The Effects of High-Frequency Hearing
Loss on Low-Frequency Components of the
Click-Evoked Otoacoustic Emission
Owen D. Murnane*†
John K. Kelly*
Abstract
Click-evoked otoacoustic emission (CEOAE) input/output (I/O) functions were
measured in ears with normal hearing and in ears with sensorineural hearing
loss above 2000 Hz. The low- to midfrequency CEOAEs obtained from the
ears with high-frequency hearing loss were significantly reduced in level compared to the CEOAEs obtained from the ears with normal hearing even though
there were no significant group differences in the 250–2000 Hz pure-tone
thresholds. The findings are discussed within the context of two hypotheses
that explain the low- to midfrequency reduction in transient-evoked otoacoustic
emission (TEOAE) magnitude: (1) subclinical damage to the more apical
regions of the cochlea not detected by behavioral audiometry, or (2) trauma
to the basal region of the cochlea that affects the generation of low-frequency
emissions. It is proposed that localized damage at basal cochlear sites affects
the generation of low- to midfrequency CEOAE energy.
Key Words: Click-evoked otoacoustic emission, high-frequency hearing loss,
transient-evoked otoacoustic emission
Abbreviations: CEOAE = click-evoked otoacoustic emission; EOAE = evoked
otoacoustic emission; I/O = input/output; OHCs = outer hair cells; TBOAE =
tone-burst-evoked otoacoustic emission; TEOAE = transient-evoked otoacoustic emission; SSOAE = synchronized spontaneous otoacoustic emission
Sumario
Se midieron las funciones de input/output (I/O) para emisiones otoacústicas
evocadas por clicks (CEOAE) en oídos con audición normal y en oídos con
hipoacusias sensorineurales por encima de los 2000 Hz. Las CEOAE de baja
a media frecuencia obtenidas a partir de los oídos con hipoacusia de alta frecuencia fueron significativamente reducidas en su nivel, comparadas con las
CEOAE obtenidas de los oídos con audición normal, aunque no existieron
diferencias significativas de grupo en los umbrales tonales de 250-2000 Hz.
Los hallazgos se discuten dentro del contexto de dos hipótesis que explican
la reducción en las frecuencias bajas a medias, en emisiones en la magnitud de las otoacústicas evocadas por transitorios (TEOAE): (1) daño sub-clínico
a las regiones más apicales de la cóclea, no detectadas por la audiometría
conductual, o (2) trauma a la región basal de la cóclea que afecta la generación de emisiones de baja frecuencia. Se propone que el daño localizado
a los sitios basales de la cóclea afecta la generación de la energía de las
CEOAE de baja a media frecuencia.
*James H. Quillen VA Medical Center, Mountain Home, Tennessee; †Departments of Surgery and Communicative Disorders,
East Tennessee State University, Johnson City, Tennessee
Reprint requests: Owen D. Murnane, Audiology (126), James H. Quillen VA Medical Center, Mountain Home, TN 37684;
Phone: 423-979-3653; Fax: 423-979-3403; E-mail: owen.murnane@med.va.gov
Portions of this paper were presented at the annual meeting of the Association for Research in Otolaryngology, St. Petersburg
Beach, FL, February, 2000.
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Journal of the American Academy of Audiology/Volume 14, Number 9, 2003
Palabras Clave: Emisión otoacústica evocada por clicks, hipoacusia de alta
frecuencia, emisión otoacústica evocada por transitorios
Abreviaturas: CEOAE = emisión otoacústica evocada por clicks; EOAE = emisión
otoacústica evocada; I/O = input/output; OHC = células ciliadas externas; TBOAE
= emisión otoacústica evocada por burst tonal; TEOAE = emisión otoacústica
evocada por transitorios; SSOAE = emisión otocústica espontánea sincronizada.
E
voked otoacoustic emissions (EOAEs),
first detected by Kemp (1978), are
low-level sounds generated within the
cochlea in response to auditory stimuli that
travel from the inner ear laterally through the
middle ear into the ear canal where they can
be recorded by a miniature microphone. It is
generally accepted that the cochlear outer
hair cells (OHCs) are an integral component
in the production of EOAEs as OHCs and
EOAEs share a similar physiological
vulnerability to ototoxicity (Brown et al,
1989), noise exposure (Anderson and Kemp,
1979), hypoxia (Rebillard and LevigneRebillard, 1992), and genetic disorders
(Horner et al, 1985). EOAEs, therefore, are
associated with the same cochlear processes
as those responsible for normal-hearing
sensitivity and frequency selectivity. Although
the clinical utility of EOAEs in the
identification of hearing loss has been
established (Kemp et al, 1990; Gorga et al,
1993, 1996, 1997, 1999; Prieve et al, 1993;
Hurley and Musiek, 1994; Kimberley et al,
1994; Glattke et al, 1995; Stover et al, 1996;
Hussain et al, 1998; Vinck et al, 1998; Dorn
et al, 1999; Harrison and Norton, 1999), some
issues concerning the processes involved in
the generation of EOAEs remain unclear.
One of these issues is related to the frequency
specificity of transient-evoked otoacoustic
emissions (TEOAEs) and the notion that
TEOAEs are generated by independent
frequency channels (Probst et al, 1986; Xu et
al, 1994; Prieve et al, 1996).
TEOAEs are typically elicited by click
stimuli (CEOAEs). Clicks have broadband
amplitude spectra that stimulate a wide
region of the basilar membrane and produce
an emission with a similarly broad amplitude
spectrum. TEOAEs also can be evoked by
tone bursts (TBOAEs) that have a narrower
bandwidth and contain energy predominantly
around the nominal frequency. The amplitude
526
spectrum of the TBOAE generally contains
energy that corresponds to the stimulus
spectrum (Elberling et al, 1985; Probst et al,
1986; Norton and Neely, 1987). When
measured in the same ear, Probst and
colleagues (1986) observed that the amplitude
spectrum of summed TBOAEs was similar to
the amplitude spectrum of the CEOAE. In a
similar study, Xu et al (1994) measured
TEOAEs obtained with individual tone bursts
at 1000, 2000, and 3000 Hz and for a complex
stimulus that consisted of a digital addition
of the three single tone-burst stimuli. When
the responses to the individual tone bursts
were combined and compared with the
response to the tone-burst complex, the
amplitude spectra were similar. The apparent
linear correspondence between stimulus and
response spectra observed in these studies
lends support to the notion that TEOAEs
are evoked by a number of independent
generators that are distributed along the
cochlear partition.
The above hypothesis also has been
tested using subjects with high-frequency
hearing loss and normal low- to midfrequency
thresholds. If TEOAE frequency channels
are independent, then the low- to
midfrequency TEOAEs obtained from
subjects with high-frequency hearing loss
(presumably partially damaged cochlea)
would be similar to the low- to midfrequency
TEOAEs obtained from subjects with normal
hearing sensitivity across the entire range of
audiometric frequencies (presumably intact
cochlea). In this regard, somewhat conflicting
results have been obtained. Prieve et al (1996)
observed that TBOAE and CEOAE inputoutput functions were essentially identical in
regions of normal hearing both for subjects
with normal hearing and for subjects with
normal low- to midfrequency hearing and
high-frequency hearing loss. In addition,
there was no significant difference in TEOAE
Effects of High-Frequency Hearing Loss on CEOAEs/Murnane and Kelly
group delay between the subjects with normal
hearing and the subjects with hearing loss.
Prieve et al concluded that the data supported
the view that TEOAE frequency channels
were independent.
In contrast to the Prieve et al data, several
studies have shown a reduction in low- to
midfrequency TEOAE level obtained from
subjects with high-frequency hearing loss
compared to subjects with normal hearing
(Hauser et al, 1991; Avan et al, 1997; Kowalska
and Sulkowski, 1997). Similarly, Arnold et al
(1999) found that the 4 to 8 kHz DPOAE levels
were significantly correlated with the average
pure-tone thresholds from 11 to 20 kHz and
that ultra-high-frequency hearing accounted
for a significant proportion of the variance in
DPOAE levels from 4 to 8 kHz. Avan et al
(1991) and Avan and Bonfils (1993)
demonstrated that TEOAE threshold and
DPOAE amplitude were significantly
correlated with the audiometric threshold at
least one octave above the TEOAE frequency
and one octave above the geometric mean of
the DPOAE primary frequencies. The temporal
characteristics of the TEOAE waveform also
have been shown to be dependent on the status
of the basal cochlea (Avan et al, 1993).
Conflicting results also have been reported
for guinea pig. Avan et al (1995) and Withnell
et al (2000) observed significant reductions
in low-frequency TEOAE magnitude following
basal cochlear trauma, whereas the reductions
observed by Ueda (1999) were negligible. Thus,
it is not clear if localized damage at remote
(basal) cochlear sites affects the generation of
low- to midfrequency TEOAE energy in the
human cochlea.
The purpose of this study was to
reexamine the independence of TEOAE
frequency channels by comparing the CEOAE
levels obtained from a group of subjects
having sensorineural hearing loss restricted
to the higher audiometric frequencies with the
CEOAE levels obtained from a group of
subjects with normal hearing across the range
of audiometric frequencies. In contrast to
previous studies, the pure-tone thresholds
of the subjects with high-frequency hearing
loss were statistically matched (250–2000
Hz) with those from subjects with normal
hearing, and CEOAEs were obtained for
stimulus levels from 60 to 85 dB pSPL. In
addition, attempts were made to balance the
subject groups in terms of the following
factors that have been shown to influence
CEOAE level: (1) the number of right ears,
(2) the number of males versus females, and
(3) the number of ears having synchronized
spontaneous otoacoustic emissions (SSOAEs)
(Robinette, 1992; Prieve and Falter, 1995).
METHODS
Subjects
Click-evoked otoacoustic emissions
(CEOAEs) were measured in one ear of two
groups of adults. The normal hearing (NH)
group consisted of 23 subjects (18 males and
5 females; 10 right ears and 13 left ears)
between the ages of 28 and 62 years [Mean (M)
= 47.4 yrs., standard deviation (SD) = 8.9]
with pure-tone thresholds ≤ 30 dB HL (ANSI,
1996) at the octave frequencies from 250 to
8000 Hz as well as at the interoctave
frequencies of 3000 and 6000 Hz. The hearing
loss (HL) group consisted of 23 subjects (22
males and 1 female; 10 right ears and 13 left
ears) between the ages of 40 and 76 years (M
= 55.1 yrs., SD = 9.4) with pure-tone thresholds
≤ 30 dB HL at the octave frequencies from 250
to 2000 Hz and high-frequency sensorineural
hearing loss. Two ears in the NH group had
synchronized spontaneous otoacoustic
emissions (SSOAEs) whereas SSOAEs were
not observed in the HL group.
In addition to pure-tone threshold data,
each subject met the following inclusion
criteria: (1) no history of middle-ear disease,
(2) no excessive cerumen in the ear canal, (3)
normal middle-ear function as determined by
226 Hz acoustic admittance measures
[tympanometric peak pressure ±100 daPa;
static admittance within published norms
(Holte, 1996)], and (4) presence of an
ipsilateral 1000 Hz acoustic reflex in the test
ear. The test ear was selected in order to
minimize threshold differences at the octave
frequencies 250 through 2000 Hz between the
NH group and the HL group. Although
etiology of the hearing loss was not considered
as an inclusion criterion, the majority of the
subjects in the HL group had a positive
history of military noise exposure.
Procedures
CEOAEs were recorded using the
ILO88/96 Otodynamic Analyser hardware
and software version 5.60Y (Bray and Kemp,
527
Journal of the American Academy of Audiology/Volume 14, Number 9, 2003
1987; Kemp et al, 1990). The subjects were
seated in a reclining chair in a double-walled
sound booth. CEOAEs were measured using
the nonlinear method of stimulus
presentation and synchronous time-domain
averaging. Two waveforms (A and B), each
consisting of 1040 artifact-free responses,
were obtained at six stimulus levels from 60
to 85 dB pSPL in 5 dB increments. The click
stimuli were presented at a rate of 50/sec, and
the default response window of 2.5 to 20.5
msec postclick was used. The artifact rejection
level was set at a single value for each subject
within the range of 40 to 45 dB pSPL in an
attempt to keep noise levels constant within
and between subjects.
The CEOAE levels were calculated using
the ILO88/96 software by analyzing the
correlated portions of the A and B waveforms
into half-octave bands centered at 750, 1000,
1500, and 2000 Hz. The corresponding noise
levels were calculated as the average difference
between the A and B waveforms in the same
half-octave bands. Unlike some otoacoustic
emission measurement systems, the noise
floor estimate is not determined by the
background acoustical/electrical noise but by
some other proprietary factor in the ILO88/96
software or hardware with a much lower
effective level. Although the measurement
method is valid, it prevents the computing of
accurate means and standard deviations of
CEOAE level when the CEOAE level is below
the corresponding noise level. The calculations
performed by the software often yield
inaccurate and large negative CEOAE-level
values. To limit the effects of this factor, the
noise-level estimate was imposed as an
effective “noise floor” by setting the value of
any half-octave band CEOAE level that was
below the corresponding noise level equal to
the noise-level value.
Data Analysis
A mixed-model analysis of variance
(ANOVA) with repeated measures was
computed separately for audiometric
thresholds and for CEOAE response levels
(Abacus Concepts, SuperANOVA, version 1.11).
Differences were considered to be statistically
significant if p < 0.05. All p-values reported
were adjusted using the Greenhouse-Geisser
estimate of epsilon to correct for the inherent
correlation of repeated measurements.
528
Figure 1 Mean audiometric thresholds for Groups
NH and HL. The error bars represent ±1 SD of the
mean. Based on a mixed-model ANOVA (two groups,
four frequencies), there were no significant differences
in threshold between groups for the octave frequencies from 250 to 2000 Hz, and there was no significant interaction of group by frequency.
RESULTS
M
ean hearing thresholds for each group
are shown in Figure 1. There were no
significant differences in mean thresholds
between the NH group and the HL group for
the octave frequencies from 250 to 2000 Hz
based on a 2 x 4 (group x frequency) mixedmodel ANOVA with repeated measures on
the second factor. There was no significant
difference in either a group effect or
frequency-by-group interaction.
The mean half-octave band CEOAE
response level is plotted as a function of
stimulus level for each group in Figure 2.
Each panel shows the data for a different
half-octave band. The circles represent the
data for the NH group, and the squares
represent the data for the HL group. The
solid line represents the corresponding mean
residual noise level plus one standard
deviation for the NH group, and the dashed
line represents the corollary for the HL group.
For each half-octave band, the input-output
functions for both groups demonstrated an
increase in CEOAE response level with an
increase in stimulus level. The mean response
levels for the NH group were higher than the
response levels of the HL group at each halfoctave band and at each stimulus level. The
difference in mean CEOAE response levels
between the NH group and the HL group
increased as the half-octave band center
frequency increased.
Effects of High-Frequency Hearing Loss on CEOAEs/Murnane and Kelly
Figure 2 Mean half-octave band CEOAE response
level as a function of stimulus level for Groups NH (circles) and HL (squares). Each panel shows the data for
a different half-octave band center frequency. The
solid line without symbols connects the corresponding
mean residual noise level plus one standard deviation
for Group NH, and the dashed line without symbols
represents the corollary for Group HL. The error bars
represent ±1 SD of the mean.
The lowest stimulus level for which the
mean CEOAE response level was higher than
the noise level for both groups at all four
half-octave bands was 75 dB pSPL. Only the
CEOAE response levels obtained at 75, 80,
and 85 dB pSPL, therefore, were selected for
statistical analysis. A 2 x 4 x 3 (group x halfoctave band x stimulus level) mixed-model
ANOVA was performed (the repeated
measure was CEOAE response level for three
stimulus levels and four half-octave bands).
The results of the ANOVA are listed in Table
1. Although there were no significant
differences in mean pure-tone thresholds
between the two groups for the octave
frequencies from 250 to 2000 Hz, ANOVA
results indicated that the CEOAE response
level for the NH group was significantly
higher than the HL group (F (1,44) = 11.664,
p = 0.0014). In addition, CEOAE response
level was significantly different depending on
stimulus level (F (2,132) = 96.049, p < 0.0001)
Table 1
Summary Table for Mixed-Model ANOVA
Source
SS
df
MS
3140.28
1
3140.28
11846.38
44
269.24
Stimulus level
1549.65
2
Half-octave band
2887.29
F
p*
Between Subjects
Group
11.66
0.0014
774.83
96.05
0.0001
3
962.43
33.97
0.0001
5.55
2
2.77
0.34
0.6244
584.66
3
194.89
6.88
0.0006
Stimulus level * Half-octave band
69.01
6
11.50
3.47
0.0114
Group * Stimulus level * Half-octave band
80.17
6
13.36
4.03
0.0048
Error
Within Subjects
Group * Stimulus level
Group * Half-octave band
Note: The repeated measure was CEOAE level for three stimulus levels (75, 80, and 85 dB pSPL) and four half-octave
band center frequencies (750, 1000, 1500, and 2000 Hz). One grouping factor (Group NH or Group HL) was used.
* p-values adjusted using the Greenhouse-Geisser estimate of epsilon
529
Journal of the American Academy of Audiology/Volume 14, Number 9, 2003
DISCUSSION
T
Figure 3 Mean CEOAE response level (averaged
across 75, 80, and 85 dB pSPL) as a function of halfoctave band center frequency for Groups NH (circles)
and HL (squares). The error bars represent ±1 SD of
the mean.
and half-octave band center frequency (F
(3,132) = 33.972, p < 0.0001). Post-hoc means
contrasts indicated that all pair-wise
comparisons for stimulus level (p < 0.0001)
and half-octave band center frequency (p ≤
0.0210) were significant.
The interaction between half-octave band
center frequency and stimulus level was
significant (F (6,88) = 3.470, p = 0.0114),
indicating that the change in CEOAE
response level (averaged across the two
groups) as a function of stimulus level was
dependent on the half-octave band center
frequency. The group and stimulus level
interaction was not significant, indicating
that the change in CEOAE response level
(averaged across the four half-octave bands)
as a function of stimulus level was of the
same magnitude for both subject groups. In
contrast to the group by stimulus level
interaction, the interaction between group
and half-octave band center frequency was
significant (F (3,88) = 6.879, p = 0.0006) and
is illustrated in Figure 3 in which the mean
CEOAE response level (averaged across the
three stimulus levels) is plotted as a function
of the half-octave band center frequency for
each group. The mean CEOAE response level
for the NH group was higher than the HL
group at each half-octave band, and the
magnitude of the difference in CEOAE
response level between the two groups
increased as a function of half-octave band
center frequency.
530
he low- to midfrequency CEOAEs
obtained from ears with high-frequency
hearing loss were significantly reduced in
level compared to those obtained from ears
with normal-hearing thresholds across the
range of audiometric frequencies. These
findings are in agreement with similar studies
using both animal and human subjects.
Hauser and colleagues (1991) measured clickevoked and tone-burst-evoked OAEs in a
group of subjects with normal hearing across
the range of audiometric frequencies and in
a group of hearing-impaired subjects with
normal hearing through 2000 Hz and
moderate-severe high-frequency sensorineural
hearing loss. The subjects with hearing loss
showed reduced emission amplitudes in
regions of normal hearing compared to the
subjects with normal hearing. Avan et al
(1997) evaluated CEOAE amplitude in
subjects with normal hearing through 4000 Hz
and varying degrees of ultra-high-frequency
(8000–16000 Hz) hearing loss. Results showed
a significant negative correlation between
CEOAE amplitude in the 1000–4000 Hz
region and the average ultra-high-frequency
hearing thresholds. In a study of workers
exposed to high levels of industrial noise
resulting in high-frequency hearing loss,
Kowalska and Sulkowski (1997) found that
the CEOAE amplitude in regions of normal
hearing was reduced by 3 dB compared to
that of a nonexposed control group with
normal hearing.
Prieve et al (1996) concluded that TEOAE
frequency channels were independent. They
measured click-evoked and tone-burst-evoked
OAE input/output (I/O) functions and group
delays using subjects with normal hearing
from 250–8000 Hz and subjects with normal
hearing at low- to midfrequencies and hearing
loss at high frequencies. The click-evoked
and tone-burst-evoked OAE I/O functions
were essentially identical in regions of normal
hearing for the normal-hearing subjects as
well as for subjects with high-frequency
hearing loss. In addition, there was no
significant difference in group delay between
the subjects with normal hearing and the
subjects with hearing loss. It should be noted
that only within-group comparisons of clickevoked and tone-burst-evoked OAE I/O
functions were made; no direct comparisons
between I/O functions for the subjects with
Effects of High-Frequency Hearing Loss on CEOAEs/Murnane and Kelly
normal hearing and the subjects with hearing
loss were presented. On closer examination
of their Figure 4, it is apparent that the I/O
functions obtained from the subject with
high-frequency hearing loss were reduced in
level compared to those of the subject with
normal hearing at each stimulus level and at
each 1/3-octave band center frequency at
which hearing sensitivity was normal (500,
1000, and 2000 Hz). In addition, the difference
in CEOAE and TBOAE response levels
between the subject with normal hearing
and the subject with hearing loss increased
as the 1/3-octave band center frequency
increased. When viewed in this manner, the
findings for these two subjects were similar
to the results obtained in the present study.
One important difference between the current
study and the Prieve et al study concerns
the audiometric thresholds of the subjects
with hearing loss. In the present study, the
pure-tone thresholds of the subjects with
hearing loss were statistically matched with
those of the normal-hearing subjects at the
octave frequencies from 250–2000 Hz, and the
cutoff frequency for the high-frequency
hearing loss was 2000 Hz in all subjects. In
contrast, the pure-tone thresholds of the
hearing-impaired subjects in the Prieve et al
study were not statistically matched with
the normal-hearing subjects, and their cutoff
frequencies varied from 500 to 4000 Hz.
Several hypotheses have been proposed
to explain the reduction in the low-frequency
emission components in ears with highfrequency hearing loss. Avan et al (1991,
1995) suggested that the low-frequency
reduction may be due to either: (1) subtle or
subclinical damage to the more apical regions
of the cochlea not detected by behavioral
audiometry, or (2) trauma to the basal region
of the cochlea that affects the generation of
low-frequency emissions. Supporting the
hypothesis that subclinical damage to the
cochlea is revealed earlier by OAE measures
than by pure-tone audiometry are the findings
that significant loss of OHCs in the apical
cochlea went undetected by pure-tone
audiometry (Prosen et al, 1990; Nicol et al,
1992) and the reduction in EOAE magnitude
observed in noise-exposed, audiometrically
normal ears (Attias et al, 1995; Lucertini et
al, 2002). Consistent with the notion that
remote changes in the basal region of the
cochlea affect the generation of low-frequency
emissions, Avan et al (1995) and Withnell et
al (2000) observed a reduction in lowfrequency TEOAE magnitude following
acoustic trauma to the basal cochlea of the
guinea pig.
Yates and Withnell (1999) recorded
CEOAEs in normal-hearing guinea pigs with
high-pass click stimuli and observed that the
response spectrum was comprised of
frequencies not present in the stimulus.
Furthermore, following acoustic trauma to the
base of the cochlea that resulted in highfrequency hearing loss, low-frequency
CEOAE level was substantially reduced if the
click stimulus contained energy within the
range of frequencies affected by the trauma
(Withnell et al, 2000). These findings suggest
that the basal region of the cochlea
contributes to the generation of low-frequency
CEOAE components in the form of
intermodulation distortion products and
provide a reasonable basis for the reduction
in low-frequency TEOAE magnitude observed
in human subjects with high-frequency
hearing loss.
Additional observations demonstrating
the influence of the basal cochlea on lowfrequency CEOAE components are evident in
data concerning the utility of CEOAEs in
the identification of hearing loss. The
accuracy of classification of audiometric status
(normal hearing versus impaired hearing)
using CEOAE signal-to-noise ratio was
improved using a multivariate approach to
data analysis in which the signal-to-noise
ratios at multiple CEOAE frequency bands
were used to predict audiometric status at a
single frequency (Hussain et al, 1998).
Specifically, accuracy was improved when
the CEOAE signal-to-noise ratios at higher
frequencies (2000 and 4000 Hz) were used to
predict the audiometric status at a lower
frequency (1000 Hz) in comparison to a
univariate approach in which the CEOAE
signal-to-noise ratio at 1000 Hz was used to
predict audiometric status at the same
frequency. In contrast, there was little or no
improvement in accuracy over the univariate
approach when the CEOAE signal-to-noise
ratios at lower frequencies (1000 and 2000
Hz) were used to predict the audiometric
status at a higher frequency (4000 Hz).
Hussain et al suggested that the observed
correlation across frequency might reflect
some influence of the basal cochlea on lowfrequency emission components.
The results of the present study
531
Journal of the American Academy of Audiology/Volume 14, Number 9, 2003
demonstrate that the low- to midfrequency
CEOAEs obtained from ears with highfrequency hearing loss are significantly
reduced in level compared to those obtained
from ears with normal hearing even though
there were no statistically significant group
differences in pure-tone thresholds in the
region of normal hearing (250–2000 Hz).
These findings are not consistent with the
notion that CEOAEs are evoked by
independent generators within the cochlea
and indicate that localized damage at basal
cochlear sites affects the generation of lowto midfrequency CEOAE energy. It was
assumed that the normal low- to
midfrequency pure-tone thresholds for the
hearing loss subjects in this study reflected
normal OHC function in the corresponding
regions of the cochlea since the factors that
produce high-frequency hearing loss (e.g.,
noise) typically operate in a systematic
manner from high to low frequencies
(Hawkins and Johnsson, 1976). Additional
factors (gender, number of right ears, and
number of ears with SSOAEs) were
considered in the subject selection process in
order to minimize their influence on any
observed group differences in CEOAE level.
However, the presence of subclinical damage
to the more apical regions of the cochlea
cannot be ruled out in studies using human
subjects. Therefore, it is not possible to
determine unequivocally if the low-frequency
reduction in CEOAE level is due to subclinical
damage to the more apical regions of the
cochlea or to remote changes in the basal
cochlea. Moreover, it is conceivable that both
mechanisms contribute to the reduction in
low-frequency CEOAE magnitude observed
in ears with high-frequency hearing loss.
Acknowledgment. This work was supported by a
Merit Review from the Medical Research Service,
Department of Veterans Affairs to the first author.
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