Evoked Potentials and Intraoperative Monitoring

David B. Macdonald

Charles C. Dong

INTRODUCTION

Evoked potentials are time-locked bioelectric signals conducted partly or entirely through the central nervous system (CNS) in response to specific stimuli. They are valuable for diagnostic testing and for intraoperative monitoring (IOM). By detecting and localizing conduction disturbances, diagnostic evoked potentials extend and complement the clinical evaluation of multiple sclerosis and several other diseases, although MRI advances diminish this role. They can also assist coma prognosis and pediatric vision, hearing, or CNS evaluations. Intraoperative evoked potentials enable functional mapping and monitoring that can avoid neurologic injury, and this is now the most frequent application.

This chapter summarizes the principles, methods, and clinical utility of the most common modalities: visual evoked potentials (VEPs), short-latency brainstem auditory evoked potentials (BAEPs), short-latency somatosensory evoked potentials (SEPs), and motor evoked potentials (MEPs). We assume that readers know the relevant neuroanatomy and pathology. Other dedicated textbooks contain more detailed information and include additional modalities.¹^,²^,³^,⁴^,⁵^,⁶^,⁷^,⁸

BASIC PRINCIPLES

Evoked Potential Generation

By transiently exciting a specific sensory organ, nerve, or CNS structure, the stimulus initiates a time-locked sequence of propagating action potentials in the selected pathway’s axons and localized postsynaptic potentials in its neurons or muscle fibers.³^,⁴^,⁹^,¹⁰^,¹¹^,¹²^,¹³^,¹⁴^,¹⁵ These elemental responses summate and volume conduct to generate compound surface evoked potentials consisting of sequential peaks of known or putative anatomical origin. The number of peaks and their polarities, latencies in ms from stimulus initiation, interpeak intervals (IPIs) in ms, and amplitudes in µV or mV are modality specific and technique dependent.

Propagating long nerve or tract impulses generate traveling evoked potentials with latencies that vary with stimulus-recording site distance. Short nerve or tract impulses and gray matter or muscle postsynaptic potentials generate stationary responses with latencies that vary with stimulus-generator distance. Superficial generators produce near-field evoked potentials with amplitudes that increase with recording electrode proximity, while deep structures generate far-field responses that vary less with electrode location.

Averaged Evoked Potentials

Even with optimal recording conditions, VEPs, BAEPS, and SEPs have low signal-to-noise ratios (SNRs) because their <1-20 µV signals are smaller than spontaneous EEG, EMG, and ECG “background noise” that obscures individual responses.³^,⁴^,¹⁴^,¹⁶ Extracting them requires averaging of multiple stimulus repetitions, known as sweeps (ie, the tracing that sweeps across the oscilloscope screen with each stimulus). The number of sweeps (N) needed to generate an interpretable signal depends on the signal and the background it is competing against. N can range from ≤200 for relatively high SNR (≥ -10 dB) to ≥2000 for very low SNR (≤ -20 dB). Responses that are time locked to the stimulus summate and average in, though they may be modified by jitter (variability in response latency), while random noise amplitude declines as N increases. The amplitude of background noise is divided by

; hence, more stimulation always improves the signal relative to background, but the noise never reaches zero.

Thus, averaged evoked potentials are estimates distorted by jitter and residual noise. Their reproducibility in superimposed independent averages determines accuracy and verifies that apparent peaks are actual responses rather than residual
noise.³^,⁴^,¹⁴^,¹⁷ Confident interpretation requires moderate to high reproducibility, while low reproducibility indicates that the signal should be interpreted with caution and nonreproducible traces should be considered unreliable (Table 19.1, Fig. 19.1).

TABLE 19.1 Averaged evoked potential reproducibility classification

Reproducibility	Signal Amplitude Variation	Waveform Fit
High	<20%	Nearly exact
Medium	20%-30%	Approximate
Low	30%-50%	Loose
Nonreproducible	>50% or inapparent signal	Divergent
Amplitude variation = (maximum – minimum)/maximum. Waveform closeness-of-fit determines reproducibility by itself when signals are inapparent or absent. Modified from MacDonald DB, Dong C, Quatrale R, et al. Recommendations of the International Society of Intraoperative Neurophysiology for intraoperative somatosensory evoked potentials. Clin Neurophysiol. 2019;130(1):161-179, with permission.

Unaveraged Evoked Potentials

Muscle MEPs are an exception because their 50 µV to several mV amplitudes result in very high SNR and single-trial fidelity.¹³^,¹⁵^,¹⁸ They also exhibit intrinsic trial-to-trial amplitude and morphology variability that would violate the averaging principle of approximate signal invariance. Unaveraged muscle MEPs are advisable for both reasons, and superimposing two or more verifies that they are time-locked responses rather than random muscle potentials.

General Methods

This section summarizes general methods and safety principles.³^,⁴^,¹¹^,¹²^,¹³^,¹⁴^,¹⁵^,¹⁷^,¹⁹^,²⁰ Subsequent sections describe modality-specific techniques. Methods vary slightly between studies performed in the electrophysiology laboratory (“lab studies”) and in the surgical suite (IOM).

Electrodes

The technologist attaches stimulating and recording electrodes at standard peripheral and/or scalp sites for each modality. Surface electrodes are safe and effective after skin preparation with mildly abrasive gel to desquamate the high-impedance outer epidermal layer. This enhances common-mode electric interference rejection by achieving low, balanced impedances of <5 kΩ in the lab and <2 kΩ in the electrically noisy operating room. Reusable scalp EEG cup electrodes filled with conductive paste or gel are suitable for lab studies and also for IOM when fixed with collodion. Disposable single-use peripheral adhesive electrodes are effective in both situations. Reusable rigid bar electrodes for peripheral nerve stimulation are safe in the lab but not for IOM because they risk sustained-pressure skin necrosis. One must clean and disinfect reusable electrodes after use.

FIGURE 19.1. Averaged evoked potential reproducibility (RP) classification illustrated with median nerve SEPs. AV, signal amplitude variation (%). (Modified from MacDonald DB, Dong C, Quatrale R, et al. Recommendations of the International Society of Intraoperative Neurophysiology for intraoperative somatosensory evoked potentials. Clin Neurophysiol. 2019;130(1):161-179, with permission.)

Needle electrodes are unsuitable for lab evoked potentials, but sterile single-use needles inserted after induction and skin antisepsis are popular for IOM because of their rapid application and <5 kΩ impedance. “Corkscrew” needles self-secure in the scalp, and tape secures straight needles at peripheral sites. However, they risk needlestick incidents and rare but serious burns because their small surface areas generate highenergy density and heat if they conduct stray electrosurgery current. Consequently, a few programs limit their use to techniques justified by greater efficacy, such as intramuscular needle recordings that maximize muscle potential amplitudes.²¹ One should handle needles by the stem, never recap them, and discard them in a sharps box after use.

Some IOM recordings require sterile single-use invasive electrodes, such as subdural strips, probes, or spinal epidural electrodes. Their small but potentially serious risks of infection, hemorrhage, or trauma are only justifiable when noninvasive methods are insufficient. These electrodes are discarded after use.

Recording Leads

Bundling together recording leads further enhances common-mode noise rejection because nearby wires pick up similar electromagnetic interference that cancels out in differential amplifiers. Tight lead braiding to maximize noise rejection is advisable in the operating room.

Stimulation

The technician must select stimulus intensity with care. Evoked potential latencies decrease and amplitudes increase as stimulus intensity increases from threshold to supramaximal levels that are too strong for patients to tolerate. Consequently, lab studies use a standard suprathreshold intensity comfortable for most patients. Since tolerance is not an issue for patients under anesthesia, IOM can employ supramaximal stimuli to enhance response amplitude and stability.

Stimulus frequency is also important. To avoid synchronizing the evoked potential response with power line interference and “locking in” line noise, the stimulus frequency should not divide evenly into 50 or 60. A rate slightly off from a number that evenly divides into the line frequency (eg, 5.1 Hz) ensures that line noise averages out. Also, since faster stimuli speed data acquisition but reduce some response amplitudes, lab studies use a standard submaximal rate to balance recording time and amplitude. However, IOM can employ faster stimuli if they do not overly depress signals.

Recording Parameters

The recording time base should contain all of the measured signal components and a postresponse segment. Notch filters should be turned off to avoid “ringing” artifact that can distort or simulate responses, and the low- and high-frequency filters should be selected so they do not affect signal frequency content while rejecting lower- and higher-frequency noise. Finally, the digital sampling rate must be more than double the high-frequency filter to avoid aliasing.

STATISTICAL CONSIDERATIONS

Diagnostic Testing

There are important statistical issues for diagnostic studies that compare patient results to normal limits defined in a control sample from the normal population.¹⁷ For example, age-matched control groups are critical because latency and amplitude evolve with age, especially in children. In addition, gender-matched control groups are advisable for VEPs, since males have longer mean response latency, possibly due to larger average head size. Furthermore, height-adjusted latency limits are relevant for SEPs and MEPs.

Defining normal limits with parametric statistics like mean ± 2.5-3 standard deviations requires a normal distribution. This is true for latencies and IPIs, but not for amplitudes and amplitude ratios that have marked positive skew. One can mathematically transform amplitude data to a more normal distribution, but then inverse transform limits may seem excessive. Thus, amplitude limits are usually ill defined, and only the absence of an obligate (normally always present) peak is unambiguous.

For the above reasons, latency and IPI are the primary diagnostic measures and amplitude is secondary. With normal latency and IPI, one interprets amplitude cautiously. However, marked amplitude deviations may be relevant, and the absence of obligate peaks in a clean recording is abnormal.

Comparing patient results to normal controls depends on using exactly the same techniques for both. Since methods vary, labs generally collect normal data to define their own limits. This is particularly important for VEPs, which are sensitive to lab-specific factors. Using published BAEP or SEP reference data requires ensuring identical technique.

Intraoperative Monitoring

The approach to IOM differs from diagnostic studies. Normal limits do not exist because of anesthesia. Instead, one analyzes evoked potential time series in waveform stacks and trend plots, with patients as their own controls. This is valid because amplitude and latency are relatively stable in an individual. It also means that one can and should optimize technique for each patient to maximize the speed and accuracy of surgical feedback.¹⁴^,¹⁶^,²² The goal is to quickly and reliably confirm functional integrity or detect impending neurologic injury and initiate intervention to reverse it.

Intraoperative pathology causes acute axonal or neuronal failure that reduces amplitude with less effect on latency; there may also be an increase of threshold stimulus intensity.¹³^,¹⁴^,²³^,²⁴^,²⁵^,²⁶ Demyelination prolongs latency with less effect on amplitude, but this subacute-chronic process does not develop during surgery. Thus, amplitude is the primary IOM consideration and latency is secondary; threshold elevation may also be relevant.

One must first rule out confounding factors that are nonsurgical causes of evoked potential deterioration.¹³^,¹⁴ They include anesthesia, baseline drift, other systemic influences, and limb ischemia or pressure. Thus, warning criteria for impending neurologic damage mainly consist of amplitude reduction unexplained by confounding factors. They range from percentage decrements to disappearance, depending on modality, reproducibility, and surgical circumstances. Some programs use acute stimulus threshold elevation for muscle MEPs.

REVIEW

19.2: Based on statistical issues, primary evoked potential measurements are:

a. Amplitude for diagnostic studies and latency for IOM

b. Latency for diagnostic studies and amplitude for IOM

c. Latency for both diagnostic studies and IOM

d. Amplitude for both diagnostic studies and IOM

e. Latency and amplitude for diagnostic studies and amplitude for IOM

View Answer

19.2: b. Latency is the primary measure for diagnostic studies, since amplitude may vary considerably between patients and for technical reasons. For IOM, amplitude is the primary measure since patients serve as their own controls, and neurologic injury affects amplitude more than latency.

VISUAL EVOKED POTENTIALS

Retinal activation with visual stimuli produces stationary near-field occipital VEPs that enable visual pathway assessment from the optic nerve to the cortex. The presumed generators are the visual cortex and possibly the geniculocalcarine tract.

Diagnostic VEP Testing

This section summarizes diagnostic VEP methods and interpretive recommendations from comprehensive sources.³^,⁴^,¹²

Stimuli

Pattern reversal stimuli produce consistent results in alert collaborative patients able to maintain visual focus. The stimulus is a black-and-white checkerboard pattern with the “checks” (squares) reversing color at ≈2 Hz. Patients sit a measured distance from the display monitor and keep their focus on its center. They wear their glasses or contact lenses because check contrast is important, and the technologist documents their corrected visual acuity. Monocular tests are performed for each eye while covering the other one.

The pattern is usually presented full-field, or occasionally hemifield, to address specific questions. It is critical to calibrate and maintain check luminance and contrast. Another important factor is the visual angle subtended by each check, determined from selected check size and eye-screen distance. Small 12-16′ checks test central vision but may not generate a good response when there is poor visual acuity or defocusing, while large 40-50′ checks are less sensitive to small changes in the fovea but good for testing peripheral vision, and medium 16-32′ checks are a good initial compromise for routine use.

Flash stimuli produce variable responses, but are necessary for patients who are too young or ill to collaborate with pattern reversal technique or who have severely impaired visual acuity. The flash source is a strobe light placed 30-45 cm in front of the patient’s preferably open eyes; light-emitting diode (LED) goggles are an alternative. Normally, the flash rate is ≈1 Hz, and testing is monocular.

Recording

The American Clinical Neurophysiology Society¹² recommends the Queen Square System recording sites and montages shown in Table 19.2. Additional inion and midparietal (5 cm above midoccipital) channels may disclose inferior or superior response displacement, which is a rare normal variant. Recording an electroretinogram (ERG) from periocular electrodes can assist flash VEP interpretation.

A 1- to 100-Hz recording bandwidth and 250- to 500-ms time base are suitable. Due to relatively high SNR, VEPs may be visible in single sweeps (EEG photic responses and lambda waves are raw VEPs), and 100-200 sweep averaging is usually sufficient.

TABLE 19.2 Recommended VEP montages for diagnostic testing

	Pattern Reversal VEPs			Flash VEPs
	Full-Field	Left Hemifield	Right Hemifield	Flash VEPs
Channel 1	LO-MF	LO-MF	LT-MF	LO-Ref
Channel 2	MO-MF	MO-MF	LO-MF	MO-Ref
Channel 3	RO-MF	RO-MF	MO-MF	RO-Ref
Channel 4	MF-Ref	RT-MF	RO-MF	Cz-Ref
MO, midoccipital 5 cm above the inion; LO and RO, lateral occipital 5 cm to the left and right of MO; LT and RT, temporal sites 5 cm lateral to LO and RO; MF, midfrontal 12 cm above the nasion; Ref, single or linked earlobe or mastoid reference. From American Clinical Neurophysiology Society. Guideline 9B: guidelines on visual evoked potentials. J Clin Neurophysiol. 2006;23(2):138-156.

Response

Full-field pattern reversal stimuli produce three midoccipital peaks designated N75, P100, and N145, with N or P for negative (conventionally upward) or positive (downward) polarity, and numbers for typical latency (Fig. 19.2A). There may also be a midfrontal N100. The P100 is the principal peak, while the others serve to identify it and to define peak-to-peak amplitude.

With left or right hemifield stimuli, the N75, P100, and N145 are at midoccipital and lateral occipital sites ipsilateral to the stimulated hemifield, while oppo-site-polarity peaks appear at contralateral lateral occipital and temporal sites. This is because the contralateral mesial occipital response dipole projects across the midline and appears maximally at the ipsilateral (to stimulation) occipital electrodes. Full-field VEPs are the sum of both occipital responses.

Flash stimuli produce early a and b ERG peaks followed by up to six alternately negative and positive midoccipital peaks labeled I-VI (Fig. 19.3A). The occipital peaks exhibit marked latency and amplitude variability between individuals and arousal states.

FIGURE 19.2. Full-field pattern reversal VEPs. A. Normal results in a 35-year-old. B. Asymmetric P100 delay (left 189 ms, right 163 ms) and marked left amplitude reduction established neuromyelitis optica in a 15-year-old with transverse myelitis. Gray traces are independent averages for judging reproducibility; black traces are grand averages for measurement.

FIGURE 19.3. Flash VEP examples. A. Normal result in a 15-year-old. B. Absent flash VEP with preserved ERG in a 9-month-old with neurodegenerative white matter disease and suspected blindness. A₁₂, linked earlobe reference.

Interpretation

Clinical examination should rule out retinal and ocular disease before attributing VEP abnormalities to visual pathway dysfunction. One should also exclude poor visual fixation, defocusing, and drowsiness.

Analysis begins with each eye’s midoccipital P100 latency and its amplitude in all three occipital channels. Amplitude measurements may be peak (from baseline) or peak to peak, but must be the same as applied for normal controls. Then, one calculates the interocular latency difference and amplitude ratio (maximum/minimum midoccipital amplitude) and each eye’s interhemispheric amplitude ratio (maximum/minimum lateral occipital amplitude).

Monocular P100 latency prolongation or an excessive interocular latency difference indicates prechiasmal dysfunction on the longer-latency side (Fig. 19.2B). “Excessive” means >2.5 or 3 standard deviations from the mean of normal recordings performed in the same laboratory; in practice, an interocular latency difference of more than 10 ms is usually abnormal. Symmetric bilateral P100 latency prolongation indicates bilateral dysfunction, which is not localizable.

Amplitude interpretation is perilous with normal latency. Absence of response needs confirmation by additional midparietal and inion recording with a 500-ms time base (to ensure the response is not just greatly delayed), and equivocal amplitudes may indicate further testing with different check sizes or hemifield stimulation. Monocular P100 amplitude reduction or an excessive interocular amplitude ratio suggests prechiasmal dysfunction on the lower-amplitude side (Fig. 19.2B). Symmetric bilateral P100 amplitude reduction suggests bilateral unlocalized dysfunction. Finally, an excessive interhemispheric amplitude ratio may suggest prechiasmal dysfunction when monocular, and chiasmal or postchiasmal dysfunction when bilateral, but requires additional testing.

Occasionally, there is an ambiguous “W” response with two positive peaks. In this situation, one can estimate P100 latency with the intersection of lines drawn through the initial and final slopes. This may be a normal variant or a sign of partial visual pathway disturbance; additional testing (particularly hemifield testing) may help localize the problem.

Hemifield pattern reversal VEPs are mostly done to clarify full-field results or for suspected postchiasmal lesions. Guidelines for their more complex interpretation are available elsewhere.¹²

Marked variability limits flash VEP interpretation. The only definite abnormality is the absence of any occipital response (Fig. 19.3B). In this case, ERG presence implies central visual pathway dysfunction, while absence implies retinal disease without excluding additional central dysfunction. Flash VEP presence indicates that the occipital cortex receives visual input but does not demonstrate perception. Large latency or amplitude deviations well beyond normal limits may suggest visual pathway dysfunction, but need cautious interpretation.

Disorders

Optic neuritis is a frequent cause of monocular or bilateral visual loss. It may be part of or progress to more widespread demyelinating disease. Nearly all affected eyes have VEP abnormalities that partially improve with subsequent clinical recovery.²⁷ Patients with optic neuritis should have brain and spinal cord MRI followed by cerebrospinal fluid testing if imaging suggests multiple sclerosis.²⁸

Multiple sclerosis consists of CNS demyelinating lesions separated in space and time. Since optic nerve lesions are common and may be subclinical, monocular or bilateral VEP abnormalities can aid diagnosis. About 30%-40% of multiple sclerosis patients with no history of optic neuritis have abnormalities.²⁹

Neuromyelitis optica consists of transverse myelitis and optic neuritis. Since it may initially present with spinal cord but no visual symptoms, VEP evidence of optic nerve malfunction can establish the diagnosis (Fig. 19.2B).³⁰

Cortical blindness is a bioccipital stroke syndrome than can cause abnormal or absent pattern reversal and flash VEPs. However, results may be surprisingly normal, presumably because damage or disconnection prevents visual perception even though surviving cortical islands respond to visual input.³¹

Functional blindness is a rare conversion disorder. Since diagnosis requires excluding pathology, normal VEPs are supportive but do not exclude cortical blindness. These patients may have spurious pattern reversal VEP findings if they do not visually fixate, and flash VEPs may then be normal, but again do not rule out cortical pathology.

Pediatric visual assessment can be difficult in infants and noncommunicative young children. Flash VEP studies may contribute to their evaluation (Fig. 19.3B).

Intraoperative VEPs

Early attempts to monitor intraoperative flash VEPs using inhalational anesthesia and standard LED goggles produced inconsistent results. However, recent reports describe reliable VEPs during brain surgery using total intravenous anesthesia (TIVA) and high-luminance LEDs in goggles or silastic eyelid discs.³²^,³³^,³⁴^,³⁵ These methods might also help avoid rare ischemic optic neuropathy during spine surgery.³⁶ Nevertheless, their general usefulness remains to be seen.

BRAINSTEM AUDITORY EVOKED POTENTIALS

Cochlear activation with auditory stimuli produces BAEPs that enable auditory system assessment from the auditory nerve to the mesencephalon. Putative generators include the auditory nerve and brainstem auditory tracts and nuclei.

Diagnostic BAEP Testing

This section summarizes diagnostic BAEP methods and interpretive recommendations from several sources.³^,⁴^,¹¹^,³⁷^,³⁸^,³⁹

Stimulus

The stimuli are broadband clicks containing a wide range of frequencies to excite most cochlear receptors. They come from a flat frequency response headphone speaker driven by 0.1-ms electric pulses. As the headphone diaphragm oscillates, it alternately presses the air forward (condensation) or pulls air away from the ear (rarefaction). Initial sound pressure is negative with rarefaction clicks, positive with condensation clicks, and alternately negative and positive with alternating clicks. Subtle response differences necessitate click-specific normal limits.

The stimulus rate is 8-10 Hz because faster stimuli reduce early peak amplitudes. It is important to calibrate and maintain click intensity in dB peak-equivalent
sound pressure level (peSPL). Test intensity is typically 60-80 dB above normal hearing level (the mean hearing threshold of healthy young adults) or sensation level (the patient’s ear-specific hearing threshold). The technologist tests each ear separately, with contralateral 60 dB peSPL white noise masking to avoid stimulating the opposite cochlea through bone conduction.

Recording

For upgoing peaks (using the standard convention that input 1 negativity produces an upward deflection), the montages are Ai-Cz and Ac-Cz, where Ai and Ac are the ipsilateral and contralateral earlobe or mastoid. Some labs obtain upgoing peaks with reversed convention and derivations, and a few prefer down-going peaks with standard convention and reversed derivations. A 10- to 15-ms time base and 10- to 30-Hz to 2500- to 3000-Hz bandwidth are suitable. Since these <1-2 µV signals have very low SNR, averages regularly need 1000-4000 sweeps to reproduce.

Response

There are five stationary peaks labeled waves I-V (Fig. 19.4A). Wave I is a negative near-field distal auditory nerve potential from Ai, and the subsequent waves are positive far-field potentials mainly from Cz. Wave II arises from the proximal auditory nerve and possibly cochlear nucleus. Putative origins of other waves are III—cochlear nucleus, lateral lemniscus, and superior olivary complex; IV—superior olivary complex and lateral lemniscus; and V—lateral lemniscus and inferior colliculus. More generally, wave III comes from the lower pons, and waves IV and V come from the upper pons and midbrain. These localizations are summarized in Table 19.3.

Waves II and III are occasionally missing, and waves IV and V form a variable complex in which either they are distinct peaks, IV is a wavelet on the ascent to V, V is a wavelet on the descent from IV, or there is a single fused peak. The Ac-Cz channel helps identify peaks because it has no wave I and often shows better IV-V separation (Fig. 19.4).

The BAEP threshold is the lowest intensity that produces a response, usually only wave V. With increasing intensity, other waves appear and all peaks show increasing amplitude and decreasing latency but stable IPIs. Latency-intensity testing records BAEPs from high intensity to 0 dB in 10- to 20-dB steps (Fig. 19.5).

Interpretation

Clinical examination and preferably audiometry should rule out ear disease and peripheral hearing loss before attributing BAEP abnormalities to retrocochlear dysfunction, and one should remove excessive earwax before testing.

FIGURE 19.4. BAEP examples. A. Normal responses in a 6-year-old. B. Bilateral I-III and I-V delay in a 6-month-old with suspected hearing impairment. In both recordings, Ac-Cz has typically wider wave IV-V separation no wave I.

Analysis begins by measuring wave I, III, and V latencies and wave I and V amplitudes in Ai-Cz. Then, one calculates the I-III, III-V, and I-V intervals and the V/I amplitude ratio. Normal results even with missing wave III indicate cochlear reception and auditory transmission to the midbrain, but do not establish normal puretone hearing or auditory perception. Audiometric peripheral hearing loss can delay all peaks without altering IPIs or cause absence of wave I or even of all peaks when severe.

Absence of all waves (unexplained by severe peripheral hearing loss or technical failure) indicates retrocochlear dysfunction involving at least the distal acoustic nerve. Absence of waves after I, II, or III indicates dysfunction beyond the relevant structure. Reduced V/I amplitude ratio suggests retrocochlear dysfunction but requires caution when this is the only abnormality.

Prolonged IPIs signify dysfunction between corresponding structures: I-III, distal acoustic nerve and pons (Fig. 19.4B); III-V, pons and midbrain; and I-V, distal acoustic nerve and midbrain. Either or both of the first two may explain the latter, while I-V delay with absent wave III indicates unlocalized retrocochlear malfunction. Increased interside IPI differences have similar significance, but their interpretation requires audiometric results.

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