9 Evoked Potentials: Search in This Book

Primer on Multiple Sclerosis (2 edn)
Barbara S. Giesser (ed.)
https://doi.org/10.1093/med/9780199341016.001.0001
Published: 2016 Online ISBN: 9780190226305 Print ISBN: 9780199341016
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CHAPTER
9 Evoked Potentials 
Marc R. Nuwer
https://doi.org/10.1093/med/9780199341016.003.0009 Pages 141–162

Published: January 2016
Abstract
Visual evoked potentials, brainstem auditory evoked potentials, and somatosensory evoked potentials
are established clinical tests that are useful for the diagnosis of multiple sclerosis. Motor evoked
potentials, cognitive event-related potentials, and vestibular evoked potentials also are used clinically
to test additional pathways and functions. These objective, reproducible tools can identify clinically
silent lesions, predict clinical deterioration risk, and localize levels of impairment. They di er from
magnetic resonance imaging in that they assess function rather than anatomy and thereby ll a
complementary role in clinical care. They also are useful in therapeutic trials because they can predict
outcomes in parallel with, or earlier than, clinical examinations.
Keywords: visual evoked potential, brainstem auditory evoked potential, somatosensory evoked
potential, motor evoked potential, cognitive event-related potential, vestibular evoked potential,
therapeutic trial, multiple sclerosis
Subject: Neurology
Collection: Oxford Medicine Online
Introduction
Evoked potentials (EP) are nervous system electrical potentials evoked by certain brief stimuli. For 40 years
certain EP tests have helped clinically to diagnose multiple sclerosis (MS) (Comi et al., 1998, 1999; Fuhr &
Kappos, 2001; Leocani & Comi, 2000; Leocani, Medaglini, & Comi, 2000. As a research tool, they can explore
the pathophysiology of demyelination and serve as a tool for MS therapeutic trials (Emerson, 1998; Nuwer,
Packwood, Myers, & Ellison, 1987).
Evoked potentials are sensitive, objective, and reproducible. They easily are quanti ed to two to three
signi cant gures. Evoked potentialscan detect “silent lesions,” physiological impairment without
accompanying signs or symptoms that can provide evidence of an additional lesion. The tests are objective
because they require only that the patient lie quietly or watch a video screen. The patient’s cooperation does
not alter EP results. Test scoring is standardized. Evoked potentials are reproducible in that they yield the
same values when tested again. The standard scoring is quanti ed to two or three signi cant gures for
comparison with normal values. These precisely quanti ed measurements facilitate their use with
parametric statistics, a substantially more powerful research tool than categorical variables.
Evoked potentials are electrical potentials (voltages) evoked by brief stimuli. After each stimulus, nerve
volleys travel along the peripheral and central nervous system pathways of the stimulated sensory or motor
modality. These axon volleys are delayed or blocked by regions of demyelination (Raminsky, 1981; Sears &
Bostock, 1981; Sedgwick, 1983; Waxman, 1981; Waxman & Ritchie, 1981). Beyond the level of demyelination,
the recordable EP signals are delayed, attenuated, or absent. The peaks’ generator sites are known, so the EP
reader can determine the level of impairment. Four traditional EP modalities assess speci c paths: central
visual, brainstem auditory, lemniscal sensory, and corticospinal motor pathways (Cowan et al., 1984; Hess,
Mills, Murray, & Schriefer, 1987; Mills & Murray, 1985). Event-related potentials measure cognitive
processing speed (Goodin, Desmedt, Maurer, & Nuwer, 1994). New modalities assess brainstem vestibular
re ex pathways (Gabelić et al., 2013; Gazioglu & Boz, 2012; Rosengren & Colebatch, 2011).
Evoked potentials also are used to diagnose other neurological disorders. Brainstem auditory EPs screen
infants for hearing impairment (Starr, Amlie, Martin, & Sanders, 1977). In comatose patients, EPs assess
degree and location of impairment (Cant, Hume, Judson, & Shaw, 1986; Karnaze, Marshall, McCarthy,
Klauber, & Bickford, 1982) and assess prognosis (Young, 2009). They can help distinguish among some
hereditary–degenerative neurological conditions that have speci c patterns of EP changes (Nuwer,
Perlman, Packwood, & Kark, 1983). In the operating room, EPs can monitor the nervous system, allowing
early identi cation of complications and allowing for early intervention (Nuwer, 2008). They can help
separate peripheral from central levels of sensory impairment, analogous to the clinical use of deep tendon
re exes to separate central from peripheral motor pathway impairment.
Visual Evoked Potentials
Visual evoked potentials (VEP) use strobe ash or a checkerboard pattern. Flash was described earlier
(Richey, Kooi, & Tourtellotte, 1971). Pattern reversal checkerboard VEP technique is more sensitive for
detecting optic neuritis (Halliday, McDonald, & Mushin, 1972). In the pattern reversal technique, each black
and white checkerboard square reverses shade twice each second. The patient is tested one eye at a time in a
p. 142 darkened room. The test measures time from the moment of checkerboard reversal to presence of an
occipital scalp peak at around 100 ms, named P100. Results from 100 separate stimulus presentations are
averaged together before making measurements. The P100 event measures time for axon volleys to travel
from the eye along the optic nerve, chiasm, optic tract, optic radiations, directly through the periventricular
white matter for rather long distances, and eventually reaching occipital cortex. Finally an electrically
positive P100 peak is seen generated by striate cortex (Figure 9.1).
Figure 9.1:
Abnormal visual evoked potentials with a delayed P100 seen as a down-going peak at 140 ms. Normal is <105 ms. The three
channels are from the right, midline, and le occipital scalp.
Delayed conduction may occur at several points along this pathway in MS patients. Delays at the optic nerve
are well known. Less appreciated are the VEP delays that may occur along the optic tract and radiations,
especially in the periventricular white matter. Prechiasmatic optic neuritis can be separated from the
postchiasmatic lesions by comparing results from each eye. Interocular P100 latency di erences are
attributed to optic neuritis.
Visual evoked potentials are more sensitive than even a careful clinical visual function examination for
detecting demyelination (Brooks & Chiappa, 1982; Chiappa, 1990; Kupersmith, Nelson, Seiple, Carr, &
Weiss, 1983). Neuro-ophthalmologic examinations always were normal when the VEP was normal (Brooks
& Chiappa, 1982). Even when the VEP was abnormal, various clinical examinations were often normal for
visual elds by confrontation or formal testing, with normal pupillary re exes, and many patients had
normal optic fundi and no red desaturation.
The checkerboard VEP technique is abnormal in almost all patients with a history of optic neuritis. In a
summary of the literature (Asselman, Chadwick, & Marsden, 1975; Cant, Hume, & Shaw, 1978; Celesia &
Daly, 1977; Chiappa, 1980; Collins, Black, & Mastaglia, 1978; Diener & Scheibler, 1980; Duwaer & Spekreijse,
1978; Halliday, McDonald, & Mushin, 1973a, 1973b; Hennerici, Wenzel, & Freund, 1977;Hume & Cant, 1976;
Kjaer, 1980a; Lowitzsch et al., 1976; Mastaglia, Black, & Collins, 1976; Matthews, Small, Small, & Pountney,
1977; Nilsson, 1978; Purves, Low, Galloway, & Reeves, 1981; Rigolet, Mallecourt, LeBlanc, & Chain, 1979;
Shahrokhi, Chiappa, & Young, 1978; Tackmann, Strenge, Barth, & Sojka- Raytsche , 1979; Trojaborg &
Petersen, 1979;van Buggenhout, Ketelaer, & Carton, 1982; Walsh, Garrick, Cameron, & McLeod, 1982;
Wilson & Keyser, 1980; Wist, Hennerici, & Dichgans, 1978), Chiappa (1990) found that >90% of optic
neuritis patients had abnormal VEPs, and close to 100% in many published series. When there was no
clinical evidence for optic neuritis, the VEPs still were abnormal in 51% of 715 patients with MS.
Visual evoked potentials improve partially after an optic neuritis or postchiasmatic demyelination episode,
but they do not usually return to normal (Jones & Brusa, 2003; Matthews & Small, 1979). An initial 30ms
delay improves gradually over months to a 16ms delay (Brusa, Jones, & Plant, 2001; Jones & Brusa, 2003),
improved but still abnormal. Visual evoked potentials help the clinician to decide whether a history of visual
changes years ago was from optic neuritis; if the VEP is normal, the episode was not optic neuritis.
For patients presenting with a clinically isolated spinal or brainstem lesion, VEP can determine whether
optic neuritis occurred in the past. This search for a silent second lesion is an established use of VEPs
(Polman et al., 2005).
A controversial report suggested that VEPs in neuromyelitis optica (NMO) di ered from those in MS (Neto
et al., 2013). The report suggested that NMO VEPs showed decreased amplitude rather than delays. However,
the report’s gure did show a P100 delay in NMO. Some loss of VEP amplitude also is well known in the acute
p. 143 phase for more severe optic neuritis symptoms. Visual evoked potentials ndings do not clearly
di erentiate between NMO and other demyelinating diseases.
Other disorders can a ect VEPs. Some hereditary-degenerative neurological disorders, for example,
Friedreich ataxia (Nuwer et al., 1983) and adreno-leukodystrophy (Mamoli, Graf, & Toi , 1979), as well as
B12 de ciency (Krumholz, Weiss, Goldstein, & Harris, 1981), neurosyphillis (Lowitzsch & Westho , 1980),
and other disorders (Streletz, Chambers, Bae, & Israel, 1981) can slow VEP latencies. These changes usually
are mild or moderate bilateral delays. Severe delay or an interocular latency di erence usually is from
demyelination. Mild to moderate symmetrical delays could be bilateral demyelination, or they might be
from another disorder, con rming an abnormality but nonspeci c for the pathology.
Several useful MS VEP facts are notable:
• Idiopathic optic neuritis (ON) patients often develop MS (Ghezzi, Martinelli, Rodegher, Za aroni, &
Comi, 2000; Rodriguez, Siva, Cross, O’Brien, & Kurland, 1995).
• Initial VEPs are abnormal in nearly all eyes a ected with ON (Bee, Lin, Wang, & Sheu, 2003;
Frederiksen & Petrera, 1999; Frederiksen, Petrera, Larsson, Stigsby, & Olesen, 1996; Jones & Brusa,
2003).
• Visual evoked potential is abnormal in the clinically una ected eye in 25% to 35% of ON patients (Bee
et al., 2003; Frederiksen & Petrera, 1999; Frederiksen et al., 1996; Jones & Brusa, 2003; Simó, Barsi, &
Arányi, 2008), greatly increasing the likelihood that those idiopathic ON patients will progress to MS.
• Visual evoked potential is more sensitive than MRI to con rm optic nerve, chasm, and optic tract
symptomatic demyelination (Farlow, Markand, Edwards, Stevens, & Kolar, 1986; Frederiksen et al.,
1996;Martinelli et al., 1991; Paty et al., 1988).
• Magnetic resonance imaging (MRI) is more sensitive than VEP (Farlow et al., 1986; Frederiksen,
Larsson, Olesen, & Stigsby, 1990; Frederiksen et al., 1996; Martinelli et al., 1991; Paty et al., 1988) to
nd a second lesion in the asymptomatic eye in ON patients.
• Brain MRI has a high yield of abnormalities in other brain areas (Giesser et al., 1987; Lee et al., 1991;
Paty et al., 1988), whereas VEP is sensitive only along the visual axis.
• The length of the MRI-detected demyelination correlated with the severity of VEP delay (Davies,
Williams, Haq, Pelosi, & Hawkins, 1998).
• The amount of VEP delay does not predict the amount of MRI-detected long-term atrophy (Hickman et
al., 2003).
• Time needed for resolution of optic nerve gadolinium enhancement correlates with time for VEP
latency improvement (Youl et al., 1991).
The American Academy of Neurology evidence-based assessment of VEPs recommends the technique as
useful to identify patients at increased risk for developing clinically de ned MS (Gronseth & Ashman, 2000).
Visual evoked potential was adopted into the MacDonald criteria for diagnosis of MS (Polman et al., 2005).
When evaluating for possible MS those patients presenting with acute or chronic spinal cord lesions,
multimodality EPs have a high yield of abnormalities (69% sensitivity) and fewer false positives than MRI
(5% false positives for EPs, 9% for MRI). Abnormal VEP clari es that demyelination is the likely cause of
enhancing spinal MRI lesions (McDonald, 1988). The diagnostic yield for VEP in that circumstance was
moderately low (7%–28%), so it is often normal and not speci cally helpful for predicting which spinal
lesions patients will progress to MS (Cordonnier et al., 2003; Miller et al., 1987).
Visual EPs help understand the physiology of demyelination. Analogous to the Uhtho phenomenon, heat
alters VEPs (Bajada, Mastaglia, Black, & Collins, 1980; Persson & Sachs, 1980; Regan, Murray, & Silver, 1977)
in ways that can be studied precisely. Hyperventilation can increase VEP amplitudes (Davies, Carroll, &
Mastaglia, 1986), corresponding to clinical observations that hyperventilation, alkalosis, and hypocalcemia
can transiently improve clinical de cits. The calcium channel blocker verapamil (Gilmore, Kasarskis, &
McAllister, 1985) and the potassium channel blocker 4-aminopyridine (Jones, Heron, Foster, Snelgar, &
Mason, 1983) can improve VEPs transiently.
An investigational VEP technique tests each small portion of the visual eld. Known as multifocal VEPs
(Fraser et al., 2006a, 2006b; Grover et al., 2008; Hood et al., 2004a, 2004b), these can better de ne central
p. 144 scotomas better than optical coherence tomography (Laron et al., 2010). Multifocal VEPs correlate with
EDSS (Blanco et al., 2014) as do traditional full- eld VEPs. Routine VEPs also can show evidence of a central
scotoma, which presents with a bi d (doubled) P100 peak (Rousse , Tzvetanov, & Rousseva, 2005).
Studies of VEP along with an ophthalmic examination, optical coherence tomography, scanning laser
polarimetry, and pattern electroretinogram showed a decreased retinal nerve bre layer on the a ected eye
(Garcia-Martin et al., 2011;-Rodriguez-Mena et al., 2013; Tugcu et al., 2013). These worsen over time as MS
progresses, and correlate with disability and quality of life (Garcia-Martin et al., 2013).
Visual evoked potentials can help study genetic predisposition to MS (Nuwer, Visscher, Packwood, &
Namerow, 1985). Some asymptomatic rst-degree relatives of MS patients have mild VEP abnormalities. A
genetic predisposition toward subclinical pathology may underlie this (e.g., subclinical optic nerve edema
without demyelination). Epidemiology of MS tells us that most such abnormalities are unlikely to develop
into frank clinical MS. Some additional factors must be needed to convert such subtle processes into clinical
MS.
Overall, checkerboard reversal pattern VEP helps the clinical evaluation of patients with possible MS.
Abnormalities commonly occur in these visual pathways even in patients with no visual signs or symptoms.
Visual evoked potentials are more sensitive than MRI to detect optic neuritis. A VEP clari es whether history
of a previous visual event was optic neuritis. They can also identify a silent second lesion in the visual
pathway in patients with clinically isolated brainstem or spinal cord syndromes.
Brainstem Auditory Evoked Potentials
Brainstem auditory evoked potentials (BAEPs) record at the scalp signals generated in the brainstem.
Signals are evoked by 100-microsecond clicks delivered through earphones. The signals are generated by
pons and midbrain nuclei and tracks associated with auditory localization, not speech discrimination.
The eighth cranial nerve generates wave I. That peripheral peak is normal in patients with MS who have no
hearing problem. The BAEP’s four central peaks are labeled II through V (Figure 9.2). Wave II is generated by
the cochlear nucleus. Wave III is generated around the superior olive and trapezoid body in the lower pons.
Waves IV and V arise from lateral lemniscus bilaterally in the upper pons to lower midbrain. Internuclear
ophthalmoplegia is the most common clinical sign corresponding to BAEP abnormalities. Table 9.1 shows
the correlation among BAEP, signs, and symptoms.
Figure 9.2:
Brainstem auditory evoked potentials, identifying the five main peaks waves I through V (in Roman numerals).
From Nuwer, M. R., Amino , M., Goodin, D., Matsuoka, S., Mauguiere, F., Starr, A., & Vibert, J. F. (1994b). IFCN recommended
standards for brain-stem auditory evoked potentials. Electroencephalography and Clinical Neurophysiology, 91, 12–17.
Table 9.1. Correlation between Degree of BAEP Abnormality and Multiple Sclerosis Patient Signs and Symptoms
Correlation with Abnormality
In BAEPs History
0.41 Diplopia
0.23 Dysphagia
0.16 Vertigo
0.12 Hearing impairment
0.10 Dysarthria
0.03 Facial sensory impairment
Physical Signs
0.39 Ocular dysmetria or gaze paresis
0.32 Nystagmus
0.29 Facial weakness
0.25 Dysarthria
0.23 Facial sensory loss
0.21 Slow tongue movements
0.09 Other brainstem signs
0.04 Subjective hearing threshold
Source: From Nuwer, M. R., Packwood, J. W., Ellison, G. W., & Meyers, L. W. (1988). A parametric scale for BAEP latencies in
multiple sclerosis. Electroencephalography and Clinical Neurophysiology, 71, 33–39. 10.1016/0168-5597(88)90017-2
BAEP, brainstem auditory evoked potential.
p. 145 Typical BAEP abnormalities in MS patients are delayed waves III to V and decreased amplitude or absent
wave V. Figure 9.3 illustrates progressively greater degrees of BAEP abnormalities among patients with MS.
Figure 9.3:
Examples of various degrees of abnormality in the brainstem auditory evoked potential test in multiple sclerosis. The upper
evoked potential traces are less a ected, and the lower traces are more a ected. Demyelination prolongs latencies with loss of
amplitude and eventual absence of peaks II to V.
From Nuwer, M. R., Packwood, J. W., Ellison, G. W., & Meyers, L.W. (1988). A parametric scale for BAEP latencies in multiple
sclerosis. Electroencephalography and Clinical Neurophysiology, 71, 33–39. 10.1016/0168-5597(88)90017-2
Other neurological disorders also a ect BAEP, such as tumors (Brown, Chiappa, & Brooks, 1981; House &
Brackmann, 1979), ischemia (Brown et al., 1981), and some hereditary–degenerative neurological disorders
(Nuwer et al., 1983). Therefore, BAEP abnormalities are not pathognomonic of MS. Abnormalities just
indicate impairment at the pons or lower midbrain.
Chiappa (1990) summarized results from many published reports (Barajas, 1982; Chiappa et al., 1980b;
Elidan, Sohmer, Gafni, & Kahana, 1982; Fischer, Blanc, Mauguiere, & Courjon, 1981; Green, Price, &
Woodbury, 1980; Green, Walco , & Lucke, 1982; Hausler & Levine, 1980; Hutchinson, Blandford, Glynn, &
Martin, 1984; Kayamori, Dickins, Yamada, & Kimura, 1984; Khoshbin & Hallett, 1981; Ko er, Oberascher, &
Pommer, 1984; Lacquanti, Benna, Gilli, Troni, & Bergamasco, 1979; Mogensen & Kristensen, 1979; Parving,
Elbering, & Smith, 1981; Prasher, Sainz, Gibson, & Findley, 1982; Purves et al., 1981; Robinson & Rudge,
1977a, 1977b, 1980; Shanon, Himmelfarb, & Gold, 1981; Stockard & Rossiter, 1977; Stockard & Sharbrough,
1980; Tackmann & Ettlin, 1982; Tackman, Strenge, Barth, & Sojka-Raytsche , 1980), and 46% of 1000
patients with MS had abnormal BAEPs (Table 9.2). Among patients without brainstem symptoms or signs,
38% had clinically silent BAEP abnormalities.
Table 9.2. Rates of Abnormalities for Evoked Potentials in Multiple Sclerosis: Aggregate Results of 26 to 31 Separate Research
Series
VEP BAEP SEP
No. of patients 1950 1006 1006
No. of research series 26 26 31
Rates of EP abnormality
Definite MS 85% 67% 77%
Probable MS 58% 41% 67%
Possible MS 37% 30% 49%
Asymptomatic patients 51% 38% 42%
All patients 63% 46% 58% (upper extremity)
76% (lower extremity)
Source: From Chiappa, K. H. (1990). Evoked potentials in clinical medicine. (2nd ed.). New York: Raven Press.
BAEP, brainstem auditory evoked potential; EP, evoked potential; MS, multiple sclerosis; SEP, somatosensory evoked potential;
VEP, visual evoked potential.
p. 146 Brainstem auditory evoked potentials were more sensitive for intrinsic pontine lesions than rst
generation MRI (Baum, Scheuler, Hegerl, Girke, & Schörner, 1988; Comi et al., 1987, 1989; Cutler, Amino ,
& Brant-Zawadzki, 1986. Recent MRIs perform better. The advantage of brain MRIs is in nding lesions in
many places, whereas BAEP is speci c to a limited part of the brainstem. Among studies directly comparing
the two tests, brain MRI was abnormal among 68% to 83% of patients, whereas BAEP was abnormal among
41% to 50% (Comi et al., 1989; Filippini et al., 1994; Giesser et al., 1987; Gilmore, Kasarskis, Carr, & Norvell,
1989).
A new evoked potential technique for the brainstem assesses the vestibular system. These record the
electromyographic (EMG) responses to click auditory stimulation similar to the BAEP. Recordings are made
from the sternocleidomastoid (cervical vestibular re ex) and orbicularis oculi (oculo-vestibular re ex).
Both re exes are prolonged in patients with MS (Gabelić et al., 2013; Gazioglu & Boz, 2012;Rosengren &
Colebatch, 2011). The oculo-vestibular re ex was abnormal in 69% of patients with MS and correlated with
internuclear ophthalmoplegia signs (Rosengren & Colebatch, 2011).
Overall, BAEP can con rm that cranial nerve signs or symptoms are due to central brainstem impairment,
as opposed to impairment along the peripheral pathways. The test is sensitive to pons and lower midbrain
impairment.
Somatosensory Evoked Potentials
Somatosensory testing begins with a brief electrical stimulus to the median nerve at the wrist or posterior
tibial nerve at the ankle. Recordings are made using electrodes over the brachial plexus or lumbar spine,
cervical spine, and scalp. The somatosensory evoked potentials (SEP) travel along the posterior columns,
medial lemniscus, and internal capsule.
Median nerve SEP peaks are generated at brachial plexus, mid-cervical cord, cervicomedullary junction,
upper midbrain or thalamus, and Rolandic ssure (Figure 9.4). The main potentials of posterior tibial nerve
SEPs are from lumbar spinal cord and Rolandic ssure. Comparison among these peaks reveals the
anatomical level of lemniscal pathway disruption. This is useful when approximate anatomical localization
is valuable.
Figure 9.4:
Examples of the peaks seen in normal short latency. (A) median nerve and (B) posterior tibial nerve, somatosensory evoked
potential testing. Negative potentials are upward deflections here. Recording sites EPi and EPc are at shoulders; C5Sp and T12
over the spine; PF, K, and IC at popliteal fossa, knee, and iliac crest; Ci, Cc, C′z, and Fz on scalp. The several standard peaks are
identified here.
From Nuwer, M. R., Amino , M., Desmedt, J., Eisen, A. A., Goodin, D., Matsuoka, S., … Vibert, F. F. (1994a). IFCN recommended
standards for short latency somatosensory evoked potentials. Electroencephalography and Clinical Neurophysiology, 91, 6–
11. 10.1016/0013-4694(94)90012-4
In Chiappa’s (1990) summary of results among clinical studies in MS (Abbruzzese et al., 1980; Anziska,
Cracco, Cook, & Feld, 1978; Chiappa, 1980; Chiappa et al., 1980b; Dau, Petajan, Johnson, Panitch, &
Borenstein, 1980; Diener & Scheibler, 1980; Dorfman, Bosley, & Cummins, 1978; Eisen & Nudleman, 1979;
Eisen & Odusote, 1980; Eisen, Paty, Purves, & Hoirich, 1981; Eisen, Purves, & Hoirich, 1982; Eisen, Stewart,
Nudleman, & Cosgrove, 1979; Ganes, 1980; Green et al., 1980; Hausler & Levine, 1980; Kazis, Vlaikidis,
Xafenias, Papanastasiou, & Pappa, 1982; Kjaer, 1980a, 1980b; Larrea & Mauguiere, 1988; Mastaglia, Black,
Edis, & Collins, 1978; Matthews & Esiri, 1979; Matthews & Small, 1979; Namerow, 1968, 1970; Noel &
Desmedt, 1980; Purves et al., 1981; Small, Matthews, & Small, 1978; Stockard & Sharbrough, 1980;
Tackmann et al., 1980; Trojaborg & Petersen, 1979; Trojaborg, Bottcher, & Saxtrup, 1981; van Buggenhout,
Ketelaer, & Carton, 1982;Walsh, Garrick, Cameron, & McLeod, 1982; Weiner & Dawson, 1980, median nerve
SEP was abnormal in 42% of patients with MS without sensory signs or symptoms; and abnormal in 75% of
patients who did have sensory signs or symptoms. Posterior tibial SEPs had somewhat higher rates of
clinically silent abnormalities (Table 9.2). Delays in SEP correlated with the expanded disability status scale
(EDSS) ndings (Koehler, Faldum, & Hopf, 2000). Abnormalities in SEP parallel clinical measures of limb
impairment in patients with MS (Nociti et al., 2008).
Various neurological disorders can a ect SEPs. Peripheral e ects can be identi ed by measuring central
conduction separately from peripheral conduction, which is checked at the brachial plexus or lumbar spinal
cord. Some hereditary–degenerative neurological conditions can impair central sensory conduction (Nuwer
et al., 1983); so can B12 de ciency (Fine & Hallet, 1980; Misra, Kalita, & Das, 2003). Focal ischemia, tumors,
and cervical myelopathy can disrupt central lemniscal conduction. Central delay of SEP is not speci c to MS
(Cruccu et al., 2008).
Brain MRI tests a much wider area of brain and spinal anatomy, so that the MRI is more sensitive than either
median or posterior tibial nerve SEP in MS. In two direct comparisons, 48% to 54% of patients with early
MS had an abnormal median nerve SEP, and 61% to 72% had abnormal posterior tibial nerve SEPs, whereas
brain MRI more often had abnormalities among the same patients (Comi et al., 1989; Gilmore et al., 1989).
In a series of patients with spinal cord symptoms being evaluated for MS, 67% (31/46) had an abnormal
cervical MRI, whereas 57% (26/46) had abnormal SEPs (Miller et al., 1987).
p. 147 The American Academy of Neurology evidence-based assessment of SEPs recommends the technique as
possibly useful to identify patients at increased risk for developing clinically de nite MS (Gronseth &
Ashman, 2000).
Overall, SEPs are a useful tool for detecting clinically silent lesions, and they can contribute to the diagnosis
of MS. They provide a sensitive way to assess the lemniscal spinal and intracranial pathways.
Motor Evoked Potentials
p. 148 Cerebral neurons can be discharged by a brief electrical stimulus. This can be delivered through the intact
skull. Considerable voltage is needed to drive transcranial electrical currents from the scalp through the
skull to the cortex. In awake patients such electrical stimulation is painful.
An ingenious painless solution is to use a powerful magnetic device held above the scalp. Each stimulus is a
brief, extremely intense magnetic eld. The skull is a resistor for electrical currents, but magnetic elds
pass unimpeded through the intact skull. Faraday’s law of electromagnetic induction describes that such an
abrupt change in a magnetic eld creates an electrical potential. The brief intense magnetic eld above the
scalp evokes an electric current in the cerebral cortex strong enough to discharge neurons (Barker,
Freeston, Jalinous, & Jarratt, 1986; Barker, Jalinous, & Freeston, 1985). This can be focused in a particular
small region under the magnetic stimulator. The speci c cortical region stimulated is chosen by locating the
magnetic coil over the corresponding scalp.
Clinicians studying motor pathways now use magnetically stimulated motor evoked potentials (MEPs).
These have been evaluated in MS and other neurological disorders (Merton & Morton, 1980; Merton,
Morton, Hill, & Marsden, 1982). Motor evoked potentials are sensitive to corticospinal impairment early in
the course of MS (Rico et al., 2009). Markedly prolonged central motor conduction times are seen in most
tested patients with MS (Cowan et al., 1984; Cruz-Martinez, González- Orodea, López Pajares, & Arpa,
2000; Dan, Christiaens, Christophe, & Dachy, 2000; Di Lazzaro, Oliviero, & Pro ce, 1999; Firmin, Müller, &
Rösler, 2012; Hess, Mills, & Murray, 1986; Hess et al., 1987; Ingram, Thompson, & Swash, 1988; Jones,
Streletz, Raab, Knobler, & Lublin, 1991; Mayr, Baumgartner, Zeitlhofer, & Deecke, 1991; Mills & Murray,
1985; Ravnborg, Liguori, Christiansen, Larsson, & Sørenson, 1992; Segura, Garcea, & Gandolfo, 1994). In
MS, lower-extremity MEPs are abnormal more often than upper-extremity MEPs. Exercise increases the
abnormality rate (Nielsen & Norgaard, 2002; Perretti et al., 2004). Motor EPs are well suited for identifying
silent lesions in patients with MS. They are an objective measure for MS therapeutic trials (Andersson,
Siden, & Persson, 1995; Kandler et al., 1991a, 1991b). Motor EP correlates well with MRI lesions in cervical
corticospinal tracks (Cruz-Martinez et al., 2000). Delayed MEP conduction does correlate well with the
Expanded Disability Status Scale (Kale, Agaoglu, Onder, & Tanik, 2009). They correspond less well with
speci c physical signs of weakness per se (Humm, Magistris, Tru ert, Hess, & Rosler, 2003; Segura et al.,
1994).
Ongoing muscle activity is disrupted by some MEPs. The duration of this disruption is known as the silent
period. Ongoing investigations suggest that this is dependent on spinocerebellar pathways. A prolonged
silent period may be a sign of cerebellar involvement in patients with MS (Tataroglu, Genc, Idiman, Cakmur,
& Idiman, 2003). Other MEP techniques evaluate fatigue using repetitive stimulation (Brasil-Neto, Cohen, &
Hallett, 1994; Liepert, Kotterba, Tegentho , & Malin, 1996; Petajan & White, 2000; Schubert, Wohlfahrt,
Rollnik, & Dengler, 1998). Some relationships are seen between MS symptoms and MEP ndings (Fuhr &
Kappos, 2001).
Central motor conduction tests also can be abnormal in other neurological disorders. Slowed MEPs were
found in 85% of patients with amyotrophic lateral sclerosis (Berardelli, Inghilleri, Formisano, Accornero, &
Manfredi, 1987; Hugon et al., 1987), whereas their SEPs were normal. Patients with hereditary motor and
p. 149 sensory neuropathy patients had delayed central conduction when they had clinical signs of corticospinal
disease (Claus, Waddy, Harding, Murray, & Thomas, 1990).
Event-Related Potentials
Cognitive processes can be measured by special EPs known as event-related potentials (ERPs). These mark
certain internal recognition events and decision-making processes. P300, the most common ERP, uses the
auditory oddball paradigm (Goodin et al., 1994). A series of brief tones is presented, most at one pitch
intermixed with occasional (rare) tones at a di erent pitch. The patient is asked to count silently the rare
tones. An extra positive polarity potential occurs around 300 ms after each rare tone (Figure 9.5). That peak,
measured over the scalp vertex, is referred to as the P300. It corresponds to the brain recognizing the rare
tone, “Oh, that’s it! Count it!”
Figure 9.5:
P300 event-related potential test recorded from the scalp vertex. A: Stimulation with the frequently presented 1000 Hz
tones. Primary auditory peaks are present. B: Stimulation with the rare 2000 Hz tones. Primary auditory peaks N1 and P2 are
present plus the P300 peak seen here at 365 ms.
The P300 ERP peak latency is delayed in dementia but not in depression. In MS patients, P300 often is
delayed (Amino & Goodin, 2001), as are earlier primary auditory cortical peaks. The results may be a
combination of primary sensory system and cognitive processing speed delays. P300 delay in MS is worse
among patients with secondary progressive MS (Ellger et al., 2002). Visual P300 also is often abnormal
(Sailer et al., 2001). Serial ERP studies in MS measured progression of the P300 cognitive processing delays
over time (Gerschlager et al., 2000), and in children and adolescents with MS (Lori et al., 2011).
Multimodality Evoked Potential Testing
It is worthwhile to compare EP modalities with each other, and to compare EPs with MRI and cerebrospinal
uid (CSF) ndings. Chiappa (1990) summarized results from several thousand patients among 26 to 31
published reports of VEP, BAEP, and SEP in patients with MS (Abbruzzese et al., 1980; Anziska et al., 1978;
Asselman et al., 1975; Barajas, 1982; Cant et al., 1978; Celesia & Daly, 1977; Chiappa, 1980; Chiappa et al.,
1980a, 1980b; Collins et al., 1978; Dau et al., 1980; Diener & Scheibler, 1980; Dorfman et al., 1978; Duwaer &
Spekreijse, 1978; Eisen & Nudleman, 1979; Eisen & Odusote, 1980; Eisen et al., 1979, 1981, 1982; Elidan et al.,
1982; Fischer et al., 1981; Ganes, 1980; Green et al., 1980, 1982; Halliday et al., 1973a, 1973b; Hausler &
Levine, 1980; Hennerici et al., 1977; Hume & Cant, 1976; Hutchinson et al., 1984; Kayamori et al., 1984; Kazis
et al., 1982; Khoshbin & Hallett, 1981; Kjaer, 1980a, 1980b; Ko er et al., 1984; Lacquanti et al., 1979; Larrea
& Mauguiere, 1988; Lowitzsch et al., 1976; Mastaglia et al., 1976, 1978; Matthews & Esiri, 1979; Matthews &
Small, 1979; Matthews et al., 1977; Mogensen & Kristensen, 1979; Namerow, 1968, 1970; Nilsson, 1978; Noel
& Desmedt, 1980; Parving et al., 1981; Prasher et al., 1982; Purves et al., 1981; Rigolet et al., 1979; Robinson &
Rudge, 1977a, 1977b, 1980; Shahrokhi et al., 1978; Shanon et al., 1981; Small et al., 1978; Stockard & Rossiter,
1977; Stockard & Sharbrough, 1980; Tackmann & Ettlin, 1982; Tackmann et al., 1979, 1980; Trojaborg &
Petersen, 1979; Trojaborg et al., 1981; van Buggenhout et al., 1982; Walsh et al., 1982; Weiner & Dawson,
1980; Wilson & Keyser, 1980; Wist et al., 1978 (see Table 9.2). Visual evoked potentials had the most
abnormalities and BAEPs the fewest. Abnormality rates of SEPs were similar to VEPs, even higher in the
possible and probable MS categories. Lower extremity SEPs were abnormal more often than median nerve
SEPs. Silent lesions, that is, SEP abnormalities, despite no signs or symptoms in that sensory modality, are
seen in one-third to one-half of patients with MS.
Among patients with a more severe degree of MS, SEPs are most likely to be abnormal compared with VEP or
BAEP. In one study (Nuwer et al., 1987) of chronic progressive MS, median nerve SEPs were abnormal in
93%, VEPs in 75%, and BAEPs in 48% of patients (Table 9.3). Similar results have been reported in children
with MS (Brass et al., 2003; Pohl et al., 2006).
Table 9.3. Evoked Potential Findings Among 101 Patients with Chronic Progressive Multiple Sclerosis (Le and Right Sides
Scored Separately)
Pattern Visual EPs
Median P100 latency 119 ms (normal <105)
Number normal 50/202 (25%)
Present but abnormal 132/202 (65%)
Absent 20/202 (10%)
Median P100 amplitude 4.0 microV
Brainstem Auditory EPs
Median I–V interpeak latency 4.4 ms (normal <4.6)
Median V/I amplitude ratio 64% (normal >50%)
Wave V present but abnormal 24/202 (12%)
Wave V absent 63/202 (32%)
All peaks absent 2/202 (1%)
Median Nerve Somatosensory EPs
Number N9 absent 0/202
N13 absent 70/202 (35%)
N20 absent 115/202 (57%)
N20 latency 26 msec
N20 amplitude 0.8 microV
Source: From Nuwer, M. R., Packwood, J. W., Myers, L. W., & Ellison, G. W. (1987). Evoked potentials predict the clinical changes in
multiple sclerosis drug study. Neurology, 37, 1754–1761. 10.1212/WNL.37.11.1754
Note: Small adjustments to normal limits for individual patients were made for age, gender, and height (details not shown here).
Absent peaks were excluded from median latency determination here. Somatosensory normal limits were N20-N9 <10.5 ms,
N20-N13 <7.0 ms plus N13-N9 <4.3 ms; absolute latencies of N20 were not used when assessing normality.
p. 150 Comparing MEPs with sensory EPs, lower extremity SEPs were abnormal most often (75%), followed by
lower-extremity MEPs (65%), VEPs (64%), upper-extremity MEPs, and SEPs (56% and 52%), and nally
BAEPs (39%) (Filippi et al., 1995). In another study of early relapsing-remittting MS (Jung, Beyerle, &
Ziemann, 2008), the lower-extremity MEPs were most sensitive (68%), followed by VEP (62%) and then
lower-extremity SEPs (57%).
Patients with chronic progressive MS had the highest rate and greatest degrees of EP abnormalities. Other
reports noted worse MEPs among secondary progressive than relapsing-remitting MS (Facchetti et al.,
1997), and that MEPs were abnormal more often than SEPs (Andersson et al., 1995).
How useful are EPs for patients being evaluated for a diagnosis of MS? Abnormal EPs are found commonly
among patients who eventually are found to have a diagnosis of MS, and usually are normal among patients
who do not have MS. Multimodal EPs were abnormal in 90% to 92% of patients who eventually were
diagnosed with MS (Gajofatto et al., 2010; Hume & Waxman, 1988). Among speci c EP modalities and MRI
among patients who eventually were diagnosed with MS (Ravnborg et al., 1992), the MRI was positive in
88%; MEP, 83%; VEP, 67%; SEP, 63%; and BAEP, 42%. Evoked potentials do not distinguish among types of
demyelinating disorders such as between NMO and MS. Abnormal EPs were occasionally seen in other
disorders, so they are pathognomonic for MS only for asymmetrical VEP delays (De Seze et al., 2001).
Patients with possible MS had a 71% chance of clinical progression over 2 to 3 years if they had abnormal
EPs, but only a 16% chance if their EPs were normal (Hume and Waxman, 1988). The presence and degree of
EP abnormalities at rst presentation predicted EDSS at 3 to 14 years later: The worse the initial EPs, the
worse the disability years later (Fuhr, Borggrefe-Chappuis, Schindler, & Kappos, 2001; Invernizzi et al.,
2011; Jung et al., 2008; Kallmann et al., 2006; Leocani et al., 2006; Margaritella et al., 2012; Pelayo et al.,
2010; Schlaeger et al., 2012a, 2012b, 2014).
Magnetic resonance imaging is considered more reliable than CSF or EPs for predicting a future diagnosis of
MS (Polman et al., 2005), yet EPs do provide helpful information (Filippini et al., 1994; Ghezzi, Torri, &
Za aroni, 1996; Ghezzi et al., 1999, 2000). When compared directly, both were abnormal in at least 70%
patients with de nite or probable MS (Baum et al., 1988; Comi et al., 1987, 1989; Cutler et al., 1986; Farlow
et al., 1986; Giesser et al., 1987; Gilmore et al., 1989; Guerit & Argile, 1988; Hume & Waxman, 1988;
Rodriguez et al., 1995. Brainstem auditory evoked potentials were more sensitive than MRI for detecting
pontine lesions (Baum et al., 1988; Cutler et al., 1986). Visual evoked potentials are better than MRI at
detecting optic nerve lesions. Magnetic resonance imaging shows a multiplicity of lesions or classical MS
p. 151 distribution of lesions more e ectively than multimodal EPs (Cutler et al., 1986; Farlow et al., 1986).
Magnetic resonance imaging and sensory EPs were similarly e ective in predicting an MS diagnosis, its
course, and severity (Guerit & Argile, 1988; Hume & Waxman, 1988; Lee et al., 1991; O’Connor, Marchetti,
Lee, & Perera, 1998). An abnormal VEP makes eventual diagnosis of MS signi cantly more likely among
patients with a radiologically isolated syndrome (Lebrun et al., 2009). Magnetic resonance imaging and
MEP taken together were more e ective at predicting disability than either alone (Kalkers et al., 2007).
Multimodal EPs were more useful to assess disease progression, because EP abnormalities are more strictly
related to disability than MRI lesion burden (Leocani & Comi, 2008). Evoked potentials were considered
useful to identify therapeutic nonresponders, to assess patients with ambiguous new symptoms, to con rm
a dubious relapse, and to measure disease progression.
Compared with oligoclonal banding and other CSF abnormalities, multimodal sensory EPs were slightly
more likely to be abnormal in early or possible MS (Bartel, Markand, & Kolar, 1983; Cosi et al., 1987; Ganes,
Brautaset, Nyberg-Hansen, & Vandvik, 1986; Hume & Waxman, 1988; Irkec, Nazhel, & Kocer, 2001; Lee et
al., 1991; Miller, Burke, & Bever, 1983; Trojaborg et al., 1981). Evoked potential abnormality is more accurate
for predicting MS progression than are CSF changes. Patients with normal results on both EP and CSF
studies are most likely to remain stable over time.
In a formal technology assessment, the American Academy of Neurology (AAN) looked at EPs in MS
(Gronseth & Ashman, 2000). They used a structured literature review to assess the usefulness of EPs to
identify clinically silent lesions in patients with suspected MS. The reports recommend using VEPs and SEPs
to search for clinically silent lesions. Visual evoked potentials were scored as probably useful and SEPs as
possibly useful in predicting progression from initial evaluation to clinically de nite MS within a few years.
For BAEPs, there is a trend toward usefulness to search for silent lesions, but the magnitude of an e ect is
less than for VEPs and SEPs. The reports note that there are other reasons for using EPs in MS beyond just
searching for silent lesions. They may aid in localizing lesions, con rm clinically ambiguous lesions or the
organic basis of symptoms, and suggest demyelination as the cause of a suspicious lesion.
In these days of limited health care resources, it is appropriate to compare resource utilization. The United
States Medicare Professional Fee Schedule allows 11.09 relative value units (RVUs) for brain, 11.10 for
cervical, 11.11 for thoracic, and 11.07 for lumbar MRIs with and without contrast. Each sensory EP test
(visual, auditory, and upper and lower somatosensory EPs) averages only 4.22 RVUs, far less than the
expense of MRI testing.
Overall, the di erent tests are complementary to each other, with MRI assessing anatomy and EPs assessing
physiology (Cruccu et al., 2008). Evoked potentials, MRI, and CSF studies have their own niches in the
diagnostic evaluation paradigms.
Use of Evoked Potentials in Multiple Sclerosis Therapeutic Trials
Evoked potentials are useful as measuring tools in MS therapeutic trials (Nuwer et al., 1987). Evoked
potential testing is easily repeated at modest costs. Grouped EP data track accumulated disease burden
(Brigell, Kaufman, Bobak, & Beydoun, 1994; Hennerici et al., 1977; Nuwer et al., 1987). Evoked potentials
tend to worsen progressively in MS. They can detect the physiological remnants of previous demyelination
that may have become inapparent on MRIs. The gradual progression of EPs provides an objective, quanti ed
measure that parallels progression in EDSS (Guerit & Argile, 1988; Hume & Waxman, 1988; Koehler et al.,
2000; Lee et al., 1991; Leocani & Comi 2008; Niklas, Sebraoui, Hess, Wagner, & Then Bergh, 2009; O’Connor
et al., 1998). Because the EPs detect clinically silent lesions, they are not redundant with any signs or
symptoms detectable by physical examination or history.
In therapeutic trials EPs ought to be scored in terms of the actual latency values. Test–retest di erences
ought to be measured by direct, careful comparison of EP traces themselves, not by completely separate
scoring of the individual traces. This substantially reduces the trial-to-trial interpretation variability
(Nuwer et al., 1987; Thomae et al., 2010). Year-to-year comparisons can be carried out using parametric
statistics. This is far superior to the better/worse/unchanged, changed/unchanged, or normal/abnormal
scoring that is used in some MS trials.
Evoked potentials reliably can measure and predict courses in groups in MS patients (Fuhr et al., 2001). They
were valuable in several therapeutic trials. In a trial of azathioprine and steroids, VEP and SEP predicted the
p. 152 3-year study outcome at year one (Nuwer et al., 1987). In a trial of azathioprine, antilymphocite globulin,
and steroid (Mertin et al., 1982), VEPs deteriorated in the control group but were stable in the
immunosuppressed group. Visual evoked potentials reliably tracked clinical progress in interferon studies
(Anlar, Kisli, & Tombul, 2003; Sipe et al., 1984; Weinstock-Guttman, Baier, & Stockton, 2003). Similar
improvements were seen for MEPs in a steroid and cyclophosphamide study (Manova, Kostadinova,
Chalakova-Atanasova, Temenlieva, & Petrova, 2001), where it paralleled the EDSS. Visual evoked potentials
and SEP were improved or stable during Natalizumab treatment but not during a pretreatment baseline year
(Meuth, Bittner, Seiler, Göbel, & Wiendl, 2011). Steroid therapy showed P300 (Filipovic, Drulovic,
Stojsavljevic, & Levic, 1997) and MEP (Fierro et al., 2002) improvement, and multimodality EPs correlated
with clinical disability scores (La Mantia et al., 1994). Evoked potentials paralleled clinical ndings for
plasmapheresis (Dau et al., 1980; Gordon et al., 1985; Khatri, McQuillen, Harrington, Schmoll, & Ho mann,
1985; Sorensen et al., 1996; Weiner & Dawson, 1980).
Other studies found change neither in clinical scores nor in EPs. Those drugs may be ine ective in MS, for
example, hyperbaric oxygen (Harpur et al., 1986; Neiman, Nilsson, Barr, & Perkins, 1985) and acyclovir
(Lycke et al., 1996).
Overall, EPs are cost-e ective tools that can add easily measured and quanti ed statistical signi cance to
the results of an MS therapeutic trial.
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Primer on Multiple Sclerosis (2 edn)

Barbara S. Giesser (ed.)

https://doi.org/10.1093/med/9780199341016.003.0009 Pages 141–162

Visual Evoked Potentials

Several useful MS VEP facts are notable:

Correlation with Abnormality

0.12 Hearing impairment

0.03 Facial sensory impairment

0.39 Ocular dysmetria or gaze paresis

0.29 Facial weakness

0.23 Facial sensory loss

0.21 Slow tongue movements

0.09 Other brainstem signs

0.04 Subjective hearing threshold

BAEP, brainstem auditory evoked potential.

VEP BAEP SEP

No. of patients 1950 1006 1006

No. of research series 26 26 31

Definite MS 85% 67% 77%

Probable MS 58% 41% 67%

Possible MS 37% 30% 49%

Asymptomatic patients 51% 38% 42%

All patients 63% 46% 58% (upper extremity)

76% (lower extremity)

Somatosensory Evoked Potentials

Motor Evoked Potentials

Pattern Visual EPs

Median P100 latency 119 ms (normal <105)

Number normal 50/202 (25%)

Absent 20/202 (10%)

Median P100 amplitude 4.0 microV

Brainstem Auditory EPs

Median I–V interpeak latency 4.4 ms (normal <4.6)

Median V/I amplitude ratio 64% (normal >50%)

Number normal 105/202 (52%)

Wave V present but abnormal 24/202 (12%)

Wave V absent 63/202 (32%)

All peaks absent 2/202 (1%)

Median Nerve Somatosensory EPs

Number normal 15/202 (7%)

Number N9 absent 0/202

N13 absent 70/202 (35%)

N20 absent 115/202 (57%)

N20 latency 26 msec

N20 amplitude 0.8 microV

Use of Evoked Potentials in Multiple Sclerosis Therapeutic Trials

Nuwer, M. R. (2008). Intraoperative monitoring of neural function. Amsterdam: Elsevier.

© Oxford University Press

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