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FIGURE2.12Arteriesofthespinalcord.
FIGURE2.13Arterialsupplyandvenousdrainageofthespinalcord.
PosteriorSpinalArteries
Thepaired posterior spinalarteries derived fromthevertebral arteriesdescend
on the posterior surface of the spinal cord just medial to the posterior roots
(Figure 2.12). The arteries receive variable contributions from the posterior
radiculararteries.Atpointsalongthecord,theposteriorspinalarteriesbecome
sosmallthattheyappeartobediscontinuous.Thearteriessupplybloodtothe
posterior one-third of the spinal cord. The peripheral portions of the lateral
funiculi are supplied by the arterial vasocorona, which is formed by an
anastomosisbetweentheanteriorandposteriorspinalarteries(Figure2.13).
FIGURE2.14 Diagram showing the extent of the lesion in anterior
cord(spinalartery)syndromeandassociatedneurologicsigns.
RadicularArteries
Thesegmentalvesselsthatpassthroughtheintervertebralforaminadivideinto
posteriorandanteriorradiculararteries,whichfollowtheposteriorandanterior
roots, respectively (Figure 2.13). At variable levels, the radicular arteries
continue coursing medially until they anastomose with either the anterior or
posteriorspinalarteries.Theanteriorradiculararteriescontributetotheanterior
spinalartery,andtheposteriorradiculararteriescontributetotheposteriorspinal
arteries.Inthelumbarregion,oneanteriorradiculararteryisquitelargeandis
knownasthearteryof Adamkiewicz(Figure2.12).Thisarteryisusuallyfound
ontheleftandentersthevertebralcanalbyfollowingananteriorrootateithera
lowthoracicorupperlumbarlevelbeforeanastomosingwiththeanteriorspinal
artery.ThearteryofAdamkiewiczreinforcesthecirculationtotwo-thirdsofthe
spinalcord,includingthelumbosacralenlargement.Occlusionofthisarterymay
seriously compromise spinal cord circulation, which could lead to infarct and
paraplegia.
Thegreatestdistancebetweenradiculararteriesthatcontributessignificantly
totheanterior andposterior spinalarteriesisfoundat thethoracic levelofthe
spinal cord. At this level, occlusion of just one radicular artery could lead to
significant infarct of spinal tissue. The T1–T4 levels of the thoracic cord are
particularlyvulnerabletoinfarctfollowingocclusionofaradicularartery.Spinal
cordsegmentL1isanothervulnerableregion.
FIGURE 2.15 Collateral circulation of the spinal cord. When
posteriorintercostalsare tiedoffsurgically,bloodflowstothespinal
cord via internal thoracic and lateral thoracic (not shown) artery
anastomoseswithposteriorintercostalarteries.
FIGURE 2.16 Veins of the spinal cord and the vertebral venous
plexus.
CollateralCirculationoftheSpinalCord
Severe trauma to the vertebral column on the left at the thoracic level can
fracturethebodiesofoneormorevertebrae.Asurgeonoftenmustmobilizethe
descendingaortatotherighttoexposethefracturedvertebralbodies,removethe
bonyfragments,andstabilizethespine.Theaortaismobilizedbyfirsttyingoff
severalposteriorintercostalarteriesclosetotheiroriginfromtheaorta,severing
thearteriesinthisregion,andthenmovingtheaortatotheright(Figure 2.15).
Theupperthoracicspinalcordisparticularlyvulnerabletoinfarctifbloodflow
into the cord from an important segmental vessel is interrupted. The above
surgicalprocedure, however,does not interrupt the flow of blood through the
intervertebral foramen, and thus to the spinal cord, because of collateral
circulation. This collateral circulation results from the anastomosis of the
internal thoracic artery (a branch of the subclavian artery) with the posterior
intercostal artery. As soon as blood flow from the aorta is interrupted, blood
begins retrograde flow from the internal thoracic artery through the posterior
intercostal artery and into the spinal cord (Figure 2.15). Although this is not
showninthefigure,HollinsheadandRosse(30)havesuggestedthatthelateral
thoracic artery (a branch of the axillary artery)alsohas anastomoses with the
posterior intercostals and thus provides a second source of blood flow to the
spinalcordundertheseconditions.
VeinsoftheSpinalCord
Ingeneral,thedistributionpatternoftheveinsofthespinalcordissimilartothat
ofthespinalarteries(Figure2.16).Threelongitudinallyorientedposteriorspinal
veinsandthreeanteriorspinalveinscommunicatefreelywitheachotherandare
drained by anterior and posterior radicular veins, which join the internal
vertebral(epidural)venousplexuslyingintheepiduralspace(Figure2.16).This
plexusofveinspassessuperiorlywithinthevertebralcanalthroughtheforamen
magnum to communicate with the dural sinuses and veins within the skull
(Figure2.16).Theinternalvertebralvenousplexusalsocommunicateswiththe
externalvertebralvenousplexusontheexternalsurfaceofthevertebrae.
Therearenovalvesinthespinousvenousnetwork.Thus,bloodflowingin
thesevesselscouldpassdirectlyintothesystemicvenoussystem.Forinstance,
whenintra-abdominalpressureisincreased,bloodfromthepelvicvenousplexus
passessuperiorlyviathe internal vertebral plexus. When the jugular veins are
obstructed, blood leaves the skull by this same plexus. Because the prostatic
plexusiscontinuouswiththevertebralvenoussystem,neoplasmsoriginatingin
theprostateglandmaymetastasizeandlodgeinvertebrae,spinalcord,brain,or
skull(31).
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3
PathologyoftheSpinalCord
RonaldC.KimandMariPerez-Rosendahl
INTRODUCTION
Thischapterisstructuredtoprovideanoverviewofthemorphologicfindingsin
thosedisordersthat physiciansengaged inthepracticeofspinal cordmedicine
aremostlikelytoencounter.Itiswrittenwithanemphasisonclinicopathologic
correlationandinsuchamannerastoprovidethepractitioner,wherepossible,
withaninsightintopathogeneticmechanisms.
SPINALVASCULARDISEASE
SpinalArterialInfarction
Althoughallofthearterialbloodsupplytothespinalcordisultimatelyderived
fromtheaorta,itisprovidedbyonlyseventoeightradiculomedullarybranches
(1). Because the cervical and upper two to three thoracic spinal segments are
relatively richly supplied, arterial infarction in this region rarely occurs. The
middle thoracic (T4–T8) region, however, is typically dependent on a single
radiculararterythatusuallyentersthespinalcanalnearthevertebralbodyofT7,
andthethoracolumbarregionislargelydependentonasinglemajorartery,the
artery of Adamkiewicz, which enters usually on the left side, accompanying
spinalnerverootsoriginatinganywherefromT8toL3(2).Forthisreason,the
spinal cord from T5 downward is particularly susceptible to arterial
insufficiency.
Theradiculomedullaryarteries,uponentryintothespinalcanal,ramifyover
the surface of the spinal cord to form a perimedullary arterial network that
coalesces into a single anterior and two posterior spinal arteries that send
centripetally directed branches into the underlying white matter. The internal
portion of the spinal cord is supplied by sulcal arteries coursing through the
anterior median fissure and sending branches directed centrifugally,
predominantly into gray matter. Because of the relatively rich anastomotic
arterialnetworksupplyingthewhitematter,incontrasttotheend-arterialsupply
of the gray matter, severe systemic circulatory impairment tends to produce
damagemainlytothegraymatter(3).
Arterial infarction of the spinal cord develops most commonly as a
consequence of factors arising outside of the spinal canal (e.g., profound
systemic circulatory impairment [shock or cardiac arrest] or surgical crossclamping or disease of the aorta or its major branches). Under these
circumstances,themostcommonpatternofdamageisonethatislimitedlargely
to the gray matter from upper to mid-thoracic levels downward (Figure 3.1),
presumably because of the protective effect of the perimedullary anastomotic
networkexertedonthespinalwhitematter(4).Clinically,therewillbepersistent
flaccidparaplegia(becauseofsparingofthecorticospinaltracts)andlossofpain
andtemperatureperception(becauseofinterruptionofthelateralspinothalamic
pathways), with relative sparing of posterior column (proprioceptive) function
(thisbeentermed“AnteriorCordSyndrome”).
Operativeinterruptionofamajorintercostalarterialfeeder(suchasligation
ofthearteryofAdamkiewiczduringribresectioninpreparationforthoracotomy
for aortic surgery) will result in noncavitary ischemic atrophy of the ventral
portion of the spinal cord (Figure 3.2) (5). In this situation, lower extremity
weakness is usually of upper motor neuron (UMN) type (i.e., with spasticity)
becauseofdamagetothelateralcorticospinaltracts.
SpinalVascularEmbolicDisease
Occlusionoftheanteriorspinalartery(ASA)withresultantcavitaryinfarctionin
itsterritoryofsupplyisrelativelyuncommonbut,whenitoccurs,isusuallythe
resultofatheromatousorfibrocartilaginousembolism(3).Atheromatousemboli
(Figures 3.3 and 3.4) tend to appear in relatively elderly subjects with severe
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