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Auditory Brainstem Response Wave I Prediction
of Conductive Component in Infants and Young
Children
Carol L. Mackersie
David R. Stapells
Albert Einstein College of Medicine, Bronx, NY
City University of New York
Wave I latencies were used to predict the
magnitude of conductive components in 80
infants and young children (122 ears) with
normal hearing, conductive hearing loss due to
otitis media or aural atresia, sensorineural
hearing loss, and mixed hearing loss. Two
prediction methods were used. The first method
based predictions on a 0.03-ms wave I latency
delay for each decibel of conductive hearing
loss. The second method was based on a
regression analysis of wave I latency delays
and the magnitude of conductive component for
A
udiologists involved in the assessment of hearing
in infants and difficult-to-test patients are often
unable to obtain reliable behavioral information
regarding hearing sensitivity. In such instances, auditory
brainstem response (ABR) testing is used to obtain further
information. As in any hearing evaluation, when a hearing
loss is identified through ABR testing, it is important to
estimate the degree of cochlear involvement. In behavioral
testing, this is normally accomplished through boneconduction testing; however, bone-conduction ABR testing
is not routinely done in the clinic.
Latency measures obtained from the ABR to air-conducted stimuli provide a potential source of information not
available from the behavioral air-conduction audiogram.
Latencies increase as stimulus intensity decreases (for
review, see Hall, 1992, pp. 126–133), and conductive hearing
loss reduces the effective intensity arriving at the cochlea.
Consequently, ABR latencies are often prolonged in cases of
conductive hearing loss. It is a commonly held belief that
these ABR latency shifts can be used to predict the extent of
conductive involvement with reasonable accuracy.
The relationship between ABR latency and the magnitude of conductive loss has been examined for both wave I
(Berlin & Gondra, 1976; Chisin, Gafni, & Sohmer, 1983;
Conijn, van der Drift, Brocaar, & van Zanten, 1989;
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July 1994 AJA
the subjects in this study with normal cochlear
status. On average, these prediction methods
resulted in prediction errors of 15 dB or greater
in over one-third of the ears with hearing loss.
Therefore, the clinical use of wave I latencies to
predict the presence or magnitude of conductive impairment is not recommended for infants
and young children. Instead, bone-conduction
ABR testing is recommended as a direct
measure of cochlear status when behavioral
evaluation is not possible.
Eggermont, 1976; Fria & Sabo, 1979; Mendelson, Salamy,
Lenoir, & McKean, 1979; Salomon & Elberling, 1988) and
wave V (Borg, Löfqvist, & Rosén, 1984; Chisin et al.,
1983; Conijn et al., 1989; Fria & Sabo, 1979; McGee &
Clemis, 1982; van der Drift, Brocaar, & van Zenten, 1988;
van der Drift, van Zenten, & Brocaar, 1989; Yamada,
Yagi, Yamane, & Suzuki, 1975). There are at least two
methods that have been used to predict conductive hearing
loss using wave I and wave V latency delays. One method
is based on the horizontal shift from the normal wave I or
V latency-intensity (LI) function. For example, Yamada et
al. (1975) extended a horizontal line from the latency value
at normal threshold (10 dB for their subjects) to the point
of intersection with the subject’s LI function, and then
calculated the difference (in dB) between the normal
threshold and the intensity at the point of intersection. A
second method, using wave I latency, estimates the
magnitude of the conductive component from the latency
delay at a single intensity, where each 0.3-ms delay from
the mean of normal latency values corresponds to 10 dB of
conductive loss (Fria & Sabo, 1979).
Results from these studies have been mixed. Predictions
for ears with known conductive hearing loss have been
reasonably good. For example, van der Drift et al. (1989)
reported that predictions of magnitude of conductive loss
1059-0889/94/0302-0052 © American Speech-Language-Hearing Association
based on wave V latencies were within 16 dB in 95% of
the conductive hearing losses examined. Yamada and
coworkers reported that predictions based on wave V
latencies were within 15 dB in 83% of their cases (Yamada
et al., 1975). McGee and Clemis (1982) reported that
predictions were generally within 10 dB for ears with otitis
media (OM) or artificially induced (i.e., occluded) hearing
loss; however, there was a tendency to overestimate the
magnitude of conductive loss in ears with ossicular chain
disorders.
When studies included subjects with sensorineural or
mixed hearing losses, results were not as favorable. This is
closer to the clinical situation in which the type of hearing
loss would not be known at the time of testing. The data of
van der Drift and his colleagues show overlap between
categories of conductive and cochlear hearing loss for
ABR thresholds of 40 dB nHL and less (van der Drift et
al., 1988). These investigators subsequently reported that
they were unable to differentiate between cochlear and
mixed hearing loss (van der Drift et al., 1989). Chisin et al.
(1983) examined the relationship between wave I and V
latencies and hearing loss in ears with conductive, sensorineural, and mixed losses. Moderate correlations were
reported between the air-bone gap (average at 0.5, 1, and 2
kHz) and waves I and V latencies; however, their best
correlation for this relationship (.59 for mixed losses, using
wave I) accounts for only 35% of the variance. In addition,
these correlation coefficients were not significant for
sensorineural hearing losses using wave I or for mixed
hearing losses using wave V, suggesting that in the
presence of reduced cochlear sensitivity, the relationship
between the magnitude of conductive component and
latency delay is even weaker.
Several studies have compared wave V versus wave I
latencies for prediction of conductive loss (Chisin et al.,
1983; Conijn et al., 1989; Fria & Sabo, 1979). Conijn et al.
(1989) reported that correlations between latency and
conductive loss were similar for waves I and V. In contrast,
Chisin et al. (1983) showed that correlation coefficients
based on wave I latencies were slightly better in the
majority of cases. Fria and Sabo (1979) compared predictions based on wave V latency and wave I latency delays in
school-aged children who had indications or history of
otitis media (OM). The magnitude of conductive impairment was estimated from wave V latencies using the
technique described by Yamada et al. (1975), whereas for
wave I latencies, predictions were based on a 0.3-ms delay
equalling 10 dB of conductive loss. Fria and Sabo (1979)
reported a 20-dB error in prediction for 20% of the cases
using wave I latency delays, and for 10% of the cases using
wave V latency delays.
Waves I and V latency delays have also been used to
predict the presence of otitis media in younger subjects for
whom audiometric information was unavailable. Fria and
Sabo (1979) used waves I and V latency delays to evaluate
the sensitivity for detection of OM in 12 infants and
toddlers ranging in age from 4 to 39 months. Sensitivity
was good for both measures (wave I—82%; wave V—
100%); however, the specificity was much poorer using
wave V latencies (wave I—100%; wave V—25%), with a
tendency for wave V to overpredict the presence of otitis
media. The poor specificity using wave V latencies was
attributed to age-related variability and maturational
changes associated with wave V latency. Mendelson et al.
(1979) also reported that wave I delays were superior to
wave V in predicting the presence of otitis media. Given
the findings of Mendelson et al. (1979) and Fria and Sabo
(1979), it is generally believed that wave I latency is more
appropriate than wave V latency for predictions of conductive loss in infants and young children.
In addition to the disparities between studies described
above, there are still unresolved issues that must be
addressed before applying a predictive technique in a
clinical setting. First, techniques predicting the magnitude
of conductive component would be applied primarily to
infants, yet the studies cited above examined only a few
infants. This was presumably because of the difficulty in
obtaining a measure of cochlear sensitivity in infants, and
thus in estimating the actual conductive component. Those
studies that included infants did not differentiate the results
of infants and older subjects. Second, conductive component predictions need to be accurate for patients with all
types of hearing loss; thus, further study of these predictions is needed in infants with conductive, sensorineural,
and mixed losses.
The purpose of the present study was to extend the work
of Fria and Sabo (1979) to include infants and young
children with otitis media, aural atresia, mixed hearing
loss, and sensorineural hearing loss. The predictions of
conductive component were determined from wave I
latency delays. Wave V latency delays were not considered
in this paper due to the variability associated with
brainstem maturation. Classification of cochlear status in
ears with hearing loss was determined using brainstem
responses to bone-conducted tones (Foxe & Stapells, 1993;
Stapells, 1989; Stapells & Ruben, 1989).
Methods
Subjects
Clinic files were examined for 80 infants and young
children (122 ears) seen for auditory brainstem response
evaluations in the Auditory Evoked Potential Laboratories
of the Albert Einstein College of Medicine. Subjects
ranged in age from 2 weeks to 96 months, with a mean age
of 22 months (standard deviation [SD] = 23 months), and a
median age of 11.5 months. Data were categorized into the
following categories of hearing loss: normal hearing,
conductive hearing loss–otitis media, conductive hearing
loss–atresia, sensorineural hearing loss, and mixed hearing
loss. The primary determinants for group placement were
responses to air- and bone-conducted stimuli. Normal
hearing ears (N = 13) were defined as those in which
auditory brainstem responses were present to air-conducted
2,000-Hz tones or clicks presented at 20 dB nHL (Stapells,
1989; Stapells & Foxe, 1990; Stapells, Gravel, & Martin,
1993; Stapells, Picton, & Durieux-Smith, 1994). Ears with
conductive hearing loss (N = 71) were those in which ABR
thresholds to air-conducted clicks or 2,000-Hz tones were
elevated (i.e., threshold 30 dB nHL or greater) with ABRs
July 1994 AJA
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to bone-conducted 2,000-Hz tones present at the normal
screening intensity of 30 dB nHL. The differences in
normal criteria for air- (20 dB nHL) and bone-conducted
(30 dB nHL) stimuli reflect the differences of normal
infants’ responses to air- and bone-conducted stimuli (Foxe
& Stapells, 1993; Stapells & Ruben, 1989). Ears with
conductive hearing loss were subdivided into otitis media
(N = 55) and atresia (N = 16) categories according to
etiology. Ears with sensorineural hearing loss (N = 35)
were those in which ABR thresholds for air- and boneconducted stimuli were both elevated, and bone-conduction thresholds were not more than 10 dB better than airconduction thresholds. Ears with mixed hearing loss (N =
3) were those in which ABR thresholds for air- and boneconducted stimuli were both elevated, and the boneconduction thresholds were more than 10 dB better than
the air-conduction thresholds.
In nine ears, bone-conduction ABR results were not
available, and behavioral results were used to categorize
the type of loss. In three of these ears, behavioral thresholds were used because ABR threshold information (air- or
bone-conducted) was not available. There was a total of 28
ears for which both ABR and behavioral results were
available, and behavioral thresholds confirmed the degree
and category of hearing loss for all of these ears. In total,
there was behavioral confirmation of hearing loss category
and threshold for 37 ears. In the remaining 85 ears,
behavioral audiometric results were inconclusive due to the
developmental status of the child.
ABR Recordings
Two-channel recordings were obtained using gold-plated
cup electrodes placed at the vertex (noninverting) and on
each mastoid (inverting). A fourth electrode placed on the
forehead served as ground. Interelectrode impedances were
3,000 Ω or less. The EEG was amplified and filtered (30–
3,000 Hz, 12 dB/octave). Trials containing amplitudes
exceeding ±25 µV were automatically rejected. The EEG
was monitored on an oscilloscope throughout the test session,
and testing proceeded only when subjects were asleep.
Subjects aged less than 6 months were tested in natural sleep,
and those aged 6 months and older were tested under chloral
hydrate sedation prescribed by a physician.
Responses were recorded to high-intensity rarefaction
clicks presented at a rate of either 19.1 (81% of ears) or
61.1 per second. An intensity of 80 dB nHL was used for
the majority of subjects; however, intensities up to 100 dB
nHL were used when necessary in order to obtain a clear
and replicable wave I.
Responses to air-conducted clicks or 2,000-Hz tones
were recorded at lower intensities either to establish
normal hearing or to determine ABR thresholds. Threshold
searches (10-dB steps) for air-conducted stimuli were
conducted only for those ears not exhibiting responses at
the normal air-conduction intensity of 20 dB nHL. Thresholds to 61.1 per second rarefaction clicks were obtained for
eight ears. For the remaining 111 ears with ABR thresholds, 2,000-Hz (“2-1-2 cycle”) tones were presented at a
rate of 39.1 per second (Stapells, 1989; Stapells & Foxe,
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July 1994 AJA
1990; Stapells et al., 1994). The use of different stimuli
reflects a change in clinic protocols over the course of the
data collection period.
Brainstem responses to bone-conducted 2,000-Hz tones
were recorded either to determine bone-conduction ABR
thresholds or to establish normal cochlear sensitivity.
Stimuli were presented through a Radioear B70A oscillator
placed on the temporal bone in a superoposterior auricular
position and held in place with 350–450 grams of force.
Threshold searches (10-dB steps) for bone-conducted
stimuli were conducted only for ears with both elevated
air-conduction thresholds and no response at the normal
bone-conduction intensity of 30 dB nHL. The 30 dB nHL
criterion for normal was used because all normal infants in
previous studies showed responses at this intensity (Foxe
& Stapells, 1993; Stapells & Ruben, 1989). Whenever
masking was not used during bone-conduction ABR
testing, ipsilateral/contralateral response asymmetries were
used to determine ear-specific responses. Further details of
our bone-conduction stimuli and technique for ABR testing
are given in our recent papers (Foxe & Stapells, 1993;
Nousak & Stapells, 1992; Stapells, 1989; Stapells &
Ruben, 1989).
Testing was performed in a double-walled soundattenuating room (IAC). A minimum of two replications of
2,000 trials each was obtained for each condition. Additional replications were obtained when necessary to
confirm the presence of the response.
Tympanometry was performed on 92% of the ears (97/
106, excluding the 16 atretic ears), with a 220-Hz probe
tone used for subjects 6 months of age and older and a 660Hz probe tone for subjects aged less than 6 months
(ASHA, 1991; Marchant et al., 1986). Ipsilateral acoustic
reflex testing was conducted whenever possible. In 95% of
these ears, tympanometric findings were consistent with
the hearing loss category, as were the physical findings for
all 16 atretic ears.
Data Analysis
Wave I latency was measured for each subject’s data.
Latency delays were calculated using the laboratories’
normative database, which was obtained from a larger
group of normal subjects who are not included in this
study. Latency delay was calculated by subtracting from
each subject’s wave I latency the mean of the normative
data for a given rate/intensity combination.
The magnitude of the conductive component was
determined for each ear. Because bone-conduction
threshold searches were not carried out for ears with
conductive hearing loss, bone-conduction results were not
used for the determination of the magnitude of conductive
components. The exception to this was the mixed hearing
loss group that included only three ears. For the conductive
hearing loss categories (otitis media and atresia), the
conductive component was calculated as the air-conduction
threshold minus 10 dB, as ABR thresholds tend to overestimate the behavioral thresholds by approximately 10 dB
(e.g., Elberling & Don, 1987; Kodera, Yamane, Yamada,
& Suzuki, 1977; Picton, Stapells, & Campbell, 1981;
Suzuki, Kodera, & Yamada, 1984; Yamada et al., 1975).
For the group with mixed hearing loss only, the difference
between the air-conduction and bone-conduction ABR
thresholds was used to estimate the magnitude of the
conductive component. A conductive component of 0 dB
was used for ears in the normal hearing and sensorineural
hearing loss categories.
Linear regression analyses were carried out on the
combined data for normal ears and those with conductive
hearing loss, using wave I latency delay and the conductive
component as the variables. The conductive component
was then predicted for individual subjects using two
methods. First, using the method proposed by Fria and
Sabo (1979), the conductive component was derived by
dividing the wave I latency delay by 0.03 ms (based on
0.3-ms latency delay per 10 dB of conductive hearing
loss). Second, the conductive component was predicted
using the regression equation from our data analysis.
Results
ABR air-conduction thresholds and corresponding wave
I latency delays are plotted in Figure 1. Each point represents one ear. Average and standard deviation ABR
thresholds were 43.5 ± 12.2 dB nHL for the ears with otitis
media, 63.1 ± 10.1 dB nHL for the ears with atresia, 66.7 ±
15.3 dB nHL for the ears with mixed loss, and 50.4 ± 18.7
dB nHL for those with sensorineural hearing loss. All ears
in the normal group had clear responses at 20 dB nHL and,
therefore, thresholds less than or equal to this intensity.
The average wave I latency delay for the normal-hearing
group is 0.06 ms (SD = 0.2 ms), indicating no overall
difference from our larger normative database. There is an
overall trend for wave I latency to increase with increasing
hearing loss; however, the range of latency delay is quite
large for any specific threshold level. This is true even
FIGURE 1. Wave I latency delay from the mean of the normative data as a function of air-conduction threshold for normal
hearing, otitis media, atresia, mixed, and sensorineural
hearing loss. The number of ears in each group is shown in
parentheses. Shown are ABR thresholds to 2,000-Hz brief
tones (111 ears), ABR thresholds to clicks (8 ears), and
behavioral thresholds to 2,000-Hz pure tones (3 ears).
within specific hearing loss groups. Ears with sensorineural
loss (open squares) tend to show smaller wave I delays;
however, there are several with large delays. Of importance, there is considerable overlap of data between groups
for a given magnitude of latency delay or for a given
threshold. Note, for example, the overlap between latency
delay for otitis media and sensorineural hearing loss for a
40 or 60 dB nHL threshold. Finally, the range of the
normal ears’ latency delays overlaps that of conductive
hearing losses having thresholds as great as 70 dB nHL.
All except one of the normal ears showed wave I
latencies within our clinical norms (i.e., ±2.5 SD of the
mean). The one exception showed a prolonged wave I
latency of 1.98 ms (0.44 ms delay). Despite this delayed
latency, this 7-month-old infant showed clear responses to
2,000-Hz air-conducted tones at 20 dB nHL, with normal
wave V latencies. The response to 80 dB nHL clicks (19.1
per second) showed normal waves III and V latencies.
Further, acoustic immittance results were consistent with
tympanic membrane mobility.
The linear regression carried out on the data for the
normal ears and ears with conductive hearing loss resulted
in the equation
Y = 14.32026 + 25.67061 * X
where X is the wave I latency delay (in ms), and Y is the
magnitude of the conductive component (in dB). Although
statistically significant, the correlation coefficient for these
data indicates that the equation accounts for only 45% of
the variance (r = .67, df = 82, p < .001).
The magnitude of error in prediction (in dB) for each
ear with hearing loss was determined using the prediction
formula (0.03 ms/dB of conductive component) employed
by Fria and Sabo (1979) and the resulting regression
equation shown above. These results are shown in Table 1.
Error was calculated using the conductive component
minus the predicted conductive component. Negative
numbers indicate that the prediction overpredicted the
magnitude of the conductive component; positive numbers
indicate underpredictions.
Wave I latency delays predicted conductive components
in some normal ears because of the range of latencies
observed in subjects with normal hearing. As shown in Table
1, the range of prediction “errors” (i.e., anything other than
0 dB) in normals is large, spanning a 22-dB range using the
0.03 ms/dB equation. The regression equation resulted in
an average overprediction of 16 dB in the normal group,
largely due to the 14.3-dB constant in the equation.
For all hearing loss, the average predicted conductive
component was within 5 dB of the measured conductive
component for both prediction methods, however, the
range of errors was greater than 80 dB for both techniques.
The worst predictions were found in ears with sensorineural components. This is because these prediction methods
do not take into account wave I latency delays produced by
cochlear hearing loss.
Figure 2 shows, for each group and prediction method,
the percentage of ears in which the prediction error (i.e.,
the absolute value of the error) is equal to or exceeds 10,
15, 20, and 30 dB. Overall, the error in prediction for all
July 1994 AJA
55
TABLE 1. Prediction error in dB (conductive component minus predicted conductive component) for the two equations.
NORMAL
ALL HL
OM
ATRESIA
SNHL
MIXED
13
109
55
16
35
3
-2.07
-1.00
6.42
-15 to 7
4.61
2.00
15.99
-29 to 58
11.35
12.00
15.69
-19 to 58
10.56
15.00
12.32
-12 to 34
-7.71
-5.00
9.80
-29 to 10
-6.77
-6.33
3.02
-10 to -4
Prediction:
Y=14.32026 + 25.67061 * X
Mean
-16.00
Median
-15.00
Standard deviation
5.00
Range
-26 to 17
-5.04
-8.00
15.91
-37 to 46
2.00
2.00
13.89
-25 to 46
5.88
9.50
11.25
-15 to 28
-20.29
-18.00
7.61
-37 to 7
14.33
15.00
3.06
-11 to -17
N
Prediction:
Y = X / 0.03
Mean
Median
Standard deviation
Range
Y = conductive component (dB)
X = wave I latency delay from normal (ms)
hearing losses was 15 dB or greater in 35% and 39% of the
ears for predictions determined using the 0.03 ms/dB
equation and regression equation, respectively. The
regression equation provided the best predictions of
conductive component for ears with conductive hearing
loss, but resulted in large errors in ears with sensorineural
components. In contrast, the 0.03 ms/dB equation resulted
in the smallest errors in prediction for the ears with
sensorineural hearing loss, with the largest prediction
errors for the conductive groups.
Discussion
The results of this study suggest that, at best, wave I
latency delay accurately predicts (i.e., less than 15 dB
FIGURE 2. Percentage of all impaired ears and for each
hearing loss group in which the error in prediction (conductive component minus predicted conductive component) was
≥10, ≥15, ≥20, and ≥30 dB.
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July 1994 AJA
error) the magnitude of conductive involvement in only
61% to 65% of hearing losses. Thus, in approximately one
out of three cases, clinicians attempting to estimate the
magnitude of conductive component using wave I latency
delays are likely to err in their prediction by at least 15 dB.
In one out of every 12 patients, this error will be 30 dB or
greater.
Predictions were better for some categories of hearing
loss than others. Predictions were within 15 dB in 76% of
the ears with otitis media using the regression equation,
which is only slightly poorer than the 80% predictive
accuracy reported by Fria and Sabo (1979) for their 10
school-aged subjects. However, using the 0.03 ms/dB
equation recommended by Fria and Sabo (1979), only 55%
of the ears with otitis media in the present study were
within 15 dB.
Prediction of conductive components from airconduction ABR latency delays has several disadvantages.
First, the range of wave I latencies in normal ears is large
(1.41 to 1.98 ms for the 13 subjects with normal hearing in
this study), resulting in considerable overlap with some of
the hearing loss groups. Thus, as Eggermont has noted, the
minimum amount of conductive impairment that can be
detected is about 20 dB, and the inaccuracy of predictions
for conductive losses exceeding this amount is also about
20 dB (due to the 20-dB range in latencies seen for normal
subjects) (Eggermont, 1982, 1983). Second, differentiation
between conductive, sensorineural, and mixed hearing
losses is complicated by the fact that wave I and V
latencies are often prolonged in cases of cochlear hearing
losses (e.g., Coats, 1978; Eggermont, 1982; Elberling,
1981). Wave V latencies are also often prolonged in
retrocochlear hearing losses (for review, see Hall, 1992).
Predictions based on wave I latency, however, have the
advantage of not being influenced by post-term maturational changes (Schwartz, Pratt, & Schwartz, 1989) and
infrequently by retrocochlear pathology (Eggermont,
1976). However, wave I is frequently absent in ears with
hearing loss (Hall, 1992, p. 389; Picton & Durieux-Smith,
1988).
Predictions from previous studies that restricted
analyses to subjects with known conductive hearing loss
have been reasonably good. When evaluating infants in a
clinical situation, however, one rarely knows the type of
hearing loss prior to evaluation. In the case of an infant
with otitis media, one may be tempted to rely on a combination of tympanometry and latency-based predictions to
arrive at a diagnosis of conductive hearing loss. The danger
of this approach is illustrated in the following example.
One 6-month-old subject in this study presented with a flat
tympanogram and elevated ABR air-conduction threshold
(40 dB nHL). Based on a wave I latency delay of 0.82 ms,
both equations would have predicted that the hearing loss
was conductive, however a bone-conduction ABR threshold of 50 dB nHL was obtained, indicating a sensorineural
hearing loss. Relying on the acoustic immittance results
and air-conduction ABR predictions rather than a direct
measure of cochlear sensitivity would have resulted in a
misdiagnosis of the nature of the child’s hearing loss. This
example underscores the importance of obtaining a direct
measure of cochlear sensitivity by obtaining responses to
bone-conducted stimuli. Otitis media often coexists with
sensorineural hearing loss and does not always result in
substantial air-bone gaps. Sensorineural hearing loss often
results in prolonged latencies, further complicating these
predictions.
Neither of the prediction methods accurately estimated
the conductive components for all types of hearing loss.
The regression equation gave better predictions for ears
with conductive hearing loss, but showed large errors in
ears with sensorineural components. The opposite pattern
was found using the 0.03 ms/dB equation.
Because of the use of bone-conduction stimuli, the
cochlear status of all the infants and children with impaired
hearing in the present study was known, allowing for
determination of appropriate therapeutic intervention.
Further, armed with the bone-conduction information, it
was possible to provide parents with more definitive
information regarding their child’s hearing loss and
recommended course of intervention.
Although not yet widely used by clinicians, there are
very few difficulties in recording the ABR to boneconducted stimuli. Care must be taken to ensure that the
oscillator is adequately placed and the applied force is
appropriate (Stuart, Yang, & Stenstrom, 1990; Yang &
Stuart, 1990; Yang, Stuart, Stenstrom, & Hollett, 1991).
There appear to be maturational differences in responsivity
to bone-conducted stimuli such that these stimuli may be
effectively more intense for neonates and young infants
(Foxe & Stapells, 1993; Nousak & Stapells, 1992; Yang,
Rupert, & Moushegian, 1987). Normal response levels are
thus determined from infant response detectability rather
than adult normal hearing levels (Stapells & Ruben, 1989).
Masking of the contralateral ear during bone-conduction
ABR testing may not be as critical as in adults because
there appears to be greater interaural attenuation of boneconducted stimuli in infants (Yang et al., 1987). Further,
large ipsilateral/contralateral ABR asymmetries observed
in infants may be used to determine the ear of response
origin (Foxe & Stapells, 1993; Jahrsdoerfer, Yeakley, Hall,
Robbins, & Gray, 1985; Stapells & Ruben, 1989). It should
be noted that studies are in progress concerning the ABR to
BC stimuli. In addition to the 28 ears in this study with
both BC ABR and reliable behavioral audiograms, further
studies of subjects with known audiograms are required to
confirm the accuracy of the ABR to BC stimuli.
Recent studies (Foxe & Stapells, 1993; Gorga,
Kaminski, Beauchaine, & Bergman, 1993; Kramer, 1992;
Nousak & Stapells, 1992; Stapells & Ruben, 1989; Stuart
et al., 1990; Yang & Stuart, 1990; Yang, Stuart, Mencher,
Mencher, & Vincer, 1993; Yang et al., 1991) as well as
current ASHA guidelines support the clinical use of
auditory brainstem responses to bone-conducted stimuli.
Specifically, the ASHA guidelines recommend that when
“air-conducted ABR is elevated, an ABR to boneconducted stimuli should be considered” (ASHA, 1991).
Although they recommend the inclusion of acoustic
immittance testing as part of each evaluation, these
guidelines caution that acoustic immittance data alone are
not sufficient for middle-ear assessment (ASHA, 1991).
The results of the present study do not support the use
of wave I latency-based predictions of conductive component for individual patients. Rather, as is the standard for
behavioral audiometry, direct measures of cochlear
sensitivity should be obtained by recording the ABR to
bone-conducted stimuli.
Acknowledgments
This work was supported by USPHS NIDCD Clinical Center
Grant No. 8 P50 DC00223, and by NICHD Mental Retardation
Research Center Grant HD01799.
References
American Speech-Language-Hearing Association. (1991).
Guidelines for the audiologic assessment of children from
birth through 36 months of age. Asha, 33(Supplement 5), 37–
43.
Berlin, C. I., & Gondra, M. I. (1976). Extratympanic clinical
electrocochleography with clicks. In R. J. Ruben, C. Elberling,
& G. Salomon (Eds.), Electrocochleography (pp. 457–469).
Baltimore: University Park Press.
Borg, E., Löfqvist, L., & Rosén, S. (1984). Evaluation of pure
tone audiograms in brainstem audiometry of patients with
conductive loss. In A. Starr, C. Rosenberg, M. Don, & H.
Davis (Eds.), Sensory evoked potentials 1. An international
conference on standards for auditory brainstem response
(ABR) testing (pp. 105–109). Milan: CRS Amplifon.
Chisin, R., Gafni, M., & Sohmer, H. (1983). Patterns of
auditory nerve and brainstem-evoked responses (ABR) in
different types of peripheral hearing loss. Archives of
Otorhinolaryngology, 237, 165–173.
Coats, A. C. (1978). Human auditory nerve action potentials and
brain stem evoked responses. Latency-intensity functions in
detection of cochlear and retrocochlear abnormality. Archives
of Otolaryngology, 104, 709–717.
Conijn, E. A. J. G., van der Drift, J. F. C., Brocaar, M. P., &
van Zanten, G. A. (1989). Conductive hearing loss assessment in children with otitis media with effusion. A compariJuly 1994 AJA
57
son of pure tone and BERA results. Clinics in Otolaryngology,
14, 115–120.
Eggermont, J. J. (1976). Electrocochleography. In W. D. Keidel
& W. D. Neff (Eds.), Handbook of Sensory Physiology 5(3).
(pp. 625–704). New York: Springer-Verlag.
Eggermont, J. J. (1982). The inadequacy of click-evoked
auditory brainstem responses in audiological applications.
Annals of the New York Academy of Sciences, 388, 707–709.
Eggermont, J. J. (1983). Audiologic disorders. In E. J. Moore
(Eds.), Bases of auditory brain-stem responses (pp. 287–315).
New York: Grune & Stratton.
Elberling, C. (1981). Analysis and interpretation of auditory
brainstem responses in man. Sensus, 1, 89–101.
Elberling, C., & Don, M. (1987). Threshold characteristics of
the human auditory brain stem response. Journal of the
Acoustical Society of America, 81, 115–121.
Foxe, J. J., & Stapells, D. R. (1993). Normal infant and adult
auditory brainstem responses to bone-conducted tones.
Audiology, 32, 95–109.
Fria, T. J., & Sabo, D. L. (1979). Auditory brainstem responses
in children with otitis media with effusion. Annals of Otology,
Rhinology, and Laryngology, 89, 200–206.
Gorga, M. P., Kaminski, J. R., Beauchaine, K. L., &
Bergman, B. M. (1993). A comparison of ABR thresholds
and latencies elicited by air and bone conducted stimuli. Ear
and Hearing, 14, 85–94.
Hall, J. W. III. (1992). Handbook of auditory evoked responses.
Needham, MA: Allyn and Bacon.
Jahrsdoerfer, R. A., Yeakley, J. W., Hall, J. W., Robbins, K.
T., & Gray, L. C. (1985). High resolution CT scanning and
auditory brain stem response in congenital aural atresia:
Patient selection and surgical correlation. Otolaryngology,
Head and Neck Surgery, 83, 292–298.
Kodera, K., Yamane, H., Yamada, O., & Suzuki, J. (1977).
Brainstem response audiometry at speech frequencies.
Audiology, 16, 469–479.
Kramer, S. J. (1992). Frequency specific auditory brainstem
responses to bone-conducted stimuli. Audiology, 31, 61–71.
Marchant, C. D., McMillan, P. M., Shurin, P. A., Johnson, C.
E., Turczyk, V. A., Feinstein, J. C., & Panek, D. M. (1986).
Objective diagnosis of otitis media in early infancy by
tympanometry and ipsilateral acoustic reflex thresholds. The
Journal of Pediatrics, 109, 590–595.
McGee, T. J., & Clemis, J. D. (1982). Effects of conductive
hearing loss on auditory brainstem response. Annals of
Otology, Rhinology and Laryngology, 91, 304–309.
Mendelson, T., Salamy, A., Lenoir, M., & McKean, C. (1979).
Brain stem evoked potential findings in children with otitis
media. Archives of Otolaryngology, 105, 17–20.
Nousak, J-M. K., & Stapells, D. R. (1992). Frequency specificity of the auditory brain stem response to bone-conducted
tones in infants and adults. Ear and Hearing, 13, 87–95.
Picton, T. W., & Durieux-Smith, A. (1988). Auditory evoked
potentials in the assessment of hearing. Neurologic Clinics, 6,
791–808.
Picton, T. W., Stapells, D. R., & Campbell, K. B. (1981).
Auditory evoked potentials from the human cochlea and
brainstem. Journal of Otolaryngology, 10(Supplement 9), 1–41.
Salomon, G., & Elberling, C. (1988). Estimation of inner ear
function and conductive hearing loss based on
electrocochleography. Advances in Audiology, 5, 46–55.
Schwartz, D. M., Pratt, R. E. Jr., & Schwartz, J. A. (1989).
Auditory brainstem responses in preterm infants: Evidence of
peripheral maturity. Ear and Hearing, 10, 14–22.
Stapells, D. R. (1989). Auditory brainstem response assessment
58
July 1994 AJA
of infants and children. Seminars in Hearing, 10, 229–251.
Stapells, D. R., & Foxe, J. (1990). Frequency-specific ABRs in
infants: Normative results. Asha, 32, 176.
Stapells, D. R., Gravel, J. S., & Martin, B. (1993). ABR
thresholds to tones in notched noise obtained from infants and
young children with sensorineural hearing loss. Abstracts of
the Association for Research in Otolaryngology Midwinter
Meeting, 16, 59.
Stapells, D. R., Picton, T. W., & Durieux-Smith, A. (1994).
Electrophysiologic measures of frequency-specific auditory
function. In J. T. Jacobson (Ed.), Principles and applications
in auditory evoked potentials (pp. 251–283). Needham Hill,
MA: Allyn and Bacon.
Stapells, D. R., & Ruben, R. J. (1989). Auditory brainstem
responses to bone-conducted tones in infants. Annals of
Otology, Rhinology and Laryngology, 98, 941–949.
Stuart, A., Yang, E. Y., & Stenstrom, R. (1990). Effect of
temporal area bone vibrator placement on auditory brain stem
response in newborn infants. Ear and Hearing, 11, 363–369.
Suzuki, J. I., Kodera, K., & Yamada, O. (1984). Brainstem
response audiometry in newborns and hearing impaired
infants. In A. Starr, C. Rosenberg, M. Don, & H. Davis (Eds.),
Sensory evoked potentials 1. An international conference on
standards for auditory brainstem response (ABR) testing
(pp. 85–93). Milan: CRS Amplifon.
Van der Drift, J. F. C., Brocaar, M. P., & van Zanten, G. A.
(1988). Brainstem response audiometry I. Its use in distinguishing between conductive and cochlear hearing loss.
Audiology, 27, 260–270.
Van der Drift, J. F. C., van Zanten, G. A., & Brocaar, M. P.
(1989). Brainstem electric response audiometry: Estimation of
the amount of conductive hearing loss with and without use of
the response threshold. Audiology, 28, 181–193.
Yamada, O., Yagi, T., Yamane, H., & Suzuki, J-I. (1975).
Clinical evaluation of the auditory evoked brain stem
response. Aurix-Nasus-Larynx, 2, 97–105.
Yang, E. Y., Rupert, A. L., & Moushegian, G. (1987). A
developmental study of bone conduction auditory brain stem
response in infants. Ear and Hearing, 8, 244–251.
Yang, E. Y., & Stuart, A. (1990). A method of auditory
brainstem response testing of infants using bone-conducted
clicks. Journal of Speech Language Pathology and Audiology,
14, 69–76.
Yang, E. Y., Stuart, A., Mencher, G. T., Mencher, L. S., &
Vincer, M. J. (1993). Auditory brain stem responses to air
and bone conducted clicks in the audiological assessment of
at-risk infants. Ear and Hearing, 14, 175–182.
Yang, E. Y., Stuart, A., Stenstrom, M. A., & Hollett, S. (1991).
Effect of vibrator to head coupling force on the auditory brain
stem response to bone-conducted clicks in newborn infants.
Ear and Hearing, 12, 55–60.
Received March 22, 1993
Accepted December 15, 1993
Contact author: David R. Stapells, PhD, Albert Einstein College
of Medicine, Rose F. Kennedy Center, Rm. 817, 1410 Pelham
Parkway, Bronx, NY 10461
Key Words: wave I latency, conductive impairment,
auditory brainstem response, hearing loss, infants and
children