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Original Research—Otology and Neurotology
Acoustic Reflex Screening of Conductive
Hearing Loss for Third Window Disorders
Robert S. Hong, MD, PhD1,2,3,4,
Christopher M. Metz, DO5, Dennis I. Bojrab, MD1,2,3,4,
Seilesh C. Babu, MD1,2,3,4, John Zappia, MD1,2,3,4,
Eric W. Sargent, MD1,2,3,4, Eleanor Y. Chan, MD1,2,3,4,
Ilka C. Naumann, MD1,2,3,4, and Michael J. LaRouere, MD1,2,3,4
No sponsorships or competing interests have been disclosed for this article.
Abstract
Objective. This study examines the effectiveness of acoustic
reflexes in screening for third window disorders (eg, superior semicircular canal dehiscence) prior to middle ear exploration for conductive hearing loss.
Study Design. Case series with chart review.
Setting. Outpatient tertiary otology center.
Subjects and Methods. A review was performed of 212 ears
with acoustic reflexes, performed as part of the evaluation
of conductive hearing loss in patients without evidence of
chronic otitis media. The etiology of hearing loss was determined from intraoperative findings and computed tomography imaging. The relationship between acoustic reflexes and
conductive hearing loss etiology was assessed.
Results. Eighty-eight percent of ears (166 of 189) demonstrating absence of all acoustic reflexes had an ossicular
etiology of conductive hearing loss. Fifty-two percent of
ears (12 of 23) with at least 1 detectable acoustic reflex had
a nonossicular etiology. The positive and negative predictive
values for an ossicular etiology were 89% and 57% when
acoustic reflexes were used alone for screening, 89% and
39% when third window symptoms were used alone, and
94% and 71% when reflexes and symptoms were used
together, respectively.
Otolaryngology–
Head and Neck Surgery
2016, Vol. 154(2) 343–348
Ó American Academy of
Otolaryngology—Head and Neck
Surgery Foundation 2015
Reprints and permission:
sagepub.com/journalsPermissions.nav
DOI: 10.1177/0194599815620162
http://otojournal.org
Received August 19, 2015; revised October 14, 2015; accepted
November 10, 2015.
T
he acoustic reflex refers to the contraction of the stapedius muscle in response to an intense acoustic stimulus. It can be indirectly measured in the clinical
setting by means of an impedance bridge. The reflex arc consists of sound stimulating the cochlea, resulting in stimulation
of the eighth cranial nerve, ventral cochlear nuclei, superior
olive, and facial nerve and, ultimately, contraction of the stapedius muscle.1 It involves crossed and uncrossed pathways,
whereby stimulation of 1 ear with a high-level sound stimulus will result in contraction of the stapedius muscles of both
ears in a individual with normal physiology.
The majority of patients with significant conductive hearing
loss, with otherwise normal otoscopic examination results, will
have an ossicular etiology of hearing loss. However, there
have been reports of patients undergoing middle ear exploration with the intraoperative finding of a normal ossicular
chain, despite a significant conductive hearing loss.2,3 For
many years, these patients were considered as having an
‘‘inner ear conductive hearing loss.’’4-6 More recently, it has
been found that third window disorders, such as superior semicircular canal dehiscence and a dilated vestibular aqueduct,
can also cause a conductive hearing loss,7-9 and many patients
1
Michigan Ear Institute, Farmington Hills, Michigan, USA
Department of Otolaryngology–Head and Neck Surgery, Wayne State
University, Detroit, Michigan, USA
3
Neurotology Division, St John Providence Health System, Novi, Michigan,
USA
4
Department of Surgery, Oakland University William Beaumont School of
Medicine, Rochester, Michigan, USA
5
Osteopathic Division, St John Providence Health System, Madison Heights,
Michigan, USA
2
Conclusion. Acoustic reflex testing is an effective means of
screening for third window disorders in patients with a conductive hearing loss. Questioning for third window symptoms should complement screening. The detection of even
1 acoustic reflex or third window symptom (regardless of
reflex status) should prompt further workup prior to
middle ear exploration.
Keywords
acoustic reflex, otosclerosis, superior semicircular canal
dehiscence, conductive hearing loss, third window
This article was presented at the 2015 AAO-HNSF Annual Meeting & OTO
EXPO; September 27-30, 2015; Dallas, Texas.
Corresponding Author:
Robert S. Hong, MD, PhD, Michigan Ear Institute, 30055 Northwestern
Hwy, #101, Farmington Hills, MI 48334, USA.
Email: [email protected]
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Otolaryngology–Head and Neck Surgery 154(2)
with previously unclear causes of conductive hearing loss have
been found to have such a third window disorder.10-13 One
potential way to avoid middle ear surgery in patients whose
hearing loss is caused by a third window disorder is to obtain
high-resolution computed tomography (CT) imaging of the
temporal bone.14 However, this is not performed routinely, due
to the high rates of success of middle ear exploration and to
the added cost and radiation involved with imaging.
An alternative that may be considered to assess for a
third window disorder is to obtain acoustic reflexes prior to
middle ear exploration. In patients considering surgical correction of conductive hearing loss, one would expect acoustic reflexes to be absent in the affected ear if the etiology is
secondary to otosclerosis.15,16 In contrast, in patients with
conductive hearing loss due to a third window disorder, the
acoustic reflex should remain present, as the ossicles are
normal.9 For patients whose reflexes are not consistent with
an ossicular etiology, imaging can be ordered to assess for a
third window disorder.
At our institution, we routinely measure acoustic reflexes
at 4 stimulus frequencies (500, 1000, 2000, and 4000 Hz)
for each ear. Thus, a total of 8 measurements of acoustic
reflex threshold are relevant when one is evaluating the likelihood of an ossicular etiology of a particular ear’s conductive hearing loss. What are ill defined are the exact criteria
that should be used to trigger further workup for a third
window disorder. How many acoustic reflexes need to be
present to recommend imaging for a third window disorder?
Does the magnitude of the acoustic reflex threshold matter,
when present? Is it possible for all acoustic reflexes to be
absent and still have a third window disorder responsible for
the conductive hearing loss? If so, are there other factors to
consider to mitigate the risk of unnecessary middle ear
exploration? In addressing these questions, we hope to
improve our ability to avoid middle ear surgery for patients
whose conductive hearing loss is not due to an ossicular
etiology.
Methods
The cases of 720 consecutive patients who had acoustic
reflexes performed at a tertiary otology center from July
2011 to April 2014 were screened in a retrospective review.
The study was approved by the Providence Hospital and
Medical Centers Institutional Review Board (study No.
636292). From these, 192 patients contributing 212 ears
were included in the study, based on the following inclusion
and exclusion criteria.
Inclusion criteria included the following:
Acoustic reflexes obtained in context of consideration of middle ear exploration for conductive hearing loss
Evidence of etiology of conductive hearing loss—
including (1) middle ear surgery documenting the
status of the ossicles AND postoperative documentation of hearing status or (2) high-resolution CT
imaging of temporal bone
Exclusion criteria were as follows:
Prior middle ear surgery on the ear with the conductive hearing loss
Chronic otitis media, including tympanic membrane
perforation or cholesteatoma (based on history,
physical examination, or imaging findings)
Incomplete acoustic reflex data relevant for a particular ear’s conductive hearing loss
Given the above, the majority of patients who were
excluded from this study were those with a conductive hearing loss who did not have surgical exploration of the ear
and did not have CT imaging, as the etiology of the hearing
loss could not be determined.
Classification of conductive hearing loss. The etiology of conductive hearing loss was separated into the following categories: (1) ossicular abnormalities, (2) third window
disorders, (3) both ossicular and third window etiologies,
(4) other etiology, and (5) unknown etiology.
To be classified as having an ossicular etiology, an ear
needed to meet 1 of the following criteria. First, if an ear
underwent middle ear surgery, there needed to be an intraoperative finding of an ossicular abnormality (eg, ossicular
fixation or discontinuity) deemed responsible for the hearing
loss. Furthermore, if surgical correction of this abnormality
was attempted, there needed to be confirmation of hearing
improvement postoperatively, in the form of either closure
of the average air-bone gap (ABG) after surgery to \20 dB
or documentation of subjective hearing improvement (in a
few instances where the audiogram not available). Second,
if an ear did not undergo surgery, it needed to have a highresolution CT scan of the temporal bone that demonstrated
either evidence of otosclerosis or lack of evidence of a third
window disorder.
To be classified as having a third window disorder, an
ear needed to demonstrate semicircular canal dehiscence or
a dilated vestibular aqueduct on CT imaging. Diagnosis of
these entities was based on review of the local neuroradiologist’s report of CT findings, followed by review of images
by the attending otologist during the patient encounter as
documented in the patient chart. With respect to the diagnosis of superior semicircular canal dehiscence, all scans
obtained at our home institution had the recommended
views in the Stenvers and Poschl planes; CT scans obtained
from outside institutions were reformatted by the attending
otologist at the time of the patient visit using OsiriX software (Pixmeo Sarl, Bernex, Switzerland) in the Stenvers
and Poschl planes if such views were not already available.
To be classified under other etiology, there needed to be
a clearly defined alternative etiology for conductive hearing
loss, as was true in one case of an encephalocele (seen on
CT imaging and intraoperatively).
To be classified as having an unknown etiology, there
needed to be a lack of evidence of ossicular etiology (ie,
intraoperative finding of normal ossicles and/or lack of
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Hong et al
345
improvement in hearing postoperatively despite attempted
surgical correction) and lack of evidence of a third window
disorder (ie, normal CT temporal bone).
Audiometry. All testing was performed in a soundproof
booth. Pure tone audiometry was performed from 250 to
8000 Hz for air conduction and 250 to 4000 Hz for bone
conduction, with masking as appropriate. Conductive hearing loss was calculated from the 4-tone average ABG measured at 500, 1000, 2000, and 4000 Hz.
Acoustic reflex thresholds were measured at 500, 1000,
2000, and 4000 Hz for each ear with both ipsilateral and
contralateral presentation of the sound stimulus. Reflexes
were assessed with the GSI Tympstar Middle Ear Analyzer
(Grason-Stadler, Eden Prairie, Minnesota). All stimuli were
presented with the auto-timing GSI default setting, with a
train of 8 repeated pure tones over 1.5 seconds. Stimuli
were initially presented at 80 dB and increased in 5-dB
increments up to 120 dB, until a reflex was measured. If an
acoustic reflex was not detected at 120 dB, then the acoustic
reflex was regarded as not being present. A total of 8 acoustic reflexes were relevant for evaluating the conductive
hearing loss in a given ear. For example, for right conductive hearing loss, reflexes were relevant at each frequency
for the right ipsilateral condition (sound stimulus to right
ear, probe in right ear) and left contralateral condition
(sound stimulus to left ear, probe in right ear).
Results
A total of 192 patients contributing 212 ears met inclusion
criteria for the study, with 20 patients contributing both ears.
Their average age was 47.5 years, and there were 121
women and 91 men. The laterality of the ears was 110 left
and 102 right ears. The average ABG prior to any surgical
intervention for all ears in this study was 22.8 dB, with those
with an ossicular etiology having a statistically significantly
larger ABG (23.8 dB) than those with a third window disorder (17.2 dB; t test, P = .003). The etiology of conductive
hearing loss is shown in Table 1. Of the ears included in this
study, 186 of 212 underwent middle ear surgery, which
included several ears where the diagnosis of a nonossicular
etiology of hearing loss was not obtained until after surgery.
Out of 212 ears, 189 demonstrated no response to all
acoustic reflexes, and 23 had at least 1 detectable acoustic
reflex. Of the ears found to have absent acoustic reflexes at
all frequencies tested, an ossicular etiology of hearing loss
was found in 88% (166 of 189 ears) and a third window
etiology in 10% (18 of 189). This excludes 4 ears that had
evidence of both etiologies and 1 ear that had evidence of
neither. Of the ears found to have at least 1 detectable
acoustic reflex, an ossicular etiology of hearing loss was
present in 48% (11 of 23 ears), and a third window abnormality was present in 39% (9 of 23). This excludes 1 ear that
had evidence of both, 1 ear that had evidence of neither,
and 1 ear that had an encephalocele as the source of the
conductive hearing loss. Thus, overall, for patients with at
least 1 detectable acoustic reflex, a nonossicular etiology
Table 1. Etiology of Conductive Hearing Loss.
Conductive Hearing Loss Etiology
Ossicular abnormality
Otosclerosis
Other ossicular abnormality
Third window disorder
Superior semicircular canal dehiscence
Dilated vestibular aqueduct
Both ossicular and third window disorder (including above)
Other (eg, encephalocele)
Unknown
Ears, n
171
11
29
3
5
1
2
was present in 52% (12 of 23 ears). The number of detectable acoustic reflexes for ears with only an ossicular
abnormality and those with only a third window disorder
are shown in Figure 1. There was no statistical correlation
found between either the number of detectable reflexes or
the magnitude of these reflexes, when detected, and the
etiology of conductive hearing loss.
For patients with no response to any acoustic reflexes,
the prevalence of symptoms suggestive of third window disorders was examined. No such symptoms were found in
82% (155 of 189 ears), including 144 ears with an ossicular
etiology, 8 ears with a third window etiology, 2 ears with
both etiologies, and 1 ear with an unknown etiology. The
symptom of dizziness was found in 14% (26 of 189 ears),
including 17 ears with an ossicular etiology, 8 ears with a
third window disorder, and 1 ear with both. The symptom
of pulsatile tinnitus was present in 7% (13 of 189 ears),
including 8 ears with an ossicular etiology, 4 ears with a
third window disorder, and 1 ear with both. The symptom
of autophony was present in 2% (3 of 189 ears), including 1
ear with an ossicular etiology and 2 ears with a third
window disorder. Overall, 35% (12 of 34) of ears with dizziness, pulsatile tinnitus, and/or autophony and no response
to any acoustic reflex were found to have a nonossicular
etiology of conductive hearing loss.
For patients with at least 1 detectable acoustic reflex, the
prevalence of symptoms suggestive of third window disorders was also examined. No such symptoms were found in
83% (19 of 23 ears), including 10 ears with an ossicular
etiology, 6 ears with a third window etiology, 1 ear with
both etiologies, 1 ear with an unknown etiology, and 1 ear
with an encephalocele. The symptom of dizziness was
found in 13% (3 of 23 ears), with all 3 ears with a third
window disorder. The symptom of pulsatile tinnitus was
present in 4% (1 of 23 ears), with this ear having an ossicular etiology. The symptom of autophony was not found in
any ears. Overall, 75% (3 of 4) of ears with dizziness, pulsatile tinnitus, and/or autophony and at least 1 detectable
acoustic reflex were found to have a third window disorder.
In summary, the results presented in Table 2 demonstrate the value of acoustic reflexes as compared with the
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Otolaryngology–Head and Neck Surgery 154(2)
Figure 1. Number of acoustic reflexes present. The number of acoustic reflexes detected (of 8) per ear is shown for those with conductive hearing loss secondary to an ossicular abnormality and a third window disorder.
Table 2. Performance of Acoustic Reflexes vs Third Window Symptoms as a Screening Tool for Conductive Hearing Loss (in Percentages).
Positive predictive value
Negative predictive value
Sensitivity
Specificity
Acoustic Reflexes
Third Window Symptoms
Both
89
57
94
36
89
39
87
43
94
71
94
69
use of third window symptoms as a screening tool for determining that an ossicular abnormality is solely responsible
for conductive hearing loss. A true positive is defined as a
correct determination of an ossicular etiology of hearing
loss. A true negative is defined as a correct determination
that an ossicular etiology is not solely responsible for hearing loss. From the table, it can be seen that the use of third
window symptoms alone in screening is almost as effective
as using acoustic reflexes alone. However, the most effective screening method is to use a combination of acoustic
reflexes and the presence of third window symptoms to
screen, where a CT scan is obtained for all patients that
have either at least 1 detectable acoustic reflex or third
window symptom (regardless of acoustic reflex result).
Ordering imaging in these cases would allow us to increase
the positive predictive value to 94%, as we would correctly
diagnose the etiology of conductive hearing loss in 12 additional ears (Table 2). The cost of such an algorithm would
be that a negative CT scan would be ordered in 12%, as 22
ears with an ossicular abnormality and absence of all acoustic reflexes also had dizziness, pulsatile tinnitus, and/or
autophony.
Discussion
This study demonstrates that it is important to obtain acoustic reflexes and inquire about the presence of third window
symptoms in all patients prior to middle ear exploration.
While reflexes alone and history alone can serve as screening tools for third window disorders, the combination of the
two is most effective in minimizing the risk of unnecessary
middle ear surgery. The results of this study suggest that the
detection of even 1 acoustic reflex relevant to a particular
ear’s conductive hearing loss should prompt further workup
with CT imaging. Furthermore, it is important to realize that
it is possible for all acoustic reflexes to be absent and still
have a third window disorder responsible for the conductive
hearing loss. Asking about third window symptoms and
obtaining a CT scan when such symptoms are present help
to mitigate the risk of a negative middle ear exploration in
such a scenario. It has been suggested that vestibular
evoked myogenic potentials may also play a role in the
screening process for third window disorders prior to
middle ear exploration.17 Additional research is required to
determine what combination of history, acoustic reflexes,
and/or vestibular evoked myogenic potentials is most effective for screening for third window disorders in such
patients.
With ossicular etiologies of conductive hearing loss,
acoustic reflexes change as the disease progresses. With otosclerosis as an example, the reflexes may be initially
normal. As stapes fixation progresses, reflex amplitudes will
decrease, and thresholds will increase, until eventually the
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Hong et al
347
reflexes can no longer be detected.16 In this study, all patients
had advanced-enough disease (average ABG = 22.8 dB)
where surgical exploration was considered and where one
may have reasonably expected all reflexes to be absent.
Nevertheless, some ears with ossicular etiologies had detectable acoustic reflexes, so reflex testing is not infallible. At
our institution, we do not routinely assess for the presence of
the biphasic ‘‘negative on/off ’’ effect that has been described
with early otosclerosis.18 It is possible that the addition of
this assessment may further improve the value of acoustic
reflexes in differentiating among etiologies of conductive
hearing loss.
The retrospective nature of this study requires that the
results be interpreted with a degree of caution. First, the
number of patients with third window symptoms may be
underestimated. In particular, patients who present with hearing loss where an ossicular etiology is highly suspected may
not always have documented if they experience autophony or
pulsatile tinnitus. Second, given that we practice at a tertiary
otology referral center, the CT scans obtained came from a
large number of different facilities and were of variable quality. This may have introduced variability in the accuracy of
the radiologic diagnosis of ossicular and third window disorders. Third, the number of patients with third window disorders and thus combined etiologies may be underestimated. In
this study, the majority of patients with otosclerosis did not
have a CT scan performed. It was assumed that if they had an
intraoperative finding of stapes fixation, postoperative hearing
improvement, and no CT scan, the cause of their hearing loss
was due solely to an ossicular etiology. However, the prevalence of third window disorders in the general population has
been reported to be between 3% and 9%.19-21 Thus, we suspect
that if every patient received imaging prior to middle ear
exploration, we would find a higher rate than the 2% (5 of
212 ears) of concurrent ossicular and third window disorders
found in this study.
One question brought up by this study is how to address
patients with significant conductive hearing loss for whom
there is evidence (eg, from a preoperative CT scan) for both
otosclerosis and a third window disorder. In this study, 5
ears were found to fit into this category, all of which had
concurrent otosclerosis and superior semicircular canal
dehiscence. Of these ears, 2 underwent stapedectomy surgery and had a successful postoperative hearing outcome; 1
underwent middle ear surgery with no postoperative change
in hearing; and 2 did not have surgery because of the concurrent presence of a third window disorder.
When one considers middle ear exploration for concurrent
otosclerosis and third window disorders, there are 2 relevant
issues to address. The first is if hearing can be improved significantly with middle ear surgery, given the concurrent presence of a third window disorder. The literature is sparse but
supports our findings that in some cases, significant closure
of the ABG can be achieved.22,23 The second issue is whether
there is an increased risk of sensorineural hearing loss following stapedectomy because of a concurrent third window disorder. We are not aware of any reports of sensorineural
hearing loss following stapedectomy attributed to semicircular
canal dehiscence. There are a few case reports linking intraoperative stapes gusher and postoperative sensorineural hearing
loss to dilated vestibular aqueduct,24,25 but most of these cases
had other inner ear malformations present. Therefore, it seems
reasonable to offer middle ear exploration to patients with concurrent otosclerosis and third window disorders, as long as
they are counseled that there may not be complete closure of
the ABG after surgery.
Acknowledgments
We thank Nancy M. Jackson, PhD, for her help with statistical
analysis.
Author Contributions
Robert S. Hong, design of study, analysis of data, drafting of
work, final approval of version to be published, agreement to be
accountable; Christopher M. Metz, acquisition of data, drafting
of work, final approval of version to be published, agreement to be
accountable; Dennis I. Bojrab, design of study, critical revision,
final approval of version to be published, agreement to be accountable; Seilesh C. Babu, design of study, critical revision, final
approval of version to be published, agreement to be accountable;
John Zappia, design of study, critical revision, final approval of
version to be published, agreement to be accountable; Eric W.
Sargent, design of study, critical revision, final approval of version
to be published, agreement to be accountable; Eleanor Y. Chan,
design of study, critical revision, final approval of version to be
published, agreement to be accountable; Ilka C. Naumann, design
of study, critical revision, final approval of version to be published,
agreement to be accountable; Michael J. LaRouere, design of
study, critical revision, final approval of version to be published,
agreement to be accountable.
Disclosures
Competing interests: None.
Sponsorships: None.
Funding source: None.
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