductal grey, OPMDIS, 62perineal pain see pelvic painperiosteum, myofascial trigger point

(TrP) pain syndrome, 88pharmacotherapy, CRPS, 105–6physical factors, MTrPs, 292–4physiological reactions, needling, 136–7physiotherapy

CRPS, 106low-back pain, 298–9osteoarthritis, 329–30

PID see prolapsed intervertebral disc

piriformis syndrome, low-back pain,304, 304–6

placebosanalgesia, 153–4credible, 151currently employed, 152–3inactivated laser, 152non-invasive needling, 152–3pain-suppression, scientific

evaluation, 149–54PSD, 152–3TENS, 152

plantar fasciitis, lower limb pain, 321point specificity, pain-suppression, 150post-thoracotomy pain, chest pain, 183post-traumatic headache, 268

case studies, 268posterior cervical muscles, neck pain,

212, 213posterior chest wall myofascial TrP

activity, 179–83postural disorders correction, 137–140,

138–40neck pain, 218

prolapsed intervertebral disc (PID),low-back pain, 281–2, 283–7

see also disc prolapsepronator teres muscle, wrist and hand

pain, 241–2, 242prostatectomy, scrotal pain, 356PSD see Park Sham Devicepsychogenic pain, 46psychological factors, MTrPs, 292–4psychotherapy, CRPS, 106

Q

quadratus lumborum muscle, low-back pain, 302, 302–3, 303

quadriceps femoris muscles, lowerlimb pain, 316, 316–17

R

radiculopathic chronic low-back pain,294–7

radiculopathic compression, motornerves, myofascial trigger point(TrP) pain syndrome, 77

radiographic findings, whiplash, 215radiography, low-back pain, 280–1,

284–5Raynaud’s phenomenon, FS, 92rectus abdominis muscle

anterior chest wall MTrP painsyndrome, 175

posterior chest wall myofascial TrPactivity, 179–80

referred pain, 32, 33, 35abdominal pain, 350anatomical distribution, 35–6anterior chest wall MTrP pain

syndrome, 166–75, 168arm pain, 226, 232–3, 232–3capsulitis, 192–3cardiac pain, 166, 167–77early observations, 32–6extensor carpi radialis brevis

muscle, 237, 238extensor digitorum muscle, 237, 237knee, 334–5low-back pain, 275, 281–2, 291,

301–6, 301–6, 351myofascial trigger point (TrP) pain

syndrome, 77, 81–3neck pain, 213, 224relevance, trigger point

acupuncture, 36saline injections, 32–6shoulder pain, 224supinator muscle, 236, 236wrist and hand pain, 235–8, 235–8

reflex sympathetic dystrophy (RSD)see complex regional painsyndrome

repetitive strain injury, wrist and handpain, 248

research, AA, 113–16restless leg syndrome, FS, 92, 142reticular formation, brainstem, 54rheumatoid arthritis, 339ten Rhijne, Willem, 13–17rhomboid muscles, neck pain, 213–14,

214rib fracture, chest pain, 178rostral projections to the periaqueductal

grey, OPMDIS, 62–3rostral ventromedial medulla (RVM),

OPMDIS, 62rotator cuff tendinitis, shoulder pain,

187–8RSD (reflex sympathetic dystrophy)

see complex regional painsyndrome

RVM see rostral ventromedial medulla

S

sacroiliac joint, low-back pain, 306sagging shoulders, shoulder pain, 217saline injections

MTrPs, 129, 132referred pain, 32–6

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scalene muscleanterior chest wall MTrP pain

syndrome, 166–9, 168TrPs activity, 224

scapulocostal syndrome, neck pain, 211scapulohumeral syndrome, neck pain,

211scientific evaluation

blinding, 154future clinical trials, 156–8future therapeutic advances, 158needle stimulation strength, 155number of treatment sessions, 155numbers required, 156pain-suppression, 149–58placebos, 150–4prospective participants, 158randomization, 154results assessment, 156trial protocols, 156–7trials design, 155–6see also clinical trials

scrotal pain, 356case studies, 355, 356

SDN see superficial dry needlingsegmental/non-segmental

acupuncture, 120sensations, needle-evoked, 137sensory receptors

muscle, 48–50skin, 47–8

serotonin levels, FS, 94–5serotonin role

AA, 116migraine, 25

serratus anterior muscle, anterior chestwall MTrP pain syndrome, 175,176

serratus posterior superior muscle,posterior chest wall myofascialTrP activity, 179, 179–80, 180

Shaw, D, 41short-leg syndrome

knee, 334low-back pain, 282

shoulder girdle, neck pain, 217–18shoulder-hand syndrome, wrist and

hand pain, 247shoulder pain, 187–203

biceps muscle, 199, 200bicipital tendinitis, 189capsulitis, 189–192coracobrachialis muscle, 198, 198deltoid muscle, 196–224, 197, 199, 203frozen shoulder see capsulitisinfraspinatus muscle, 194–5, 195, 196latissimus dorsi muscle, 200–1levator scapulae muscle, 196

referred pain, 224rotator cuff tendinitis, 187–8sagging shoulders, 217soft tissue disorders, 187–203subacromial bursitis, 188–9subscapularis muscle, 203–4, 203supraspinatus muscle, 193, 193–4,

194, 196teres major muscle, 200–2, 202teres minor muscle, 195–7tilting shoulders, 217trapezius muscle, 196triceps muscle, 201

Simons, David, 42, 42skin disinfection, 136sleep apnoea, FS, 142sleep disturbance

FS, 142myofascial trigger point (TrP) pain

syndrome, 84sleep, non-restorative, FS, 91Smythe, H A, 42–3Snell, Simeon, 24soft tissue disorders, shoulder pain,

187–203soleus muscle, lower limb pain,

319–20, 320, 321spatial disorientation, whiplash, 215spinal fusion, low-back pain, 287spinal stenosis, low-back pain, 295spinal supports, low-back pain, 298–9spinal terminals, OPMDIS, 62splenius cervicis, neck pain, 211–12, 212spondylolisthesis, low-back pain, 294spondylosis, cervical

arm pain, 223–4neck pain, 208–9

sprainsjoints pain, 331knee, 335

Standards for Reporting Interventionsin Controlled Trials ofAcupuncture (STRICTA), 157

sternalis muscle, anterior chest wallMTrP pain syndrome, 169–70, 170

sternocleidomastoid muscleanterior chest wall MTrP pain

syndrome, 167, 168head and face pain, 266–8

steroid injections, 129–30capsulitis, 191lateral epicondylalgia, 228–9osteoarthritis, 330

stimulation-produced analgesia,descending systems, 61

stressalleviation, 141MTrPs, 141

STRICTA see Standards for ReportingInterventions in Controlled Trials

of Acupuncturestructural disorders correction, 137–41,

138–40studies see clinical trials, scientific

evaluationsubacromial bursitis, shoulder pain,

188–9subclavius muscle, anterior chest wall

MTrP pain syndrome, 170, 171subscapularis muscle, shoulder pain,

203–4, 203substance P, FS, 95substantia gelatinosa, 52, 56–7Sun Ssu-mo, 9–10superficial dry needling (SDN)

FS, 132information, for patients, 134cf. Japanese shallow needling, 135mechanisms, 119–20MTrPs, 119–20, 132–4review, 131–2training, 145

supinator muscle, referred pain, 236,236

supraspinatus musclearm pain, 224neck pain, 224paraesthesia, 224shoulder pain, 193, 193–4, 194, 198TrPs activity, 224

T

TCAPs see traditional Chineseacupuncture points

Teale, T Pridgin, 24temperomandibular joint, head and

face pain, 261–5temporalis muscle, head and face pain,

269, 269–70ten Rhijne, Willem, 13–17tender point injections, fibromyalgia

syndrome (FS), 144–5tender spots, 166tendinitis

bicipital tendinitis, 189referred pain, 192–1rotator cuff tendinitis, 187–9secondary activation, myofascial

TrPs, 192–203tennis elbow see lateral epicondylalgiatenosynovitis, wrist and hand pain,

243TENS see transcutaneous electrical

nerve stimulation

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tension-type headaches, 259–60acupuncture, 260clinical manifestations, 259–60MTrPs, 260pharmacotherapy, 260

teres major muscle, shoulder pain,198–200, 202

teres minor muscle, shoulder pain,195–7

testicular pain, 354, 356, 357thermography, myofascial trigger point

(TrP) pain syndrome, 88–9thoracic outlet syndrome, arm pain,

227–8thoracotomy scar pain, chest pain, 183–4thumb pain, 244–7

case studies, 245–7tibialis anterior muscle, lower limb

pain, 318Tietze’s syndrome, chest pain, 178–9tilting shoulders, shoulder pain, 217tissue dystrophy, CRPS, 103Titsingh, Isaac, 22toe pain, 323–4, 324torticollis

case studies, 269head and face pain, 268–9

traditional Chinese acupuncturepoints (TCAPs)

knee, 333lateral epicondylalgia, 234–5manual acupuncture, 144cf. MTrPs, 119

transcutaneous electrical nervestimulation (TENS), 116–21

acupuncture-like, 118analgesia tolerance, 118conventional, 117, 117intercostal pain, nerve section, 183placebos, 150therapeutic acupuncture, 118–19

transmitted strain, neck pain, 217trapezius muscle

neck pain, 212–13, 213shoulder pain, 196

traumaFS, 92myofascial trigger point (TrP) pain

syndrome, 73post-traumatic headache, 268

trauma-induced myofascial TrPcephalagia, head and face pain,266–8

Travell, Janet, 35, 41–2, 42, 166trials, clinical see clinical trials;

scientific evaluationtriceps muscle

arm pain, 226–7

shoulder pain, 201trigeminal neuralgia, head and face

pain, 265trigger finger

case studies, 243wrist and hand pain, 243

trigger point acupunctureearly observations, 32–6referred pain, 32–6saline injections, 32–6, 129, 132

trigger points (TrPs)abdominal pain, 343, 350–3anterior chest wall MTrP pain

syndrome, 166–80deactivating techniques, 132, 134,

218–9elbow, 229–33identification, 219infraspinatus muscle, 224knee, 331–2, 332lateral epicondylalgia, 228–35low-back pain, 280, 290neck pain, 214–18primary activation, neck pain, 214–8scalene muscle, 225secondary activation, shoulder

pain, 192supraspinatus muscle, 224whiplash, 214–15wrist and hand pain, 242–7see also myofascial trigger points

U

ulnar nerve entrapment, 240case studies, 241

ultrasound, low-back pain, 298

V

Valleix, F, 39–40vaso-vagal attacks, 135vastus lateralis muscle, lower limb

pain, 317, 316–17, 318vastus medialis muscle, lower limb

pain, 316–17, 317viscera damage, 136visceral pain referral, myofascial

trigger point (TrP) painsyndrome, 77

W

Ward, Dr T Ogier, 23–4water injection, MTrPs, 132

Western world, 19th century, historicalreview, 21–7

wet needling techniquesMTrPs deactivation, 128–30review, 131–2

wheal/flare, 136–7whiplash

case studies, 216, 217, 218cognitive impairment, 215emotional disturbances, 216facet joint damage, 215head pain, 215late whiplash syndrome, 216neck pain, 214–17paraesthesia, 215radiographic findings, 215spatial disorientation, 215TrPs, 214–15

Whitty, C W M, 35wrist and hand pain, 235–47

brachial pain disorders,multifactorial, 247–8

carpal tunnel syndrome, 243case studies, 237cubital tunnel syndrome, 240finger pain, 247forearm extensor muscles, 236–8forearm flexor muscles, 238–40hand muscles, 245Heberden’s nodes, 247multifactorial brachial pain

disorders, 247–8neuralgic amyotrophy, 247osteoarthritis, 337palm pain, 246palmaris longus muscle, 241, 242pronator teres muscle, 241–2, 242referred pain, 236–8, 236–8,

240–2repetitive strain injury, 247–8shoulder-hand syndrome, 248tenosynovitis, 243thumb pain, 244–7trigger finger, 246TrPs activity, 242–7

Wyke, B, 35–6

Y

Yin/Yang, 5–11

Z

zygomaticus major musclehead and face pain, 270, 271

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acupuncture, trigger points and musculoskeletal pain (elsevier 3rd ed)

Health & Medicine

pain management

pain specialists

phenomena of pain

musculoskeletal pain

practice of treatment

firstclass book

nature of muscle pain

trigger point treatment