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withcutaneousreflexesgenerallyprecedingDTRs(53,54).Thefirststepinthe
earlyexaminationofSCIpatientsinvolvesdetectionofthepresenceorabsence
ofdelayedplantarresponse(DPR)achievedbyadministeringastrongstimulus
tothesoleofthefootwithabluntinstrument,movingfromtheheeltothetoes.
In a 1999 prospective study of reflex recovery in patients admitted within 24
hoursofSCI(55),Koandhiscolleaguespresentedthefirstsignificantpatternof
reflex recovery, observing that the DPR returned first, followed by the
bulbocavernosus(BC)and cremasteric (CR) reflexes in the first few days and
subsequentlythe DTRs,that is,ankle andkneejerkreflexes,by 1to 2weeks.
Theyfurtherconcludedthat(1)thecontinuedpresenceofDPRfor48hoursor
more indicates poor prognostic significancefor neurological recovery,and (2)
the evolution of reflexes over several days following injury may be more
relevanttoprognosis than their presence or absence on the day of injury. The
DPRwasconsistentlyseeninsevereinjuriesbutwasseenfarlessoftenandfora
muchshorterduration inthose withAISDSCI.Prognosis forambulation was
diminished in those with AIS A, B, or C SCI who continue to demonstrate
presenceoftheDPRformorethan2days.
FIGURE9.1PercentAISconversionfrominitialexamination(within
<3daysto30daysofSCItothe1-yearanniversarydateafterSCI).
AIS, ASIAImpairment Scale; ASIA, American Spinal Injury Association; SCI, spinal cord
injury.
Source:Kirshblum SC, Botticello AL, Dyson-Hudson TA, et al. Patterns of sacral sparing
componentsonneurologicrecoveryinnewlyinjuredpersonwithtraumaticspinalcordinjury.
Arch Phys Med Rehabil. 2016;97(10):1647–1655. doi:10.1016/j.apmr.2016.02.012; Fawcett
JW, CurtLA, Steeves JD,et al. Guidelinesfor the conduct of clinicaltrials for spinalcord
injury as develop by the ICCP panel: spontaneous recovery after spinal cord injury and
statistical power needed for therapeutic clinical trials. Spinal Cord. 2007;45:190–205.
doi:10.1038/sc.2014.194; American Spinal Injury Association/International Medical Society
of Paraplegia (ASIA/IMSOP). International Standards for Neurologic and Functional
ClassificationofSpinal CordInjury,Revised2000.Chicago,IL:ASIA;LeeBA,LeibyBE,
Marino RJ. Neurological and functional recovery after thoracic spinal cord injury. J Spinal
CordMed. 2016;39(1):67–76. doi:10.1179/2045772314Y.0000000280; Marino RJ, Burns S,
GravesDE,et al. Upper andlower extremity motor recovery aftertraumaticcervical spinal
cord injury: an update from the National Spinal Cord Injury Database. Arch Phys Med
Rehabil.2011;92:369–375.doi:10.1016/j.apmr.2010.09.027;SpiessMR,MullerRM,RuppR,
etal.ConversioninASIA Impairment Scale during the firstyearaftertraumaticspinalcord
injury.JNeurotrauma.2009;26:2027–2036.doi:10.1089/neu.2008.0760
ThepresenceoftheBCreflexinapatientwithanuppermotorneuronlesion
has no prognostic significance, since it is usually present in these cases. Its
persistent absence for more than several days is suggestive of a lower motor
neuron (LMN) injury, which does have implications for the return of
independent bowel, bladder, and sexual function. While the majority of LMN
injuries occur at the T12-S5 levels, a notable percentage of T9-11 injuries
demonstrateabsenceoftheBCreflexaswellastheDTRs(56).
Calancieetal.(57)examined229acuteSCIsubjectswithkeyfindingsnoted
in crossed adductor responses in combination with close examinationof DTR
amplitudes.Intheirstudy,thecrossedadductorresponsewasneverobservedin
individuals who remained motor complete. In contrast, only three individuals
withcervicalmotor incompleteSCIfailedtodemonstratethecrossed adductor
response when follow-up occurred beyond the first 3 months of injury.
Furthermore, the amplitude of the DTRs was diminished in motor-complete
subjectsrelativetoincompleteparticipants.Bycombiningtheamplitudeofthe
DTRsandthepresenceorabsenceofthecrossedadductorresponse,theauthors
wereabletopredictwith100%accuracywhichoftheindividualswouldremain
motorcomplete.
TheFour-PhaseModelofReflexRecovery
In2004,Ditunnoetal. (54)postulatedan evolvingfour-phasemodelofreflex
recovery,markedbyhyperreflexia,whichisthoughttoresultfromthecreation
ofnewsynapseswithinthespinalcord,andtheresultantspasticitythatoccursas
thesynapsesarereestablished.Thefourphasescanbebrieflydescribed:
1. Areflexia/hyporeflexia(0–1day):Involvesinitialrecoveryofcutaneous
polysynapticreflexessuchastheBCandanalwinkandcremasteric
reflexes.ItincludestheDPRifthecaseissevere,andanexamineris
fortunatetoobserveitstransientpresence.Incervicallesions,thisphase
mayinvolvebradyarrhythmias,atrioventricularconductionblock,and
hypotension,arisingfromimpairedsympatheticinnervationandthe
presenceofvagalnerve-mediated,parasympatheticpredominance.Spinal
neuronhyperpolarizationalsooccursduringthistimefromtheinterruption
ofpathwaysofspinalmotorneuronsandinterneurons,lossofnormal
backgroundsupraspinalexcitation,increasedspinalinhibition,andreduced
neuronalmetabolism.
2. Initialreflexreturn(1–3days):Cutaneousreflexes(bulbocavernosus,anal
wink,andcremastericreflexes)increaseinstrength,andDTRsremain
absentinmostpatients,butthetibialHreflexcanreturn(58).
Physiologically,thisphaseinvolvesinactivity-dependentreceptor
upregulationandN-methyl-D-aspartate(NMDA)receptorupregulation
alongwithdenervationsupersensitivity.
3. Earlyhyperreflexia(4–30days):ReappearanceofDTRswithAchilles
reflexgenerallyprecedingpatellarreflexoccursinthisperiod,andthe
reemergenceoftheBabinskireflexfollowsshortlyaftertheanklejerk
appears.Improvementinbradyarrythmiasandhypotensionisseen,butat
thesametimethepatientbecomesatriskforautonomicdysreflexia
(althoughphase4hasmoreofthis).Mechanismsofrecoveryincludenew
synapsesgrowntocompensateforvacatedsynapticsites,withmost
occurringbyshort-axonedinterneuronsaswellaslimitedgrowthbylongaxonedinterneurons.
4. Spasticityandhyperreflexia(1–12months):CutaneousreflexesandDTRs
nowbecomehyperesponsiveandcanbeinitiatedwithminimalstimuli.
Detrusorfunctionmayrangefromareflexiatodysenergia(co-contractionof
detrusorandurethralsphincterinamaladaptivepattern).Mechanismsof
recoveryinthisphaseinvolvenewsynapsegrowthbylong-axonedneurons
suchas1Aafferentsandinterlimbafferentswithassistancefromaxon
transportforcertainaspectsofsynapsegrowth.
THEROLEOFIMAGINGFORPROGNOSISAND
FUNCTIONALRECOVERY
MRIhascontributedmorethananyotherimagingmodalitytoourunderstanding
ofnaturalhistoryfollowingSCI,andtheclaritywithwhichMRIisabletodepict
the anatomy of the spinal cord is unmatched. Specifically, MRI has made it
possible to assess intracanalicular and paraspinal soft tissues, including the
spinalcorditself(59–69).Despitethis,theclinicalindicationsforperformingan
MRIevaluationofthespineinthesettingoftraumaremaincontroversial.
MRI, however, has been proven helpful in the acute period for excluding
occult ligamentous/soft tissue injury, vertebral thrombosis, and for confirming
acute bony injury. It has also been used to exclude a neurological injury in
uncooperative, obtunded, or malingering patients. There is unequivocal
agreement that an MRI examination in the acute period is warranted in any
patientwhohasapersistentmyelopathyfollowingspinaltrauma(65,66,70).
MRIFindingsofSCI
MRI routinely demonstrates intramedullary hemorrhage and edema following
SCI.Inanimalstudies,thecombinationofMRIlesionlength,cordcaliber,and
extentofwhitematterpreservation(incrosssection)isrelatedtobothfunctional
status and pathologic findings at autopsy (71–73). The MRI appearance of
experimentally induced SCI has also been used to explain the variability in
functionaldeficitamonganimalssubjectedtoidenticalinjuries(71).
SpinalCordHemorrhage
Posttraumaticspinal cord hemorrhage on MRI is definedas thepresence of a
discrete focus of hemorrhage within the substance of the spinal cord
(intramedullary).Themostcommonlocationiswithinthecentralgraymatterof
thespinalcord,centeredatthepointofmechanicalimpact(60,62,65,68,74,75).
Drawingfrom experimental and autopsystudies,the underlying lesion ismost
oftenhemorrhagicnecrosisofthespinalcord.Truehematomyeliaisrare(75).
Immediatelyfollowinginjury,deoxygenatedhemoglobin(deoxyhemoglobin)
is the most common hemoglobin species generated (60,62,64,68,75–77). The
presenceof deoxyhemoglobin, representing hemorrhagicnecrosis of the spinal
cord(62–64,78), is depicted on high-field-strength MRI scannersasadiscrete
area of hypointensity on T2-weighted and gradient echo images (59–
62,64,68,70,74,77–80). Free radicals and oxidative stress in the lesion site
eventually cause deoxyhemoglobin to evolve into methemoglobin, a form of
hemoglobin unable to carry oxygen. After conversion to methemoglobin, the
hemorrhagic component of the SCI is depicted as increased signal on T1weightedMRIimages.Animalevidencesuggeststhatparenchymalhemorrhages
develop rapidly in the spinal cord after injury (81), but evidence of blood on
imaging is not immediately apparent. In the brain, methemoglobin appears
approximately 3 to 5 days after an initial hemorrhage. In the spinal cord,
conversionto intracellular methemoglobinmaybe delayed for 8daysor more
followinginjury,duetolocalhypoxia/hypoperfusionanddelayeddegradationof
deoxyhemoglobin.
SpinalCordEdema
Spinal cord edema is defined on MRI as a focus of abnormal high-signal
intensity on T2-weighted images (70). This signal abnormality is thought to
reflecta focalaccumulationof intracellularandinterstitial fluidinresponse to
injury (61,62,64–67,69,70,82,83), although microhemorrhage may also be a
contributingfactor.Theextentofedemaisbestdefinedbyusingthemid-sagittal
longrepetitiontime(TR)images.AxialT2-weightedimagesoffersupplemental
informationregardingtheinteractionofspecificstructuresinthecrosssection.
Edematypicallyinvolvesavariablelengthofspinalcordaboveandbelow the
level of injury, with discrete boundaries adjacent to uninvolved parenchyma.
Spinal cord edema is invariably associated with some degree of spinal cord
swelling.Posttraumaticspinalcordhemorrhagealwayscoexistswithspinalcord
edema; however, the converse is not always true; that is, edema can occur
withoutMRI evidence ofintramedullary hemorrhage. Inthesetting oftrauma,
edemawithin the spinal cord has beenreferredto as a contusion; when blood
products are present, the term of hemorrhagic contusion is used instead
(74,76,79,80,84).Cord edema alone connotes a morefavorableprognosis than
cordhemorrhage(64,74,84–86).
Factorsaffecting thelength of spinalcordedema include ageandthe time
frominjurytoimaging.Patientageisinverselyproportionaltolengthofspinal
cordedema(87),whiletimetoimagingisdirectlyproportionaltoedemalength.
InpatientswithcompletecervicalSCI,thelengthofspinalcordedemaincreases
approximatelyone vertebral segment every 30 hours during thefirst 72hours
post-injury(88). It isnot known how long ittakes for edema to first develop
aftertraumaticSCI.Recently,Aoyama et al. (89) described a patient who fell
andsustained a completeSCIat the C4 level.A MRI taken120minutes after
injury had no signal changes in the cord on T1- or T2-weighted images. A
postoperative MRI 8 hours after injury detected an increased signal on T2weighted images in the same area where intraoperative ultrasoundindicated a
hyperechoiclesion.
ClinicalSignificanceofSpinalCordMRIFindings
Theanatomiclocationofthe hemorrhage corresponds closely to the NLI, and
the presence of intramedullary hemorrhage implies a poor prognosis
(60,62,64,74,77,85,90–92).Zohrabianetal.(89)foundthattheupperboundary
ofhemorrhage showed a stronger correlation to the NLI than either the upper
boundary of edema or lesion epicenter. Use of multiple regression analysis
suggestedthatthecombinationof lesion epicenter and edema length were the
bestpredictorsof NLI (89). Patients withBrown-Séquardsyndrome following
bluntcervical traumaoften haveedema limitedtothehemicordon theside of
greaterweakness(93).PatientswithCCStypicallyhaveevidenceofcordedema
butnothemorrhageatthelevelofinjury(94).Therefore,MRImeasuresmaybe
usedasanobjectivemeasureoftheNLIandcansuggestthepatternandseverity
ofinjurywhendeterminationbyclinicalexaminationisnotpossible.
Theimagingparameters associated with neurological deficit and prognosis
are spinal cord hemorrhage, spinal cord edema, and spinal cord compression.
Using multiple regression analysis, Flanders et al. (95) assessed the utility of
MRIforpredictingmotorfunctionindependentoftheinitialclinicalevaluation.
Initialmotorscores,thepresenceofhemorrhage,andthelengthofedemawere
independentpredictors of the final motor score and theproportion ofmuscles
with useful function at 1 year. The addition of MRI parameters to the initial
clinicalinformationimprovedthepredictivepowerofthemodelby16%forthe
upperextremitiesand34%forthelowerextremities.
SpinalCordHemorrhageasaPredictorofNeurologicDeficitandRecovery
While it was initially thought that detection of intramedullary hemorrhage on
MRI was predictive of a complete SCI, the increased sensitivity and spatial
resolution of current MRI techniques has shown that small amounts of
hemorrhageareidentifiableinincompletelesions(60).Subsequently,ithasbeen
shownthattheseverityofneurologicaldeficits is determined by the extent of
cord edema and cord hemorrhage (80). Detection of a sizable focus of blood
(>10mminlengthonsagittalimages)inthespinalcordistypicallyindicativeof
acompleteneurological injury(84). Boldinetal.(96)foundthat patientswith
hemorrhagesmeasuringgreaterthan4mmincranial–caudallengthshowedno
clinicalimprovementatfollow-up,whereasthosewithhemorrhagesunder4mm
hadincompleteinjuriesandexhibitedclinicalimprovementatfollow-up.These
results suggest that there may be an absolute threshold for lesion size that
predictsneurologicalrecovery.
Schaefer et al. (97) correlated the appearance of the admission MRI to
changeintotalmotorscores,findingthattetraplegicpatientswithhemorrhagic
lesionsfailedtoshowsignificantimprovementinmotorscoresatfollow-up.Ina
similar study of 24 tetraplegic subjects, Marciello et al. (85) correlated the
presence or absence of intramedullary hemorrhage with changes in upper
extremityandLEmotorscores.Forpatientswithspinalcordhemorrhage,only
16% of upper-extremitymuscles and 3% of LE muscles improved toa useful
grade(≥3/5)atfollow-up,andonly7%ofpatientsimprovedoneormoremotor
levels. In comparison, for patients without MRI evidence of spinal cord
hemorrhage, 73% of upper-extremity and 74% of LE muscles improved to a
usefulgradeand78%ofsubjectsimprovedoneormorelevels.
SpinalCordEdemaasaPredictorofNeurologicDeficitandRecovery
Cordedema alone connotes amorefavorable prognosis than cord hemorrhage
with edema (64,74,84–86). The length of spinal cord edema is directly
proportional to the initial neurological deficit (62,80). Schaefer et al. (80,97)
reportedthatcordedemaextendingmorethanthespanofonevertebralsegment
was associated with greater initial neurologic deficit than smaller areas of
edema.Theseinvestigators also stated that patients with edema alone on MRI
hadagreaterimprovementintotalmotorscorecomparedtopatientswithboth
hemorrhageandedema.
In addition, patients with small areas of edema (less than one vertebral
segment in length) demonstrated the largestimprovement in total motorscore
(72% recovery), whereas larger areas of edema showed less recovery (42%).
Thisfindingwasconfirmedinastudyof104cervicalSCIpatientsfollowedfor
1yearpost-injury.Individual manualmuscletestscores were recorded for the
upper and lower extremities at acute hospital admission and 12 months postinjury. Motor recovery rates for the upper and lower extremities were also
determined.Lesionlengthwasdirectlyproportionaltoneurologicalimpairment
atthetimeofinjury(p<.001).NonhemorrhagicMRI(edematous)lesionswere
associatedwithhigher motorrecovery ratesinthelowerand upperextremities
andhadahigherproportionofmuscleswithusefulmotorfunction(95).
SpinalCordCompressionandRelationshiptoNeurologicDeficit
Silbersteinetal.(90)reportedthatfindingsassociatedwithseverespinetrauma
suchas spinalfractures, subluxation,ligamentous injury, prevertebralswelling,
and epidural hematoma were associated with severe clinical deficits at
presentationandapoorprognosis.Incontrast,Flandersetal.(62)foundthatthe
presenceoffractures,discherniation,andligamentousinjurywasnotpredictive
of the neurological deficit; however, the presence of residual spinal cord
compressionbybone,disc,orfluidwaspredictiveofahemorrhagicspinalcord
lesion,forwhichfunctionaloutcomeappearstobelessfavorable.Suchfindings
suggest that residual compression may be an important factor in determining
recovery and provide some support for early decompression following SCI
(59,62,98).
Clearly,thereisarelationshipbetweentheextentofspinalcordcompression
and neurological injury (99). Rao and colleagues (100) performed a critical,
evidence-based analysis of the existing literature. Reviewed studies included
bothquantitativeandqualitativeassessmentsofthespinalcanalandspinalcord
dimensions. Preexisting mid-sagittal canal stenosis (developmental or
congenital) was associated with a more severe neurological deficit following
cervicalinjury,mostnotablewhenthemid-sagittalcanaldiameterwas10mmor
less.InanotherstudyofcervicalSCI,theanteroposteriordiameterofthespinal
canal was again smaller in patients with complete (10.5 mm) and incomplete
injuries (13.1 mm) compared to patients with no deficits (16.7 mm) (101).
Hayashi et al. (102) found that 30% of patients with severe spinal cord
compression(defined as a two-thirds reduction in spinal corddiameter) hada
completemotor deficitat thetime ofinjurycomparedto20% ofpatients with
mildspinalcordcompression(definedaslessthanone-thirdreductioninspinal
cord diameter). More importantly, 90% of patients with mild spinal cord
compressionimprovedbyoneormoreAISgradescomparedto30%forpatients
withseverespinalcordcompression.
Miyanjietal.(103)usedquantitativeassessmenttodeterminewhetherMRI
correlated with initial neurological status and clinical outcomes in 100
consecutive cervical SCI patients. Complete motor and sensory deficits were
associatedwithspinalcordcompressionaswellasspinalcanalcompromisewith
a higher incidence of intramedullary hemorrhages, lesion length, soft tissue
injury, stenosis, and cord swelling. Initial cord compression, intramedullary
hemorrhage, and extent of cord swelling were predictive of poor neurological
outcomesatfollow-up.SubjectswithincompleteSCI(AISgradesB,C,orD)or
minimal deficits (AIS grade E) had a mean lesion length of 20 mm or less,
whereasthosewithcompleteinjurieshadameanlengthof40mm.
LimitationsofConventionalMRIintheEvaluationof
SpinalCordInjury
MRI is currently the best imaging modality for the evaluation of spinal cord
parenchyma but lacks the ability to differentiate edema from axonal injury.
While MRI provides valuable information about location and basic injury
characteristics,watercontent(edema)andhemorrhagedonotnecessarilyreflect
axonintegrityandfunction.ThislimitationisapparentinanimalmodelsofSCI.
Followingaspinalcordcontusioninadultrats,therewasnocorrelationbetween
magnitudeofneurologicalrecoveryandlesionsize(volume),whetherevaluated
by T2-weighted abnormal signal (edema) or T2 hypointensity (hemorrhage)
(83). In another study usingadult rat spinal contusions, water contentand T2
signal did not always change significantly in injured areas (101); therefore,
conventional MRI techniques may underestimate the degree of injury.
Additionally,somesmallareasofhemorrhagemaynotbevisibleonT2images.
TheutilityofimagingofchronicSCIhasbeenlimitedtoassessingposttraumatic
syringomyeliaandmyelomalacia(104–109).
AdvancedMRI techniques suchasdiffusion MRI,functionalMRI (fMRI),
and MR spectroscopy (MRS) could provide important information about
function and axonal integrity of damaged spinal cord parenchyma. To date,
however, the clinical application of these techniques has been limited. The
technicalchallengesaresubstantial;specificallythesmallsizeofthespinalcord,
its close proximity to bony structures, and reduction in image quality due to
pulsationofcerebrospinalfluidandrespiratorymotion.Themostpromisingof
theseadvancedMRItechniquesisdiffusiontensorimaging(DTI).DTIprovides
aquantitativeassessment offree waterdiffusionwithinanatomicstructures.In
normally myelinated neurons, water diffuses predominantly along the
longitudinalaxisoftheaxon.Cellularmembranesandmyelininhibitdiffusivity
perpendiculartothelongaxisoftheaxon.Thesecomponentscanbemeasured
andareusedtoassesstheintegrityoftheaxonitselfand/orpreservationofthe
myelin sheath. Injured animal and human spinal cords show predictable
diffusivity characteristics with a decrease of diffusion longitudinally and
increased transverse diffusion. These diffusion characteristics correlate with
neurologic function and can serve as a noninvasive biomarker of neurologic
recovery (110–112). Preliminary studies show promise (112–114); however,
largerdefinitivestudiesarestillneededtoclarifytheroleofdiffusionMRIfor
predictingfunctionandneurologicalrecovery.
FUNCTIONALRECOVERY
Ambulation
A primaryconcernof SCIpatients(and theirfamilies)is whetherthey will be
abletoregaintheabilitytowalk.Ambulation,likeotherfunctionaloutcomes,is
dependent on many factors in addition to neurologic function. When the
populationofindividualswithSCIisstudiedasawhole,expertsgenerallyagree
thatonlyaminorityofindividualsareabletoambulatefollowingSCI.Beyond
the basic question of whether a patient will be able to ambulate or will rely
solelyonawheelchair,thereisthequestionofthedegreeofambulatoryfunction
thatcanbeattained.
In the 1970s, Stauffer divided ambulatory status into four categories:
community ambulatory, household ambulatory, exercise ambulatory, and
nonambulatory(44).Communityambulatorscantransferthemselvesoutofbed
orawheelchair,walka “reasonable”distance (laterestimatedat>150feet), in
and out of the home without assistance from another person. Persons in this
categoryuseambulationastheirprimarymeansofmobilityinthecommunity,as
opposed to a wheelchair. Household ambulators may or may not require
assistancewithtransfersfrombedorwheelchair;theyareabletoambulateinthe
homewithrelativeindependencebutareunabletoambulateoutsideofthehome
forany significant distance. These individuals frequently use a wheelchair for
mobility outside the home. The exercise ambulator attains functional mobility
with a wheelchair and can ambulate only under closely controlled conditions.
Considerablephysical assistance is also requiredtoambulate.Individuals who
are nonambulators rely exclusively on a wheelchair. Both community and
householdambulationareconsidered“functional”ambulation,whereasexercise
ambulationisconsidered“nonfunctional.”
Thetypeof gait pattern utilized depends on the degreeofneurologicloss.
Waters(11)hasdeterminedthatonly5%ofindividualswithcompleteparaplegia
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