eMedicine Specialties > Neurology > Electroencephalography and Evoked Potentials

Clinical Utility of Evoked Potentials

Author: Leslie Huszar, MD, Consulting Staff, Department of Neurology, Indian River Memorial Hospital
Contributor Information and Disclosures

Updated: Apr 18, 2006

Introduction

Evoked responses measure the electrophysiological responses of the nervous system to a variety of stimuli. Almost any sensory modality can be tested in theory; in clinical practice, however, only a few are used on a routine basis. The ones most often encountered are the visual evoked responses (VEP, both flash and checkerboard types), short-latency somatosensory evoked responses (SSEP), and short-latency brainstem auditory evoked responses (BAER, BAEP). Late-evoked responses are used for studying higher cortical functions, such as P300 in Alzheimer disease. The clinical usefulness of the late-evoked responses is limited by the experimental paradigm and they are not used routinely or widely in general clinical neurology. Nevertheless, the late responses show promise and may gain more inroads in clinical use in the near future. Some centers have developed testing paradigms for olfactory and taste-evoked responses as well.

The clinical use of evoked potentials (EPs) has changed over time. Progressive advances in imaging technology have limited the frequency of evoked-response studies in clinical practice. Current use of MRI technology is mostly responsible for this. The basic difference that persists is that the MRI largely remains an imaging, structural, or anatomical test, while the EP explains the functionality of certain pathways of the nervous system. The MRI scan gives more accurate information about structural problems, while the EP gives us information about the physiology of a certain anatomical pathway with much less spatial or localizing information. Under given circumstances they may be complementary. However, most clinical questions are answered better by MRI of the pertinent neurological structures. Recently, SSEP has shown promise in predicting outcome in postanoxic coma.

Types of EPs in every day clinical use include (1) VEP, usually pattern-shift checkerboard visual evoked responses, (2) SSEP, short latency, somatosensory evoked responses, and (3) BAEP, short latency brain stem evoked responses.

Visual Evoked Potential

The VEP tests the function of the visual pathway from the retina to the occipital cortex. It measures the conduction of the visual pathways from the optic nerve, optic chiasm, and optic radiations to the occipital cortex. (The author has assumed that the reader is familiar with the anatomy of the optic system.) The most important fact to consider is that, although the axons from the nasal half of the retina decussate at the optic chiasm, the temporal axons do not. Therefore, retrochiasmatic lesions may not be detected by full-field checkerboard stimulation. VEPs are most useful in testing optic nerve function and less useful in postchiasmatic disorders. In retrochiasmatic lesions, the MRI is a more useful test. Partial-field studies may be useful in retrochiasmatic lesions; however, they are not performed routinely in clinical settings. Also note that the macula projects to the occipital pole, while the rest of the retina projects to the mesial calcarine cortex.

The VEP is very useful in detecting an anterior visual conduction disturbance. However, it is not specific with regard to etiology. A tumor compressing the optic nerve, an ischemic disturbance, or a demyelinating disease may cause delay in the P100; only additional clinical history and, often, MRI are needed to uncover the etiology. The usual waveform is the initial negative peak (N1 or N75), followed by a large positive peak (P1 or P100), followed by another negative peak (N2 or N145). Maximum value for P100 is 115 milliseconds (ms) in patients younger than 60 years; it rises to 120 ms thereafter in females and 125 ms in males. Even though published norms are available in the medical literature, each individual laboratory should have its own norms to control for lab-to-lab variability in technique.

The W morphology, in the author's experience, is most often an individual variation, although decreasing the stimulation frequency from the ubiquitous 2 Hz to 1 Hz usually converts the W shape into a conventional P100 peak. Check size and alternation rate are factors in this; the responses can be manipulated to a W or a conventional P100 response by changing these parameters. Large checks tend to produce VEPs similar to those produced by flash stimulation.

Factors influencing VEP

The usual VEPs are evoked by checkerboard stimulation and, because cells of the visual cortex are maximally sensitive to movement at the edges, a pattern-shift method is used with a frequency of 1-2 Hz. The size of the checks affects the amplitude of the waveform and the latency of the P100. In addition, pupillary size, gender, and age all affect the VEP. Visual acuity deterioration up to 20/200 does not alter the response significantly; large checks may be required. In some studies, women have slightly shorter P100 latencies. Sedation and anesthesia abolish the VEP. Some subjects, by "fixating" beyond the plane of stimulation, may alter or suppress P100 altogether.

Certain drugs, such as carbamazepine, prolong VEPs. The effects of carbamazepine and sodium valproate monotherapy on VEPs were studied in 18 epileptic children by Yuksel et al. Pattern-reversal VEPs were determined before administration of the antiepileptic drugs and after 1 year of therapy. The VEP amplitude showed no consistent changes after 1 year of therapy, but VEP P100 latencies were significantly prolonged after 1 year of carbamazepine therapy. The conclusion was that carbamazepine slows down central impulse conduction.

According to Trip et al, atrophy of the optic nerve was correlated with decreased VEP amplitude (Trip, 2006).

Technical aspects

Checkerboard pattern (or less often, flash) is used as stimulation. Responses are collected over Oz, O1, and O2 and with hemifield studies at T5 and T6 electrodes using the standard EEG electrode placement. Monocular stimulation is used to avoid masking of a unilateral conduction abnormality. Sedation should not be used, and note should be taken of medications that the patient is taking regularly. Testing circumstances should be standardized, including seating distance of 70-100 cm from the monitor screen, giving a check size of approximately 30 seconds of visual angle. The vision should be corrected to the extent possible in case of a visual problem. Pupil size and any abnormality should be noted. The P100 waveform is at its maximum in the midoccipital area. Stimulus rates of 1-2 Hz are recommended, and filter setting should be 1- to 200-Hz bandwidth (outside limit is 0.2-300 Hz).

The recommended recording time window (ie, sweep length) is 250 ms; 50-200 responses are to be averaged. A minimum of 2 trials should be given. The responses are averaged and the P100 positive polarity waveform that appears in the posterior head region is analyzed. The mean latency is about 100 ms. Normative data should be assembled on a lab-by-lab basis.

Pitfalls

Check size of 27 seconds of visual angle may result in normal P100 latency in a patient with cortical blindness; smaller checks (ie, 20 seconds of visual angle or less) should be used to demonstrate the abnormality. If cortical blindness is suspected, large checks should not be used.

In conditions such as retinal disease or refractory errors, the amplitude may be smaller and, at very small check sizes, the latency may increase. For this reason proper refraction is of great importance.

Since the VEP measures the pathway from the retina to area 17, a normal P100 does not exclude lesions of the visual pathway beyond area 17. For this reason, the VEP may be normal in patients with the diagnosis of cortical blindness. Note that, in such cases, the VEP is useful, ruling out disease up until area 17 in patients with a normal response. The usefulness of VEP is limited in malingering and hysterical visual loss. It is useful when a normal VEP is recorded, but abnormal responses are of limited diagnostic value in such cases. Baumgartner et al reported that as many as 5 of 15 healthy subjects were able to suppress their pattern VEPs.

Effects of physiological changes of serum glucose level

Sannita et al evaluated the correlation between amplitude and latencies of the pattern-reversal VEP and serum glucose level in healthy volunteers. Pattern VEP and serum glucose levels were obtained at 2-hour intervals during an 8-hour experimental session. At serum glucose concentrations within the physiological range of variability (55-103 mg/dL), the P100 latency increased with increasing serum glucose level, with a 6.9% estimated latency difference between lower and higher glucose concentrations.

VEP generator site

The generator site is believed to be the peristriate and striate occipital cortex. Prolongation of P100 latency is the most common abnormality and usually represents an optic nerve dysfunction. VEP is clearly more sensitive than physical examination in detecting optic neuritis. Ikeda et al studied generators of VEP by dipole tracing in the human occipital cortex. Current source generators (dipoles) of human VEP to pattern-onset stimuli were investigated. A visual stimulus, a checkerboard pattern, was presented for 250 ms in each of the 8 quadrants. Central and peripheral parts of each of the 4 quadrant fields were evaluated. The VEPs, consisting of initial positive-late negative waves, were recorded mainly on the occipital region contralateral to stimulated visual fields. The initial positive waves of VEP were divided into 2 components: (1) early component with approximate peak latency of 70-90 ms and (2) late component with approximate peak latency of 100-120 ms.

The results from these analyses of VEP indicated topographic localization of the dipoles around the calcarine fissure. This was comparable to the retinotopy of the human occipital lobe based on clinicopathologic studies. In order to examine the feasibility of multicenter studies, Brigell et al described the pattern VEP using standardized techniques. They concluded that the peak latency of pattern-reversal VEP is a sensitive measure of conduction delay in the optic nerve caused by demyelination. To establish whether pattern-reversal VEP could be standardized adequately for use as a measure in multicenter therapeutic trials for optic neuropathy or multiple sclerosis (MS), stimulus and recording variables were equated at 4 centers; pattern-reversal VEPs were recorded from 64 healthy subjects and 15 patients with resolved optic neuritis.

The results showed equivalent latency and amplitude data from all centers, indicating that the VEP test can be standardized satisfactorily for multicenter clinical trials. Further, the authors concluded that the N70 and P100 peak latencies and N70-P100 interocular amplitude difference were sensitive measures of resolved optic neuritis.

Abboud et al studied left-right asymmetry of VEPs in brain-damaged patients. The left-right asymmetry in the potential amplitude on the scalp was studied in patients after stroke by using flash VEP. The VEP amplitude was smaller over the ischemic hemisphere than over the intact hemisphere. This finding indicates that the left-right asymmetry in scalp VEPs of patients after brain damage may be a result of changes in the conductivity of the volume conductor, due to the ischemic region between the source and the electrodes.

Interhemispheric transfer of visual information

Ipata et al assessed interhemispheric visual transfer of information in humans. Estimates of interhemispheric transfer time ranged between 5.77 and 12.54 ms, depending upon the type of component and the location of the electrode sites. More anterior locations yielded shorter values and overall transfer time tended to be 7 ms shorter for the N70 component than for the P100 component.

Optic neuritis

The VEP characteristically shows an increase in P100 latency of the involved side. The use of steroids in this condition has been controversial. Trauzettel-Klosinski et al observed the effect of oral prednisone on VEP latencies in acute optic neuritis. Forty-eight patients with acute optic neuritis were treated orally either with methylprednisolone (100 mg/day initially, dosage reduction every 3 days; n=15) or with thiamine (100 mg/day; n=33) in the control group, 36 of them in a double-blind procedure. Oral methylprednisolone resulted in a faster improvement in VEP latency in the initial phase but had no benefit after 12 weeks or 12 months.

Elvin et al used Doppler ultrasonography, MRI, and VEP measurements to study abnormal optic nerve function. VEP assessments were performed in 16 patients. Patients with impairment of visual acuity and a prolonged VEP initially had a more swollen nerve and increased flow resistance in the affected optic nerve. Statistically significant side-to-side differences were found in the optic nerve diameter and in the resistance to flow in the central retinal artery between the affected and unaffected eyes.

Optic neuritis versus ischemic optic neuropathy

Atilla et al found that VEP amplitude decrease was more significant in ischemic optic neuropathy, while optic neuritis showed more significant latency prolongation.

VEP in adrenoleukodystrophy

Adrenoleukodystrophy is an X-linked metabolic disorder with very long-chain fatty acid (VLCFA) accumulation and multifocal nervous system demyelination, often with early involvement of visual pathways. Kaplan et al found that pattern-reversal VEPs were abnormal in 17% of the men with adrenoleukodystrophy; no evidence indicated that reduction of VLCFA levels improved or retarded visual pathway demyelination.

Optic neuropathy due to HTLV-1

Yukawa et al found delayed P100 latencies in 7 of 46 eyes in patients with uveitis due to the virus.

Pattern-reversal VEP in classic and common migraine

Shibata et al recorded pattern-reversal VEP to transient checkerboard stimulus in 19 patients with migraine with visual aura (ie, classic migraine), 14 patients with migraine without aura (ie, common migraine) in the interictal period, and 43 healthy subjects. Latencies and amplitudes of pattern-reversal VEPs in each group were analyzed. In patients with classic migraine, P100 amplitude was significantly higher than in healthy subjects, whereas latencies of pattern-reversal VEPs did not differ significantly. No significant differences were noted in latency between the common migraine group and healthy subjects or in latencies and amplitudes of pattern-reversal VEP between the classic migraine and common migraine groups.

Zgorzalewich found prolongation of P100 and N145 latencies and reduction in amplitude in migraine patients in one hemisphere.

These results suggest that patients with classic migraine may have hyperexcitability in the visual pathway during interictal periods and that the increased amplitude of pattern-reversal VEPs after attacks may be due to cortical spreading depression.

Szabela et al found abnormal VEP in 22% of type 2 diabetics.

With abnormal VEP, some of the differential diagnostic considerations are as follows:

• Optic neuropathy
• Optic neuritis
• Ocular hypertension
• Glaucoma
• Diabetes
• Toxic amblyopia
• Glaucoma
• Leber hereditary optic neuropathy
• Aluminum neurotoxicity
• Manganese intoxication
• Retrobulbar neuritis
• Ischemic optic neuropathy
• Multiple sclerosis
• Tumors compressing the optic nerve - Optic nerve gliomas, meningiomas, craniopharyngiomas, giant aneurysms, and pituitary tumors

Normal VEP virtually excludes an optic nerve or anterior chiasmatic lesion.

Clinical usefulness of VEPs includes the following:

• More sensitive than MRI or physical examination in prechiasmatic lesions
• Objective and reproducible test for optic nerve function
• Abnormality persists over long periods of time
• Inexpensive as compared with to MRI
• Under certain circumstances, may be helpful to positively establish optic nerve function in patients with subjective complaint of visual loss; normal VEP excludes significant optic nerve disorder

Summary

The VEP is preferable in optic nerve and anterior chiasmatic lesions, while MRI is clearly superior in retrochiasmatic disease. Note that the VEP is nonspecific as to the underlying etiology and pathology.

Brainstem Auditory Evoked Potential

BAEP or BAER measures the function of the auditory nerve and auditory pathways in the brain stem (see Image 1). The short-latency BAER generally is used for clinical purposes. The test can be performed under sedation or under general anesthesia. Standard broadband click stimulation is used on the ear tested, while the contralateral ear receives masking noise of 30- to 40-dB lesser intensity. Monoaural stimulation is used. The click intensity should be 65-70 dB above click perception threshold. A repetition rate of about 10 Hz should be used.

Electrode placement

An electrode is placed on each ear lobe and at Cz. Whether nuclei or tracts, or both, generate the peak latencies is not known. Generators currently are postulated to be as follows:

• Wave I - Action potential of the cranial nerve (CN) VIII
• Wave II - Cochlear nucleus (and CN VIII)
• Wave III - Ipsilateral superior olivary nucleus
• Wave IV - Nucleus or axons of lateral lemniscus
• Wave V - Inferior colliculus

Factors influencing peak latencies of BAERs include age, sex, auditory acuity stimulus repetition rate, intensity, and polarity. Rarefaction (ie, earphone diaphragm moves away from the eardrum) produces an increase in wave I amplitude. In severe hearing loss, all waveforms may be delayed, wave I may be absent with waves II through V delayed, or all waveforms may be absent. Note that in patients with hearing loss BAER still can be obtained to assess central conduction time by increasing stimulation intensity.

BAEPs are useful in estimating or aiding in the assessment of hearing loss. The most commonly used method for this is evoked response audiometry. The frequency of stimulation is 50-70 Hz, and at least 3 different intensities should be used. Wave V latency shifts are used to estimate the amount of hearing loss.

In children, especially those younger than 2 years, the BAEP can be used to screen those who might benefit from auditory amplification in order to achieve more normal speech and language development. However some children with a normal BAER have abnormal hearing. Kileny showed middle latency abnormalities in some of these cases. The role of BAEP nevertheless is to identify those patients who could benefit from a hearing aid. Obviously with normal BAEP a hearing aid would not be useful to correct the hearing loss.

Kern et al studied effects of insulin-induced hypoglycemia on the auditory brainstem response (ABR) in humans. ABRs were examined in 30 healthy men during euglycemia and after 20 minutes and 50 minutes of steady-state hypoglycemia of 2.6 mM induced with insulin. Hypoglycemia increased interpeak latencies III-V and I-V, whereas changes in the latency of wave I were not significant.

Technical aspects - Filter band pass 100-3000 Hz

The first 10 ms are averaged, and 2-4000 responses may be averaged. At least 2 separate trials should be performed. The recording montage is at least, and usually, a 2-channel montage: channel 1 is ipsilateral ear to vertex, and channel 2 is contralateral ear to vertex. Because of relative vertex positivity, the waveforms are recorded as upward deflections. The normal response is a series of waveforms within a time window of 10 ms.

Clinically, the first 5 waves are used, with more significance placed on waves I, III, and V. Peak and interpeak latencies are measured, side-to-side differences are calculated, and wave I-V ratios may be used. Audiometry is very helpful and should be done within a reasonable time interval of the BAER. This helps delineate any hearing loss that might influence the test results. Hearing loss in the 2000- to 4000-Hz frequency range is especially important, since it may delay the BAER.

Neonatal BAEP: Recording the neonatal BAEP is technically different from recording that of adults. The skin is very sensitive, and special nonallergenic tape should be used to fix the electrode. Collodion or other irritant chemicals are to be avoided. To avoid collapse of the earlobe and obstruction of the auditory canal in premature babies, the earphone should be held slightly above the ear. The earphone is best held by hand, and the recording preferably should be performed with the neonate asleep. This helps reduce the high-frequency components of the EEG that might interfere with BAEP recording. Because of the slower response, sweep should be set at 15-20 ms and the low-frequency cutoff filter at 20-30 Hz.

BAEPs predominantly activate the pathways in the brain stem ipsilateral to the side of click stimulation. In particular, mid-upper pontine lesions tend to lead to ipsilateral BAER abnormalities. The structures involved in generation of BAER may be more concerned with sound localization than with hearing itself.

Clinical usefulness

BAEPs are very resistant to alteration by anything other than structural pathology in the brainstem auditory tracts. BAEPs are not affected significantly by barbiturate doses sufficient to render the EEG "flat" (ie, isoelectric) or by general anesthesia (although Garcia-Larrea et al have reported BAEP loss with combined lidocaine and thiopental infusion). Disorders of the peripheral vestibular system do not affect BAEP. Thus, 21 patients who had labyrinthine diseases (ie, Ménière disease, labyrinthitis, vestibular neuronitis) had no BAEP interwave latency abnormalities using the limits employed for clinical neurological purposes.

Cerebellopontine angle lesions (acoustic neuromas)

BAEP may be abnormal when audiometry fails to disclose a lesion. The characteristic findings are increased I-V and increased I-III interpeak latencies ipsilateral to the lesion. Meningiomas and other cerebellopontine angle tumors may not produce any abnormalities until they are large enough to be externally compressive.

Demyelinating disease

An abnormal response may be seen with higher frequency in symptomatic patients; sometimes, however, a positive test may be recorded in the absence of clinical brainstem symptomatology.

Migraine headaches

Zgorzalewicz found significant prolongation of waves III and IV. The finding would support that the brainstem contributes to the pathomechanism of migraine.

Multiple sclerosis

BAEP should be considered if the clinical symptom implicates a lesion outside of the brain stem. In this case an abnormal BAEP would further support the diagnosis of MS. If, however, the clinical sign (eg, diplopia) points to the brain stem, BAEP abnormality is merely confirmatory. In various studies about 20% of the population tested for a second lesion have an abnormal BAEP and about half of these go on to develop MS in the next 1-3 years.

Purves et al reported pattern-shift VEP to be abnormal in 45%, SEP abnormal in 35%, and BAEP in 14% of patients without brainstem signs. Combining all 3 modalities, 97% of patients with definite MS, 86% of patients with probable MS, and 63% of patients with possible MS had abnormal findings on at least one of these tests. Similar findings were reported by Ferrer et al. Kjaer reported 38% abnormal BAEPs in patients with silent lesions, while 50% of these patients had an abnormal VEP and only 13% an abnormal SEP.

Kjaer also reported 22 patients with only spinal symptoms; 55% of these showed an abnormal BAEP.

Chiappa found that the BAEP is positive in 21% of clinically unsuspected cases. Most authors have concluded that, of the 3 tests, BAEP yields the smallest percentage of patients, but it still adds to the detection rate because it is abnormal in a different subset of patients.

Brainstem tumor

Bilateral prolongation of latencies and interpeak latencies may be seen. Gordon et al evaluated the efficacy of ABR as a screening test for small acoustic neuromas by performing a prospective trial to determine the diagnostic sensitivity of BAER in these tumors. Randomly selected patients (n=105) with surgically proven acoustic neuromas underwent preoperative BAER tests within 2 months of surgery. A test result was considered abnormal when the interaural wave I-V latency difference was greater than 0.2 ms, the absolute wave V latency was abnormally prolonged, or waveform morphology was abnormal or absent.

Of the 105 patients tested, 92 (87.6%) had an abnormal BAER result and 13 (12.4%) had completely normal waveforms and wave latencies. Eighteen patients had tumors greater than 2 cm in total diameter. Of these, 12 had tumors 2.5 cm or larger and 6 had tumors between 2.1 and 2.4 cm. All of these 18 patients had abnormal BAER results. Of 29 patients with tumors 1.6-2 cm in size, 25 (86%) had abnormal BAERs. Of 45 patients with tumors in the range of 1-1.5 cm diameter who underwent preoperative BAER, 40 (89%) had an abnormal response. In 13 patients with tumors 9 mm or smaller, only 9 (69%) had an abnormal ABR finding.

These data show that BAER sensitivity decreases with decreasing tumor size. Therefore, MRI scanning is the preferred study because the accuracy for detection of tumor smaller than 1 cm through BAER is 70%. Nevertheless, BAER is useful in patients who have implanted medical devices (eg, pacemakers) that prevent MRI scanning.

Meningomyelocele

Taylor et al studied BAER and VEP in infants with meningomyelocele; 47 infants were included in the study to determine whether EPs reflect early neurological status and whether BAER and VEP have prognostic value in neurological outcome. The infants, aged 1 day to 3 months, were tested while still in hospital after the meningomyelocele repair.

Normal BAEPs were found in 41% and normal VEPs in 62% of the patients. BAEPs were abnormal in all infants studied who had symptomatic Arnold-Chiari malformation (n=9); VEPs were abnormal in only 55% of symptomatic infants. VEPs did not appear to be sensitive enough to have prognostic value in these infants. Nevertheless, BAEPs were consistently abnormal in patients with symptomatic Arnold-Chiari malformation and showed a positive predictive value of 88% and accuracy of 84% in predicting central neurological sequelae.

Brainstem stroke

The response is variable; some lesions cause abnormal latencies while some do not (eg, negative BAER in lateral medullary syndrome).

Respiratory insufficiency following encephalitis

Schwarz et al showed prolonged interpeak latencies (I-III, I-V, III-V, IV-V) and delayed absolute latencies of waves II, III, V, and I, at least on one side, in the BAEP. The auditory pathways are near the respiratory control centers in the brain stem; therefore, the electrophysiologic abnormalities of wave III and the IV-V complex may be a reflection of the disturbed central control of ventilation.

Prediction of posttraumatic coma in children

BAEP and SEP studies were performed within 72 hours of admission in 127 children with severe head injury in order to predict the outcome of posttraumatic coma. Outcomes were categorized as brain death or survival. On first assessment, 50 comatose children had normal BAEP and SEP. About 78% survived and 22% deteriorated and died. Forty-five had abnormal findings; 69% of them improved and survived, whilst 31% deteriorated and died. All 32 children who did not have recordable BAEP and SEP died. These data suggest that BAER is a useful test in predicting neurological outcome in this setting.

Childhood speech disorders

Maassen et al found that children with speech and language deficit showed abnormal auditory evoked potentials in 95% of his study group.

Comatose patient

BAEP can be done while the patient is sedated. It can be used as a prognostic indicator. Survival is unlikely in the absence of BAEP. The brain-dead patient has invariably abnormal BAEPs—either the absence of all waveforms or the presence of wave I and the absence of all subsequent waveforms.

Summary

The most common uses of BAEP are in MS and in acoustic neuroma. It is a useful screening test, with limitations; MRI scanning may be preferable when a small lesion is under consideration. Increased I-III interpeak latency indicates a lesion from CN VIII to the superior olivary nucleus, while increased III-V interpeak latency suggests a lesion from the superior olivary nucleus to the inferior colliculus ipsilateral to the ear stimulated. Intraoperative monitoring during cerebellopontine angle tumor surgery may be helpful in aiding the surgeon to preserve as much function as possible.

Somatosensory Evoked Potentials

History

The first evoked response measurement is credited to Richard Caton, Liverpool, England, in 1913, but he could not record his results because he had no camera. About 34 years later, the first human scalp recording was accomplished. Major improvements included introduction of the first signal averager (by Dawson in 1954) and of the first modern averager, in 1958.

Origin of somatosensory evoked potential

The actual SEP is considered to be the result of summated effects of action potentials and synaptic potentials in a volume conductor. The short-latency SEP (SLSEP) is considered to be generated from volleys traversing the large-fiber sensory system (ie, posterior columns and medial lemnisci). Studies have shown that simply changing the size and shape of volume conductor can create voltage differences at the surface.

Physiological basis

Predominantly large-diameter group Ia fibers and group II cutaneous afferents are responsible for SEPs. The modality used in the majority of instances is electrical stimulation, due to its ease of delivery and quantification, even though other types of sensory stimuli have been tried with success. When a mixed nerve is stimulated, Ia muscle afferents are activated. In the spinal cord, the dorsal columns are predominantly responsible for conduction of the activity that generates the SEP. The lemniscal and thalamocortical pathways are involved in the brain. Extralemniscal pathways also may play a role.

To test the physiological basis of SEP, Drews et al investigated the contribution of group I muscle afferent activation in the production of H reflexes and SEP in man. Electrical stimuli were applied to the tibial nerve in the popliteal fossa to study how the information is transferred from group I muscle afferents to motor neurons and to the somatosensory cortex. For control purposes, identical stimuli were applied to the skin. The SEP evoked by skin stimulation alone had a peak latency that was 5 ms longer than the SEP to transcutaneous nerve stimulation. The threshold intensity to evoke an H reflex was at least twice as high as the threshold for an SEP.

In most subjects, H reflex was correlated with SEP size. If 2 identical stimuli were applied to the posterior tibial nerve with an interval of 1 second, the second H reflex was 30% smaller than the first one. The corresponding SEPs were reduced only slightly. Postactivation depression presumably results from intrinsic properties of synapses of group I muscle afferents.

Stimulation techniques

Mixed nerve stimulation - Need not be supramaximal; a small twitch is sufficient

Stimulus duration - 2-300 microseconds, some prefer longer

Repetition rate - Usually 3 Hz (some patients tolerate only 1-2 Hz); no change in SEP until 15-Hz stimulation frequency; no need for random stimuli (but may be needed to trigger off ECG)

Cutaneous nerve stimulation - Used with the trigeminal and lateral femoral cutaneous nerves; to study segmental innervation disturbance, dermatomal studies may be used. Dermatomal SEPs may be technically difficult and therefore are not used routinely. Current MRI technology largely replaced dermatomal SEP studies in suspected radiculopathies and spinal cord lesions. In expert hands, however, they may have value in selected cases.

Dermatomal SEPs are discussed later in this article since they played a significant role historically in the development of the SEP technology and contributed significantly to the understanding of neurophysiology.

Recording and filtering

Surface or needle electrodes may be used.

Montages - Cephalic bipolar, referential

Upper extremities

• Channel 1 - C3/C4 referenced to Fz
• Channel 2 - Second cervical spinous process to Erb point
• Channel 3 - Fz to contralateral cortex

Lower extremities

• Channel 1 - L1, L3 to hip
• Channel 2 - Cz- Fpz

Filter - General setting 10-2500 Hz

Generators of median SEP

• Erb point = brachial plexus
• N11, N13 = dorsal column, nucleus cuneatus
• P14 = medial lemniscus
• N18 = subcortical
• N20 = primary sensory cortex
• P22 = primary motor cortex

Buchner et al researched the origin of P16 of the median nerve SEP. Following median nerve stimulation, several monophasic peaks were recorded at the scalp in the 15- to 18-ms time range. Source analysis using 3 different methods modeled a source near the center of the head with an orientation toward the activated hemisphere and a peak activity at 16 ms after the stimulus. Magnetic recordings detected no signals in this time range, which confirmed that the source had a subcortical location. From dipole localization, assigning the exact origin of the P16 source to either the subthalamic level or the thalamocortical radiation was not possible, because of the limited spatial resolution at the center of the spherical head model.

An estimate of the conduction velocity of the medial lemniscus pointed toward a subthalamic origin. The P16 source was preserved in 2 patients with a lesion of the thalamocortical radiation and the ventral thalamus. Further evidence for a subthalamic location of P16 was derived from the physical mechanisms generating far-field potentials.

Normal upper limb (median nerve) SLSEP

For this test, 4 channels generally are used but at least 3 channels are needed, as follows:

• Erb point to Fz
• Nuchal midline C2 spine electrode to Fz
• Contralateral somatosensory area scalp electrode to Fz
• Extra channel - Erb point to the contralateral scalp. Polarity is arranged so that active electrodes, Erb point, cervical, and cortical result in an upward deflection, representing negativity. Fz is used as the reference electrode for the upper extremity EP. This electrode location on the scalp is not inactive. It may attain electronegativity at 19-20 ms after stimulation that is equal or nearly equal to that at the contralateral cortical site and abolishes N19 in Cc-Fz derivation.

Generators of tibial SEP

• N22 = dorsal gray and root entry zone at lumbosacral spine
• N29 = nucleus gracilis
• P31 = brain stem
• N34 = brain stem
• P37 = primary sensory cortex

Role of age, height, and limb length

Vaney et al studied the role of physical parameters in relation to the median nerve SEP. SEPs following stimulation of the median nerves of 25 medical students were recorded along with their height, age, and upper limb length. Three major positive and negative peaks were recorded as follows:

• P1 (16 ms), N1 (20 ms)
• P2 (28 ms), N2 (33 ms)
• P3 (43 ms), N3 (50 ms)

N1 and P1 were correlated significantly with height and limb length. The authors concluded that SEP studies might be affected by physical parameters including age, height, and limb length.

Role of sleep

Noguchi studied the changes of frontal and parietal SEP in the awake state and compared them with SEPs in different stages of sleep in 10 healthy adult subjects. Frontal and parietal SEP components were affected differently as sleep stages progressed. The amplitudes of frontal components were increased in sleep, whereas the amplitudes of parietal components were decreased in sleep. The most discordant changes occurred in stages III/IV. The amplitudes for the frontal N18-P22-N30 complex and parietal N20-P26-N32 complex increased from stage II to stages III/IV, while those for frontal N30-P40 and parietal N32-P40 decreased. P14 and frontal N18 latencies did not change significantly. The further latencies showed progressive prolongation from the awake state to slow-wave sleep.

The SEP waveforms and latencies in rapid eye movement (REM) sleep were similar to those in the awake state. Amplitudes for frontal peaks remained slightly higher and amplitudes for parietal peaks slightly lower. Apparently both excitatory and inhibitory influences may mediate these sleep stage–related changes.

Note that significant neuropathy may be a complicating factor in acquiring SEP, and the development of cortical potentials may be irregular, delayed, dispersed, and with a poor amplitude. Generally some of these difficulties can be overcome by increasing the number of samples collected.

N/P13 deflection

Most human clinicopathologic correlations suggest that the N/P13 waveform is generated in the lower medulla, probably in the dorsal column nuclei. The negativity recorded in the Fz-Cc derivation (N19) is the difference in negativity between the 2 electrode sites and thus is a "derived" waveform. N19 generally is believed to originate in the primary sensory cortex; however, good human clinicopathologic data are available to suggest that much of N19 is generated in the thalamus.

Chiappa et al and Goldie et al published data on a series of patients with instructive lesions, indicating that much of the negativity after 15 ms was generated in the thalamus. Regli and Despland studied 50 patients who had acute infarctions and found N19 preserved in small lesions confined to the postcentral gyrus but absent in large lesions involving the underlying white matter and thalamus. Epileptogenic lesions of the sensory cortex often produce augmentation of P22 but not of N19.

These data suggest that the negative deflection appearing between 16-19 ms after stimulation of the median nerve at the wrist probably is generated in the thalamus. With lower limb stimulation (ie, posterior tibial nerve at the ankle), the widespread negative activity seen at 25-30 ms also is believed to be generated in the thalamus. The subsequent positive activity (N/P37) probably is generated in the primary sensory cortex. When using lower limb stimulation, absence of the cauda equina potential (LP) suggests the presence of a lesion at or below that level. Technical considerations (eg, muscle artifact) also may obscure the LP potential.

Clinical interpretation is based on the time interval between "peaks" of the waves. Registering a good Erb point or cauda equina potential is important to allow measurement of central conduction times. Side-to-side comparisons of latencies can be useful in clinical diagnosis. Like BAEPs, SEPs are fairly resistant to changes by widespread influences other than structural pathology in somatosensory tracts. Barbiturate doses (sufficient to render the EEG isoelectric) and general anesthesia do not significantly alter the SLSEPs.

Yiannikas et al found that both SEPs and electromyography (EMG) are of limited clinical utility in patients presenting with symptoms but without neurological signs of root compression in cervical spondylosis. In patients with clinical signs of neurological deficit, EMG and SLSEPs may be helpful or confirmatory. In patients with clinical evidence of myelopathy, performing SLSEPs from both upper and lower extremities may be informative and may reveal or disprove a conduction block. Patients with syringomyelia often have abnormal central conduction time following upper limb stimulation. In cervical spondylosis, an abnormal latency difference may be noted between brachial plexus (EP) and lower medullary (N/P13) components following upper limb stimulation.

Le Pera et al showed selective abnormality of the N13 spinal SEP to dermatomal stimulation in patients with cervical monoradiculopathy. Scalp SEPs to dermatomal stimulation have proved to be only partially useful in the diagnosis of monoradiculopathy, mostly in cases without motor impairment. The aim of the study was to test the sensitivity of the spinal N13 potential in uncovering lesions of single cervical roots.

The author studied 5 patients suffering from cervical monoradiculopathy by using a recording technique allowing specific recording of the genuine N13, which probably is generated by dorsal horn cells. No patient showed signs of muscle impairment, and needle EMG findings were always normal. In 4 patients, the N13 SEP was absent following stimulation of the dermatome corresponding to the damaged root, while both the lemniscal P14 and the cortical N20 components were normal. SEP recorded after stimulation of upper limb nerves showed no abnormality in any of these patients. Apparently loss of N13 potential after dermatomal stimulation could be due to deafferentation of dorsal horn neurons; the N13 is particularly sensitive to initial root compression. A montage allowing recording of the genuine N13 SEP, therefore, can improve the sensitivity of dermatomal SEP recording in patients with suspected cervical monoradiculopathies.

Multiple sclerosis

The SEP is positive in a significant number of patients with MS. The abnormalities may include prolonged latencies or lack of development of the SEP altogether. Lower extremity studies are more frequently abnormal because of the longer pathway. Upper limb SLSEPs are abnormal in about 40-60% of all patients with MS. Lower limb SLSEPs have an abnormality rate of approximately 70%, presumably because of the greater length of CNS white matter involved.

Eisen et al reported abnormal results in trigeminal nerve stimulation in 41% of patients with MS. Abnormalities of trigeminal SLSEPs also have been reported in patients who had MS, Wallenberg syndrome, cerebellopontine angle tumors, trigeminal neurinomas, or meningeal sarcoidosis with facial paralysis.

Approximately one third of SLSEP abnormalities in MS are unilateral. One fifth of the bilateral abnormalities are asymmetric. Some patients with MS show loss of N/P13 with preservation and normal latency of N19; this pattern is difficult to explain if SLSEP generator sources are assumed to be linked in series.

Comparisons of the 3 evoked potential stimulus modalities have found visual and somatosensory testing to be of approximately equal sensitivity for revealing clinically unsuspected lesions, with auditory testing being one half to one third less sensitive; the 3 tests are complementary.

Lumbosacral disk disease

Sitzoglou et al described dermatomal SEP studies in evaluating patients with lumbosacral disk disease. Twenty-four patients with unilateral radiculopathy were studied. All patients had clinical signs and symptoms of disk prolapse and positive findings on neuroradiologic testing. The latency and the amplitude of the first positive SEP waveform were measured and peripheral nerve conduction studies and EMG were performed. Clear dermatomal SEP abnormalities were identified that correlated with radiculopathy in as many as 83% of studied cases. EMG was positive in ~63% of the same subjects. Thus, dermatomal SEPs may complement routine electrophysiological testing of patients with radiculopathy and may provide a sensitive noninvasive technique for defining the level of disk prolapse.

Tsonidis et al reported on the diagnostic value of dermatomal SEPs by correlating the neurophysiological data to clinical, neuroradiological, and operative findings in lumbar disk protrusion. Twelve patients with lumbar disk disease treated surgically were analyzed. Diagnostic workup included history, neurologic examination, routine lumbar spine films, and CT and MRI of the lumbar spine, in addition to neurophysiological investigations, especially conduction velocity studies, and standard SEPs and dermatomal SEPs. The retrospective study disclosed correlation of the SEPs after dermatomal stimulation and surgical findings in 83% of cases.

Cervical syringomyelia

Wagner et al monitored median nerve SEPs in 28 patients with cervical or cervicothoracic syringomyelia. Intraoperative median nerve SEPs were monitored. Analysis was focused on SEP components—N13 (spinal cord), P14 (brain stem), and N20 (cortex). N13 was absent in ~87% of patients because of a combined effect of syringomyelia and general anesthesia, and did not recover.

P14 showed a significant intraoperative latency increase in 2 patients; this was irreversible in 1 patient who had a postoperative worsening of sensory function. N20 showed no significant alterations. Pure motor deficits after surgery were not predicted by SEP monitoring. Thus, intraoperative P14 recordings helped to identify, and thereby prevent, injury to the dorsal columns, whereas N13 recording did not contribute to the intraoperative monitoring of spinal cord function in syringomyelia.

Patients with cervical cord syrinxes may show abnormalities in median nerve SEPs, indicating a lesion in the upper cervical cord, with relative sparing of lower limb SEPs.

Spondylosis

Berthier et al evaluated the effects of spondylosis on SEP to ascertain its potential role in the presurgical assessment of cervical myelopathy in patients with MRI abnormalities and clinical findings of either segmental spinal cord or dorsal column dysfunction. Using median and tibial nerve SEP, no clear correlation was found between the severity of MRI abnormalities and that of clinical presentation or SEP abnormalities. Some patients with MRI evidence of cervical cord impingement or intramedullary T2 hyperintensity showed normal SEPs, while 8 of 13 patients without evidence of cord narrowing or T2 signal abnormality showed abnormal SEPs.

This discrepancy may suggest that MRI and SEPs evaluate different aspects of the disease process. On the basis of this study, the SEP does not appear to be a good measure of anatomical deficit; however, spinal cord dysfunction detected by SEP may be present in patients with an unremarkable MRI image. SEP recording may therefore be useful in the presurgical assessment of symptomatic patients without MRI evidence of cervical cord compression.

Lyczak et al reported abnormal SEPs in 56% of patients with cervical myelopathy. The tibial nerve's SEPs were used, and abnormal central conduction times (CCT) were observed. A significant reduction of the abnormalities occurred after surgery. Abnormal SSEPs before the surgery correlates with the severity of myelopathy, and improvement in SSEPs following surgery correlated strongly with clinical improvement.

L5/S1 radiculopathy

Dumitru and Dreyfuss applied strict criteria to define a group of 20 patients with a unilateral/unilevel L5/S1 radiculopathy. They concluded that the clinical utility of both segmental and dermatomal SEPs is dubious in patients with known unilateral/unilevel L5 and S1 nerve root compromise. Castello et al studied the effects of lumbar nerve root decompression on SEP. They found a significant improvement in postoperative SEP latency in patients with lateral recess stenosis.

Intraoperative SEP

The basis of intraoperative SEP as a representative index of motor function is based on the fact that the vascular compromise that may cause motor dysfunction or loss affects the lateral corticospinal tract and the dorsal spinocerebellar tract also.

In general terms, the regions of both motor and sensory pathways (lateral corticospinal tract and dorsolateral spinal cord and the alpha motor neurons) are served by the same vascular supply.

Intraoperative SEP poses a special challenge and requires cooperation with the operating room staff and also special equipment and careful attention to limit electrical noise. Careful checking of the ground is important, as is good shielding. The list of interfering factors is long and includes electrocautery equipment, nerve stimulators, and electric drills. Anesthetic agents and level of anesthesia also are interfering factors.

• Access to the patient is important, but the recording should not interfere with the operative procedure. A baseline recording should be done prior to the operation to establish the patient's own normal value under less stressful circumstances.
• The operative plan and what the surgeon expects from the monitoring needs to be discussed in advance. Communication with the entire staff is important.
• Make note of preexisting diseases such as diabetes that may interfere with successful SEP testing.

Stimulus pulse duration was evaluated by Luk et al, who found that stimulus duration of 0.3 ms is the recommended choice for tibial SEPs during intraoperative monitoring. Stimulus duration affected amplitude but not latency.

SEP monitoring during lumbosacral spinal stenosis is a well-known procedure. Weiss found that, even in routine surgical procedures, monitoring the SEP along with EMG helps the surgical team to avoid neurogenic complications.

Recording motor evoked potential (MEP) and SEP during thoracoabdominal aortic surgery to assess ischemia of spinal cord has been valued by a number of authors as a procedure to lower risk of postoperative neurological injury. Polo et al found SEP and MEP useful in scoliosis surgery to assess hypotension-related anoxic cord injury.

Weigand et al found SSEP monitoring to be useful in thoracoabdominal aortic endovascular stent grafting in order to prevent spinal cord anoxia.

Arrington et al used similar methods in pelvic fractures and acetabular surgery. They found that combined somatosensory and motor recording prevented damage to the sciatic nerve.

Mills et al found that monitoring radial nerve SEP was helpful in humeral nailing procedures.

Schwartz et al reported that monitoring ulnar SEP is predictive of brachial plexus injury during surgery for correction of scoliosis. However Deutsch et al found that the false-negative rate was 9% for SEP in anterior spinal surgical approaches.

Minahan et al recently showed that both SEP and neurogenic MEP could miss a spinal cord lesion during intraoperative monitoring. In their 2 cases, posterior column function was preserved on the clinical examinations although the patients were paraplegic. They concluded that neurogenic motor responses, while generally useful, are not reliable indicators of spinal cord motor function.

Baba et al reported the results of spinal cord EP monitoring for cervical and thoracic compressive myelopathy. Epidural spinal cord EPs were recorded in 95 patients undergoing surgery for cervical and/or thoracic compressive myelopathy. Abnormal spinal cord EPs correlated significantly with the severity of spinal cord compromise and symptoms, such as myelopathy. All of the thoracic myelopathy cases and 91% of the cervical myelopathy cases exhibited abnormal evoked responses. The preoperative EPs were not clearly helpful in predicting outcome; however, postoperative early recovery of the EPs correlated with clinical improvement.

Acute transverse myelitis

Few studies have been done evaluating the role of EP changes in acute transverse myelitis. Misra et al studied 10 patients with lower limb and upper limb weakness with detailed clinical, MRI, and neurophysiological evaluation; median and tibial SEPs, MEPs of upper and lower limbs, and concentric needle EMG. MRI and MEPs were useful in assessing the clinical outcome; however, the role of SEP was limited.

Tuberculous myelopathy

Misra et al investigated the value of SEP and MEP changes in patients with Pott paraplegia. MEP and SEP correlated with respective motor and sensory impairments, as well as with the outcome.

Intracranial neoplasm

Rowed et al used SEP to identify the somatosensory cortex to help remove intracranial neoplasms and spare eloquent cortex. SEPs were recorded in response to contralateral median nerve stimulation from the cortical surface. Polarity reversal of SLSEP waves was used to identify the position of the central sulcus in 46 consecutive craniotomies for removal of metastases, gliomas, or meningiomas located in, near, or overlying sensorimotor cortex. SEPs were recorded successfully in 43 of 46 cases (94%), with demonstration of polarity reversal in 42 of 43 (98%) cases. SEP localization led to modification of 14 of 42 (33%) procedures, most frequently because of either displacement or involvement of sensorimotor cortex by tumor. Six patients (14%) developed new neurological deficits, but none of these were attributable to incorrect identification of sensorimotor cortex. Routine use of this technique should be considered in all procedures for lesions located near the central sulcus.

Diabetic polyneuropathy

Use of SEP in diabetes is mainly confirmatory. It also can be used in selected cases for whom the central conduction time is needed. In general, the SEP is prolonged in patients with clinically significant diabetic neuropathy. Palma et al studied SEPs in individuals with non-insulin-dependent diabetes who had different degrees of neuropathy. The wrist-Erb point conduction velocity is decreased and the Erb point-N13 interpeak latencies are increased in patients with diabetes. The N11-N13, N13-N20, and N13-P22 interpeak latencies are within the normal range. The wrist to Erb point conduction velocity was proportional to the degree of neuropathy. The degrees of neuropathy have no influence on the EP-N13 interpeak latency. Although SEP may be confirmatory, it is not used often, since routine nerve conduction studies readily yield the diagnosis in diabetic neuropathy.

Giant SEPs have been reported in cortical reflex myoclonus. Kofler et al described enlarged cortical responses in 14 patients with progressive supranuclear palsy. They attributed this to cortical hyperexcitability. Since frontal lobe dementia is frequently present in patients with progressive supranuclear palsy, striatofrontal deafferentation and intracortical disinhibition may explain the increase in the size of the SEP.

Ferri et al observed large-amplitude middle latency SEPs in children with benign epilepsy of childhood with centrotemporal spikes. The mechanism of this is not known. An age-related decrease in amplitude and lack of SEP after age 12 years were noted. The findings may be interpreted as maturational changes.

Rinsho described a 66-year-old woman with corticobasal degeneration, cortical reflex myoclonus with related cortical spike, aphasia, clumsiness, and dystonia with rigidity. The right side was affected, and median nerve stimulation elicited a giant SEP over the left scalp. He also described a 58-year-old woman with reflex myoclonus cortical myoclonic tremor and a giant cortical SEP. In a study of 2 patients with corticobasal degeneration, one showed a giant SEP and one did not.

Striano et al studied a family with cortical tremor, myoclonus, and epilepsy and found giant SEP potentials and enhanced long latency reflex I. Genetic study revealed linkage on chromosome 2p.

Valeriani studied cortical myoclonus and concluded that the initial giant SEP corresponds to physiologic potentials evoked in healthy subjects, while the late giant SEP could be explained by hyperpolarization that follows the postsynaptic excitation of the early components. Tsuda described Lafora body myoclonus with giant SEP. Positron-emission tomography revealed no increase in glucose metabolism in the somatosensory cortex.

Ugawa reported that the dipole responsible for the giant SEP is localized in the sensory cortex. Some patients showed the localization for the dipole in the superior frontal gyrus in the paracentral lobule.

In a study by Schmitt et al, increased amplitude of SEP was noted in all cases of ceroid lipofuscinosis.

Myoclonus and giant SEP have been described in herpes simplex encephalitis. Triggs described giant SEP with anterior spinal artery syndrome. The hypothesis has been advanced that this is due to lack of inhibition of the anterolateral inhibitory influences on the dorsal column medial lemniscal system.

Saitoh described giant SEP in the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (ie, MELAS syndrome). Lu reported dyssynergia cerebellaris myoclonica in 3 brothers in whom alcohol decreased both the myoclonus and the giant SEP amplitude.

Vitamin B-12 deficiency

Both upper and lower limb SEPs have been found abnormal in patients with vitamin B-12 deficiency, often showing no components or only the peripheral EP peak.

Puri et al reported that serum vitamin B-12 level correlated well with the latencies of P37 (P <0.005) and sural SNAP (P <0.006). On treatment, normalization of P100, MRI signal, N 20 and partial recovery of P37 latencies was seen at 6 months, 9 months, and 1 year, respectively.

Hyperthyroidism

Takahashi and Fujitani studied median SEPs in 14 patients; they found that the N19-P23 amplitude was significantly higher in the patients than in the healthy controls.

Hypothermia

Guerit et al studied the use of the SEP to determine the optimal degree of hypothermia during circulatory arrest. They sequentially recorded subcortical (P14) and cortical (N20) SEPs in 32 patients undergoing deep hypothermic circulatory arrest. Under normal hemodynamic conditions, hypothermia initially produced N20 disappearance at a mean nasopharyngeal temperature of 20.4 +/- 2.6 degrees C (range 14.5-26.1 degrees C) and P14 disappearance at a mean of 16.9 +/- 2.0 degrees C (range 12.4-20.2 degrees C). On rewarming, P14 reappeared at mean temperatures of 19.3 +/- 4.0 degrees C (range 13.5-29.2 degrees C) and N20 at a mean of 21.1 +/- 4.1 degrees C (range 14.3-29.6 degrees C).

The delay of SEP reappearance after restoration of blood flow correlated significantly with cardiac arrest duration (r=0.74 for P14, and r=0.62 for N20; P <0.01). Neurological recovery was uneventful in 23 patients; 5 patients presented with neurological sequelae (minor or transient in 4; no recovery from anesthesia and death after 48 hours in 1), and 4 patients died during operation. Twenty-three of 24 surviving patients in whom P14 disappeared when the hypothermia was deep enough to cause cardiac arrest (duration was 17-94 min) had a normal neurological outcome. By contrast, all surviving patients in whom cortical SEPs disappeared at higher temperatures presented neurological sequelae. In conclusion, the neurophysiological monitoring of brainstem activity, as provided by SEPs, enables determination of the optimal temperature for hypothermic circulatory arrest.

Carotid endarterectomy monitoring

Duffy et al compared the results of cerebral oximetry and EP monitoring in carotid endarterectomy. Decrease in SEP amplitude of 50% and in rSO₂ of 10% were considered clinically significant. Compared with SEPs, rSO₂ had a sensitivity of 50% and a specificity of 96%. Clinical experience with this evolving technology is ongoing. Its role in neurovascular procedures has yet to be established. Fiori and Parenti performed electrophysiological monitoring for selective shunting during carotid endarterectomy. In 255 endarterectomies for severe carotid stenosis, 2-channel EEG and SEPs were monitored.

They found that computerized EEG is an easily interpretable method of monitoring and reveals rapidly developing cerebral ischemia but that severe SEP changes can occur in spite of a normal EEG pattern when cerebral ischemia has a slow onset. SEP monitoring is a slower method of recording but it can give a finer distinction of less severe cerebral ischemia.

Myotonic dystrophy

Patients have a prolonged interpeak latency between the Erb point and N/P13, indicating a sensory system involvement in this disorder.

Epidural sensory block

Zaric et al evaluated epidural sensory block by thermal stimulation, laser stimulation, and recording of the SEP. The existence of differential sensory block during epidural analgesia has been confirmed by some authors and disputed by others. The zone of anesthesia was smaller than the zone of any other investigated variable. The cranial spread of analgesia and motor block was lower than that of laser-assessed block. Partial block of laser perception and thermal perception lasted longer than analgesia and motor block. No consistent segmental or temporal differences were found between the thermal test and laser methods.

During epidural block, prolongation of latencies and reduction in amplitudes of SEP produced at the most cranial analgesic dermatome did not differ significantly from those produced at the anesthetic dermatome. No differential block of small nerve fibers was found during epidural analgesia by thermal test and argon laser stimulation. Recording of SEPs did not demonstrate significant difference between responses from the sites with most superficial and with most intense sensory block.

Postanoxic coma

Zandbergen et al found short latency evoked potentials (SSEP) and neuron-specific enolase (NSE) to be correlated with poor outcome. Patients unconscious at 72 hours and having an abnormal SSEP had poor outcome. Even after 24 hours, the predictive value of the SSEP was very strong.

Stroke

Tzvetanov et al attempted to answer the predictive value of median SSEP in the early phase of stroke. The results were mixed.

Summary Of The Role Of Evoked Potentials

During the last decade, the rapid advancement in MRI technology has diminished the utilization of electrophysiologic testing modalities. A part of this is justified because of the high yield and generally good correlation of MRI findings to the underlying pathology. Also, MRI is often able to visualize the pathological anatomy underlying a disease state. Nevertheless, in some instances the disturbance is not readily visible by an imaging modality or MRI is neither feasible nor cost-effective. For such eventualities, EPs are uniquely suited.

• In a wide variety of primary and secondary visual system diseases, VEP testing provides a sensitive extension of the clinical examination.
• MRI is a highly accurate localizing modality, while VEP is useful primarily in assessing optic nerve function in the anterior (prechiasmatic) portion. It is lateralizing but not localizing to the lesion.
• BAEP is useful in acoustic neuroma, but in the past few years MRI has clearly surpassed the yield of BAEP in small lesions, and in most cases MRI is clearly superior. However, MRI may not be applicable in every patient (ie, an increasingly larger percentage of elderly are equipped with pacemakers), while BAEP can be done in patients with a variety of implanted devices. BAEP shows good "anatomical definition."
• While SEP is limited in spatial localization, it is a good functional tool; its primary use is to determine compromised CNS conduction. It may help confirm symptoms when little physical findings are noted. It may reveal asymptomatic lesions, thereby aiding the workup of suspected MS.
• Use of SEP and MRI modalities may be complimentary. SEP showed limited usefulness in spinal disorders. Degenerative disk disease, spinal stenosis, and compressive lesions show poor physioanatomical correlation. SEP may confirm or reject the presence of a suspected conduction block. BAEPs and SLSEPs may be able to establish an anatomical region where the conduction disturbance or block occurs. They provide a sensitive tool for assessment of brainstem auditory and somatosensory tracts and nearby structures. Abnormalities demonstrated by these tests are etiologically nonspecific and must be integrated carefully into the clinical situation by a physician familiar with the clinical use and limitations of these tests.

With advancing technology and increasing frequency of certain implants and medical devices in patients, the population of patients who are unable to undergo MRI scanning is growing. For these patients, evoked response studies may be a suitable avenue for diagnosis. Finally, intraoperative EPs may provide timely information in the operating room that may benefit neurosurgical or neurovascular surgical outcomes.

Multimedia

(Enlarge Image)

Media file 1: Normal brainstem auditory evoked potentials (BAER).

Keywords

VEP, VER, BAER, BAEP, SEP, SLSEP, visual evoked responses, short-latency somatosensory evoked responses, short-latency brainstem auditory evoked responses

• Search for CME/CE on This Topic »