SEMINARS IN NEUROLOGY-VOLUME

10, NO. 2 JUNE 1990

Sensory Evoked Potentials in Clinical Practice

The use of sensory evoked potentials (SEPs) in clinical neurologic practice has changed with the advent of increasingly sophisticated neuroimaging techniques. However, by and large, imaging techniques have allowed better understanding of structure of the central nervous system rather than function. SEPs still provide a quantitative measure of function of certain pathways within the nervous system. Somatosensory evoked potentials (SSEPs) provide the means to study the somatosensory system of the peripheral and central nervous systems noninvasively. Brainstem auditory evoked potentials (BAEPs) permit study of brainstem pathways and also allow assessment of hearing. Visual evoked potentials (VEPs) are a means by which one may extend physical examination of the visual system, hence, EPs continue to be a valuable diagnostic aid to the clinician. In this review we will examine short-latency SSEPs after median nerve (MN-SSEP) and posterior tibia1 nerve (PTN-SSEP) stimulation, BAEPs, and VEPs, with respect to generator sources, principles of interpretation, and common clinical applications.

NEURAL GENERATORS OF EVOKED POTENTIALS EPs recorded from the body's surface are either near field or far field in nature. That is, the generator source is close to or distant from the site of recording. T h e generators may be in gray matter or white matter. Generators in gray matter produce postsynaptic potentials (PSPs), which may be near field or far field. For example, near field PSPs are probably responsible for cortical components of SSEPs and VEPs.

White matter generates compound action potentials (APs), which are propagated through fiber tracts. T h e latencies of the propagated APs increase proportionate to the distance from point of stimulation and hence are dependent on recording electrode position. These are recorded only in close proximity to the fiber tract itself, and thus are termed "near-field potentials" (NFPs). Because they are close to site of origin, amplitude is relatively large (greater than 1 FV). Other EPs may be recorded at long distances from the point of propagation and are generated when a traveling impulse (signal) passes through a certain anatomic site or fixed point along the nerve. These are farfield potentials (FFPs). Most of the BAEP is an FFP. It was previously considered that FFPs reflected the approaching volley recorded beyond the point of termination of an active fiber' (Fig. 1). More recently, it has been suggested that FFPs are generated because of abrupt changes in geometry of tissue surrounding the n e r ~ e , or ~.~ change in the medium through which the volley is transmitted, or change in the direction of the fiber^.^ Potentials are labeled according to polarity and mean latency from a sample of the normal population. As one would expect, latencies change with body growth and nervous system maturation. Hence labels differ between children and adults. For purposes of discussing generator sources, adult terminology will be used for SSEPs.

SOMATOSENSORY EVOKED POTENTIALS Neural generators of MN-SSEPs and PTNSSEPs which have been delineated in adults are reviewed below, they are probably applicable to chil-

Associate Professor, Director, Clinical Neurophysiology Program, Departments of Neurology a n d Pediatrics, University of Kentucky Medical Center, Lexington, Kentucky Dr. Gilmore is a recipient of CIDA 1 KO8 NS1005. Reprint requests: Dr. Gilmore, Director, Clinical Neurophysiology Program, Department of Neurology, University of Kentucky Medical Center, Lexington, K Y 40536-0084 Copyright O I990 by Thieme Medical Publishers, Inc., 381 Park Avenue South, New York, NY 100 16. All rights reserved.

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Robin L. Gilmore, M.D.

SEMINARS IN NEUROLOGY Referential Recording

Bipolar Recording

Traveling Impulse I

VOLUME 10, NUMBER 2 JUNE 1990

Table 1. Presumed Generators of MN-SSEPs Component

Origin

P9

Brachial plexus

N9

Brachial plexus

P11

Dorsal root entry zone

N11

Dorsal root entry zone

P13-PI 4

Brainstem lemniscal pathways or composite of cervical dorsal horn synaptic activity and brainstem lemniscal pathways

N20

Subcortical region and sensory cortex

P23

Sensory cortex

.----I

+ Far Field Polential

Presumed Generators of PTN-SSEPs

Figure 1. Schematic model of generation of fat-field potential and the difference between referential and bipolar recordings. Far-field potential (rounded positive potential) is generated when an impulse crosses at a site where the geometry surrounding the nerve fiber changes. Referential recording registers both far-field and traveling impulse (pointed negative potential), whereas far-field potential is canceled with bipolar recording because of equipotentiality between the two electrodes. (From Yamada.' Reprinted with permission.)

Component

dren. Available evidence625 is summarized in Tables 1 (MN-SSEP) and 2 (PTN-SSEP).

p l e x u ~ .The ~ ~ 'P11 ~ is believed to be generated presynaptically from the dorsal root entry zone.4," The P13 component arises in structures caudal to the thalamus, probably in brainstern lemniscal pathways.12 Desmedt and Cheron13 recorded P13 in anterior neck and proposed a horizontally oriented dipole arising from the PSPs in the interneuron of the dorsal horn. T h e N19 generator source is not precisely understood. Some have suggested that it is thalamic in origin,14 whereas others have supported thalamocortical or cortical source^.].^.^^.^^ The P23 clearly arises from somatosensory c ~ r t e x . ~

MEDIAN NERVE SSEPs

When MN-SSEPs are recorded from the scalp with a noncephalic reference, three positive potentials P9, P11, and P13, are obtained regardless of recording site (see Fig. 2, Channels 1 and 3). These are believed to be FFPs. Two later components are also recorded, the N19 (sometimes known as the N20) and P23 (not labeled in Figure 2). T h e P9 arises from the distal portion of the brachial

Origin

N8

Tibial nerve action potential

N19

Cauda equina

N22

Lumbar cord gray matter

N27

Gracile nucleus

P37

Mesial sensory cortex

B Ldt

Figure 2. A: Normal median nerve somatosensory evoked potential. B: Abnormal median nerve somatosensory evoked potential. On the left in channel 1, note the absence of the obligatory P13, and from channel 2 the absence of the obligatory N19. On the right, note the absence of the obligatory PI3 and the prolongation of N19 to 25.0 msec. (From Gilmore et aLa4Reprinted with permission.)

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Table 2.

SENSORY EVOKED POTENTIALS IN CLINICAL PRACTICE-GILMORE

POSTERIOR TZBZAL NERVE SSEPs

There are less standard EP component designations for PTN-SSEPs than for MN-SSEPs. Following PTN stimulation, electrodes over the popliteal fossa record the electronegative peripheral nerve AP N8 (see Fig. 3). Electrodes over the lower spine record two electronegative potentials: the N 19 and the N22. Only the N22 is shown in Figure 3. The N19 represents the afferent volley in the cauda equina.ls The N22 is a stationary potential and probably reflects postsynaptic activity of internuncial neurons in the gray matter of the spinal cord.18 Electrodes over the cervical spine record another, later stationary potential, N27. This component may reflect postsynaptic activity in the gracile nucleus.lg The P37 is the first major scalp component and reflects the ipsilaterally oriented cortical surface electropositivity. The electronegative end of the dipole may be recorded contralaterally.'0~21 There is a great deal of intersubject variability in the topography of the P37 in adults22and, especially, children.23This is probably related to known anatomic difference in the location of the primary sensory area for the leg.24When the leg area is located at the superior edge of the interhemispheric fissure, the cortical generator for P37 (P28) is vertically oriented and its amplitude is maximal close to the vertex. When the leg area is located more deeply in the fissure, the cortical generator is more horizontally turned and the P37 (P28) projects i p ~ i l a t e r a l l y . ~ ~ - ~ ~

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Figure 3. A: Normal posterior tibial nerve somatosensory evoked potential. B: Abnormal posterior tibial nerve somatosensory evoked potential. On the left in channel l , note the absence of the obligatory P37. In channel 2 there is a questionable N27; however, this is not an obligatory potential. (From Gilmore et aLE4Reprinted with permission.)

rons. The short duration of most BAEP peaks suggests that they derive from APs rather that PSPs. From a vertex to ipsilateral ear derivation (Cz-Ai), a waveform with five to seven electropositive peaks is recorded in normally hearing subjects (see Fig. 4). These waves are labeled I-VII: only I, 111, and V are recorded reliably enough to be used in standard clinical practice. Wave I, in contradistinction

BRAINSTEM AUDITORY EVOKED POTENTIALS Most human BAEP peaks are composites of contributions of multiple generatomZ6BAEPs are the summation of activities of several pools of neu-

Figure 4. A: Normal brainstem auditory evoked potential. B: Abnormal brainstem auditory evoked potential with prolongation of the I-V interpeak interval to 4.48 msec. (From Gilmore et Reprinted with permission.)

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VOLUME 10, N U M B E R 2 JUNE 1990

to the later waves, is actually a negative wave, re- ulus. Its greatest amplitude is usually near the midcorded at the ear being stimulated and appearing line occipital electrode. There is a consensus that simultaneously with the AP of the electrocochleo- PlOO elicited in response to a transient checkergram. Wave I reflects the volley of eighth nerve board pattern reversal (shift) stimulus arises in the APs generated by the stimulus in the segment of occipital cortex (see Fig. 5). It is presumed that the nerve close to the cochlea. T h e origin of wave these are NFP from the visual cortices."' However, I1 remains controversial. Posible generators in- it is unclear whether it is exclusively produced by clude the distal eighth nerve, the proximal eighth area 17 or 18 or by a combination of cortical neunerve, and the cochlear nucleus andlor its out- ronal pools. It has been pointed out that the activf l o ~ . " ~ Based '~ on human lesion data, the major ity from area 17 and from extrastriate areas is generators of wave 111 are in the caudal pontine overlapping in time and produced in contiguous tegmentum, probably involving the superior oli- areas," making analysis of generators difficult. vary complex. Wave 111 is likely a composite and may be altered by lesions of either side, although PRINCIPLES OF INTERPRETATION it is usually more abnormal following stimulation of the ear ipsilateral to the major pathology.'!'~"" SOMATOSENSORY EVOKED POTENTIALS T h e principal generators of wave IV must be close to those of wave V, since both of those waves are Although several methods have been sugusually either affected or unaffected. Lesions of gested for recording EPs, the reader is referred the midpons, rostra1 pons, or mesencephalon are to the American EEG Society Guidelines.""or associated with absent waves IV and V.","%liniSSEPs, the presence of certain components is concally, unilateral abnormalities of wave V are most sidered obligatory-their absence is abnormal. For often associated with ipsilateral path~logy."'~""~":'~~" MN-SSEP, the P9, P13, and N19, and for PTNWaves VI and VII may be generated by activity in SSEP the N8 and P37 are obligatory in the adult. the medial geniculate, in the inferior colliculi, and/ Additionally, in the child, the N22 (PTN-SSEP) is or in the distal auditory radiations. obligatory. One may use height- adjusted and, as VISUAL EVOKED POTENTIALS

In standard clinical practice today, the most commonly recorded VEP is that elicited in response to a checkerboard reversal stimulus. It is positive at occipital scalp locations, appearing approximately 100 msec after the pattern shift stim-

necessary, age-corrected normative data for the latencies of peaks, or one may calculate conduction ("propagation") velocities over the peripheral nerves and central fibers. American EEG Society Guidelines recommend the use of velocity calculat i o n ~ . "However, ~ there are legitimate objections to this method, since there is a potential for error in

P loo 153.0

188

Figure 5. A: Normal visual evoked potential. B: Abnormal visual evoked potential with latency of PI00 prolonged to 153.0 msec. (From Gilmore et aI.O4Reprinted with permission.)

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SEMINARS I N NEUROLOGY

SENSOKY EVOKED POTENTIALS IN CLINICAL PRACTICE-GILMORE

BRAINSTEM AUDITORY EVOKED POTENTIALS

Waves I, 111, and V are considered obligatory, and the absence of any of these three is abnormal. T h e absence of all three is also abnormal, but since this abnormality may be associated with diversely different conditions ranging from brain death to Guillain-Barr6 syndrome to profound hearing loss, one must be very cautious in the interpretation. As always when interpreting a clinical neurophysiologic study, the context of the study is important. Absolute amplitude criteria have little use in the interpretation of BAEPs, although the relative amplitude ratio VII has been considered by some authorities to be useful provided a sufficiently high stimulus intensity is used. Absolute latencies of the waves I, III, V, and the 1-111, 111-V, and I-V IPLs (the I-V IPL is also known as the CCT) are probably the most standard criteria. Another criterion is the I-V IPL interaural difference. Absolute latencies and IPLs are dependent on many factors, including, but not limited to, stimulus intensity, patient temperature4' gender,." hearing function, and maturation4' (the last two are considered later). Unlike SSEPs and VEPs, BAEPs are little affected by the level of alertness per se. Between young and old adults, there is a mild effect of age on absolute latencies and IPLs. There is a much more dramatic effect of age when comparing the infant with the adult.." T h e BAEP can be recorded in the preterm newborn from approximately 30 weeks postconceptional age (PCA). T h e absolute latencies and IPLs are markedly prolonged relative to adult values. From 30 to 44 weeks PCA, there is roughly 0.2 mseclweek decrease in wave V latency. During the same time period, there is a 0.14 msecl week decrease in the I-V IPL."-4"'These agedependent changes continue until approximately 18 months PCA. These rapid changes require the

use of age-specific normative data. T h e changes in the I-V IPL have been attributed to myelination, with associated increasing fiber diameter and increasing synaptic efficiency. Hearing loss, of course, has a marked effect on the BAEP. In the normally hearing ear, as stimulus intensity increases, the latencies of I, 111, and V decrease (see Fig. 6A). One may develop a latency-intensity (L-I) function or curve for waves I and V (see Fig. 7). Close to hearing threshold (20 2 10 dB) wave V will appear. Since V appears closer to threshold than I, it is the L-I function of V that is used more commonly. However, an absent wave V at 20 + 10 dB is abnormal (in a technically adequate record). If V should appear at a higher stimulus intensity, this finding is referred to as an "elevated threshold," which also suggests a hearing loss (see Fig. 6B). With a conductive hearing loss, there is a proportional increase in the absolute latencies of all components. T h e conductive hearing loss increases the latency of V by a similar time over the entire range of intensities. When this is plotted as an L-I function, there is a parallel shift of the curve by an amount proportional to the hearing loss (see Fig. 8). Sensorineural hearing loss may be associated with high thresholds, attenuated or absent wave I, or both. This type of hearing loss may also be associated with a characteristic L-I function in which at lower stimulus intensities there is a large difference in wave V latency between the patient and control subjects with the difference diminishing as stimulus intensity is increased. Thus, at low stimulus intensities, the L-I function appears very steep, and then at higher intensities, the function becomes parallel to the normal L-I function. If one wishes to distinguish the type of cochlear hearing loss further, an electrocochleogram can be recorded using extratympanic electrodes: the summating potential (SP) and cochlear nerve AP are elicited. T h e amplitude of these electronegative potentials can be compared. Cochlear hearing loss not associated with hair cell loss (such as that associated with Meniere's disease) produces elevated SPIAP ratio^.^'

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the measurement of distance as a requisite for the calculation.'" Relative latencies (interpeak intervals or latencies [IPL]) may also be used. A commonly used IPL for the MN-SSEP is the N19-P13, also known as the central conduction time (CCT). Another commonly used CCT is the P37-N22 of the PTN-SSEPs. Since CCTs are also used in the interpretation of BAEPs, one must be careful to specify which modality one is referring to when using "CCT." Sleep has an effect on the short-latency SSEPS.',"~There appears to be a slight prolongation of the cortical response in adults, but in infants and children the effect of sleep is more dramatic. There is attenuation and prolongation of the components of the cortical response: the younger the child, the more marked the

VISUAL EVOKED POTENTIALS T h e PlOO of the VEP is the peak of interest for clinical interpretation. PlOO latencies and amplitudes are affected by a number of technical and subject variables, many of which are beyond the scope of this article. Two important issues, effects of maturation and level of attention, will be discussed. T h e amplitude of the PlOO has not been a reliable measure, presumably because of the large

189

3 0 wks

190

3 1 wks

3 2 wks

35 wks

18 months

Figure 7. Latency-intensity functions or curves for various postconceptional ages (PCA) and for 18 months postterm.

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Figure 6. A: In the normally hearing ear, the latency of wave V decreases as stimulus intensity increases. B: The condition in which wave V first appears at a higher than normal threshold is referred to as an elevated threshold and is abnormal. It may be seen with either conductive or sensorineural hearing loss.

SENSORY EVOKED POTENTIALS IN CLINICAL PRACTICE-GILMORE

bined with BAEPs in providing useful information. In one group of comatose children with hypoxic insults. BAEP and MN-SSEP were better predictors of chronic vegetative state than the EEG and clinical assessment." In cases of children with brainstem pathology conditions, the combined recordings of BAEP and MN-SSEP together have provided more information than either test alone.54 De Meirleir and Taylor55 reported SSEPs in children who were comatose from various causes. Their patients with bilaterally absent cortical SSEPs had extremely poor outcomes: they either died or developed severe spastic quadriplegia.55Patients who had unilaterally abnormal cortical SSEPs were later found to have residual hemiparesis. Those patients who had normal outcomes had normal or only mildly abnormal SSEPs, which Figure 8. Latency-intensity function for wave V shown normalized within a few days. in Figure 6B. This is consistent with a conductive hearing T h e role of SSEPs in evaluation of patients loss. with suspected brain death is somewhat controversial. Patients fulfilling the clinical criteria of brain death have no waves arising from structures above normal variability of amplitude. T h e absolute lathe lower m~dul1a.l"~~ Approximately ~" 60 to 70% tency of PlOO is a very useful criterion. Since each of patients will have a lower medullary potential eye is tested individually, the interocular difference present, but 30 to 40% will not. In these latter is also an important criterion; it may, in fact, be the cases, it will not be possible to ascertain that the most sensitive indicator of optic nerve dysfunction. signal reached the central nervous system, and Age affects PlOO latency somewhat: there is little change in latency that is age-related until the fifth hence the MN-SSEP does not contribute to the didecade;" thereafter, latency increases at about 2 agnosis, either positively or negatively. In one of msec per decade. Unlike the SSEP and BAEP, the the cases reported by Anziska and Cracco," an SEP VEP is affected by level of attention to the stimu- component thought to be generated rostrally to lus. Some have found that focusing on the periph- the lower medulla was recorded. However, Oken ery of the stimulus rather than its center can and Chiappa" have raised the possibility that the did not fulfill all generally accepted criteria produce significant latency changes.47 C h i a ~ p a ~patient ~ of brain death. BAEPs in adults are extraordinarily believes that those maneuvers that produce the resistant to toxic and metabolic encephalopathies; most marked changes are easily detected by obserthus, normal potentials can be recorded from pavations of the technologist. tients in deep barbiturate coma. Hepatic and renal failure also have no or little effect on the BAEP. T h e use of checkerboard pattern VEPs in CLINICAL APPLICATIONS states of altered consciousness is precluded by the technical need to have alert, attentive patients. For COMA AND PROGRESSIVE ENCEPHALOPATHIES patients with encephalopathies who do not have T h e value of MN-SSEPs for prognosis has altered states of consciousness, VEPs may be been examined in comatose infants, ~hildren,~"."~) abnormal with diffusely prolonged latencies. For and adults.~4..j~.x Hume and Cant"' studied SEPs in instance, patients with subacute combined degenprognosis following head injury associated with eration may have abnormally prolonged PlOOs bicoma. They found that, for a large group of pa- l a t ~ r a l l yPatients .~~ with alcoholism" and with renal tients, the bilateral absence of scalp-recorded com- disease") have also been reported to have abnormal ponents was highly indicative of a fatal outcome; VEPs. responses that were attenuated or absent over one side suggested residual neurological deficit. In the ASSESSMENT OF HIGH-RISK NEWBORNS evaluation of patients with anoxic-ischemic coma, Brunko and Zegers de Bey1 found that no patients Assessing and establishing a prognosis for with absent cortical responses had recovery of cog- high-risk newborns (HRN) can be quite difficult. nition."' SSEPs are especially helpful when com- Assessment via EPs is attractive because it is non-

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18 months

191

invasive, can be done at the bedside, and gives quantitative information that can be acquired serially. There is an increasing number of studies that have evaluated the SSEP in this setting. All patients with persistent abnormalities had clinical evidence of brain injury. Laget et al" studied infants and children from 14 days to 13 years of age with motor deficits. They reported that the SSEP was more accurate than the EEG in localizing or lateralizing the lesion. Lutschg et alG2combined SSEPs and BAEPs to study 10 asphyxiated babies at 3 months of age, all with abnormal tone on physical examination and severe leukomalacia on computed tomography (CT). Although BAEPs were normal or only slightly abnormal, there were no cortical components recorded. More recently, G ~ r k evalue ~ ~ ated the prognostic value of the SSEP in infants with cerebral palsy and with neurodegenerative and metabolic diseases of the central nervous system. Many infants had prolonged or absent cortical potentials; all of these infants demonstrated fixed handicaps after the first year of life. T h e author concluded that the SSEP was a valuable early indicator of severe motor impairment. Majnemer et al'j4 assessed healthy newborns and HRNs. This group found that approximately one third of newborns who were highly at-risk for neurologic and/ or developmental sequelae had abnormal SSEPs consisting of prolongation of absolute cortical latency or C C T , . ~absence ~ of the scalp recorded Potentials. Patients were subsequently tested at 2 to 3 of age: those with prolonged latencies at birth and later normal latencies had mild neurologic deficits; those with absent potentials initially and 3 months later had spastic quadriparesis.

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VOLUME 10, N U M B E R 2 JUNE 1990

with Parkinson's disease" and Huntington's chorea (HC)70also have abnormal VEPs. Patients with HC also have abnormal SSEPS.~') Rossini et a171 have found abnormal SSEPs in patients with several other neurodegenerative disorders including Friedreich's ataxia (FA), hereditary motor-sensory neuropathies I and I1 (HMSN), familial spastic paraplegia (FSP), olivopontocerebellar atrophy (OPCA), and ataxia telangiectasia (AT). Patients with FA, OPCA, HMSN-11, and AT had impaired central conduction. This has been vertified by others.72Patients with OPCA usually had normal MN-SSEPs, but all SSEPs from the lower extremities were abnormal. The patients with HMSN-I1 and AT usually had normal MNSSEPs with increased CCT of SSEP after- lower extremity testing. BAEP abnormalities have been reported in spinocerebellar degenerations and in some cases of subacute combined degeneration. VEPs are abnormal in a high proportion of cases of FA and may, in fact, be used to distinguish it from other spinocerebellar degenerations. Metabolic disorders such as aminoacidopathies, neuronal storage diseases, and organic acidemias may demonstrate mild prolongations of CCT of SSEPs and BAEPs. STRUCTURAL AND COMPRESSNE LESIONS

Structural and compressive lesions may also rise to abnormal SSEPs, depending of the site. Intrinsic cervical spine lesions such as those seen in spinal cord gliomas and Arnold-Chiari malformations are associated with SSEP abnormalities, which have correlated with the severitv of clinical involvement. Patients with extrinsic lesions such as NEURODEGENERATNE DISORDERS spinal canal stenosis and foramen magnum stenoSeveral investigators have reported abnormal- sis secondary to achondroplasia have also been ities in EPs in a variety of neurodegenerative dis- studied.73Nelson et a17%tudied the MN-SSEPs and o r d e r ~ . ~ ~Abnormalities -~' of spinal and cortical PTN-SSEPs of 23 patients who had achondroplasia components of SSEPs have been found. Severe ab- with and without symptoms. All symptomatic panormalities have been described in patients with tients had at least one abnormal SSEP, and 44% (7 polioencephalopathies (disorders primarily affect- of 16) of asymptomatic patients also had abnormal ing gray matter) and leukodystrophies. In most of SSEPs. They suggested that SSEPs might serve to these disorders, the peripheral components of alert the clinician to potential problems early in the SSEPs are normal while more rostral compo- course so that decompressive surgery could be nents have been delayed or a b ~ e n t .In ~ ~patients .~~ done before serious neurologic compromise ocwith metachromatic leukodystrophy, peripheral curred. and more rostral components are abnormal in As might be anticipated, structural spinal cord SSEPs. In these patients, BAEPs and VEPs are also lesions not involving the cervical spine are frefrequently abnormal." Tobimatsu and coworkers68 quently associated with abnormalities in PTNhave demonstrated that MN-SSEPs are valuable S S E P S .For ~ ~ the evaluation of patients with myeloin differentiating adrenomyeloneuropathy (AMN) dysplasia and occult spinal dysraphism, Cracco and from adrenoleukodystrophy (ALD). In both of C r a ~ c o were ~ ~ among the first to demonstrate the these conditions CCT is prolonged, but in AMN utility of recording the spinal components of the peripheral potential is prolonged also. Patients SSEPs. The large spinal potential normally re-

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SEMINAKS I N NEUKOLOGY

SENSORY EVOKED POTENTIALS IN CLINICAL PRACTICE-GILMORE

MULTIPLE SCLEROSIS

The clinical usefulness of SEPs in multiple sclerosis (MS) is based on their ability to demonstrate abnormal sensory function when the history andlor physical examination, or both, are equivocal and on their ability to reveal the presence of clinically silent malfunction in a sensory system. There has been a large number of studies of SEPs in patients with MS. Of approximately 1000 patients in the literature with varying classifications of MS, 58% had abnormal upper extremity SSEPs and 76% had abnormal lower extremity SSEPs." One fifth to one half of patients without brainstem symptoms or signs demonstrated evidence of clinically silent lesions on BAEP testing.82 Of these 1000 patients, 7 15 had no clinical evidence of optic nerve involvement; of these 7 15,51% had VEP abnormalities." Although the use of MRI has changed the role of SEPs in the diagnosis of MS, it appears that MRI and SEPs (paraclinical studies) are complementary and not mutually exclusionary. There has been much interest in comparing MRI of the optic nerve and VEPs in the evaluation of patients with s ~ s pected MS. Miller et alN"reported on their experience using the advanced technology of short inversion time inversion recovery (STIR) to image the optic nerve. They found that VEPs in the symptomatic eye were 100% sensitive, but STIR-MRI detected lesions in only 84%. In the asymptomatic

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corded over lower thoracic spine is displaced eye, VEPs were again more sensitive than MRI. caudally in these children. Others have recorded Thus, they concluded that VEP remained the preabnormal PTN-SSEPs in patients with tethered ferred investigation for demonstrating abnormalities in optic neuritis. spinal cord syndrome (TSCS).40 One of the more important issues in considStructural brainstem lesions such as neoplasms have been frequently associated with both MN- eration of cost-effectiveness is which of the paraSSEP4 and PTN-SSEPi" abnormalities. They are clinical studies (MRIs and SEPs) increase diagnosprobably most helpful when used in conjunction tic yield in patients suspected of having MS. To with BAEPs. In brainstem gliomas, the incidence answer this question, Gilmore et als4 compared of BAEP abnormalities appears to approach 100% MRI and SEPs directly in 58 patients. They found when the lesion involves the p o n ~ . ~In ~ .the ~ ' ex- that the MRI was more sensitive, but SEPs, espeperience of some, BAEPs are more sensitive than cially VEPs and PTN-SSEPs, provided essential C T at detecting brainstem gliomas, although prob- complementary information in evaluating these ably not more sensitive than magnetic resonance patients. Thus, there is still a significant role for imaging (MRI).7''BAEPs remain a very useful and SEPs. This appears to be the case because SEPs can cost-effective means of screening for acoustic neu- assess areas currently not imaged or not imaged romas. In the evaluation of children suspected of well by MRI. As these techniques continue to harboring supratentorial brain tumors SSEPs have evolve. these issues should be reexamined. been found useful in detecting tumor r e ~ u r r e n c e . ~ " PERIPHERAL LESIONS Compression of the anterior visual pathways produces distortion of the VEP wavefbrm. AlPeripheral nerve plexus and root lesions can though neuroimaging studies are likely to be the also be assessed with SSEPs. In patients with Erb's most sensitive diagnostic tool, the VEP may be palsy, when there is a root avulsion but the dorsal used to follow patients with optic nerve g l i ~ m a s , ~ "root ganglion is intact, a peripheral potential is reand patients with pseudotumor ~ e r e b r i . ~ ~ corded and more rostral components are abnormal." If there is a plexus lesion, the peripheral potential and more rostral components are absent. Schiff et alH5reported abnormal SSEPs in patients with Guillain-BarrC syndrome. Combinations of prolongation or absence of peripheral potentials and more rostral potentials of MN-SSEP and PTN-SSEPs have been reported by ~ t h e r s . ~ " SEPs are a useful, reliable means of assessing somatosensory, brainstem auditory, and visual systems. By providing a means by which to examine portions of the nervous system inaccessible to clinical examination and by assessing function rather than structure, they are a valuable adjunctive neurophysiologic technique. T h e factors of complex maturational changes in the CNS and body growth complicate the interpretation of SEPs. In many clinical conditions SEPs have been useful in diagnosis and prognosis.

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