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CLINICALSYNDROMESOFSPINALCORD
INJURY
Multiple clinical syndromes of SCI have been described in the literature and
includecentralcord, Brown–Sequard, anterior cord, posterior cord, CE, conus
medularis,anddiscompletesyndromes. The majority of these syndromes have
remained largely unchanged since they were originally described, with the
exceptionof central cord syndrome.Noneof the clinical syndromedefinitions
contain precise, quantitative criteria such as percentage of muscles with a
specificfinding.
Central cord syndrome (CCS) is the most common of the clinical
syndromes,accountingforapproximately50%ofincompleteinjuriesand9%of
alltraumatic SCI (53).Thisis characterized by greater motor weaknessinthe
upperextremitiesgreater than the lower extremities, in associationwithsacral
sparing(54).Atthelevelofinjurythereislowermotorneuron(LMN)weakness
as well as sensory loss, with upper motor neuron (UMN) paralysis below the
lesionlevel.In addition to the motor weakness, other features include bladder
dysfunctionandvarying sensory loss below the level of thelesion.CCSmost
commonly occurs in older persons with cervical spondylosis who suffer a
hyperextensioninjury,typicallyfromafall,followedbymotorvehiclecrashes.
However,CCS may occur in persons of any age and is associated with other
etiologies,predisposingfactors,andinjurymechanisms.Thepostulatedcommon
mechanism of injury involves compression of the cord both anteriorly and
posteriorlybydegenerativechangesofthebonystructures,withinwardbulging
oftheligamentumflavumduringhyperextensioninanalreadynarrowedspinal
canal (53–58). Occurring with or without fracture or dislocation, CCS was
initially described as caused by hemorrhage to the central cord. However,
subsequentresearchnotesthatthefindingsofthissyndromearepredominately
due to white matter lesions, with potential further gray matter involvement
(when accompanied with LMN findings in upper extremities) (55–57). The
findingsoftheupperextremitiesbeingrelativelymoreinvolvedthanthelower
extremitieswasinitiallypostulatedasduetoamorecentrallocationoffibersof
the upper limb within spinal cord motor tracts (with the lower limbs more
peripherallylocated)(54,58).Thishasbeenchallengedwithmorerecentstudies
being supportive of a disproportionate distribution of the corticospinal tract
contributingtohandandupperextremityfunction,therebyanyinjurytothetract
leadingtomoreaccentuatedsymptomsintheseareas(59).
ThedefinitivediagnosticcriteriafortraumaticCCSremainsundefined,with
surveys demonstrating lack of consensus on the degree of upper extremity
weakness or lower extremity sparing required for classification (60,61).
Research has demonstrated that upper and lower extremities recovery is not
significantlyalteredevenwithgreatermotordiscrepanciesbetweenthetwo,and
theAISremainsmostpredictiveofrecovery(62).
CCS usually has a favorable prognosis (53,63–65). The typical pattern of
recovery occurs earliest and to the greatest extent in the lower extremities,
followedby bowel andbladder function, upperextremity(proximal), andthen
intrinsic (distal) hand function. The prognosis for functional recovery of
ambulation,activitiesofdailyliving(ADL),andbowelandbladderfunctionare
dependent upon the patient’s age, with a less optimistic prognosis in older
patientsrelativetoyoungerpatients(63,64).Patients<50yearsofagearemore
successfulin achieving independent ambulationthan older patients (87%–97%
vs. 31%–41%). Similar differences were seen between the younger and older
patients in independent bladder function (83% vs. 29%), independent bowel
function(63%vs.24%),anddressing(77%vs.12%).However,forpersonswith
initialneurologicalexaminations(within 72hours)withaclassificationof AIS
Dtetraplegia,prognosisfortherecoveryofindependentambulationisexcellent,
evenforthosewhoseageis>50(66).
Wheninitially describedin the1950s,surgicaldecompressionof CCSwas
discouraged as potentially leading to worse functional outcomes. While
decompression is now accepted, controversy regarding the role of timing of
surgicalinterventioncontinues inCCS. Retrospectivereviews todate havenot
demonstratedfunctionalimprovementassociatedwithearlydecompression(67–
69), though a single ambispective study has shown motor improvement at 6
monthsfor select CCSpatientswho received decompression priorto24 hours
afterinjury(69).
A syndrome with similar clinical features of upper extremity paresis or
paralysis with minimal to no lower extremity involvement is “cruciate
paralysis” (70–75). This may occur with fractures of C1 and C2, with
neurologicalcompromiseofthebrainstematthecervicomedullaryjunction(71)
asopposedtoCCSthatisusuallylocalizedinthemid-tolowersegmentsofthe
cervical spinal cord (i.e., C4–C5). Respiratory insufficiency occurs in roughly
25% of patients and cranial nerves can also demonstrate deficits. Overall, the
prognosis for cruciate paralysis is excellent, with studies noting over 50% of
patients with complete recovery (71). Wallenberg proposed an anatomical
explanation for this clinical syndrome (76), suggesting that the decussating
fibersoftheupperlimblayinamorerostral,medial,andventrallocationinthe
cervicomedullaryjunctioncomparedtoamorelateralandcaudallocationofthe
lower limb decussating fibers. Therefore, injury to the canal where the upper
extremityfibers travel alone after decussation causes preferential injury to the
upperlimbs.Neuroanatomicalevidencetosupportthishypothesis,however,has
notbeenfound(77).
Brown–Sequard syndrome (BSS) is characterized by asymmetric paresis
withhypoalgesiamoremarkedonthelesspareticsideandaccountsfor2%to
4%ofalltraumaticSCI(76–82).IntheclassicpresentationofBSS,thereis(a)
ipsilaterallossofallsensorymodalitiesatthelevelofthelesion,(b)ipsilateral
flaccidparalysisat the level ofthelesion, (c) ipsilaterallossof position sense
and vibration below the lesion, (d) contralateral loss of pain and temperature
belowthelesion,and(e)ipsilateralmotorloss(UMN-mediated)belowthelevel
ofthelesion.Almost90%ofthesecasesareinthecervicallevel,and66%are
classifiedasAISD(53).
Understandingtheunderlyingneuroanatomy allows for an insight into this
constellation of signs. Spinothalamic tract decussation within the spinal cord
leadsto contralateral loss ofpainand temperature when injured.Corticospinal
anddorsalcolumntractsdecussatewithinthebrainstem,explainingforclinical
findings of loss ofmotor,proprioception and vibration sense ipsilateral to the
lesion.
AlthoughBSShastraditionallybeenassociatedwithknifeinjuriesthatcause
cord hemisection, a variety of etiologies including those that result in closed
spinalinjurieswithorwithoutvertebralfracturesmaybethecause(81–83).In
addition,neoplasticcausesandintramedullaryinflammatorylesions,suchasin
multiple sclerosis, can result in partial or complete BSS. In clinical practice,
however,onlyalimitednumberofpatientspresentwithpureBSS.Moreoften,
patientspresentclinicallywith acombinationof featuresfromBrown–Sequard
and CCS, with relatively varying degrees of ipsilateral hemiplegia and
contralateral hemianalgesia. This has been termed Brown–Sequard plus
syndrome(81).
Despitethevariationinpresentation,considerableconsistencyisfoundinthe
prognosis of BSS. Recovery usually takes place in the ipsilateral proximal
extensorsandtheninthedistalflexors(84,85).Motorrecoveryofanyextremity
havingapain/temperature sensorydeficitoccursbeforetheoppositeextremity,
andthesepatientsmayexpectfunctionalgaitrecoveryby6months.
Nearly, 75% to90% of patients ambulate independently at dischargefrom
rehabilitation and 70% perform functional skills and ADL independently
(53,79,83). The most important predictor of function is whether the upper or
lowerlimbisthepredominantsiteofweakness:whentheupperlimbisweaker
than the lower limb, patients are more likely to ambulate at discharge (81).
Recovery of bowel and bladder function is also favorable, with continence
achievedin82%and89%,respectively,inonestudy(81).
Theanteriorcordsyndrome(ACS)accountsfor2.7%oftraumaticSCIand
involves a lesion affecting the anterior two-thirds of the spinal cord while
preservingtheposteriorcolumns.ACSmayoccurfromretropulseddiscorbone
fragments(86),directinjurytotheanteriorspinalcord,ormostcommonlywith
vascularinjuryorocclusionoftheanteriorspinalarterythatprovidestheblood
supplytotheanteriorspinalcord(87).Thiscanoccurduringsurgerytotheaorta
(especiallywith clampingabove therenalartery) orother processesthatcould
decreasebloodflowtothespinalcord(i.e.,vertebralburstfracture).Thereisa
variablelossofmotoraswellaspinpricksensationwitharelativepreservation
oflighttouch,proprioception,anddeep-pressuresensation.Usuallypatientswith
ACShaveonly10%to20%chanceofmusclerecovery,andeveninthosewith
somerecovery,thereispoormusclepowerandcoordination(88).
The posterior cord syndrome is the least frequent of incomplete SCI
syndromes and has been omitted from recent versions of the International
Standards. It is characterized by preservation of pain, temperature, and touch
appreciationwith varying degrees of motor preservationandan absence of all
dorsal column function. Prognosis for ambulation is poor, secondary to the
proprioceptivedeficits.
Conus Medullaris and Cauda Equina Injuries (Table 5.5): The conus
medullaris,whichistheterminalsegmentoftheadultspinalcord,liesattheL1
vertebraeandendsattheinferioraspectoftheL1vertebrae.Thesegmentabove
theconusmedullarisistermedtheepiconus,consistingofspinalcordsegments
L4–S1. Nerve roots extend from the conus medullariscaudallyas the CE. As
nerverootsandUMNaretightlyconsolidatedinthisregion,injuriestotheconus
medullaris and epiconus can present clinically withvariedfindings. Typically,
lesions to the epiconus primarily affect the lower lumbar roots with relative
sparing of sacral reflex arcs. This translates clinically into UMN findings in
sacral segments with spasticity likely developing in toe flexors, ankle plantar
flexors,andhamstringsandinpatientshavingpositivebulbocavernosusreflexes.
LowerconusmedullarislesionsaffectingneuralsegmentsS2andbelowwill
presentwith LMNdeficits ofthe analsphincterand bladderdue todamageof
the anterior horn cells of S2–S4. These lower conus lesions are clinically
indistinguishablefrom CE injuries (see the followingparagraph). Bladderand
rectalreflexesarediminishedorabsent,dependingontheexactlevelandextent
ofthelesion.Thereisparalysisofthebladderdetrusormuscleduetodestruction
of the preganglionic parasympathetic (PS) fibers, with retention of urine and
overflow incontinence. In men, there is failure of penile erections and
ejaculation due to the destruction of the preganglionic PS neurons and the
somaticmotorventralhorncells,respectively.Emissionofsemencanstilloccur
because the motor fibers to the ductus deferens and seminal vesicles have
sympatheticinnervation.Motorstrengthinthelowerlimbsmayremainintactto
a variable degree, depending on degree of injury to nerve roots arising from
morerostralsegments(L2–S1).Thelumbarnerverootsmaybesparedpartially
ortotally inthe conusmedullaris, referredtoas“rootescape.” Ifthe rootsare
affectedastheytravelwiththesacralcordinthespinalcolumn,thiswillresult
inLMNdamagewithdiminishedorabsentreflexes.Insomeconusinjuries,the
kneereflexesmaybepreserved,but theanklereflexes willbeaffected.Inlow
conuslesions,the S1segment isnotinvolvedandtherefore,theankle reflexes
arenormal, afindingaccounting formostinstances offailureto recognizethe
clinical syndrome. Due to the small size of the conus medullaris, lesions are
more likely to be bilateral as compared to those of the CE. With conus
medullarislesions,recoveryofcompletelyparalyzedmusclesislimited.
InjuriescaudaltotheL1vertebrallevelpredominantlydonotcauseinjuryto
thespinalcord,butrathertotheCEornerverootletssupplyingthelumbarand
sacralsegmentsoftheskinandmusclegroups.CaudaEquinaSyndrome(CES)
thereforeisa LMN syndrome that presents with patchy and often asymmetric
findings of lumbosacral impairment ranging from complete flaccidity to
seemingly unaffected due to the relative mobility of these neural segments.
Atrophy and flaccid paralysis of lower extremity musculature (L2-S2) and
varyingsensorylossinradicularpatternsiscommon.Additionally,lossofdeep
tendonreflexesandbowel/bladderinvolvementisseenfrequently.Patientsmay
classicallyhave “saddle anesthesia” (loss of sensation in theupper innerlegs,
inneraspectsofthebuttocksandperineumregions)withaccompanyinglossof
bulbocavernosusand analwinkreflexes. WithsignificantLMN componentsto
this syndrome, prognosis for recovery is better than incomplete UMN
syndromes.Thisislikelyduetotheresiliencyofthenerverootstoinjury,with
earlydeficitspotentiallyduetoneurapraxiademonstratingprogressiverecovery
over weeks to months. As CE rootlets are histologically peripheral nerves,
regenerationispossible.
SeparationofCEandconuslesionsinclinicalpracticeis difficult,because
theclinicalfeaturesaswellaslevelsofinjuryoftheselesionsoverlap(53).(See
Table 5.5.) Isolated conus lesions are rare since the roots forming the CE are
wrapped around the conus. Traumatic SCI will likely produce a combination
syndromeorapureCElesion.TheconusmaybeaffectedbyafractureofL1,
whereasafractureofL2orlowerimpingessolelyontheCE.Sacralfracturesas
well as fractures of thepelvic ring also damage the CE, as well as the sacral
plexus.Bulletwoundscanpenetratethebonystructurestotraumatizethecauda
andconus.Intrinsictumorsoftheconusmedullariscanselectivelydamagethe
conus.
Caudaequinalesions can be considered as multiple radiculopathiesandas
such electrodiagnostic studies may be helpful in the diagnosis. The
electromyographic abnormalities in cauda lesions would be widespread and
bilateral (but often asymmetrical). Other methods of studying root or nerve
function (H-reflexes, F waves, root stimulation, somatosensory evoked
potentials)maybeusedtoaidindiagnosis.Conusmedullarislesionswillcause
electricalabnormalitiesinmuscleswheretheLMNsareaffected.
SCIclinicalsyndromescanbetheresultofbothtraumaticandnontraumatic
etiologies. CCS and conus medullaris syndromes are most likely due to falls,
whereas motor vehicle crashes are the primary etiology for BSS. In contrast,
AnteriorCordandPosteriorCordsyndromesaremorefrequentlytheresultofa
nontraumaticinjury. CES is almost equally due to traumatic and nontraumatic
etiologies(53).
DISCOMPLETEINJURIES
Neurological pathways within the spinal cord may be spared even after a
neurologicallycompleteinjuryonclinicalexam.Theterm“discompleteinjury”
was introduced by Dimitrevic and colleagues (89,90) to describe a clinically
complete SCI with neurophysiological evidence of residual function and
connectivity between above and below the injury. Subsequent studies have
demonstrated degrees of intact localization with quantitative sensory testing
below the neurological level of injury in complete injuries (AIS A) without
sparingofclinicalmotor,LTor sharp/dulldiscrimination(91–95). Finnerupet.
al. performed quantitative sensory testing below the level ofinjury (including
thermalstimulation,pressure,pinchandpainsensitivity)in24subjectswithAIS
A (with no sparing of voluntary motor function or preserved sharp/dull
discriminationorLTsensationbelowtheinjury)andfoundthat50%hadvague
localizedsensation tothe stimuli(95).All patientshadno cortical responseto
lowerextremity(posteriortibialnerve)SSEP.Therewasnorelationshipbetween
the presence of this sensory perception with levelofinjury or etiology. There
was also no correlation between the presence of sensory perception with the
presenceorseverityofspasticityorchronicneuropathicpain(95).
Neuropathologicalstudiesfoundasimilarpercentage(50%)ofanatomically
discompleteinjuriesinpersons withclinicalcompleteinjuries(89,91).Further,
recentresearchonepidural stimulation in clinically complete injuries suggests
the presence of such latent tracts (96). However, it is still unclear where the
spared information travels and what the preservation of these pathways
represents.KnowledgeofretainedneuralcommunicationacrossaSPImayhave
consequences for treatment strategies and enhancing functional recovery and
furtherstudyisneeded.
CONCLUSION
PerformanceofanaccurateexaminationasrecommendedbytheISNCSCIwill
allow the professional to classify the individual using the ASIA Impairment
Scale. Using consistent terminology and definitions will allow for improved
communicationbetweenclinicians,researchers,andpatients.
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