anatomia medula espinal

SPINAL CORD ANATOMY,LOCALIZATION, ANDOVERVIEW OF SPINALCORD SYNDROMESGregory Gruener, Jose Biller

ABSTRACTSpinal cord syndromes are “unique” clinical presentations that localize lesions tothe spinal cord by their pattern of anatomic dysfunction while implying their underlyingetiology. Recognizing these patterns and their significance is best accomplished byrelearning and appreciating the relevant anatomy and relationships, which are themajor focus of this review. This clinical-anatomic background will provide the frame-work for the clinical topics that follow in this issue.

ANATOMY OF THE SPINALCORD

Relationship to the VertebralLevels and SpineThe typical vertebra consists of a co-lumnar body with a larger transversethan anterior-posterior diameter andserving as the primary support for thespine. The vertebral arch extends fromthe body, forming a protective enclo-sure, and consists of a pedicle on ei-ther side that unites posteriorlythrough the two laminae. Three pro-cesses arise from the vertebral arch,laterally the transverse and posteriorlythe spinous, serving as the attachmentsite for muscles (Figure 1-1). Fourseparate articular processes, a superiorpair extending cranially and an infe-rior pair extending caudally, serve todirect or limit movement to specificdirections by articulating with the ver-tebra above and below (Figure 1-2).

A notch in the inferior aspect of thepedicle will contribute to the boundaryof the intervertebral foramen when ad-jacent vertebrae are articulated andthrough which the spinal nerve and in-tervertebral vessels will pass.

An intervertebral disc is interposedbetween each vertebral body and con-sists of alternating, crisscrossing bandsof fibrous connective tissue, the annu-lus fibrosus, which surround a gelati-nouslike core, nucleus pulposus. Thevertebral discs will contribute 25% of theheight of the vertebral column. Severalligaments and fibrous attachments ofmuscles help to bind together and en-close the vertebral column. The mostprominent are the anterior longitudinal(along the anterior aspect of the bodies),the posterior longitudinal (along theirposterior aspect), the ligamentum fla-vum (posterior wall of spinal canal), andthe interspinous ligament.

The fused periosteum of the cra-

Relationship Disclosure: Dr Gruener has received personal compensation for speaking engagements withMedical Education Resources, Inc. Dr Biller has nothing to disclose.Unlabeled Use of Products/Investigational Use Disclosure: Drs Gruener and Biller have nothing todisclose.

KEY POINT:

� A notch in theinferior aspect ofthe pedicle willcontribute to theboundary of theintervertebralforamen whenadjacentvertebrae arearticulated andthrough whichthe spinal nerveandintervertebralvessels will pass.

Copyright © 2008, American Academy of Neurology. All rights reserved.

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nium and meningeal layer of the duramatter will separate caudal to the fo-ramen magnum, forming an anatomic

space, epidural space, which extendsthe length of the spinal column (Fig-ure 1-3). Within this space reside fatty

FIGURE 1-1 Functions of the constituent parts of a vertebra.

Reprinted with permission from Grant JCB. An atlas of anatomy. 6th ed. Baltimore: Williams &Wilkins, 1972.

FIGURE 1-2 Lateral view of a lumbar (second) vertebra.

Sup � superior; Inf � inferior.

Modified with permission from Grant JCB. An atlas of anatomy. 6th ed. Baltimore: Williams &Wilkins, 1972.

‹ SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

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Continuum: Lifelong Learning Neurol 2008;14(3)

tissue and the vertebral venous plexus.The separation of these fused layers ofconnective tissue allows the vertebralcolumn to move separately relative tothe dural sac that surrounds the spinalcord and roots. The dorsal and ventralroots will enter a dural sleeve at thelevel of their intervertebral foramina,lateral to the dorsal spinal ganglia, fus-ing to form the spinal nerves. A layerof pia mater surrounds the surface ofthe spinal cord, and between it and theinner layer of the arachnoid tissue isthe subarachnoid space. Between suc-cessive nerve roots, a bandlike exten-sion of the pia mater will arise fromthe surface of the spinal cord, dentic-ulate ligament, attaching to the duraand serving to anchor the spinal cord(Figure 1-4). The ventral nerve rootslie anterior and the dorsal nerve rootsposterior to this ligament.

The spinal cord is cylindrical inshape, but flattened dorsoventrally. Itis widest at the cervical enlargement,and a second enlargement occurs inthe lumbosacral level of the cord, bothreflecting the innervation levels of thelimbs. At birth the spinal cord typicallyextends to the lower border of L3. Byadulthood its tip is usually at the L1-2vertebral disk level but can end at T12or descend to the lower border of theL2 vertebrae.

Each segment of the spinal cordusually has a set of dorsal (sensory)and ventral (motor) rootlets thatemerge and join together to form theircorresponding root; dorsal roots havetheir corresponding ganglia (dorsalroot ganglia). The dorsal and ventralroots will fuse to form the spinal nerveas it exits from the spinal canal. Thespinal nerves then divide into individ-ual branches. There are usually 31pairs of spinal nerves: eight cervical,12 thoracic, five lumbar, five sacral,and usually one coccygeal (Figure1-5). The first pair of spinal nerves willexit between the skull and the atlas(C1), the next six above their respec-

tively numbered vertebrae (C2through C7), but C8 above the T1 ver-tebrae. The remaining spinal nerveswill exit below the vertebrae of thecorresponding number. The spinalnerves will have a dorsal root ganglionusually located within the interverte-bral foramen. C1 lacks a cutaneoussensory dermatome. Below the L1 ver-tebra, lumbar and sacral spinal nerveroots need to descend in order toreach their point of exit; this collectionof spinal roots is called the caudaequina. The cord will terminate in athin-walled sac covered by pia mater,the filum terminale, which fuses withthe periosteum of the dorsal surface ofthe coccyx.

The gray matter of the spinal cordcan be divided into a posterior column

KEY POINT:

� At birth thespinal cordtypically extendsto the lowerborder of L3. Byadulthood its tipis usually at theL1-2 vertebraldisk level butcan end at T12or descend tothe lower borderof the L2vertebrae.

FIGURE 1-3 Spaces associated with the spinal meninges.

Modified with permission from Fitzgerald MJ, Gruener G,Mtui E. Clinical neuroanatomy and neuroscience. 5th ed.London: Saunders, 2007:49. Copyright © 2007, Elsevier.

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(or horn), a lateral column, and ananterior column (or horn) that respec-tively “divide” the adjacent white mat-ter into a posterior, lateral, and ante-rior funiculus. At the junctionbetween white and gray matter areshort ascending and descending axonsthat arise from small neurons withinthe spinal cord gray matter and com-prise the intrinsic or intersegmental re-flex pathways, proprius bundles (orsystem) or fasciculi proprii and arenamed by their location. While theposterior funiculi primarily consist ofascending sensory fibers, they alsocontain their descending collateral fi-bers, which serve to further integrateintrinsic spinal reflexes and form theirown distinct, but small, fasciculi.

Within the gray matter of the spi-nal cord cell groups can be identified(right portion of Figure 1-6), withthose in the posterior horn participat-ing in sensory pathways and those inthe intermediate and anterior hornsserving motor functions. In addition,layers of synaptic inputs within thespinal cord have also been identified.These are called Rexed laminae andare labeled I to X (left side of Figure1-6). Those within the posterior horn,

laminae I through V, more clearlydemonstrate a laminated appearance.

Major Ascending TractsThe diagrammatic representation ofboth ascending and descending tractswithin the spinal cord reflects a levelof certainty that, while useful for com-prehension, oversimplifies a morecomplex anatomic distribution and an-atomic variations that likely exist(Nathan et al, 1990; Nathan et al, 1996;Nathan et al, 2001). Indeed, the con-cept of a tract as a homogenous groupof fibers is also an oversimplification.Despite their shortcomings, however,such generalizations have proven tobe clinically useful.

The sensory pathways and tractswe will first review are responsible fortransmitting sensory information thatis perceived (conscious) as well asnonconscious sensation. The dorsalroot ganglia contribute nerve fibersthat at the dorsal root entry zone willfurther segregate into a medial groupof large-diameter fibers, which will en-ter the posterior funiculi of the spinalcord, and a lateral group of small-di-ameter myelinated and unmyelinatedfibers. This segregation is modality

KEY POINT:

� The first pair ofspinal nerveroots will exitbetween theskull and theatlas (C1), thenext six abovetheir respectivelynumberedvertebrae (C2through C7), butC8 above the T1vertebrae. Theremaining spinalnerves will exitbelow thevertebrae of thecorrespondingnumber.

FIGURE 1-4 Relationships of the sixth cervical spinal nerve.

Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy andneuroscience. 5th ed. London: Saunders, 2007:171. Copyright © 2007, Elsevier.


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specific and will give rise to the majorascending tracts within the spinal cord(Figure 1-7). This lateral group of fi-bers will divide into short ascendingand descending branches within thetract of Lissauer and predominantlysynapse on neurons within laminae Iand II of the posterior horn.

The posterior column–medial lem-niscal pathway receives its input fromthe largest group of sensory receptors(neuromuscular spindles and Golgitendon organs) entering through themedial portion of the dorsal root entryzone. These fibers form a laminationwithin the posterior column, and mostmedial are those originating from thelower extremity and trunk, fasciculusgracilis, carrying sensory informationfrom the lower extremity; and laterallyis the fasciculus cuneatus, carryingsimilar sensory information from theupper trunk and limb (Figure 1-8). Asthese fibers enter the posterior columnthey bifurcate and one branch ascendsto the medulla where it will synapseonto its second-order neuron withinthe nucleus gracilis or cuneatus.Those neurons will then project acrossthe midline in the sensory decussation,continuing their ascent to the thalamusas the medial lemniscus. The third-order neurons of this pathway willthen arise from the thalamus andproject to the somatic sensory cortex.The other branch of that initial bifur-cation of entering fibers will synapsewithin the posterior gray horn laminaeII, III, and IV at various levels (theascending branch also gives off collat-erals to the dorsal gray horn). The tra-ditional functions of this system arebelieved to be relaying conscious pro-prioception as well as discriminativetouch. Yet, its role in supporting themotor cortex as it carries out its intri-cate and precise digital movementsmay better or more accurately charac-terize its function and importance(Davidoff, 1989).

The other major conscious sensory

pathway is the anterolateral spinotha-lamic tract (Figure 1-9). This tractarises from neurons in laminae I, II, IV,and V that receive excitatory as well asinhibitory input from neurons withinthe substantia gelatinosa (lamina II).The axons that arise from those neu-rons cross in the anterior commissureof the spinal cord and arrange them-selves in the anterolateral locationwithin those spinal cord funiculi.There are two divisions, and the mostanterior is the anterior spinothalamictract, which has a somatotopic organi-zation and mediates the sensory mo-

FIGURE 1-5 Vertebral column, spinal cord, and nerverelationships.

Modified with permission from Moore KL, Dalley AF.Clinically oriented anatomy. Philadelphia: LippincottWilliam & Wilkins, 1999:478.

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dality of touch and pressure. The lat-eral spinothalamic tract is lateral andposterior, somatotopically as well as

modality arranged with cervical repre-sentation most medial and sacral mostlateral; pain, tickle, and itch sensorymodalities are more peripheral whiletemperature is more medially repre-sented within this tract. These tractsascend, merge within the brainstem asthe spinal lemniscus, are joined laterby the trigeminal lemniscus (afferentsfrom the head), and together terminatewithin the thalamus. Their third-orderneurons will also project to the so-matic sensory cortex. The spinoreticu-lar tract arises from neurons withinlaminae V to VII and accompanies thespinothalamic pathway, both as acrossed and uncrossed tract, terminat-ing within the brainstem. It serves asan arousal system for the cerebral cor-tex (through the reticular activatingsystem), and it helps to interpret thenature of a stimulus (pleasurable ornot).

The spinocerebellar tracts providenonconscious proprioception (Figure1-8). Fasciculus gracilis collaterals pro-vide information from lower limb pri-mary afferents (especially muscle spin-dle), synapse upon the posteriorthoracic nucleus in lamina VII (ex-tends from T1 through L1 spinal cordlevels, previously called the dorsal nu-cleus or Clarke column), and give riseto the posterior spinocerebellar tract.The tract ascends and reaches the cer-ebellum through the inferior cerebel-lar peduncle. A similar group of affer-ents from the fasciculus cuneatusprovides information from the upperlimb and synapses on the accessorycuneate nucleus, which gives rise tothe cuneocerebellar tract. It alsoreaches the cerebellum through the in-ferior cerebellar peduncle. The follow-ing two spinocerebellar tracts will pro-vide information about the state ofinternuncial function in regard to spi-nal cord reflexes and arise from theintermediate gray matter of the spinalcord. (1) The anterior spinocerebellartract arises from the lower spinal cord

FIGURE 1-6 Spinal cord laminae and cell groups(midthoracic level).

Reprinted with permission from Fitzgerald MJ, GruenerG, Mtui E. Clinical neuroanatomy and neuroscience. 5thed. London: Saunders, 2007:182. Copyright © 2007,Elsevier.

FIGURE 1-7 Primary afferent neuron targets in theposterior horn.



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and will initially cross, ascend to thesuperior cerebellar peduncle, crossagain to its side of origin, and termi-nate within the cerebellum. (2) Fromthe upper half of the spinal cord therostral spinocerebellar tract will as-cend and, through the inferior cerebel-lar peduncle, enter the cerebellum.

The remaining tracts to be consid-ered include the spinotectal tract,which ends in the superior colliculus,runs with the spinothalamic tract, andbrings somatic sensory information tothe superior colliculus. The spinooli-vary tract projects to the inferior oli-vary nucleus and through its effects onthe contralateral cerebellar cortex willmodify motor activity.

Major Descending TractsThe motor cell types within the ante-rior gray horns are of two types: (1)Alpha motor neurons (physiologicallydefined as tonic or phasic in regard tothe physiologic/functional type ofmuscle fibers they innervate) supplythe extrafusal skeletal muscle fibers,and (2) gamma motor neurons supplythe intrafusal muscle fibers of neuro-muscular spindles. The motor unitcomprises an individual alpha motorneuron, its axon, and all the musclefibers (varying from a few to hun-dreds, dependent on the precision ofthe movement) it will subsequently in-nervate. Recurrent axons of alpha mo-tor neurons excite inhibitory internun-cial neurons, Renshaw cells, whichserve to inhibit their own firing (recur-rent inhibition). At each segmentallevel of the spinal cord, however, al-pha motor neurons also receive nu-merous inhibitory (usually on theirsoma) as well as excitatory (throughsynapses on their dendritic trees) in-puts. These inputs arrive from bothsupraspinal pathways as well asthrough the propriospinal neurons (lo-cal) and their pathways. Most of thesefibers and inputs will exert an inhibi-tory effect on alpha motor neurons. If

those effects are abolished by a cordlesion, the disproportionately stronginfluence of the spinal intrinsic circuitswill lead to the clinical phenomenonof spasticity.

Figure 1-10 demonstrates the co-lumnar organization of motor neuronsinto groups that then innervate mus-cles with similar function. Those mostmedial innervate the axial muscula-ture, and moving traversely throughthose groups of neurons, they alsomove from the innervation of proximalto distal limb muscles and finally to theintrinsic muscles of the hand or foot.Another result of this neuronal organi-

FIGURE 1-8 Ascending pathways (upper cervical level).

GF � gracile fasciculus; CF� cuneatefasciculus; PLT � posterolateral tract;

PSCT � posterior spinocerebellar tract; RSCT � rostralspinocerebellar tract; LSTT � lateral spinothalamic tract;ASCT � anterior spinothalamic tract; SOT � spinoolivarytract; ASTT � anterior spinothalamic tract; ST �spinotectal tract; SRT � spinoreticular tract.

Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinicalneuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:187.Copyright © 2007, Elsevier.

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zation is alpha neurons innervating ex-tensor muscles lying ventral or anteriorto those that innervate flexor muscles.Dysfunction of these neurons results inthe clinical features of weakness, atro-phy, and fasciculations, as well asareflexia when their loss is marked.

The long descending tracts (corti-cospinal, reticulospinal, tectospinal,vestibulospinal, raphespinal) andaminergic and autonomic pathwayswill terminate on interneurons, whichinfluence alpha and gamma motorneuron function. The rubrospinal tractis small and lies anterior to the lateralcorticospinal; in humans its role is un-clear. Similar to sensory pathways, thediscrete locations indicated within theaccompanying diagrams are used assimplifications and conceal a morecomplex and variable distribution ofthese pathways that explains the dis-crepancy at times encountered be-tween clinical findings and visualizedanatomic lesions.

The majority of fibers that give riseto the corticospinal tract have their or-igin in primary motor cortex (perhaps50%), but supplementary motor cortexand premotor cortex, as well as so-matic sensory cortex, also contribute.Some of these projections will end onbrainstem nuclei (corticobulbar orcorticonuclear), while those from sen-sory cortex project onto sensory nucleiin the brainstem and spinal cord thatmodulate their transmission of sensoryinformation. Those fibers that reachthe medulla form the pyramids, visibleon its ventral surface. Seventy percentto 90% of these fibers cross the ventralmidline in the pyramidal decussation,giving rise to the lateral corticospinaltract within the spinal cord. A soma-totopic organization results with fibersdestined for the sacral area most lateraland those to the cervical, medial (Fig-ure 1-11). The remaining fibers de-scend uncrossed either within the lat-eral corticospinal tract (uncrossed

KEY POINTS:

� The dorsal rootgangliacontribute nervefibers that willfurthersegregate at thedorsal root entryzone into amedial group oflarge-diameterfibers that willenter theposterior funiculiof the spinalcord and alateral group ofsmall-diametermyelinated andunmyelinatedfibers.

� The traditionalfunctions of theposteriorcolumn–mediallemniscal systemare believed torelay consciousproprioceptionand to mediatediscriminativetouch. Yet, itsrole insupporting themotor cortex asit carries out itsintricate andprecise digitalmovements maybetter or moreaccuratelycharacterize itsfunction andimportance.

FIGURE 1-9 Spinothalamic pathways (sensory modalities, upper cervical level).

Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy andneuroscience. 5th ed. London: Saunders, 2007:187. Copyright © 2007, Elsevier.


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lateral corticospinal tract) or the ma-jority adjacent to the anterior medianfissure as the anterior corticospinaltract to innervate paraspinal and axialmuscles. At the appropriate level fi-bers will cross through the anteriorwhite commissure to provide theircontralateral innervation.

All corticospinal neurons appear ex-citatory with glutamate as their neuro-transmitter. The corticospinal tract inner-vates not only alpha and gamma motorneurons, but also Renshaw cells, excita-tory and inhibitory internuncials, and,through presynaptic inhibition, sup-presses some sensory transmissionwithin the spinothalamic tract in volun-tary movement. The proximity of thelateral corticospinal tract to the motorneurons that innervate distal limb mus-cles supports its role in facilitating theperformance of skilled movements andthe belief that an isolated pyramidal le-sion “only” results in flaccid paralysisand loss of skilled motor function of thedistal limb muscles.

The reticulospinal tracts, throughshared internuncials with the cortico-spinal tract, act upon motor neurons ofaxial as well as proximal limb muscles.They are considered part of the extra-pyramidal system of motor control(with the lateral vestibulospinal andtectospinal tracts) and are involved inlocomotion as well as posture. Themedullary reticulospinal tract is be-lieved to act on flexor motor neuronsand the pontine reticulospinal tract onextensor motor neurons.

The tectospinal tract arises frombrainstem tectum and orients the headto visual or auditory stimulation. Thelateral vestibulospinal tract originatesin the lateral vestibular nucleus (ofDeiters) and helps in maintaining thecenter of gravity for the body. Theraphespinal tract originates from itsnucleus in the medulla and modulatessensory transmission from its positionwithin the Lissauer tract. The aminer-gic pathways arise from their cellgroups within the pons and medulla

KEY POINT:

� The lateralspinothalamictract issomatotopically,as well asmodality,arranged withcervicalrepresentationmost anteriorand sacral mostposterior. Pain,tickle, and itchsensorymodalities aremore peripheralwhiletemperature ismore mediallyrepresentedwithin this tract.

FIGURE 1-10 Anterior gray horn cell column and somatotopic organization.

Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London:Saunders, 2007:192. Copyright © 2007, Elsevier.

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and have inhibitory effects on sensoryneurons and facilitatory effects on mo-tor neurons through a widespread dis-tribution in the spinal cord gray mat-ter. The central autonomic pathwaysarise from the hypothalamus as well asassociated brainstem nuclei, terminat-ing on neurons within the intermedio-lateral cell columns.

Vascular Supply of the SpinalCordThe arterial blood supply to the spinalcord comprises three longitudinallyoriented vessels as well as contribu-tions from numerous radicular vessels(Bowen and Pattany, 1999). A rich vas-cular plexus (arterial or pia vasoco-rona or plexus) arises from anastomo-ses between these vessels along thesurface of the spinal cord and fromwhich medullary vessels penetrateinto both the white and gray matter.These penetrating vessels are end ar-teries and do not anastomose further.

The anterior spinal artery arisesfrom the union of the anterior spinalbranches of the vertebral artery anddescends within the anterior medianfissure of the spinal cord down to theconus medullaris. Its largest caliber isat the lumbosacral area, and smallestat the thoracic area, which is also con-sidered its watershed area. The twoposterior spinal arteries also originatefrom the vertebral arteries but descendalong the line of attachment of thedorsal nerve roots, posterolateral sul-cus, on either side. At the conus med-ullaris, the anterior and posterior spi-nal arteries communicate thoughanastomotic branches (Figure 1-12).

Thirty-one pairs of small radiculararteries enter every intervertebral fora-men supplying their correspondingnerve roots. Some of these are largerand also supply the spinal cord, ra-diculomedullary branches. There maybe six to 10 such arteries, and throughtheir anterior radicular branch theycontribute to the anterior spinal artery.The cervical and first two thoracic seg-ments receive these arteries frombranches of the vertebral and thyro-cervical trunk, T3 to T7 spinal cordusually from an intercostal artery, andthe remainder of the spinal cord re-ceives the largest and most constantartery of Adamkiewicz (arises from aleft-sided intercostal or lumbar artery,usually at the T9 through L2 spinelevel), which supplies the lumbar en-largement and conus medullaris. Theposterior spinal arteries receive contri-butions from 12 to 16 posterior radiculararteries, including a radicular branchfrom the artery of Adamkiewicz.

The intrinsic arterial supply of thespinal cord consists of a centripetal(posterior spinal arteries and the an-terolateral plexuses) and a centrifugal(anterior sulcal arteries) system (Fig-ure 1-13). The centripetal system isformed from radial arteries directed in-ward and supplying the posteriorwhite columns, and through shorter

KEY POINT:

� The longdescendingtracts(corticospinal,reticulospinal,tectospinal,vestibulospinal,raphespinal),and aminergicand autonomicpathways willterminate oninterneurons,which theninfluence alphaand gammamotor neuronfunction.

FIGURE 1-11 Descending pathways (upper cervical level).



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radial penetrating vessels the periph-eral rim of perhaps one-third to one-half of the spinal cord. The centrifugalsystem arises from sulcal arteries of theanterior spinal artery that pass backinto the anterior medial sulcus andthen turn right or left to supply theadjacent gray and white matter. Smallerbranches from the anterior spinal artery

also contribute to the arterial vasoco-rona that envelops the spinal cord andthrough their short penetrating arteriessupply the anterior rim of the spinalcord. In general, the centrifugal system(anterior spinal artery) supplies the an-terior two-thirds of the spinal cord.

Analogous to the arterial bloodsupply, venous drainage of the spinal

KEY POINTS:

� The majority offibers that giverise to thecorticospinal tracthave their originin primary motorcortex, butsupplementarymotor cortex andpremotor cortex,as well assomatic sensorycortex, alsocontribute.

� Within thepyramidaldecussation,70% to 90% offibers willdecussate andgive rise to thelateralcorticospinaltract. Asomatotopicorganizationdevelops withfibers to thesacral area mostlateral and thoseto the cervical,medial.

� Thirty-one pairsof smallradicular arteriesenter everyintervertebralforamensupplying theircorrespondingnerve roots.Some of theseare larger andalso supply thespinal cord,(radiculomedullarybranches). Theremay be six to 10such arteries,and throughtheir anteriorradicular branchthey contributeto the anteriorspinal artery.

FIGURE 1-12 Arterial supply of the spinal cord.

Reprinted with permission from Moore KL, Dalley AF. Clinically oriented anatomy. Philadelphia:Lippincott William & Wilkins, 1999:487.

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cord also involves a longitudinal sys-tem of veins, the larger posterior spinalvein and the anterior. Through a cir-cumferentially arranged venous anas-tomosis, coronal venous plexus, withinthe pia mater on the spinal cord’s sur-face, they are connected (Figure1-14). The anterior spinal vein willcommunicate superiorly with the ve-nous system of the brainstem and in-feriorly end at the dural sac in thesacrum. The posterior spinal veincommunicates with radicular veins atthe cervical level and extends down tothe conus medullaris. At each spinalcord segment small radicular veinsdrain the nerve roots, but at some lev-els larger veins, medullary veins, willarise from the anterior median spinal

FIGURE 1-13 Arterial supply of a spinal cord segment.

Reprinted with permission from Haerer AF. DeJong’s: the neurologic examination. 5th ed. Philadelphia: Lippincott Company,1992:582.

FIGURE 1-14 Venous drainage of a spinal cord segment.

Krauss WE. Vascular anatomy of the spinalcord. Neurosurg Clin N Am 1999;10(1):9–15.

Reprinted with permission from Mayo Foundation for Medical Educationand Research. All rights reserved.


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vein. There are approximately 10 to 20anterior veins and a similar number ofposterior medullary veins, asymmetricin location and not concomitant withthe medullary arteries. The largest arein the lumbar region: the great ante-rior medullary vein (usually accompa-nying the nerve roots between T11and L3) and the great posterior medul-lary vein usually at L1 or 2. The pos-terior half of the spinal cord will draininto the posterior and the anterior halfinto the anterior medullary veins.These medullary veins follow andpenetrate the dura with the nerve rootand in the intervertebral foramen willunite with the radicular veins, internaland external vertebral plexus to formthe intervertebral vein that drains bloodfrom the spine and spinal cord. Prior totheir exit from the dura matter, theseveins are valveless (Gillilan, 1970;Krauss, 1999).

The cervical intervertebral veinswill drain into the deep cervical andvertebral veins and will empty into thesuperior vena cava through the bra-chiocephalic and subclavian vein. Atthe thoracic cord they will connect

with the intercostal veins and then viathe azygos and hemiazygous veins willenter the superior vena cava. The re-mainder of the venous drainage fromthe spinal cord can follow a similarpathway or, through the azygous andhemiazygous veins, enter the commoniliac veins and then the inferior venacava.

Within the spinal canal’s epiduralspace is also a longitudinally and cir-

FIGURE 1-15 Vertebral venous plexus.

Modified with permission from Moore KL, Dalley AF.Clinically oriented anatomy. Philadelphia: LippincottWilliam & Wilkins, 1999:466.

FIGURE 1-16 Cord transection (modalities involved).

Reprinted with permission from Souayah N, Khella S. Neurology examination & board review.New York: McGraw Hill, 2005:44.

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cumferentially arranged anastomosisof valveless veins, the internal venousplexus (anterior and posterior) (Figure1-15). It communicates with the spinalcord through the medullary and radicu-lar veins, and vertebral body through abasivertebral vein, but it also drains to aseparate plexus that surrounds the ver-tebra, the external vertebral plexus (an-terior and posterior divisions). Throughthe previously mentioned routes, it willeventually empty into the superior orinferior vena cava.

SPINAL CORD SYNDROMES

A syndrome (symptom complex) rep-resents a complex of signs and symp-toms that appear in combination andpresent as a clinical picture. It mayhave a specific cause, disease, or in-herited abnormality, but this is not arequirement and at times has resultedin some confusion in the use and di-agnostic significance of the term. Someof the reported etiologies for the respec-tive syndromes are listed in Table 1-1.

TABLE 1-1 Spinal Cord Syndromes and Their Etiologies (Representative Examples)

Etiology Complete CordTransection

Brown-SequardSyndrome

Anterior Spinal ArterySyndrome

Vascular *Aortic dissection,*vasculitis, *atherosclerosisof the aorta

Inflammatory orinfectious

*Postinfectious,*multiple sclerosis,*postvaccinal

Traumatic Traumatic spineinjury, herniated disc

*Traumaticspine injury

Iatrogenic ortoxin

Epidural hematoma(anticoagulants)

Postoperative spine, aortaor thoracic surgery,postoperative spinalarteriovenousmalformation surgery,decompression injury

Metabolic

Endocrine

Neoplastic Tumor, paraneoplastic Intramedullarytumors

Degenerative orHereditary

Cervical spondylosis

HTLV-I � human T-cell leukemia virus I; HAM � human T-cell lymphotropic virus–associated myelopathy.

*“Classic” or most common associated etiologies.


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Complete Cord TransectionA complete cord transection disruptsthe sensory tracts ascending from be-low the level of the lesion and thedescending tracts from above (Figure1-16). However, as many such lesionsare incomplete, the clinical deficit willreflect the extent of the injury. Onphysical examination a sensory levelwill be detected, using pinprick loss,and is the most valuable finding thatidentifies the spinal cord as the site ofthe lesion. While sensory loss is ex-pected to involve all modalities below

the level of the lesion, the actual spinalcord level involved may be higher andthe presence of radicular pain or seg-mental paresthesias may serve as amore accurate localizer. Radiation ofpain may also occur, and with cervicalspinal cord lesions pain can radiate intothe arms, thoracic into the chest or ab-domen, and lumbar or sacral spinal cordinto the legs. Careful examination foroverlying vertebral spine tendernessmay suggest an underlying destructiveprocess such as a neoplasm or infectionas the etiology, and pain that lessens

KEY POINT:

� In cordtransection, themost valuablefinding thatidentifies thespinal cord as thesite of the lesion ispinprick sensation.The actual spinalcord level involvedmay be higher;the presence ofradicular pain orsegmentalparesthesias mayserve as a moreaccurate localizer.

PosterolateralColumn Syndrome

Central Lesion PosteriorColumnSyndrome

Anterior HornCell Syndrome

CombinedAnteriorHorn CellPyramidalSyndrome

HIV HTLV-1 (HTLV–associated myelopathy,HAM, or tropicalspastic paraplegia)

*Neurosyphilis Poliomyelitis,West Nile virus

HTLV-1

Late sequelae ofspinal cord injury

Epidural spinalcord compression

Nitrous oxidemyeloneuropathy

Postradiation

*Vitamin B12 deficiency*Copper deficiencymyeloneuropathy

Hexosaminidasedeficiency

Intramedullary spinalcord tumors

Cervical spondylosis *Syringomyelia *Spinal muscularatrophies(hereditary motorneuropathies)

*Amyotrophiclateral sclerosis

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with sitting or standing is suggestive of amalignancy. While further historical de-tails may be helpful, laboratory and ra-diologic studies are necessary to moredefinitively identify an etiology.

Weakness, either paraplegia or tet-raplegia, occurs below the level of thelesion, owing to the interruption of thedescending corticospinal tracts. Ini-tially, the paralysis may be flaccid andareflexive because of spinal shock, buteventually, hypertonic, hyperreflexiveparaplegia or tetraplegia occurs withbilateral extensor toe signs, loss of su-perficial abdominal and cremastericreflexes, and extensor and flexorspasms (Adams and Hicks, 2005). Atthe level of the lesion lower motorneuron signs (paresis, atrophy, fas-ciculations, and areflexia) in a seg-mental distribution and reflectingdamage to the local anterior horn cellsor their ventral roots may be demon-strated. These lower motor neuronsigns may be quite subtle in thoraciclesions but can localize a lesion to aspecific spinal cord level. Urinary andrectal sphincter dysfunction with in-continence, sexual dysfunction, andsigns of autonomic dysfunction such

as anhidrosis, trophic skin changes,impaired temperature control, and va-somotor instability below the level oflesion can also be demonstrated(Cases 1-1 and 1-2).

Brown-Sequard SyndromeA hemisection of the spinal cord re-sults in this characteristic syndrome(Tattersall and Turner, 2000) (Figure1-17). Loss of pain and temperaturesensation occurs contralateral to theside of injury due to interruption of thecrossed spinothalamic tract, but usu-ally a clinical sensory level is one ortwo segments below the level of thelesion, reflecting the ascending natureof this crossing tract (Nathan et al,2001). Below the site of the lesionthere is ipsilateral loss of propriocep-tive function due to interruption of theascending fibers of the posterior col-umns, but such modalities of sensationmay also arise from within the spino-cerebellar tracts as well (Davidoff,1989). Ipsilateral weakness below thelesion reflects the interruption of thedescending corticospinal tract. In aslowly progressing lesion hyperre-flexia and an extensor toe sign will beelicitable, while in an acute lesionthose findings may initially be absent.Damage to the ventral roots or anteriorhorn cells results in segmental lowermotor neuron findings at the level ofthe lesion, but these are clinically dif-ficult to identify in thoracic spinal cordlesions. Finally, if spinal root irritationoccurs, radicular pain, again at the siteand side of the lesion, may be experi-enced and more clearly define the spi-nal cord level.

Anterior Spinal ArterySyndromeThe vascular nature of this syndromeis manifested in its abrupt onset withthe deficit occurring within minutes orhours from its initiation (Novy et al,2006). Clinically the syndrome pre-sents with back or neck pain and at

FIGURE 1-17 Hemisection of the cord (Brown-Sequardsyndrome).

Reprinted with permission from Souayah N, Khella S.Neurology examination & board review. New York:McGraw Hill, 2005:46.


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times in a radicular pattern, usuallyfollowed by a flaccid paraplegia andless commonly tetraplegia. Urinaryand bowel incontinence are usuallypresent. A sensory level to tempera-ture and pinprick is found that reflectsthe involvement of the spinothalamictracts bilaterally, but posterior columnmodalities of sensation remain rela-tively intact (Figure 1-18). Althoughthe thoracic spinal cord may be ananatomic watershed zone with respectto regional blood supply (Figure1-19), the lumbosacral cord neuronsappear to be more susceptible to isch-emia (Duggal and Lach, 2002). Theinitial motor presentation progressesfrom a flaccid paraplegia to one ofspasticity with hyperreflexia and Bab-inski signs (Case 1-3).

Central LesionsIn this and in the syndromes discussedbelow, the underlying pathologic pro-cess is usually an insidious one, and thefeatures of the disease develop over anextended period of time. When fully de-veloped, the specific syndrome is moreclearly recognized, but early during theprocess features may be incomplete,leading to difficulty and a delay in rec-ognizing the syndrome.

This syndrome results from a patho-logic process in and around the centralcanal, initially involving those tracts thatcross through the gray matter (anteriorand lateral spinothalamic tracts) (Figure1-22). The resulting sensory impairment istermed a dissociated sensory loss (loss ofpain and temperature sensation with pres-ervation of position, vibration, and touch).The typical site of involvement in the cer-vical spinal cord and theparticular sensorymodalities initially involved result in a clin-ical presentation in which sensory loss oc-curs in a vest- or shawl-like pattern overthe upper extremities and shoulders. Asthe size of the lesion increases, other fibertracts will be involved, dependent on thedirection and extent of the pathologic pro-cess. With extension anteriorly, a flaccid

FIGURE 1-18 Arterial spinal artery syndrome.


FIGURE 1-19 Arterial supply of the spinal cord and“watershed” areas.

Reprinted with permission from Bradley WG, Daroff RB,Fenichel GM, Marsden CD, editors. Neurology in clinicalpractice. Volume II. 3rd ed. Boston: ButterworthHeinemann, 1999:1226.

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Case 1-1A 64-year-old right-handed man was brought to the emergency department after having fallendown a flight of steps. He was not able to move his limbs. His medical history included coronaryartery disease, status post–coronary artery bypass graft, diabetes mellitus, and schizophrenia,but no clear motor difficulties prior to this incident. He remembers that during the fall he hit hisshoulders as he slid down the steps, but he experienced no loss of consciousness. Afterward hewas aware of “pain all over,” but most of his discomfort was in both upper extremities and“electrical” in quality. Before being brought to the emergency department he noted thatpassive movements of his headintensified his upper extremity pain, butno associated worsening of his sensorysymptoms occurred.

On examination his vital signs werenormal and he was in a rigid cervicalcollar. He had abrasions over both upperextremities. He was awake, alert, andfollowed all commands. His cranial nerveexamination showed no clearabnormalities. He was able to shrug hisshoulders but unable to lift his armsfrom the bed; proximal strength in theupper extremities was 2-3/5 and distalwas 0/5. Lower extremity motorexamination demonstrated weakness ofhip flexion at 4-/5, and the other motorgroups were 4/5. His tone appeared tobe normal. Reflexes were depressed, butthere appeared to be a right andperhaps a left extensor toe sign. Sensoryexamination demonstrated a decrease inpinprick up to the C4 level on the rightand a patchy decrease in pinprick overthe distal part of his left lowerextremity; sacral sensation to pin wasintact. Position sense appeared to beintact in his extremities. Rectal tone wasnormal; a urinary drainage catheter wasin place.

Routine cervical spine x-raysdemonstrated no clear fractures orprevertebral soft tissue swelling. Extensive degenerative changes were noted at multiple levels.An MRI of the cervical spine demonstrated spinal stenosis, worse at C3-4, and neuroforaminalstenosis from C3 to C5. There was an increase in spinal cord T2 signal intensity from C3 to C5without enhancement, which was interpreted as edema (Figure 1-20). Over the next 12 hours hislower extremity strength improved and his sensory deficits appeared to retract, but upperextremity strength remained significantly impaired. No improvement with steroids was noted.His persistent deficit and underlying cervical spine stenosis led to the recommendation forcervical spine surgery.

Comment. Spinal cord trauma presents with different anatomic syndromes that includetransection, cervicomedullary syndromes with high cervical spine lesions, anterior or posteriorcord syndromes, Brown-Sequard syndrome, conus/cauda equina syndrome, or, as in this case, acentral cord syndrome. Recovery and manifestations are related to the site and extent of thetrauma and underlying mechanisms, eg, presence of preexisting spinal stenosis. These influenceeventual outcome and dictate immediate management.

FIGURE 1-20 Cervical spine MRI (sagittal view, T2weighted).


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Case 1-2A 43-year-old woman with no prior medical history began to develop episodic vertigo and“jumpiness” in her eyes when she was in her late 30s. Attributed to vertigo, the symptompersisted but did not result in a disability. It was not until several years later that she began tonotice numbness over both of her hands, unaccompanied by neck or radicular pain. Sheattributed this to carpal tunnel syndrome precipitated by her administrative and secretarialwork. It was the gradual involvement of ambulatory difficulties and an acute worsening overthe last several months that led her to seek further evaluation.

Her general physical examinationand vital signs were normal. Cervicalspine examination and hairline werenormal; there was no spinal scoliosis.Her cranial nerve examinationdemonstrated a left Horner syndrome,and rotary nystagmus was evident onhorizontal as well as downward gaze.She had weakness predominantly inthe distal lower extremities, more soon the left side and to a 4�/5 degree,but her tone appeared to be increasedin all extremities. Sensory examinationshowed a decrease in pinprick over theright extremity that extended ontothe upper thorax; similar, but less-marked, findings were found on theleft, suggesting a “shawl-like” pattern.Her reflexes were generally increased,and she demonstrated bilateralBabinski signs.

An MRI scan of her brain andcervical spinal cord demonstrated aChiari type-one malformationassociated with syringomyelia. Sheunderwent foramen magnumdecompressive surgery, upper cervicalspine laminectomy, and fusion andshunt placement (fourth ventricle toupper cervical spine). Thepostoperative cervical spine MRI scanis shown in Figure 1-21. Since surgeryher neurologic deficit has remainedrelatively stable, but recently she has begun to experience lower extremity radicular painsecondary to lumbar degenerative disc and neural foraminal stenosis.

Comment. The insidious nature of this patient’s deficit initially delayed her seeking furtherclinical evaluation. However, the presence and pattern of her nystagmus, bilateral upperextremity sensory impairment, and cortical spinal tract involvement suggest an intramedullaryspinal cord lesion that may extend into the brainstem. The onset of syringomyelia is ofteninsidious, and symptom onset occurs between the ages of 25 and 40. A presentation withisolated findings may delay identification while the combination of brainstem dysfunction (eg,vertigo, oscillopsia, dysphonia, and facial sensory loss), dissociated sensory loss in the extremities,and later involvement of upper and lower motor neurons usually suggest the diagnosis.Radiologic confirmation is necessary for definitive diagnosis. Surgical interventions and extentare dependent on the assumed etiology and preexisting neurologic deficit. Decompressionsurgery or shunting procedures may be required in selected cases.

FIGURE 1-21 Cervical spine MRI (sagittal view, T1weighted).

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paralysis with fasciculations and atrophyoccurs as the anterior horns and their mo-tor neurons are affected. Lateral extensioninvolves the corticospinal tracts, resultingin spastic paralysis of muscles below thelesion, while posterior extension involvesthe posterior columns with disruption oftheir sensorymodalities. The laminationofthe lateral spinothalamic tract results in fi-bers conveying sensation from the sacrumto be more laterally/superficially placedwithin the spinal cord and are often pre-served for an extended period of time

with central spinal cord lesions, represent-ing a form of sacral sensory sparing.

At times an acute cervical spinalcord injury, especially after hyperex-tension injuries of the neck, results in aunique neurologic presentation thatsignifies an injury to the central por-tion of the spinal cord (distinguishedfrom the man-in-the-barrel syndromereported after ischemic cerebral le-sions within the border zone betweenanterior and middle cerebral arteriesand cruciate paralysis, a syndrome of

KEY POINTS:

� The sensoryimpairment incentral cordlesions is termeda dissociatedsensory loss (lossof pain andtemperaturesensation withpreservation ofposition,vibration, andtouch).

� The laminationof the lateralspinothalamictract results infibers conveyingsensation fromthe sacrum to bemore laterally/superficiallyplaced withinthe spinal cord.These are oftenpreserved for anextended periodof time withcentral spinalcord lesions(sacral sensorysparing).

Case 1-3A 67-year-old right-handed woman was brought to the emergencydepartment by her husband. Without any clear precipitants, she hadawakened with severe low back pain, accompanied by radicular paindown both lower extremities, and abdominal discomfort. She had gone toher toilet but was unable to raise herself. While being transported to theemergency department she developed urinary incontinence and laterbowel incontinence.

On evaluation, her vital signs and cardiac and vascular examinationswere normal. Her examination was significant for lower extremityparaplegia and hyporeflexia. Plantar stimulation elicited no response; aBeevor sign was present. She demonstrated a sensory level to pinprick upto T10, decreased temperature to L1, and normal position sense. Sacralsensation to pinprick was absent; rectal tone was absent, and a urinarydrainage catheter was in place (initially 1000 cc of urine had beendrained). There was no tenderness to percussion over the spine, andstraight-leg raise was negative. Her pain resolved over 2 days.

Steroids were initially administered because of the possibility of spinalcord compression, and an emergent MRI of the entire spine wasperformed as well as imaging of the aorta. Both were normal. Over theensuing weeks her lower extremity strength improved, and hyperreflexia,as well as bilateral Babinski signs, appeared. However, her ambulationremained impaired. Her sensory deficits lessened, and although her bowelincontinence improved she required periodic urinary catheterization.

Comment. While this initial clinical presentation suggested a spinal cordinfarction and an anterior spinal artery syndrome, a compressive spinalcord or conus/cauda equina lesion required exclusion. Aortic dissection canalso cause spinal cord ischemia/infarction, and such an evaluation isrequired as soon as possible. Usually (67%) of the time MRI demonstratesa T2-weighted abnormality, but a normal study does not exclude a spinalcord infarction, which then becomes a diagnosis of exclusion. Back or neckpain and radicular pain can occur at symptom onset (59%), resolving inseveral days, but later neurogenic pain can develop. In the majority ofspontaneous cases (70%) an etiology is not discovered, but the possibilityof mechanical stress-induced vascular compromise has been suggested insome cases. Prognosis is related to the extent of the injury, butambulation usually remains impaired (Novy et al, 2006).


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brachial diplegia after medullary lesions).Such individuals at first may be quadri-plegic, but recovery of lower extremitystrength often occurs early, and theprognosis may be better because of apredominantly white matter injury (Col-lignon et al, 2002). However, a uniquepattern of weakness that is more pro-nounced in the arms, worse distally thanproximally, characterizes the syndromeand the unique site of injury. Urinarydysfunction, as well as patchy sensoryloss below the level of the injury or up-per and lower levels of sensory loss (sus-pended sensory level), can be demon-strated (Cases 1-1 and 1-2).

Posterolateral ColumnSyndromeInvolvement of the posterior and lateralcolumns of the spinal cord will lead to apattern of sensory loss that predominantlyinvolves the modalities of position and vi-bratory sense and a motor syndrome ofspastic paralysis that reflects involvementof the corticospinal tract (Figure 1-23).This pattern of dysfunction leads to a sen-sory ataxia with a positive Romberg sign,while pain and temperature sensation re-main intact because of preservation of thespinothalamic tracts. A spastic-ataxic gaitreflects this constellation of fiber tract dys-function.

This pattern of involvement usu-ally develops insidiously, reflectingthe underlying pathologic processes.In the syndrome known as subacutecombined degeneration, related to adeficiency of vitamin B12 or copper,the initial neurologic manifestationsmay be those of limb paresthesia, pre-dominantly involving the feet, fol-lowed later by the development of themore distinctive posterior column andcorticospinal tract deficits. The completefeatures of this syndrome usually de-velop over an extended period of time.

Posterior Column SyndromeA process involving the posterior columnsis characterized by loss of position sense,vibration sense, and two-point discrimina-tion. These deficits occur distal to the le-sion. The lack of proprioceptive informa-tion and feedback to the motor systemaffects those muscle groups required fordiscriminative movements, resulting in asensory ataxia. While vision can partiallycompensate for this loss of proprioceptiveinformation when the eyes are open,ataxia worsens when they are closed, re-sulting in the presence of a Romberg sign.The gait is described as ataxic (or stomp-

FIGURE 1-22 Syringomyelia (modalities involved).


FIGURE 1-23 Posterolateral column syndrome.


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ing) in character, and the deficit can bemore prominent in darkness or with eyeclosure as visual cues no longer can assistin maintaining balance. The affected limbsmay become hypotonic but usually arenot weak. At times other spinal cord le-sions can produce a truncal ataxia butwithout the associated proprioceptive dif-ficulties. In such cases, spinocerebellartract dysfunction, as a manifestation of spi-nal cord compression, appears to be re-sponsible for this clinical syndrome.

With dysfunction of the posterior col-umns in the cervical region, neck flexionmay elicit an electric-like sensation thatradiates down the back or into the arms(Lhermitte sign). It is thought to representincreased mechanosensitivity of the dorsalcolumns with neck flexion further activat-ing those sensory pathways. The symp-tom is most frequently associated with spi-nal cord involvement in multiple sclerosis.

Anterior Horn Cell SyndromeDamage to the motor anterior horn cellsleads to an ipsilateral flaccid paralysis ac-companied by atrophy and fasciculations.Because larger muscles are supplied bymotor neurons from more than one seg-ment, damage to a single spinal cord seg-ment may lead only to muscular weak-ness rather than complete paralysis of theaffected motor group (Figure 1-10).When the lateral horns are involved, adecrease in sweating and vasomotor func-tions may also be demonstrated, as the

cell bodies of the sympathetic neurons areinvolved.

Combined Anterior Horn Cell–Pyramidal SyndromeThis syndrome is perhaps best exempli-fied by ALS. These lesions produce a com-bination of flaccid and spastic paralysis.Damage to the anterior horns or lowermotor neurons will result in a flaccid pa-ralysis with atrophy and fasciculations,while a lesion of the lateral corticospinaltract or upper motor neurons results in aspastic paralysis with associated hyperre-flexia and Babinski sign (Figure 1-24).The degree of injury to either site can behighly variable and reflected in the clinicalpresentation. If one site is more or pre-dominantly affected, an additional lesionin the other at the same level may notproduce noticeable effects.

INTRAMEDULLARY VERSUSEXTRAMEDULLARY CORDLESIONSNeoplasms arising within the spinalcanal tend to produce their symptomsand signs in a slow and progressivemanner, although an acute presenta-tion can occasionally be encountered.When arising from lesions within thespinal cord (intramedullary), symp-toms often begin within the vicinity ofthe central canal. Sensory symptomsare initially less localizing and dissoci-ation of sensory loss can occur. Early

KEY POINTS:

� Dysfunction inthe posteriorcolumnsyndrome ischaracterized bya sensory ataxiawith a positiveRomberg signwhile pain andtemperaturesensation remainintact becauseof preservationof thespinothalamictracts.

� Withdysfunction ofthe posteriorcolumns in thecervical region,neck flexion mayelicit an electric-like sensationthat radiatesdown the backor into the arms(Lhermitte sign).

FIGURE 1-24 Combined anterior horn cell–pyramidalsyndrome.



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evidence of lower motor neuron find-ings, later accompanied by corticospi-nal tract findings, characterizes theselesions, and their clinical presentationcan mimic a syrinx. Extramedullarylesions can arise from the dura andadjacent structures (extramedullaryintradural) or can have an extraduralsite of origin such as the vertebral bod-ies or extradural space (extramedul-lary extradural). Spontaneous pain,especially in a radicular pattern, canbe a presenting feature and suggeststhe level of involvement. Subsequentmotor and sensory changes are usuallyslow to develop, and because of theasymmetric nature of such lesions a

Brown-Sequard pattern may appear.The features of either type of clinicalsyndrome are described and con-trasted in Table 1-2.

CONUS MEDULLARIS VERSUSCAUDA EQUINA LESIONSThe close anatomic localization of the co-nus medullaris and overlying caudaequina makes distinction of either syn-drome difficult, and at times involvementof both structures occurs. A symmetricpattern of sensory loss andmotor dysfunc-tion is more consistent with a conus than acauda equina lesion. The clinical featuresof both conditions are further describedand contrasted in Table 1-3.

KEY POINT:

� A moresymmetricpattern ofsensory loss andmotordysfunction ismore consistentwith a conusthan a caudaequina lesion.

TABLE 1-2 Clinical Features of Intramedullary VersusExtramedullary Spinal Cord Lesions

Symptoms andSigns

Extramedullary Intramedullary

Spontaneous pain Radicular in type anddistribution; an earlyand importantsymptom

Burning in type andpoorly localized

Sensory deficit Contralateral loss ofpain and temperature;ipsilateral loss ofproprioception

Dissociation ofsensation; patchydistribution

Changes in pain andtemperaturesensations overperineum (saddle area)

More marked than atlevel of lesion

Less marked than atlevel of lesion

Lower motor neuroninvolvement

Segmental Widespread withatrophy andfasciculations

Upper motor neuroninvolvement

Prominent, early Late, minimal

Muscle stretch reflexes Increased early,markedly

Late, minimal changes

Corticospinal tractsigns

Early Late

Trophic changes Usually not marked Marked

Data from Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 5th ed. Philadelphia: LippincottWilliams & Wilkins, 2007:111.Data from Haerer AF. DeJong’s the neurologic examination. 5th ed. Philadelphia: Lippincott Williams & Wilkins,1992:588.

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TABLE 1-3 Clinical Features of Conus Medullaris and CaudaEquina Lesions

Symptoms andSigns

Conus Medullaris Cauda Equina

Spontaneous pain Not common orsevere; bilateral andsymmetric; overperineum and thighs

May be mostprominent symptom;severe and radicular intype; unilateral orasymmetric; overperineum, thighs, legs,and back

Sensory deficit Saddle distribution;bilateral, usuallysymmetric; dissociationof sensation

Saddle distribution;may be unilateral andasymmetric; allmodalities affected; nodissociation ofsensation

Motor loss Symmetric; notmarked; fasciculationsmay be present

Asymmetric; moremarked; atrophy mayoccur; usually nofasciculations

Reflex loss Only Achilles reflexabsent

Patellar and Achillesreflexes may be absent

Bladder and rectalsymptoms

Early and marked Late and less marked

Trophic changes Decubitus common Decubitus less marked

Sexual function Erection andejaculation impaired

Less markedimpairment

Onset Sudden and bilateral Gradual and unilateral

Data from Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 5th ed. Philadelphia: LippincottWilliams & Wilkins, 2007.Data from Haerer AF. DeJong’s the neurologic examination. 5th ed. Philadelphia: Lippincott Williams & Wilkins,1992:591.


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REFERENCES AND SELECT READINGS

Note: There are many general textbooks of neuroscience, neuroanatomy as wellas clinical neurology that you may have found useful. The following recom-mendations represent our “bias” and are driven by familiarity with and theusefulness we have found in the following general resources for teaching andreview.

Adams MM, Hicks AL. Spasticity after spinal cord injury. Spinal Cord 2005;43(10):577–586.

Bowen BC, Pattany PM. Vascular anatomy and disorders of the lumbar spine and spinalcord. Magn Reson Imaging Clin N Am 1999;7(3):555–571.

Bradley WG, Daroff RB, Fenichel GM, Marsden CD, editors. Neurology in clinical practice.Volume II. 3rd ed. Boston: Butterworth Heinemann, 1999:1226.

Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 5th ed. Philadelphia:Lippincott Williams & Wilkins, 2007.

Collignon F, Martin D, Lenelle J, Stevenaert A. Acute traumatic central cord syndrome:magnetic resonance imaging and clinical observations. J Neurosurg 2002;96(1 suppl):29–33.

Davidoff RA. The dorsal columns. Neurology 1989;39(10):1377–1385.

Duggal N, Lach B. Selective vulnerability of the lumbosacral spinal cord after cardiacarrest and hypotension. Stoke 2002;33(1):116–121.

Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed.London: Saunders, 2007.

Gillilan LA. Veins of the spinal cord. Anatomical details; suggested clinical applications.Neurology 1970;20(9):860–868.

Grant JCB. An atlas of anatomy. 6th ed. Baltimore: Williams & Wilkins, 1972.

Haerer AF. DeJong’s the neurologic examination. 5th ed. Philadelphia: Lippincott,Williams & Wilkins, 1992.

Krauss WE. Vascular anatomy of the spinal cord. Neurosurg Clin N Am 1999;10(1):9–15.

Moore KL, Dalley AF. Clinically oriented anatomy. Philadelphia: Lippincott Williams &Wilkins, 1999.

Nathan PW, Smith M, Deacon P. Vestibulospinal, reticulospinal and descendingpropriospinal nerve fibres in man. Brain 1996;119(pt 6):1809–1833.

Nathan PW, Smith M, Deacon P. The crossing of the spinothalamic tract. Brain2001;124(pt 4):793–803.

Nathan PW, Smith MC, Deacon P. The corticospinal tracts in man. Course and location offibres at different segmental levels. Brain 1990;113(pt 2):303–324.

Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: clinical andimaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol 2006;63(8):1113–1120.

Souayah N, Khella S. Neurology: examination & board review. New York: McGraw Hill, 2005.

Tattersall R, Turner B. Brown-Sequard and his syndrome [erratum published in Lancet2000;356(9226):344]. Lancet 2000;356(9223):61–63.

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