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a
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S. M. Kayaalp et al.
b
Fig. 14.11 (a) This was a 5-year-old male patient who had a history of
immunodeciency and bone marrow transplant. Histopathologic examination showed bilateral otitis media with effusion. (b) Higher magni-
cation showed the continuation of effusion from serous to sero-mucoid
and mucoid character in the middle ear
Fig. 14.13 This histopathologic section shows a dimeric membrane
intact with serous effusion in the middle ear. A brocystic granulation
tissue is seen around the round window niche and sinus tympani
Fig. 14.12 This was an 18-month-old patient with bilateral chronic
otitis media and meningitis. Fibrocystic granuloma, cholesterol granuloma, and residual mesenchyme can be seen behind the intact tympanic
membrane. Purulent labyrinthitis showed biolm structures in the inner
ear. The concept of chronic silent (masked) otitis media depends on the
basis of clinical and otopathological evidence of chronic infection in
the middle ear cleft in the absence of obvious pathologic ndings in the
tympanic membrane
14 Translational Histopathology inOtitis Media: TheReal Evidence-Based Medicine!
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141
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Paparella MM.Round window membrane and labyrinthine pathological changes: an overview. Acta Otolaryngol. 2005;125(1):9–15.
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Patulous Eustachian Tube
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andtheDifferential Diagnosis
ofAutophony
BryanK.Ward, CarrieL.Nieman, andDennisS.Poe
15
There are three primary functions of the Eustachian tube,
including (1) ventilating and equalizing pressure in the middle ear; (2) draining secretions from the middle ear by gravity or by mucociliary clearance; and (3) protecting the
middle ear from sounds and reux of pathogens and contents from the nasopharynx [1]. This third function of the
Eustachian tube is often overlooked. The Eustachian tube
functions as a dynamic valve that is closed in its resting
position and opens intermittently due to muscular action.
Patulous Eustachian tube dysfunction can occur when the
Eustachian tube is in a persistently opened state. The middle
ear is no longer protected from the transmission of internal
sounds and nasopharyngeal material. This chapter will
review the diagnosis and management of patulous
Eustachian tube dysfunction as well as consider the differential diagnosis of autophony for disorders that may overlap
with the clinical presentation of patulous Eustachian tube
dysfunction.
Introduction: Patulous Eustachian Tube
Dysfunction
A patulous Eustachian tube was initially described by
Hermann Schwartze in 1864 when he noticed that a patient’s
tympanic membrane was moving with breathing [2]. There
have been numerous subsequent reports of patients in whom
B. K. Ward · C. L. Nieman
Department of Otolaryngology-Head and Neck Surgery, Johns
Hopkins University School of Medicine, Baltimore, MD, USA
e-mail: bward15@jh.edu; cnieman1@jhmi.edu
D. S. Poe (*)
Department of Otolaryngology-Head and Neck Surgery, Boston
Children’s Hospital, Boston, MA, USA
e-mail: dennis.poe@childrens.harvard.edu
ipsilateral nasal breathing evoked excursions of the tympanic
membrane, and this was associated with having patulous
Eustachian tube dysfunction [3–7]. The common symptoms
that patients report are a sense of aural fullness, hearing their
nasal breathing loudly in their ears, and hearing that their
own voice can be perceived as abnormally loud or distorted
on the affected side. These two latter symptoms are called
autophony. Some common descriptions that patients provide
are that they feel that their voice sounds like it has an “echo”
or that they sound like they are speaking “in a bucket or barrel.” Sometimes patients will change their voice in response
to this feedback, and it may be noticed by others. Patients
with patulous Eustachian tube dysfunction can report hearing their heartbeat loudly in the affected ear when the other
symptoms occur. Typically, the symptoms all occur together,
and they are often intermittent. Commonly, there are triggers
for the symptoms, such as public speaking, singing, yawning, or exercise. Anecdotally, symptoms can occur more frequently after drinking beverages containing caffeine or when
taking diuretics or decongestant medications. There is also
often a relief in symptoms when patients lie supine. An
explanation for this is the dilation of the venous plexus
around the Eustachian tube lumen [8]. Similar effects can
occur if patients apply gentle pressure to their ipsilateral
jugular vein or when lying supine with their head below the
level of the heart.
The cause of patulous Eustachian tube dysfunction is a
concave defect longitudinally through the valve within the
cartilaginous portion of the Eustachian tube, usually located
in the membranous (anterolateral) wall. Less commonly,
there can be a deciency in the cartilaginous (posteromedial)
wall. In a normal situation, there is typically a convex bulge
of the membranous wall, and this can be observed via nasopharyngoscopy (Fig. 15.1). Any deciency in the valve
region may prevent it from fully closing at rest, resulting in
impairment of the usual function of preventing reux of
sound or secretions from entering the middle ear. A patulous
Eustachian tube provides a new route for sound or nasopharyngeal secretions to access the inner ear.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. V. Goycoolea et al. (eds.), Textbook of Otitis Media, https://doi.org/10.1007/978-3-031-40949-3_15
143
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a
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B. K. Ward et al.
b
Fig. 15.1 An endoscopic examination of the left Eustachian tube. (a)
A normal examination of an Eustachian tube in the closed position with
a convex defect of the membranous wall. (b) Example of a patient with
Risk Factors forPatulous Eustachian Tube
Dysfunction
patulous Eustachian tube dysfunction with a hollowed-out concave
deformity of the membranous wall at the mucosal valve (arrow)
Eustachian tube may be multifactorial, and in addition to the
above-acquired issues, it could include congenital phenomena such as the shape of the medial cartilaginous lamina, the
In the healthy state, the usual bulge in the membranous wall
of the Eustachian tube is caused by several factors that
include mucosa, submucosa, muscle from the tensor veli
cartilage that supports the torus tubarius and cartilaginous
wall, or the lateral cartilaginous lamina that contributes to
the convex bulge in the membranous wall.
palatini muscle, the lateral cartilaginous lamina, and fat. A
depot of fat called Ostmann’s fat pad is located in the region
of the membranous wall. A deciency in any or all of these
structures can result in an increased likelihood that the valve
Diagnosis ofPatulous Eustachian Tube
Dysfunction
will open and remain open, resulting in all of the classic
symptoms of patulous Eustachian tube dysfunction. Several
conditions may alter these structures, making patulous
Eustachian tube dysfunction more likely. Allergic rhinitis is
the most commonly associated condition with patulous
Eustachian tube dysfunction [7]. Rapid weight loss is the
next most common, and it is thought to cause atrophy of
Ostmann’s fat pad. An increased resting tension of the tensor
veli palatini muscle and medial pterygoid muscle can atten
the membranous wall, increasing patency. Excessive tension
can result from temporomandibular disorders (TMD), such
as clenching of the muscles of mastication. Chronic inammation in the nasopharynx, such as from environmental
allergies or laryngopharyngeal reux, may lead to atrophy of
the secretory mucosa and submucosa. In clinical studies of
patients with patulous Eustachian tube dysfunction, clinical
diagnoses such as weight loss, chronic autoimmune or neuromuscular disorders, anxiety (possibly associated with
TMD), and a history of environmental allergy are more prevalent than would be expected. Furthermore, ndings on
nasopharyngoscopy have correlated with the underlying
diagnoses [7]. In any patient, the cause of a patulous
Clinicians can suspect patulous Eustachian tube dysfunction
when they see a patient with aural fullness by asking about
the classic symptoms of patulous eustachian tube dysfunction (autophony of voice and nasal breathing). The diagnosis
is made by observation of pressure changes transmitted to
the ear with ipsilateral nasal breathing. This pressure transmission can be observed by viewing the tympanic membrane
with otoscopy or binocular microscopy. Observation is made
for medial and lateral excursions of the tympanic membrane
while the patient occludes the contralateral nostril and
breathes through the nose, mildly deeper and faster than normal, similar to breathing while auscultating the lungs. Often,
the movements of the tympanic membrane are best seen in
the posterior-superior quadrant. These medial and lateral
excursions of the tympanic membrane with nasal breathing
are typically best seen when the patient is sitting upright. It
is important to keep in mind that the movements will not be
observed if symptoms are absent at the time of the examination. Sometimes patients can perform a maneuver to cause
the symptoms, such as yawning or exercising, prior to the
examination. On the other hand, patients may inadvertently
15 Patulous Eustachian Tube andtheDierential Diagnosis ofAutophony
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145
perform frequent snifng maneuvers to close the Eustachian
tube when it opens [9]. To maximize the chances of seeing
the tympanic membrane move with breathing, patients
should be asked to avoid snifng during the encounter.
Audiologists may be able to record these tympanic membrane excursions on tympanometry using the acoustic reex
decay setting on their audiometer. By performing tympanometry and asking the patient to perform ipsilateral nasal
breathing, the movements of the tympanic membrane can be
recorded as uctuations in the immittance that are timed with
nasal breathing [10]. Similar to examining the tympanic
membrane in the clinic, however, uctuations will not be
observed if symptoms are absent at the time of the study.
Finally, some patients may have a continuous column of air
identiable on computed tomography (CT) imaging, extending from the nasopharynx up to the middle ear. It can best be
seen by cone beam CT in the sitting position. A continuous
column of air is also diagnostic of a patulous Eustachian tube
[11].
Since the sensation of ear fullness can be present in both
patulous Eustachian tube dysfunction and obstructive
Eustachian tube dysfunction, patients with ear fullness are
often initially diagnosed with obstructive dysfunction.
Furthermore, patients with patulous Eustachian tube dysfunction may have retractions of the tympanic membrane
from repeated snifng, generating negative pressure in the
middle ear space to try to close the patulous Eustachian tube
[12]. A strong sniff can generate a negative pressure in the
nasopharynx, forcing air out of the middle ear space and
closing the Eustachian tube by a Bernoulli effect. This can
result in temporary relief of symptoms of the patulous
Eustachian tube, but it can also result in retraction pockets,
middle ear effusions, and cholesteatoma. Ordinarily, patients
with negative middle ear pressure would be expected to try to
improve their symptoms by performing a nasal Valsalva
maneuver, forcing air from the nasopharynx to the middle
ear (auto insufation). Any patient with repeated snifng
despite evidence of negative pressure should be evaluated for
patulous Eustachian tube dysfunction.
Finally, adding to the complexity of the diagnosis of patulous Eustachian tube dysfunction is that patients may fall
along a spectrum of Eustachian tube dysfunction. As discussed above, the Eustachian tube is a valve that, for some of
its functions, must open intermittently to ventilate the middle
ear, while others stay closed to protect the middle ear from
reux of sound or nasopharyngeal secretions. In any person,
there may be episodes in which the Eustachian tube is too
frequently open, causing symptoms associated with patulous
Eustachian tube dysfunction, and subsequently, episodes in
which the Eustachian tube becomes closed too often (obstructive). The transition between obstructive and patulous dysfunction most commonly occurs in allergic rhinitis patients.
Initially, they may have obstructive dysfunction, but over
time, atrophy of the valve may occur, causing patulous dysfunction, even while there may still be evidence of inammation elsewhere in the nose, nasopharynx, or torus tubarius.
During exacerbations of allergic disease, obstructive dysfunction could recur, but during periods of quiescence or
overmedicated for allergies, patulous symptoms may resume.
Patients may alternate between these conditions, yet only
report that they consistently have a “blocked ear.” Therefore,
the diagnosis of patulous Eustachian tube dysfunction
requires a high index of suspicion.
Treatment ofPatulous Eustachian Tube
Dysfunction
When treating patients with patulous Eustachian tube dysfunction, the primary aim is to restore competence to the
functional valve of the Eustachian tube to facilitate its closure more frequently. Patients should be made aware of
behaviors that can make their symptoms less noticeable.
Some will already have noticed that when they lie supine or
put their head below the level of the heart, the symptoms are
lessened. Similarly, gentle pressure on the neck ipsilateral to
the symptoms can cause temporary venous congestion
around the Eustachian tube, alleviating symptoms temporarily. Gentle snifng can decrease symptoms in some patients,
but strong snifng as practiced by some patients should not
be recommended due to the long-term effects on the tympanic membrane of inducing frequent negative pressure in
the middle ear, such as tympanic membrane retractions and
cholesteatoma.
The initial management of patulous Eustachian tube dysfunction is to discontinue any treatments with the potential to
exacerbate symptoms. Dehydration makes symptoms more
likely to occur. Therapies such as decongestants, diuretics,
and caffeine should be discontinued if possible [13]. It may
be helpful to increase oral water intake or to improve local
hydration by delivering normal saline to the area with nasal
saline drops. Topical estrogen drops (non-FDA approved) or
irritants delivered to the surface of the Eustachian tube can
help induce mucosal thickening and may be effective rstline agents [14, 15]. Patients need to be instructed on how to
best apply the drops to the nose in order to deliver them to
the surface of the Eustachian tube. We instruct patients to lie
on their backs with their heads hanging 15°. After applying
the drops, the head is turned approximately 45° to the side
being treated to take on a nearly Hallpike position, except
that the head is only hanging 15°. For example, when applying drops to the right nostril, the patient should lie supine.
They then place the drops in the right nostril and rotate their
head 45° to the right side to allow them to drain to the surface
of the Eustachian tube. For irritants like hypertonic saline or
ascorbic acid, patients often report feeling a twinge of irrita-
146
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B. K. Ward et al.
tion or pain that radiates toward the ear being treated when
the drops contact the orice of the Eustachian tube. This is
often followed by relief of symptoms of variable duration.
Patients are instructed to apply the drops as needed, generally three drops at a time. Hypertonic saline can be prepared
at home with two teaspoons of table salt in a cup of water
(~2.4dL), varying the concentration if desired. Ascorbic acid
preparations generally provide the maximal irritation that
most patients would readily accept. They can be used three
drops daily or, two to three times daily for 2months in an
attempt to obtain lasting benets. Although weight loss has
been associated with the onset of symptoms in some patients,
it appears that weight gain is not an effective method for
reducing symptoms and should only be recommended if the
patient is medically underweight [7].
Surgical Management ofPatulous
Eustachian Tube Dysfunction
The majority of patients with patulous Eustachian tube dysfunction can be managed with behavioral changes and mucosal irritants, as described above [7]. Surgical treatments for
patulous Eustachian tube dysfunction can be divided into
two categories: (1) procedures that aim to modify the vibratory functions of the tympanic membrane (mass loading) to
decrease symptoms such as autophony of voice and nasal
breathing; and (2) procedures aimed at decreasing the diameter of the lumen of the valve of the Eustachian tube.
Procedures toModify theTympanic Membrane
Tympanostomy tubes have been reported as helping to alleviate symptoms in up to 54% of patients in one series [16];
however, symptoms of altered hearing and aural fullness
may also be exacerbated by placing a tympanostomy tube
[17]. Patients with frequent snifng will be unable to alleviate their symptoms with a tympanostomy tube in place and
should be counseled about this prior to placement. It may be
that, when effective, tympanostomy tubes apply a mass load
to the tympanic membrane or modify its vibratory features in
a way that minimizes symptoms of autophony. Other groups
have reported success with mass-loading the tympanic membrane using a variety of materials, such as tape, paper strips,
eggshells, or putty-like adhesives [18–22]. We have observed
that mass loading is more likely to be benecial in patients in
whom autophony of breathing or the sensation of tympanic
membrane excursions are the dominant symptoms. We place
one or more layers of adhesive skin closure strips, cut to
about 4mm in diameter, onto the posterior and superior tympanic membranes. These strips can stay in place for several
weeks.
The above methods of addressing patulous Eustachian
tube dysfunction are temporary, and symptoms are expected
to recur once the materials migrate off the tympanic membrane with the normal epithelial migration of the ear canal
skin. If patients report temporary relief, however, they may
be more likely to benet from a tympanostomy tube.
Alternatively, mass loading by performing a tympanoplasty
using auricular cartilage could provide enduring relief of
symptoms [19, 21].
Procedures toDecrease theDiameter
oftheLumen oftheValve
oftheEustachianTube
The other major category of procedures for patulous
Eustachian tube dysfunction aims to address the Eustachian
tube directly (Fig.15.2). One approach includes inserting a
shim to ll a gap in the valve of the Eustachian tube [13,
23–25]. Prior to the procedure, a CT scan is always per-
formed to ensure there is no bony dehiscence of the internal
carotid artery, as this would be contraindicated for this procedure. The shims may be inserted either via the nasopharynx or via the middle ear. For the nasopharynx insertion, a
transnasal or combined transnasal and transoral approach is
used to access the Eustachian tube. A non-FDA-approved
shim is constructed using a 14-gauge or, less commonly,
16-gauge angiocatheter. Molten bone wax is aspirated into
the angiocatheter, and this is trimmed to a size such that the
full length of the Eustachian tube is included, plus an additional 5 mm. The nal length is usually between 38 and
42mm. After the wax hardens within the angiocatheter, it is
trimmed to the appropriate size, placed within a piston-like
insertion tool, and then inserted slowly into the nasopharyngeal end of the Eustachian tube via the oral or nasal cavity,
using endoscopic guidance via the nasal passage. Although
the shim is advanced into the Eustachian tube like the balloon catheter during balloon dilation of the Eustachian tube,
the shim is advanced through the isthmus to hold it in place,
while a balloon catheter does not pass the isthmus. Once the
shim is inserted, the tympanic membrane is inspected to
ensure the shim is not contacting the tympanic membrane.
Following the nasopharyngeal placement of a shim, approximately 75% of patients can expect to have relief of symptoms at 1year following the procedure; however, there is a
risk that the shim can become dislodged in about 10% of
cases and that about 50% of patients will develop a middle
ear effusion that can be managed with tympanostomy tubes
[26]. Shims have also been placed via a trans-tympanic
approach, inserting the shim into the bony Eustachian tube.
Using binocular microscopy, an otolaryngologist can place
the shim by raising an anterior tympanomeatal ap, as initially described by Bluestone [23], or via a myringotomy.
15 Patulous Eustachian Tube andtheDierential Diagnosis ofAutophony
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147
Fig. 15.2 Procedures to decrease the diameter of the Eustachian tube
via the nasopharyngeal approach are shown, including insertion of a
shim (upper panel), injection of calcium hydroxyapatite (middle panel),
Materials used have included angiocatheters constructed
similar to those described above [27, 28] and custom silicone
plugs [29]. In either the nasopharyngeal approach or the
transcanal approach, the procedure is reversible via a clinic
visit, either by performing a myringotomy or nasopharyngoscopy and removal using sinus forceps.
Other attempts to narrow the lumen of the Eustachian
tube have included injecting agents like calcium hydroxyapatite paste (non-FDA-approved) or performing procedures
on the cartilaginous portion of the Eustachian tube to augment the soft tissue and facilitate closure of the valve.
Calcium hydroxyapatite is a permanent ller material that
can be injected beneath the surface of the mucosa. A needle
is guided either transorally or transnasally and inserted just
immediately beneath the mucosa, near the concave defect in
the membranous wall of the Eustachian tube. Larger defects
and those in which there is a defect at the 12 o’clock position
(i.e., roof) in the Eustachian tube may not respond as well to
the injection technique. Other injected materials have been
reported, including morselized cartilage [30], fat [31],
and reconstruction of the Eustachian tube valve by augmentation of the
membranous wall (lower panel)
absorbable gelatin [32], Teon paste [33], and polydimethylsiloxane elastomer [34]. Teon has been abandoned following instances of cerebral embolus and death, potentially
related to intravascular injection.
There have been additional methods described in which
the Eustachian tube valve is reconstructed to narrow its
lumen [26, 35, 36]. These procedures involve using combined transnasal and transoral approaches. The goal of the
procedure is to narrow the diameter of the lumen without
obliterating it entirely. Most commonly, incisions are made
in the mucosa along the cartilaginous wall, beginning at the
torus tubarius. Less commonly, the membranous wall may
be augmented. Submucosal aps are elevated, and materials
are inserted into the pocket to reduce the diameter of the
lumen [37]. The incisions are then closed. Still, other techniques have been developed, addressing the tensor veli palatini muscle or its tendon [38, 39]. Complete obliteration of
the Eustachian tube can relieve symptoms [6, 26], but,
chronic middle ear effusions are expected, at least initially.
In instances of excessive closure of the valve, the effusion
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could become thick and mucoid, frequently occluding tympanostomy tubes. Total obliteration of the Eustachian tube is
reserved only for patients who have failed multiple prior
attempts to improve symptoms, as they would require permanent ventilation through the tympanic membrane and
there is an increased risk of developing troublesome mucoid
effusions.
The Dierential Diagnosis ofAutophony
From the time we begin to speak, we grow accustomed to the
sound of our own voice, a combination of bone-conducted
sounds transmitted directly from our vocal cords through
bone to our ears combined with feedback from reections of
our self-generated acoustic sounds in the environment. This
sensation is “normal.” The lack of bone-conducted sound is
the reason why our own voices sound distorted when we rst
hear recorded versions of them played back to us.
Psychophysical experiments have taught that distortions in
the perception of one’s own voice can greatly affect the way
one speaks. For instance, we raise the volume of our voices
in the presence of background noise, known as the Lombard
effect [40]. If one hears their own voice played back in a
delayed manner, it begins to cause discomfort. Small delays
(<10ms) will distort the sound, medium delays (10–30ms)
will cause a hollow sound to the voice, and larger delays
(>30ms) are perceived as an “echo,” with delays >200ms
resulting in difculty communicating [41]. These studies
support the idea that even a subtle variation in the way either
bone- or air-conducted sounds reach our ear can signicantly
alter the comfort we experience when we perceive our own
voice. Autophony is the term used to describe the enhanced,
distorted perception of one’s own voice.
Any method by which the sound of one’s own voice
becomes distorted can cause a sensation of autophony.
Patients with patulous Eustachian tube dysfunction describe
their own voice as sounding like they are speaking “in a
bucket,” and symptoms correlate temporally with the other
symptoms of patulous Eustachian tube dysfunction, suggesting the opening in the Eustachian tube alters the transmission
of sounds to the middle ear, resulting in a perceived distortion to one’s voice. A loss in conductive hearing will cause
distortion in the air-conducted component of one’s own
voice. This can be assessed by occluding the ear canal and
speaking. Excessive cerumen, middle ear effusions, or ossicular chain abnormalities would cause a similar distortion.
These alternative causes of autophony can be identied by
pure tone audiometry, tympanometry, and a careful physical
examination, including binocular microscopy. Patients with
patulous Eustachian tube dysfunction typically do not have
conductive hearing loss on pure tone audiometry, and conventional tympanometry is often normal.
Superior Semicircular Canal Dehiscence
Syndrome andOther Third Mobile Window
Syndromes
Altered mechanics within the inner ear can also cause distortion in one’s own voice. For instance, diplacusis is the
sensation of hearing two tones simultaneously. Patients
with Meniere’s disease occasionally report that some
sounds in the affected ear can be perceived as having two
tones, and this has been associated with the presence of
endolymphatic hydrops [42]. Diplacusis can be disturbing,
and similar to conductive hearing loss, the symptoms occur
for both external and internal noises. However, patients
with patulous Eustachian tube dysfunction often report that
external sounds are often undisturbed, yet internal sounds,
notably the sound of their own voice, are distorted. Another
inner ear disorder that can alter the mechanics of acoustic
transmission in the inner ear is superior semicircular canal
dehiscence syndrome (SCDS) [43]. Like patients with patulous Eustachian tube dysfunction, patients with SCDS
report that their own voice is disturbed but that their hearing for external sounds is minimally affected. Because of
the overlap in symptoms of autophony, aural fullness, pulsatile tinnitus, and sensitivity to internal noises, SCDS is
often in the differential when evaluating a patient with
patulous Eustachian tube dysfunction and will be reviewed
in greater detail.
SCDS has been modeled as a “third mobile window” syndrome. In a healthy state, there are two mobile windows in
the inner ear: the oval and round windows. Vibrations of the
tympanic membrane are transmitted through the ossicles to
the inner ear at the oval window and are decompressed at the
round window. In this way, acoustic energy is transmitted
through the cochlea, facilitating normal hearing. There may
be additional openings into the inner ear, caused either by
surgeons or by disease processes. An extra opening or dehiscence in the superior semicircular canal is the best understood of these disorders. In some patients, an anatomic
dehiscence in the superior semicircular canal can serve as a
third mobile window and cause symptoms of superior semicircular canal dehiscence syndrome. The extra opening in the
superior semicircular canal functions to shunt acoustic
energy entering the oval window away from the round window and toward the dehiscence [44]. This causes an apparent
increase in thresholds for low-frequency air-conducted
sound on audiometry as this acoustic energy is shunted away
from the cochlea. This alternate pathway traverses the sensory epithelium of the utricle and superior semicircular
canal, causing the sound- and/or pressure-induced vertigo
that patients report when exposed to loud low-frequency
sounds. At the same time, the dehiscence creates a new lowimpedance pathway into the inner ear for bone-conducted
sounds. This allows patients with SCDS to hear
15 Patulous Eustachian Tube andtheDierential Diagnosis ofAutophony
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bone- conducted sounds better than normal, leading to symptoms of autophony, pulsatile tinnitus, audible eyeball movements, footfalls, chewing, etc.
Risk Factors forSuperior SCDS
The etiology of SCDS remains unknown, but there are two
primary theories about its cause. The rst is that SCDS is a
congenital phenomenon, based on a large temporal bone
study that found an anatomic dehiscence over the superior
semicircular canal in approximately 0.5% of specimens
without bony remodeling [45]. Furthermore, the otic capsule
bone continues to develop several years after birth, with
higher rates of anatomic dehiscence in young children [46].
Patients tend to present in their fourth and fth decades of
life; however, as many as a quarter of patients note an inciting traumatic event such as a head injury, noise exposure, or
a strong Valsalva just prior to the onset of symptoms [47].
Others have suggested that SCDS may develop from progressive erosion of the bone over the superior semicircular
canal and have pointed to the observation that patients with
SCDS often have numerous defects in the tegmen [48]. The
etiology may involve a combination of a congenital opening
and progressive thinning of the bone or dura overlying the
superior semicircular canal, eventually leading to the onset
of symptoms.
Diagnosis ofSuperior SCDS
The International Classication for Vestibular Disorders
recently published diagnostic criteria for SCDS [49]. For a
diagnosis of SCDS, patients must have (1) at least one symp-
tom consistent with a third mobile syndrome; (2) evidence of
pressure transmission through the third mobile window on
physiologic testing; and (3) the presence of dehiscence on
high-resolution CT imaging. The symptoms that can be best
attributed to a third mobile window include bone conduction
hyperacusis (including autophony and abnormally loud
internal noises like eye movements), sound or pressureinduced vertigo, and pulsatile tinnitus. There are several sensitive and specic diagnostic tests for SCDS. Classically,
patients with SCDS have eye movements in the plane of the
dehiscent semicircular canal when loud sounds or pressure
are applied to the affected ear [43]. Additional diagnostic
tests have become available, including the observation of
negative or better-than-normal bone conduction thresholds
on pure tone audiometry and enhanced responses on ocular
or cervical vestibular-evoked myogenic potential (VEMP)
testing. Patients with SCDS must also have anatomic dehiscence on high-resolution temporal bone CT imaging with
multiplanar reconstruction in the plane of the affected semicircular canal (Fig. 15.3). Due to the frequent overlap of
symptoms of SCDS with patulous Eustachian tube dysfunction and the observation that more patients with patulous
Eustachian tube dysfunction than would be expected also
have SCDS [7], any patient with symptoms consistent with
SCDS should undergo a high-resolution temporal bone CT
scan to evaluate for a possible third mobile window syndrome. Additional vestibular or VEMP testing can then be
performed if an anatomic dehiscence is discovered. In
patients with conductive hearing loss, stapedial reex testing
should be performed to distinguish SCDS from other diagnoses that cause conductive hearing loss, like otosclerosis.
Stapedial reexes should be present in patients with SCDS
and absent in patients with other causes of conductive hearing loss.
Fig. 15.3 Computed tomography imaging reconstructed in the plane of the superior semicircular canal and orthogonal to the canal, demonstrating
a dehiscence (arrows)
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Treatment ofSuperior SCDS
While there are no known medical treatments for SCDS, there
are effective surgical interventions. Many patients (about half
in our experience), however, are content to have an explanation for their symptoms and do not pursue surgical intervention. Surgery is offered when patients meet the diagnostic
criteria for SCDS and nd their symptoms debilitating. The
original series by Minor etal. described plugging the superior
semicircular canal via the middle cranial fossa approach [43].
The aim of surgery is to eliminate the pathophysiology of the
third mobile window. Early attempts at resurfacing alone without plugging the affected canal led to recurrences of symptoms, and plugging was therefore preferred. Surgeons have
used a variety of materials, including autologous tissues such
as fascia, bone dust, bone chips, bone wax, or bone dust with
brin glue. Often, the oor of the middle fossa is then resurfaced using calcium hydroxyapatite cement. Patients generally do well after surgery to plug the affected canal, with
improvements in autophony [50], dizziness handicap [51], and
overall health-related quality of life [52]. The transmastoid
approach to plugging the canal has also been used with excellent results [53, 54]. Following surgery to plug the affected
canal, patients have a reduction in the function of the affected
superior canal, and about one-third of patients have a temporary reduction in the function of all three semicircular canals
[55]. Profound hearing loss is a rare complication, occurring
in fewer than 3% of cases, but approximately 25% of patients
can have a high- frequency hearing loss [56]. The long-term
recurrence rate following plugging is generally low, and most
patients are content with the improvement in symptoms [57].
Conclusions
Autophony can be a debilitating symptom and seems to be
particularly bothersome for patients with patulous Eustachian
tube dysfunction and superior semicircular canal dehiscence
syndrome. A careful history and physical examination can
help differentiate the causes of autophony, but additional diagnostic testing may be needed. The workup typically begins
with pure-tone audiometry and tympanometry. Additional
evaluations such as nasopharyngoscopy, CT imaging, and
vestibular-evoked myogenic potentials can help aid the diagnosis. Fortunately, there are excellent treatment options for
both patulous Eustachian tube dysfunction and SCDS.
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