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The spine is a complex structure with bony, ligamentous,

muscular, and neurologic components. Knowledge of theanatomy and associated pathology of the spine is essentialfor treating patients with spinal disorders. The focus of thischapter is to develop an understanding of the anatomic andmore specifically the functional relationships between thesecomponents.

Overview of the Vertebral Columnand Spinal Cord

The human spinal column consists of 33 vertebrae separatedinto five anatomic regions. These regions include 7 cervical(C1-7), 12 thoracic (T1-12), 5 lumbar (L1-5), 5 sacral (S1-5), and 4 coccygeal bones (Fig. 5-1). In utero developmentplays a large part in the formation of the adult spine, contrib-uting to the primary curvatures: kyphosis in the thoracic andsacral regions. Late in utero, after the development of theprimary curvatures and continuing through early childhood,the secondary curvatures of the spine develop (Fig. 5-2). Thecervical and lumbar lordosis becomes significant because ofthe gravitational forces created by the weight of the headand upright posture.1 The positions taken by the cervicaland lumbar spine allow for horizontal gaze while standing inan upright posture.

The development and maintenance of spinal anatomy andposture are not static and vary individually. Variations withintervertebral discs and vertebral bodies can be potentiated by

congenital anomalies, age-dependent vertebral changes andosteophyte formation, traumatic injuries, neurologic disor-ders, and paraspinal muscle imbalances. Commonly occurringvariations include sacralization of the fifth lumbar vertebra orlumbarization of the first sacral vertebra, Klippel-Feil anomalyin the cervical spine, and anomalous nerve root anatomy. Amyriad of reactive changes may be seen as a response to spinaldeformity. The flexibility of the spine may allow a patient tocompensate for a deformity in one region with a change incurvature in another. However, a deformity may become soprofound that an individual may be severely disabled.

The flexibility of the spine varies from region to region andis based on anatomic constraints. The cervical spine offersthe greatest flexibility because of the requisite mobility of

the head. This is in contrast to the rigidity of the thoracic

spine due to its association with the chest wall.2 Unique

articulations in the cervical region afford flexibility such asthose found between the skull-atlas and atlas-axis (C1-2).Flexibility at other regions of the spine is influenced by carti-laginous discs between vertebral bodies and apophyseal jointsfound dorsal to the vertebral arches, all developed in a man-ner to provide optimum stability, flexibility, and mobility.The center of gravity of the spinal column and that of thebody do not pass through the same points. The former beginscranially at the odontoid process of the axis and passes cau-dally through the sacral promontory.3 The latter passes ven-tral to the sacral promontory caudally. Disability may occurif the center of gravity deviates from the normal position.Studies have found that when the center of gravity passes toofar ventral to the sacrum so the work required to maintainerect posture is significantly increased, lumbar muscle fatigueand pain result.

Normal physiologic function is supported by the ligamentsand joint capsules of the spine. The ligaments of the spinalcolumn are composed of elastin and collagen3,4 and may spanseveral segments. The anterior longitudinal ligament (ALL)spans the entire length of the spinal column, extending fromthe ventral border of the foramen magnum (basion), where itis known as the anterior atlanto-occipital membrane, to thesacrum. The ALL spans 25% to 33% of the ventral surface ofthe vertebral bodies and intervertebral discs, supporting theannulus fibrosus and preventing hyperextension. The ALL isarranged in three layers: the outermost spanning four to fivelevels, the middle layer spanning three levels and connectingvertebral bodies and intervertebral discs, and the innermost

layer binding adjacent vertebral discs. The posterior longi-tudinal ligament (PLL) begins as the tectorial membrane atC2 and extends to the sacrum. The PLL runs within the ver-tebral canal and flares at the level of the intervertebral discwhere it is interwoven with the annulus fibrosus and narrowsat the vertebral bodies, where it is loosely attached. The lay-ers of the PLL are similar to the ALL but function to preventhyperflexion.

Interspinous and supraspinous ligaments provide stabilityto the dorsal elements of the spinal column. Ligamenta flavaconnect spinal laminae in a discontinuous fashion and areintertwined with the facet joint capsule. The proximal inser-tion of the ligamentum flavum is the ventral part of the cra-nial lamina extending to the dorsal part of the caudal lamina.

Laterally, the ligamentum flavum is in contact with the ventral

Functional Anatomy of the Spine

CHAPTER 5

Zabi Wardak | Elizabeth Demers Lavelle | Brian J. Kistler | William F. Lavelle



SECTION 2 | The Fundamentals56

capsule of the facet joint. These attachments are significantwhen excision of the ligamentum flavum is necessary to allevi-ate spinal stenosis. The microscopic anatomy of the ligamen-tum flavum is unique due to its approximately 80% elastincontent. This is the source of the yellow appearance and thenickname “yellow ligament.” The elasticity of the ligamen-tum flavum allows it to stretch during flexion without limitingmotion and allows it to become taut when returning to neutraland during extension. As a person ages, the elastin is replacedwith a higher percentage of collagen, causing it to become less

elastic, which may lead to buckling into the spinal canal.The spinal cord is a 40- to 45-cm long structure extending

from the foramen magnum to the L1-2 spinal level. The cordtransitions at this point into a collection of nerve roots knownas the cauda equina. Spinal nerve roots exit neural foraminaand consist of a dorsal sensory and ventral motor root, with theexception being C1 and C2 contributions to the spinal acces-sory nerve. The outermost membranes, or meninges, whichcover the spinal cord, are the dura, arachnoid, and pia—theinnermost layer of the meninges. Suspension of the spinalcord is accomplished by the dentate ligaments, which inter-connect the innermost pia with the outermost dura matter.The spinal cord is divided into regions much like the spine:8 cervical, 12 thoracic, 5 lumbar, and 5 sacral regions and

1 coccygeal region. The nomenclature of the nerve roots is as

follows: the first seven cervical nerves exit above their namedvertebrae, with the eighth cervical nerve and all spinal nervesbelow exiting below their named vertebrae.

The spinal cord is part of the central nervous system andlike the brain it is mapped in a somatotopic arrangement.The corticospinal tracts are responsible for motor function.Within these tracts control of the hands is found medially andcontrol of the feet is found laterally. The spinothalamic tractstransmit sensory information, with hand sensation found

ventromedially and sacral sensation dorsolaterally. Lumbarregions of the posterior columns of the spinal cord have sacralsegments located medially and upper lumbar regions laterally.

Spinal canal dimensions provide adequate space for thespinal cord in all segments except for the midthoracic region.Here, the risk of neural tissue impingement during surgicalinstrumentation is increased. The lumbar region has a con-sistent spinal canal size and, along with the cauda equina,the anatomy functions to limit nervous tissue damage due totrauma or degenerative changes.5

Decreases in canal dimensions may result in radiographicand clinical spinal stenosis. These decreases in canal size maybe either congenital, generally presenting at a younger age, oracquired, presenting at a later age due to degenerative changes.

Stenosis is a self-perpetuating loop often beginning with disc

Atlas (C1)

Cervicalvertebrae

Thoracicvertebrae

Lumbarvertebrae

Axis (C2)

C7

T1

T12

L1

L5

Sacrum(S1-5)

FIGURE 5-1. A dorsal view of the spine demonstrating the cervical,thoracic, and lumbar regions.

Atlas (C1)

Cervicalvertebrae

Thoracicvertebrae

Lumbarvertebrae

Axis (C2)

C7

T1

T12

L1

L5

Sacrum(S1-5)

FIGURE 5-2. A lateral view of the spine demonstrating the cervical,thoracic, and lumbar regions. The primary thoracic kyphosis andsecondary cervical and lumbar lordosis are illustrated.



5 | Functional Anatomy of the Spine 57

degeneration leading to alterations in mechanical stress thatcause facet joint degeneration and ligamentous changes, with anend result of a decrease in the canal space. Spinal stenosis maylead to changes in intradural pressure that diminish the blood

flow to nerve roots and alter axonoplasmic flow. Acute nerveroot constrictions have substantial edema, which can slow elec-trical conduction and nutrient transport and which are more sub-stantial than chronic conditions. There is also an inflammatorycomponent to stenosis that alters neuropeptide concentrations.

Vertebrae

The intricate design of the vertebrae provides stability to thespinal column along with support and protection for the spi-nal cord and associated nerve roots. The compressive forcesare significant in a stacked column, and the cortical lamellaeare arranged vertically to aid in resisting these forces. The

cancellous bone found in the inner trabeculae allows for acompromise between strong mechanical support and limitingvertebral weight. All of the structures coincident with thevertebral bodies act to bear weight in compression. The ante-rior column functions to transfer body weight to the pelviswhile standing in an erect posture. Dorsal elements of thespinal column serve to protect the spinal cord. The dorsal ele-ments also function as a tension band and a lever, transferringmuscular contractions of the paraspinal musculature throughthe anterior and middle columns of the spine.

The dorsal bony elements include the pedicles, whicharise from the superior aspect of the vertebral body and formthe lateral walls of the spinal canal. The laminae extend fromthe pars interarticularis and fuse to form the dorsal wall of thespinal column. The junction of the laminae, where the spi-nous processes arise, support functional stability of the spinewith their ligamentous and muscular attachments. The rela-tionship between the transverse processes and the dorsal ele-ments is unique to the specific spinal region where they arefound. Cervical transverse processes arise from the junctionof the vertebral body and pedicle. The shape of cervical spi-nous processes are bifid, resulting in the great flexibility ofthe cervical region. Thoracic and lumbar transverse processeshave a different anatomic relationship with the dorsal ele-ments, arising from the junction of the pars interarticularisand pedicle. Stability and motion to the spine are also pro-vided by transverse processes with their unique ligamentousand muscular attachments.

Flexion, extension, and rotation of the spine are sup-

ported, facilitated, and restricted by the facet joints. A facetjoint consists of a superior articular process with an articulat-ing surface projecting dorsally, which is met by the adjacentvertebra’s inferior articular process that projects its articulat-ing surface ventrally. The synovial joint formed by the twoprocesses consists of a thin layer of hyaline cartilage betweenmatching articulating surfaces, lined with synovium and sur-rounded by a joint capsule. Although limited in size, the facetjoints provide constraints to extremes of spinal motion.

Atlas (C1) and Axis (C2)

The first cervical vertebra is unique in its articulation withthe occipital condyle of the cranium. This articulation is the

basis for significant flexion and extension of the head.

Another unique aspect of the atlas is that although it lacks atrue ventral body it still supports the cranium by the superiorfacet surfaces of the lateral masses (Fig. 5-3A). The caudalfacet surfaces of the lateral mass articulate with the supe-

rior facets of the axis (Fig. 5-3B). The transverse process ofthe atlas houses the vertebral artery within the transverseforamina. Superior and inferior oblique muscles attach to thetransverse process. The atlas is hydrostatically held betweenthe cranium and axis. The anterior and posterior occipitalmembranes attach to the atlas and also contribute to stability.They are continuations of the anterior longitudinal ligamentand ligamentum flavum, respectively.

The axis is the second cervical vertebra. The articulationbetween the atlas and axis, known as the atlantoaxial joint,contributes to the majority of cervical rotation and stabilityto the upper cervical region. Unlike the atlas, the axis doeshave a true vertebral body and a unique structure knownas the odontoid process projecting cranially from its dorsal

aspect (Figs. 5-4A–C). The alar, cruciform, and transverseligaments are anchored to the odontoid process. Further sta-bility of the cervical region is contributed to by the muscularattachments at the spinous process of the axis, which includethe rectus major and inferior oblique muscles. Like the atlas,a transverse foramen encases the vertebral artery.

Ligamentous anatomy of the cervical spine is unique, pro-viding support for the head and maintaining stability despitethe tremendous flexibility of this region. Ligaments exist both

Posteriorarch

Posteriortubercle

Anterior

tubercle

Anterior

archA

B

Vertebralforamen

Superior

articular

surface of

lateral mass(for occipital

condyle)

Transverse

foramen

Transverse

process

Lateralmass

Articular

facet for

dens

Posterior

tubercle

Anterior

tubercle

Anterior

arch

Vertebral

foramen

Inferior

articular

surface oflateral mass

(for axis

articulation)

Transverse

foramen

Transverse

process

Articular

surface

for dens

FIGURE 5-3. The anatomy of the atlas (C1) demonstrating its uniqueosseous anatomy with noted lack of an anterior body and large

lateral masses. Superior (A) and inferior (B) views.




within and outside of the spinal canal. Much of the stabil-ity of the craniocervical region is provided by the ligamentswithin the spinal canal, which are ventral to the spinal cord.These are arranged in three layers. The tectorial membraneis the most dorsal of these ligaments and is a continuation ofthe PLL, attaching dorsally to the cruciate ligament at thebasiocciput. The cruciate ligament is the middle layer andfunctions to constrain ventral translation between C1 andC2. It is a complex ligament with both horizontal and verticalbands. The odontoid ligament, or apical ligament, is the mostventral of the inner ligaments and extends from the lateralaspect of the odontoid to the medial aspect of the occipital

condyles. Outside of the spinal canal are fibroelastic bands

extending from the foramen magnum to C1. From the ventralportion of the foramen magnum extends the anterior atlanto-occipital membrane. From the dorsal foramen magnum arisesthe posterior atlanto-occipital membrane. Because these are

thin bands, their contribution to the strength of the cervicalspine is limited.

Subaxial Cervical Vertebrae (C3-7)

The remaining cervical vertebrae share anatomic featuresand may be considered separately from the atlas and axis.They are the smallest in size compared with all other regionsof the spine and begin the trend of gradually increasing insize with each successively lower level. Descending down thespine, more body weight is supported, which is why the ver-tebrae increase in size. The end plates of the vertebrae in thisregion are concave superiorly and convex inferiorly, and theyarticulate to form the uncovertebral joints (joints of Luschka)

(Fig. 5-5). These joints are often the site of arthritic changes,which can cause nerve root impingement. The position of thesubaxial cervical spine affects the relative size of the neuralforamen (Figs. 5-6A–C). Clinically, this is demonstrated bythe Spurling maneuver. If the volume of the neural foramenis compromised by an osteophyte or disc fragment, pain canbe elicited by tilting the head toward the affected side, whichfurther reduces the foramen volume.

Pedicles are short and arise from the midpoint of the ver-tebral bodies. The laminae are fairly narrow. The spinousprocesses are bifid, with C7 being the largest (Fig. 5-7). Thetransverse processes, like the atlas and axis, have vertebralforamen that transmit the vertebral artery. The majority ofindividuals have vertebral arteries passing through the trans-verse foramen of C1-6, but in 5% of cases these arteries passthrough the foramen at C7.6 The facet joints are horizontal,and the facet capsule is weak, which allows for the mobilityof the cervical spine.

The ligamentum nuchae is the primary ligamentous struc-ture in the dorsal cervical spine outside of the spinal canalwith attachments to the spinous processes. Descending pastC7, the ligamentum nuchae transitions into the supraspinousligament, which extends to the lumbosacral region, endingbetween L3 and L5.

Dens

Dens

Spinous

process

Transverse

process

Dens

A

B

C

Transverse

process

Transverse

process

Body

Pedicle

Inferior

articularfacet

for C3

Anterior

articularfacet

(for arch

of atlas)

Superior

articular

facet for

atlas

Superior

articularfacet for

atlas

Superior

articular

facet for

atlas

Lateralmass

Lateralmass

Transverse

process

Vertebral

foramen

FIGURE 5-4. The anatomy of the atlas (C2) demonstrating its uniqueosseous anatomy with its large anterior dens that allows for 50%of the cervical spine’s rotation through its articulation with theatlas. Lateral (A), superior (B), and anterior (C) views.

Uncus(uncinateprocess)

Intervertebralforamen (for

spinal nerve)

Interarticularpart

Zygapophyseal joint

FIGURE 5-5. Dorsal view of the anatomy of the atlas subaxial cervi-

cal spine.




The range of motion measure at the cervical spine canvary due to age, gender, and method of measurement. Visualestimation and radiography are the primary methods used tomeasure cervical range of motion. Studies of these measure-ment techniques on active cervical range of motion havefound that, on average, the cervical spine has a total of 151degrees of rotation, a total of 86 degrees of lateral bending,and a total of 126 degrees of flexion-extension. When con-sidering motion in only one direction, leftward and rightwardrotation and lateral bending are, on average, half the totalvalues, whereas the cervical spine has, on average, a greaterrange of extension than flexion.7

Thoracic Vertebrae

The thoracic region of the spine contains the largest numberof vertebrae, which continue to increase in size from T1 toT12. The first four thoracic vertebrae maintain some cervicalfeatures, and the last four possess some lumbar features, main-taining a smooth transition between the adjacent regions.

The superior vertebral notch is the cervical feature of T1, andthe lumbar features of T12 include lateral direction and infe-rior articular processes. Laminae in the thoracic region arebroader than in the cervical spine and overlap, whereas the

transverse processes increase in size as they progress down thethoracic spine8 (Fig. 5-8). The spinous processes of the tho-racic vertebrae are variably arranged in horizontal, oblique,or overlapping vertical arrangements. Horizontal spinousprocesses are found at T1-2 and T11-12 and oblique spinousprocesses at T3-4 and T9-10, with the rest of the thoracicvertebrae possessing overlapping, vertical spinous processes(Fig. 5-9). Thoracic facets are primarily arranged in a coronalplane but develop a sagittal orientation near the junction ofthe lumbar vertebrae. There is less free space in the spinalcanal in the thoracic region compared with both cervical andlumbar regions.

A characteristic feature of the thoracic vertebrae is therelationship with the ribs.9 The ribs articulate with unique

costal facets—found where the vertebral body and ped-icle meet—as well as on transverse processes, with T10-12being exceptions to facets on transverse processes. The tho-racic spine has maximum stiffness relative to all regions ofthe spine, which is a function of the relationship betweenthe rib and vertebrae combined with support from accessory

A B C

FIGURE 5-6. The alignment of the cervical spine greatly affectsthe volume of the neuroforamen. A, The subaxial cervical spinepositioned in lateral bending. B, The relative volumes of the neu-roforamina (arrows ) change with the concave side significantlydecreasing in volume. C, The convex side increases relatively involume. This becomes important in patients with a cervical discherniation and an already compromised neuroforamen.

Spinousprocesses Intervertebral

foramina (forspinal nerves)

Intervertebral joints(symphysis)

Zygapophyseal joints

FIGURE 5-7. A lateral view of the subaxial cervical spine. Most strik-ing are the orientation of the cervical facet joints and the bifidnature of the spinous processes, which allow for the extremes of

cervical motion.

Vertebralforamen

Inferiorarticularprocess

Superiorarticularprocess

Lamina

Spinousprocess

Pedicle

Transverseprocess

FIGURE 5-8. The dorsal osseous anatomy of the thoracic spine. Thelarge transverse processes are distinctive. Due to the presenceof the rib cage (not shown), the thoracic spine is the least mobile

spinal segment.




ligaments.9 The “junctional” regions of the spine, such asC7-T1 and T12-L1, are sites of transition from a rigid spinalregion to one with maximal spinal motion. These junctionalsites are often the sites of natural and iatrogenic pathology.

Lumbar Vertebrae

Descending down the spinal column, we come to the larg-est vertebral bodies—the lumbar vertebrae (Fig. 5-10). These

vertebrae progressively increase in diameter when approach-ing the sacrum and are greater in transverse width relative toanteroposterior diameter. Within the lumbar region are sub-regional variations in the anatomy of the vertebrae. These areattributed to the greater weight and forces that these verte-brae must distribute as the spinal column transitions into thepelvis. The L1-2 vertebral bodies have greater depth dorsally,whereas L4-5 vertebral bodies have greater depth ventrally(Fig. 5-11). The two subregions are balanced by the L3 ver-tebral body, which provides a transitional point between thetwo. Vertebral body angulation and translation are affectedby these locoregional differences in anatomy during flexionand extension. These variations produce changes in interver-tebral disc height and foramen cross-sectional area, which are

functionally linked to motion during flexion and extension.

Superiorcostalfacet

Spinousprocess

Pedicle Transversecostalfacet

Vertebralbody

FIGURE 5-9. A lateral view of the thoracic spine. The vertebral bod-ies increase in size from cranial to caudal as the body impartsgreater weight and forces on the spinal column.

Vertebralcanal

Transverseprocess

Lamina

Spinousprocesses

Vertebralbody

FIGURE 5-10. A dorsal view of the osseous anatomy of the lumbarspine.

Intervertebraldisc

Superiorarticularprocess

Mammillaryprocess

Transverseprocess

Spinousprocess

Inferiorarticularprocess

Inferiorvertebral

notch

Superiorvertebral

notch

Articularfacet forsacrum

Intervertebralforamen

Auricularsurfaceof sacrum

Sacralhiatus

Sacralcornu

Vertebralbody

FIGURE 5-11. A lateral view of the osseous anatomy of the lumbar

spine.




The variations may be associated with susceptibility at lum-bar regions for disc herniation, spinal canal stenosis, andother pathology. Cadaveric studies have shown that in theL4-5 region, flexion results in a greater dorsal disc bulge thanin the L1-2 region. The cross-sectional area of the foramenin the lumbar region shows that compared with a neutralposition, flexion increases the area by 12% (15 mm2) andextension decreases the area by 15% (19 mm2). The vertebralbodies move closer ventrally and further apart dorsally duringflexion, which increases the dimensions of the spinal canal;the opposite occurs during extension.10

The cross-sectional area of the nerve root is linked to flex-ion and extension as well. The nerve roots traverse beneaththe lateral recess of the pedicles and articular facets throughthe intervertebral foramina. Ventral borders of the nerveroot are the vertebral body and intervertebral disc, dorsalborders are lamina and facets, and both superior and inferiorborders are adjacent pedicles. Because of the locoregional dif-ferences in anatomy of the lumbar region, flexion and exten-sion movements alter these borders and result in changesin nerve root cross-sectional area (Figs. 5-12A–C). Thesechanges can be associated with susceptibility to nerve rootimpingement. Cadaveric studies have found that the neutralcross-sectional area of the L1-2 nerve root is 28.31 ± 10.48 mm;in flexion it increases to 32.37 ± 9.92 mm, and in extension itdecreases to 22.97 ± 7.52 mm.10

Pedicles in the lumbar region arise from the rostral aspectof the vertebral body. They can be visualized behind the facet

of the named vertebra and supra-adjacent vertebra. The diam-eter of the L1 pedicle is approximately 9 mm with a medialangle of 12 degrees,11 which requires consideration withscrew placement. Lumbar facets have a sagittal orientation,which limits axial rotation. The L5-S1 facet is unique, with acoronal orientation that resists anteroposterior translation.2

Sacrum and Coccyx

Five vertebrae, costal ligaments, and transverse processes arefused to create the sacrum. The sacral bodies are separatedby transverse lines. Nerves emerge from rounded dorsal andventral foramina that are lateral to the vertebral bodies. Theunique fusion of vertebrae in the sacrum provides strength

and stability to the pelvis, and through articulation with the

ilea at the sacroiliac joints the weight of the body is distrib-uted to the pelvic girdle. The coccyx is the terminal portionof the spinal column and commonly referred to as the “tailbone.” It can be found as a single fused bone, or the first coc-

cygeal element may be separated from the others. There areno dorsal elements to the vertebrae in the coccyx. The pri-mary function of the coccyx is to serve as a site of attachmentfor pelvic muscles.

Vertebral End Plates

The vertebral end plates are composed of cortical bone ofthe vertebral body and cartilage of the intervertebral disc.Approximately 1.3 mm of cortical bone of the vertebral bodyforms a concave surface that is fused to the thin cartilaginoussurface of the intervertebral disc by a layer of calcium knownas the lamina cribrosa. Because the intervertebral discs lack a

blood supply, nutrients are acquired via passive diffusion fromthe vertebral end plates. The largest avascular space in thehuman body is the L4-5 disc space. With aging, the diffusioncapacity of the end plate decreases and the disc’s nutrition iscompromised, narrowing the disc space and increasing sus-ceptibility to pathology.

Intervertebral Discs

The intervertebral discs are a vital component of the spine,contributing to stability, resisting loads in all directions, andrestricting intervertebral motion. Twenty-three intervertebraldiscs are found, starting between C2 and C3 and extendingdistally to L5-S1. The discs account for roughly 20% to 33%of the vertebral column height and show regional variationsmuch like the osseous structures, such as increasing in cross-sectional size when descending down the spine. The shape ofthe discs varies based on region of the spine, ellipsoid in thecervical and lumbar regions and resembling a rounded trian-gle in the thoracic region. In addition to the cartilaginous endplates, the disc components include an annulus fibrosus andthe nucleus pulposus. Each component is linked to the othersuch that pathology of one affects the ability of the others tocarry out their physiologic functions.

The cartilaginous end plate is a thin layer of hyaline carti-lage that allows nutrient passage via diffusion to the minimallyoxygenated disc center. The annulus fibrosus is composed ofan outer layer of alternating type I collagen fibers and an

inner fibrocartilage component. With torsion, the alternatingcollagenous fibers become taut while others are lax, whichcontributes to limitations in motion. This unique structureforms an attachment along the periphery of the vertebralbody that maintains spinal stability in combination with thedorsal structures and the soft tissues.

The nucleus pulposus is bounded peripherally by theannulus fibrosus and both superiorly and inferiorly by the endplates. It is made up of negatively charged proteoglycan mol-ecules and collagen. The negative charge makes the nucleushydrophilic, which contributes to the extensive water com-ponent of the disc. Height and resistance to axial loadsis maintained by the hydraulic properties of the fluid sur-rounded by end plates and the annulus fibrosus. Maintenance

of disc height keeps the ligaments and capsules of the spine at

A B C

FIGURE 5-12. The positioning of the lumbar spine can greatly affectspinal canal volume. A, The neuroforamen volume (arrows ) inthe neutral position. With lumbar extension (B), the neural fora-men decrease in size, and with lumbar flexion (C), the foramenincrease in size.




optimal length and allows them to function physiologically.With aging, the distinct regions of the intervertebral disc areno longer present, and the proteoglycan content and hydra-tion decreases. As disc height diminishes, increased demands

are placed on the annulus fibrosus, thus increasing suscepti-bility to tears and subsequent herniation. Dorsal structuresare also affected by the loss of disc height, including facetsubluxation and hypertrophy, which may predispose an indi-vidual to nerve root compression.

Muscles

With the majority of body weight ventral to the vertebralbody, the musculature of the back is crucial to balancingthe forces placed on the vertebral column. The muscles canbe divided into extrinsic and intrinsic back muscles. Theextrinsic back muscles include the latissimus dorsi, trapezius,

rhomboid, and serratus posterior muscles. The latissimus dorsimuscle, innervated by the thoracodorsal nerve, is the mostprominent and arises from the spinous processes of the infe-rior six thoracic vertebrae and fans out to the axilla, function-ing to raise the trunk when the arms are fixed. The trapeziusmuscle, innervated by the accessory nerve, is attached to thespinous processes of C7-T12 and functions in scapular move-ment. The rhomboids, innervated by the dorsal scapularnerve, are attached to the spinous processes of C7-T1 (minorrhomboid muscle) and T2-5 (major rhomboid muscle) andinsert on the scapula. They too function in scapular move-ment. The serratus posterior muscle has two parts: a superiorpart innervated by intercostal nerves and attached to thespinous processes of C7-T3, and a caudal part innervated bythoracic spinal nerves and attached to the spinous processesof T11-L2. The two parts function to elevate and depress theribs, respectively.

The intrinsic muscles of the back are superficially thesplenius capitis and cervicis muscles, innervated by the dor-sal rami of the cervical nerves. The splenius capitis muscleis attached to the ligamentum nuchae and spinous processesof C7-T4 and inserts on the occiput. The splenius cervicismuscle is attached to the spinous processes of T3-6 andinserts on the transverse processes of C1-4. The two musclesfunction to laterally flex the neck. The intermediate layer ofintrinsic back muscles are the erector spinae muscles, whichare a trio of columns. From lateral to medial, they are the ilio-costalis, longissimus, and spinalis muscles. The columns over-lap and have a common broad tendon attached to the iliac

crest, sacrum, sacroiliac ligaments, and lumbosacral spinousprocesses. The erector spinae muscles are the chief exten-sors of the spinal column and are innervated by the dorsalrami of spinal nerves. The deep layer of intrinsic muscles are

the semispinalis, multifidus, and rotatores muscles. All areinnervated by the dorsal rami of the spinal nerves. There arethree semispinalis muscles: capitis, cervicis, and thoracis. Thesemispinalis capitis muscle attaches to cervical and thoracic

transverse processes and inserts on the occiput. It functionsto extend the head. The semispinalis cervicis and thoracismuscles attach to transverse processes and insert on the spi-nous processes of the more superior vertebrae, respectively.They function to extend their respective region of the spine.The multifidus and rotatores muscles stabilize and rotate thevertebrae.

Anomalous Anatomy

Variants of normal spinal anatomy are not uncommon andcan have dramatic effects on the regular function of the spine.Cervical spine anomalies can result in progression of degen-

erative changes, an example being the Klippel-Feil anomaly.The classic triad of Klippel-Feil is a short neck, low dorsalhairline, and limited neck motion. It is due to the fusionof adjacent cervical vertebrae, which alters the physiologicforces the spine is constructed to handle. Lumbar vertebraeanomalies can lead to functional changes in a region that isalready susceptible to pathology. The presence of abnormalnumbers of lumbar vertebrae can accelerate degenerativechanges or increase susceptibility to herniation. This is com-monly found with the presence of only four lumbar segmentsor the presence of a sixth lumbar vertebra. Nerve root anoma-lies such as conjoined nerve roots increase the risk of injuryfrom disc herniation, trauma, or iatrogenic injury during sur-gical procedures.

KEY REFERENCES

Benzel E: Stability and instability of the spine. In Benzel E, editor:Biomechanics of spine stabilization: principles and clinical practice , New York,1995, McGraw Hill, Inc, pp 25–40.

Panjabi MM, Duranceau J, Goel V, et al: Cervical human vertebrae.Quantitative three-dimensional anatomy of the middle and lower regions.Spine (Phila Pa 1976) 16:861–869, 1991.

Panjabi MM, Takata K, Goel V, et al: Thoracic human vertebrae. Quantitativethree-dimensional anatomy. Spine (Phila Pa 1976) 16:888–901, 1991.

Vollmer DG, Banister WM. Thoracolumbar spinal anatomy. Neurosurg Clin North Am 8(4):443–453, 1997.

White AA, Panjabi MM: The basic kinematics of the human spine. A reviewof past and current knowledge. Spine (Phila Pa 1976) 3:12–20, 1978.

Woodburne RT: Essentials of human anatomy, ed 7, Oxford, England, 1982,Oxford University Press.

REFERENCES

The complete reference list is available online atexpertconsult.com.



CHAPTER

21Surgery of Peripheral

Nerves

Geoffrey P. ColeJoseph R. Smith

BASIC ANATOMY AND METABOLISMOF PERIPHERAL NERVES

Peripheral nerves include motor, sensory, and autonomic

fibers. Cell bodies for peripheral motor nerve fibers are

located in the anterior horns of the spinal cord. The cell

bodies of the preganglionic sympathetic nerves are located at

the intermediolateral cell column from T1-L2. The cell

bodies of the peripheral sensory nerve fibers are located inthe dorsal root ganglia just outside the spinal canal.

Nerve fibers are composed of a central axon surrounded

by a single layer of Schwann cells. (See Fig. 21-1.) About a

fifth of the nerve fibers are myelinated.1 The myelin is

contained within the Schwann cells in a multilayered spiral

concentric sheath. The outer basement membrane of the

Schwann cell, seen only by electron microscopy, is referred

to as the endoneural sheath. Schwann cells are sequentially

located so that many may cover an individual axon.

Points of junction of Schwann cells are called nodes of

Ranvier, where, in myelinated nerves, there is a brief seg-

ment of axon without myelin. (See Fig. 21-2.) This has

physiological significance in that conduction along a mye-linated nerve fiber is much more rapid because the nerve

action potential in a myelinated nerve "jumps" from one

node to another (saltatory conduction) rather than traveling

directly along the entire length of the axon, as in the case of

unmyelinated fibers.

Individual nerve fibers—and their Schwann cell sheaths in

the case of myelinated axons—are surrounded by a thin

tubule of collagen fibers, the endoneurium.

Groups of nerve fibers are collected into bundles, or

fascicles, encircled by the perineurium, another collagen

sheath. (See Fig. 21-3.) Variable numbers of fascicles will

be collected together to form a nerve surrounded by an

external epineurium.Within the external epineurium and between the fascicles

is the internal epineurium. There may be one, a few, or

numerous fascicles within a nerve.

Peripheral nerves are supplied by external segmental

blood vessels that give off segmental branches that supply

intrinsic longitudinal vessels. (See Fig. 21-4.) Microvessels

run within the epineurium and perineurium, but only capil-

laries are found in the endoneurium.2 Preservation of the

more complex external blood supply takes on considerable

importance when one is attempting to develop free vascular-ized grafts.3

There is significant positional change in the fascicular

pattern throughout the length of nerves, so that the cross-

sectional localization of a given fascicle may change over

just the course of a few millimeters.4 This exchange in

pattern is much more prevalent in proximal segments of

nerves than distal.

There are also major positional changes in the motor and

sensory fascicles that travel to various segments of the

arm—within and just distal to the brachial plexus. Most of

this cross-sectional positional change has occurred by the

time the level of the elbow is reached. In fact, fascicles

innervating a digit may travel for several centimeters in theforearm with very few positional changes.5

Metabolism of peripheral nerves is focused at the cell

body, from which axoplasm and transmitter substances are

transported toward the nerve terminals,6-7 Similarly, unused

transmitter substances are transported back to the cell body.8

Exact mechanisms of transport are unclear, but rates have

been determined. Some materials prepared in the cell body

are transmitted at a rate of 1 to 6 mm per day, whereas

transmitter substances move much more rapidly, up to 410

mm per day.9-10 Retrograde transport is reported to occur at a

more constant rate of about 240 mm per day.8-10

Metabolism at the cell body increases significantly at the

time of interruption of a peripheral nerve. The degree of augmentation depends, to some extent, on the distance of

419



420 CHAPTER 21

Figure 21-1 Microscopic anatomy of myelinated peripheralnerve fiber.

Figure 21-3 Anatomy of peripheral nerve. Note endoneurium

within fascicles, between fibers. Fascicles bound by perineureum.Nerve bound by epineurium.

interruption from the cell body.1'6 The rate of transport

down the axon may not increase, but the amount of axo-

plasm will. The amount of transmitter substance decreases.

However, if the axonal injury is proximate to the nerve cell,

retrograde degeneration will involve the neuronal cell bodyand cell death will occur.

It is most likely that the trophic effects of a nerve dependto some extent on axonal transport." Regeneration acrossa site of interruption also depends on the distance betweenthe proximal and distal stumps, as well as on the trophicfactors that direct axons into their appropriate distal neuraltubes.".12

REACTION OF PERIPHERAL NERVESTO INJURY

Metabolism within the cell body of a nerve that has beeninjured is altered within hours.i The size of the cell body

Figure 21-2 Node of Ranvier and cross-sectionalview of myelinated axon.

increases, Nissi substance breaks up, and the nucleus mi-grates to the periphery of the cell body.

There is an increase in both ribonucleic acid (RNA) and

the elements required for axon synthesis. Production of neurotransmitters decreases. Lipid synthesis increases signif-

icantly to reconstitute the Schwann cell membrane.

After injury to a peripheral nerve, some cells may die,depending in part on the distance of the injury from the cell

body: the nearer the injury to the cell body the greater is thechance of cellular death.

Wallerian degeneration occurs in fibers distal to axonalinterruption. Similar changes also occur retrograde for vary-

ing distances proximal to an injury, depending more on the

severity of the injury than the location of the next proximal

node of Ranvier.13

This type of retrograde change may

account for some cellular deaths.'Multiple sprouts from a single severed axon occur within

24 h of transection of a peripheral nerve. These sprouts areinitially unmyelinated, even when the axon of origin is

myelinated. Growth cones that consist of filopodia developon each axonal sprout.

14 They reach out for contact with an

appropriate substrate—preferably fibronectin and laminin,

both components of the basal lamina of Schwann cells.

15

If the sprouts do not make appropriate contact, they willretract and advance again toward a more appropriate sub-strate. While there is usually loss of regenerating units at the

site of a nerve repair, the multiplicity of sprouts results in anincreased number of axons crossing a nerve repair.

The sprouts from myelinated nerve fibers eventually be-

come myelinated, and the number of sprouts will decreasedepending on whether contact is made with a distal tubule.

16

Eventually, this number approaches normal.' If the regener-

ating axons become lost in the extraepineural environment, a

neuroma will form.

Following division of a nerve and wallerian degeneration of

the distal segment, Schwann cells begin to proliferate andphagocytose debris, while myelin degenerates.* The endo-

neurial tubes collapse and are now merely stacked processesof Schwann cells known as bands ofBungner. The Schwann



SURGERY OF PERIFERIAL NERVES 421

Figure 21-4 Vascular supply toperipheral nerve.

cells are organized into columns. The regenerating axons as-

sociate themselves with the layers of basal lamina, which may

be considered potential tubes. Sprouts may enter inappropriate

tubes, leading to misdirection and nonfunctional units.

The final result of reinnervation will depend on the num-

ber of axons that become associated with columns of Schwann cells to reinnervate appropriate end organs. Resid-

ual bands of Bungner are endoneural tubes that have failed

to be reinnervated.

Muscle fibers undergo atrophy several weeks after dener-

vation. The denervated fibers, on cross section, become

rounded, and the nuclei, normally located at the periphery of

muscle fibers, move to the center.17

(See Pig. 21-5.)

Muscle fibers are normally typed I or II depending on

whether they are "fast" or "slow," with variation in the

amount of stain they take up. The type of nerve fiber

innervating a muscle determines the type of the muscle fiber.

After denervation, the types of muscle fibers become ran-

domly distributed.

REINNERVATION OF THE INJUREDPERIPHERAL NERVE

Motor end plates are not altered for more than a year after

denervation; however, the distribution of acetylcholine re-

ceptors changes markedly.18 While acetylcholine receptors

are normally located in the center of the length of muscle

fibers, after dencrvalion, fibers develop supersensitivity

throughout their course. With reinnervation, motor fibers

will reform neuromuscular junctions at the original endplates, but, in addition, innervating axons will send projec-

tions to adjacent muscle fibers so that a group of neighbor-

ing muscle fibers may receive innervation from the same

axon. This will determine the type of muscle fibers demon-

strated on histologic examination.

Questions have arisen about the feasibility of implanting

transected ends of nerves into muscle. Studies demonstrate

that this procedure results in reinnervation of some musclefibers, but the reinnervation is not as efficient as reinnerva-

tion through distal segments of a motor nerve.19

There is no question about the effect trophic factors have

on reinnervation. Implantation of a sensory nerve in a dener-

vated muscle will result in axons of sensory fibers growing

into muscle fibers; however, if the muscle is innervated,

axonal growth of sensory fibers into nerve sheaths going to

the muscle will be inhibited.20

'21

Cutaneous sensation has a greater potential for recovery

from denervation than does motor function. Paccinian and

Meissner corpuscles arc the receptors attached to quickly

adapting nerve fibers mediating touch and vibration from

glabrous (nonhairy) skin. Merkel neurites are more slowlyadapting fiber receptors mediating touch and pressure. These

undergo changes after denervation, but nonnervous elements

survive and may be reinnervated years after denervation.22-23

Sensory receptors of hairy skin are located at the base of hair

follicles. Sensations of pain, touch, and temperature recover

after denervation. Peripheral to central recovery of deaffer-

ented areas occurs if there is no axonal regeneration of the

injured nerve elements. But if regeneration occurs, there

should also be central-to-peripheral recovery of sensory

function. Recovery begins at the edges of transplanted skin

and proceeds toward the center.24'25

Transplanted digits may develop nearly normal sensation.

The degree of recovery depends on the status of the donornerve, the recipient nerves, and the type and quantity of

sensory end organs.26



422 CHAPTER 21

Figure 21-5 Motor end plateson muscle fibers.

THE EVOLUTION OF SURGERY ONPERIPHERAL NERVES

The evaluation and treatment of patients with peripheral nerve

injuries has evolved and improved over the years. Quantum

leaps in the clinical scientific basis for handling lesions of

peripheral nerves have taken place at the time of great wars.

Weir Mitchell, while Commander of the United States

Army Hospital for Injuries and Diseases of the Nervous

System during the 1860s in the American Civil War, began

his famous work on partial nerve injuries, out of which came

his classical description of causalgia.27

—World War II became the laboratory for Sidney Sunder-

land to advance the diagnosis and treatment of peripheral

nerve lesions. Beginning in 1940 and lasting a decade,

Sunderiand was Professor of Anatomy at the University of

Melbourne and Visiting Consultant of Peripheral Nerve In-

juries to the 115th Australian General Military Hospital and

the Commonwealth Repatriation Department in Melbourne.Here he was able to maintain a 10-year chain of unbroken

records on 365 patients.28

The American military contribu-

tion to peripheral nerve injury during World War II was led

by Bames Woodhall, who compiled and presented data from

the Peripheral Nerve Registry.29

Ducker. Kempe, and Hayes

advanced the science of handling nerve injuries by including

their experience from the Vietnam War and reviewing the

metabolic basis for treatment of such lesions.6

INITIAL EVALUATION OFPERIPHERAL NERVE LESIONS

When a patient presents with a peripheral nerve lesion, three

important factors should be noted in the first examination.

The physician must determine (1) the type of injury, (2) the

time the injury occurred, and (3) the clinical condition of the

patient at the time of the examination. Each of these compo-

nents is essential to the understanding of what has happened

to the nerve, how much deterioration has occurred, and how

much recovery can be expected. This baseline examination

is used to judge improvement or deterioration at subsequent

evaluations. It also becomes the reference for determining

improvement or deterioration after surgery involving the

peripheral nerve.

CLASSIFICATION OF PERIPHERALNERVE INJURY

TYPES OF INJURY

A peripheral nerve, or group of nerves, may be injured in

many ways. A stab wound to the forearm resulting in a

laceration of the ulnar nerve is a dramatic and obvious injury

to the nerve, as opposed to the subtle and discrete nature of a

slowly developing compression of a root or peripheral nerve.

A nerve may also be crushed (acute severe compression),

contused, stretched or avulsed, accidentally injected, ther-

mally injured, damaged from shock waves (forces around a

projectile), or rendered ischemic (e.g., Volkman's ischemic

contracture). Examples of each type of injury include the

following:

1. The median nerve is compressed by the flexor retinacu-lum, resulting in the clinical presentation of carpal tun-

nel syndrome.



SURGERY OP PERIPHERAL NERVES 423

The S 1 nerve root is compressed with a hemiation of

the L5-S1 disk, resulting in a loss of the Achilles reflex,

decreased sensation of the lateral aspect of the foot, and

decreased plantar strength.

2. A nerve is contused by the sudden onset of blunt force.

Trauma to the arm that may fracture the humerus may

also contuse the radial nerve in the arm. Also, a severe

crush injury to a nerve may occur in relation to massive

limb trauma.

3. Peripheral nerves may be lacerated by an assortment of

objects: a knife, the sharp edges of a broken window,

unintentional laceration by an angiographer's needle or

a surgeon's scalpel. The laceration may divide the

whole nerve or divide only a portion of the fascicles.

4. Motorcyclists thrown from their vehicles and landing on

the head and shoulder will stretch several roots or

nerves within the brachial plexus. If the stretch injury tothe brachial plexus is particularly severe, the nerve

root(s) may be detached or avulsed from the spinal cord.

Pelvic dystocia during delivery of an infant may result

in an Erb's (C5-C6) palsy or, more rarely, both an Erb's

and Klumpke's (C7-T1) palsy. Erb's palsy leaves the

upper extremity adducted at the shoulder, extended at the

elbow, and pronated. The biceps reflex is absent.

Klumpke's palsy results in absence of flexion of the wrist

and fingers and only minimal extension of the elbow.

5. Nerves are also affected by extreme cold and heat.

Severe freezing (over a 2- to 3-day period) results in

necrosis of the affected segment, with eventual regener-

ation of new, thinner fibers. This process of recoverytakes approximately 3 months.30 Transient freezing or

cooling causes lesser degrees of disruption to nerve

fibers that ranges from mild conduction blocks to in-

terruption of the axons with wallerian degeneration.

Severe bums may damage peripheral nerves at the

time of the injury or lead to loss of function at a later

date because of the constrictive fibrosis that is asso-

ciated with destruction of adjacent tissues. This pro-

duces nerve lesions of varying severity.28

6. Even though a missile may not directly strike a nerve

during its course through an extremity, the nerve may

still be injured by the shock waves that spread out

around the missile tract, thereby damaging tissue which, may include the neural elements.

7. Ischemic injury. Limb trauma with sufficient hemor-

rhage or swelling may render nerves variably ischemic

as they pass within involved muscles.

8te Injection injury. Improperly placed needles may enter

the radial nerve in the arm or the sciatic nerve in the

buttock. If the injection is not aborted when the patient

reports pain with introduction of the needle, serious

injury with painful neuroma may result.

ANATOMIC-PHYSIOLOGIC CLASSIFICATION

In 1943, Seddon described three classifications of nerve

injury according to extent of disruption of axons and their

supporting tissues: neurapraxia, axonotmesis, and neurotme-

sis.31

Neurapraxia is an injury to the nerve where the nerve

tissue remains intact but the surrounding myelin sheath at

the site of injury may be disrupted. The result is slowed

conduction velocity lasting weeks to months. Axonotmesis is

an injury where the axon and surrounding myelin are

disrupted but the surrounding perineurium and epineurium

remain intact. In order for this injury to recover, regeneration

of the axon and resultant reinnervation of the target organ

are necessary. Neurotmesis is a complete disruption of the

nerve such as would result from a laceration. Recovery

occurs only if the nerve ends are brought together and the

neurons regenerate along their length and reinnervate the

target organ.

Sunderland further categorized nerve injuries according to

degree.

32

In a first degree injury, there is interruption of conduction at the site of injury, but preservation of the

anatomical components of the nerve trunk, including the

axon. This is equivalent to neurapraxia of Seddon. The block

in conduction is fully reversible. Time of recovery of sen-

sory and motor function is essentially the same for both

proximal and distal function.

With second degree injury, the axon is severed or the

axon below the level of the lesion fails to survive; however,

the endoneurial tube is preserved despite wallerian degener-

ation. The end organ becomes isolated until the axon re-

grows, but the axon invariably returns to the end organ it

originally innervated. Reinnervation follows a pattern deter-

mined by the distance the axon must regrow (i.e., proximalto distal, as opposed to neurapraxia).

Regrowth of sensory fibers may be followed by Tinel's

sign. This sign is positive when tapping along the nerve

elicits distal paresthesias in the sensory distribution of the

nerve. But it is important to note that although a distally

migrating Tinel's sign is evidence of functional recovery in

a second degree injury, it is not necessarily a sign of func-

tional recovery in the case of a more severe injury, because

it may be elicited when only C fibers regenerate.

In third degree injury, the trauma is more severe. There is

some disorganization of the internal structure of the fasci-

cles. There may be intrafascicular fibrosis, which can prove

an obstacle to regeneration. There may also be some loss of continuity of endoneural tubes so that some regenerating

axons are no longer confined to the tubes they originally

followed, and new anomalous patterns of innervation occur.

Recovery may be incomplete.

A fourth degree injury results in bundles of nerve fibers

being so disorganized that they are no longer sharply demar-

cated from the epineurium in which they are embedded. The

continuity of the nerve trunk persists, but the involved

segment is converted into a tangled strand of connective

tissue, Schwann cells, and regenerating axons that may

eventually form a neuroma. Recovery is often out of the

question for that part of a nerve that undergoes fourth degreeinjury.

Fifth degree injury implies loss of continuity of the nerve



424 CHAPTER 21

FlllKIIOIUI

dl»rtxAlUtgmlcil/ Ktliophyilologlcalbiili

Prounwil/ ncanry

Diagram (sw footnote)

Physiologicalconduction block,type a'

Ptiysiotogicafconduction Uodi.lypeb'

Local

Localconduction Mock,

Local conductionblockMotor function andproprioception mainlyaffected.Some sensation andsympathetic functionmay be preserved'

Loss of nerveconduction at level ofiiijmyaiid wilhm [Jn.lalnerve segment

Loss of nerveconduction at level ofinjury and within distalnerve seamen!

Loss of nerveconduction at level ofInjury and within distalnerve segment

Loss of nefveconduction at level ofinlury and within distal

nerve segment

Intraneural circulatoryarrest.Metabolic (ionic) block

with no nerve fibrepathology

Intraneural edema.Metabolic block withlittle or no nerve fibrepathology. Increasedendoneurial fluidpressure (EFP)

Local myelin damage.primarily thic k.myelinated fibresAxonal continuitypreserved. Nowallerian degeneration

Loss of axonalcontinuity, wallenandeaeneialiun.Endoneurial tubespreserved

Loss of axonalcontinuity andendoneurial tubes;perineurium intact

Loss of axonaicontinuity.endoneurial tubes andperineurium.EpinBurium intact

Transection or ruptureof entire nerve trunk

Immediately reversible

Reversible within daysor weeks

Reversible withinweeks to months

Recovery requiresaxonal regeneration.Correct orientation ofgrowing fibres sinceendoneurial tubes are

preserved. Correcttargets will bereinnervated

Endoneurial pathwaysdisrupted anddisoriented, bleedingand oedema lead toscarring. Axonalmisdirection. Poorprognosis. Surgerymay be required

Rupture and totaldisorganization ofguiding elements of thenerve trunk.Intraneural scaf formation. Axonalmisdirection. Poorprognosis. Surgeryrequired

Recovery requiressurgical adaptation andco-aptatlon ot nerve

ends. Prognosisdependent on thenature of the injury aswell as local andgeneral factors (cfch.6)

At s ar Sunderiand s classifications.BW2

Figure 21-6 Caricature of levels of nerve

injury related to train. (Reprinted with permission

from the publisher, Churchill Livingstone, from

Nerve Injury and Repair by Goran Lundborg,

Table 31, pp 78-79, 1988.)

trunk. Distances of interruption vary, but the nerve

ends remain separated- Scar tissue and separation of the

nerve ends provides a formidable barrier to spontaneous

recovery.

A sixth category of nerve mjuyy described by Sonderiand—

and emphasized by Mackianin and Delloa in 1988—is a

combination of the above Injuries.s'28 Some fibers escape

injury while others experience various degrees of deteriora-

tion. Sunderland pointed out that it would be unlikely for all

of a nerve to be crushed with a combination of first, and

fourth, or fifth degree injuries to thai same nerve, but that

mixed injuries are common, especially with penetrating

wounds.

Figure 21-6 is a visual analogy of the various levels of

nerve injury to a train running along a track supplied by

energy. The rails correspond to a nerve fiber, the track to the

endoneural tube, and the train to the electric impulse travel-

ing along the fiber. The electric wire corresponds to micro-vessels providing the blood supply to the nerve.

The physiological conduction block at the top of the page

demonstrates what happens if the local energy supply is

interrupted. The train cannot move in spite of an intact nerve

fiber. The moment the energy supply is restored (electric

wire repair), the train starts moving again, as in a first degree

injury.If the electric wire system is more severely damaged as in

a second degree injury, illustrated by the falling tree, then

the repair takes longer. Still, the rail is intact. In the example

of neurapraxia, or Sunderland's first degree injury, the train

is stopped because of local damage to the rail (demyelinat-

ing block), while more distal parts of the rail, as well as the

energy supply system, remain intact. Repair of local damage

takes up to 6 or 8 weeks.

In the illustration for axonotmesis, or Sunderland's second

degree injury, the rail is damaged and has disappeared distal

to the level of injury. The track is still intact and new rails

can easily be laid in the correct position. In the example of

neurotmesis, or Sunderland's third through fifth degree inju-ries, the rail as well as the track are destroyed. The result is a

great deal of misdirection.33



SURGEKY OF PERIPHERAL NERVES 425

FACTORS INFLUENCING RECOVERYFROM PERIPHERAL NERVE INJURY

ESTABLISHING TIME AND NATURE OF INJURY

Vhen evaluating the patient with a peripheral nerve injury,establishing the time of injury is important. This is usuallyeasy to determine, but in some cases may not be clear.Symptoms of a compressive lesion may have an insidiousonset which a patient only notices after several months. The

deficits after a crush injury may not be present immediately

but may present weeks to months later when scarring in the

extremity renders the nerve dysfunctional. The same sort of

delayed presentation may take place after a gunshot woundadjacent to a nerve.

Simple lacerations are injuries that usually do not presenta problem in determining the time of the nerve injury. Thisis not, however, always the case. A large bloody laceration

to the arm may result in injuries to many structures (skin,

muscles, arteries, and veins) that require immediate atten-

tion. This may distract the physician from recognizing apossible deficit due to injury of a nerve. Only later may thedeficit be recognized.

This can lead to a problem for a later examiner. Did the

nerve lesion occur at the time of the accident, or was it an

iatrogenic lesion that occurred during repair of the patient'sother injuries? The question can have both legal and clinicalimplications.

Determination of the time of injury is essential in estimat-ing the timing of recovery. The degree of recovery is alsocritical in determining the future management of a peripheralnerve injury. For example, recovery of sensory or motorfunction indicates continued conservative management,

whereas a distally migrating Tinel's sign or recovery of

autonomic function in the absence of sensory or motorrecovery requires surgical exploration.

RATES OF REGENERATION

Axons of peripheral nerves regenerate at predictable rates.

Various factors affect the rate of regeneration. After nervesare anastomosed, several days to weeks are required for anaxon to cross the site of anastomosis, but once axons reach

the distal nerve sheath, regeneration occurs at the rate of 1 to1.5 mm per day or 2.5 to 4.5 cm per month, depending on

the particular nerve and the distance of the injury from the

cell body.34

-35

-30

In general, axon regeneration near the cellbody is more rapid than regeneration at greater distances.

IMPAIRMENT OF REGENERATION

If a transected nerve is not anastomosed with its distalsheath, axons will grow into surrounding tissue, but theirgrowth is disorganized and individual axons rarely reach the

appropriate end organ. Recovery will be slow and rarely

functional. More devastating is the developing of scarring

that may result in a painful neuroma at the proximal end of a

lacerated nerve.If a nerve trunk remains intact (in continuity) but its

internal structure is severely disrupted (e.g., high velocity

missile wound, severe compression, or other complex injury), then organized regeneration is unlikely.

TIMING OF SURGICAL INTERVENTION

Another factor important in determining whether reinnerva-tion after injury will be successful is the timing of surgical

intervention.

1. Lacerations. Repair within first 48 h. If injury is severaldays old, wait about 2 weeks for edema to subside.

2. Blunt trauma. Allow at least 6 weeks for evidence of recovery from a possible neurapraxic injury.

Since peripheral nerve regenerates about 1 in. per monthand motor end plates are reinnervated with difficulty 1 year

or more after denervation, surgery must be planned accord-

ingly. For example, with a blunt injury to the sciatic nerve,surgical intervention should occur as soon as possible if no

clinical evidence of recovery is seen within 6 to 8 weeksafter injury. Early repair may provide recovery of plantarflexion of the foot and a very functional lower extremity.

Delaying 3 or 4 months might result in diminished or absentrecovery of plantar flexion of the foot. On the other hand,one can afford to observe a patient with distal median nerve

injury for 3 or 4 months and still obtain a good surgicalresult.37

Denervated muscle fibers also degenerate. Although theremay be fibrillations as long as 10 years after a human

muscle has been denervated, thickening of the muscle sheath

may cause difficulty with end-plate formation. In summary,the longer the period after an injury before repair, the poorer

the results. Still, there are some rare exceptions when re-markable response to reinnervation has occurred 2 to 3 yearsafter injury of a peripheral nerve.

In cases where the neurological deficit is initially incom-plete—i.e., where motor function of all involved muscles isparetic but present and sensory function is diminished but

present—the injury is most likely neurapraxic. If there iscomplete loss of function of the entire nerve or any of its

divisions, the injury may be neurapraxic, axonotmetic, or

neurotmetic.A period of observation is required before one can con-

clude that exploration is indicated. During this time, neuro-logical recovery in the case of Sunderland's first, second,

and third degree injuries will occur. Proximal and distalrecovery will be simultaneous in the case of neurapraxic

injuries. If the injury is proximal to the next most distalmuscle group, it may require several months of observation

to distinguish between axonotmesis and neurotmesis; i.e.,



426 CHAPTER 21

reinnervation will occur in the case of axonotmetic or second

degree injuries.

If the distance between injury and the next most distal

muscle group is greater than 12 in.—e.g., injury to the tibial

division of sciatic nerve in the thigh—one might not have

the luxury of 3 to 4 months for observation and might have

to explore within 8 to 12 weeks after injury.

By the process of elimination, fourth degree injuries

(where scarring fills the perineurium) and fifth degree inju-

ries will not improve. In the case of neurotmetic (third,

fourth, and fifth degree) lesions, a surgical approach is

indicated either to (1) establish with nerve action potentials

that there is physiological continuity and, in the latter case,

remove the damaged segment and anastomose cleanly cut

ends primarily or use an interposition graft, or (2) if the

nerve is anatomically disrupted (fifth degree injury) to do a

primary neurorrhaphy (repair) and place a cable graft be-tween the proximal and distal nerve ends.40

COMMON NERVE INJURYSYNDROMES

Specific syndromes of deficits due to peripheral nerve le-

sions have been selected for presentation because of theirfrequency, including carpal tunnel syndrome, ulnar neuro-

pathy from compression at the elbow, radial nerve injury in

the spiral groove, and peroneal nerve entrapment at the

fibular head.

CARPAL TUNNEL SYNDROME

Carpal tunnel syndrome occurs when the median nerve is

compressed beneath the flexor retinaculum. The anatomy of

the median nerve is illustrated in Fig. 21-7. The carpal

tunnel may be thought of as an inverted table—with the

carpal bones forming the tabletop, and the hook portion of

the hamate, the pisiform, the tubercle of the trapezium, and

the distal pole of the scaphoid forming the table legs.' The

flexor retinaculum is stretched over the legs of this meta-

phoric table.Median nerve compression may occur in pregnancy, amy-

loidosis, diabetes, thyroid disease, and arthritis. The patient

complains of pain at the wrist and into the thumb and index

fingers. The pain usually occurs at night and may awaken

the patient.

On examination, the thenar muscle group may demon-

strate atrophy. The sensory deficit is over the palmar surface

of the thumb, index, middle, and thenar half of the ring

fingers. A Tinel's sign is present at the wrist approximately

50 percent of the time; therefore, it is of little diagnostic

value. The nerve conduction velocity will slow as the first

finding, and later, the EMG will show increased terminallatencies beyond the normal of 3.5 ms or a significant

asymmetry on the two sides.

Conservative treatment may be effective. Placing the wrist

at rest relieves the nocturnal pain of carpal tunnel syndrome

in some patients with mild symptoms. Patients are placed in

a "cock-up" splint that they may wear constantly or only ai

night. Relief may be temporary or continuous over a pro-

longed period. In patients with persistent symptoms and

prolonged latency of the median nerve at the wrist by nerve

conduction studies, decompression by division of the flexor

retinaculum is indicated.

ULNAR ENTRAPMENT AT THE ELBOW

Ulnar entrapment at the elbow has also been called tardy

ulnar palsy. The name originated from a paper written by

Davidson and Horowitz in 1955 entitled "Late or Tardy

Ulnar Nerve Paralysis." They wrote: "The classical pictureof later ulnar neuritis occurs ten or more years after an injury

to the elbow joints, usually in childhood."38

Patients present with pain and numbness in the ulnar side

of the hand. Clinical examination reveals a Tinel's sign as

the ulnar nerve travels over the medial epicondyle or as the

nerve passes through the cubital tunnel. The cubital tunnel is

defined by Mackinnon and Dellon as the fascial covering

that is frequently loose and variable in its proximal extent

at the level of the medial epicondyle and the olecranon—

extending distally to a point between the two heads of the

flexor carpi ulnaris, which is frequently tight.'

In the presence of appropriate physical findings, the diag-

nosis is confirmed by nerve conduction velocity studies andelectromyography. The first findings are slowed conduction

velocities followed by prolonged motor latencies. Neurotme-

sis can result from injury to the nerve. The ulnar nerve

anatomy is illustrated in Fig. 21-8. ;

RADIAL NERVE INJURY

Fractures of the midshaft of the humerus sometimes result in

a radial nerve injury as this nerve travels in the spiral groove

of the humerus. The patient develops weakness in all mus-

cles of the extensor compartment of the forearm. Character-

istic wrist and finger drop makes the diagnosis fairly easy.Usually, function of the triceps muscle is normal, innerva-

tion to the triceps having exited from the radial nerve

proximal to the spiral groove. Electromyography 2 to 3

weeks after the injury will aid in the diagnosis. The injury is

usually neurapraxic or axonotmetic and will resolve. Explo-

ration of the radial nerve is warranted in the injury that

shows no improvement within 3 to 4 months following the

humeral fracture.

PERONEAL NERVE INJURY

Compression of the peroneal nerve commonly occurs as the

nerve crosses in the area of the fibular neck. The nerve is



SURGERY OF PERIPHERAL NERVES 427

Figure 21-7 Anatomy of median nerve.

vulnerable to injury as it crosses the fibula through the

opening in the peroneus muscle. Direct blunt trauma, frac-

ture of the neck of the fibula, repeated compression from

crossing the legs, or pressure from leaning on one side may

cause paresis in the distribution of the peroneal nerve. Pain

laterally in the leg and foot is a common symptom. Some

patients may present with a painless foot drop, i.e., loss of

motor function without sensory changes.

BRACHIAL PLEXUS INJURIES

The brachial plexus presents a challenge diagnostically and

therapeutically. The anatomy is complex and has been illus-

trated in Fig. 21-9.

Table 21-1 provides a study guide that lists the branches

of the brachial plexus and the muscles they innervate. With

the exclusion of compressive injuries, the brachial plexus

injuries may be classified as open or closed.

Open injuries may accompany serious, or even fatal,

vascular or pulmonary injuries.39 Management of these

problems must precede surgery on the brachial plexus. The

decision to explore the brachial plexus depends on severalfactors. If the injury is by a sharp object (knife, glass,

needles, or other sharp object), it warrants early surgical

intervention as described in the section on timing of surgical

intervention. Blunt injuries may be observed for a variable

period of time, depending on the proximal or distal location

of the injury. When repaired, a lesion to the upper or middle

trunk, lateral cord, musculocutaneous nerve, posterior cord,

or axillary nerve has the greatest chance for the return of

useful function because of the proximal muscles they inner-

vate.40 Gun shot wounds in the region of the brachial plexus

may require a waiting period of up to 3 months to help

establish the degree of neural injury. When serial examina-

tions during this time demonstrate persistent deficits, indi-

cating type IV and V lesions, operative intervention is indi-

cated. Evidence of lost neural tissue during an initial

exploration for repair of other injuries is an indication for

early grafting, after allowing local edema to resolve.

Closed injuries of the plexus can be further subdivided

into supraclavicular and infraclavicular injuries. Infraclavi-

cular injuries have a better prognosis and are usually the

result of bony injuries in the shoulder region. Clavicular

fractures or callus formation may compress the plexus. Su-

praclavicular injuries usually occur after high-speed motor

vehicle accidents, often when a rider is thrown from a

motorcycle, resulting in severe stretch injuries or avulsion of roots from the cord.

Damage ranges from nerve root avulsion through more



428 CHAPTER 21

Figure 21-8 Anatomy of ulnar nervefrom elbow distally.

distal neurotmetic injuries to neurapraxic lesions. An upper prognosis. The Homer's syndrome results from injury to the

plexus lesion that also presents with a Homer's syndrome upper sympathetic chain located near the dorsal root ganglia

(myosis, ptosis, and anhydrosis of the face) has a poor of C8 through T2. In a blunt injury, this strongly suggests

Figure 21-9 Anatomy of brachial plexus.



Nerve

Axillary

Long thoracic nerve

Dorsal scapular nerve

Lower subscapular nerve

Supiascapular nerve

Musculocutaneous

Radial

Median

Ulnar

Table 21-1NERVE SUPPLY OF MUSCLES OF THE UPPER EXTREMITY

Muscle

DeltoidTeres minor

Serratus anterior

Levator scapulaeRhomboid minor

Rhomboid major

Teres majorSubscapular (also from upper

scapular nerve)

Supraspinatus

Intraspinatus

Biceps brachiiCoracobrachialisBrachialis

Three heads of tricepExtensor pollicis brevisExtensor pollicis long usExtensor indicisSome branches of brachialis

and brachioradialisExtensor carpi radialis longusExtensor carpi radialis brevisExtensor digitorumExtensor carpi ulnaris

AnconeusSupinatusAbductor pollicis longus

Pronator teresPronator quadratu sFlexor carpi radialisFirst and second lumbricaTisAbductor pollicis brevisFlexor poll icis brevis

(superficial head)Opponcns pollicisFlexor digitoru mFlexor pollicis longusLateral half of flexor digitorum

profundus

Flexor carpi ulnarisMedial half of flexor

digitorum profundusThird and fourth lumbricalisPalmer interosseiDorsal interosseiAdductor pollicisAbductor digiti minim iFlexor digiti minim iOpponens digiti minimiFlexor policus brevis (deep

head)

avulsion. A flail or weak arm at the time of injury should be

supported against gravity to prevent possible additional

damage. In a complete brachial plexopathy, resulting from

avulsions of the roots and causing a flail arm, grafting of

intercostal nerves to the distal end of the musculocutaneous

nerve may provide useful elbow flexion when combined

with a distal limb prosthesis.41

Diagnostic evaluation after a brachial plexus injury should

include plain cervical spine films. (Fractured cervical trans-

verse processes provide good presumptive evidence of nerve

injury.) Cervical myelography or magnetic resonance imag-

ing of the cervical spine usually demonstrates traumatic

pseudomeningoceles at the site of avulsed nerve roots. These

studies should be carried out 2 to 4 weeks after the injury.

Surgical management of pain in association with avulsion of

the brachial plexus is discussed in Chap. 24.

Injury to the lumbar plexus is not as common as brachialplexus injury. This plexus is better protected in its retroperi-

toneal and pelvic location. It is most frequently involved in

penetrating injuries. Fig. 21-10 demonstrates the nerves of

the lumbar plexus.

SURGICAL PROCEDURES

Nerve lesions of type IV in Sunderland's classification, or

neuromas in continuity, are explored in order to determine

the extent of that nerve's injury. Intraoperative action poten-

tials on the isolated or individual fascicles will establishwhich fascicles are not functioning. Decompression or exter-

nal neurolysis of a nerve may relieve entrapment. Examples

of this are division of the flexor retinaculum overlying the

median nerve at the wrist, transposition of the ulnar nerve,

and peroneal nerve decompression.

A lacerated nerve is usually repaired primarily, or an

autologous interposition graft may be needed if the repair is

delayed. Prognosis for the extent of recovery is based on two

factors: (1) At each site of anastomosis approximately 10

percent of the axons will not cross; therefore, in general,

external recovery is better with primary neurorrhaphy com-

pared to cable grafting. (2) Primary repair of the two ends of

the injured nerve leads to better recovery if the anastomosis

is not under tension. Tension can be released by the place-

ment of an appropriate interposition graft, by rerouting of

the anastamosed nerve, or by limb flexion.

There is debate as to whether epineural or intrafascicular

repair is preferable.42.43-44-45 (See Fig. 21-11.) Despite both

laboratory and clinical investigations, neither technique has

proven superior.46 Fascicular repair is technically more chal-

lenging but is more traumatic to the nerve because of the

necessary dissection. In a few instances, this technique may

be better, but epineural repair appears appropriate for most

cases. Fascicular repair should be used in a nerve that is cut

distally where a clear distinction can be made between thesensory and motor divisions of the nerve.46-47 This can only

be done in the first 48 to 72 h. Surgery may be performed



430 CHAPTER 21

Figure 21-10 Anatomy of lumbosacral plexus.

under local anesthesia, with distal motor fascicles and proxi-

mal sensory fascicles identified by direct stimulation.Nerves should be anastomosed primarily under minimal

tension, using 7-0 to 10-0 prolene sutures through the epin-eurium alone. This technique requires magnification. The

deep side of the anastomosis should be performed first, after

two sutures are placed at each side of a line bisecting thehorizontal axis for orientation. This also aids in rotation of

(he nerve, which is necessary for placement of the othersutures. The superficial repair is accomplished last.

A difficult and technically demanding technique using

vascularized nerve grafts has been developed by Julia Ter-

zia. She recommends it for anastomosis of a nerve in anextremely scarred bed where vascularity is known to be

poor.48

Interposition or cable grafts are used to repair an injurednerve when a length of the nerve has been destroyed.Sources for harvesting grafts include the sural nerve, theantebrachial cutaneous nerve, and occasionally the lateral

femoral cutaneous nerve. Any extremity that the injuredpatient might have lost may be an excellent donor source.

Good material for grafting will support axon regeneration

Figure 21-11 Epineural and intrafascicular repair.




while directing that growth toward the intended distal target

nerve and, ultimately, its target organ. Functional recovery is

the goal in all surgical repairs of peripheral nerves.

Other materials have proven effective in achieving thatresult. Sensory nerve repair has been accomplished using

basal laminal grafts of muscle. The pectoralis muscle fibers

are harvested, frozen in liquid nitrogen, thawed, and used to

repair the injured digital nerve. Allograft (tissue from an

unrelated donor) material has been used with limited success

in rats. Mackinnon and Hudson have extended this work to

human beings, but immunosuppression was used.49 They

subsequently discontinued the immunosuppression. The pa-

tient experienced excellent recovery of sensation but no

return of motor function.

DECOMPRESSIVE PROCEDURES

A description of some of the decompressive nerve proce-

dures follows.

Carpal Tunnel Release Anesthetic techniques which

have been described for division of the flexor retinaculum

include: axillary block, local nerve block, and the Bier

block. Local infiltration with 0.5% lidocaine containing

1:200,000 epinephrine has been our most common choice.

This may be supplemented with intravenous sedation in

anxious patients.The incision is located 6 mm to the ulnar or medial side

of the thenar crease. A zigzag extension is used to carry the

incision across the wrist in order to avoid a scar which

restricts motion. The wound is held open with a self-retain-

ing retractor. Subcutaneous fat is retracted and hemostasis

obtained, using bipolar cautery. The palmar fascia is opened

in the long axis of the hand, and the deep transverse carpal

ligament is opened sharply with a scalpel, taking care to

preserve the branches of the median nerve to the muscles at

the base of the thumb. (See Fig. 21-12.)

The median nerve, once exposed, is protected with a no. 4

Penfield dissector as the incision is carried proximally to thedistal portion of the antebrachial fascia and distally until the

fat around the superficial palmar arch is encountered. A

portion of the flexor retinaculum may be removed for patho-

logic examination.

The closure is accomplished in two layers, using absorbable

sutures in the subcutaneous layer and nylon interrupted sutures

on the skin. A bulky fluff gauze dressing is applied, along with

an elastic wrap. The patient is instructed to move the fingers

frequently but should not remove the dressing until the first

postoperative visit, 10 to 12 days after surgery, when the

sutures are taken out. If there is increasing pain or swelling, the

patient should be seen as soon as possible. Patients are allowed

to return to work 3 to 4 weeks after surgery. Postoperativevisits should be scheduled for removal of sutures and at inter-

vals of 3 months for up to a year.

Ulnar Nerve Transposition After the diagnosis of

compression of the ulnar nerve at the elbow is made, a

decision as to how to treat the lesion must follow. Treatment

options include transposition of the nerve along with correc-tions of bony and ligamentous lesions at the elbow, medial

epicondylectomy, removal of any compromising soft tissue

mass, or simple transposition of the ulnar nerve. Transposi-

tion of the ulnar nerve will be described here.

Local infilt ration, block, or general anesthesia may be used.

The patient may be positioned supine with the arm out-

stretched while the surgeon and his assistant are on either side

of the extremity. An alternative positioning is illustrated in Fig.

21-13. This is a more comfortable position for the patient who

is awake, and it also makes accessible the entire segment of the

ulnar nerve to be dissected. With the patient in the supine

position, it is difficult to fully externally rotate the arm in order

to dissect the ulnar nerve away from the medial epicondyle.The lateral decubitus position avoids this problem.

The "lazy omega" incision is used on the skin. (See Fig.

21-13.) This creates a skin flap that entirely covers the trans-

posed nerve. Once the skin and subcutaneous tissues have been

elevated, the fascia between the medial head of the triceps and

the medial intermuscular septum is divided.

The ulnar nerve is dissected free, being retracted with a

loop of umbilical tape or, preferably, a loop usually used for

retraction of blood vessels. Dissection continues distally

until the nerve is released from the cubital tunnel. Branches

of the ulnar nerve, which innervate the proximal flexor carpi

ulnaris, must be separated by interfascicular dissection and

preserved.

The nerve may be transposed over the medial epicondyle

to a bed fashioned in the flexor pronator fascia. (See Fig.

21-13.) The skin flap is then sutured to the fascia to act as a

splint for the transposed nerve; 3-0 Vicryl sutures are used in

this step. (See Fig. 21-13.) The skin is closed with in-

terrupted sutures. A sterile dressing with an elastic bandage

is applied. Sutures are removed 1 week later.

Peroneal Nerve Decompression Decompression of the

peroneal nerve is illustrated in Fig. 21-14. The skin incision

is carried out on the lateral aspect of the proximal leg. The

common peroneal nerve is found proximal and posterior tothe head of the fibula. The nerve is followed to its point of

entrapment, which is usually where the nerve runs through a

tunnel roofed by the peroneus longus muscle.

Swelling of the nerve is usually noted just proximal to the

point of entrapment. The sharp edge of the arch of the peroneus

longus is incised. The deep peroneal nerve is followed to the

extensor digitorum muscle to ensure that it is free.

Harvesting of the Sural Nerve for Cable Graft The

technique for harvesting the sural nerve is illustrated in Fig.

21-15. The lower extremity is positioned so that the lateral

aspect of the leg is exposed. Once the leg is prepared, an

incision is planned 1 cm lateral and parallel to the Achillestendon.

The incision is begun 1 cm proximal to the lateral malleo-



432 CHAPTER 21

Figure 21-12Carpal tunnel release.

lus and extended proximally. The sural nerve is found justsuperficial to the deep fascia and deep to the lesser saphen-

ous vein. The nerve, once identified, is freed by sharpdissection. Proximal and distal ends are divided with a razor

blade over a wooden spatula. If the patient is awake, a

conduction block with xylocaine should be performed proxi-

mally before transecting the nerve, in order to prevent pain.

B has a less cellular pattern, consisting of a loose arrange-ment of spindle cells and a watery, clear, mucinous matrix.

The eighth cranial nerve is involved more than all other

cranial nerves. Schwannomas may be completely removed

from peripheral nerves with minimal damage to the nerve.

However, this is not the case when the tumor involvescranial nerve VIII. (See Chap. 11 on tumors of cranial

nerves and coverings.)

TUMORS OF PERIPHERAL NERVES

A classification of tumors of peripheral nerves has beenprovided by Harkin and Reed.50 (See Table 21-2.) Surgeonswho are planning an approach to neoplastic lesions of peripheral nerves should be familiar with schwannomas,

neurofibromas, fatty infiltration of the median nerve, lipofi-

broma, intraneural lipomas, intraneural ganglia, and intran-

eural hemangiomas.

NEUROMAS

Neuromas occur either as solitary tumors or as a part of neurofibromatosis. The neurofibroma is also a nerve sheath

tumor but is differentiated from the schwannoma in thatnerve fibers run through the tumor. Excision of this tumor

routinely results in neurological deficits.

SCHWANNOMAS

Schwannomas arise from the Schwann cell sheath. They mayoccur on any nerve encased in a sheath of Schwann cells.

The microscopic pathology of these tumors has two char-acteristic patterns: Antoni A and Antoni B. Antoni A is thedensely cellular form, with cells aligned in palisades. Antoni

NEUROFIBROMATOSIS

Neurofibromatosis (von Recklinghausen's Disease) is an au-

tosomal dominant genetic disorder that has varying degrees

of manifestation. Its cardinal features include cafe-au-lait

spots of the skin and neurofibromas within the peripheral,

autonomic, and central nervous systems. Four types of thedisease have been described, including central, peripheral,

visceral, and forme fruste.50




Figure 21-13 Transposition of ulnar nerve.

TUMORS OF NONNEURAL ORIGIN

Tumors of nonneural origin include Upofibromatosis of the

median nerve, which usually presents as a soft mass in the

palm during childhood or early adulthood. Carpal tunnel

release offers only temporary relief. Extensive microsurgical

neurolysis is more efficacious, since the tumor is outside thenerve. Removal of large amounts of the tumor may be

accomplished with preservation of function. Intraneural lipo-

mas, hemangiomas, and gangliomas have been described,

Figure 21-14 Decompression of peroneal nerve.



434 CHAPTER ;

Figure 21-15 Harvesting sural nerve.

presenting as a mass, with neurological symptoms, or

both.51-56 Removal of these masses is possible without loss

or interruption of function.

Table 21-2CLASSIFICATION OF TUMORS OF

PERIPHERAL NERVES

I. Neoplasms st nerve staeatli originA. Benign primary nerve sheath tumors

1. Schwannoina2. Neurofibroina

B. Malignant primary nerve sheath tumors,

1. Malignant schwannoina2. Nerve sheath fibrosarcoina

II. Neoplasms of nerve cell originA. NeuroblastomaB. GanglioneuromaC. Pheochroniocytorna

III. Tumors metastatic to peripheral nerves

IV. Neoplasms of nonneural originA. Lipofibromatos is of the median nerveB. Intraneural lipoma, h emangio ma, ganglion

V. Nonneoplasms

A. Traumatic neuromaB. Compressive neuroma (Morion's neuro ma. Bowler'sthumb)

CAUSALGIA AND PAINFULTRAUMATIC NEUROMAS

Injury to a peripheral nerve may result in loss of function

supplied by the nerve, but it may also cause painful seque-

lae. The pain may result from a pressure-sensitive neuroma

or an incomplete nerve injury that produces causalgia (from

the Greek kausis, meaning "burning," and algos, meaning

"pain"),

Causalgia is an intense, constant, burning pain. The

slightest movement of the affected extremities may cause

paroxysms of the pain. Changes in the autonomic function to

the affected extremity are apparent. The hand, for example,

will be colder or warmer, bluer or pinker, and usually moremoist than the contralateral, unaffected hand. In typical

causalgia of the hand due to incomplete median nerve injury,

a stellate ganglion block may be of diagnostic and therapeu-

tic benefit. A series of stellate ganglion blocks may increase

the duration of relief and even cause the condition to abate.

However, there may be pitfalls to the interpretation of such

blocks, and a short course of an oral alpha blocking agent

may be equally effective in temporarily or permanently

stopping such pain. (See section on sympathectomy in

Chap. 24.)

If sympathetic blockade gives only temporary relief, sur-

gical sympathectomy should be considered, provided a thor-

ough psychological evaluation has ruled out any significantpsychopathology. If causalgia involves the upper extremity,

;the lower half of the stellate ganglion and the upper two or




three thoracic sympathetic ganglia are moved, using a trans-

axillary or posterior approach (see Ref. 40 in Chap. 24).

In patients with painful neuromas, relief of the pain is

sometimes difficult to achieve. For this reason, many treat-

ment options have evolved. Kline and Nulson advocate

sharply sectioning the nerve proximal to the neuroma and

embedding the freshly sectioned nerve end in adjacent deep

soft tissue.40 This has, on occasion, led to reoperation to

resect a new neuroma. Recurrence of the painful neuroma is

less likely if the freshly sectioned nerve end is placed in a

protective environment deep in the limb and surrounded by

muscle.40

If the pain is related to a neuroma in continuity, there is

complete loss of motor function of more than 3 but less than

12 mo duration, and intraoperative nerve action potentials

indicate no regeneration across the site of injury, the neur-

oma should be excised and a primary neurorrhaphy or cablegrafting performed. If there is intraoperative nerve action

potential evidence of recovery of function, an external and

possibly an internal (interfascicular) neurolysis should be

performed. If there is clinical or EMG evidence of recovery,

adequate time for regeneration to complete itself should be

allowed.40 As in all cases of chronic pain, a thorough psy-

chological evaluation should be done before finalizing plans

for surgery.

SUMMARY

In patients with peripheral nerve injuries, concurrent injuries

that might be life-threatening must be treated first, and then

the peripheral nerve injury approached systematically. The

type of injury, its time of occurrence, initial deficit, and

degree of recovery expected are important issues in estab-

lishing the treatment plan, which may range from skilledobservation to extensive surgical intervention.

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34. Seddon HJ, Medawar PB, Smith H: Rate of regeneration of peripheral nerves in man. J Physiol (Lond) 102:191-215,1943.

35. Sunderland S: Rate of regeneration sensory nerve fibers. Arch Neurol Psychiatr 58:1-6, 1947.

36. Sunderland S: Rate of regeneration of motor fibers in the ulnarand sciatic nerves. Arch Neurol Psychiatr 58:7-14, 1947.

37. Yahr MD, Beebe GW: Recovery of motor function, in Wood-hall B, Beebe GW (eds): Peripheral Nerve Regeneration.

Washington, U.S. Government Printing Office, 1956, chap 3,pp 71-202.

38. Davidson AJ, Horwitz MT: Late or tardy ulnar-newe paralysis. J Bone Joint Surg 17:844-856, 1935.

39. Nelson KG, Jolly PC, Thomas PA: Brachial plexus injuriesassociated with missile wounds of the chest: A report of 9cases from Viet Nam. J Trauma 8:268-275, 1968.

40. Kline DG, Nulson FE: Acute injuries of peripheral nerven, IYoumans JR (ed): Neurological Surgery, 2d ed. PhiladeI(l3E-Saunders, 1982, chap 75, pp 2362-2429.

41. Yeoman PM, Seddon HJ: Brachial plexus injuries: TreamionBof the flail arm. J Bone Joint Surg 43B:493-500, 1961.

i

42. Bora FW: Peripheral nerve repair in cats: The fascicular sw;-- J Bone Joint Surg 49A:659-666, 1967.

43. Kutz JE, Shealy G, Lubbers L: Interfascicular nerve repairOrthoped din North Am 12:277-286, 1981.

44. Kline DG, Hudson AR, Bratton BR: Experimental study of fascicular nerve repair with and without epineurial closure. / Neurosurg 54:513-520, 1981.

45. Edshage S: Peripheral nerve suture: A technique for improvedintraneural topography. Evaluation of some suture materials

Acta Chir Scand (suppi) 331:1-104, 1964.46. Orgel MG, Terzis JK: Epineural vs. perineurial repair: An

untrastructural and electrophysiological study of nerve regener-ation. Plast Reconstruct Surg 60:80-91, 1977.

47. Levinthal R, Brown WJ, Rand RW: Comparison of fascicular.interfascicular and epineural suture techniques in the repair of

simple nerve lacerations. J Neurosurg 47:744—750, 1977.48. Terzis JK, Smith KL: The Peripheral Nerve: Structure, Func-

tion, and Reconstruction. New York, Raven, 1990, pp 129-131.

49. Mackinnon SE, Hudson, AR: Clinical application of peripheralnerve transplantation. Plast Reconstr Surg. 90:695-699, 1992

50. Harkin VC, Reed RJ: Tumors of the Peripheral Nervous Sy-tem. Washington, Armed Forces Institute of Pathology, 196-pp 67-97.

51. Morley GH: Intraneural lipoma of the median nerve of thecarpal tunnel. J Bone Joint Surg 46B:734-735, 1964.

52. Mikhail IK: Meidan nerve lipoma in the hand. J Bone Joint Surg 46B:726-730, 1964.

53. Kojima T, Ide Y, Marumo E, et al: Hemangioma of mediannerve causing carpal tunnel syndrome. Hand, 8:62-65, 1976.

54. Losli EJ: Intrinsic hemangiomas of the peripheral nerves: Areport of two cases and a review of the literature. Arch Pathol53:226-232, 1952.

55. Purcell FH, Gurdjian ES: Hemangiomata of peripheral nerveswith report of a case of cavernous hemangioma of the sciaticnerve. Am J Surg 30:541-544, 1935.

56. Barrett R, Cramer F: Tumors of the peripheral nerves andso-called "ganglia" of the peroneal nerve, din Orthop27:135-146, 1963.

STUDY QUESTIONS

I. A 21-year-old male loses control of his motorcycle when

it strikes a parked vehicle. He is thrown over the vehicle and

hits a tree. He does not remember the accident, but when he

regained consciousness, he has severe pain over the left

clavicle. He can flex his fingers weakly but cannot flex his

elbow or abduct or rotate his shoulder. He can hold his arm

extended. He has anesthesia over the shoulder and down the

lateral and thenar sides of his arm and forearm, respectively.

X-rays reveal that the clavicle is fractured.

1. What is the differential diagnosis? 2. How can the

various diagnoses be determined? 3. Assuming avulsion of

the fifth and sixth cervical nerve roots, what might be done

to reinnervate the shoulder and arm? 4. Assuming avulsion

of the upper roots of the brachial plexus, what might the

EMG of the forearm show the day after the injury? A month

later? 5. When might one expect to see beginning recovery

of motor function, assuming the injury is due to stretching of

the upper brachial plexus?

II. A 45-year-old female falls on some ice, sustaining a

Colles fracture of the right wrist, which is treated with

reduction and a cast. After the cast is removed, the patient

begins to notice numbness of the hand. She awakens at night

with pain, gets up, and moves the hand about to be able to

go back to sleep for a while.

She begins to notice atrophy of the muscles at the base of

the thumb. Examination reveals hypalgesia over the palmar



169

C H A P T E R 10

Physiology of the Cerebrospinal Fluidand Intracranial Pressure

Anthony Marmarou† ■ Andrew Beaumont

The exquisite sensitivity of the central nervous system to physicaland chemical injury has led to an ingenious series of protectiveand homeostatic systems that shroud, nurture, nourish, andmaintain maximal function. These systems include rigid physicalprotection in the form of skull bones, hydraulic shock absorptionin the form of cerebrospinal fluid (CSF), substrate supply andcellular homeostasis in the form of a rich vascular supply with

continuous turnover of extracellular fluid, and protection fromexternal noxious substances by the blood-brain barrier. These highly developed protective systems can become

detrimental, however, under certain pathologic conditions. Inparticular, encasement of brain tissue in a rigid structure (theskull) places an important constraint on the refined interplaybetween cerebral homeostatic processes, namely, volume regula-tion. Noncompressible matter such as fluid, when added to a rigidcontainer, will generate pressure; in the case of the centralnervous system, this results in the intracranial pressure (ICP).Under pathologic conditions, the intracranial volume and there-fore ICP can rise, which presents a serious threat to the centralnervous system. Furthermore, the effects of raised ICP canfurther contribute to the primary pathologic process.

A wide range of neurosurgical problems—including congeni-tal lesions, neoplasms, metabolic and infectious syndromes,

infarction, hemorrhage, and trauma—requires evaluation andtreatment for elevated ICP. Effective clinical treatment of prob-lems relating to raised ICP demands a detailed understanding ofthe physiologic mechanisms that generate and maintain normalICP, the perturbations that lead to an elevated ICP, and themeans by which elevated pressures can be reduced.

HISTORICAL CONSIDERATIONS Although problems with brain swelling and the effects of remov-ing pieces of skull were understood even in the times of Galen,Hippocrates, and the early Egyptian physicians, modern thinkingabout volume regulation inside the skull began with the writingsof George Kellie and his mentor, Alexander Monro, who workedin Edinburgh at the turn of the 19th century. Monro,1 in hisseminal work on the brain and nervous system, wrote:

For, as the substance of the brain, like that of other solids of ourbody, is nearly incompressible, the quantity of blood within thehead must be the same, or very nearly the same at all times,

whether in health or disease, in life or after death, those cases onlyexcepted in which water or other matter is effused, or secretedfrom the blood vessels; for in these a quantity of blood, equal inbulk to the effused matter, will be pressed out of the cranium.

Some years later, at a meeting of the Medico-Chirurgical Societyof Edinburgh, George Kellie2 presented a report in which headvanced this idea and stated:

If these premises be true, it does not then appear very conceivablehow any portion of the circulating fluid can ever be withdrawnfrom within the cranium, without its place being simultaneously

occupied by some equivalent; or how anything new or exuberantcan be intruded without an equivalent displacement.

These ideas later became recognized as the Monro-Kelliedoctrine, which is formalized physiologically later. Subsequentadvances in understanding ICP came with the ability to effec-tively monitor ICP under different circumstances. Quincke3 first

described lumbar puncture for the relief of “brain pressure” in1911. However, it was not until the work of Guillaume and Janny 4 in 1951 that ICP was continuously monitored. Lundberg5 later published results from a large series of patients in which hedescribed several of the fundamental concepts used today in clini-cal ICP monitoring, including the Lundberg A, B, and C waves.

ICP monitoring today is considered commonplace in neuro-surgical practice. ICP values are used as a measure of disease, asan indication of treatment response, and to monitor cerebralperfusion.

NORMAL INTRACRANIAL PRESSURE The upper limit of normal ICP in adults and older children isusually given as 15 mm Hg, although the usual range is 5 to

10 mm Hg. Transient physiologic changes resulting from cough-ing or sneezing often produce pressures exceeding 30 to50 mm Hg, but ICP returns rapidly to baseline levels.

ICP can be measured by low-volume displacement transduc-ers to interface with CSF pathways in the intraventricular, intra-parenchymal, subdural, or epidural spaces. The ICP waveform isnormally pulsatile and can be divided into three major compo-nents (Fig. 10-1). The baseline or average level is commonlyreferred to as the ICP; rhythmic components superimposed onthis level are associated with cardiac and respiratory activity. Tocompletely describe ICP, one should specify the magnitude ofthe baseline or “steady-state” level and the amplitude and peri-odicity of the pulsatile components. Changes in these pulsatilecomponents can be one of the earliest signs that the ICP is begin-ning to rise, as a reflection of the increased conductance of pres-sure waves through a “tightening” brain.

Cardiac and respiratory activity creates pulsatile componentsby cyclic changes in cerebral blood volume. Left ventricular con-traction contributes the cardiac component, which has a fre-quency similar to the peripheral arterial pulse. The exact vesselsthat transmit the peripheral pulse remain to be established. Earlystudies suggested that the choroid plexus and pial arteries wereresponsible,6 although more recent analysis has implicated thehigh-compliance venous blood vessels.7

The respiratory contribution to the ICP waveform arises as aresult of fluctuations in arterial blood pressure and cerebral

venous outflow during the respiratory cycle, generated by pres-sure changes in the thoracic and abdominal cavities. Duringinspiration, there is a fall in arterial blood pressure and an increasein pressure gradient from cerebral veins to central venous capaci-tance vessels. This gradient drives cerebral venous return, which

is therefore increased on inspiration, with a concomitant drop incerebral blood volume. Mechanical ventilation and intrathoracic†Deceased.



170 SECTION I INTRODUCTION TO NEUROLOGICAL SURGERY

parameters that are features common to any hydrodynamicsystem: the internal (intracranial) fluid volume, the elastance ofthe system, the contribution from the atmosphere, and the ori-

entation of the craniospinal axis relative to the gravitational vector.Pressure (P) is defined as force (F) per unit area (A). Pressures

are usually reported in units of either millimeters of water (mmH2O) or millimeters of mercury (mm Hg). This convention arosebecause a fluid column will exert a pressure at its base propor-tional to the height of the column (h), the density of the fluid (ρ),and the gravitational constant ( g ). Because, for a given fluid, g and ρ are constant, pressures can be compared by relation to theheight of a given fluid. ICP is variably expressed in either milli-meters of mercury or millimeters of water. Dividing the pressurein millimeters of water by 13.6 yields the equivalent pressure inmillimeters of mercury; this constant is based on the ratio of thedensity of water to mercury. The SI unit for pressure is the pascal(Pa), which is defined as 1 newton (N)/square meter; 1 kilopascal(kPa) is 7.5 mm Hg or 102 mm H 2O.

In actual fact, three different pressures contribute to ICP:atmospheric pressure, hydrostatic pressure, and filling pressure. Atmospheric pressure is the component resulting from transmit-ted atmospheric pressure to the brain, and therefore absolute ICP

varies with altitude. This pressure is principally transmittedthrough the vasculature10; however, ICP is typically reportedrelative to atmospheric pressure, and this component is ignored.

As with any column of fluid, the skull and spinal canal experi-ence hydrostatic pressure caused by the weight of their contents.

The contribution of hydrostatic pressure depends on the weightof fluid and tissue above the point of measurement, divided bythe cross-sectional area at that level. For example, lumbar CSFpressure is greater in the sitting position compared with thelateral decubitus position11,12 as a result of the hydrostatic differ-ence; increasing degrees of head-down tilting further increase thecontribution of hydrostatic pressure.

The filling pressure of the system is determined by the volumeof the intracranial contents and the elastance of the enclosingstructures. The intracranial contents consist of blood, brain,CSF, and any pathologic masses. Elastance is a system parameterthat is defined by the pressure change per unit of volume change,13 namely, the corresponding pressure change for any given volumeincrease in craniospinal contents (Fig. 10-3A ). The relationshipis not necessarily linear across all volumes and not necessarilyconstant under all physiologic conditions. Compliance is theinverse of elastance, and both measures are useful for understand-ing the physiology of ICP. Elastance arises as a combined resultof both distention and displacement. In other words, as volumeis added to the system, there are two principal routes for com-pensation, either expansion or loss of volume. In a physiologicsense, this can occur either by distention of the spinal dura materor by displacement of CSF and blood. These concepts areexpounded on subsequently in the discussion of non–steady-statedynamics. Atmospheric pressure, hydrostatic pressure, and fillingpressure all contribute to the concept of steady-state dynamics.

STEADY-STATE DYNAMICSIn the absence of disease, baseline ICP and the amplitude of thepulsatile components of ICP remain constant despite a variety oftransient perturbations. As alluded to previously, the skull shouldbe considered a rigid container of noncompressible elements.ICP therefore depends on the relative constancy of total volumeinside the skull, contributed to by CSF, blood, and brain tissue.

The ability of the dural coverings to distend is very limited;therefore, any change in volume of one of the three intracranialcomponents must occur at the expense of the other two if ICP

is to be maintained. The following equation describes thisrelationship:

disease may considerably alter the respiratory contribution to theICP waveform.

If the ICP waveform is examined in more detail and at ahigher chart speed, the waveform of highest frequency can beseen to consist of as many as five smaller peaks. Three of theseare relatively constant (Fig. 10-2): the percussion wave (W1), thetidal wave (W2), and the dicrotic wave (W3).7,8 The percussion

wave is the most constant in amplitude and derives from pulsa-tions in large intracranial arteries.9 The tidal wave has a more

variable shape and is thought to arise from brain elastance. Thetidal wave and the dicrotic wave are separated by the dicroticnotch, which corresponds to the dicrotic notch in the arterialpulse waveform.

PHYSICAL PRINCIPLESICP is synonymous with CSF pressure and is defined as the pres-sure that must be exerted against a needle introduced into theCSF space to just prevent escape of fluid. ICP depends on several

Respiratory pulse

Cardiac pulse

INTRACRANIAL PRESSURE WAVEFORMS20

Baseline

0

10

0

m m H g

FIGURE 10-1 Normal intracranial pressure (ICP) waveform. The base-line pressure level is affected by rhythmic components caused bycardiorespiratory activity. Mean arterial blood pressure fluctuationwith heart rate causes small-amplitude rapid pulsation, and respirationcauses larger amplitude fluctuations of lower frequency. ICP is com-pletely described only by information about both the baseline leveland the pulsatile components.

NORMAL INTRACRANIAL PRESSURE

WAVEFORM AT RAPID CHART SPEED

0

2

4

6

8

10

W1

W2

W3

FIGURE 10-2 Normal ICP waveform at rapid chart speed. Several

small components can be seen, the most constant of which are thepercussion wave (W1), the tidal wave (W2), and the dicrotic wave (W3).



C H A P T E R 10 Physiology of the Cerebrospinal Fluid and Intracranial Pressure 171

within the intracranial compartment that are considered part ofthe steady state.

General Physiology of the Cerebrospinal FluidIn the adult, approximately 87% of the typically 1500-mL intra-cranial space is occupied by the brain, 9% by compartmental CSF(ventricles, cisterns, and subarachnoid space), and 4% by blood.14

The extracellular space is in direct contact with CSF and formsapproximately 15% of the total brain volume.15 Total CSF isconsidered to include compartmental CSF and the extracellularspace.

Cranial CSF volume as assessed in humans by Tanna andcolleagues16 was found to have a mean of 164.5 mL, with arange of 62.2 to 267 mL. Ventricular volume also varies consider-ably, as assessed with magnetic resonance imaging, from 7.49 mLto 70.5 mL, with a mean of 31.9 mL. Reasons for such

variation are not clear; however, the amount of CSF in anyorganism reflects a dynamic balance between production andclearance.

CSF is principally produced by the choroid plexuses, whichare invaginations of the pia mater into the ventricular cavities,specifically in the roofs of the third and fourth ventricles and the

walls of the lateral ventricles. At these points, fronds of denselybranching blood vessels are invested by pia mater and covered byspecialized ependymal cells, the choroidal epithelium. The sur-faces of cells in this structure are densely covered with villousprocesses to increase the surface area. A second site of CSF pro-duction is the ventricular ependyma, the proportional contribu-tion of which arguably ranges from 50% to 100%.17,18

For a considerable time, CSF was described as an ultrafiltrateof plasma, implying that hydrostatic pressure within blood vesselsforced protein-free fluid through interendothelial spaces.19 However, close analysis of the composition of CSF (Table 10-1)shows multiple differences in composition at the ionic level,

which is strongly against the idea of a simple filtration or dialysisprocess. CSF, in general, has a higher sodium, chloride, and

V V V V

V

CONSTANT

CSF BLOOD BRAIN OTHER

INTRACRANIAL SPACE

+ + +

=

= ( )

This relationship encapsulates the concept of the Monro-Kellie doctrine. The presence of an abnormal component, suchas a tumor or hematoma (represented by V OTHER in the equation),demands reciprocal changes in the volumes of brain, blood, orCSF to maintain ICP at physiologic levels. Even the physiologicstate is far from static; it is rather a dynamic equilibrium. Con-

stant changes induced by the heartbeat, systemic blood pressure,fluid status, and intrathoracic pressure invoke transient changes

0

–8 0 8

Compliance =.14

b

PRESSURE-VOLUME CURVE

Normal adult

(ICP vs 2V)

Compliance =.62

a

2V (mL)

I C P ( m m H

g )

16 24

10

20

30

40

50

60

70

80

90

0

4

6

8

10

20

40

60

80

–8 0 8

PVI = 25 mL

(Calculated volume

to raise ICP = 10)

PRESSURE-VOLUME INDEX (PVI)

Normal adult

(ICP vs 2V)

L o g I C P ( m m H

g )

16 24B

A

FIGURE 10-3 The pressure-volume curve and the pressure-volumeindex describe the response of ICP to the addition of volume. A, Thenormal curve shows how compliance changes as greater volumes areadded. The CSF system is in the phase of spatial compensation atpoint a compared with spatial decompensation at point b. B, Graph-ing log ICP against volume change allows calculation of the pressure-volume index, which is widely used as a description of intracranialcompliance.

TABLE 10-1 Concentrations of Solutes (mEq/kg H2O)in Plasma and Lumbar Cerebrospinal Fluidin Humans

SUBSTANCE PLASMA CSF

Sodium (Na+) 150 147

Potassium (K +) 4.63 2.86

Magnesium (Mg2+) 1.61 2.23

Calcium (Ca2+) 4.7 2.28

Chloride (Cl−) 99 113

Bicarbonate (HCO3−) 26.8 23.3

Amino acids 2.62 0.72

Osmolality 289.0 289.0

pH 7.397 7.30

Cl−, Na+, and K + from Fremont-Smith F, Dailey ME, Merritt HH, et al.

The equilibrium between cerebrospinal fluid and blood plasma: I. The

composition of the human cerebrospinal fluid and blood plasma. ArchNeurol Psychiatry . 1931;25(6):1271-1289; Mg2+ and Ca2+ from Hunter G,

Smith HV. Calcium and magnesium in human cerebrospinal fluid. Nature.

1960;186:161-162; HCO3− and pH from Bradley RD, Semple SJ. A

comparison of certain acid-base characteristics of arterial blood, jugular

venous blood and cerebrospinal fluid in man, and the effect on them of

some acute and chronic acid-base disturbances. J Physiol . 1962;160:381-

391; osmolality from Hendry EB. The osmotic pressure and chemical

composition of human body fluids. Clin Chem. 1962;8:246-265.




model that analyzes the physiologic mechanisms of (1) CSF for-mation, (2) volume storage or compliance, and (3) fluid absorp-tion (Fig. 10-4).28,29

The formation of CSF can be depicted as a pump that con-tinuously introduces fluid into the CSF spaces of the neural axis. The rate of formation of fluid (If ) is considered constant andindependent of the pressure that has to be pumped against, inaccordance with observations that the rate of CSF formation isaffected minimally, if at all, by changes in the ICP. The fluidenters a compliant storage space, which can expand to accom-modate the added volume, and proceeds through outflow path-

ways to be absorbed across the arachnoid villi into the dural venous sinuses. The compliance mechanism is represented by anelement (C) that decreases its compressibility with increasing

volume, much like the resistance offered by a rubber balloon atmaximal inflation. Both the resistance of the CSF channelsleading to the arachnoid villi and the resistance of the villi to fluidflow are combined into a single resistance element (R o). Thiscomponent represents the total resistance to the outflow of the

CSF, which under normal conditions remains fixed and indepen-dent of ICP. The final element of this model is the dural sinuspressure (Pd). Fluid crossing the arachnoid villi must overcomethis exit pressure.

From this conceptual framework, a theory has been developedto describe the interaction of the formation, storage, andabsorptive elements in the steady state. First, both pressure and

volume are in equilibrium, and there can be no net increase ordecrease in the total volume of the CSF. The CSF formed mustpass through the absorptive elements so that no net fluid isstored.

Because all fluid formed passes through the resistive element(R o), a pressure gradient will be developed across the absorptiveelement that is equal to the product of fluid formation (I f ) andthe fluid resistance (R o). The greater the magnitude of flow orresistance, the greater the pressure gradient (If × R o). As long as

the system is in equilibrium, the pressure of the CSF spaces mustbe of sufficient magnitude to drive fluid through the arachnoid

villi at the same rate it is being formed. This requires that theCSF pressure (ICP) be equal to the sum of the pressure gradientacross the absorptive element (If × R o) and the exit pressure. Theequation

ICP I R Pf o d= ×( ) +

shows that the steady-state ICP is proportional to three param-eters: (1) the rate of CSF formation, (2) the resistance to CSFabsorption, and (3) the dural sinus pressure. When these param-eters remain constant, ICP is unchanged, and the complianceelement does not actively participate in ICP regulation.

An increase in CSF formation, outflow resistance, or venouspressure at the site of fluid absorption can alter this dynamicequilibrium and result in elevated ICP. Mathematical modelinghas shown that the contribution of the product of CSF formationrate and outflow resistance (If × R o) is approximately 10% of thetotal ICP.29 The remainder is attributed to the magnitude of thedural sinus pressure (Pd). With this distribution, the outflowresistance would have to increase markedly to cause a significantrise in the ICP. However, much smaller elevations of sagittalsinus pressure (Pd) caused by venous sinus obstruction would betransmitted directly to the CSF system, thus raising resting ICP.From the equation, it is clear that changes in these elements canoccur independently of each other.

If Pd rises, CSF absorption can remain constant, and a shift toa new ICP equilibrium can occur. This concept is supported bythe work of Johnston,30 who demonstrated normal CSF resis-tance in the presence of raised ICP induced by venous obstruc-

tion.4,30

In this case, there is no net change in the CSF volumeand presumably no change in the compliance element.

magnesium concentration than one would expect in a plasmafiltrate. The concentrations of potassium, calcium, urea, andglucose are lower. The overall osmolality is, however, similar.

Current thinking therefore holds that a simple filtration processis modified by energy-dependent secretion and reabsorptionprocesses.

Estimates of the rates of CSF production can be made experi-mentally by examining the clearance or turnover of injected sub-stances,20 by marker dilution techniques,21 or by ventriculocisternalperfusion.22 Estimates with these techniques have yielded valuesin the range of 0.35 to 0.37 mL/min for humans. 23,24 Morerecently, flow voids in magnetic resonance signal within the CSFsystem have been used to estimate CSF production rates. Fein-berg and Mark 25 estimated the flow of CSF through the aqueductin humans, which should in principle equate to the flow of CSFsecretion in the lateral and third ventricles, as 0.48 mL/min.

There are variations in absolute rates of CSF production,however, that clearly relate to the absolute weight of choroidplexus tissue in each subject. Furthermore, rates of CSF produc-

tion follow a diurnal variation, with peak production rates in thelate evening and early morning.26

Because there is a constant production of CSF, there must beremoval of CSF at the same rate. CSF circulates from choroidplexus, through the ventricles, to the cisterna magna, basal cis-terns, and subarachnoid space. The principal site of physiologicCSF drainage is into the dural venous system, through the dural

venous sinuses. Evaginations of the arachnoid membrane pro-trude into the lumen of the dural veins and form the arachnoidgranulations or villi. This forms a valvular connection betweenthe subarachnoid space and the dural sinus so that blood cannotreflux into CSF. A higher hydrostatic pressure in the subarach-noid space drives the bulk flow of fluid in the forward direction,therefore draining CSF volume. Studies of these structures haverevealed that they can allow molecules up to several microns topass, but only unidirectionally.27 CSF reabsorption has been

shown to cease at CSF pressures of less than 5 mm Hg. 23

Cerebrospinal Fluid Dynamics The nonpulsatile volume of CSF at any point in time is depen-dent on a balance between the rate of formation, the rate ofabsorption, and the volume sink in the skull. The interactionsbetween these parameters can be addressed by a mathematical

I formation P

R

Formation Absorption

I absorbed

b

a

c

I (t)PdStorage

I storage

FIGURE 10-4 Equivalent electrical circuit showing the principalfactors that govern ICP. CSF formation is represented as a currentsource (I formation), CSF storage is represented by a capacitativeelement (C). Resistance to CSF outflow is represented by a resistiveelement (R), and dural sinus pressure is Pd. This framework has allowedaccurate description of CSF dynamics. (From Marmarou A, Shulman

K, Rosende RM. A nonlinear analysis of the cerebrospinal fluid systemand intracranial pressure dynamics. J Neurosurg. 1978;48:332-344.)




mal blood collection, increased CBV, and a strong vasomotorreaction to the ensuing injury.36

Brain tumors provide a slowly increasing V OTHER , which pro-

vides time for the organism to make compensatory changes. Therefore, ICP problems with tumors occur less commonly;however, a sudden change in intracranial volume (such as a hem-orrhage into the body of a tumor) in a system that is alreadycompensated and therefore dynamically stressed can have disas-trous results. Also, prolonged periods of increased hydrostaticpressure (such as lying down) can create substantial increases inICP in such patients. This phenomenon, coupled with the diurnal

variation in CSF secretion, may underlie the early morning head-aches and nausea experienced by these patients.

Other clinical conditions can result in an elevated ICP, includ-ing hydrocephalus, idiopathic intracranial hypertension, menin-gitis, and arteriovenous malformations. In several of theseconditions, a direct addition of intracranial volume is not theprimary cause. For example, in hydrocephalus, an impaired CSFdrainage system causes CSF accumulation. The cause of elevated

ICP in idiopathic intracranial hypertension is not known,although again, CSF production and drainage have been impli-cated as has elevated venous pressure.37 Meningitis can influenceICP in several patterns, either by blocking CSF drainage path-

ways or by stimulating marked cerebral edema. Arteriovenousmalformation, in contrast, represents a significant increase in

V BLOOD that can secondarily create V OTHER if it is involved in ahemorrhagic event.

Brain edema is a specific pathologic process arising in responseto a wide range of cerebral pathologic changes. It is defined asan increase in the brain tissue water content and therefore canbe thought of as contributing to V OTHER or V BRAIN. At the turn ofthe 20th century, Reichardt 38 reported differences between a dryswollen brain and a wet edematous brain. Klatzo39 subsequentlypaved the way for all future discussions of edema by introducingthe terms cytotoxic and vasogenic to indicate intracellular and extra-

cellular water accumulation, respectively. The latter of these istraditionally associated with an open blood-brain barrier andfluid leakage. However, this division is a simplification for tworeasons. First, for brain tissue water to rise, even under cytotoxicconditions, water has to enter the tissue from an external source,the most likely of which is blood vessels. Therefore, even cyto-toxic edema has a “vasogenic” origin. It is the pathologic causeand the final site of edema accumulation that must distinguishthese phenomena. Furthermore, studies in traumatic brain injuryhave suggested that the vasogenic component of injury may havebeen overemphasized40,41 and that the importance of a disruptedblood-brain barrier lies in the provision of a low-resistancepathway for movement of water to cells that are swelling cyto-toxically.42 The predominance of traumatic cellular edema hasbeen supported by studies in head-injured patients.43 Cytotoxicand vasogenic edema may not, therefore, be separable entities,and a recently proposed classification of edema based on theterms intact barrier and open barrier may have merit.44

Several possible alterations in intracranial volume are dis-cussed in the preceding paragraphs. When such changes occurrapidly or exceed the ability for compensation by reciprocal

volume reductions, ICP may begin to rise. Under these condi-tions, more descriptors of ICP are required than in the steadystate.

Intracranial Pressure in Idiopathic“Normal-Pressure” Hydrocephalus

The term normal-pressure hydrocephalus was introduced in thethesis of Solomon Hakim in 1964 and the description later pub-

lished in the landmark article by Adams and coworkers.45

Together, they are credited with describing a specific syndrome

Pulsation Models of CommunicatingHydrocephalus: A New Concept

The pulsation of ICP has been the subject of study for many years. More recently, it has been considered to be an integral partof a new concept of hydrocephalus whereby the ICP pulse ismore than a CSF reflection of the cardiac and respiratory pulsa-tion. In the new concept, the flow of the arterial pulsations intothe cranium is considered to be sequential, beginning from thelarge subarachnoid arteries at the skull base to the small arteriolesin the parenchyma. Pulsations are dissipated into the subarach-noid CSF and into the choroidal arteries and ventricular CSF.

These pathways are arranged in a series-parallel array of arteriesand CSF spaces. The bulk flow of blood that remains after thepulsations have been filtered out continues through the capillarypathways and represents a windkessel mechanism.31 Most impor-tant, this model provides an alternative view to the “bulk flowtheory” causing ventricular enlargement. Increased impedance topulsations in the subarachnoid space increases pulsations in the

blood flow to the choroidal arteries and the choroid plexus,thereby increasing the pulsations in the ventricular CSF. The ventricular pulsations exceed those in the subarachnoid space,and it is theorized that a transmantle pulse pressure gradient andsubsequent ventricular expansion result. This theory is now beingexplored by mathematical models and experimental studies in thelaboratory and in the clinical setting.32,33 Future work will focuson demonstrating that this model accounts for the pathologicchanges seen in communicating hydrocephalus.

Cerebral Blood Volume and Flow The other dynamic component of the equation representing the Monro-Kellie doctrine is cerebral blood volume (CBV). CBVand cerebral blood flow (CBF) are essentially functions of thecerebral arteriovenous pressure difference and cerebrovascular

resistance, which is largely determined by vessel caliber. Although,as described previously, there are rhythmic changes in blood

volume as a result of the cardiorespiratory cycles, both CBV andCBF are maintained within narrow limits by the process of auto-regulation. Vascular tone is influenced by both physical (force)and chemical (pH, Pco2) signals, with the aim of maintainingCBF across a wide range of both arterial blood pressures (50 to160 mm Hg) and levels of tissue metabolism (Paco2, 20 to 70).

The mean normal adult CBF is 53 mL/100 g per minute.

NON–STEADY-STATE DYNAMICS The preceding processes maintain a constant ICP while there isno CSF accumulation or other change in intracranial volume.Unfortunately, many pathologic states, such as hematoma, tumor,hydrocephalus, and cerebral edema, are associated with changesin intracranial volume, which can, in turn, cause elevated ICP.

The most common clinical cause of raised ICP is traumaticbrain injury, the pathology of which encompasses several possible

V OTHERS. Brain edema contributes extra volume to the intracra-nial contents in the form of water. Trauma may induce intrace-rebral collections of blood in extradural, subdural, subarachnoid,or intraparenchymal locations, which each contribute extra

volume. Furthermore, trauma may induce changes in V BLOOD asa result of disrupted autoregulation and hyperemia. The extentto which elevated CBV contributes to ICP after traumatic braininjury seems small, however, compared with edema.34

Subarachnoid hemorrhage after rupture of an intracranialaneurysm differs from other intracranial hemorrhage. Bleeding

with arterial pressure can potentially cause ICP to rise instanta-neously, and as ICP approaches the mean arterial blood pressure,

bleeding slows, but cerebral perfusion pressure is critically low.35

The cause of this rise in ICP is a combination of intraparenchy-




–2

–2 0 2 4 6 8

0 2 4 6 8

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2V (mL)

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PO

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I C P ( m m H

g )

I C P ( m m H

g )

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NORMAL ADULTPVI = 25 mL

AFTER TBIPVI = 10 mL

FIGURE 10-6 Pressure-volume curves from a normal adult ( A) andan adult with cerebral edema (B). In the pathologic state, the curve issteeper and the pressure-volume index (PVI) is greatly reduced as aresult of VOTHER. TBI, traumatic brain injury.

compliance is to plot ICP logarithmically against volume, whichgives a straight line.50 Its slope is the pressure-volume index(PVI), or the calculated volume in milliliters needed to raise ICPby a factor of 10 (Fig. 10-6A ). In normal adults, PVI is 25 to30 mL.51 When compliance is reduced by a pathologic process,PVI diminishes, and therefore small volume changes result in

much greater pressure changes. Values less than 13 mL are con-sidered clearly abnormal.52 PVI is age dependent, although

associated with patients in whom ventricular enlargementoccurred in the absence of elevated ICP and who presented withgait disturbance, dementia, and incontinence. Current guidelinesfor diagnosis and management of idiopathic normal-pressurehydrocephalus are now available.46 According to these guidelines,the lumbar pressures for idiopathic normal-pressure hydrocepha-lus range from 60 to 240 mm H2O. This range was arrived by

consensus in a meeting of experts on the basis of their experienceand what was reported in the available literature. Later, in a studyof 151 patients diagnosed with idiopathic normal-pressure hydro-cephalus, it was confirmed that the lumbar pressure measured inthese patients varied over a wide range47 (Fig. 10-5). Thus, theterm normal-pressure hydrocephalus has been questioned as pres-sures varied considerably from the so-called normal pressuredefined by Ekstedt.48 Interestingly, the median pressure found by

Marmarou47 in patients with idiopathic normal-pressure hydro-cephalus correlates well (9.0 mm Hg) with the value of thenormal resting pressure by Ekstedt (10.0 mm Hg).

Pressure-Volume Relationships

The relationship between intracranial volume and ICP is notlinear. Volume-pressure relationships can be depicted by graph-ing the response of ICP to volume added into the neural axis (seeFig. 10-3). In the normal adult, Ryder and coworkers49 showedthat this relationship describes a hyperbolic curve. Along the flatportion of the curve, increases in volume affect ICP minimallybecause compensatory mechanisms can effectively maintain ICPin a normal range. This part of the curve is called the period ofspatial compensation. As volume is added, the pressure changesper unit volume become increasingly large, and compliancelessens; this portion is called the period of spatial decompensa-tion. Above 50 mm Hg, and as ICP approaches mean arterialpressure, the curve tends to flatten again; thus, the completecurve is not hyperbolic but rather sigmoid.

The reciprocal of the slope of this curve (∆ V/ ∆P) representsthe compliance of the system, which is maximal in the period ofspatial compensation. The slope of the pressure-volume curve

rises rapidly during spatial decompensation, and therefore com-pliance falls. Another method of expressing information about

<3

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OPENING ICP DISTRIBUTION IN NPH PATIENTS

11–<13

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Median = 9.0

FIGURE 10-5 Distribution of lumbar pressure in patients with idio-pathic “normal”-pressure hydrocephalus (NPH). Pressure varied overa wide range, calling normal-pressure hydrocephalus into question.The median pressure of 9.0 mm Hg was slightly lower than the average10.0-mm Hg lumbar pressure found in patients without normal-pres-sure hydrocephalus.




normal infants have PVIs below 10 mL, and the adult PVI of25 mL is reached at around 14 years of age.

PVI can be measured clinically by infusion or withdrawal of

small boluses of fluid in the CSF space, with concomitant mea-sures of the pressure response. CSF outflow resistance can alsobe calculated from the rate decay of the pressure peak after abolus infusion. A complete description of resistance measurementtechniques is found in the report of Eklund and colleagues. 53

Methods of continuous PVI measurement have been devised withuse of multiple time-averaged small-volume pulses.54 Althoughthese methods generate less pressure perturbation, they tend tounderestimate compliance as measured with the conventionaltechnique.

The compensatory abilities of brain, blood, and CSF at anygiven point on the pressure-volume curve are dependent on theirrespective volumes, their ease of egress from the skull, and thelevel of ICP at which the interactions are occurring, coupled withthe rigidity of the skull. Although the brain occupies 80% of theintracranial space, this volume is effectively available for compen-

sation only when increases in V OTHER occur slowly. With morerapid changes, brain shifts and herniations are more likely tooccur. Although blood and CSF occupy less of the intracranialspace, their total volume can be reduced more rapidly.

These concepts become more complex, as do most models, when they are applied to clinical practice. Although short-termchanges cause movement along a single pressure-volume curve,changing intracranial dynamics can create a new pressure-volumecurve with time (Fig. 10-6B). Increases in CBV and cerebraledema are also likely to play a role in producing these dynamicpressure-volume interactions.55 Thus, knowledge of the absolutepressure coupled with some expression of the slope of the ICP

volume curve at any given time point provides a more completedescription of the stability or instability of ICP.

Effects of Elevated Intracranial PressureUnder non–steady-state conditions, failure of compensationmechanisms ultimately results in an elevated ICP, the pathologicconsequences of which can be severe. First, continued perfusionof the brain relies on a cerebral arteriovenous pressure gradient.ICP is transmitted to the compliant cerebral veins, and thereforethe cerebral perfusion pressure (CPP) is defined as the arterialinflow pressure minus ICP. If ICP increases, CPP falls; and if thelower limit of autoregulation is exhausted, CBF will begin to fall.

The autoregulatory reserve may be defined as the differencebetween the CPP at a given moment and the lower limit ofautoregulation. Considering that the lower limit of autoregula-tion is within the range of 50 to 70 mm Hg, the autoregulatoryreserve for a CPP of 90 would be 20 to 40 mm Hg. Thus, a CPPbelow the autoregulatory threshold exhausts the autoregulatoryreserve.56-60 When CPP decreases, the wall tension of reactivebrain vessels decreases, thereby increasing the transmission of thearterial pulse wave to the intracranial contents.61 Similarly, whena reduction of CPP is caused by increased ICP, brain compliancedecreases,29,62 which also serves to increase pulsatile transmission.

Taken in concert, a decrease in CPP results in an increase of bothblood pressure and ICP pulsatility. This relationship is highlypredictive for fatal outcome63 because as the ICP pulse amplitudelevels off or starts to decrease, it implies that the cerebral vesselsare no longer pressure reactive.

By use of these principles, it is clear that the correlationbetween spontaneous waves of blood pressure and ICP is depen-dent on the autoregulatory reserve. The correlation coefficientbetween changes in blood pressure and ICP is defined by Czos-nyka61 as the pressure reactivity index. An example of the use ofthe pressure reactivity index is illustrated in Figure 10-7. Exam-

ples of time-related changes of the pressure reactivity index areshown, in which the index increases from relatively low values

A

B P

[ m

m H

g ]

I C P

[ m m H

g ]

F V

[ c m / s e c ]

P R x

A B P

[ m m H g

]

I C P

[ m m H

g ]

F V

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P R x

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+1

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B 20 min

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FIGURE 10-7 Examples of the use of the pressure reactivity index toassess autoregulatory reserve and to predict patient outcome.

A, Mean arterial blood pressure (ABP), ICP, middle cerebral artery flowvelocity (FV), and pressure reactivity index (PRx) in a patient with a fatalincrease in ICP. The pressure reactivity index rises with ICP increaseand remains high. B, Comparable data from a patient experiencing aplateau wave in ICP with subsequent recovery. It is notable how thepressure reactivity index falls with recovery and reduction in ICP.(Courtesy of M. Czosnyka.)

(no association) to values approaching 1.0 (strong positive asso-ciation). These values were calculated from a period of 1-hourterminal increase in ICP from 60 to 90 mm Hg in a head-injuredpatient who died (Fig. 10-7A ). Figure 10-7B illustrates a transientchange in pressure reactivity index during the period of an ICPplateau wave with rapid recovery when ICP returned to baseline.In summary, the pressure reactivity index provides a practicalmeans of assessing the degree of autoregulation and is useful inelucidating the contribution of the cerebrovasculature to mecha-nisms causing ICP rise.

Furthermore, in many pathologic cases, autoregulation is dis-turbed so that the response curve is shifted to the right and ismore linear (Fig. 10-8). This reduces the autoregulatory reservefor any given CPP. If the autoregulatory reserve is exhausted,CBF begins to fall, which ultimately causes tissue ischemia. Isch-emia creates cytotoxic edema, which, in turn, contributes to theICP elevation and low CPP. Clearly, a vicious circle of edemaand ICP elevation can ensue if treatment attempts do not prevent

this. A marked rise in ICP that will not respond to available treat-ments is called refractory ICP.




Vital signs may also change under conditions of elevated ICP. The Cushing response, defined as arterial hypertension and bra-dycardia, arises as a result of either generalized central nervous

system ischemia or local ischemia due to pressure on the brain-stem.67 Bradycardia is possibly mediated by the vagus nerve andcan occur independently of hypertension. Abnormal respirationmay also arise,68 depending in part on the anatomic location ofany lesion. Cheyne-Stokes respiration arises from damage to thediencephalic region, and sustained hyperventilation occurs inpatients with dysfunction of the midbrain and upper pons.69 Mid-pontine lesions cause slow respiration; pontomedullary lesionsresult in ataxic respirations; upper medullary lesions cause rapid,shallow breathing; and with greater medullary involvement,ataxic breathing predominates.

Herniation Syndromes

Tissue herniation is the most serious complication of raised ICP.Central herniation and uncal herniation cause the central syn-

drome and the uncal syndrome, respectively.70

The central syn-drome displays progressive dysfunction of structures in a rostralto caudal direction. Diencephalic structures are involved early,

which may cause a change in behavior or even loss of conscious-ness. Diencephalic involvement also alters respiration, causinginterruptions of sighing, yawning, or pausing; Cheyne-Stokesrespiration may appear. Pupils become small, with a poor reactiv-ity to light. A unilateral lesion can cause contralateral hemipare-sis, with ipsilateral paratonia and decorticate responses. Withprogressive midbrain involvement, respiration becomes tachyp-neic, and the pupils fall into a midline fixed position. Internuclearophthalmoplegia may arise, and motor examination will showbilateral decerebrate posturing. As the pons becomes involved,respiration remains rapid and shallow. Motor examination revealsflaccid extremities with bilateral extensor plantar responses. Withprogressive medullary involvement, respiration slows and

becomes irregular with prolonged sighs or gasps. As hypoxiaensues, the pupils dilate, and brain death follows shortlythereafter.

In sharp contrast, the uncal syndrome often begins with aunilaterally dilated and poorly reactive pupil, which can ariseeven in the presence of a normal conscious level. The pupil willthen fully dilate with external oculomotor ophthalmoplegia. Ifmidbrain compression ensues, consciousness may be impaired,followed by contralateral decerebrate posturing. On occasion,posturing or hemiparesis may occur ipsilateral to the lesion as aresult of pressure on the contralateral cerebral peduncle on theedge of the tentorium cerebelli.71 If the uncal syndrome is allowedto progress, extensor plantar response appears bilaterally, along

with dilation of the contralateral pupil. Finally, patients willdevelop hyperpnea, midposition pupils, impaired oculovestibularresponse, and bilateral decerebrate rigidity. From this point, pro-gression is as for the central syndrome.

Other compression and herniation syndromes may arise,including unilateral hemiparesis and hemianesthesia with com-pression of cortical structures or compression of the anteriorcerebral artery with subfalcine herniation of the cingulate gyruscausing contralateral leg weakness. Although no less distressingfor the patient, these symptoms represent a much lesser emer-gency than either the central or uncal syndrome does.

INTRACRANIAL PRESSURE MONITORINGSeveral published clinical trials show that monitoring of ICP,under situations in which ICP may be high, either facilitatesoutcome or promotes aggressive management.72-74 There isstrong clinical evidence that careful control of ICP is important,75

and maintaining CPP under many different pathologic circum-stances is of benefit for outcome.60 An understanding of the

A second problem with increased ICP arises from the genera-tion of pressure gradients.64,65 CSF will conduct the pressuregenerated by an increased volume in one region of the brain toothers. There are specific anatomic sites where such pressuregradients may cause movement of brain tissue into an abnormalanatomic location—so-called herniation. Several types of hernia-tion have been described, including downward transtentorial(central and uncal), subfalcine, upward transtentorial, and

transforaminal.66 Each syndrome has a characteristic clinicalcorrelate.

Anatomically, in central transtentorial herniation, downwardshift of the hemisphere and basal ganglia compresses and dis-places the diencephalon through the tentorial incisura. Subse-quent displacement of the brainstem will stretch the paramedianbranches of the basilar artery, which, in turn, will contribute tothe marked diencephalon and brainstem dysfunction. In uncalherniation, the uncus and hippocampal gyrus shift medially intothe tentorial notch, which distorts the brainstem and createssignificant dysfunction. Subfalcine herniation of the cingulategyrus is caused by expansion of one hemisphere causing a move-ment of the cingulate gyrus under the falx cerebri. Cingulateherniation may compress the internal cerebral veins or the ipsi-lateral anterior cerebral artery. Lesions in the posterior fossadiffer slightly in that they may cause upward transtentorial her-niation as well as downward transforaminal herniation.

Symptoms and Signs of Elevated

Intracranial Pressure The degree of effect of a given ICP depends greatly on the natureand anatomic location of the underlying pathologic condition.

The cardinal symptoms and signs of raised ICP include headache, vomiting, and papilledema. Vomiting without any associatednausea is especially suggestive of intracranial disease. Varyingdegrees of cranial nerve palsies may arise as a result of pressureon brainstem nuclei (particularly abducens palsies). Papilledemais a reliable and objective measure of raised ICP, with goodspecificity. However, its sensitivity is observer dependent, and

symptoms suggestive of intracranial disease in the absence ofpapilledema should not be ignored.

CEREBRAL BLOOD FLOW IN RESPONSE TOCHANGES IN CEREBRAL PERFUSION PRESSURE

CPP (mm Hg)

C B F ( m L / 1 0 0 g / m i n )

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FIGURE 10-8 Cerebral autoregulatory curves. Normal autoregula-tion maintains cerebral blood flow across a range of mean arterialblood pressure. Disturbed autoregulation causes a shift of the curve

to the right and introduces a more linear component (i.e., cerebralblood flow is less stable with rising mean arterial blood pressure). Ifautoregulation is completely abolished, cerebral blood flow rises lin-early with mean arterial blood pressure.

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