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7
ElectrodiagnosticEvaluationofSpinal
CordDisorders
MarkA.Lissens,RyanSolinsky,andStevenKirshblum
INTRODUCTION
Invariousdisordersofthespinal cord,itmaybeimportanttoobtainobjective
information regarding the neurophysiological function of the spinal tracts.
Electrodiagnostic assessments have implications for both the diagnosis and
prognosis of an individual following spinal cord injury (SCI). The sensory
(ascending tracts) and the motor (descending tracts) can each be evaluated
electrodiagnostically with somatosensory-evoked potentials (SEPs) and motor
evokedpotentials(MEPs),respectively.
SOMATOSENSORY-EVOKEDPOTENTIALS
Methodology
SEPs are elicited with electrical stimulation delivered transcutaneously to a
mixed or sensory nerve or delivered to a given dermatome. This stimulation
excites the type Ia and II afferent nerve fibers. Stimuli are monophasic,
rectangular pulses of shortduration (100–300 μs) at a rate of 3 or 5 Hz.The
stimulationintensityshouldbegreaterthan2to3timesthesensorythresholdor
slightlyabovemotor thresholdif amixednerveisbeing stimulated.Toreduce
thepatient’sdiscomfort,theskincontactimpedanceshouldbe5kΩorless.
In clinical settings, the most commonly stimulated nerves are the median,
ulnar,andtheposterior tibial,but anyaccessible nervecan bestimulated. SEP
responsesarerecordedwitheithersurfaceorneedleelectrodes.Responsesfrom
the nerve proximal to the site of stimulation, including varied areas over the
spineandthescalp(accordingtotheInternational10/20System(1)),arefurther
recorded.Stimulusartifactisreducedbyplacementofagroundelectrodeonthe
stimulatedlimb.Muscleandmovementartifactscanbereducedbysedationof
thepatient.
SEPs are extracted from background (cerebral) activity by means of
computationalaveraging,withthenumberoftrialstobeaverageddependingon
the recording quality, background noise, and size of the signal of interest.
Usually between 300 and 4000 individual trials are required. At least two
averagesshouldbeobtainedtomakesurethattheSEPfindingsarereproducible
withabandpassfilterof30to3000Hzcommonlyused(2–7).
The SEP responses are characterized by a certain polarity at the active
electrode with respect to the reference electrode and also by post stimulus
latency time. The voltage changes reflect the activation of sources within
differentpartsofthecentralnervoussystem(CNS).Therearemanyvariationsin
nomenclature,butthemosttypicallabelsforSEPstudiesusethepolarity(Por
N,forpositiveornegative)andexpectedlatency(inmilliseconds),forexample
P14orN20(Figure7.1).
When performing studies in the upper limb, the most consistent measure
utilized is at Erb’s point (N13/P13–P14), reflecting the voltage difference
recordedbetweenthecervicalspineandthemidfrontalscalp(Fz),andanN20in
recordingsmadebetweenthecontralateralhandareaofthescalp(C3’ontheleft
scalp/C4’ on the right scalp) and Fz. The cervical N13 most likely reflects
postsynaptic activity in the spinal cord, whereas P14 reflects activity in the
medial lemniscus. The N20 is likely generated in the primary somatosensory
cortex.
Similarly,P37andN45componentsarefoundinrecordingsoverthevertex
ofthescalp(Cz)withrespecttoacephalicreferencefollowingstimulationofthe
posteriortibialnervesin thelower extremities(Figure 7.2). The N20andN45
componentsarefollowedbyanumberofdifferentpeaksaccordingtothesiteof
recording over the scalp and most likely reflecting distinct corticalgenerators
(2).Comparable tothe cervicalN13,a negativepotential canbe detectedover
thecaudaequinaandoverthethoracolumbarspine.Thisisthoughttoberelated
predominantlytopostsynapticactivityinthelumbarspinalcord(8).
Finally, the central somatosensory conduction time (CSCT) can be
determinedasbeingthetimeintervalbetweenthemajornegativepeakidentified
inthespine(e.g.,N13forthecervicalspineorN23forthethoracolumbarspine)
andtheinitialmajornegativepeakofthecorticalresponse(e.g.,N20orN37).
Thismeasurecanbehelpfulindetectingslowedtransmissionthroughthecentral
neuroaxis,forexamplebetweenthecervicomedullaryjunctionandthecortex(as
maybeseenwithcentralinvolvementinvariousneuropathies,SCI,spondylotic
myelopathy,etc.).
InadditiontoabsoluteSEPcomponentandintercomponentlatencies,sideto
sidelatencydifferencesarealsotakenintoaccount.Responsesareconsideredto
beabnormaliftheseexceedthemeanvalueforcontrolsubjectsbymorethan2.5
or3standarddeviations.Lessstringentcriteriamayleadtohigherfalse-positive
results. The presence or loss of specific components is also important in
determining SEPabnormality.SEPamplitudeand morphology changes on the
otherhand are lessreliablebecause of thewidevariability in normalsubjects.
Side-to-side amplitude differences of more than 50%, however, may be of
significance,andfurtherevaluationisoftenneeded.
FIGURE7.1SEPsrecordedfromvariouslocationsalongthesensory
pathwayfollowingelectricalstimulationoftheulnarnerveatthewrist.
SEPs,somatosensory-evokedpotentials
FIGURE7.2SEPsrecordedfromvariouslocationsalongthesensory
pathwayfollowingelectricalstimulationoftheposteriortibialnerveat
theankle.
SEPs,somatosensory-evokedpotentials.
ClinicalApplications
Altered SEPs are not specific for the age or the nature of the underlying
pathologyandprovide limitedinformationof the exact location of the lesions
proximaltothedorsalrootganglion.Onebenefitoftheseevokedpotentialtests
is that the electrodiagnostic changes occur simultaneously with developing
neurologicdeficitsfollowingSCI.Thisdiffersfromotherelectrodiagnosticsthat
may take weeks to evolve. Although SEP abnormalities are etiologically
nonspecific, they can be very helpful in the diagnosis of numerous spinal
disorders including traumatic SCI, spondylotic myelopathy, spinal cord
compression,radiculopathy,andmultiplesclerosis.Furthertheymaybeutilized
indeterminingprognosis,evaluatingtreatment,andinfollowinguppatientsby
monitoringneurologicalrecovery,aswellasforintraoperativemonitoring.
SEPs have been shown in SCI to have prognostic value in the acute and
subacute stages (2,4,9–12). Although less specific, SEPs may be sensitive in
predictingoutcomeintheacutephase,asabsentSEPsareassociatedwithapoor
prognosis. When present, and to a greater extent if latency times are within
normallimits,abetterprognosisforneurologicalrecoverycanbeexpected.The
specificityofthisassessmentmayincreasewhencombiningSEPswithMEPs
Incervicalspondyloticmyelopathy,SEPscanbehelpfulintheevaluationof
the severity and level of the lesion, especially when combined with other
electrodiagnostictechniques.SEPs are also useful in the follow-up of patients
aftersurgeryorrehabilitationtreatments(13–15).
Intheintensivecareunit,patientsincomaareunlikelytorecoverfromtheir
conditionwhenthecorticalresponsesoftheSEPsarebilaterallyabsent.Thisis
especiallytrueforatraumatic(e.g.,anoxic)comainadultpatients(5,16–18).In
patients with dual diagnosis of traumatic brain injury and SCI, this becomes
particularly relevant. Unfortunately, thepresenceof complete SCI may impair
thissignalacquisition,makingcomarecoveryprognosisdifficult.Conversely,in
a comatose patient with suspected SCI, SEPs allow early quantification of
deficitsandmayhelpguideinterventionswhilethepatientisstillinthecoma.
Inmultiplesclerosis,SEPscanreflecttheupperlimbmotorperformance:a
significantlongertimetocompleteafingerdexteritytest(9-HPT)wasobserved
in patients with abnormal SEPs; patients with undetectable N20 or P14
responsesperformedthe9-HPT in a significant longer time thanpatientswith
detectableresponses(19).Further,selectstudieshavedemonstratedthatchanges
inSEPscorrelatetooveralldisabilityevolutioninmultiplesclerosis,especially
whenpairedwithotherevokedpotentials(20,21).
SEPshavebeenshowntobeveryusefulforintraoperativemonitoring,for
exampleinspinaldeformitysurgery(22)andvascularoperations(23,24).
Dermatomalsomatosensoryevokedpotentials(dSSEPs)havebeenshownin
somecasestoexhibitobjectiveevidenceofclinicallysignificantchangeswhere
other electrodiagnostics have remained normal (25). Similarly, dSSEPs paired
with electrical perception thresholds have also been advocated by some as an
objective measure of sensation following SCI (26). In addition to accurate
quantification,these tests have notable implications for trackingsafetyofnew
researchinterventionsforSCI.
Given their objective nature, SEPs also have roles in differentiation of
potential conversion disorder or malingering. These multipleuses for SEPs in
assessmentofconductionthroughthespinalcordemphasizetheirimportancefor
bothclinicalandresearchpurposes.
MOTOR-EVOKEDPOTENTIALS
Differing from SEPs, MEPs may be elicited by either cortical electrical or
magnetic stimulation. Due to the higher, and often painful, electrical stimulus
needed to elicit MEPs compared to SEPs, magnetic stimulation has gained in
popularity (27–36). The technique of transcranial magnetic simulation with
recordingoftheevokedresponsesorMEPson theexaminedmusclesprovides
reliableinformationabout thefunctionalintegrityandconductionpropertiesof
the corticospinal tracts and motor control in the diagnostic and prognostic
assessment of various neurological disorders. It further allows providers to
follow the evolution of motor control and to evaluate the effect of different
therapeuticprocedures.Changesinconductionspeedmaysuggestremyelination
orreconnectionofthecorticospinaltractwithintheinjuredspinalcord(37).
PrinciplesofMagneticStimulation
A magnetic field is generated by passing an electric current through a coil of
wire. Amagnetic pulse produced from an electric current pulse will induce a
current in an electrically conductive region, such as the human body. If the
inducedcurrent isof sufficientamplitude andduration, itwillstimulate neural
tissueinitsvicinityinthesamewayaswithconventionalelectricalstimulation.
Currently,twotypesofmagneticstimulatorsareavailable:monophasic(such
astheMagstim200stimulator)andpolyphasic(suchastheCadwellstimulator),
whichmodifythewayinwhichcerebralstructuresareexcited.
Electricalandmagnetictranscranialmagneticstimulationactivatethe brain
atdifferent sites(38). Whereas the electrical stimulusexcitesthe corticospinal
neuronsdirectly,themagneticstimulusexcitestheseneuronstranssynaptically,
explaining the extra delay of a few milliseconds in magnetic stimulation as
comparedtoelectricalstimulation.
PhysiologicalMechanisms
Transcranialstimulationprovidesthefirstobjectivelaboratory measurementof
corticospinal tract function in humans without surgical exposure. The MEP
procedureconsistsoftranscranial stimulation followed by measurement of the
compound muscle action potential (CMAP) from different limb and trunk
muscles.
Magnetic stimulation allows providers to safely, easily, and effectively
stimulate most neural structures, unimpeded by fat and bone, and without
discomfort to the patient. Responses following magnetic stimulation can be
recordedin a standard fashionfromeither the nerve orthemuscle, and signal
averaging is usually not necessary. CMAPs from various muscles can be
obtainedinresponsetomagnetictranscranialmotorcortexstimulation,as well
asnerveroot,plexus,andperipheralnervestimulation.
When the CNS is stimulated, several adjustments can be made. The
stimulation threshold can be reduced by approximately 30%, the response
amplitudecanbeincreasedandtheresponselatencyreducedbysome1to6ms
(usually about 1–2 ms) through preactivation of the target muscle. This
technique,referredtoas“facilitation,”hasbeendescribedinconsiderabledetail
(38–40)andwasnotedinanearlystageoftheoriginaltranscutaneouselectrical
stimulationstudiesofMertonandMorton.Thistechniqueisequallyprominent
withmagneticbrainstimulation(41).
The relationship between background force and CMAP amplitude is
approximately linear with electrical stimulation, whereas a small background
contractionontheorderof5%ofmaximumhasastrikingfacilitatingeffectwith
magneticstimulation.
There are several different processes of facilitation. It is probable that
facilitationoccurs bothat spinalandcortical levels.When attentionisfocused
on accurate force production in a particular muscle, thenfacilitation occursat
smallforces. Thisis likelytoinvolve corticalmechanisms. Presumablyduring
spinal facilitation, more spinal motor neurons are recruited by an unchanged
descending volley because their excitability is raised by the descending
voluntaryinput,whereasthecorticalfacilitationdependsonanactualincreasein
thedescendingvolleycausedbythemagneticstimulus.
Responselatencyshorteningduringvoluntarycontractionislikelytoreflect
theapplicationofthesizeprincipleofHenneman:thefirstcorticomotoneuron
cellstofire during a voluntary contraction are those thatconductmostslowly
and with increasing contraction larger, faster conducting neurons are recruited
(42).Moreover,singlemotorunitstudieshavedemonstratedinhumansthatthe
first motor units to be stimulated magnetically are the first to fire under
voluntarycontrolandareofrelativelylonglatency(41).Laterlargerunitswith
fasterconductingaxonshaveshorterlatencies.
When comparing muscle responses to magnetic stimulation with those
electricallyinduced,magneticresponsesareoflongeronsetlatencybyaround2
ms (in hand muscles), are of simpler waveform, shorter duration, and larger
amplitude. These differences suggest that electrical and magnetic stimulation
activate the motor pathways at different sites. It is probable that electrical
stimulationexcitescorticospinalneuronsdirectlyandthatmagneticstimulation
actstranssynaptically.
Thesynapticdelayfordischargebythemotoneuronhastwocomponents:the
excitatorypostsynapticpotential(EPSP)delay(±0.3ms)andthedelayforthe
EPSP to reach firing level. With strong stimulation of the motor cortex, the
number of corticospinal neurons discharging, and thus the amount of spatial
summationofEPSP,areincreased,therebyshorteningthedelayformotoneurons
to attain firing level. When the muscle is relaxed, the motoneuron requires
increasedexcitationtoreachfiringlevel,suchascouldbeprovidedbytemporal
summation of motoneuron EPSPs elicited by direct and indirect corticospinal
discharge. The need for indirect corticospinal discharge would impose an
additionaldelayintheCMAPattributable to cortical synaptic delays and thus
largely account for the difference observed (± 2 ms) in CMAP latency in
contractedandrelaxedmuscle,whichcanbeperformedwhenthereisnooronly
asmallresponseduringrelaxation.
Another phenomenon (inhibitory) is the interruption of the ongoing
voluntarymuscle contraction producedbymagnetictranscranial stimulation of
the motor cortex. This phenomenon appears as the absence of EMG signal
lasting about 100 to 150 ms, which is defined as the “silent period” (43–46).
Thissilentperiod(seeFigure7.3)isproducedbyamixtureofcorticalandspinal
inhibitoryeffects.Approximately,thefirst50msofthesilentperiodaredueto
bothcorticalandspinalmechanisms.Afterthisfirst50ms,spinalmechanisms
areprogressivelyless important and the cortical inhibitory mechanismsacton
theneuralelements of the corticomotoneuronal system at motorcorticallevel.
Notably, amagneticstimulus given duringthesecond half ofthesilent period
does not produce MEP while electrical stimulation evokes almost unchanged
muscleresponses.Inotherwords,theunexcitabilityofthemotorcortexaftera
second magnetic stimulus indicates that the motor cortex per se is inhibited,
whereas the excitability with electrical stimulation implies that corticospinal
axonsandspinalmotoneuronsarenotinhibited(43,44,47).
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