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patientshascomefrompublichospitalssuch as the VAafter WWII and from
militaryhospitalsinWWIandWWII.Inthosesituations,thepayerwasalsothe
providerofcare,assuringcoordinatedcareandfundingatasinglesite.Butthese
systemsofcareappliedonlytomembersofthemilitaryorveteranswithcovered
injuriesandoftendidnotintegrateacutesurgicalcarewithrehabilitation.
InWWImilitaryfacilitiesdirectedbySurgeonGeneralWilliamGorgas,R.
TaitMcKenzie,JoelGoldthwait,andFrankGrangerwouldensure coverageof
rehabilitationservicesas wellasnecessarysurgicalandmedicalcare,although
not necessarily in a fully integrated model system (9). In 1936 Munro would
establishanSCI centerat BCHutilizingtherehabilitationresources developed
by Granger in the 1920s. In 1944, financing was provided for Munro’s SCI
patients by Liberty Mutual Insurance Company through its worker’s
compensationcoverage,underwhichitdirectedSCIpatients tospecial centers
(57). Workers Compensation insurers have a special incentive to provide
integrated care including comprehensive medical and vocational rehabilitation
services, because rehabilitation and a return to work reduces the long-term
outlaysforincomesupportandmedicalexpensesaswellasmedicalcarewhich
workers compensation carriers are obliged to cover.During WWII, Rusk and
Kessler would develop comprehensive rehabilitation programs in Army and
Navy hospitals for severely disabled patients (19,58). After WWII, Paul
Magnuson, Medical Director of the VA, established affiliations between VA
hospitalsandacademichealthcenterswithrequiredrehabilitationservicesinall
VAhospitals, establishing a gold standard for acute rehabilitation care of SCI
andotherseveredisabilitiesalthoughnotintegratinginitialsurgicalcare(37,44).
In the late 1940s, the Mine Workers Health and Welfare Fund directed their
severely disabled members to specialized rehabilitation centers providing
surgical,medicalandcomprehensiverehabilitationservices,butoftenthisonly
occurredyears after theinitialinjury (19,58). Beginninginthe mid- 1950s,as
described previously, Mary Switzer led the RSA (then referred to as the
Vocational Rehabilitation Administration) in financing comprehensive
rehabilitation services and rehabilitation research, but achieved only limited
federalandstatefundingforvocationalrehabilitation(37).Inthe1970s,J.Paul
Thomas and John Young would found a national demonstration program for
model SCI centers financed by RSA. However, financing of surgical and
medical services was the responsibility of other payers. In Canada,
comprehensiveSCIcareandfinancingwereledby auniquepartnershipofthe
CanadianVeteransAssociation,itslocalhospitals,andtheCanadianParaplegic
Association,initiallyformedbyveteransandservingbothveteransandcivilians
(59).
The availability of Medicare coverage for Social Security Disability
Insurance beneficiaries in 1972 enabled appropriate financing of surgical,
medical,andmedicalrehabilitationservicesforSCI;moreover,enactmentofthe
Prospective Payment System in 1983 incentivized expansion of rehabilitation
programs and SCI services. However, comprehensive rehabilitation services
including vocational, social, and psychological rehabilitation, as well as longterm follow-up were not available, especially given financial constraints on
rehabilitation payments in the 1990s (37). Private insurers and employers’
concerns with the cost of health and rehabilitationservices alsoledto private
insurancecoveragelimitsbeginninginthelate1980s.
Thefragmented medicalcaresystem referredtoby Donovan inhis Munro
Lecture(5)andothersismirroredinthefinancingavailableforSCIcareinthe
UnitedStates.Thebestfinancingforcomprehensivecareremainsinmilitaryand
veteran’sfacilitiesaswellaswithafewinsurersintheWorkersCompensation
programthatdirectpatientstocomprehensiveSCIcenters.
CONCLUSION
Asthishistorydemonstrates,thenihilist“nottotreat”attitude,whichprevailed
for millennia, gave way in the early part of the 20th century to succeeding
decades of remarkable achievement in SCI care. However, the roots of
Rehabilitation Medicine, which the pioneers wedded to medical and surgical
caretoachievethisrevolutioninWWII,wereexhibitedacenturyagoinWWIin
GermanyandtheUnitedStates.Effortstoestablishcomprehensiverehabilitation
oftheSCIpersonwasfurtherfacilitatedbytheestablishmentoftheSCIModel
Systemsinthepast50years,whicheliminatedfragmentationandprovidedcare
fromthemomentofinjurytolifelongfollow-upinfundedprograms.Inaddition,
education, research, and advocacy organizations have emerged,advancing the
visionof pioneers, bringingever-increasing attentionto the importanceofSCI
medicine.
Yettheseaccomplishmentshavebeentemperedbycontinuingchallengesto
the fragmentation of care due to limitations of financial and organizational
resourcestosegments of our society and the international community. History
teachesus that advancesin knowledge appliedwithvision, determination,and
optimism by dedicated professionals in partnership with consumers will
hopefullyprevail.
ACKNOWLEDGMENTS
Recognition and appreciation of assistance to Richard E. Verville, Dan
Lammertse, Kristian Ragnarsson, John Russell Silver, Avi Ohry, Margaret
Hammond,andCarolynKinney
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2
Development,Anatomy,andFunctionof
theSpinalCord
HarryG.Goshgarian
This chapter is written for physicians and other practitioners who care for
patients with spinal cord injury (SCI), and thus does not include all of the
macroscopicandmicroscopicdetailsofhumanspinalcordanatomythatmaybe
included in standard medical texts. Only major topics are discussed and,
wheneverpossible,theissuesarecoveredfromaperspectivethatisrelevantto
spinalcordmedicine.Forinstance,inthediscussionofthedevelopmentofthe
spinalcord,abriefdescriptionofdefectsinneuraltubeclosure(spinabifida)is
included.Moreover,althoughthefunctionofseveralascendinganddescending
spinal pathways is discussed, emphasis is placed only on those that are most
relevant to SCI. Finally, although the standard medical text description of the
arterialbloodsupplytothespinalcordisincluded,thereisalsoadiscussionof
howanunderstandingofthedistributionpatternofthesearteriesmayleadtoa
diagnosis of anterior cord syndrome. Details regarding the intrinsic
neuroanatomicorganizationofthegrayandwhitematterhavebeenomitted,but
referencesareincludedattheendofthechaptersothatareadermaypursuethis
informationifitshouldbecome necessary. This chapter is organized into four
major sections, which cover the embryonic development, gross anatomy,
neuroanatomicorganization,andbloodsupplyofthespinalcord.
EMBRYONICDEVELOPMENT
The formation of the human spinal cord begins during the third week of
gestation. Soon after gastrulation, the process that establishes all three germ
layers (ectoderm, mesoderm, and endoderm), the axial portion of the
neuroectoderm(neuroepithelium)thickenstoformtheneuralplatedorsaltothe
mesodermalnotochordalplate(Figure2.1A,top).Theneuralplatethickensand
eventuallyforms the neural groove(Figure2.1B, middle). The lateral margins
(folds)oftheneuralgroovecontinuetothickenapproaching each other at the
midline. As the neural plate thickens laterally,a group of cells appears along
each edge (crest) of the neural folds (Figure 2.1B middle). These ectoderm
neuralcrest cellsextendalong thelengthof theneuralgroove. Eventually, the
neural groove closes and forms the neural tube. The neural crest cells then
migratelaterally toultimately giveriseto thedorsalroot gangliaofthe spinal
nerves and other cell types (Figure 2.1C bottom). At about the same time as
neuraltubeclosure,themesodermofthenotochordal plateis transformedinto
thenotochord(Figure 2.1C, bottom). Both events occur at the 7to 10 somite
stageofdevelopment.Theclosureoftheneuraltubeoccursatthecervicallevel
of the future spinal cord and progresses both rostrally and caudally (Figure
2.1D). The junctional zones (at which neuroepithelial closure takes place)are
known rostrally as the anterior neuropore and caudally as the posterior
neuropore(Figure2.1D).Finalclosureoftheanteriorneuroporeoccursatthe18
to20somitestageofdevelopment(25thday),whiletheposteriorneuroporeof
the lumbosacral spinal cord closes two days later at the 25 somite stage.The
closure of the neuroepithelium results in the spinal canal and cephalic brain
vesicles.Theensuingmitosisofthesurroundingneuroepithelialcellsoccursin
thefluid-filledhumoralenvironmentofthecerebrospinalventricularsystem.
Mitosisoftheneuroepithelialcellsaroundthespinalcanalgivesrisetothe
primitivenervecells,orneuroblasts,intheembryonicspinalcord.Collectively,
thesecellsformthemantlelayeraroundtheneuroepitheliallayer(Figure2.1C).
Themantlelayerwilldevelopintothefuturegraymatterofthespinalcord.The
peripheral marginal layer contains nerve fibers which grow out from the
neuroblasts and will form the future white matter of the spinal cord. During
gestational weeks (GW) 3.5 and 4.5,the continuing mitosis of neuroepithelial
cellsresultsinadorsalandventralthickeningoneachsideoftheneuraltube.
There is a longitudinal groove in the central canal, the sulcuslimitans, which
markstheboundarybetween the dorsal and ventral thickenings (Figure2.1C).
Theventralthickeningsareknownasthebasalplatesandtheseformthefuture
ventralhornsormotorareaofthespinalcord.Thedorsalthickeningsarethealar
platesand these form the future dorsalhorns(sensoryarea) of the spinal cord
(Figures2.1C).Thedorsalandventralmidlineportionsoftheneuraltubeform
theroofandfloorplates,respectively(Figure2.1C).Theseareasdonotcontain
neuroblasts,butratherserveassubstratesforaxonscrossingthemidlineofthe
spinalcord.Theroofplateregionwillformthefuturedorsalgraycommissure,
whilethefloorplatewillformthefutureventralgraycommissureofthespinal
cord.
AtGW5.5, an intermediate thickening of the mantle layer is visible. This
willultimatelyformtheintermediatehornofthespinalcordandwillbethesite
ofpreganglionicsympatheticneuronsfoundatallthoraciclevels(T1–T12)and
thefirsttwolumbarlevels(L1–L2).
FIGURE2.1Stagesofspinalcorddevelopment.
Bytheendofthefirsttrimesterofdevelopment,theneuroepithelialcellsthat
surround the central canal are replaced by ependymal cells signaling the
cessation of further neurogenesis. Motoneuron clusters in the ventral horn
segregate into medial and lateral groups, and there is an expansion of the
intermediate interneuronal field, a deepening of the dorsal funiculus, and a
furthergrowthanddifferentiationofthedorsalhorn.Theventralmediansulcus
deepensconsiderablyandissurroundedbytheventromedialfuniculus.
Followingthecessationofneuroblastproduction,gliablastsareformedfrom
the neuroepithelium. These cells migrate from the neuroepithelial layer to the
mantle and marginal layers where they form both fibrous and protoplasmic
astrocytes. Another glial cell type, most likely formed from gliablasts, is the
oligodendroglialcell.Thiscell,whichisfoundprimarilyinthemarginallayer,is
responsibleformyelinatingaxonsthatremainwithinthecentralnervoussystem
(CNS). The oligodendrocyte should be distinguished from the Schwann cell
whichisderivedfromtheneuralcrest.TheSchwanncellmyelinatesaxonsinthe
peripheral nervous system (PNS). Finally, during the second half of
development, a third type ofglial cell, the microglial cell isderived from the
mesenchyme.Microgliaare the main phagocytic cells in the CNS. During the
last 2 to 3 weeks of the first trimester, the gray matter of the spinal cord
approximatesitscharacteristicadultconfiguration.
Thespinalcord lengthensover threefoldduringthesecondhalf ofthe first
trimester(Figures2.2A–C).Infact,byGW11(67mm),thelengthofthespinal
cordmatchesthatofthevertebralcolumn.Bythistime,thespinalnerveshave
passed through the intervertebral foramina at almost right angles and have
establishedconnections withthe developing dermatomesand myotomesofthe
body somites. Starting at the beginning of the second (e.g., GW 14, 111mm
Figure2.2C)andprogressingthroughthethirdtrimesterofdevelopment,thereis
a disparate growth of the vertebral column and spinal cord with the vertebral
column growing faster in length. The greater rate of growth of the vertebral
columnrelativetothespinalcordcontinuesbeyondbirthuntiltheelongationof
thebodystopsduringadolescence.
The end result of the disparate growth of the spinal cord and vertebral
columnisthattheendofthespinalcordisfoundatapproximatelythelevelof
thefirstlumbarvertebraintheyoungadult.Thus,thespinalcordoccupiesthe
vertebralcanalintherostral2/3ofthevertebralcolumnintheadult.Theneural
connections between the spinal cord and body somites established during the
firsttrimester are maintained duringthesecond and third trimester (aswellas
postnatally) by the elongationof the central processes of the dorsal roots and
ventralrootswithinthevertebralcanalaswellastheelongationoftheperipheral
nerves in the body. The resultant anatomy of the spinal cord and the clinical
significanceofthisanatomywillbedescribedlaterinthischapter.
FIGURE2.2Thelengthofthespinalcordinrelationtothevertebral
columnatthreedevelopmentalperiods.
GW,gestationalweek.
Furtherdevelopmentofthespinalcordduringthesecondandthirdtrimesters
involves the establishment and growth of fibers systems that interconnect the
spinal cord with supraspinal centers, the proliferation of glia throughout the
spinalcord,andthemyelinationofdevelopingascendinganddescendingtracts.
Theexpansionofthewhitematterrelativetothegraymatterisaslowprocess
that progresses over the entire second and third trimesters. The white matter
enlargesin specific regionsofthespinal cord and myelination followsshortly
thereafterintheseregions.Myelinationdoes not occur uniformly in the white
matter. Itis first seen in thelateral aspect of the fasciculuscuneatus (i.e., the
“collateralizationzoneofthedorsalroot”)(1)andinthewhitematteradjacentto
the ventral horn (i.e., the “inferior circumferential fasciculus”) (1). The latter
area contains the propriospinal and intraspinal tracts whose fibers “close” the
intersegmentalreflexcircuitsofthespinalcord.Thenextmyelinatingtractsare
found in the fasciculus gracilis and medial aspect of fasciculus cuneatus, the
ventromedial and ventral funiculi, and the marginal fasciculus. The tracts in
theselatterareascontainascendingexteroceptiveandproprioceptivefibersand
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