aaem minimonograph 19: somatosensory evoked potentials

Key words: somatosensory evoked potentials; cerebral potentials; spinalpotentials; nerve stimulation; sensory lesions

Muscle Nerve 21: 277–290, 1998

AAEM MINIMONOGRAPH 19:SOMATOSENSORYEVOKED POTENTIALS

MICHAEL J. AMINOFF, MD, FRCP 1 and ANDREW A. EISEN, MD 2

1 Department of Neurology, University of California at San Francisco, San Francisco,California, USA2 Department of Medicine, University of British Columbia, Vancouver,British Columbia, Canada

Received 11 August 1997; accepted 5 September 1997

More than 40 years have elapsed since the first so-matosensory evoked potential (SEP) was recordedfrom humans,21 and 15 years have passed since theclinical role of SEPs was reviewed as an AmericanAssociation of Electrodiagnostic Medicine (AAEM)minimonograph. At that time, interest in SEPs wasreaching its zenith, and a vast literature had alreadyaccumulated. The subsequent development of so-phisticated imaging techniques has impacted on therole of SEPs in the clinical setting, making it timelyto review this aspect as the end of the century isapproached. This minimonograph considers currentconcepts of the physiologic basis of the SEP, dis-cusses the different techniques available to elicit andrecord it, and critically analyzes its clinical utility.

The peripheral electrical stimulus routinely usedto elicit an SEP activates predominantly—if not en-tirely—the large-diameter, fast-conducting group Iamuscle and group II cutaneous afferent fibers.55 Se-lective intrafascicular stimulation has provided evi-dence for a direct muscle afferent fiber (Ia) projec-tion to the human somatosensory cortex.43 However,when a mixed nerve is stimulated, both group Iamuscle afferents and cutaneous group II afferentscontribute to the resulting SEP.55 Its amplitude isalmost maximal when the peripheral nerve actionpotential is only 50% of its maximum.35 This trans-lates into a requisite stimulus intensity of about twice

sensory threshold. It is also possible to elicit SEPsusing a variety of mechanical stimuli.63,105 This al-lows selective activation of specific sensory modali-ties, but the SEPs elicited are often of small ampli-tude and may require many hundreds of responsesto be averaged. This limits the clinical utility of me-chanically elicited SEPs.

The SEP is greatly attenuated or abolished whenthe dorsal columns are selectively ablated in ani-mals,18 indicating that within the spinal cord the SEPis mediated predominantly via these tracts. Con-versely, cord lesions that do not interrupt the dorsalcolumns are associated with a relatively normal SEP.Loss of posterior column function in humans is al-most invariably accompanied by a grossly abnormalSEP.47 Some SEP components may, however, reflectextralemniscal activity; they have been evoked in catsafter selective dorsal column transection by stimulithat are sufficient to excite small-diameter periph-eral fibers,76 and tourniquet-induced ischemia in hu-mans abolishes short-latency before long-latency SEPcomponents, suggesting that they are mediated bydifferent centrally conducting tracts.119

Although in general the SEP is best recordedover the somatosensory cortex, topographic map-ping indicates that several of its components arewidely distributed over the scalp, and some are maxi-mally recorded outside the somatosensory cortex.112

Because the SEP monitors more than just the so-matosensory pathways, abnormalities recorded incertain primary diseases of the motor system (such asamyotrophic lateral sclerosis) should not cause con-cern.

*Correspondence to: American Association of Electrodiagnostic Medi-cine, 421 First Avenue S.W., Suite 300 East, Rochester, MN 55902, USA

CCC 0148-639X/98/030277-14© 1998 American Association of Electrodiagnostic Medicine. Publishedby John Wiley & Sons, Inc.

AAEM Minimonograph 19: SEPs MUSCLE & NERVE March 1998 277

STIMULATION TECHNIQUES

Mixed Nerve Stimulation. Because electrical stimu-lation of a mixed nerve initiates a relatively synchro-nous volley that elicits a sizable SEP, it has becomethe standard for clinical use. The stimulus intensityrequired to elicit an SEP of maximum amplitudeneed not be supramaximal. The ideal stimulus in-duces a mixed nerve action potential that is justgreater than 50% of its maximum amplitude andclinically produces a slight muscle twitch. Too high astimulus is counterproductive, producing occlusionof Ia impulse traffic by other converging afferentimpulses.43 The occurrence of occlusion may de-pend on the limb that is stimulated.44 When occlu-sion occurs, a percentage of the initial volley is inef-fective, and the SEP is accordingly lower inamplitude. A stimulus of short duration (200–300µs) is popular, but longer duration (1000 µs) pulsesof appropriately lower intensity may be appropriatebecause they preferentially activate the type Ia and IIafferents.113 A repetition rate of 5.1 Hz is conve-nient. Faster rates may be tolerable to the patientand do not alter the SEP until they exceed 15 Hz.Troublesome electrocardiographic artifact,particularly relevant with noncephalic referential re-cordings of SEPs elicited from the legs, can be obvi-ated by triggering the stimulus off the electrocardio-gram. In general, SEPs elicited by lower limbstimulation have the added advantage of testing thefunctional integrity of much of the length of thespinal cord, an important consideration in suspectedmultiple sclerosis and other myelopathies that maynot be detected by imaging techniques.

Cutaneous Nerve Stimulation. Virtually any acces-sible cutaneous nerve can be stimulated to elicit anSEP. With cutaneous nerve stimulation, however, thepotentials are smaller than those evoked by mixednerve stimulation, and the small far-field compo-nents are difficult to record.25,30 Use of cutaneousnerve stimulation should be considered when it isnecessary to: (1) assess the integrity of specific cuta-neous nerves, such as the lateral femoral cutaneousnerve,116 which are not readily studied by conven-tional techniques; (2) measure peripheral sensoryconduction when this is not otherwise possible be-cause the sensory nerve action potential (SNAP) iseither absent or very small25,30; (3) evaluate isolatedroot function, because of the increased segmentalspecificity of cutaneous stimulation4,29; and (4) as-sess dubious patchy numbness for medicolegal rea-sons, by stimulating homologous areas of ‘‘involved’’and normal skin supplied through cutaneous termi-nals.22

Dermatomal Stimulation. Dermatomal stimulationis even more segmentally specific than cutaneousnerve stimulation, because cutaneous nerve stimula-tion invariably activates fibers from more than onedermatome. However, with dermatomal stimulationthe ascending volley is very desynchronized, and thissometimes makes the SEP difficult to interpret. Der-matomal stimulation has been used most often toassess function of the lumbosacral roots. For L5, themedial side of the first metatarsophalangeal joint orthe dorsal surface of the foot between the first andsecond toes is stimulated. For S1, the lateral side ofthe fifth metatarsophalangeal joint is stimulated.Care must be taken to avoid stimulus spread toneighboring dermatomes, underlying muscle (whichinduces activity of Ia afferents), and digital cutane-ous nerves. This can be achieved if the stimulus iskept at 2.5 × sensory threshold, which gives about80% of the maximum amplitude. Normative data forthe L5 and S1 dermatomes are well established.4

Motor Point Stimulation. A single muscle motorpoint can be stimulated to elicit SEPs.31 This isachieved by using a monopolar needle electrode forstimulation. A long-duration (1.0 ms), low-intensitystimulus preferentially activates the Ia afferents thatexit in the same bundle as the alpha motor fibers atthe motor point. This method allows stimulation ofproximal (large) muscle Ia afferent input.

Paraspinal Stimulation. The paraspinal region atsequential levels along the vertebral column can bestimulated to elicit SEPs.51 This method ‘‘obviates’’peripheral input from long nerves in the limbs andmore readily identifies lesions of the spinal cord.The stimulus is applied simultaneously to both sides,2 cm lateral to the midline, at an intensity that in-duces a small visible muscle twitch. Potentials arerecorded over the scalp (Cz–Fz). The afferent volleyis primarily initiated in the cutaneous branches ofthe primary dorsal root rami, with some contributionfrom the paraspinal Ia afferents.

In normal subjects, the value for spinal cord con-duction velocity between T12 and T1 is approxi-mately 64 m/s. However, it is better to refer to con-duction time, which over the same segments is 5.4 ±1.6 ms.51

RECORDING AND FILTERING OF SEPs

Surface or needle electrodes can be used for record-ing SEPs. There is no difference in the resultant SEP.The latter, although easily inserted into the scalp,are not popular because of their higher impedance,the discomfort of their insertion, and the theoretical

278 AAEM Minimonograph 19: SEPs MUSCLE & NERVE March 1998

risk of infection. Recording montages are either ‘‘ce-phalic bipolar’’ or ‘‘referential.’’ In a cephalic bipo-lar montage both electrodes are placed on the head,while in a referential montage the reference elec-trode is placed off the head. A cephalic bipolar mon-tage is relatively noise-free and is satisfactory for rou-tine clinical use. However, there is cancellation ofthe small-amplitude, far-field potentials, which canonly be recorded with noncephalic references (e.g.,the opposite mastoid, shoulder, arm, hand, or knee,or the linked mastoids or earlobes). Recording withboth types of montage is advantageous (see Fig. 1).

The number of channels (recording derivations)used should be dictated by the specific reason forperforming the SEP. For example, in field distribu-tion studies, 16 or more channels may be useful,whereas one channel is sufficient when the SEP isbeing used to measure peripheral conduction veloc-ities.

With a bipolar cephalic derivation, near-field po-tentials, which are characteristically of negative po-larity and of relatively large amplitude, are recorded.Their amplitude falls rapidly when the electrode ismoved only a short distance from the generatorsource. Certain small-amplitude far-field potentials

may be recorded with bipolar cephalic derivations,37

but referential recording is required for properidentification. Far-field potentials are small in ampli-tude, recorded with equal ease and amplitude over awide area of the scalp, and usually positive andmonophasic at the active electrode, reflecting a mov-ing front approaching the recording electrode.Kimura and coworkers showed that under some cir-cumstances far-field potentials may be biphasic andof either polarity.67 The posterior tibial near-fieldpotential is also positive in polarity.

Small-amplitude components of the SEP arecomposed of both high and low frequencies, andfiltering can be problematic. Too wide a bandpassresults in a ‘‘noisy’’ SEP, while a restrictive bandpassattenuates either the high- or low-frequency compo-nents, depending on the settings chosen. There is no‘‘correct’’ filter setting—the choice is best related tothe particular task. For general purposes, a relativelybroad bandpass (10–2500 Hz) is suitable. Restrictivefiltering of between 150 and 300 Hz to 3000 Hz en-hances high-frequency, small-amplitude, near- andfar-field components, but does so at the expense ofthe low-frequency components.74,75

Analog-restrictive filtering induces phase shift of

FIGURE 1. Normal SEP elicited by stimulation of the left median nerve and recorded over the Erb’s point region, fifth cervical spine, andscalp. EPi, ipsilateral Erb’s point; EPc, contralateral Erb’s point; CV5, fifth cervical spinous process; C38 and C48, scalp placementshalfway between C3 and P3, and C4 and P4, respectively. The bottom trace shows the Erb’s point potential, the second channel showsmainly the stationary cervical potential, the third channel shows the subcortical far-field potentials (especially P14 and N18), and the topchannel shows the N20 potential.


components and may induce distortion of compo-nents. Digital filtering, designed for zero phase shift,does not induce phase shift or distortion of compo-nents37 and does not create ‘‘new’’ peaks. Digitalfiltering does however greatly enhance peaks thatare normally present. This is of particular promisefor SEPs evoked by leg stimulation, when the small-amplitude components, usually difficult to recog-nize, become easily identifiable.

MEASUREMENT OF THE SEP

The latency, interpeak latency, amplitude, morphol-ogy (presence or absence of components), and dis-persion of the SEP can be measured, and side-to-sidecomparisons can be made. Latency is easily mea-sured and standardized, whereas other characteris-tics (e.g., morphology or dispersion) may be difficultto assess. Latency varies with limb length. Interpeaktransit (conduction) times are reliable parametersindependent of limb length and usually indepen-dent of peripheral nerve disease. Central afferentpathways do not mature at the same rate as periph-eral pathways, and adult values for conduction veloc-ity are not attained until 7 or 8 years of age.15 Agingis associated with prolongation of SEP latencies.24,62

This is not simply a reflection of slowed peripheralconduction, because central conduction times arealso slowed significantly.

Absolute and interpeak latency are consideredabnormal when they are more than 3 SDs ratherthan 2 or 2.5 SDs above the normal mean. Less sta-tistical strictness is valid if the results are related toage and height. In fact, however, latency is seldomrelated to age and height in clinical laboratories.Absolute and interpeak latencies are easily measuredbut frequently are normal in the face of obviousclinical impairment. Care is required to distinguishbetween a delayed and an absent component; whena component is absent, the subsequent componentmay be mistaken for the missing potential.

Absolute amplitude of SEP components is vari-able, but a side-to-side difference exceeding 50%is usually abnormal, providing the clinician can becertain that the disease is unilateral. An excessiveinterside amplitude difference is nonspecific and in-dicates either central conduction block or consider-able neuronal/axonal loss. However, complex facili-tatory and occlusive interactions leading to ‘‘centralgain’’ can prevent amplitude reduction in the SEP,masking axonal or neuronal loss.35,89 SEP amplitudeincreases in the elderly,24 and ‘‘giant’’ potentialstypify hereditary myoclonic epilepsy.101 SEPs evoked

by dermatomal—as opposed to nerve—stimulationare much more variable in amplitude.

The morphology (shape) and dispersion of theSEP are difficult to quantitate, but both may be ab-normal before or in the absence of latency prolon-gation or amplitude reduction. Computer-assistedmethods for quantifying both dispersion and mor-phology of the SEP have been described.36

NEURAL GENERATORS OF THE SEP

It is generally accepted that the different compo-nents of the SEP predominantly reflect sequentialactivation of neural generators excited by the as-cending volley. This concept is appealing because itprovides a rational base for interpreting an absent orabnormal component in relation to a specific ana-tomic lesion. However, factors other than neuralgenerators (synapses in relay nuclei) are importantin the origin of some SEP components, especially thesmall far-field potentials recorded using noncephalicreferences. In particular, the stationary far-fieldpeaks, for example P9, P11, P13, and P14, evoked bymedian nerve stimulation reflect propagated volleysof action potentials traveling in axons67 and can berecorded as the traveling volley approaches, but be-fore it actually reaches, the active recording elec-trode. This results from physical changes in the sur-rounding volume conductor,66,67 including theresistance or impedance of the volume conductor,sites of axonal branching, and anatomic orientationof the traveling impulse.66,67

Of the far-field potentials in the median andtibial SEPs, it seems likely that relay nuclei are re-sponsible only for the generation of P13/14 (me-dian) and P31 (tibial) components, with the otherpotentials probably reflecting electrophysicalchange in the surrounding volume conductor.The near-field N20 (median) and P38 (tibial) com-ponents are neurally generated, but it is likely thatthey reflect multiple and even independent thalamo-cortical projections.16,112,118 Certainly, from studiesusing digital filtering, it appears that there are ‘‘toomany components’’ for available ‘‘generators.’’37

SEP components are designated by their polarityand normal latency. The numerical latency valuesascribed to each component are summarized inTable 1, which also indicates current views of theorigin of specific, early latency, SEP componentselicited by median and tibial nerve stimulation andrecorded over the scalp.40,117

Little is known about the anatomic substrates ofthe middle (and longer) latency components of the


SEP. They exhibit considerable intertrial variability,and their amplitude and latency are affected bysleep, level of consciousness, habituation, and cog-nitive function. Nevertheless these components mayhave some clinical relevance. Isolated abnormality ofthe contralateral P40–N60 in the median SEP hasbeen described in multiple sclerosis and with deepsubcortical lesions involving thalamic nuclei otherthan the primary sensory nuclei.117

Long-latency components are distributed bilater-ally, being of greatest amplitude at the vertex. Thesecomponents relate to nonspecific thalamocorticalprojection systems involved in habituation, adapta-tion, and arousal. These components are of largeamplitude, being between 10 and 40 µV, so that asfew as 50 averaged epochs are required to obtain ameasurable response. Unfortunately their recoverytime takes several seconds, necessitating a stimulusrepetition rate that is lower than once every 5 s toavoid significant attenuation of the response.

Spinal SEPs. Using a vertical and horizontal arrayof electrodes placed over the neck and referred to anoncephalic reference, the cervical SEP elicited bymedian nerve stimulation consists of three distinctcomponents41: (1) the proximal plexus volley (PPV),with a latency of about 10 ms; (2) the dorsal columnvolley (DCV), reflecting the volley in the dorsal col-umn, with a latency of about 12 ms; and (3) thecervical N13/P13, which is possibly generated at the

level of the dorsal gray of the cervical cord. With acephalic reference these three components becomefused, but the latency difference between its peakand the N20 cortical SEP gives a ‘‘central conductiontime’’ between the lower brain stem and cortex thatmeasures about 5.5 ms.

Using a knee or iliac crest reference, SEPs elic-ited by tibial nerve stimulation can be recorded overthe thoracolumbar spine. The components of theSEPs correspond to those described above for thecervical SEPs elicited by median nerve stimulation.Posterior tibial nerve stimulation at the ankle evokesa traveling wave, N18, that can be recorded over thelower lumbar spine immediately after the volley haspassed the sacral plexus and is the scalp-recordedfar-field P18 potential. This plexus-propagated volleyis the equivalent of the PPV recorded over the neckwith median nerve stimulation. A second distinct po-tential, N22, can also be recorded over the lowerspine. It is a stationary peak and its latency remainsconstant. Its amplitude is maximal over the lowerthoracic spine (T10–L1). N22 probably representspostsynaptic activity in the lumbar gray matter gen-erated in response to inputs from axon collaterals.40

A third negative traveling wave, N24, whose latencyshortens from caudal ro rostral thoracic cord, is evi-dent over the lower thoracic cord. It reflects a prop-agated volley in the dorsal columns and is equivalentto the DCV potential recorded over the neck withmedian nerve stimulation. Spinal SEPs may not be

Table 1. Origin of far-field and near-field SEP components.

Generator Comments

Median nerveFar-field potentials

P9 Just distal to brachial plexus Sometimes bilobed P9a and P9b (depending onarm position)

P11 Dorsal root entry (presynaptic)P13/P14 Medial lemniscus (postsynaptic) P13 may reflect synaptic activity of dorsal horn

interneuronsN18 Between upper pons and midbrain N18 remains intact after thalamic lesions

Near-field potentialN20 Area 3b in the posterior bank of rolandic fissure Diagnostically the most useful peak to measureP22 Motor area 4 Increases with ageP27 Parietal cortexN30 Supplementary motor area Decreases with age

Tibial nerveFar-field potential

P18 Sacral plexus Analogous to median P9P31 Gracile nucleus Analogous to median P14N34 Brain stem Analogous to median N18

Near-field potentialP38/N38 Primary somatosensory cortex Analogous to median N20

Multiple cortical generators are involved

This reflects the authors’ view; differing opinions exist.


recordable in all normal subjects, and their absencemust be interpreted with caution.

SEPS IN DISORDERS OF THE PERIPHERAL ANDCENTRAL NERVOUS SYSTEM

Although SEPs may reveal or localize a lesion involv-ing the somatosensory pathways, they are simply anextension of the clinical examination and do notindicate the underlying disease process. Normalfindings do not exclude an organic basis for symp-toms. Despite these limitations, SEP studies may behelpful diagnostically and to determine the extent ofpathologic involvement in different disorders.

Peripheral Nervous System.Disorders of the Peripheral Nerves. SEPs may be

helpful in evaluating the peripheral nervous systemwhen nerve conduction studies (NCSs) are inappli-cable because of the proximal site or severity of pa-thology. Peipheral sensory conduction velocity canbe measured by SEPs with comparable results tothose from conventional NCSs. The nerve is stimu-lated at two or more sites and the responses are re-corded over the scalp. Scalp-recorded SEPs may beabsent or delayed in the presence of polyneuropa-thies and mononeuropathies.9,47 Scalp-recordedSEPs may be important for identifying peripheralnerve lesions when SNAPs are unrecordable periph-erally. Parry and Aminoff recorded robust SEPs onstimulation of each of 15 nerves from which SNAPswere absent or grossly attenuated as a result of ac-quired demyelinating peripheral neuropathies.89 In11 instances there was slowed afferent conductionvelocity (determined from the SEPs), but in fournerves conduction velocity was within the normalrange despite slowed motor conduction. The inabil-ity to record peripheral SNAPs in such cases mustreflect pathologic dispersal of impulses, in whichcontext the preservation of cortically generated SEPsprobably results from reorganization and synchroni-zation of afferent volleys at different synaptic lev-els.25,31,35,89 If this is the case, the responses of a fewnormally conducting surviving axons must accountfor the misleadingly normal values for conductionvelocity sometimes obtained by the SEP technique.89

Focal nerve lesions can be diagnosed by scalp-recorded SEPs,23 but this is only helpful when thelesion is too proximal to be recognized by conven-tional techniques, such as in meralgia pares-thetica.108 Some physicians have also used the SEPtechnique to follow recovery after peripheral nervetransection injuries—the SEP may be present whenperipheral SNAPs cannot be elicited.

The SEP findings have been used to diagnose

Guillain–Barre syndrome when distal conduction isnormal. The aim is to demonstrate conduction slow-ing in the proximal segments of peripheral nerves.10

In this regard, some physicians have found SEPs tobe more sensitive than F waves,115 whereas othershave found the converse.88,96 Aminoff and associ-ates, in a study of 44 nerves in 15 patients with Guil-lain–Barre syndrome, found F-wave abnormalitiesmore frequently than SEP abnormalities, especiallywhen peripheral conduction was normal.88 The au-thors therefore believe that SEP studies are best re-served for occasions when both peripheral and F-wave studies are normal in patients with suspectedGuillain–Barre syndrome.

SEPs may have some role in the evaluation ofpatients with distal axonopathies, but this remains tobe established.

Plexus Lesions. The prognosis of brachial plexusinjuries influences clinical outcome; a postgangli-onic lesion—unlike root avulsion—sometimes re-quires operative treatment and may be followed byrecovery. Conventional NCSs can suggest the site ofinjury. Preserved SNAPs despite clinical sensory lossindicate a preganglionic lesion. Recording over thescalp and spine of SEPs following stimulation of up-per limb nerves has been suggested by some physi-cians to improve the electrophysiologic evaluation ofplexus lesions, based on the belief that N13 attenu-ation reflects the total damage, whereas N9 attenu-ation reflects the extent of postganglionic damage.61

Jones and coworkers compared the preoperativeelectrophysiologic findings with the site of the lesionat surgery in 16 patients with unilateral traction le-sions of the brachial plexus.61 The electrophysi-ologic findings correctly localized the lesion in only8 instances; in 3, the findings suggested a purelypostganglionic lesion in roots that were subsequentlyfound to be ruptured preganglionically. Moreover, adiscrepancy sometimes occurred between the SEPand peripheral SNAP findings, perhaps because ofrecoil of an avulsed root from the spinal cord with itsganglion attached; this would affect the size andshape of the N9 potential recorded from about theclavicle, but not the distal SNAP.61

The segmental level of proximal plexus lesionshas been delineated by recording SEPs to stimula-tion of the median, radial, and ulnar nerves at thewrist,109 or the musculocutaneous nerve proximal tothe wrist.107 With multiple root avulsions, there maybe no spinal or scalp-recorded SEPs; with C7 rootinvolvement, responses to radial nerve (but not me-dian and ulnar nerve) stimulation may be abnor-mal.109 Cervical and cortical SEPs from musculocu-


taneous nerve stimulation are especially likely to beattenuated or absent with C5 and C6 root lesions.107

A preganglionic lesion may be partially or com-pletely obscured electrophysiologically by coexistingpostganglionic pathology, thereby limiting the utilityof SEPs for evaluating plexus lesions. Moreover, theinformation derived from SEP studies concerningthe site and extent of plexus injury can usually beobtained by needle electromyography (EMG). Nev-ertheless, the finding of attenuated (but present)peripheral SNAPs and absent spine and scalp SEPs isimportant in suggesting that multiple root avulsionshave occurred in addition to more peripheral le-sions.6

At operation, the appearance of the brachialplexus may be misleading, especially when disruptednerve fascicles appear intact. Intraoperative stimula-tion of specific roots, with recording of the responsesfrom the contralateral scalp, is therefore helpful inindicating whether there is functional continuitywith the cord.70,106 Similarly, when ruptured nervesare to be repaired by grafting, cortical responses tostimulation of the proximal stump indicate that asecond more rostral lesion is unlikely,70 and an ab-sent response suggests a poor outcome.

Thoracic Outlet Syndrome. Characteristic electro-physiologic changes may occur in patients with neu-rogenic thoracic outlet syndrome. This is an uncom-mon disorder. In many patients suspected to haveneurogenic thoracic outlet syndrome, there is noclinical or electrophysiologic abnormality in conven-tional studies. The SEP findings in such patients arevariable. Both the authors’ findings,6 and those re-ported from the Mayo Clinic,120 indicate that SEPstudies are of limited value for the diagnosis of theneurogenic variety of thoracic outlet syndrome. Insome patients there may be abnormalities of the ul-nar-derived SEP, such as an absent or markedly at-tenuated N13 response despite a relatively normalN9 peak, or a small delayed N9 peak with or withoutabnormalities of the N13 or N20 or prolonged inter-peak intervals. In one instance, the authors foundthe only abnormality was marked attenuation of theN20 component.6

In patients with the nonneurogenic syndrome,the authors and others have found normal median,ulnar, or radial SEPs.6,68,120 However, in one study,12 of 18 patients, most of whom had no clinical defi-cit, were found to have abnormal ulnar SEPs, withsmall N9 potentials despite preserved distal ulnarSNAPs, a finding difficult to explain on pathophysi-ologic grounds.59 In another study, 13 of 19 patientswith suspected thoracic outlet syndrome had abnor-mal SEPs evoked by median or ulnar nerve stimula-

tion,48 but the clinical and electrophysiologic find-ings were not detailed, and interpretation is furthercomplicated because diagnostic criteria for the SEPabnormalities were not provided.

The published evidence is thus conflicting con-cerning the role of SEPs in the evaluation of sus-pected thoracic outlet syndrome, but in the authors’view, SEPs are of limited utility in diagnosing theneurogenic disorder and of no established value indiagnosing the nonneurogenic variety.

Cervical Spondylotic Myeloradiculopathy. SEPs donot distinguish spondylosis from other cervical le-sions. Patients with pain and paresthesias but noneurologic signs frequently have normal median orulnar SEPs, whereas those with objective clinical defi-cits may have abnormal SEPs, with delayed or lostcomponents, regardless of whether there is a my-elopathy.39,45 The nature of the SEP abnormalitydoes not indicate either the severity or long-termprognosis of the neurologic disorder, and some pa-tients with a spondylotic myelopathy have normalSEPs.39,45 Thus the findings are no better than care-ful clinical examination in determining severity andprognosis of cervical spondylosis, and do not help inthe selection of patients for surgery.

It has been suggested that fibers ascending fromthe lumbosacral region are more likely to be affectedby cervical compression than fibers arising from theupper limbs.85 It is not yet established, however,whether recording sural SEPs in patients without amyelopathy helps to indicate those at risk of a clini-cal cord deficit.

Epidurally recorded SEPs have been recorded inpatients with cervical spondylosis but should not beused routinely for evaluating patients or in selectingpatients for surgery.

Radiculopathy. There are reports that peronealor tibial SEPs are abnormal in many patients with anisolated lumbosacral radiculopathy, but this is sur-prising, because stimulation of a multisegmentalnerve should not lead to an SEP abnormality in thepresence of an isolated root lesion. Aminoff and col-leagues have found normal peroneal SEPs in all oftheir patients with a compressive L5 or S1 root le-sion.4

Eisen and coworkers stimulated cutaneous nervesto improve the segmental specificity and recordedthe SEPs in patients with myelographically provencervical or lumbosacral radiculopathies.32 Among 28patients, only 16 (57%) had abnormal SEPs, particu-larly amplitude reductions and abnormal morphol-ogy; a prolongation in latency was uncommon.

Others subsequently reported that SEPs elicitedby cutaneous nerve stimulation were more reward-


ing in detecting root involvement.91 Among 27 pa-tients with low back pain, unilateral radicular symp-toms, and abnormal lumbosacral computerizedtomography (CT) scans, SEP abnormalities werefound in 21 patients; in 15 patients there was noassociated clinical deficit or other electrophysiologicabnormality. This suggested that the SEP was usefulfor detecting subclinical root pathology. More re-cently, however, Seyal and associates found with thesame technique that scalp-recorded SEPs were ab-normal in only 20%—and lumbar responses in50%—of patients with lumbosacral radiculopathiesand accompanying radiologic abnormalities.100

Thus, the preponderance of studies casts doubt onany role for SEPs elicited by cutaneous nerve stimu-lation in the diagnosis or prognosis of radiculopa-thies.

SEPs can be elicited by dermatomal stimulationin the L5 or S1 territory.4,5,98 Scarff and colleaguesreported abnormalities in 92% of patients with sur-gically verified L5 or S1 root compression, but theircriteria of abnormality were apparently derived arbi-trarily.98 Aminoff and associates studied 32 normalsubjects and 19 patients with unilateral lumbosacralradiculopathy, and found that in only 5 patients wasthe lesion localized correctly by this technique.4

When the SEP was abnormal there was usually loss ormarked attenuation of the response; latency abnor-malities were uncommon. Needle EMG was gener-ally the most useful electrophysiologic means ofevaluating root lesions, but dermatomal SEPs some-times revealed unsuspected root dysfunction or ab-normalities when other electrophysiologic studieswere normal.5

Katifi and Sedgwick claimed that with dermato-mal SEP studies they predicted correctly the pres-ence of root compression in 19 of 20 patients,64 butthey used generous criteria for abnormality andmade multiple statistical comparisons of the datafrom their patients, most of whom had extensive dis-ease.3 Thus, they correctly identified 25 of 34 rootsthat were involved at surgery (their “gold” standard),but incorrectly identified another 12 roots that werenot compressed.3 In fact, they accurately and com-pletely predicted on electrophysiologic grounds theoperative findings in only 4 of 20 patients, a yieldsimilar to that of Aminoff and associates.4,5 A morerecent study by Dumitru and Dreyfuss also suggestedthat dermatomal SEPs are of limited diagnostic util-ity in patients with suspected unilateral L5 or S1 ra-diculopathy, because they do not have both a highsensitivity and a high specificity.28 They appear to beless accurate and sensitive than EMG and anatomic(imaging) studies.95

Dermatomal SEPs have also been used to evalu-

ate patients with lumbar spinal stenosis, and may bemore helpful in this context than when used toevaluate isolated compressive root lesions (W.C. Sto-lov, personal communication). A detailed account ofthis work and a comparison of the yield of dermato-mal SEPs and needle EMG, however, has yet to bepublished.

Central Nervous System. The SEP findings may de-tect and localize central somatosensory lesions butare not pathognomonic of specific diseases.1

Detection of Lesions in Central Somatosensory Path-ways. Multiple Sclerosis. The presence of SEP abnor-malities may reveal subclinical somatosensory lesionsand thereby establish that multiple lesions are pre-sent. An SEP abnormality may also indicate thatvague sensory complaints have an organic basis, es-pecially when the findings on clinical examinationare equivocal.

The likelihood of finding an SEP abnormality isgreater in patients with definite multiple sclerosis(MS) than in patients with possible MS. The inci-dence of abnormalities in patients with definite MSis about 80% regardless of whether there is any clini-cal sensory disturbance,46,77,102,111 but among pa-tients with possible MS the incidence of subclinicalSEP abnormalities is only about 25–35%. The yield ishighest from SEPs elicited by stimulation of a nervein the legs.1 An SEP abnormality is more likely ifthere is a clinical sensory disturbance in the stimu-lated limb, although the electrophysiologic findingthen provides little further information than ob-tained by clinical examination. SEP abnormalitiesare also more common when there are pyramidalsigns in the stimulated limb20 or legs.103 In patientswith a pyramidal deficit, however, an SEP abnormal-ity may not reflect a separate pathologic lesion butmerely an extensive lesion involving both motor andsensory pathways.

Among the different evoked potential techniquesfor detecting subclinical involvement of afferentpathways in patients with suspected MS, the highestyield is with SEPs; brain stem auditory evoked poten-tials (BAEPs) are the least useful.52,65,93,111 The basisof such differences is unknown but may reflect thelength and extent of the tracts being tested or dif-ferential susceptibility to pathologic involvement.

Abnormalities of the SEP may include delay orabsence of various components or an altered re-sponse-morphology. In the median SEP, a commonabnormality is loss of the cervical (N13) componentwith preservation of the later components. Thus, inone study the cervical response was abnormal in 41%of patients with suspected MS, and the yield in-creased to 50% when the cortical response was con-


sidered as well.38 The corresponding number for pa-tients with definite MS was 87% and 73%,respectively. The cervical SEP abnormalities encoun-tered most often were absence, attenuation, and in-creased dispersion of the response; only very occa-sionally was there an increase in latency. Centralconduction time, as calculated from the interpeaklatency of various components of the SEP, com-monly shows significant side-to-side difference in pa-tients with MS.33 In normal subjects, there is no sig-nificant change in the median SEP when bodytemperature is raised by 1°C, apart from a slight re-duction in latency resulting from increased periph-eral conduction velocity.79 Among patients with MS,by contrast, an initially normal cervical response maybecome abnormal, or—less commonly—an initiallyabnormal response may normalize. In many pa-tients, especially when the N13 is already abnormal,it becomes disorganized and attenuated.79

Subclinical SEP abnormalities are not diagnosticof MS. Such SEP abnormalities may also be found inother disorders such as vitamin B12 and vitamin Edeficiency states,42,69 hereditary spinocerebellar de-generations,87,90 and hereditary spastic paraple-gia.110 The electrophysiologic findings, therefore,must always be interpreted in relation to the clinicalcontext.

It is not clear whether evoked potential tech-niques are useful for monitoring disease progressionand evaluating experimental therapies for MS. Ami-noff and associates found a poor correlation be-tween clinical and electrophysiologic changes overtime, as well as an excessive variability between testsessions of the response to stimulation of a clinicallyinvolved afferent pathway in patients with definiteMS and a stable clinical deficit.2 Similar findingshave been reported by others for SEPs.72,80 Changesin previously abnormal evoked potentials do not nec-essarily reflect the site of new lesions, and the elec-trophysiologic changes occurring during clinical ex-acerbations may be in pathways uninvolved clinicallyby the relapse.

Thus SEPs may be diagnostically helpful in pa-tients with MS by establishing the presence of mul-tiple lesions when this is clinically inapparent. Thismultiplicity of lesions is not, however, pathogno-monic of MS and must be considered together withany other clinical and laboratory findings. Any rolefor SEPs in following the course of MS or its re-sponse to treatment appears limited.

Evoked potential techniques and magnetic reso-nance imaging (MRI) are probably equally sensitivein detecting lesions in patients with definite MS, butMRI is superior when the diagnosis is not definite.19

However, patients without clinical evidence of MS

may have MRI abnormalities resembling those inMS, so the MRI findings alone cannot establish thediagnosis. Further, evoked potential studies, particu-larly if used selectively in individual cases, are lessexpensive than MRI. Finally, the electrophysiologicfindings may clarify the underlying pathophysiology.In certain patients with abnormal tibial SEPs, forexample, the P38 (P40) and succeeding negativityare absent, and the first component recorded on thescalp is a positive wave with a latency closely approxi-mating that of the P50, suggesting that conductionblock (rather than delay) has occurred.34

SEPs may be abnormal in various disorders of thecentral nervous system, other than MS, that inter-rupt the somatosensory pathways. They are normal,however, when only spinothalamic function is im-paired.

Spinal cord dysfunction. Patients with spinal cordtumors or malformations or with spinal arteriovenousmalformations may have abnormal SEPs if the pos-terior columns are involved.73 In patients with re-paired spinal dysgraphic lesions, serial SEP studieshave sometimes been used to facilitate early detec-tion of clinically significant retethering, but the find-ings do not correlate well with clinical status and areof questionable utility.71

An upper cervical myelopathy occurs in achondro-plasia due to a small foramen magnum, and may leadto abnormal median or peroneal SEPs.84 In onestudy, SEPs were abnormal in all patients with neu-rologic symptoms or signs and in 44% of patientswithout neurologic dysfunction. In several of thesepatients, CT scans showed significant stenosis at theforamen magnum. Thus SEPs may have some use asa monitor of cord function in achondroplasia.

SEPs have also been used to monitor the effectsof radiation on the spinal cord. The findings havesuggested that subclinical cord dysfunction may fol-low radiotherapy for lung cancer even at conven-tional dose schedules.26

A variety of SEP abnormalities has been de-scribed in Friedreich’s ataxia, including mild latencyprolongation, and broadening or fractionation ofthe cortical response.78 Nuwer and colleagues foundin Friedreich’s ataxia that SEPs elicited from upper-limb nerves generally have delayed N20 peaks, butthat the Erb’s point potential is either normal oronly minimally delayed when present.87 In somecases the Erb’s point potential may be markedly at-tenuated.60

In patients with hereditary spastic paraplegia or he-reditary cerebellar ataxia, there may be loss of spinalor cortical components or marked cortical delay,even when there is no clinical sensory loss.110 Inthese disorders and Friedreich’s ataxia, there may


also be abnormality of the visual and auditory evokedpotentials.90 In olivopontocerebellar atrophy, SEPsmay be normal,87 attenuated, or absent.56

SEPs may be abnormal in patients infected withthe human immunodeficiency virus (HIV). Patients withacquired immune deficiency syndrome (AIDS) mayhave delayed cortical responses to tibial nerve stimu-lation, suggesting slowed spinal conduction. In non-AIDS patients, spinal latency and conduction timefrom gluteal crest to T12 tend to increase overtime.104 Again, others have reported that in somepatients with subclinical HIV infection, SEPs are ab-normal and may suggest a conduction defect in cen-tral somatosensory pathways.13 Whether SEP studieshave any clinical or prognostic relevance in this con-text is not established. In human T-cell lymphotropicvirus (HTLV)-I-associated myelopathy/tropical spas-tic paraparesis, lower-limb SEPs may provide impor-tant information; central sensory conduction timecorrelates with disability and may reveal subclinicallesions of afferent pathways.83 Lower-limb SEPs maybe unrecordable in patients with Pott’s paraplegia.82

Brain stem lesions. SEPs are normal in Wallen-berg’s syndrome,86 but are usually abnormal whenthe medial lemniscus is involved. They may be ab-normal in the ‘‘locked-in’’ syndrome due to pontineinfarction.86 The SEP findings do not distinguish re-liably between intra- and extra-axial lesions of thebrain stem.17

Thalamic lesions. The SEP findings in patientswith thalamic pathology tend to parallel the clinicalfindings, usually but not invariably being abnormalwhen there are significant clinical deficits.57 Laterallesions affect particularly the tibial SEP, and moremesial lesions affect the median SEP.12 The SEP issometimes relatively preserved with slowly growingnoninfiltrating extrinsic tumors involving the thala-mus, whereas extrinsic mass lesions compressing thethalamus acutely may abolish both median and tibialSEPs. The SEP is generally markedly abnormal inpatients with intrinsic thalamic tumors and a clinicalsensory deficit.12

Hemispheric lesions. In patients with predomi-nantly unilateral cerebral lesions, there is a correla-tion between the clinical and electrophysiologicfindings.47 SEPs are often normal in patients with nosensory deficit and abolished in those with moderateor severe cortical sensory loss. In some patients, how-ever, there is a discrepancy between the clinical andSEP findings—SEPs are normal despite cortical sen-sory deficits or absent despite preserved sensation.

Mauguiere and coworkers found that completeparietal lesions produced contralateral hemianesthe-sia without pyramidal signs, and eliminated the pa-

rietal N20–P27–P45 complex but not the prerolan-dic P22–N30 complex, indicating that the N20 andP22 components have separate generators.81 Smallpostcentral lesions causing astereognosis (with oth-erwise preserved sensation) reduced or abolishedthe N20 and P27 components without affecting theP22–N30 complex.

Recent work suggests that the electrophysiologicfindings are no better than a detailed neurologicexamination in predicting outcome from stroke,49

despite earlier suggestions to the contrary.SEPs as a Guide to Prognosis. Coma. In 36 coma-

tose patients with preservation of some brain stemfunction, Goldie and colleagues found the Erb’spoint response and the N13/N14 cervical responseto median nerve stimulation were preserved.50 Pa-tients with bilateral loss of the N20–P22 responseeither died or remained in a vegetative state. Unilat-eral loss of the N20–P22 responses was associatedwith a variable clinical outcome: death, a persistentvegetative state, or recovery of a functional level.Among patients with bilaterally preserved N20–P22responses, 56% became functional, 25% remainedin a vegetative state, and 19% died. Loss of the cor-tical N20–P22 responses therefore suggests a poorprognosis.

Among patients in posttraumatic coma, there isan association between the degree of abnormality inthe median SEP and clinical outcome. Hume andCant examined the scalp-recorded SEP findingssoon after onset of posttraumatic coma.58 Bilateralloss of median SEPs was believed to suggest a fataloutcome, and consistently asymmetric responses (inamplitude and latency) or a unilaterally absent SEPwere regarded as indicating the probable develop-ment of a severe residual deficit. The SEP findingspredicted the outcome corfectly in 38 of the 49 pa-tients studied in the first 84 h after coma onset. How-ever, the SEP findings sometimes changed when re-corded serially, and the outcome did not correlatewell with the SEP results in every test period. Forexample, 44 patients ultimately did badly (i.e., diedor were left with a severe deficit), and 10 of themsometimes had normal SEP findings, while 3 hadnormal SEPs on every recording. Similarly, amongthe 31 patients who did well, 15 had abnormal SEPson at least one occasion. Thus the SEP findings maynot be as useful as originally hoped in providing asatisfactory prognostic guide in individual cases.

Among patients in anoxic–ischemic coma, thefindings in one study revealed that none of 30 pa-tients with absent cortical SEPs recovered cognition.The presence of normal SEPs did not reliably predictrecovery, however. Some patients with normal corti-


cal SEPs several hours after cardiac arrest recoveredcognition, whereas others did not.11 The SEP find-ings corresponded to some extent with brain stemfunction. One or several brain stem reflexes wereabsent on initial examination in a majority of pa-tients with lost cortical SEPs but in only 20% of thosewith preserved SEPs. In another study, involving 60patients in coma for more than 6 h after cardiacarrest, the association of a Glasgow coma score ofless than 8 at 48 h with abnormal or absent earlycortical components of the median SEP was highlypredictive of a bad outcome.8

In locked-in syndrome, the SEP findings varyconsiderably in different patients and are of littlediagnostic help.54

Brain Death. SEPs are more important thanBAEPs in evaluating patients with suspected braindeath, because all responses to auditory stimulationare often absent, possibly for technical reasons orfrom deafness.50 With median nerve stimulation, bycontrast, most patients have cervical (N13/N14) butnot later responses, indicating that input reaches thecord-medulla but does not generate cerebral activitymore rostrally. This suggests an important role forSEPs in the evaluation of suspected brain death. Theuse of special recording derivations (midfrontal tomedian nasopharyngeal) for obtaining the medianSEP may be helpful in distinguishing between comaand brain death, but this requires further study.114

Spinal Injuries. SEP changes may occur with spi-nal injury.27,97,99 Responses to stimulation of a nervein the legs may be normal, delayed, small, or lost,depending on the extent and severity of the lesionand the timing of the examination.

It may not be possible to record any cortical re-sponse during the acute stage after incomplete trau-matic cord lesions,99 so an absent SEP does not re-liably permit early distinction of complete fromincomplete lesions. Preserved responses or theirearly return after injury, however, indicates an in-complete lesion and therefore a better prognosisthan otherwise, although functional recovery maystill be poor.97

Use of SEPs to Prevent or Minimize Neurological-Problems. SEPs have been used intraoperatively to

monitor cord function, but their utility in this con-text is unclear and beyond the scope of the presentminimonograph.

Defining the Extent of Neuropathologic Involvementin Neurologic or Neuromuscular Disorders. SEP ab-normalities have been found in patients with amyo-trophic lateral sclerosis,53,94 and this accords with pre-vious clinical and pathologic reports of sensoryinvolvement in this disorder. Polo and colleagues

have found the SEP elicited from both upper andlower limbs to be abnormal in patients with bulbo-spinal neuronopathy (Kennedy’s syndrome).92 SEPstudies have suggested that in diabetics, central affer-ent transmission—as well as peripheral nerve con-duction—may be affected.14 Median SEPs may beabnormal in dystrophia myotonica, reflecting periph-eral or central conduction delays in about one thirdof cases.7 There seems to be no relationship, how-ever, between the SEP findings and severity of theclinical disorder.

Some patients have sensory symptoms but no ob-jective clinical deficits, suggesting that symptoms arenot organic in origin. In such a circumstance, anabnormal SEP indicates that symptoms have an or-ganic basis. Normal SEPs and peripheral sensoryNCSs may support suspicions that symptoms are notorganic, but do not establish this with certainty. In-deed, SEPs may be normal in patients with pure sen-sory stroke due, for example, to lacunar infarcts.

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aaem minimonograph 19: somatosensory evoked potentials

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