Download Limitations of Pure-Tone Audiometry in the Detection of

Limitations of Pure-Tone Audiometry
in the Detection of Nonorganic
Hearing Loss: A Case Study
Zarin Mehta
Wichita State University, KS
P
ure-tone audiometry continues to be the
mainstay of modern audiology and the most
used procedure to diagnose auditory disorders.
Hearing sensitivity levels obtained with pure-tone audiometry using appropriate psychophysical protocols and
analysis procedures are generally reliable. One of the
factors that can affect test reliability of pure-tone audiometry, however, is the interrelationship with client performance; if the client cannot or does not want to cooperate,
ABSTRACT: Detection of a nonorganic hearing loss
(NOHL) can pose a challenge for the clinical audiologist,
especially if the diagnosis is dependent solely on
behavioral testing. Detection can become particularly
difficult if the NOHL is manifested at an unconscious
level, as presented in this case study of a 48-year-old
woman who was diagnosed with a bilateral severe-toprofound sensorineural hearing loss and fitted with
monaural amplification based on pure-tone audiometric
data. Several years after the initial diagnosis, a
nonorganic component was detected based on physiologic test procedures and confirmed by a psychiatric
evaluation. This case demonstrates the importance of the
use of physiologic measures such as otoacoustic emissions, the middle ear muscle reflex, and auditory
brainstem response testing as a cross-check for behavioral assessment and the incorporation of these tests in
routine clinical practice.
KEY WORDS: adjustment disorder, auditory evoked
potentials, conversion disorder, middle ear muscle reflex,
nonorganic hearing loss, otoacoustic emissions
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the test results can be questionable. The reliability of puretone audiometry becomes particularly vulnerable when
dealing with a nonorganic hearing loss (NOHL). An NOHL
appears greater in magnitude than may be explained on the
basis of any known auditory pathology (Martin, 2002). The
presence of an NOHL, in most instances, is related to some
kind of personal gain, which may be the expectation of
monetary compensation, a need to gain attention from
others, or, especially in children, an excuse for poor
academic performance (Rintelmann & Schwan, 1999).
Although the classic literature suggests that there are no
characteristic audiometric patterns that typify NOHLs
(Chaiklin, Ventry, Barrett, & Skalbeck, 1959; Ventry &
Chaiklin, 1965), one aspect of NOHL that is widely
accepted in the literature is the high incidence of a true
underlying hearing loss among adults diagnosed with
NOHL (Chaiklin & Ventry, 1963; Gelfand & Silman, 1985,
1993). Further, in most cases of NOHL, it seems that these
individuals use an internalized loudness-based anchor to
present with the “exaggerated” hearing loss (Gelfand &
Silman, 1985, 1993; Martin, Champlin, & McCreery, 2001).
Typically, the exaggerated behavioral responses will show
discrepancies between the different test results, which is
not the case for most organic hearing losses. Common
discrepancies include lack of reliability across test sessions;
wide threshold ranges; speech recognition threshold (SRT)
pure-tone average (PTA) disagreement, with the SRTs being
considerably better; half-spondee responses; bone conduction thresholds poorer than air conduction thresholds; and
lack of cross hearing (Gelfand & Silman, 1993; Martin et
al., 2001).
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Audiologic assessment of an NOHL can pose a major
challenge for the clinical audiologist, with the diagnosis
becoming even more problematic when that hearing loss is
manifested at an unconscious level as a symptom of a
psychological disturbance or disorder. An example of such
a condition that is cited most commonly in the literature is
a conversion disorder or a psychogenic hearing loss.
Hysterical deafness is an older term used to describe a
conversion disorder (Martin, 1986). These terms imply that
the patient may have an emotional or psychological
disorder resulting from a psychological conflict or need
(Wolf, Birger, Shoshan, & Kronenberg, 1993).
Although there is some disagreement within the profession regarding conversion hearing loss, whether it is a
true clinical entity (Beagley & Knight, 1968; Cohen et al.,
1963; Wolf et al., 1993) or whether every NOHL is
feigned (Goldstein, 1966), the psychiatric literature
recognizes the presence and nature of conversion disorders. According to the American Psychiatric Association’s
(APA’s, 1994b) Diagnostic and Statistical Manual of
Mental Disorders (DSM–IV), a conversion disorder is a
somatoform disorder with the symptoms or deficits
affecting voluntary motor or sensory function, including
hearing, that suggest a neurological or other general
medical condition. The symptoms do not conform to
known anatomical pathways or physiological mechanisms
but instead follow the individual’s conceptualization of a
condition. The DSM–IV (APA, 1994b) definition indicates
a temporal relationship between a psychologically stressful
situation and the appearance or exacerbation of the
symptom. The symptom or deficit may be acute or
chronic, often it is recurrent, and it is not intentionally
produced or deliberately feigned. An associated feature of
conversion disorder is la belle indifference (the relative
lack of concern about the nature or implication of the
symptom). It is more prevalent in rural populations, in
individuals of lower socioeconomic status, and in individuals less knowledgeable about medical and psychological concepts. Conversion disorders appear more frequently
in women, with reported ratios varying from 2:1 to 10:1,
and often with an accompanying personality disorder of
the histrionic type. In women especially, the symptoms
appear much more commonly on the left side than on the
right side of the body. In men, conversion disorder is
often seen in the context of industrial accidents or the
military, in which case it must be carefully differentiated
from malingering (APA, 1994b).
As a group, individuals who manifest an NOHL demonstrate certain emotional and psychosocial characteristics.
According to Trier and Levy (1965), they tend to score
lower on all measures of socioeconomic status. They also
score lower on tests of verbal intelligence and demonstrate
a greater degree of clinically significant emotional disturbances. In an early study, Gleason (1958) reported that
these individuals, as a group, typically tend to display
emotional immaturity, instability, and an inadequate
response to social demands. They also tend to manifest a
reliance on denial mechanisms and appear to have a
diminished sense of confidence in their abilities to meet the
needs of daily living (Martin, 2002).
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The majority of individuals with NOHL are diagnosed
within a relatively short time or the functional component
resolves when the expectation of the personal gain has been
met. There have been some cases cited in the literature,
however, where the NOHL was not diagnosed and these
individuals were referred for a cochlear implant. The
NOHL component was eventually identified by the cochlear
implant assessment team with considerable time and
expense spent on the diagnosis (Spraggs, Burton, &
Graham, 1994).
Although the literature is replete with examples of cases
of NOHL, the present case is somewhat unique because the
individual had been in the health care system for at least 6
years before discovery of the NOHL. During that period, she
had several audiologic evaluations and had been diagnosed
with a profound sensorineural hearing loss in the right ear
and a moderately severe sensorineural hearing loss in the left
ear, had been fitted with monaural amplification, and had
been under the care of an otolaryngologist—without the
nonorganic nature of the hearing loss being detected.
CASE STUDY
In 1998, JD,1 a 48-year-old homeless woman, was
referred to a Midwest university’s speech and hearing clinic
by her case manager at the local vocational rehabilitation
(VR) district office. In 1992, JD had been fitted with an inthe-ear hearing aid in the left ear by an audiologist
working in a local otolaryngology clinic. During the 9
months before referral to the university clinic, the VR case
manager had referred JD to four hearing aid dispensers for
free hearing evaluations. A pure-tone threshold assessment
had been performed at all four sites. The test results
indicated a profound bilateral sensorineural hearing loss
with no response to pure tones at output limits of the
equipment. The VR case manager also had referred JD to a
local otolaryngologist who had evaluated JD in 1996. In his
report, the otolaryngologist had stated that JD’s current
audiogram showed a bilateral sensorineural hearing loss
with no response to pure tones, which was not in agreement with her 1996 audiogram when she had presented
with a profound sensorineural hearing loss in the right ear
and a moderately severe sensorineural hearing loss in the
left ear. The otolaryngologist reported no change in her
medical history and no medical indication for the significant change in hearing. He added that JD had “normal”
speech but responded to his questioning through a sign
language interpreter. He recommended repeating the puretone test. No physiologic assessment other than
tympanometry, which was completed only at the otolaryngology clinic, was performed at any of the test sites. The
VR case manager had reliability concerns regarding JD’s
behavioral test results because she did not believe that JD’s
speech was consistent with a profound bilateral sensorineural hearing loss. She had, therefore, referred JD to the
university clinic for physiologic audiometric assessment.
1
JD is a pseudonym used to protect the client’s privacy.
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JD arrived for her appointment at the university clinic an
hour late dressed in a night shirt. Her face was devoid of
affect and she spoke in a barely audible whisper. JD was
able to follow directions and answer questions at normal
conversational levels without difficulty and without visual
cues, including at one point when both her ears were
plugged by immittance probe tips and the clinician’s back
was to her. She reported a history of severe and recurrent
ear infections as a child and poor hearing in her right ear
for at least 20 years. She attributed the poor hearing to
either childhood ear infections or sinus infections later in
life. She described the current hearing ability in her right
ear as “plumb gone.” She did not report any symptoms of a
balance disorder such as dizziness, tinnitus, or vertigo. The
rest of the medical history was unremarkable. The client was
currently unemployed and stated that the hearing loss did not
prevent her from working but that sometimes “it was
frustrating.” She reported some noise exposure for 2 years
while working as a seamstress at a local aircraft manufacturing plant. JD stated that she wanted the VR office to provide
her with a new hearing aid for the left ear because her
hearing had become worse in that ear. She did not have her
existing hearing aid with her and was vague as to its
whereabouts. During the initial interview and all through the
evaluation, JD exhibited an affect that was flat and appeared
indifferent to the severity of her reported disability.
All tests were performed in a double-walled IAC soundtreated booth (Industrial Acoustics Company, Inc., Bronx,
NY) with equipment calibrated according to American
National Standards Institute (ANSI, 1996) S3.6-1996
guidelines. Otoscopy revealed normally appearing pinna,
ear canal, and tympanic membrane bilaterally. Immittance
testing was performed with a GSI immittance bridge
(Grason Stadler, Inc., Fitchburg, WI). Tympanometry was
performed with a single-component (Y-226 Hz) probe tone.
The tympanogram obtained from both ears showed normal
peak compensated static admittance (peak Ytm), equivalent
ear canal volume (Vea), tympanometric width (TW), and
tympanometric peak pressure (TPP) (American SpeechLanguage-Hearing Association, 1997; Margolis & Heller,
1987; Shanks & Wilson, 1986; Shanks, Lily, Margolis,
Wiley, & Wilson, 1988; Wiley et al., 1996), which was
consistent with normal middle ear function. Tonal middle
ear muscle reflex (MEMR) levels were within normal limits
with ipsilateral and contralateral stimulation at 500, 1000,
and 2000 Hz, with no response elicited at 4000 Hz in the
left ear, which is not an uncommon occurrence at 4000 Hz
for middle-aged and older individuals (Fria, LeBlanc,
Kristensen, & Alberti, 1975; Gelfand, 1984, 1994, 2002).
Tonal MEMR thresholds, however, were slightly worse for
the left ear than for the right ear (see Table 1). Acoustic
reflex decay with contralateral stimulation was negative for
each ear at 500 and 1000 Hz.
An attempt was made to establish SRT using a GSI 10
diagnostic audiometer (Grason Stadler, Inc., Fitchburg, WI)
with TDH-50 headphones (Telephonics, Huntington, NY)
and MX 41/AR cushions. JD did not respond to any of the
spondaic word stimuli in either ear even at maximum
audiometric output. Pure-tone behavioral testing was
attempted next, with repeated instructions to the client to
respond if she heard or felt anything. JD did not respond to
the air conduction tonal stimuli even at the maximum
output of the audiometer at 1000 and 2000 Hz bilaterally,
nor did she indicate any signs of discomfort or pain at the
highest intensity level (120 dB HL). JD did respond to the
clinician talking to her through the audiometer talk-forward
up to an output level of 65 dB HL, but stopped responding
when the intensity was decreased. At that point, behavioral
testing was abandoned.
Because of the lack of behavioral responses and also
reliability concerns regarding the behavioral assessment,
transient-evoked otoacoustic emission (TEOAE) testing was
performed. TEOAEs are frequency-dispersive responses
arising within the cochlea that can be measured in the
external ear canal in response to brief stimuli such as
clicks or tone bursts (Kemp, 1978; Norton, 1993; Prieve,
Gorga, & Neely, 1996). TEOAEs are a noninvasive, rapid,
and reliable assessment measure of the peripheral auditory
system up to the outer hair cell level. A substantial body of
literature exists describing the relationship of TEOAEs to
hearing loss, with the generally accepted consensus being
that the presence of TEOAEs is consistent with a hearing
loss no greater than 30 to 40 dB HL (Glattke, Pafitis,
Cummiskey, & Herer, 1995; Harrison & Norton, 1999;
Hussain, Gorga, Neely, Keefe, & Peters, 1998). Reproducibility scores of the TEOAEs in the frequency bands from
Table 1. Tonal middle ear muscle reflex levels with ipsilateral (ipsi) and contralateral (contra)
stimulation.
Middle ear
muscle reflex
Test frequencies
500 Hz
1000 Hz
2000 Hz
4000 Hz
Stimulus right
Ipsi
Contra
Decay (contra)
80
95
Negative
75
85
Negative
85
95
110
NR
Stimulus left
Ipsi
Contra
Decay (contra)
85
95
Negative
85
95
Negative
100
100
NR
NR
Note. NR = no response.
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1.0 to 5.0 kHz, especially the reproducibility score at 2.0
kHz, appear to be the most efficient measure in separating
normal and impaired ears, regardless of frequencies affected
(Glattke et al., 1995; Harrison & Norton, 1999). The
TEOAEs in JD’s ears were evoked by an 88 dBpk click
stimulus in the right ear and an 87 dBpk click stimulus in
the left ear generated by the commercially available ILO88i
otoacoustic emission measurement system (Otodynamics,
Ltd., Herts, UK). Based on current criteria (Hall, 2000;
Hurley & Musiek, 1994), emissions were present at all five
frequency bands from 1.0 to 4.0 kHz in both ears, including an overall waveform reproducibility of 96% in the right
ear and 98% in the left ear (see Figure 1).
The auditory brainstem response (ABR) test was performed next as a cross-check to the TEOAEs and to rule out
a retrocochlear pathology using a Traveler Express SE
evoked potential system (Bio-logic Systems Corp.,
Mundelein, IL). The ABR generated from a normal otologic
and neurologic auditory system consists of a sequential
series of 5 to 7 peaks occurring within approximately 10 ms
after stimulus onset. Auditory evoked potentials, in general,
and the ABR, in particular, are extremely useful in evaluating the hearing sensitivity of clients who cannot or will not
provide valid reliable hearing thresholds using behavioral
methods. In addition, the ABR is most robust in identifying
tumors of the eighth nerve greater than 1 cm in diameter
(Chandrasekhar, Brackmann, & Devgan, 1995; Telian,
Kileny, Niparko, Kemink, & Graham, 1989), with somewhat
less success reported in diagnosing diffuse demyelinating
conditions such as multiple sclerosis (Hood, 1998).
The ABR test with JD was performed with four runs in
each ear. Two runs with a rarefaction and two runs with a
condensation click stimulus polarity at 85 dB nHL also
were completed to rule out the rare chance of an existing
auditory neuropathy (dys-synchrony) even though the
MEMRs were within normal limits (Berlin, 1999). ABR
absolute latencies (the time interval between the stimulus
onset and the peak of a waveform) and interwave latencies
(the time interval between peaks of a waveform) for both
ears were within normal limits (Hall, 1992b) (see Table 2).
It is important to remember that the ABR is a test of
synchronous neural function and not a test of hearing and
thus cannot represent true, conscious, behavioral hearing
(Hood, 1998). It is possible, however, to use this measure
to make inferences about hearing sensitivity based on the
presence of responses to sound stimuli at various levels of
intensity by plotting the latencies of wave V as a function
of intensity and, thus, obtain a latency-intensity function.
The latency-intensity function in this case could have been
useful in providing an estimation of JD’s actual hearing
sensitivity, but, unfortunately, it was not determined
because JD was getting restless, resulting in an increased
number of artifacts and decreased reliability of the ABR
test results. Table 3 provides an overview of the results of
the diagnostic tests performed at the university clinic,
demonstrating the discrepancies between the behavioral test
results and the results of the physiologic assessment
measures of the auditory system.
At the completion of the evaluation, JD was told that the
results did not indicate as severe a hearing loss as had
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been demonstrated by the previous tests and that she may
have to return for additional testing. She responded to this
statement with no change in affect and appeared indifferent
to the outcome of the evaluation. JD’s VR case manager
was informed of the results and suggested a psychiatric
evaluation rather than further audiologic evaluations.
The preliminary diagnosis of the subsequent mental
status evaluation was an adjustment disorder with mixed
emotional features. An adjustment disorder is a maladaptive
reaction to an identifiable psychosocial stressor, typically
occurring within 3 months after the onset of the stressor
and not meeting the criteria for any other specific diagnosis.
Symptoms, though usually acute and transient, may last for
years if the stressor continues (APA, 1994a). The differential
diagnosis should be made from well-delineated disorders
such as conversion disorder and depression (Gregory &
Smeltzer, 1983). The psychologist reported that JD demonstrated “slightly flattened” facial expression and affect and
spoke in a “very soft” voice but was able to communicate
with him without the aid of a sign language interpreter. He
categorized her intellectual function in the low “normal”
range with memory that was intact and within normal limits
for short-term auditory recall. JD reported to the psychologist that she had spent some time in a children’s home
during her adolescence and was treated at the state mental
hospital during her teen years. After the psychological
evaluation, JD did not report back to the VR office, and,
therefore, no follow-up psychological assessment or
treatment was performed. Because of her homeless status, it
was not possible to contact her to schedule follow-up
audiologic testing, despite repeated efforts.
DISCUSSION
Martin (2002) suggested that the function of the audiologist
is to determine the true extent of the organic component, if
present, rather than to determine the precise reason for the
nonorganic component. Audiologists, however, also need to
be aware of conditions other than a hearing loss that may
bring an individual to their clinic and when the need for
diagnostic tools beyond a pure-tone audiogram may become
necessary. This case exemplifies the importance of physiologic measures such as the tonal MEMR, OAEs, and
auditory evoked potentials such as the ABR as a crosscheck for behavioral audiologic thresholds.
One possibility for the delay in diagnosis of the NOHL
in JD’s case may have been the lack of behavioral responses. Because of the absence of behavioral responses,
the typical discrepancies between behavioral test results
were not exhibited nor could behavioral diagnostic tests for
NOHL be performed. Behavioral diagnostic tests for NOHL
include the Stenger test when a unilateral NOHL is
suspected. It is based on the Stenger principle, which states
that when auditory stimuli are presented to both ears
simultaneously, but with the stimulus presented to one ear
being louder, only the louder sound will be perceived by
the listener (Monro & Martin, 1977; Stenger, 1907; Taylor,
1949). A useful test for suspected bilateral NOHL is the
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Figure 1. The upper half of the figure displays the transient-evoked otoacoustic emission (TEOAE) data from the right ear; the lower
half displays the TEOAE data from the left ear. In the upper half of the figure, the top left box shows the temporal waveform of
the click stimulus. The top right center “Response SNR” box displays the shaded waveform of the frequency spectrum of the
emission as a cross-power correlation from the two emission waveforms. The straight band across the box is the associated noise
spectrum and is the difference between the two waveform recordings. The left middle “Response Waveform” (QuickScreen) box
displays the two overlapped emission waveforms (A and B) as a time spectrum. In the middle right “Power Analysis” box, the first
solid line represents the frequency response of the stimuli, which was flat, as desired, across the frequency range from 0 to 4 kHz.
The middle shaded waveform displays the frequency spectrum of the TEOAE response or the echo rising above the noise floor, and
the lower shaded waveform displays the noise floor. The far right panel lists the stimulus and response parameters numerically. The
top subsection, Noise, indicates that the average noise level in the external ear canal during TEOAE measurement was low (32.9
dB) and that 96% of the 260 stimuli were presented when the noise was lower than the rejection level of 47.3 dB. The middle
subsection, Response, displays a high overall waveform reproducibility of 96% as well as high reproducibility values (represented
in %) across the individual octave bands from 1 to 4 kHz and a high signal-to-noise-ratio (SNR) for the TEOAES (represented in
dB) versus the noise floor. These results indicate that TEOAES were present from 1 to 4 kHz based on the response parameters of
adults with normal hearing sensitivity. Similar results were obtained for the left ear (lower panel), indicating the presence of
TEOAEs from the 1 to 4 kHz frequency region with an overall waveform reproducibility of 98%. For a detailed analysis of OAE
stimulus and response parameters, please refer to Hall (2000).
Mehta: Limitations of Pure-Tone Audiometry
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Table 2. Results of the auditory brainstem response test with 85 dB nHL click stimulus with
rarefaction polarity.
Ear
I
Right
Absolute latency (ms)
Interwave latency (ms)
Amplitude (µV)
Left
Absolute latency (ms)
Interwave latency (ms)
Amplitude (µV)
III
V
1.88
3.60
5.08
+.15
+.17
+.15
1.72
3.76
5.32
+.12
+.14
+.19
1–III
111–V
1–V
1.72
1.48
3.20
2.04
1.56
3.60
Note. Results with the condensation polarity were similar and, therefore, were not presented in order to
maintain clarity of the data.
Table 3. Overview of the bilateral behavioral and diagnostic tests performed.
Test procedure
Stimuli used
Tympanometry
226 Hz Y
Normal
Tonal middle ear muscle
reflexes (MEMRs)
5000–2000 Hz with ipsilateral
and contralateral stimulation
Within normal
limits
Acoustic reflex decay
500 and 1000 Hz with
contralateral stimulation
Negative
Speech recognition threshold (SRT)
Spondee words presented at levels
up to output limits of the audiometer
No response
Pure-tone air conduction
1000 and 2000 Hz up to 120 dB HL
No response
Otoacoustic emissions (OAEs)
Click-evoked TEOAEs
from 1000–4000 Hz
Present
Auditory brainstem response (ABR)
85 dB nHL click stimulus with
rarefaction and condensation polarity
Absolute and
interwave latencies
within normal limits
Doerfler-Stewart test (Doerfler & Stewart, 1946), which is
performed by obtaining an SRT accompanied by background
noise, with the intensity of the background noise increased
systematically. The delayed auditory feedback (DAF) test is
another behavioral test used to diagnose NOHL. It is based
on the phenomenon that audible acoustic signals fed back to
the listener with a delay of approximately 200 ms disrupt
ongoing listening behavior that manifests as a significant
change in vocal behavior (Ruhm & Cooper, 1964). Another
behavioral assessment measure for NOHL is the Lombard
test, which is based on the observation that in the presence
of background noise, listeners will reflexively increase the
intensity of their speech in order to be heard (Shoup &
Roeser, 2000). Most of these tests were useful because they
could identify the NOHL by disrupting or distorting the
internal loudness anchor used by individuals with NOHL to
decide which stimulus level they want to respond to
(Gelfand & Silman, 1985, 1993; Martin et al., 2001). Now,
however, with the exception of the Stenger test, these tests
are almost obsolete because although they identified an
NOHL, they failed to quantify its degree.
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JD’s lack of behavioral responses to tonal stimuli was
inconsistent with the results of the physiologic tests
performed; the tonal MEMR levels were within normal
limits with ipsilateral and contralateral stimulation,
TEOAEs were present bilaterally, and ABR waveforms
showed absolute and interwave latencies within normal
limits at 85 dB nHL. An ABR latency-intensity function
would have been beneficial in determining approximate
hearing sensitivity levels. The presence of TEOAEs,
however, argues strongly and objectively for normal
cochlear integrity, at least up to the level of the outer hair
cells. Although the actual hearing sensitivity was not
established, and it is possible that JD may have had an
organic peripheral hearing loss, the presence of TEOAEs
(with the exception of individuals with auditory neuropathy) is consistent with a peripheral hearing sensitivity that
was probably no worse than a mild sensorineural hearing
loss (30–40 dB HL) for the stimulus frequencies (Hurley &
Musiek, 1994; Lonsbury-Martin, Cutler, & Martin, 1991;
Lonsbury-Martin & Martin, 2001; Stover & Norton, 1993).
The audiologic testing performed at the university clinic
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did not rule out a neurological disorder beyond the auditory
brainstem. The presence of such a condition, however, was
unlikely given that no additional symptoms had been
reported or documented since 1992. In addition, JD
appeared to have no difficulty hearing or understanding
speech even without visual cues. JD’s psychosocial profile
was consistent with that cited in the literature for individuals most likely to present with an NOHL. Further, the
preliminary diagnosis of an adjustment disorder was more
consistent with a primary psychological disorder rather than
with an auditory disorder.
Although the diagnosis of NOHL may not be difficult for
most clinicians, the challenge lies in determining the actual
hearing sensitivity and confronting the client with that
information in a manner that is not insulting and that
allows for a graceful retreat on the part of the client. The
NOHL diagnosis becomes more complicated when the
purported hearing loss is manifested at an unconscious
level, especially if clinicians are not experienced or trained
to anticipate the existence of such a condition. In the
absence of an appropriate diagnosis, individuals with
NOHL may even be referred as candidates for a cochlear
implant, as one hearing aid dispenser had recommended for
JD, with the diagnosis consuming valuable time and
expense (Spraggs et al., 1994).
The diagnosis of NOHL is often an exclusionary one made
after other medical causes of the hearing loss have been
ruled out. In the case of psychological conditions such as
adjustment and conversion disorders, it is the absence of
expected medical and laboratory findings that suggest and
support the diagnosis (APA, 1994b). Identification of recent
psychosocial stressors also can aid in the diagnosis. During
the course of the evaluation, for example, JD had mentioned
several times to the clinician her concerns regarding the
whereabouts of her daughter and granddaughter, which may
have been the current psychosocial stressor. Referral source,
a good case history, and behavioral observations can be
useful in raising the index of suspicion for an NOHL.
When responses to behavioral audiometric assessments are
not reliable, or when the results of the different components
of the basic assessment battery are not in agreement, then
physiologic tests must be performed. Tonal MEMRs are an
effective nonbehavioral tool for identifying or substantiating
the presence of an NOHL. Part of the desirability of using
tonal MEMRs comes from their routine clinical nature,
compared to other physiologic measures such as cortical
evoked potentials, which may address a wider range of
hearing disorders but are rarely used in routine clinical
practice because of well-established practical limitations
(Gelfand, 1994). Several investigators have found that
excellent agreement exists between the results of MEMR
levels, reflex decay measures, and the ABR in distinguishing
a cochlear and retrocochlear site of lesion, and they serve as
a reliable cross-check (Hayes & Jerger, 1981). When all
three measures appear normal, then the presence of a
pathology, at least up to the level of the auditory brainstem,
would be highly unlikely. Gelfand (1994) reported that
although the MEMR is an effective nonbehavioral tool for
detection of an NOHL, it cannot identify a functional
component if the volunteered thresholds are ≤60 dB HL
because the MEMR would normally be present with a
cochlear hearing loss of that magnitude. Even with this
limitation, immittance measures should be performed initially
for all routine audiologic assessments because they can
discourage pseudohypacusis (Martin, 2002) and alert the
clinician to the possible presence of an NOHL.
OAEs are another physiologic measure that can aid in
the diagnosis of an NOHL. Equipment to determine OAEs
is now available in most audiology clinics and can be used
to provide additional valuable information regarding the
status of the auditory system. The relationship of OAEs to
other physiologic measures of auditory assessment, such as
MEMR and ABR, substantiates the value of this procedure
for the diagnosis of an NOHL (Kemp, Ryan, & Bray, 1990;
Musiek, Bornstein, & Rintelmann, 1995; Robinette, 1992).
The presence of emissions obtained with volunteered
thresholds greater than approximately 30–40 dB HL
suggests an NOHL or a neural basis for the hearing loss
because evidence of OAEs is typically incompatible with a
sensory hearing loss exceeding a mild loss range, if the
loss is secondary to outer hair cell dysfunction (Musiek et
al., 1995). Limitations of TEOAEs include prevention of
recording of responses because of attenuative influences of
the external and middle ear on reverse energy transmission
and their insensitivity to disorders affecting inner hair cells
or higher levels of the auditory pathway (Norton et al.,
2000). The TEOAEs’ amplitude appears to decrease with
increasing age: Adults have an overall lower TEOAE
amplitude than children, and children have a lower amplitude than infants (Glattke et al., 1995; Prieve, Fitzgerald, &
Schulte, 1997).
Auditory evoked potentials also are a useful tool for the
diagnosis of an NOHL. The ABR test can be used as a
cross-check to volunteered responses as well as to rule out
a neurologic basis of the hearing loss, which may not be
possible through behavioral or OAE testing alone. Abnormal ABR findings indicate the possibility of a pathological
condition of the auditory nerve and brainstem pathways but
not the type of the pathology. For example, the ABR
abnormality cannot diagnose a tumor versus a vascular
lesion (Arnold, 2000). Middle and long latency auditory
evoked responses can be beneficial in effectively ruling out
neurological conditions beyond the level of the brainstem
before establishing a diagnosis of NOHL. Middle latency
auditory evoked potentials (MLAEPs) consist of a series of
auditory evoked responses that occur between 10 and 80
ms following the onset of an acoustic stimulus. By definition, MLAEPs follow the ABR and precede the long
latency auditory evoked potentials (Kraus, McGee, & Stein,
1994). Clinical uses of MLAEPs include the estimation of
frequency-specific hearing thresholds, especially in the
lower frequencies (Musiek & Geurnink, 1981; Scherg &
Volk, 1983); assessment of auditory pathway function,
including ruling out a central pathology when an NOHL is
suspected and localization of auditory pathway lesions
(Buchwald, Erwin, Read, Van Lancker, & Cummings, 1989;
Jacobson & Grayson, 1988; Kileny, Paccioretti, & Wilson,
1987; Kraus & McGee, 1988); and assessment of cochlear
implant function (Kileny & Kemink, 1987; Miyamoto,
1986). The MLAEPs are affected by low-frequency muscle
Mehta: Limitations of Pure-Tone Audiometry
65
artifacts, specifically postauricular muscle (PAM) activity
(Kileny, 1984); sleep stages, especially in children (Kraus,
McGee, & Comperatore, 1989); sedation (Schwender et al.,
1996); and neuropsychiatric history (Baker et al., 1990;
Siegel, Waldo, Mizner, Adler, & Freedman, 1984). The
utility of MLAEPs as a test of central auditory function is
limited by an incomplete understanding of the MLAEP
generating system (Kraus et al., 1994), the considerable
variation in normal waveform morphology, and the pattern
of abnormalities that may vary with differing recording
conditions (Arehole, Augustine, & Simhadri, 1995).
The long latency auditory evoked potentials (LAEPs) are
recorded in a time period from approximately 50 to 250 ms
after acoustic stimulation by a transient sound such as a
click, toneburst, or speech element at a relatively slow rate
(approximately 1 to 2 stimuli per second) and include both
exogenous and endogenous potentials (Scherg, Vajsar, &
Picton, 1989; Velasco, Eelasco, & Velasco, 1989). Exogenous auditory responses are those responses that are
generated primarily by the physical characteristics of the
stimulus; endogenous auditory responses are those that are
produced after internal processing of the stimulus has
occurred. The spectral power of the typical LAEP response
is between 1 and 15 Hz and is most evident at approximately 5 Hz. Unlike the ABR waveforms, amplitude
measures are always obtained for cortical evoked potentials.
Compared to earlier evoked potential responses, the
amplitude of the LAEP response is large at approximately 3
to 10 µvolt and sometimes even larger (Hyde, 1994). The
precise location of the LAEP neural generators is unclear,
but they probably overlap and include the areas in and
around the primary auditory cortices (Vaughan & Ritter,
1970), the auditory association cortex in the superior
temporal gyrus (Wolpaw & Penry, 1975), and the frontal
motor and/or premotor cortex under the influence of the
reticular formation and the ventral lateral nucleus of the
thalamus (Naatanen & Picton, 1987).
LAEP responses demonstrate complexity of interaction
among stimulus conditions (Stapells, 2002), attention
(Naatanen & Picton, 1987), alertness and sleep
(Osterhammel, Davis, Wier, & Hirsh, 1973; Picton &
Hillyard, 1974), drugs (Hall, 1992a), and maturation
(Kurtzberg, 1989; Sharma, Kraus, McGee, & Nicol, 1997).
The LAEP can be a useful clinical tool in the estimation of
hearing sensitivity of individuals when a nonbehavioral,
frequency-specific, and sensitive measure is needed, such as
for medicolegal and compensation assessments and the
evaluation of a suspected NOHL (Hyde, 1994). Other
potential clinical applications include nonbehavioral
measurement of frequency and temporal discrimination,
localization, speech perception, and the diagnosis of
auditory processing disorders and attention deficit hyperactivity disorders (Hyde, 1994). Clinical applications of the
LAEPs are, however, limited by considerable inter- and
intrasubject variability, state of participants, drugs, age, and
the lack of knowledge regarding precise location of neural
generators (McPherson & Ballachandra, 2000). These
responses are, however, still considered important and
promising in assessing the functioning of the higher levels
of the central auditory system.
66
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Another cortical auditory evoked potential is the P300
response, which is essentially a component within an
extended LAEP time frame. It is an endogenous cognitive
auditory response that is nonsensory specific, that is, it
occurs in response to both unimodality and multimodality
sensory stimulation (McPherson & Ballachandra, 2000). It
is recorded under special stimulus conditions, the simplest
of these conditions being an infrequent or rare stimulus
presented randomly within a series of frequent, predictable
stimuli. This response is sometimes referred to as the
P300 because it is often observed in the 300 ms region,
although it has been recorded in listeners with normal
hearing sensitivity as early as 250 ms and as late as 400
ms (Hall, 1992c).
In the literature, the amplitude and latency of the P300
has been reported as abnormal in several types of neuropsychiatric and behavioral disorders. Clinical applications
of the P300 are related to the task-relevant nature of this
response, and, therefore, it has potential for studying higher
level auditory processing skills (McPherson &
Ballachandra, 2000). It has been used successfully in the
study and assessment of children with attention deficit
hyperactivity disorders (Salamat & McPherson, 1999),
cochlear implant users as a means of determining cognition
and discrimination (Kileny, 1991), cerebral lesions in adults
(Hurley & Musiek, 1997), auditory deprivation (Hutchinson
& McGill, 1997), and dementia and Alzheimer’s disease
(Polich, 1989; St. Clair, Blackburn, Blackwood, & Tyrer,
1988). Currently, only a small percentage of clinicians are
routinely using MLAEPs and LAEPs (Martin, Champlin, &
Chambers, 1998), probably because of the available
equipment, experience of clinicians, and third-party
reimbursement issues.
Physiologic assessment measures, when used together
with behavioral observation and behavioral assessment, can
improve the diagnostic criterion of NOHL. Unfortunately,
in JD’s case, no such assessments had been performed
despite repeated audiologic evaluations over several years,
and, thus, the possible underlying psychological disorder
was not diagnosed. Early identification of the NOHL may
have led to appropriate medical intervention that could
have improved her quality of life. Audiologists are not
responsible for determining the underlying reason for an
NOHL, nor should they be judgmental of those who present
with it. It is, however, the responsibility of the audiologist
to diagnose a nonorganic component and to determine the
extent of a true organic hearing loss that may coexist with
the NOHL. It also is important for audiologists to be
informed that psychogenic hearing loss does exist and that
clinicians have an obligation to provide clinical services
that will benefit clients with this disorder, including
appropriate and timely medical referral when indicated.
ACKNOWLEDGMENT
The author had evaluated this client when she was a doctoral
student. An earlier version of this manuscript was presented as a
poster session at the 1999 annual convention of the American
DISORDERS • Volume 30 • 59–69 • Spring 2003
Speech-Language-Hearing Association in San Francisco, California.
Special thanks to Kenn Apel for his thoughtful suggestions leading
to the development of the manuscript in its present format. Thanks
to Ray Hull and Barbara Hodson for their support and editorial
help during the preparation of this manuscript.
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Contact author: Zarin Mehta, Department of Communicative
Disorders and Sciences, Wichita State University, 1845 N.
Fairmount, Wichita, KS 67260-0075. E-mail:
[email protected]
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