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posterior funiculus for all discriminatory sensation is evolving into a newer
conceptthat attributesto theposteriorfuniculusarole inthe discriminationof
those sensations that an animal must explore actively and tothespinocervical
thalamic pathway a role in the perception of sensations that are impressed
passivelyontheorganism(12).
LateralSpinothalamicTract
Oneof themostclinically importantpathways in thespinal cordisthe lateral
spinothalamic tract, which is concerned with the transmission of pain and
temperaturesensations(Figure2.11).Thistractiscloselyrelatedtotheanterior
spinothalamictract, and authors often combine the twopathways andrefer to
themtogether astheanterolateralsystem(ALS).In this chapter,thepathways
arediscussedseparatelybecauseoftheirclinicalrelevance.
Unmyelinated and thinly myelinated dorsal root fibers contributing to the
lateralspinothalamictracthavetheircellbodiesinspinalganglia.Incomingroot
fiberssynapseon neurons of the dorsal horn. The dorsal hornneuronsproject
axonsacrossthe midline in the anterior white commissure to the contralateral
lateral funiculus and thus form the lateral spinothalamic tract. The crossing
fibers of the lateral spinothalamic pathway ascend from one to two spinal
segments above their entry level before entering the tract in the contralateral
lateralfuniculus.Thefibersofthetractaresomatotopicallyarrangedwithsacral
fiberslocatedlaterallyandcervicalfiberslocatedmediallywithinthetract.Note
thatthisarrangementisthereverseoftheposteriorfuniculuspathways,inwhich
sacralfibersarelocatedmediallyandcervicalfibersarelaterallylocated.Once
formed, the lateral spinothalamic tract ascends throughout the length of the
spinalcordandbrainstemtoultimatelyterminateonneuronsoftheVPLnucleus
ofthethalamus.
Lesionsof thelateral spinothalamictract inthelateral funiculusresult ina
loss of pain and temperature sensation in the contralateral half of the body,
beginning one or two segments below the level of the lesion. This pattern of
sensorylossismarkedincontrasttothelossthatoccursfollowinginjurytothe
dorsal roots, in which there is segmental or dermatomal loss of sensation
ipsilateraltothelesion.Moreover,ifpainandtemperaturefibersareinjuredas
theycrossthemidlineofthespinalcordintheanteriorwhitecommissure,there
is a bilateral segmental loss of pain and temperature sensation in the
dermatomescorrespondingtotheaffectedspinalcordsegments.Thislastpattern
of sensory loss is the characteristic of syringomyelia, a condition caused by a
centrally located cavitation of the spinal cord that destroys the anterior white
commissure. Finally, in a Brown–Sequard lesion (hemisection of the spinal
cord),thepatientexperiencesbothacontralaterallossofpainandtemperaturein
thebody(causedbythedestructionofthelateralspinothalamicpathwayinthe
lateralfuniculus)andabilateralsegmentallossofpainandtemperature(caused
byadestruction of the anterior white commissure) thatwillbeslightlyhigher
thanthecontralaterallossofpainandtemperaturesensation,butstillbelowthe
levelofthelesion.
Inthepast,thelateralspinothalamictractwassectionedsurgicallytorelieve
intractablepain.The procedureis referredtoascordotomyandmaybecarried
outunilaterallyorbilaterally.Ifbilateralcordotomyisperformed,thelesionsare
made at slightly different levels in the spinal cord. During surgery, the
denticulateligamentisusedasalandmark;lesionsaremadejustanteriortothe
denticulate ligament to locate and transect the lateral spinothalamic tract. A
unilaterallesionofthetractresultsinanesthesiaofthebodywallandlimbs,but
not the viscera, which are bilaterally represented (12). Furthermore, the
anogenitalregionisnotmarkedlyaffectedwithunilateral lesions(13).Clinical
results have indicated that after variable periods of time following bilateral
cordotomies, there is often a return of pain and temperature sensation, thus
suggestingthattheremaybeotherpathwaysin the spinal cord to convey this
modality. Thesepathwaysmay be multisynapticand pass throughthereticular
formation (i.e., spinoreticular; 14) or involve shorter relays (i.e., spinospinal;
13).Inaddition,AffifiandBergman(13)havesuggestedthatpainsensationmay
bemediatedthroughaspinotectalpathway,andCarpenterandSutin(12)have
suggestedthatuncrossedspinothalamicfibersmayberesponsibleforthereturn
of pain and temperature sensation following unilateral lesion of the lateral
spinothalamicpathway.
AnteriorSpinothalamicTract
The dorsal root fibers convey light touch sensation and certain types of pain
impulses synapse on dorsal horn neurons. The axons of these dorsal horn
neuronscrossintheanteriorwhitecommissureoverseveralsegmentsandgather
in the lateral and anterior funiculi to form the anterior spinothalamic tract
(Figure 2.11). The course and termination of this tract in the spinal cord and
brainstemaresimilartothelateralspinothalamictract.
Functionally,“lighttouch”isdefinedasthesensationprovokedbystroking
anarea ofskindevoid of hair(glabrous skin) witha feather orwispof cotton
(13).ThistypeofsensationisconveyedtohigherCNScentersinadditiontothe
pressure sense and discriminatory tactilesensations conveyed by theposterior
funiculus. Because tactile sensation is transmitted centrally by the posterior
funiculi, the anterior spinothalamic tract, and the spinocervical thalamic tract,
clinicallythisparticularsensorymodalityisoflittlevalueinlocalizinginjuries
to the spinal cord (13). If the anterior spinothalamic tract islesioned, there is
littlelossoftactilesensibility;however,theaffectiveaspectofsensationmaybe
lost.Bilateraldestructionoftheanterolateralfuniculimaycauseacompleteloss
ofitching,tickling,andlibidinousfeeling(15);thusthisregionofthespinalcord
has been associated with one’s ability to judge the pleasant or unpleasant
character of sensation. In addition to light touch stimuli, the anterior
spinothalamic tract is thought to convey nondiscriminative pain sensations, in
contrasttothelateralspinothalamictract,whichisthoughttoconveythewelllocalizeddiscriminativepainsensations(15).
OtherAscendingTracts
There are several other ascending tracts in thespinalcord lateral and anterior
funiculi that are of little clinical significance. These tracts include the spinoolivary, spinotectal, spinoreticular, spinocortical, spinovestibular, and anterior
spinocerebellar. These multisynaptic pathways do not have a well-delineated
functionalsignificance,butmayplayaroleinfeedbackcontrolmechanismsor
inthemaintenanceofthestateofconsciousness.Formoredetailedinformation
onthesepathwaysconsultCarpenterandSutin(15).
DescendingTractsoftheLateralandAnterior
Funiculi
CorticospinalTracts
Asthenameimplies,neuronsgivingrisetothecorticospinaltractsarefoundin
the cerebral cortex. The axon ofthese neurons projects through the brainstem
andterminatesinthespinalcord.Thecorticospinaltractscomprisethelargest,
clinicallyimportantdescendingfibersysteminthehumanneuraxis.Theneurons
that give rise to the tract are located in the primary motor cortex (i.e., the
precentral gyrus or Brodmann’s area 4), the premotor cortex (area 6), the
primary sensory cortex (i.e., the postcentral gyrus or area 3, 1, 2), and the
adjacent parietal cortex (area 5, 7) (16,17). Although both sensory and motor
corticalareascontributetothetracts,theprimarymotorcortexandthepremotor
cortexgiveriseto80%ofthetracts.
At the caudal level of the medulla oblongata, the majority of the
corticospinalfiberscrossthe midlinein thepyramidaldecussationtoform the
lateral corticospinal tract, which is located in the dorsal aspect of the lateral
funiculus (Figure 2.11). The lateral corticospinal tract extends to the entire
lengthofthespinalcord.
Theuncrossedcorticospinalfibersdescendfromthemedullaintotheanterior
funiculusofthespinalcordastheanteriorcorticospinaltract(bundleofTürck)
(Figure2.11).Theanteriorcorticospinaltractextends,about10%ofthefibers,
onlytotheupperthoracicspinalcordandinnervatesneurons projectingto the
musclesoftheupperextremitiesandneck.Thefibersofthistractgenerallycross
the midline segmentally within the spinal cord before terminating on
contralateral neurons. In rare cases, fibers do not cross the midline at all and
formextremelylargeanteriorcorticospinaltracts(18).
Corticospinal fibers terminate mostly on interneurons in the spinal cord.
Evidencealsoexists for a direct projection to alpha and gamma motoneurons.
Becausethecorticospinaltractsinnervatebothalpha andgammamotoneurons,
stimulationofcorticospinalfibersleadstoaco-contractionofbothintrafusaland
extrafusal muscle fibers. Because of the co-contraction of the two types of
muscle fibers, there is increased sensitivity of the muscle spindle (intrafusal
fiber)tochangesinmusclelengthevenwhenthemuscleisshortening.
Ithasbeenestimatedthat55%ofallcorticospinalfibersendinthecervical
cord,20%inthethoracic,and25%inthelumbosacralsegments(19).Thesedata
suggestthatthecorticospinaltractshaveagreatercontrolandinfluenceoverthe
upperextremitiesthan overthe lower. Thecorticospinal tractsareessentialfor
skillandprecisioninmovementandalsofortheexecutionofprecisemovements
of the fingers. Interestingly, although the tracts are necessary for speed and
agility during precise movements, they are not necessary for the initiation of
voluntarymovement.Theyalsoservetoregulatesensoryrelayprocessesandto
determinewhichsensorymodalityreachesthecerebralcortex,asevidencedby
terminationson sensoryneurons inthespinal cord.The properfunctionofthe
corticospinaltractsisdependentontheextentoftheirmyelination.Myelination
ofcorticospinalfibersbeginsafterbirthandisnotcompleteduntiltheendofthe
firstyearoflife.
Neurons in the cerebral cortex and their axons that form the corticospinal
tracts have been referred to as upper motor neurons (UMN). The alpha
motoneurons in the spinal cord ventral horns and their axons that directly
innervateskeletalmusclearereferredtoaslowermotorneurons(LMN).Lesion
ofthelateralcorticospinaltractinthespinalcordlateralfuniculusresultsinan
UMN syndrome which includes spasticity, hyperactive deep tendon reflexes,
Babinskisign, clonus,anda lossordiminution ofsuperficialreflexes, suchas
the abdominal or cremasteric reflex. In the acute phase of an SCI involving
bilateral lesion of the lateral corticospinal tracts, a patient undergoes “spinal
shock,”inwhichthereisacompleteshutdownofneuronalactivityinthespinal
cord below the level of the injury. The signs of spinal shock include flaccid
paralysisofmuscles,hypotonia,andtheabsenceofmyotatic,bowel,andbladder
reflexes. Depending on the level of injury,there mayalso bebradycardiaand
significant lowering of blood pressure. Following a variable period (hours to
weeks),thepatientrecoversfromspinalshockandtheUMNsyndromebecomes
apparent. The mechanisms underlying the induction and recovery from spinal
shockareunknown.LMNlesionsresultinsignssimilartothoseofapatientin
spinalshock.InLMNparalysis,thereisalossofallmovement,bothreflexand
voluntary,aswellasalossofmuscletoneandsubsequentatrophyoftheaffected
muscles.Unlikethetransientdeficitsassociatedwithspinalshock,LMNdeficits
are permanent, assuming that there is no reinnervation of the denervated
structures.
Thesignsassociatedwith an UMN syndrome are not always indicative of
injuryordiseaseofthespinalcord.Inolderindividuals,thereisatendencyfor
thesuperficialabdominalreflexestobeabsent;thisoccursmoreofteninfemales
than in males (20). Although the Babinski sign is commonly associated with
injurytothecorticospinalsystem,itcanalsobeelicitedinthenewborninfant,a
sleeping or intoxicated adult, or following a generalized seizure.Interestingly,
the Babinski sign may be absentin somepatients with a known lesion of the
corticospinaltract(21).
RubrospinalTract
Theneuronsthatgiverisetotheaxonsoftherubrospinaltractarelocatedinthe
posteriortwo-thirdsoftherednucleus inthemid-brain. Theaxonsofthetract
crossinthe ventral tegmental decussation and descend to spinal levels, where
thetractformsinthelateralfuniculusmostlyanteriorto(partiallyoverlapping)
the lateral corticospinal tract (Figure 2.11). The fibersof the rubrospinal tract
terminateinthesameareasofthespinalgraymatterasthelateralcorticospinal
tract and function to facilitate flexor motor neuron activity. Because the red
nucleus receives an input from the cortex (corticorubral) and because of the
similar terminations of both tracts in the spinal cord, the rubrospinal tract is
thoughttobefunctionallyrelatedtothelateralcorticospinaltract.
Althoughtherubrospinaltractextendsthelengthofthespinalcordinmost
mammals, it only extends to the thoracic segments in man (22), is thinly
myelinated, and thought to be rudimentary. Any effect of injury to the
rubrospinaltract inpatientswill likelybemasked bythesevere motordeficits
resultingfrominjurytotheadjacentlateralcorticospinaltract.
LateralVestibulospinalTract
Theneuronsthatgiverisetothistractarefoundinthelateralvestibularnucleus
locatedatthejunctionbetweenthemedullaandpons.Theaxonsofthelateral
vestibularnucleus descenduncrossed throughthemedulla andformthe lateral
vestibulospinaltractintheanterioraspectofthelateralfuniculusalongtheentire
lengthof thespinal cord(Figure2.11).Fibers ofthetract terminatemostlyon
interneuronsinthespinalcord,buttherearesomedirectterminationsonalpha
motorneurondendrites.
The primary function of the lateral vestibulospinal tract is to facilitate
extensormuscletonetomaintainanuprightposture.Witheyesclosedandfeet
closetogether anormal individualswaysslightlyfromside toside. Balanceis
maintainedbecause,forexample,astheindividualswaystotheright,impulses
from the right semicircular canals of the inner ear activate neurons in the
ipsilaterallateralvestibularnucleus.Theseneurons,inturn,sendimpulsesalong
the right vestibulospinal tract to extensor muscles, which correct forthesway
andmove thebodyback tothemidline centerof gravity.Whenthe individual
swaystotheleft,theleftlateralvestibulospinaltractisactivated.Similarly,ifa
walking individual stumbles, reflex extension of one of the lower extremities
maypreventafall,butifafallisimminent,extensionoftheupperlimbsoften
prevents severe injury to the face and head. Under these circumstances, the
reflex extension of the limbs is also mediated by the lateral vestibulospinal
tracts.Iftheeighthcranialnerve(vestibulocochlear),lateralvestibularnucleus,
orthesemicircularcanalsareinjuredononeside,apatientwilloftenfalltothat
sideorveertothesideoftheinjurywhilewalking.Theeffectsofinjurytothe
lateralvestibulospinaltractinthespinalcord,however,aregenerallymaskedby
themoreseveredeficitsinmotorcapabilitythatresultfromconcomitantinjury
tothelateralcorticospinaltract.
MedialVestibulospinalTract
Theneuronsthatgive risetothemedialvestibulospinaltractarelocatedinthe
medialvestibularnucleusofthemedulla.Thefibersoftheseneuronsdescends
throughthemedulla bilaterallyinacompositebundleofseveral differentfiber
systems known as the medial longitudinal fasciculus (MLF). The MLF
containingthe medial vestibulospinaltractis located intheposterior aspect of
the anterior funiculus of the cervical spinal cord (Figure 2.11). Fibers of the
medialvestibulospinaltractterminateoninterneuronsin thespinalgray matter
andplayaroleinthelabyrinthineregulationofheadpositions.
ReticulospinalTracts
Theneurons that giveriseto these tractsarelocated in thecentralcore of the
brainstemknownasthereticularformation,attheleveloftheponsandmedulla.
Becauseofthedifferentoriginsandlocationsofthesetractsinthespinalcord,
theyareoftenreferredtoseparatelyasthepontineandmedullaryreticulospinal
tracts.Thepontinereticulospinaltractismostlyipsilateralanddescendsinthe
medialpartof the anterior funiculus along the entire length of the spinal cord
(Figure2.11).Thefibersterminateoninterneurons.Themedullaryreticulospinal
tractisalsoprimarilyipsilateralanddescendsthelengthofthespinalcordinthe
anterior part of the lateral funiculus (Figure 2.11).The fibers of this pathway
terminateoninterneuronsincloseassociationwiththeterminationofthefibers
of the pontine reticulospinal tract, the rubrospinal tract, and the corticospinal
tracts.
Animal studies have shown that stimulation of the brainstem reticular
formation can facilitate or inhibit voluntary movement, cortically induced
movement,andreflex activity;influencemuscletone;affectinspiratoryphases
ofrespiration;exert pressoror depressoreffectson thecirculatorysystem;and
exert inhibitory effects on sensory transmission (23). Those areas of the
medullary reticular formation giving rise to the medullary reticulospinal tract
correspond closely with the regions from which inspiratory, inhibitory, and
depressor effects are obtained (24–26). The areas of the reticular formation
related to facilitatory effects, expiration, and pressor vasomotor responses are
rostral to the medulla and extend beyond the regions that give rise to
reticulospinal fibers (27). Thus, the reticulospinal tracts may not be the
mediators of some facilitatory effects originating from neurons in the upper
brainstemreticularformation.
DescendingAutonomicPathways
Fibersbelongingtothis important descending system originate primarily from
the hypothalamus. Although there is evidence of direct projections from the
hypothalamus to the spinal cord (28), polysynaptic routes also pass through
variousregions of the reticular formation beforereachingthe spinal cord. The
descendingautonomicpathwaysarelocatedpredominantlyinthelateralfuniculi
and terminate on the preganglionic sympathetic and parasympathetic neurons
locatedintheintermediategraymatterofT1–L2andS2–S4,respectively.
Lesion of the descending autonomic pathways in SCI often leads to
significant autonomic disturbances. If injury occurs at or above the T1 level,
Horner’sSyndrome results because of injurytothesympatheticcomponent of
the descending autonomic pathways. The signs of this syndrome are seen
predominantly in the eye ipsilateral to injury and consist of miosis caused by
paralysisofthepupillarydilatormuscleandslightptosiscausedbyparalysisof
thesmoothmuscle(tarsalplate)oftheuppereyelid.Inadditiontothesignsin
theeye,thepatientmayhaveanhydrosisofthefacebecauseoftheinterruption
ofthesympatheticinnervationofthesweatglandsoftheface ipsilateraltothe
SCI(29).
When the descending autonomic pathways innervating preganglionic
parasympatheticneuronsare lesionedbilaterallyatanylevelofthe spinalcord
rostral to S2, the result is impotence and loss of normal bowel and bladder
function. However, after recovery from spinal shock, spontaneous or reflex
erectionofthepenis(orclitoris)mayoccurandbowelandbladderreflexesmay
alsoreturn.Thisis inmarkedcontrasttothedeficitsassociatedwiththeconus
medullarisandcaudaequinasyndromesexplainedearlierinthischapter.Inthese
latter cases, since the preganglionic parasympathetic neurons at S2–S4 are
destroyed or their axons are severed, this usually results in a permanently
areflexicbowelandbladderandtheabsenceofspontaneousorreflexerections.
Incontrasttoerection,ejaculationiscontrolledbypreganglionicsympathetic
neuronslocatedat theL1 andL2levelsofthespinalcord. Duringejaculation,
theseminalfluidfromtheseminalvesiclesandprostate,aswellasspermfrom
eachepididymis,flowsintotheprostaticurethraandisejectedfromthepenisby
rhythmic contractions of the smooth muscle associated with these structures.
Thus,erectioniscontrolledbyparasympathetics,andejaculationismediatedby
sympatheticneurons.Duringejaculation,dischargeofthesemenintothebladder
ispreventedbythecontractionofthesphinctervesicae,whichisinnervatedby
preganglionic sympathetics located at L1 and L2. When there is bilateral
destruction of the descendingautonomic pathways in SCI, there is not only a
lossoferection,butalsoalossofejaculation.IftheSCIisabovelumbarlevels,
reflexejaculationmay be possible in some patients after recovery from spinal
shock. Some patients may have a normal ejaculation, but without external
emissionbecauseoftheparalysisofthesphinctervesicae.
BLOODSUPPLYOFTHESPINALCORD
The spinal cord is supplied by three longitudinally oriented branches of the
vertebral arteries and multiple radicular arteries that arise from various
segmental vessels. The longitudinally oriented arteries are the anterior spinal
arteryandapairofposteriorspinalarteries.
AnteriorSpinalArtery
Ontheanteriorsurfaceofthemedulla,twobranchesfromthevertebralarteries
unite in the midline to form a single anterior spinal artery that descends the
lengthofthespinalcordintheanteriormedianfissure(Figure2.12).Thesulcal
arteriesarisingfromtheanteriorspinalarteryenterthespinalcordthroughthe
anterior median fissure. Successive sulcal arteries generally alternate in their
distributiontotheleftandrightsideofthespinalcord,butoccasionallyasingle
sulcalarterywilldistributetobothsides(Figure2.13).Thesulcalarteriessupply
theanterior two-thirdsof thespinal cordatany cross-sectionallevel. Thisis a
clinicallyimportantfeatureoftheanatomyofthespinalcord,becauseocclusion
ofthe anteriorspinal arteryoritssulcalbranches couldresult inanteriorcord
(spinalartery)syndrome(Figure2.14).Asinmostvascularproblems,theonset
ofsignsandsymptomsisrapid.Figure2.14showsthezoneofdistributionofthe
anteriorspinalarteryinthecross-hatchedarea.Theposteriorfuniculusandhorns
are spared because these areas are supplied by the posterior spinal arteries.
Initially,thereisflaccidparalysisofthemusclesinthebodybelowthelevelof
infarct because of spinal shock. In time, however, spastic paralysis and other
UMNsignsdevelopbecauseofbilateraldestructionofthecorticospinaltracts.A
variable degree of bowel and bladder dysfunction exists because of the
interruption of the descending autonomic pathways. Initially, however,
incontinence may be due to spinal shock. A cardinal sign of anterior cord
syndrome is a dissociated sensory loss characterized by a loss of pain and
temperature sensations (bilateral lateral spinothalamic tract lesion) with
preservation of kinesthesia and discriminative touch sensations (sparing of
posteriorfuniculi)inthebodybelowthelevelofinjury.Somepatientsdevelop
painfuldysesthesiasabout6to8monthsaftertheonsetofneurologicsymptoms.
Thesourceof thispain isunknown,buthasbeensuggestedto beattributedto
the activation of previously latent pathways that mediate pain sensation. The
anterior spinal artery is dependent on segmental contributions from anterior
radiculararteriesalongthelengthofthespinalcord(Figure2.12).
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