Discrepancies in Hearing Thresholds between
Pure-Tone Audiometry and Auditory Steady-State
Response in Non-Malingerers
Heil Noh,1 and Dong-Hee Lee2
Objectives: To evaluate discrepancies between pure-tone audiometry
(PTA) and auditory steady state response (ASSR) tests in non-malinger-
ers and investigate brain lesions that may explain the discrepancies, es-
pecially in cases where the PTA threshold was worse than the estimated
ASSR threshold.
Downloaded from https://journals.lww.com/ear-hearing by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD31sQqFNBnHAcNjNNRgARHrVbQXTO1UCBHsz0s3X/xV1I= on 04/26/2020
Design: PTA, speech audiometry, auditory brainstem response, ASSR,
and neuroimaging tests were carried out on individuals selected from
995 cases of hearing impairment. Among these, medical records of
25 subjects (19 males, 6 females; mean age = 46.5 ± 16.0 years) with
significant discrepancy between PTA and estimated ASSR thresholds
were analyzed retrospectively. To define acceptable levels of discrep-
ancy in PTA and ASSR hearing thresholds, 56 patients (27 males, 29
females; mean age = 53.0 ± 13.6 years) were selected for the control
group. Magnetic resonance images, magnetic resonance angiograms,
and positron emission tomograms were reviewed to identify any neuro-
logic abnormalities.
Results: Pathologic brain lesions were found in 20 cases (80%) in the
study group, all of which showed a significant discrepancy in hearing
threshold between PTA and ASSR. Temporal lobe lesions were found in
14 cases (70%), frontal lobe lesions in 12 (60%), and thalamic lesions
without the frontal or temporal lobe in 2 cases (10%). On repeated PTA
and ASSR tests a few months later, the discrepancy between ASSR
and behavioral hearing thresholds was reduced or resolved in 6 cases
(85.7%). Temporal lobe lesions were found in all 3 cases in which the
estimated ASSR threshold worsened with unchanged PTA threshold, and
frontal lobe lesions were found in all 3 cases in which the PTA threshold
improved but the estimated ASSR threshold was unchanged. No neu-
rological lesions were found in 5 cases (20%) of patients with a discrep-
ancy between ASSR and behavioral hearing thresholds.
Conclusions: Clinicians should not rely exclusively on ASSR, especially
in cases of central nervous system including temporal, frontal lobe, or
thalamus lesions. If no lesions are found in a neuroimaging study of a
patient with a discrepancy between PTA thresholds and estimated ASSR
thresholds, further functional studies of the brain may be needed. If clini-
cians encounter patients with a discrepancy between PTA thresholds and
estimated ASSR thresholds, an evaluation of brain lesions and repeat
audiologic tests are recommended in lieu of relying solely on ASSR.
Key words: Auditory steady state response, Brain lesions, Discrepancy,
Pure-tone audiometry, Malingering.
(Ear & Hearing 2020;41;663–668)
INTRODUCTION
The nature of hearing sensations is subjective. Behavioral
tests, including pure-tone and speech audiometry, are the gold
standards for clinical measurement. Owing to its subjective
1
Department of Otolaryngology-Head and Neck Surgery, St. Vincent’s
Hospital, College of Medicine, The Catholic University of Korea, Seoul,
Republic of Korea; and 2Department of Otolaryngology-Head and Neck
Surgery, Uijeongbu St. Mary’s Hospital, College of Medicine, The Catholic
University of Korea, Seoul, Republic of Korea.
0196/0202/2020/413-663/0 • Ear & Hearing • Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved • Printed in the U.S.A.
663
Copyright © 2019 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
<zdoi; 10.1097/AUD.0000000000000791>
nature, the efficacy of behavioral audiometry is often underes-
timated in uncooperative patients, especially in cases with sus-
pected conflicts of interest or secondary gain. In such cases,
many clinicians prefer to emphasize objective, electrophysio-
logical tests to determine the true hearing threshold. However,
such tests are byproducts of neural events of the central auditory
nervous system (CANS) and can only provide an estimate of true
hearing thresholds. As a result, controversy persists over which
tests are more convincing—behavioral or electrophysiological.
Together with auditory brainstem response (ABR), audi-
tory steady state response (ASSR) has been used as an alter-
native electrophysiological measurement to estimate behavioral
hearing thresholds in individuals (Picton et al. 2003; Stueve &
O’Rourke 2003; Canale et al. 2006). ASSR tests are increasingly
performed because of several advantages over ABR counter-
parts: (1) superior frequency specificity, (2) higher stimulation,
up to 120 dB hearing loss (HL), and (3) independence of sub-
jective visual inspection of the tester (Picton et al. 2003; Rance
et al. 1998; Ballay et al. 2005; Vander Werff & Brown 2005;
Dimitrijevic & Cone 2014; Gelfand 2016). Although ASSR is an
attractive tool in audiology, some evidence indicates that it may
not always accurately estimate hearing sensitivity. For example,
subcortical pathology/neuropathy reportedly can produce over-
estimates of hearing thresholds and cortical pathology/neurop-
athy may lead to underestimates of hearing difficulties.
Over the past decade, studies of the clinical usefulness of
ASSR tests have shown good correlation with behavioral hear-
ing thresholds, especially in persons with hearing loss (Ballay
et al. 2005; Canale et al. 2006; Ahn et al. 2007; Swanepoel
& Erasmus 2007; Katz 2014). Despite ASSR’s reliability as a
hearing threshold estimator, clinicians or audiologists often en-
counter cases where a significant difference is found between
ASSR-determined and behavioral hearing thresholds, ranging
from 4 to 34 dB (Aoyagi et al. 1993; Luts & Wouters 2005;
Swanepoel & Erasmus 2007; Ozdek et al. 2010; Katz 2014).
This discrepancy is important as ASSR often assists in estimat-
ing unaided thresholds in the fitting process for hard-to-test
patients as well as in selecting candidates for cochlear implants.
From a legal perspective, ASSR can give decisive information
in the form of an objective electrophysiological assessment that
can distinguish non-malingering from malingering patients.
When clinicians encounter patients with hearing loss suspected
of possible secondary gain and/or conflicts of interest, they tend to
trust objective electrophysiological assessment results over those
of behavioral audiometry. However, even though ABR and ASSR
are objective metrics, they only predict hearing levels based on
a mathematical algorithm (Ozdek et al. 2010; Hood 2014), and
audiologists should consider that an organic pathology other than
malingering may be involved. Auditory neuropathy is an organic
reason for the discrepancy between ASSR and behavioral hearing
664 Noh and Lee / EAR & HEARING, VOL. 41, NO. 3, 663–668
thresholds, especially in pediatric populations (Rance et al. 2005;
Dimitrijevic & Cone 2014). Neurologic dysfunction in the brain
offers another organic explanation for the discrepancy (Dimitri-
jevic & Cone 2014). Shinn and Musiek (2007) demonstrated that
ASSR and behavioral hearing thresholds exhibited wider discrep-
ancy in adults with neurological disorders (brainstem, sub-corti-
cal, and/or cortical lesions) than in those with normal neurologic
status. They showed that ASSR tests tended to overestimate the
degree of HL compared with actual HL.
This study aimed to evaluate the discrepancy between ASSR
and behavioral hearing thresholds in non-malingerers and to in-
vestigate explanatory variables for this discrepancy, especially
in cases where the behavioral hearing threshold was worse than
those estimated by ASSR.
MATERIALS AND METHODS
Subjects
This retrospective study enrolled all persons with hearing loss
evaluated with pure-tone audiometry (PTA), speech audiometry
(SA), ABR, ASSR, and neuroimaging studies at a university-based,
secondary referral hospital (St. Vincent’s Hospital) from 2008 to
2018. Inclusion criteria were: (1) sensorineural HL of 26 dB or
greater with a 4-frequency PTA average (average hearing threshold
levels at 500, 1000, 2000, and 4000 Hz), (2) good reliability dur-
ing PTA or SA, and (3) a 4-frequency PTA average worse than the
estimated threshold of ASSR. Exclusion criteria were (1) abnormal
auricle, external auditory canal, and tympanic membrane by oto-
scopic examination, (2) poor reliability during PTA or SA, (3) a
discrepancy larger than 10 dB HL in 4-frequency PTA average be-
tween ascending and descending methods, (4) disagreement larger
than 10 dB HL after a PTA test-retest, (5) a discrepancy larger
than 10 dB between 4-frequency PTA average and speech-recog-
nition threshold, and (6) Stenger test confirmation of malingering
(Durmaz et al. 2009) for unilateral hearing impairment.
Audiologic Tests
All audiologic tests were performed in a sound-proofed room.
PTA and SA were performed using TDH 49 supra-aural head-
phones and a calibrated GSI 61™ audiometer. For the ASSR
test, the GSI Audera system was used with the “awake” protocol,
which involves a sinusoidal stimulus with a combined ampli-
tude modulation of 100% and frequency modulation of 10% of
the carrier frequency of 250 to 8000 Hz, a fixed modulation fre-
quency of 46 Hz, an intensity of −10 to 130 dB HL, and a noise
criterion of −134.7 dBV. Estimated thresholds of ASSR were de-
termined at 0.5, 1, 2, and 4 kHz with a 97% response criterion.
Retrospective Data Collection
The study group showing significant discrepancies in
hearing thresholds between PTA and ASSR were subjected
TABLE 1.  Difference between pure-tone audiometry thresholds and estimated threshold of auditory steady state response at 0.5, 1,
2, and 4 kHz in the control group
0.5 kHz
Mean ± SD (dB HL) 9.9 ± 8.1
The 4-frequency PTA average was calculated as the average of hearing threshold levels at 0.5, 1, 2, and 4 kHz.
HL, hearing loss.
Copyright © 2019 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
to neuroimaging scans, which included at least one of mag-
netic resonance image (MRI), magnetic resonance angiogram
(MRA), or positron emission tomography (PET) assessment. A
retrospective review of medical records was then performed. All
brain images produced in the past were analyzed; if necessary,
further MRI, MRA, or PET scanning was conducted, and the
resulting images were analyzed for patients with head trauma
or other neurologic abnormality. In addition, neurological and/
or psychological evaluations for cognitive disorders were per-
formed by a neurologist and/or psychiatrist, respectively, if nec-
essary. Subjects with a history of epileptic events (Matsubara
et al. 2019) or psychological disease (Kim et al. 2019) were
excluded from follow-up.
Ethical Considerations
This study was approved by the Institutional Review Board
of St. Vincent’s Hospital (IRB #VC12RISI0134), and the re-
quirement for informed consent was waived because of the ret-
rospective nature of the study.
RESULTS
Defining the Acceptable Level of Discrepancy in Hearing
Thresholds between PTA and ASSR in the Control Group
To define an acceptable level of discrepancy in hear-
ing thresholds between PTA and ASSR, a control group was
designed. Because the general population is of mixed etiologies
that can bias the discrepancies, only confirmed cases of idio-
pathic sudden sensorineural HL were analyzed. A total of 56
such patients at the same hospital during the same study period
was selected as the control group (27 males, 29 females; mean
age = 53.0 ± 13.6 years) (Table 1). Idiopathic sudden sensori-
neural HL was diagnosed only after MRI confirmed the absence
of central brain lesions, including vestibular schwannoma.
The study defined the acceptable hearing threshold discrep-
ancy level between PTA and ASSR as: (1) a difference greater
than 20 dB HL between the PTA threshold and estimated ASSR
threshold at a frequency of 0.5 or 1 kHz, (2) a difference > 25 dB
HL between the PTA threshold and estimated ASSR threshold
at a frequency of 2 or 4 kHz, and (3) a difference greater than 15
dB HL between the 4-frequency PTA average of PTA threshold
and estimated ASSR threshold.
Factor Analysis of Cases with Significant Discrepancies
in Hearing Thresholds between PTA and ASSR
Using this criterion for significant discrepancies in hear-
ing thresholds between PTA and ASSR, we extracted the study
group from 995 cases of people with hearing loss based on PTA,
SA, ABR, and ASSR over the last 10 years. The study group
with significant discrepancies in hearing thresholds between
PTA and ASSR comprised 25 patients (19 males, 6 females;
4-frequency PTA
1 kHz 2 kHz 4 kHz average
9.9 ± 9.1 13.7 ± 11.3 13.0 ± 11.4 8.1 ± 6.7
 Noh and Lee / EAR & HEARING, VOL. 41, NO. 3, 663–668 665

mean age = 46.5 ± 16.0 years; range = 10–69 years). Results
of audiologic tests and radiologic studies of their CANSs are
summarized in Table 2. In members of the study group show-
ing significant discrepancy in hearing threshold between PTA
and ASSR, pathologic lesions in the central brain were found
in 20 cases (80%), each of which was confirmed by radiologic
studies.
Of these 20 cases, 14 (70%) had lesions of the temporal lobe.
Of 12 cases with unilateral temporal lobe lesion, the discrep-
ancy in hearing threshold between PTA and ASSR was larger in
6 cases of contralateral lesions and 6 cases of ipsilateral lesions.
Case #12, with both temporal lobe-right and frontal-right tha-
lamic lesions, showed a larger discrepancy in the left ear, while
case #20, with both temporal-left frontal lobe lesions, showed
larger discrepancy in the right ear (Table 3).
In 12 (60%) of 20 cases with lesions in the frontal lobe, 10
had frontal lesions associated with temporal lesions, and 2 had
no associated temporal lesions. Two cases with frontal lobe
lesions but no temporal lesions showed a larger discrepancy be-
tween PTA and ASSR in contralateral lesions. Unilateral frontal
and temporal lesions on the same side were found in 4 cases,
and the discrepancy was larger for the contralateral lesion in 2
cases and the ipsilateral lesion in 2 cases. Among 4 cases with
bilateral frontal and unilateral temporal lesions, the discrepancy
was larger in the contralateral temporal lesion in 2 cases and in
the ipsilateral lesion in 2 cases. Unilateral frontal and bilateral
temporal lesions were found in 2 cases, in which the discrep-
ancy was larger in the contralateral frontal lesion (Table 3).
Of these 20 cases, 2 had lesions involving the thalamus but
not the frontal or temporal lobes, and both showed a larger
discrepancy in the contralateral brain lesion, case #8, right
periventricular-thalamic lesions, and case #17, right parietal
lobe-thalamic region lesions. One case had a right frontal-both
temporal lobe-right thalamus lesion, which showed a larger dis-
crepancy in the contralateral frontal and thalamic lesions (case
#12) (Table 3).
In 7 of 25 cases in the study group, PTA and ASSR tests
were repeated with the same protocol a few months later, and
three patterns were evident. On follow-up tests, 1 case (#22)
showed the same difference in hearing threshold between PTA
and ASSR. However, in 3 cases (#2, #4, and #13), the estimated
ASSR threshold was worse, with unchanged PTA threshold
and decreased difference in hearing threshold between PTA
and ASSR. In 1 case (#13), the initial discrepancy in hearing
threshold between PTA and ASSR was resolved on follow-up at
2 months. In fact, the PTA threshold improved as time passed
and matched the ASSR threshold in 3 cases (#5, #10, and #15).
Three cases in which the estimated ASSR threshold worsened

TABLE 2.  Summary of audiologic tests and radiologic studies on central auditory pathways in the study group

Right ear Left ear

Case Follow-up
No. Age Sex Site TN Etiology PTA ASSR PTA ASSR test Central lesion in the brain
1 55 M L + trauma 94 81 93 68 − Right temporal-frontal lobe
2 42 M B + trauma 45 16 120 31 + Right temporal lobe
3 38 M B − trauma 59 35 94 74 − Right temporal-both frontal,
parietal lobes
4 50 F L + trauma 19 24 80 20 + Right temporal-frontal lobe
5 39 M L − trauma 23 30 65 29 + Right temporal-both frontal lobes
6 51 M R − trauma 60 15 38 31 − Right temporal-cerebellum
7 30 M L − trauma 8 −1 113 70 − Left cerebellum
8 69 M B + infarct 88 64 120 40 − Right periventricular-thalamus
9 53 M B + trauma 76 19 120 69 − Right temporal-frontal lobe
10 56 F B + trauma 53 31 84 31 + Left temporal lobe-frontal lobe
11 62 F L + tumor 35 28 65 50 − Right temporal-parietal lobe
12 59 M L + trauma 23 69 103 58 − Right frontal-both temporal lobes-
right thalamus
13 49 M R + trauma 93 48 34 48 + Right temporal lobe
14 42 M R + trauma 65 50 31 44 − Left frontal lobe-superior
frontal gyrus
15 74 F B + trauma 120 95 120 76 + Left temporal-both frontal lobes
16 40 M L + infarct 24 15 60 45 − Right putamen-left posterior
putamen, corona radiata
17 55 M L − infarct 20 21 96 74 − Right parietal lobe-thalamus
18 58 M B − trauma 68 15 60 44 − Left frontal-right parietal
lobe-left cerebellum
19 60 F L − trauma 53 53 45 30 − Right temporal-both frontal lobes,
corpus callosum
20 52 M R + trauma 79 60 11 10 − Both temporal lobes-left
frontal lobe
21 47 M R + trauma 111 60 21 48 − −
22 15 M L + trauma 120 101 95 41 + −
23 15 F L + trauma 8 13 78 45 − −
24 42 M B + trauma 71 25 78 38 − −
25 10 M R + trauma 86 20 0 24 − −

ASSR, auditory steady state response; F, female; L, left; M, male; PTA, pure-tone audiometry; R, right; TN, tinnitus.

Copyright © 2019 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
666 Noh and Lee / EAR & HEARING, VOL. 41, NO. 3, 663–668
TABLE 3.  Analysis of significant discrepancies in hearing thresholds between PTA and ASSR according to brain lesion
Lesions Number of cases
Temporal Unilateral lesion in 12 cases
Bilateral lesions in 2 cases
Frontal Comorbid with temporal lesion in 10 cases
 Unilateral frontal and unilateral temporal
lesions in the same side in 4 cases
 Bilateral frontal and unilateral temporal
lesions in the same side in 4 cases
 Unilateral frontal and bilateral temporal
lesions in the same side in 2 cases
Without temporal lesion in 2 cases
Thalamus Without frontal or temporal lesion in 2 cases
With frontal or temporal lesion in 1 case
ASSR, auditory steady state response; PTA, pure-tone audiometry.
(two males and one female; mean age = 47.0 ± 4.4 years) in-
volved younger patients than 3 cases in which the PTA threshold
improved (one male and two females; mean age = 56.3 ± 17.5
years). However, there was no difference in age or sex among
these three patterns (one-way analysis of variance; p = 0.113
and 0.605, respectively).
DISCUSSION
For many years, ABR has been the gold standard for esti-
mating hearing threshold as it can assess frequency-nonspe-
cific (click ABR) or specific (tone burst or tone pip ABR)
hearing thresholds. However, the main limitation of this pro-
cedure is the difficulty and subjectivity involved in interpret-
ing the responses. In addition, because results of the ABR
are only byproducts or epiphenomena of neural events that
underlie hearing, and ASSR relies on sophisticated statistics-
based mathematical detection, neither are direct hearing tests
(Ozdek et al. 2010; Hood 2014). This study clearly demon-
strates actual discrepancies between behavioral test results and
estimated ASSR thresholds in some cases in which the CANS
is injured or dysfunctional. In patients with such a discrepancy,
it is important for audiologists to remember that their role is
to measure the degree of organic HL rather than determine the
precise reason for the nonorganic results (Martin 2002), and
they should not make a hasty diagnosis of malingering based
solely on responses to behavioral tests.
This study demonstrates that estimated ASSR thresholds
seem to be better than PTA thresholds in patients with neu-
rological damage, and that indiscriminate trust in ASSR
will underestimate the actual severity of HL as well as the
underlying disability. Discrepancy in hearing threshold be-
tween PTA and ASSR was previously reported by Shinn and
Musiek (2007), but their results differed from ours. After
matching age and behavioral hearing levels between con-
trols and cases with neurological impairment of CANS,
they found that an ASSR test will overestimate the actual
degree of HL. In their study, most cases of neurological im-
pairment involved infarct of the pons and internal capsule.
However, our study analyzed cases of more diverse lesions
of the central nervous system (CNS). Despite the hypothesis
Copyright © 2019 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Side of larger discrepancy in hearing thresholds
between PTA and ASSR Case No.
Ear contralateral to brain lesion in 6 cases 1, 2, 4, 5, 11, 19
Ear ipsilateral to brain lesion in 6 cases 3, 6, 9, 10, 13, 15
12, 20
1, 3, 4, 5, 9, 10, 12, 15, 19, 20
Ear contralateral to brain lesion in 2 cases 1, 4
Ear ipsilateral to brain lesion in 2 cases 9, 10
Ear contralateral to temporal lesion in 2 cases 5, 19
Ear ipsilateral to temporal lesion in 2 cases 3, 15
Ear contralateral to frontal lesion in 2 cases 12, 20
Ear contralateral to brain lesion in 2 cases 14, 18
Ear contralateral to brain lesion in 2 cases 8, 17
Ear contralateral to frontal and thalamus lesions 12
in 1 case
of their study, they included cases in which major lesions
were found far from the CANS (pons, internal capsule, and
striatocapsular).
The ASSR to frequencies near 40 Hz has been the method
of choice for estimating hearing thresholds in adults, but such
responses are unstable or absent in sleeping infants and chil-
dren. The ASSR, recorded using a frequency modulation of
46 Hz, is believed to be generated by mechanisms similar to
the auditory middle latency response (Cone-Wesson et al.
2002). The auditory middle latency response is derived from
the inferior colliculus, the medial geniculate body of the thal-
amus, and the primary auditory cortex, which has been used
to assess auditory cortical function. Because the temporal
lobe is mainly auditory cortex, and the cortical sources of
ASSR are more active at slower rates of stimulation (Herd-
man et al. 2002), we assume that any lesions of the temporal
lobe results in decreased ASSR at a 46-Hz frequency modu-
lation rate. This assumption was also demonstrated by Shinn
and Musiek (2007), but our study showed more heterogenous
and complex results according to type of brain lesion. Of 4
cases of unilateral temporal lobe lesion alone, the discrep-
ancy in hearing threshold between PTA and ASSR was larger
than that in contralateral lesions in 2 cases and larger than
ipsilateral lesions in 2 cases.
Of 8 cases of a unilateral temporal lobe lesion with a frontal
lobe lesion, the discrepancy was larger than contralateral tem-
poral lobe lesion in 4 cases and larger than ipsilateral lesions in
4 cases. Although the contralateral effect in the auditory system
is well-known, our study failed to show any agreement between
the laterality of the temporal lobe lesion and that of larger dis-
crepancies, which is consistent with previous reports (Musiek
et al. 1999; Herdman et al. 2002). Middle and late auditory-
evoked potentials including ASSR can show weak contralateral
ear effects, and tests that yield the strongest contralateral effect
in patients with one compromised auditory hemisphere include
dichotic listening, which was not included in our study (Musiek
& Pinheiro 1985; Musiek & Chermak 2014). Another expla-
nation for this disagreement is that ipsilateral effects in unilat-
eral temporal lobe lesions may be absent because the remaining
temporal lobe generates a response that can be recorded from
the midline vertex (Herdman et al. 2002).
 Noh and Lee / EAR & HEARING, VOL. 41, NO. 3, 663–668 667
This study found that 2 cases with only thalamic lesions
showed discrepancies between PTA and estimated ASSR thresh-
olds. This coincides with the findings of Spydell et al. (1985),
who reported that the auditory 40-Hz response is reduced in
patients with brainstem or thalamic lesions. Firsching et al.
(1987) found that the auditory 40-Hz response is usually ab-
sent in comatose and brain-dead patients, consistent with the
crucial role of the upper brainstem in generating this response.
Therefore, the 40-Hz ASSR can help assess the integrity of mid-
brain structures. Our 2 cases of thalamic lesions demonstrated
an ipsilateral rather than contralateral effect on ASSR, which
is in accordance with Baran and Musiek (1999). This can be
explained by lack of crossover of most ascending fibers in the
lower brainstem to the other side, and a large portion of the
fibers are therefore ipsilateral rather than contralateral.
Two cases with only a frontal lobe lesion were included in
our study. Considering that the frontal lobe is not a part of the
central auditory pathway, this finding is interesting, but previous
reports suggest that frontal lobe lesions can involve the hear-
ing and auditory processes or influence the recording of ASSR.
Reyes et al. (2004) found that lesions involving the cingulate
and frontal lobes may be specifically involved in generating the
ASSR. Rosemann and Thiel (2018) reported that changes in ac-
tivation of frontal areas (as seen in functional MRI) influenced
audiovisual speech processing in patients with mild to moderate
hearing loss, changes of which were modulated by degree of
HL. Another explanation is that ASSR recording may be influ-
enced by technical aspects because it is involves the midline
vertex.
It is generally accepted that the ASSR has multiple genera-
tors in the brain and the contribution of the generators varies
with modulation frequency. The ASSR at rates <20 Hz is gener-
ated mainly by activity in the primary auditory cortex. When
ASSRs are elicited by stimuli between 20 and 60 Hz, the un-
derlying neural generators are located mainly in the primary
auditory cortex, auditory midbrain, and thalamus. In addition,
an ASSR elicited by stimuli at rates >60 Hz are generated pri-
marily by contributions from the superior olivary complex,
inferior colliculus, and cochlear nucleus. As for other cortical
evoked responses, ASSRs at low modulation rates show later-
ality toward the hemisphere contralateral to the stimulated ear,
although 40-Hz ASSRs show evidence of right-hemispheric
dominance (Ross et al. 2005).
No neurological lesions were found in 5 cases with a discrep-
ancy between ASSR and behavioral hearing thresholds. Follow-
ing mild traumatic brain injury or common post-concussive
brain injury, auditory symptoms such as speech-in-noise com-
plaints can occur (Hoover et al. 2017). ASSR evokes oscillatory
responses that are entrained to the frequency and phase of tem-
porally modulated stimuli, and some reports have demonstrated
that ASSR originating from different regions of CANS can
be influenced by dysfunctional brain connectivity (O’Donnell
et al. 2013; Ying et al. 2015), which means disorganization of
brain activity correlation between different neurons or neural
dyssynchrony in CANS. This hypothesis suggests that clini-
cians should not automatically suspect malingering in patients
with a normal MRI showing discrepancy between ASSR and
behavioral hearing thresholds. In cases with a discrepancy be-
tween ASSR and behavioral hearing thresholds, and if other au-
diological methods fail to prove malingering and the brain MRI
is normal, patients should be transferred to a higher referral
Copyright © 2019 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
hospital or undergo functional studies, such as functional MRI,
brain single-photon emission computed tomography, or electro-
and magneto-encephalography (Mayer et al. 2015). Three of the
five cases without a neurological lesion were children or ado-
lescents. Because our exclusion criteria were sufficiently strict
to rule out malingering even in pediatric populations, we cannot
guarantee absence of bias.
Of 7 cases who underwent repeated PTA and ASSR using
the same protocol a few months later, the discrepancy between
ASSR and behavioral hearing thresholds was smaller or re-
solved in 6 cases. Neurological lesions of the temporal lobe
were found in 3 cases in which the estimated ASSR threshold
worsened while the PTA threshold remained unchanged (right
temporal lobe in case #2, right temporal-frontal lobe in #4, and
right temporal lobe in #13). Furthermore, 3 cases in which the
PTA threshold increased but the estimated ASSR threshold re-
maining unchanged included frontal lobe lesions (right tempo-
ral-both frontal lobe in case #5, left temporal lobe-frontal lobe in
case #10, and left temporal-both frontal lobe in case #15). These
cases suggest that the estimated ASSR threshold worsened in
cases with temporal lobe lesions because ASSR includes activ-
ities from the temporal lobe of the CANS, and that the change
in PTA threshold in cases with frontal lobe lesions may result in
changes in cognitive task performance because performance in
behavioral hearing tests can depend on frontal lobe function. To
generalize this hypothesis, further study is needed.
This study has several limitations. Even though we aimed
to determine the variables characterizing the discrepancy be-
tween PTA and estimated ASSR thresholds in patients with neu-
rological impairment of the CNS, we did not have access to
vast clinical data as a result of the retrospective study design.
Second, we did not test central auditory processes including
auditory pattern/temporal ordering tasks, monaural separation/
closure tasks, binaural separation tasks, or binaural integration
tasks (Schow et al. 2000). Third, the study lacked functional
elements, such as functional MRI, brain single-photon emission
computed tomography, or electro- and magneto-encephalogra-
phy. Fourth, too few cases in which PTA and ASSR were re-
peated in the long-term were included. Although we found three
patterns on follow-up of PTA and ASSR, the number of cases
was too small for our findings to be generalized.
CONCLUSIONS
Clinicians generally rely on electrophysiological tests for
hearing if they suspect malingering, meaning that they tend to
trust the results of electrophysiological tests more than behav-
ioral hearing tests because the latter are subjective and vulner-
able to conflicts of interest or secondary gain. ASSR is superior
to ABR in those cases because of its frequency specificity. How-
ever, this study demonstrated that clinicians should not rely ex-
clusively on ASSR, especially in cases of CNS lesions. This
applies to situations in which lesions of the temporal lobe or
thalamus are found by neuroimaging studies as well as when
any lesion is found in the frontal lobe and not a part of the
central auditory pathway. It is therefore important to conduct
malingering tests and to validate the reliability of behavioral
hearing tests.
If lesions are not found in neuroimaging studies of patients
with a discrepancy between PTA thresholds and estimated
ASSR thresholds, further functional studies, such as functional
668 Noh and Lee / EAR & HEARING, VOL. 41, NO. 3, 663–668
MRI, brain single-photon emission computed tomography, or
electro- and magneto-encephalography, should be considered.
We also demonstrated that repeated behavioral as well as
electrophysiological tests for measuring hearing thresholds are
essential for patients with a discrepancy between PTA thresh-
olds and estimated ASSR thresholds.
ACKNOWLEDGMENTS
The authors have no conflicts of interest to declare.
Address for correspondence: Dong-Hee Lee, Department of
Otolaryngology-Head and Neck Surgery, Uijeongbu St. Mary’s Hospital,
College of Medicine, The Catholic University of Korea, 271 Cheonbo
Street, Uijeongbu City, Gyeonggi-do, 11765, Republic of Korea. E-mail:
leedh0814@catholic.ac.kr.
Received January 7, 2019; accepted July 15, 2019.
REFERENCES
Ahn, J. H., Lee, H. S., Kim, Y. J., et al. (2007). Comparing pure-tone audi-
ometry and auditory steady state response for the measurement of hear-
ing loss. Otolaryngol Head Neck Surg, 136, 966–971.
Aoyagi, M., Kiren, T., Kim, Y., et al. (1993). Frequency specificity of ampli-
tude-modulation-following response detected by phase spectral analysis.
Audiology, 32, 293–301.
Ballay, C., Tonini, R., Waninger, T., et al. (2005). Steady-state response au-
diometry in a group of patients with steeply sloping sensorineural hear-
ing loss. Laryngoscope, 115, 1243–1246.
Baran, J., Musiek, F. (1999). Behavioral assessment of the central auditory
system. In F. Musiek, W. Rintelmann (Eds.), Contemporary perspectives
on hearing assessment (pp. 375–415). Boston, MA: Allyn & Bacon.
Canale, A., Lacilla, M., Cavalot, A. L., et al. (2006). Auditory steady-state
responses and clinical applications. Eur Arch Otorhinolaryngol, 263,
499–503.
Cone-Wesson, B., Dowell, R. C., Tomlin, D., et al. (2002). The auditory
steady-state response: comparisons with the auditory brainstem re-
sponse. J Am Acad Audiol, 13, 173–187; quiz 225-176.
Dimitrijevic, A., Cone, B. (2014). Auditory Steady-State Response. In J.
Katz (Ed.), Handbook of Clinical Audiology (pp. 267–294). Philadel-
phia, PA: Lippincott Williams & Wilkins.
Durmaz, A., Karahatay, S., Satar, B., et al. (2009). Efficiency of Stenger test
in confirming profound, unilateral pseudohypacusis. J Laryngol Otol,
123, 840–844.
Firsching, R., Luther, J., Eidelberg, E., et al. (1987). 40 Hz–middle latency
auditory evoked response in comatose patients. Electroencephalogr Clin
Neurophysiol, 67, 213–216.
Gelfand, S. A. (2016). Essentials of Audiology. (4th ed.). New York, New
York: Thieme.
Herdman, A. T., Lins, O., Van Roon, P., et al. (2002). Intracerebral sources
of human auditory steady-state responses. Brain Topogr, 15, 69–86.
Hood, L. J. (2014). Auditory Brainstem Response: Estimation of Hearing
Sensitivity In J. Katz (Ed.), Handbook of Clinical Audiology (pp. 249–
266). Philadelphia, PA: Lippincott Williams & Wilkins.
Hoover, E. C., Souza, P. E., Gallun, F. J. (2017). Auditory and Cognitive
Factors Associated with Speech-in-Noise Complaints following Mild
Traumatic Brain Injury. J Am Acad Audiol, 28, 325–339.
Katz, J. (2014). Handbook of clinical audiology (7th Edition ed.). Philadel-
phia, PA: Wolters Kluwer.
Kim, S., Jang, S. K., Kim, D. W., et al. (2019). Cortical volume and 40-Hz
auditory-steady-state responses in patients with schizophrenia and
healthy controls. Neuroimage Clin, 22, 101732.
Copyright © 2019 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Luts, H., & Wouters, J. (2005). Comparison of MASTER and AUDERA
for measurement of auditory steady-state responses. Int J Audiol, 44,
244–253.
Martin, F. N. (2002). Psedohypacusis. In J. Katz (Ed.), Handbook of Clin-
ical Audiology (pp. 584): Lippincott Williams & Wilkins.
Matsubara, T., Ogata, K., Hironaga, N., et al. (2019). Monaural 40-Hz au-
ditory steady-state magnetic responses can be useful for identifying ep-
ileptic focus in mesial temporal lobe epilepsy. Clin Neurophysiol, 130,
341–351.
Mayer, A. R., Hanlon, F. M., Dodd, A. B., et al. (2015). A functional mag-
netic resonance imaging study of cognitive control and neurosensory
deficits in mild traumatic brain injury. Hum Brain Mapp, 36, 4394–4406.
Musiek, F., Charette, L., Kelly, T., et al. (1999). Hit and false-positive rates
for the middle latency response in patients with central nervous system
involvement. J Am Acad Audiol, 10, 124–132.
Musiek, F., Chermak, G. (2014). Handbook of central auditory processing
disorder: Auditory neuroscience and diagnosis. San Diego, CA: Plural
Publishing.
Musiek, F. E., Pinheiro, M. L. (1985). Dichotic speech tests in the detection
of central auditory dysfunction. In M. L. Pinheiro, F. E. Musiek (Eds.),
Assessment of central auditory dysfunction: Foundations and clinical
correlates (pp. 201–218). Baltimore, MD: Williams and Wilkins.
O’Donnell, B. F., Vohs, J. L., Krishnan, G. P., et al. (2013). The auditory
steady-state response (ASSR): a translational biomarker for schizo-
phrenia. Suppl Clin Neurophysiol, 62, 101–112.
Ozdek, A., Karacay, M., Saylam, G., et al. (2010). Comparison of pure tone
audiometry and auditory steady-state responses in subjects with normal
hearing and hearing loss. Eur Arch Otorhinolaryngol, 267, 43–49.
Picton, T. W., John, M. S., Dimitrijevic, A., et al. (2003). Human auditory
steady-state responses. Int J Audiol, 42, 177–219.
Rance, G., Dowell, R. C., Rickards, F. W., et al. (1998). Steady-state evoked
potential and behavioral hearing thresholds in a group of children with
absent click-evoked auditory brain stem response. Ear Hear, 19, 48–61.
Rance, G., Roper, R., Symons, L., et al. (2005). Hearing threshold estima-
tion in infants using auditory steady-state responses. J Am Acad Audiol,
16, 291–300.
Reyes, S. A., Salvi, R. J., Burkard, R. F., et al. (2004). PET imaging of the 40
Hz auditory steady state response. Hear Res, 194, 73–80.
Rosemann, S., & Thiel, C. M. (2018). Audio-visual speech processing in
age-related hearing loss: Stronger integration and increased frontal lobe
recruitment. Neuroimage, 175, 425–437.
Ross, B., Herdman, A. T., Pantev, C. (2005). Right hemispheric laterality
of human 40 Hz auditory steady-state responses. Cereb Cortex, 15,
2029–2039.
Schow, R. L., Seikel, J. A., Chermak, G. D., et al. (2000). Central audi-
tory processes and test measures: ASHA 1996 revisited. Am J Audiol,
9, 63–68.
Shinn, J. B., & Musiek, F. E. (2007). The auditory steady state response
in individuals with neurological insult of the central auditory nervous
system. J Am Acad Audiol, 18, 826–845.
Spydell, J. D., Pattee, G., Goldie, W. D. (1985). The 40 Hertz auditory event-
related potential: normal values and effects of lesions. Electroencepha-
logr Clin Neurophysiol, 62, 193–202.
Stueve, M. P., & O’Rourke, C. (2003). Estimation of hearing loss in chil-
dren: comparison of auditory steady-state response, auditory brainstem
response, and behavioral test methods. Am J Audiol, 12, 125–136.
Swanepoel, D., & Erasmus, H. (2007). Auditory steady-state responses
for estimating moderate hearing loss. Eur Arch Otorhinolaryngol, 264,
755–759.
Vander Werff, K. R., & Brown, C. J. (2005). Effect of audiometric configu-
ration on threshold and suprathreshold auditory steady-state responses.
Ear Hear, 26, 310–326.
Ying, J., Zhou, D., Lin, K., et al. (2015). Network Analysis of Functional
Brain Connectivity Driven by Gamma-Band Auditory Steady-State Re-
sponse in Auditory Hallucinations. J Med Biol Eng, 35, 45–51.