Vertigo and Imbalance: Clinical Neurophysiology of the Vestibular System
Handbook of Clinical Neurophysiology, Vol. 9
282
CHAPTER 23
Brainstem auditory evoked potentials (BAEPs)
and intraoperative BAEP monitoring
Alan D. Legatt*
*
Department of Neurology, Montefiore Medical Center and Albert Einstein College of Medicine, Bronx, NY 10467, USA
Evoked potentials are the electrical signals produced
by the nervous system in response to a sensory input.
Following a transient acoustic stimulus such as a click
or tone pip, a complex series of auditory evoked
potentials (AEPs), with latencies ranging from several
milliseconds to several hundred milliseconds, can be
recorded from the surface of the head. These signals
can be used to assess the function of the auditory sys-
tem, and also for intraoperative monitoring (IOM) of
the ear, the eighth cranial nerve, and the brainstem
auditory pathways.
Loud acoustic stimuli can also elicit neck muscle
contractions, which are thought to be mediated by
the saccule and vestibular nerve. The electromyo-
graphic signals produced by these muscle contrac-
tions, called vestibular-evoked myogenic potentials,
are discussed in Chapter 15.
23.1. Types of auditory evoked potentials
The earliest electrical signals produced in response to
auditory stimulation are generated in the inner ear.
These signals, labeled the electrocochleogram, are
discussed in Chapter 22. The AEPs generated in the
brain can be classified as short-latency AEPs, with
latencies < 10 ms, long-latency AEPs, with latencies
> 50 ms, and middle-latency AEPs, with intermedi-
ate latencies.
Middle-latency and long-latency AEPs are gener-
ated within the cerebral cortex. The long-latency
AEPs are profoundly affected by the degree to which
the subject is attending to the acoustic stimuli and
extracting information from them, e.g., by performing
*
Correspondence to: Dr. Alan D. Legatt, MD, PhD, Depart-
ment of Neurology, Montefiore Medical Center, 111 East
210th Street, Bronx, NY 10467, USA.
Tel.: þ1-718-920-6530; fax: þ1-718-920-8509.
E-mail: ALegatt@montefiore.org (A.D. Legatt)
S.D.Z. Eggers and D.S. Zee (Vol. Eds.)
# 2010 Elsevier B.V. All rights reserved
a sensory discrimination task (Linden, 2005). They
have therefore been used as probes of cognitive pro-
cesses, but their variability and the requirement for
the subject to cooperate and perform a task limits their
utility for neurologic diagnosis. Long-latency AEPs
are suppressed by anesthesia, and thus are not useful
for IOM. Middle-latency AEPs are small, subject to
contamination by myogenic signals, and variable
from subject to subject, which limits their clinical
utility. They are also markedly affected by surgical
anesthesia. This anesthetic sensitivity has led to appli-
cation of the middle-latency AEPs as an indicator of
the depth of anesthesia (Schneider et al., 2005), but
their anesthetic-related variability impedes their use
as a monitor for auditory pathway compromise during
surgery.
Most of the components of the short-latency
AEPs are generated within the brainstem. There-
fore, they are usually called ‘‘brainstem auditory
evoked potentials’’ (BAEPs), even though part of
the waveform is generated in the cochlear nerve;
there may also be a contribution from activity in
the thalamocortical auditory radiations. BAEPs
(Fig. 1) are the most useful AEPs both for diagnos-
tic purposes and for IOM. This is because they are
relatively easy to record, their waveforms and laten-
cies are highly consistent across normal subjects,
and they are relatively unaffected by surgical anes-
thesia. They can be used to identify inner ear dys-
function, eighth nerve dysfunction, or brainstem
dysfunction in patients presenting with vestibular
symptoms.
BAEPs are almost identical in the waking and
sleeping states (Campbell et al., 1992), and sedation
(Loughnan et al., 1987) produces only minor
changes in them; the differences may be due to var-
iations in body temperature rather than state-related
BAEP effects per se (Litscher, 1995). Sedation can
therefore be employed during BAEP recordings,
METHODOLOGICAL TECHNIQUES OF ASSESSMENT 283

IV
I III
II
V VI VII
Cz-Ai

IN VN

Cz-Ac

0.2 µV
1 ms
Ac-Ai

Fig. 1. Brainstem auditory evoked potentials recorded simultaneously from three different recording electrode linkages following monaural
stimulation in a normal subject. The vertical dashed lines indicate the peak latencies of waves IV and V in the Cz-Ai waveforms; these peaks
are more widely separated in the Cz-Ac waveforms. An electrical stimulus artifact is present at the beginning of each waveform. Recording
electrode positions: Cz ¼ vertex, Ai ¼ ear ipsilateral to the stimulus, Ac ¼ ear contralateral to the stimulus. Positivity at the first input is
displayed as an upward deflection in these and all other BAEP waveforms shown in this chapter. (From Legatt, 2005, with permission.)

though the use of sedation for evoked potential [ISOFLURANE]A = 2.0% BP 94/55 TNP = 35.9⬚ C
recordings has been markedly reduced due to con-
cerns about monitoring and care of patients during FP1-C3
conscious sedation (American Academy of Pediat-
rics Committee on Drugs, 1992). Surgical levels of C3-O1
anesthesia also produce relatively minor changes
in BAEPs (Stockard et al., 1992; Legatt, 2002; FP2-C4
Banoub et al., 2003) (Fig. 2), which may be more
attributable to changes in body temperature than C4-O2
to direct anesthetic effects (Markand et al., 1987;
Litscher, 1995; Rodriguez et al., 1999). T3-CZ

CZ-T4
23.2. BAEP recording techniques

The American Clinical Neurophysiology Society has EMG/ECG

published guidelines for clinical (American Clinical 15 µV
Neurophysiology Society, 2006a, b) and intraopera- 1 sec
tive (American Electroencephalographic Society, II III
1994) BAEP recordings. I IV V VI

BAER
23.2.1. Acoustic stimulation CZ +
0.25 µV
Since BAEPs are affected by stimulus parameters,
BAEPs recorded during extraoperative diagnostic 60 dBHL
click
studies should be evaluated using normative data 2 4 6 8 10 12
acquired with the same stimulus parameters. During ms
IOM, each patient serves as his or her own control; Fig. 2. Brainstem auditory evoked potentials recorded during sur-
BAEPs recorded when portions of the auditory path- gery in a patient anesthetized with isoflurane at a concentration
ways are at risk are compared to those recorded ear- sufficient to render the electroencephalogram isoelectric. The com-
ponent amplitudes were reduced somewhat, but the latencies of
lier during the same operation. Therefore, BAEP waves I through V were not significantly different from those
stimulus parameters should be held constant during recorded in this patient in the unanesthetized state. (From Stockard
IOM. et al., 1992, with permission.)
284
Clicks, produced by delivering 100 ms-duration
electrical square pulses to the acoustic transducer,
are the stimulus most often used to elicit BAEPs; brief
tone pips can also be used. Since the responses to rar-
efaction and compression clicks may differ (Emerson
et al., 1982; Schwartz et al., 1990), extraoperative
diagnostic BAEP studies should employ a single click
polarity in a given run, and the BAEPs should be com-
pared to normative data that were acquired with the
same stimulus polarity. Rarefaction clicks are gener-
ally preferable because they tend to yield BAEPs with
better definition of the components (Legatt, 2005).
Reversal of the stimulus polarity may be useful in dis-
tinguishing the cochlear microphonic from wave I of
the BAEP (see below). BAEP waveforms also contain
an electrical stimulus artifact that is synchronous with
square pulse delivered to the acoustic transducer
(Fig. 1), and arises from it by magnetic induction
and/or capacitive coupling. During IOM, when arti-
facts are often problematic, recording BAEPs to trains
of stimuli with alternating polarities may be useful to
cancel the stimulus artifact, at least in part.
Extraoperative diagnostic BAEP testing is most
often performed using headphones. The use of stan-
dard audiometric headphones ensures that the stimulus
dB nHL
0.1 µV
1 ms
Fig. 3. Generation of a latency-intensity curve. Brainstem auditory evoked potentials were recorded at progressively lower stimulus inten-
sities (left). Wave V latencies (arrows) were measured and then plotted as a function of stimulus intensity to give the latency-intensity curve
shown on the right. These recordings are from a 35-year-old woman with dizziness and tinnitus; her BAEPs and magnetic resonance imaging
were normal. (From Legatt, 2005, with permission.)
A.D. LEGATT
intensity is the same as that which was used to acquire
the normative data. The stimulus intensity should be
loud enough to elicit a clear BAEP waveform without
causing discomfort or ear damage; 60–65 dB HL is a
typical level. If hearing loss is present, the stimulus
intensity may be adjusted accordingly, so that stimula-
tion is at 60–65 dB SL. This facilitates recording of a
clear BAEP waveform so that neural conductions
within the auditory pathways can be assessed.
Reduced stimulus intensities are also useful during
BAEP recordings, when wave V latency-intensity
functions are being assessed (Fig. 3). Examination of
latency-intensity curves may help to classify a
patient’s hearing loss (Arnold, 2000). A shift of the
curve to a higher intensity level without a change in
its shape suggests conductive hearing loss, while a
change in the shape of the curve with an increased
slope suggests sensorineural hearing loss. Latency-
intensity curves may also reveal abnormalities that
are not demonstrated by BAEP recordings at the stan-
dard, relatively high stimulus intensity typically used
in BAEP studies performed for neurologic diagnosis
(Legatt et al., 1988b).
Since headphones are impractical for IOM, the
acoustic stimuli for intraoperative BAEP monitoring
8.0
65 7.5
Wave V latency (ms)
7.0
6.5
50
6.0
5.5
35 5.0
0 10 20 30 40 50 60 70
Stimulus intensity (dB nHL)
20
5
METHODOLOGICAL TECHNIQUES OF ASSESSMENT
are most often delivered using ear inserts that are
connected to the acoustic transducers with segments
of plastic tubing. The ear insert typically includes a
foam cylinder that is compressed before insertion
and then gradually expands to achieve a tight fit with
the ear canal. The time required for the acoustic signal
to propagate through the tubing typically prolongs the
latencies of all BAEP components by approximately
0.9–1.0 ms. This causes no problems in the evaluation
of the BAEPs during IOM, since each patient serves
as his or her own control and the acoustic propagation
delay is constant, but it should be taken into account if
ear inserts are used for extraoperative diagnostic
BAEP studies. During IOM, the acoustic stimulus
intensity may be difficult to control precisely due to
variability in the positioning of the ear insert, but this
again is not a problem because each patient serves as
his or her own control. The intensity setting chosen
should be loud enough to produce clear BAEPs but
not loud enough to cause ear damage.
BAEPs can also be elicited by bone-conducted
stimuli (Yang et al., 1993; Cone-Wesson and Ramirez,
1997). This is most useful for testing patients with con-
ductive hearing loss.
A stimulus rate of approximately 10/s is typical for
both intraoperative and extraoperative BAEP studies,
but a rate of exactly 10 Hz or another submultiple of
the power line frequency should be avoided. If the
stimulus rate were such a submultiple, signal averag-
ing would not reduce the inevitable line frequency
artifact, which might then obscure the BAEPs. Since
timing circuits can drift, if artifact at a harmonic of
the line-frequency appears in the averaged BAEPs
during IOM and examination of the raw data does
not show increased line frequency artifact, the stimu-
lus rate should be altered slightly.
Acoustic stimuli should always be delivered mon-
aurally, so that a normal BAEP to stimulation of one
ear does not obscure the presence of an abnormal or
absent response to stimulation of the other ear.
An acoustic stimulus delivered to one ear via head-
phones can reach the other ear via air and bone con-
duction with a volume attenuation of 40–70 dB
(Chiappa, 1997; Roeser and Clark, 2000) and gener-
ate an evoked potential via stimulation of the contra-
lateral ear, even if the ear ostensibly being stimulated
is deaf (Fig. 4). To prevent acoustic crosstalk, the
contralateral ear is masked with continuous white
noise at an intensity 30–40 dB below that of the
BAEP stimulus during extraoperative diagnostic
BAEP studies.
285
III V
II
VI
I
0.25 mV
A
V
B
C 5 ms
Fig. 4. BAEPs to monaural stimulation from a patient with one
nonfunctioning ear. (A) Stimulation of the good ear elicits a nor-
mal BAEP. (B) When contralateral noise masking is not used,
stimulation of the nonfunctioning ear produces a delayed wave V
due to air- and bone-conduction of the stimulus to the good ear.
(C) When masking noise is delivered to the good ear, stimulation
of the nonfunctioning ear does not elicit any reproducible BAEPs.
(From Chiappa et al., 1979, with permission.)
Acoustic crosstalk also occurs with ear-insert
transducers, though the signal reaching the opposite
ear is attenuated to an even greater extent, typically
70–100 dB (Roeser and Clark, 2000). During IOM,
acoustic crosstalk would not prevent recognition of
the development of new auditory pathway compro-
mise when a functioning ear is stimulated. Moreover,
most current IOM equipment can deliver interleaved
left- and right-sided stimuli and sort the responses
into separate averages, in effect acquiring averaged
BAEPs to left-ear and to right-ear stimulation con-
currently without actually stimulating both ears
simultaneously. Stimulus interleaving is not compat-
ible with continuous white noise masking of the
nonstimulated ear. For these reasons, white noise
masking is typically not used during IOM.
The BAEPs to click stimulation are generated pre-
dominantly by the region of the cochlea responding to
2000–4000 Hz sounds (Gorga et al., 1985; Van der
Drift et al., 1987); wave V may also receive contribu-
tions from lower-frequency regions of the cochlea. In
order to probe specific parts of the cochlea, BAEPs
286
have been recorded to stimulation with brief tone pips.
The pip is a brief burst of sine waves. It cannot be
abruptly stopped and started; because an audible
‘‘click’’ containing many frequencies would be pro-
duced. Instead, the sine wave stimulus is amplitude-
modulated with a rise time, plateau, and fall time to
reduce (although not eliminate) the energy content of
the stimulus at other frequencies. Acoustic masking
can also be used to obtain frequency-specific infor-
mation from BAEPs, such as by presenting the tone
pips while simultaneously administering continuous
notched noise. The latter is white noise that has been
notch-filtered to remove the basic frequency of the tone
pip. BAEP audiograms produced with such stimuli are
similar to behavioral audiograms in the same subject
(Stapells et al., 1990). Wave V is broader in the fre-
quency-specific BAEPs elicited by the lower frequen-
cies; reducing the low-cut (high-pass) analog filter in
the evoked potential averager to 30 Hz in these record-
ings may yield clearer wave Vs and more reliable
results (Arnold, 2000).
23.2.2. Recording electrode positions
Brainstem auditory evoked potentials are most often
recorded between a scalp surface electrode at the vertex
(position ‘‘Cz’’ of the International 10–20 System for
EEG electrode nomenclature) and electrodes at both
earlobes (labeled ‘‘Ai’’ ipsilateral to the stimulated
ear and ‘‘Ac’’ contralateral to it) or at both mastoids
(labeled ‘‘Mi’’ and ‘‘Mc"). Duplicate or ‘‘backup’’ elec-
trodes are useful during IOM because it is usually diffi-
cult or impossible to replace an electrode that becomes
unusable in the middle of an operation, when the
patient is positioned and draped.
A vertex-to-ipsilateral-ear (Cz-Ai) channel should
always be included in the recording montage. The
vertex-positive peaks in this BAEP waveform are
typically displayed as upward deflections and labeled
with Roman numerals according to the convention of
Jewett and Williston (1971) (Fig. 1). The downward-
pointing peaks are labeled with the suffix N according
to the peak that they follow; for example, downward
peak IN follows upward wave I. The downward
deflection following wave V labeled VN, which has
also been termed the slow negativity (SN), is typically
wider than the positive components and the earlier
negative peaks. Additional recording channels, such
as Cz-Ac and Ac-Ai, may assist in the identification
of BAEP components (Legatt, 2005). The Cz-Ac
channel is the most useful and is a recommended
A.D. LEGATT
addition to the recording montage (American Clinical
Neurophysiology Society, 2006b).
Most of the BAEP components are far-field
potentials at the skin surface, which means that small
displacements of the recording electrodes do not signif-
icantly alter the BAEP waveform. The exceptions to
this are wave I and part of wave II, which are generated
in the distal cochlear nerve (see below) and are there-
fore recorded as near-field potentials in the vicinity of
the stimulated ear. Changes in the location of the Ai/
Mi recording electrode can substantially alter these
components and therefore may be useful to make them
clearer. Ear insert stimulators used for IOM may be
covered with metal foil to serve as near-field recording
electrodes for wave I, thereby yielding a larger wave I.
If the cochlear nerve is at risk during surgery, such
as during resection of an eighth nerve tumor, and the
surgical exposure permits it, an electrode can be
placed on the proximal eighth nerve to record a
near-field compound action potential (Mller and
Jannetta, 1983; Legatt, 1991) (Fig. 5). This signal is
typically much larger than the far-field BAEP, permit-
ting signal averaging using fewer data epochs and thus
providing more rapid assessment of the cochlea and of
the cochlear nerve distal to the near-field electrode.
23.2.3. Amplification, filtering, and signal
averaging
The raw analog data should be amplified by high-input
impedance differential amplifiers with a common
mode rejection ratio of at least 80 dB (10,000:1)
(American Clinical Neurophysiology Society, 2006a).
Direct nerve recording
+
10.0 uV
0.5 uV
−
1 ms
Far-field, Cz - A2
Fig. 5. Auditory evoked potentials to right ear stimulation
recorded directly from the right cochlear nerve (top) and simulta-
neously from the scalp (bottom) during a selective vestibular nerve
section in a 26-year-old man with Ménière’s disease and intractable
vertigo. Note the differing vertical scale factors; the near-field
response is about 80 times larger than the far-field BAEP.
METHODOLOGICAL TECHNIQUES OF ASSESSMENT 287

The analog gain depends on the input window of the
analog-to-digital converter; a value of approximately
100,000 is typical.
A typical analog filter bandpass for BAEP recording
is 100–3,000 Hz or 150–3,000 Hz (3 dB points),
though low-frequency filter settings of 10–30 Hz have
also been recommended (American Clinical Neuro-
physiology Society, 2006b). While line-frequency
‘‘notch’’ filters should not be used for somatosensory
evoked potential recordings, they can be used for
BAEP recordings (Legatt, 2005).
For analog-to-digital conversion, the Nyquist crite-
rion requires a sampling rate of at least 6,000 Hz
(2  3,000 Hz) in each channel to avoid aliasing.
Sampling rates higher than that are required for accu-
rate reproduction of the BAEP waveshape and precise
measurement of peak latencies. If a 15 m epoch is
sampled using 256 points per epoch, the sampling
frequency will be approximately 17,000 Hz, which is
sufficient for good waveshape reproduction with a
high-frequency-filter setting of 3,000 Hz.
Far-field BAEPs are too small to be visible in
unaveraged raw data; thus, signal averaging is required
(Fig. 6). The improvement in the signal-to-noise ratio
is proportional to the square root of the number of data
epochs included in the average. Automatic artifact

0.5 µV
N
1 ms

32

64

128

256

512

1024

2048

4096

Fig. 6. Averaged BAEP waveforms with a progressively increasing number of data epochs included in the average (N), showing how signal
averaging improves the signal-to-noise ratio of the BAEP waveform. (From Legatt, 2003, with permission.)
288
rejection is used to exclude epochs with high-
amplitude noise from the average. During extra-
operative diagnostic BAEP studies, at least two separate
averages should be recorded and superimposed to
assess reproducibility of the BAEP waveforms.
An averaging epoch duration of 10 ms is often
used for extraoperative diagnostic BAEP recordings
in adults. However, a longer analysis time of 15 ms
may be required for recording pathologically delayed
BAEPs, BAEPs to lowered stimulus intensities (as
when recording a latency-intensity study), and
BAEPs in children, especially infants. An epoch
duration of at least 15 ms should be used during
IOM because BAEP component latencies can be pro-
longed by preexisting pathology, hypothermia, or
intraoperative compromise of the auditory system.
The choice of the number of epochs per average
depends on the signal-to-noise ratio of the raw data.
A total of 1,000–2,000 epochs per average is typical
for extraoperative diagnostic BAEP studies, but more
epochs may be required if the raw data are noisy and
the BAEPs are small. During IOM, near-field recording
from the proximal eighth nerve (Fig. 5) may permit
averaging using a much smaller number of epochs, thus
providing more rapid feedback to the surgeons.
23.3. The normal BAEP waveform
The first major upgoing peak of the Cz-Ai BAEP
after the electrical stimulus artifact is wave I. It
appears as an upgoing peak of similar amplitude in
the Ac-Ai waveform and is markedly attenuated or
absent in the Cz-Ac waveform (Fig. 1). The cochlear
microphonic may be visible as a separate peak pre-
ceding wave I, and can be distinguished from wave
I by reversing the stimulus polarity, which will
reverse the polarity of the cochlear microphonic.
Wave I may show a latency shift, but will not reverse
in polarity, as a result of this change in the stimulus.
A bifid wave I is occasionally present and repre-
sents contributions to wave I from different portions
of the cochlea. The earlier of the two peaks, which
reflects activation of the base of the cochlea, corre-
sponds to the single wave I that is typically present
in the Cz-Ai waveform. Reversal of stimulus polarity
can be used to distinguish a bifid wave I from a
cochlear microphonic followed by (a single) wave I.
In contrast to wave I, wave IN is present at sub-
stantial amplitude in the Cz-Ac channel (Fig. 1). This
downgoing deflection is usually the earliest BAEP
component in that waveform.
A.D. LEGATT
Wave II is typically the first major upward deflec-
tion in the Cz-Ac waveform, since wave I is mark-
edly attenuated or absent there. When present, wave
II is usually of similar amplitude in the Cz-Ai and
Cz-Ac channels (Fig. 1). However, wave II may be
small and difficult to identify in some normal
subjects.
A recognizable wave III is usually present in both
the Cz-Ai and Ac-Ai channels. Wave III in the Cz-
Ac waveform is usually substantially smaller than
that in the Cz-Ai waveform (Fig. 1). This difference
helps to distinguish it from wave II, which is similar
in amplitude in these two channels. A bifid wave III
is occasionally observed as a normal variant; the
wave III latency in such waveforms can be scored
as midway between the peak latencies of the two
subcomponents. Rarely, wave III may be poorly
formed or absent in a patient with a clear wave V
and a normal I–V interpeak interval; this finding is
best interpreted as a normal variant waveform.
Waves IV and V are often fused into a IV/V com-
plex with a morphology that varies from one subject
to another (Fig. 7), and may differ between the two
ears in the same subject. The IV/V complex is often
the most prominent upgoing component in the Cz-
Ai BAEP waveform. It is usually followed by a large
negative deflection that may last for several milli-
seconds and often brings the waveform to a point
below the prestimulus baseline. In distinguishing
between a totally fused IV/V complex and a single
wave IV or wave V, Epstein (1988) notes that the
former has a ‘‘base’’ that is greater than 1.5 ms in
duration, whereas the width of a single wave is less
than 1.5 ms.
When waves IV and V overlap in the Cz-Ai wave-
form, the wave V latency measurement used for
BAEP interpretation should be taken from the second
subcomponent of the IV/V complex even if this is not
the highest peak (in contrast to the amplitude mea-
surement used to calculate the IV/V:I amplitude ratio,
which is taken from the highest point in the complex).
Measurement of the peak latency of wave V may be
inaccurate if V appears only as an inflection on the
falling edge of wave IV (Fig. 7D) and impossible if
they are smoothly fused. Two approaches may be used
in such cases (Legatt, 2005). The first involves mea-
surement of wave V latency in a Cz-Ac recording
channel. The overlapping peaks are more clearly sepa-
rated there because the latency of wave IV is typically
earlier, and that of wave V is later, than in the Cz-Ai
waveform (Fig. 1). However, because of these latency
METHODOLOGICAL TECHNIQUES OF ASSESSMENT 289

IV

III

II
V I V VI
I
III
VII
I VI

A D III V
III V
IV
I IV

I II VI
II
VI
VII

B E
II
III IV
I V IV V
I
VI
II III
VI

C F

5 ms
Fig. 7. Various morphologies of the IV–V complex in Cz-Ai BAEP waveforms recorded in normal subjects. (From Chiappa et al., 1979,
with permission.)

shifts, wave V latency values measured in a Cz-Ac
waveform should be compared with normative data
in which the latency of wave V was also measured
in a Cz-Ac recording.
The other approach is to reduce the stimulus
intensity to attenuate wave IV relative to wave V
and permit accurate measurement of the peak latency
of wave V. That latency value cannot be compared
with normative data obtained at a higher stimulus
intensity, but the I–V interpeak interval can be
evaluated because it is minimally affected by
changes in stimulus intensity. Wave V is the BAEP
component most resistant to the effects of both
decreasing stimulus intensity and increasing stimulus
rate. If either of these stimulus modifications is per-
formed progressively until only one component
remains, that peak can be identified as wave V and
then traced back through the series of waveforms to
identify wave V in the BAEP recorded with the stan-
dard stimulus.
290
It is important to distinguish wave V from wave
IV. If wave V were abnormally delayed but an earlier
and larger wave IV that dominated the IV/V complex
was mistaken for wave V, the BAEP abnormality
might be missed. If the latency of an apparent wave
V is abnormally short, efforts should be made to
determine whether this peak is in fact a dominant
wave IV. Lesions that affect wave V almost always
also affect wave IV (Starr and Hamilton, 1976;
Stockard and Rossiter, 1977; Stockard et al., 1977),
but rarely wave IV may be unaltered (Fig. 8).
23.4. Generator sources of the BAEPs
Wave I of the BAEP is generated by the first volley
of action potentials in the cochlear nerve in the most
distal portion of the nerve (i.e., at its cochlear end)
(Legatt et al., 1988a). It arises from the same electri-
cal phenomenon as the N1 component of the eighth
nerve compound action potential in the electro-
cochleogram, as confirmed by simultaneous BAEP
and electrocochleogram recordings (Gersdorff,
1982). This generator produces a surface negativity
in a circumscribed area around the stimulated ear
(Hughes and Fino, 1985; Grandori, 1986); this nega-
tivity at Ai appears as a positive (upgoing) peak in
the Cz-Ai BAEP recording. An Ac-Ai recording
channel can yield a somewhat larger wave I because
its dipole source has a horizontal component that
projects a small positivity to the contralateral ear
V
I IV
II III
VI
A
0.1 µV
1 ms
B
Fig. 8. BAEPs to left ear stimulation recorded during surgery for a
basilar artery aneurysm. The aneurysm ruptured and the basilar
artery was transiently clipped to control the bleeding. The patient
suffered a brainstem infarct. (A) Clear waves I through VI were
present in these BAEPs, recorded just before the aneurysm rup-
tured. (B) BAEPs recorded after the clip was removed show a loss
of waves V and VI. Waves I through IV were unaffected. (Modi-
fied from Legatt et al., 1988a, with permission.)
A.D. LEGATT
(Legatt, 2005). Since wave I is a near-field potential
around the stimulated ear, repositioning of the Ai/Mi
recording electrode can substantially alter it; alter-
nate Ai electrode positions, or an electrode within
the internal auditory canal, can be used to obtain a
clearer wave I. Because wave I arises from the most
distal portion of the cochlear nerve, it may persist
after the nerve is sectioned at a more proximal loca-
tion, such as during surgery for eighth nerve tumors
(Raudzens and Shetter, 1982; Legatt et al., 1986)
(Fig. 9).
Although some authors have suggested source
models in which each BAEP component arises from
a single generator, research has shown that Jewett
and Williston (1971) were correct in their assertion
that most of the BAEP components are composites of
contributions of multiple generators. The complexity
of the generators of human BAEPs (Fig. 10) derives
in part from the complex anatomy of the ascending
auditory pathways, with fibers both synapsing in
and bypassing various relay nuclei (Strominger and
Strominger, 1971; Strominger, 1973; Strominger
et al., 1977). It also reflects the presence of at least
two bursts of activity in the cochlear nerve
(corresponding to the N1 and N2 components of the
eighth nerve compound action potentials in the elec-
trocochleogram), which can drive the more rostral
pathways. Because of both of these factors, several dif-
ferent structures within the infratentorial auditory
pathways may be active simultaneously, with their
contributions summating to yield the far-field BAEPs.
0.1 µV
1 ms
Fig. 9. BAEPs to left ear stimulation recorded during surgery for
left vestibular schwannomas in two different patients, showing per-
sistence of wave I (arrows) but loss of later BAEP components
after transection of the intracranial eighth nerve. The nerves were
intentionally sacrificed to permit total resection of the tumors.
(From Legatt, 2002, with permission.)
METHODOLOGICAL TECHNIQUES OF ASSESSMENT 291

AC

AC
VII?
V, VI VII?
V, VI
AR MGN V, VI?, AR
BIC MGN
VII?, SN BIC
IC IC
V V
L L
L IV IV L V
III IV
I II
I, II
III III
S S
VII
IN, IIN O O VI
C C IN IIN
C
8th Nerve N
II, III? SN
Cochlea II

Fig. 10. Diagram showing the probable generators of the human brainstem auditory evoked potentials. SN, slow negativity after wave V;
AC, auditory cortex; AR, auditory radiations; BIC, brachium of the inferior colliculus; CN, cochlear nucleus; IC, inferior colliculus; LL,
lateral lemniscus; MGN, medial geniculate nucleus; SOC, superior olivary complex. (From Legatt et al., 1988a, with permission.)

Wave II originates, in part, from the first (N1) vol-
ley in the cochlear nerve that has propagated from the
distal nerve to its proximal end and to the cochlear
nucleus. However, the activity at this point in the
auditory pathway occurs simultaneously with the sec-
ond cochlear nerve volley, the N2 component of the
eighth nerve compound action potential, in the distal
nerve (Gersdorff, 1982). The latter contributes to the
scalp-recorded BAEP in the same manner as the N1
component did when it was at the same location. This
can cause persistence of a wave II in cases where the
proximal eighth nerve has been destroyed (Legatt,
2005). With regards to the more proximal generator
of wave II, the relative contribution of activity in
cochlear nerve fibers within the proximal nerve and
of activity in cochlear nucleus neurons has been a sub-
ject of controversy (Legatt et al., 1988a).
Wave III predominantly originates in the caudal
pontine tegmentum, including the region of the supe-
rior olivary complex, though a contribution from
continued activity at the level of the cochlear nucleus
cannot be ruled out (Legatt, 2005). Ascending pro-
jections from the cochlear nucleus are bilateral, so
wave III may receive contributions from brainstem
auditory structures both ipsilateral and contralateral
to the stimulated ear. In patients with asymmetrical
lesions of the brainstem, wave III abnormalities are
usually most pronounced following stimulation of
the ear ipsilateral to the lesion (Brown et al., 1981;
Oh et al., 1981; Faught and Oh, 1985), though occa-
sionally they are more pronounced following contra-
lateral stimulation (Stockard and Rossiter, 1977).
Waves IV and V are often fused into a IV–V com-
plex, and their anatomical generators are most likely
in close anatomical proximity or overlapping, since
they are usually either both affected or both unaf-
fected by brainstem lesions (Starr and Hamilton,
1976; Stockard and Rossiter, 1977; Stockard et al.,
1977). They may, however, be differentially affected
(Stockard and Rossiter, 1977; Legatt et al., 1988a;
Hirsch et al., 1996), including by intraoperative brain-
stem damage (Fig. 8). Wave IV appears to reflect
activity predominantly in ascending auditory fibers
within the dorsal and rostral pons, just caudal to the
inferior colliculus, while wave V predominantly
reflects activity at the level of the inferior colliculus,
perhaps including activity in the rostral portion of
the lateral lemniscus as it terminates in the inferior
colliculus (Legatt, 2005). As is the case with wave
III, wave V abnormalities due to unilateral brainstem
292
lesions are usually most pronounced following stimu-
lation of the ear ipsilateral to the lesion (Brown et al.,
1981; Oh et al., 1981; Faught and Oh, 1985; York,
1986; Scaioli et al., 1988), though there are exceptions
(Zanette et al., 1990; Fischer et al., 1995).
Waves VI and VII are absent in some normal sub-
jects. While they may in part reflect activity in more
rostral structures such as the medial geniculate
nucleus, they also receive contributions from activity
in the inferior colliculus (Legatt, 2005); the latter
generator may cause persistence of these waves in
patients with auditory pathway damage rostral to
the inferior colliculus. Therefore, BAEPs cannot be
used to assess or monitor the auditory pathways ros-
tral to the mesencephalon.
23.5. Interpretation of extraoperative diagnostic
BAEP studies
BAEP component amplitudes vary considerably
across subjects, whereas latencies are highly consis-
tent. Also, waves I, III, and V are identifiable in
almost all normal subjects, whereas the other compo-
nents are more variable. Therefore, the interpretation
of extraoperative diagnostic BAEP studies is based
predominantly on the latencies of waves I, III, and
V (American Clinical Neurophysiology Society,
2006b). Once these peaks have been identified and
their latencies measured, the I–III, III–V, and I–V
interpeak intervals are calculated. The I–V interpeak
interval has been called the central transmission time
(CTT). Asymmetries of component latencies and
interpeak intervals (i.e., the differences in these mea-
sures between left ear and right ear stimulation) are
also calculated. The values in the patient’s study
are compared to those from a control population of
neurologically and audiologically normal subjects,
in whom the BAEPs were recorded using the same
stimulation and recording parameters as those used
for the patient’s study.
Although the individual component amplitudes
are not used as criteria of abnormality, one amplitude
ratio that has proved to be of clinical utility is the IV/
V:I amplitude ratio. The amplitudes of waves I and
the IV/V complex are measured, each with respect
to the most negative point that follows it in the wave-
form (I to IN and IV/V to VN), and their ratio is cal-
culated. An excessively small IV/V:I amplitude ratio
can identify as abnormal some BAEP waveforms in
which all component latencies and interpeak inter-
vals are normal (Fig. 11).
A.D. LEGATT
I II
II
IV-V VII
0.5 µV
1 ms
1.54 3.62 5.36
Fig. 11. BAEPs recorded in a 27-year-old woman with probable
multiple sclerosis. The IV–V/I amplitude ratio is 0.28 (normal is
 0.5); all absolute latencies and interpeak intervals are normal.
The stimulus intensity was 65 dB nHL. (From Legatt, 2005, with
permission.)
23.5.1. Significance of specific BAEP abnormalities
Because wave I originates in the distal portion of the
cochlear nerve, abnormalities (delay or absence) of
wave I usually reflect peripheral auditory dysfunc-
tion, either conductive or cochlear, or pathology
involving the most distal portion of the eighth nerve.
If there is no cochlear nerve volley, the brainstem
auditory pathways will not be activated. Therefore,
a BAEP waveform in which all components, includ-
ing wave I, are absent (Fig. 12E) provides no infor-
mation about the status of the brainstem auditory
pathways.
Cochlear dysfunction may reflect intracranial
pathology because the cochlea receives its blood sup-
ply from the intracranial circulation via the internal
auditory artery. This vessel, which is usually a
branch of the anterior inferior cerebellar artery
(Kim et al., 1990), passes through the internal audi-
tory canal alongside the eighth nerve. Cochlear
ischemia or infarction may result from compression
of the internal auditory artery within the canal or
from occlusion of its parent vessel (Eggermont and
Don, 1986; Ferbert et al., 1988; Legatt et al.,
1988b). Thus, wave I may be delayed or absent in
patients with basilar artery thrombosis or other poste-
rior circulation vascular disease (Stern et al., 1982;
Ferbert et al., 1988; Rao and Libman, 1995;
Yamasoba et al., 2001; Shimbo et al., 2003), acoustic
nerve tumors (Rosenhall, 1981; Raudzens and Shet-
ter, 1982) (Fig. 12D, E), or brain death (Starr,
1976; Goldie et al., 1981; Steinhart and Weiss,
1985; Facco et al., 2002) due to interference with
the blood supply to the cochlea.
METHODOLOGICAL TECHNIQUES OF ASSESSMENT
III V 2005). The latency-intensity curve may normalize fol-
I
2.92 ms 2.00 ms
A A prolonged I–III interpeak interval (Fig. 12A),
V
I either absolutely prolonged (beyond the normal lim-
B 6.78 ms
V between the distal cochlear nerve on the stimulated
C 7.30 ms
I
0.2 µV
D 1.74 ms
1 ms
E the presence of a normal CTT. In contrast, the I–III
Fig. 12. BAEPs recorded in five patients with vestibular schwan-
nomas following stimulation ipsilateral to the tumor, showing var-
ious patterns of BAEP abnormalities that can be caused by these
tumors. The stimulus intensity was increased to 85 dB nHL in all
cases. (A) The I–III interpeak interval is increased. (B) The I–V
interpeak interval is increased; wave III is not clear. (C) Wave V
is delayed; earlier peaks are not clear. (D) Only wave I is present,
and it is delayed. (E) All BAEP components are absent. (From
Legatt, 2005, with permission.)
With mild cochlear ischemia, BAEPs may be nor-
mal to standard, high-intensity stimuli but become
abnormally delayed or absent as the stimulus intensity
is lowered. Examination of latency-intensity curves
may increase the sensitivity of BAEPs for detecting
small vestibular schwannomas (Legatt et al., 1988b).
In these curves, the latency that is plotted as a function
of intensity is that of wave V, since wave I rapidly
becomes attenuated as the stimulus intensity is low-
ered whereas wave V is the last component to disap-
pear; because the I–V interpeak interval is little
affected by changes in stimulus intensity, latency
293
shifts of wave V mirror those of wave I (Legatt,
lowing resection of a small vestibular schwannoma
(Fig. 13), thereby demonstrating the reversibility of
the cochlear ischemia that had been caused by com-
pression of the internal auditory artery by the tumor.
its for this interval) or relatively prolonged (with an
excessive right-left difference) in the presence of a
prolonged CTT (I–V interpeak interval) reflects an
abnormality within the neural auditory pathways
side and the lower pons. Absence of waves III and
V (Fig. 12D) carries the same significance. Rarely,
wave III may be absent despite the presence of a
clear wave V with a normal I–V interpeak interval;
this should not be interpreted as an abnormality.
When the CTT is normal, the interpretation of a
prolonged I–III or III–V interpeak interval is less
clear. Owing to the complexity of the brainstem audi-
tory pathways, the neural activity that generates
wave V may not arise from propagation of the same
neural activity that generates wave III; the III-V
interpeak interval may therefore not actually measure
propagation of neural signals in a brainstem tract.
Thus, it is prudent to refrain from interpreting a pro-
longed III–V interpeak interval as an abnormality in
interpeak interval does reflect propagation of neural
signals from the generator of wave I to the genera-
tor(s) of wave III, since all auditory afferent activity
must pass through the distal cochlear nerve on its
way to the brainstem. Thus, it is logical to interpret
a prolonged I–III interpeak interval as an abnormal-
ity, whether or not the corresponding CTT is also
prolonged (Legatt, 2005).
Abnormality of the I–III interpeak interval is the
characteristic BAEP finding in eighth nerve lesions
such as vestibular schwannomas (Fig. 12), although
there may be a simultaneous peripheral abnormality
(Fig. 12D, E) if the internal auditory artery has been
compromised. Abnormal I–III interpeak intervals can
also result from other processes such as demyelinat-
ing disease, brainstem tumors, or vascular lesions of
the brainstem. In a patient with unilateral eighth
nerve pathology, prolongation of the I–III interpeak
interval will be found on stimulation of the ear on
the side of the lesion. In patients with unilateral
brainstem lesions and unilateral I–III abnormalities
(abnormal BAEPs to stimulation of one ear and
294 A.D. LEGATT

Fig. 13. Left: Latency-intensity curves to left ear (solid line) and right ear (dashed line) stimulation recorded prior to surgery in a 52-year-
old woman with a left-sided intracanalicular vestibular schwannoma. The wave V latency to 70 dB SL (¼ 85 dB nHL) stimulation of the
left ear was normal, but as the stimulus intensity was decreased the latency-intensity curve went outside the normal range (shaded) and then
the BAEPs disappeared (NR ¼ no response). The tumor was completely resected with intraoperative monitoring of BAEPs and facial nerve
function. Right: After the resection, the patient’s latency-intensity curves were normal bilaterally. Her audiogram was normal and her
speech discrimination score in the left ear was 100%. (From Legatt et al., 1988b, with permission.)

normal BAEPs to stimulation of the other), the ear in
which stimulation produces the abnormal BAEP
waveform is most often ipsilateral to the lesion
(Brown et al., 1981; Oh et al., 1981; Faught and
Oh, 1985), but there are rare exceptions (Stockard
and Rossiter, 1977).
Prolongation of both the III–V and I–V interpeak
intervals, or complete absence of the IV/V complex
in the presence of a wave III, reflects dysfunction
within the auditory pathways between the lower pons
and the mesencephalon. As noted above, prolonga-
tion of the III–V interpeak interval is best not inter-
preted as an abnormality if the CTT is normal.
Abnormalities in the III–V interpeak interval are
seen in a variety of disease processes involving the
brainstem, including demyelination, tumor, and vas-
cular disease. If the disease process also involves the
lower pons or eighth nerve, the I–III and the III–V
interpeak intervals may both be prolonged within the
same waveform (Fig. 14). In patients with unilateral

III IV
I V
II

A 1.98 ms 1.98 ms
0.2 µV
I II
III V 1 ms

B 4.04 ms 2.74 ms

Fig. 14. BAEPs to stimulation of each ear in a 35-year-old woman with multiple sclerosis. The I–III and III–V interpeak intervals are both
abnormally prolonged following right ear stimulation (B). BAEPs to left ear stimulation (A) are normal. (From Legatt, 2005, with
permission.)
METHODOLOGICAL TECHNIQUES OF ASSESSMENT
brainstem lesions and unilateral III–V interpeak inter-
val abnormalities, the ear in which stimulation pro-
duces the abnormal BAEP waveform is most often,
although not always, ipsilateral to the lesion (Brown
et al., 1981; Oh et al., 1981; Faught and Oh, 1985;
York, 1986; Scaioli et al., 1988; Zanette et al., 1990).
An abnormally small IV/V:I amplitude ratio
(Fig. 11) reflects dysfunction within the auditory
pathways between the distal cochlear nerve and the
mesencephalon. Because stimulus intensity affects
waves I and V differently, the amplitude ratio should
be measured at the same intensity as was used to
establish the normative data. Decreasing the stimulus
intensity attenuates wave I more than wave V,
increasing the ratio; this may cause an abnormality
to be missed. Conversely, increasing the stimulus
intensity above the normal level could increase wave
I more than wave V and give a false-positive result.
Since wave I is recorded as a near-field negativity
around the stimulated ear, suboptimal placement of
the Ai recording electrode may decrease wave I and
artifactually increase the IV/V:I amplitude ratio. Var-
iations in electrode placement are unlikely to give a
false-positive result because the IV/V complex is
predominantly recorded as a far-field potential, and
small displacements of the Cz recording electrode
will not substantially attenuate the IV/V complex.
Compromise of the brainstem that attenuates
waves IV and V can also impair the function of des-
cending inhibitory pathways within the brainstem,
causing an increase in the amplitude of wave I
(Musiek, 1986; Legatt et al., 1988a). This may
increase the sensitivity of the amplitude ratio mea-
surement because the increase in wave I and the
attenuation of the IV/V complex act synergistically
to reduce the IV/V:I amplitude ratio.
23.5.2. BAEPs in patients with vestibular symptoms
In parts of the vestibular system, such as the eighth
nerve, the neurons carrying auditory information are
in close proximity to those carrying vestibular infor-
mation, and eighth nerve lesions that cause vestibular
symptoms will most likely affect the BAEPs. Within
the brainstem, however, the auditory and vestibular
pathways diverge, and some lesions that cause ves-
tibular symptoms may not involve the auditory sys-
tem structures that generate the BAEPs. Therefore,
in a patient presenting with vestibular symptoms, an
abnormal BAEP study proves that there is dysfunc-
tion within the ear, eighth nerve, or brainstem, and
295
may help to localize that dysfunction, but a normal
BAEP study does not eliminate the possibility of
infratentorial pathology as the cause of the patient’s
symptoms.
There are many papers describing BAEP findings
in specific disease entities that may be associated
with vestibular symptoms, such as vestibular
schwannoma and multiple sclerosis, but the literature
on the yield of BAEPs in the evaluation of patients
who present with vestibular symptoms is sparse.
Ojala et al. (1988) found abnormal BAEPs in 18%
of a group of patients with dizziness; 20 of the 21
patients with abnormal BAEPs had other evidence
of CNS pathology. Welsh et al. (2002) evaluated
BAEPs in a group of 52 patients with vertigo in
whom the neurologic examination, audiometry, elec-
tronystagmography, magnetic resonance imaging of
the brain, and magnetic resonance angiography of
the cervical and cerebral vasculature were all normal
(presbycusis was permitted in the audiogram);
approximately 5% of a large patient cohort who had
presented with vestibular symptoms met these cri-
teria. BAEPs were abnormal in 13 (25%) of this
select group of patients, demonstrating dysfunction
within the infratentorial auditory system that was
presumably related to their vestibular dysfunction
but was not detected by the other diagnostic tests.
Audiograms can be normal in patients with abnormal
BAEPs because BAEPs only assess a part of the
complex brainstem auditory pathways, a subset that
subserves sound localization (Legatt, 2005).
23.6. Intraoperative BAEP monitoring
As previously noted, BAEPs can be used to assess
the auditory pathways up through the level of the
mesencephalon; they are not useful for the IOM of
the auditory pathways rostral to this. They are most
often used to monitor surgery for eighth nerve
tumors such as vestibular schwannomas (formerly
called acoustic neuromas) and for tumors or vascu-
lar abnormalities within the posterior fossa, both
extra-axial and within the brainstem parenchyma.
BAEP monitoring can help to avoid excessive
eighth nerve stretch from cerebellar retraction dur-
ing cerebellopontine angle surgery, which could
cause hearing loss.
Intraoperative monitoring of the electrocochleo-
gram has also been used during cerebellopontine
angle surgery. It may be a useful adjunct when com-
bined with BAEP monitoring, because it requires less
296
averaging (fewer epochs) than the scalp BAEPs and
thus may contribute to more rapid recognition of
cochlear dysfunction; also, it may detect cochlear
dysfunction that does not cause BAEP changes
(Ojemann et al., 1984; Levine et al., 1994; Schlake
et al., 2001). However, the electrocochleogram may
not detect cochlear nerve damage that spares its
distal end, and some patients in whom the electro-
cochleogram is preserved are deaf postoperatively
(Symon et al., 1988). Therefore, electrocochleo-
graphic monitoring by itself is not sufficient for
posterior fossa surgery.
If the structures at risk are the cochlea and the dis-
tal eighth nerve, such as during resection of an intra-
canalicular eighth nerve tumor, near-field recordings
of the compound action potential from an electrode
placed on the proximal eighth nerve (Fig. 5) may
permit monitoring with fewer epochs per average,
providing more rapid feedback to the surgeons. The
near-field recordings do not assess the eighth nerve
proximal to the recording electrode or the brainstem
auditory pathways; if the latter are at risk, then far-
field BAEPs should be monitored.
Near-field recordings of the eighth nerve com-
pound action potential can also be used to distinguish
the cochlear and vestibular divisions of the eighth
nerve during selective vestibular neurectomy, per-
formed for intractable vertigo. Due to volume-
conduction of the evoked potential within the nerve,
this localization is best performed with a bipolar
recording electrode, rather than a single near-field
recording electrode and a distant reference electrode
(Colletti and Fiorino, 1998).
23.6.1. Interpretation of intraoperative BAEP data
Extraoperative diagnostic BAEP tests are evaluated
by comparing the BAEP measurements to normative
data obtained from a control population. In order for
this comparison to be valid, the techniques used and
the state of the subjects in the patient’s study and
the control studies must be identical. This is difficult
to ensure during IOM, where the anesthetic regimen,
the body temperature, the delivered stimulus inten-
sity, and other factors will differ from patient to
patient. Therefore, during intraoperative BAEP moni-
toring each patient serves as his or her own control;
BAEPs recorded at a time when elements of the audi-
tory pathways are at risk are compared to those
recorded earlier during the same operation (Legatt,
1991).
A.D. LEGATT
As noted above, interpretation of extraoperative
diagnostic BAEP studies is predominantly based
on latency criteria because BAEP component
amplitudes vary considerably across subjects.
However, amplitudes on repeated testing in the same
subject are usually quite consistent if the recording
techniques are not altered. Moreover, intraoperative
compromise of neural pathways may cause ampli-
tude changes earlier than, or in the absence of,
latency changes. Therefore, both the amplitudes and
the latencies of the BAEP components are used in
the interpretation of intraoperative BAEPs monitor-
ing data. The amplitudes of the vertex-positive peaks
of waves I, III, and V are measured with respect to
the troughs that follow them. Typical threshold cri-
teria for the identification of an adverse BAEP
change are a 50% decrease in the amplitude of a
component (most often of wave V), or a 1 ms
increase in the absolute latency of wave V or in the
I–V interpeak interval.
23.6.2. Causes of intraoperative BAEP changes
As with any evoked potential, adverse intraoperative
changes in BAEPs can be classified into three cate-
gories: ‘‘true positive’’ changes, which reflect com-
promise of the structures that the monitoring is
intended to safeguard; changes produced by other
physiologic mechanisms such as anesthetic effects
or hypothermia; and changes due to technical pro-
blems (Legatt, 2002). These categories will be con-
sidered separately.
23.6.2.1. Technical problems
BAEPs may be lost due to technical problems such
as equipment malfunction, dislodged recording elec-
trodes, disconnected or broken wires, or operator
error (the use of incorrect protocols or settings).
The acoustic stimulus may be reduced or eliminated
if the plastic tubing through which the acoustic
stimuli reach the ear becomes kinked or dislodged,
or if liquids such as scrub soap, blood, or irrigation
fluid get into the external ear canal. This may mimic
the effects of peripheral auditory dysfunction.
Artifacts can obscure the BAEPs and prevent their
identification and measurement. Automatic artifact
rejection and avoidance of a stimulus repetition rate
that is a submultiple of the line frequency can help
to reduce artifact in the averaged BAEPs. However,
monopolar cautery and cavitational ultrasonic surgi-
cal aspirator (CUSA) devices can block recording
METHODOLOGICAL TECHNIQUES OF ASSESSMENT 297

of BAEPs without triggering automatic artifact rejec-
tion, and may require manual intervention to pause
the average until their effects have cleared (see
Legatt, 1995 for more details). If data epochs without
BAEPs are incorporated into the average, they will
cause an apparent amplitude attenuation of the
BAEPs that mimic auditory system compromise.
23.6.2.2. Physiologic effects
Anesthetic agents in the usual concentrations pro-
duce only minimal changes in BAEP amplitudes
and latencies (Stockard et al., 1992; Legatt, 2002;
Banoub et al., 2003), but BAEPs do change in
response to hypothermia. Both the interpeak intervals
and the latency of wave I progressively increase as
the patient is cooled. Component latencies and inter-
peak intervals increase by about 7% for each 1 C
drop in temperature, and at 26 C are about double
their values at normal body temperatures (Markand
et al., 1987). The latency changes are reversible upon
rewarming, but there is hysteresis — latencies at the
same temperature may differ between the cooling
and rewarming phases (Markand et al., 1990). BAEP
component amplitudes may show an initial increase
as the core temperature is lowered to the 25–30 C
range, but then decrease as the patient is cooled fur-
ther (Kusakari et al., 1984; Markand et al., 1987;
Rodriguez et al., 1995). If the temperature is lowered
enough, the BAEPs may disappear completely; the
longer-latency components usually disappear before
wave I does.
Irrigation with cold fluids can cause localized
hypothermia within the surgical field, producing
BAEP alterations in the absence of tissue damage
(Fig. 15). Irrigation with cold fluids is also undesir-
able during posterior fossa surgery because it can

09:27, 36.6°C, starting operation

10:38, 37.0°C, opening dura

11:02, 37.3°C, retracting cerebellum

11:45, 37.3°C, resecting tumor

13:05, 37.4°C, resecting tumor

13:34, 37.6°C, irrigating

14:03, 37.5°C, irrigating

14:15, 37.3°C, irrigating

14:23, 37.3°C, stopped irrigating

0.25 mV 15:07, 37.4°C, closing

1 ms

Fig. 15. BAEPs to right ear stimulation recorded during surgery for a meningioma in the right cerebellopontine angle. The BAEPs were
stable during cerebellar retraction and tumor resection. After the tumor had been removed, copious irrigation of the surgical field with cold
fluids produced a transient prolongation of the I–III interpeak interval, reflecting slowing of the conduction velocity within the eighth nerve
due to local cooling. The peaks latencies of waves I, III, and V are marked by the small diamonds, and the clock times, esophageal tem-
peratures, and surgical procedures corresponding to each of the BAEP waveforms are noted at the right. (From Legatt, 2002, with
permission.)
298 A.D. LEGATT

produce neurotonic facial EMG discharges resem-

bling those caused by facial nerve injury (Kartush 0.2 mV
I V
and Bouchard, 1992). 2 ms
Drilling of bone, such as the drilling of the roof of
the internal auditory canal during resection of an
eighth nerve tumor, will produce high noise levels in
both ears via bone conduction, and can alter the
BAEPs due to acoustic masking (Levine et al., 1994).
This should be considered when evaluating BAEPs
acquired during drilling of bone. Alternatively, BAEP
averaging can be suspended during drilling.

23.6.2.3. Localized auditory system dysfunction

Auditory system dysfunction and damage can be
caused by mechanical forces such as compression
or traction, by thermal injury from cauterization, or
by ischemia due to compromise of the blood supply
to the tissue. The pattern of BAEP changes that occur
depends on the location of the dysfunction (Legatt,
2002).
Cochlear dysfunction will cause delay and attenu-
ation of wave I (and of the proximal eighth nerve
compound action potential, if this is being moni-
tored). As wave I becomes delayed, the latencies of
later components increase in parallel, with little
change in the interpeak intervals. Cochlear dysfunc-
tion may also decrease the amplitude of wave I to
the point where it is not identifiable, resulting in a
BAEP waveform with a delayed wave V, a delayed
or absent wave III, and an absent wave I. With more
severe cochlear dysfunction, all BAEP components
are lost (Fig. 16).
The cochlea receives its blood supply from the
intracranial circulation via the internal auditory
artery, which is usually a branch of the anterior infe-
rior cerebellar artery and passes through the internal
auditory canal alongside the eighth nerve (Kim
et al., 1990). Nadol et al. (1987) wrote that damage
to this artery probably accounts for most cases of
sudden loss of all BAEP components, including wave
I, during surgery for cerebellopontine angle tumors
(Fig. 16).
Compromise of the cochlear nerve proximal to its
distal (cochlear) end will cause a prolongation of the
I–III interpeak interval (Figs 15, 17), attenuation of
waves III and V, or both. The latencies of waves III
and V increase in parallel, with relatively little
change in the III–V interpeak interval unless the
auditory pathways within the brainstem are also
affected. If the damage is severe enough, waves III
and V will be lost (Fig. 9). Changes such as these
Fig. 16. Consecutive BAEPs to left ear stimulation (earliest wave-
form at the top) recorded in a patient undergoing surgery for a left
vestibular schwannoma. A clear wave I and a poorly-formed wave
V were initially present and were stable during the initial dissec-
tion, but all BAEP components disappeared simultaneously during
dissection within the internal auditory canal and remained absent
through the end of the operation. This was most likely due to inter-
ruption of the blood supply to the cochlea via the internal auditory
artery. (From Legatt, 2002, with permission.)
have been correlated with dissection of cerebellopon-
tine angle tumors off the eighth nerve (Levine et al.,
1984). Wave I may also become delayed or disappear
if there is concurrent cochlear dysfunction due to
compromise of the internal auditory artery. If the
cochlea and the most distal portion of the cochlear
nerve are unaffected, however, wave I may persist,
if even if the eighth nerve is completely transected
(Fig. 9). Wave II could also persist in this situation
due to its contribution from the distal cochlear nerve.
Retraction of the cerebellum to gain access to the
cerebellopontine angle also moves the brainstem
away from the internal auditory meatus and stretches
the eighth nerve, which may cause hearing loss.
Intraoperative BAEP monitoring may serve to notify
the surgeons when the eighth nerve is being stretched
(Fig. 17) and the retraction needs to be reduced or
readjusted (Mller and Jannetta, 1983).
METHODOLOGICAL TECHNIQUES OF ASSESSMENT 299

1.68 4.20 6.06

2.52 1.86

0.2 µ
µV

2 ms

3.54 2.13

1.83 5.37 7.50 ms

Fig. 17. Intraoperative BAEPs to right ear stimulation recorded during surgery for a right vestibular schwannoma, showing two runs
recorded prior to (top) and after (bottom) retraction of the cerebellum. The most prominent change in the BAEPs was an increase in the
I–III interpeak interval of more than 1 msec, reflecting stretching of the eighth nerve. The smaller change in the III–V interpeak interval
may reflect effects of the retraction on the brainstem. (From Legatt, 2002, with permission.)

Complete resection of eighth nerve tumors may
require scraping fragments of tumor off the nerve,
which may cause BAEP changes either due to direct
cochlear nerve damage or to the effects of the trac-
tion on the nerve. At its distal (cochlear) end, the
cochlear nerve breaks up into fine fascicles that enter
the bony modiolus. These fascicles are mechanically
fragile, and may be avulsed if the traction on the
nerve is from the ear towards the brainstem, whereas
traction on the nerve from the brainstem towards the
ear is relatively benign (Sekiya and Mller, 1987).
The hearing loss with excessive cerebellar retraction
and eighth nerve stretching may also reflect distal
cochlear nerve avulsion.
Damage to the lower pons, around the area of the
cochlear nucleus or the superior olivary complex,
will delay waves III and V or cause them both to
be lost; wave I will be preserved if the ear and
cochlear nerve are intact. Damage to the brainstem
that is entirely rostral to the lower pons but at or
below the level of the mesencephalon will affect
wave V, but not waves I or III. Changes in wave
IV tend to parallel those in wave V, though occasion-
ally these components may be differentially affected
(Fig. 8). It should be noted that intraoperative loss of
wave V does not rule out the possibility of preserved
postoperative hearing, even if wave V remains absent
through the end of the operation (Friedman et al.,
1985; Radtke et al., 1989; Levine et al., 1994; Harner
et al., 1996). Neu et al. (1999) suggest that patients
with preserved postoperative hearing despite the loss
of wave V may be at high risk for a delayed postop-
erative hearing loss.
BAEPs assess only part of the brainstem, and may
remain unchanged during surgery that causes brainstem
damage if the damage spares the auditory pathways
(Little et al., 1987). Thus, preservation of BAEPs dur-
ing surgery on the brainstem does not guarantee a good
outcome. However, patients with significant BAEP
changes that persist to the end of the operation almost
always have new postoperative neurologic deficits (Lit-
tle et al., 1983; Manninen et al., 1994).
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