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somedescendingaxonsfromthetectumandvestibularnucleiresponsibleforthe
supraspinalcontrolofthespinalcord.
Two conspicuous areas are not myelinated at the time of birth. These are
Lissauer’s tract (the posterolateral fasciculus), which remains unmyelinated
postnatally, and the late-myelinating anterior and lateral corticospinal tracts.
These last two pathways are part of the pyramidal motor system and do not
becomecompletelymyelinateduntiltheendofthefirstyearafterbirth.Thereis
a progressive rostral to caudal gradient in the growth and myelination of the
corticospinaltractsinthenewborn.At3dayspostnatally,thefasciculusgracilis
and cuneatus and ventral funiculus in the upper cervical spinal cord are well
myelinated,butthelateralandanteriorcorticospinaltractsarenot.By4months
after birth, myelination of the lateral corticospinal tract is well under way at
upperandlowercervicallevelsofthespinalcord,butthetractisnotmyelinated
furthercaudally.Thismayberelatedtoa4-monthinfantbeingabletoraiseits
head and reach for nearby objects, but not being able to voluntarily move its
lower limbs. By the end of the first year of life, myelination of the lateral
corticospinaltractisnearlycompleteandvoluntarycontrolofthelowerlimbsis
possible.Walkingbehaviorbeginsatthistime.Foradetaileddescriptionofthe
morphological maturation of the spinal cord and how it relates to behavioral
development in the newborn, the reader should consult Development of the
HumanSpinalCordbyJ.AltmanandS.A.Bayer(2).
NEURALTUBEDEFECTS
Mostcongenital defectsofthe spinalcordresult fromabnormalclosure ofthe
neural folds during GW 3 and 4. The defects that result may involve the
meninges, vertebrae, muscles, and skin. Severe neural tube defects occur in
approximately 1/1000 births, but the incidence varies depending upon the
geographical area and may be as high as 1/100 births in some areas, such as
northernChina(3).
Whenthespinalregionisinvolved,thegeneraltermusedtodescribeneural
tube defects is spina bifida. In spina bifida, the roof of the vertebral canal
(vertebralarch)overoneormorevertebraefailstofusedorsaltothespinalcord
(Figure2.3).Thistypeofdefectmayormaynotinvolvetheunderlyingspinal
cord.Therearetwotypesofspinalbifida:spinabifidaoccultaandspinabifida
cystica.
Inspinabifidaocculta,thevertebralarchisdefective,butthisiscoveredby
skin, and the defect usually does not involve the spina cord (Figure 2.3A). It
mostoftenoccursinthelumbosacralregionandoftenisaccompaniedbyapatch
ofhairoverlyingtheaffectedregion.
Inspinabifidacystica,themeningesand,attimes,thespinalcordprotrude
throughthedefectinthevertebralarchformingacyst-likesac(Figures2.3B,C).
Spina bifida with meningocele is the term applied when only the meninges
protrude through the defect (Figure 2.3B), but when the spinal cord also
protrudesthroughthedefect,thetermusedisspinabifidawithmenigomyelocele
(Figure 2.3C). Hydrocephaly very often accompanies spina bifida cystica
becausethespinalcordistetheredtothevertebralcolumn.Thus,asthevertebral
column lengthens during development, tethering pulls the cerebellar tonsils
down into the foramen magnum and prevents the flow of cerebrospinal fluid
(CSF)outoftheventriclesintothesubarachoidspace.Spinabifidacysticacan
betreatedbyrepairingthedefect duringinuterosurgeryatabout28weeksof
gestation.Preliminaryresultsindicatethatthisapproachreducestheincidenceof
hydrocephalus, improves bladder and bowel control, and increases motor
developmenttothelowerlimbs(4).
FIGURE2.3Typesofneuraltubedefectsinvolvingthespinalcord.
There are instances in which the neural folds do not elevate during
development,butremainflattened.Inthesecases,theneuraltubedoesnotclose.
In other instances, the neural tissue folds, but there is still no closure of the
neuraltube.Thisis referredtoasspinabifidawithrachischisis(or sometimes,
myeloschisis,Figures2.3D,E).Inbothtypesofrachischisis,theneuraltissueis
exposedandbecomesnecrotic.
Theetiologyofneuraltubedefectsismultifactorial,anditisknownthatthe
likelihoodofhavingachildwithsuchadefectincreasessignificantlyafterafirst
childisbornwithadefect.Itisnowestablishedthatfolicacid(folate)reduces
theincidenceofneuraltubedefectsbyasmuchas70%if400mcgistakendaily
2monthsbeforeconceptionandthroughoutpregnancy(4).
GROSSANATOMY
ExtentandAppearance
Thespinalcord inman isroughlycylindricalinshape andis slightlyflattened
anteriorlyandposteriorly.Itbeginsatthecaudal endofthemedullaoblongata
andleavesthecranialvaultbyextendingthroughtheforamenmagnumintothe
vertebralcanal. At birth, the spinal cord terminates at the lower border ofthe
third lumbar vertebra. In adults, the spinal cord is between 42 and 45 cm in
length, weighs about 35 g, and usually terminates at the level of the
intervertebraldiskbetweenL1andL2.However,themostinferiorextentofthe
spinalcord,theconusmedullaris,maybefoundashighasT12oraslowasL3.
Thus,aspointedoutearlier,thespinalcorddoesnotextendtheentirelengthof
the vertebral canal, but rather only occupies its superior two-thirds in adults
(Figure 2.4). The basis for the discrepancy in length between the vertebral
columnand spinalcordis embryologicas explained inthe first sectionof this
chapter.
The result of this disparate growth between the spinal cord and vertebral
columnis a progressiveincreasein thelengthof spinal nerverootswithin the
vertebralcanal,withtheshortestextensionfoundatlowercervicallevelsandthe
longest found at sacral levels. Thus, in adults, upper and mid-cervical spinal
nerveshavetheshortestroots.Fromlowcervicaltosacrallevels,thedistanceis
progressivelyincreasedbetweentheintervertebralforamentransmittinganerve
andthespinalcordsegmentallevelgivingrisetotherootsofthatnerve,andany
particular spinal cord segment lies somewhat higher than its corresponding
numbered vertebra (Figure 2.5). It is important to appreciate that during
development, spinal nerves do not grow caudally in the vertebral canal to
ultimately find their way to the appropriate intervertebral foramen and body
segment.Rather,the connections aremadeearly in development, andthenthe
nerverootselongateasthecaudalhalf ofthefetusgrowsinthelaterstagesof
development.Theclinical significance of the anatomy of the “terminal end of
thespinalcord”isexplainedinthesection"TerminalEndoftheSpinalCord."
FIGURE2.4Illustrationofspinalcordshowingdivisionintograyand
whitematter.
FIGURE2.5Diagramofthepositionofthespinalcordsegmentswith
referencetothebodiesandspinousprocessesofthevertebrae.
RelationofSpinalNervesandSegmentstothe
VertebralColumn
The 31 pairs ofspinal nerves include eightcervical, 12 thoracic, five lumbar,
five sacral, and one coccygeal pair. Spinal nerves emerge from the vertebral
canalviatheintervertebralforamina.Thefirstsevencervicalnervespassoutof
intervertebralforaminaabovethevertebrahavingthecorrespondingnumber.For
example, the sixth cervical nerve passes out of the foramen above the sixth
cervicalvertebra(Figure 2.5).Because thereareeightpairsofcervicalnerves,
butonlysevencervicalvertebrae,itisbesttorememberthattheeighthcervical
nervepassesoutbelowtheseventhcervicalvertebra.Thisestablishesapattern
in which all remaining spinal nerves (thoracic, lumbar,sacral, and coccygeal)
passoutbelowthevertebrawiththecorrespondingnumber(Figure2.5).
Aknowledgeoftheanatomicrelationshipbetweenspinalcordsegmentsand
the vertebral column is important for the diagnosis and treatment of certain
spinal cord disorders, such as compression injury caused by a tumor. An
appreciationoftherelationshipofthespinalsegmenttooverlyingvertebraand
spinousprocess is necessary whenlaminectomyis contemplated to relievethe
spinalcordcompression.Asageneralrule,at the upper cervical levels of the
vertebral column (i.e., C2–C5) add 1 tothenumber of the spinous process to
indicatethe numberof theunderlying spinalsegmentat thetip oftheprocess.
Thus, the tip of the fourth cervical spinous process overlies the fifth cervical
segmentofthespinalcord.Frommid-cervicaltomid-thoraciclevels(i.e.,C6–
T6),theunderlyingspinalcordsegmentattheprocesstipisidentifiedbyadding
2tothenumberofthespinousprocess;atmid-thoracicto low-thoracic levels
(i.e., T7–T10), by adding3 to this number. The eleventh and twelfth thoracic
spinous processes overlie the five lumbar spinal cord segments, and the first
lumbar spinous process overlies the five sacral segments. The part of the
vertebralcanalformedbythelastfourlumbarvertebraeandthesacrumcontains
acollectionoflonglumbarandsacralanteriorandposteriorrootsknownasthe
caudal equina (horse’s tail) in addition to a specialization of the pia mater
knownasthefilumterminale.
SurfaceAnatomyandEnlargements
The surface of the spinal cord displays a number of longitudinally oriented
grooves (Figure 2.4). On the posterior (dorsal) surface in the midline is the
shallow posterior median sulcus. This sulcus is continuous with the posterior
median septum, a glial partition extending deeply to the gray matter. The
posterolateralsulcus is a shallow groove that demarcates the entrance of the
dorsalrootsintothespinalcordbilaterally.Inthecervicalanduppersixthoracic
spinalcordsegments,theposteriorintermediatesulcusandunderlyingposterior
intermediate septum is found between the posterior median and posterolateral
sulci on each side of the spinal cord. On the anterior (ventral) surface, the
prominent anterior median fissure penetrates the cord for a depth of
approximately 3 mm and contains the sulcal branches of the anterior spinal
arteryandvein(Figure2.4).Theanterolateralsulcusmarksthesiteatwhichthe
ventralrootfibersexitthecord.However,becausetheventralrootsexitatless
regularintervalsandarenotasnumerousasdorsalroots,theanterolateralsulcus
isnotaseasilyseenastheposterolateralsulcus.
The spinal cord is not uniform in diameter; it contains two enlargements
associated with the innervation of the upper and lower limbs. The cervical
enlargementisthemoreprominentofthetwoandisfoundattheC5–T1levels.
Thesesegmentallevelsarethesamelevelsthatgiverisetothenerverootsthat
formthe brachial plexus and thusprovideinnervation for the upperlimb.The
lumbarenlargementgivesrisetoneuronsandfibersthatformthelumbarplexus
(L1–L4) and the sacral plexus (L4–S2), both of which are involved in the
innervationofthelowerlimbs.Theseenlargementsarethenaturalresultofthe
necessary increase in neurons and their processes at these levels for the
innervationoflimbmusculatureandskin.
TerminalEndoftheSpinalCord
Asmentionedearlier,thetaperedendofthespinalcordisusuallyfoundatthe
level of the intervertebral disk between L1 and L2 and is called the conus
medullaris(Figures2.6and2.7).Theconusmedullarisconsistsofsacralspinal
cord segments. It provides sensory innervation to the saddle area, motor
innervationfor the sphincters,andparasympathetic innervation forthe bladder
andlowerbowel(i.e.,fromtheleftsplenicflexuretotherectum).Hereagainan
appreciationoftheanatomicrelationshipsbetweenthespinalcordandvertebral
columnis useful inthediagnosis of somespinalcord disorders resultingfrom
injury. Traumain the lower back at the level of the L1 vertebramayresultin
conusmedullarissyndrome,causedbyadirectinjuryoftheconusmedullarisat
thislevel(Figures 2.6and 2.7).The signs andsymptoms of thissyndrome are
permanentflaccidparalysisoftheexternalanalsphincterandfecalincontinence,
bladder distension and incontinence, impotence, and perianal or saddle
anesthesia.
The flaccid paralysis of the external anal sphincter is caused by the
destruction of the somatic lower motoneurons that innervate this voluntary
muscleattheS2–S4levels.Theseneuronsnormallyprojectaxonstothemuscle
via the inferior rectal branch of the pudendal nerve. Bladder distension and
incontinenceiscausedby paralysisof thedetrusormuscle, thesmoothmuscle
wall of the bladder innervated by the pelvic splanchnic nerves arising from
preganglionic parasympathetic neurons at S2–S4, and also by paralysis of the
urethral sphincter, the striated (voluntary) muscle innervated by the perineal
branchofthepudendalnerve(S2–S4).Asinthebowel,thebladderdysfunction
ofconusmedullarissyndromeiscausedbythedestructionofneuronsattheS2–
S4levels ofthespinal cord.Generally, thebladderis permanentlyareflexic in
conusmedullarissyndromebecauseofthelossofthesacralspinalneuronsthat
giverisetothebladderreflexes.Thus,a“spastic”or“automatic”bladderdoes
notdevelopasitwouldwhenthecordisinjuredatmorerostrallevels,atwhich,
the sacral bladder reflex circuitry is spared, and these neurons become
hyperactiveafterrecoveryfromspinalshock.
FIGURE2.6Posteriorviewoflowerendoftheduralsac.
FIGURE2.7Spinalcordinsitu.
In conus medullaris syndrome, impotence isprimarily caused by a loss of
parasympathetic neurons at S2–S4. Erection is achieved normally when
parasympatheticstimulationcausesthesmoothmuscleofthearteriesassociated
with the erectile tissue of the penis to relax. As a result, the arterial lumina
enlargeandbloodisallowedtoflowintoanddilatethecavernousspacesinthe
corpora of the penis. The bulbospongiosus and ischiocavernosus muscles are
innervatedby the deep branchofthe perineal nerve, abranchof the pudendal
nerve (S2–S4). Normally, during erection, these muscles contract and thus
compress the venous plexuses at the periphery of the corpora cavernosa,
preventing the return of venous blood. As a result, the penis becomes erect.
Because it is likely that neurons innervating the bulbospongiosus and
ischiocavernosus muscles will also be lost in conus medullaris syndrome,
paralysisorparesisofthesemusclescontributestoimpotence.
Loss of sensory neurons in the dorsal horn at S4 and S5 causes perianal
anesthesia and saddle anesthesia (i.e., anesthesia of the posterior thigh). In
conusmedullarissyndrome,thisanesthesiaiscausedpredominantlybyalossof
sensory neurons at the S2 level. In a pure conus lesion, normal sensory and
motor function is retained in the lower limb (i.e., assuming only the conus
medullarisisinjured,asinatumorlocatedattheconusmedullaris,andlumbar
rootsofthecaudaequinaarespared).IftheS1levelisspared,theanklejerkis
retained.Finally,iftheconusmedullarislesionisincomplete,someofthesigns
andsymptomsnotedabovemaynotoccur.
Lesionsofthecaudaequina(Figure2.7)belowtheL1vertebrallevelresult
incaudaequinasyndrome.Thesignsandsymptomsofthissyndromearesimilar
tothosefollowingconuslesions.However,caudaequinalesionsusuallyaffect
notonlyperipheralnervefibersfromthesacralsegmentsofthecord,butalsoa
varyingnumber ofthe lumbardorsaland ventralnerve roots.Thesensoryand
motorlosses are,as arule,moreextensiveand reachhigher spinallevels(i.e.,
thelowerlimbs)followingcaudaequinalesionswhencomparedwithlesionsof
theconusmedullaris.Furthermore,thedistributionofmotorandsensorylossis
usually more irregular because some of the nerve roots will be damaged and
otherswillbespared.
Itisimportanttonotethatbecauseoftheanatomicalproximityoftheconus
medullaris and cauda equina, a single traumatic injury is likelyto affect both
structures, thus making the determination of the injury level and the specific
syndromedifficultonthebasisofaneurologicexaminationalone.However,if
there is a tumor in the conus medullaris, this will likely affect only sacral
neurons and spare the lower limbs. In fact, the International Standards for
Neurological and Functional Classification of Spinal Cord Injury (5) define
conusmedullaris syndromeas aninjuryof thesacral cord(conus)and lumbar
nerve roots within the spinal canal that usually results in areflexic bladder,
bowel,andlowerlimbs.Interestingly,caudaequina syndromeis definedas an
injuryto the lumbosacral nerverootswithinthe spinal canal whichmayspare
thespinalcorditself(i.e.,caudaltotheconusmedullaris)(5).Inthischapter,we
define the syndromes differently and present a summary of the signs and
symptomsthatwouldoccurfollowinginjurytoeitherstructure,butnotboth,to
emphasize the anatomic and functional organization of the spinal cord. It is
noteworthy that conus medullaris syndrome and cauda equina syndrome have
beendefinedinthissamemannerinothertextbooks(6).
MeningesoftheSpinalCord
The three membranous investments of the spinal cord—the dura mater,
arachnoid,andpiamater—arecontinuouswiththemeningealinvestmentsofthe
brain.The outermostcovering, theduramater, forms a long tubularsheathof
dense,fibroelastic tissuearoundthe spinalcordand cauda equinathat extends
fromtheforamenmagnumtothelevelofthesecondsacralvertebra(Figure2.8).
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