LITERATURE REVIEW

J Neurosurg 127:1268–1276, 2017

Superior semicircular canal dehiscence syndrome

Wenya Linda Bi, MD, PhD,1 Ryan Brewster, BA,1 Dennis Poe, MD,2,3 David Vernick, MD,3
Daniel J. Lee, MD,3–5 C. Eduardo Corrales, MD,3,5 and Ian F. Dunn, MD1
1
Center for Skull Base and Pituitary Surgery, Department of Neurosurgery, Brigham and Women’s Hospital; 2Department of
Otolaryngology and Communication Enhancement, Boston Children’s Hospital; 3Department of Otolaryngology, Harvard Medical
School; 4Department of Otolaryngology, Massachusetts Eye and Ear Infirmary; and 5Division of Otolaryngology, Brigham and
Women’s Hospital, Boston, Massachusetts

Superior semicircular canal dehiscence (SSCD) syndrome is an increasingly recognized cause of vestibular and/or
auditory symptoms in both adults and children. These symptoms are believed to result from the presence of a pathologi-
cal mobile “third window” into the labyrinth due to deficiency in the osseous shell, leading to inadvertent hydroacoustic
transmissions through the cochlea and labyrinth. The most common bony defect of the superior canal is found over the
arcuate eminence, with rare cases involving the posteromedial limb of the superior canal associated with the superior
petrosal sinus. Operative intervention is indicated for intractable or debilitating symptoms that persist despite conserva-
tive management and vestibular sedation. Surgical repair can be accomplished by reconstruction or plugging of the bony
defect or reinforcement of the round window through a variety of operative approaches. The authors review the etiology,
pathophysiology, presentation, diagnosis, surgical options, and outcomes in the treatment of this entity, with a focus on
potential pitfalls that may be encountered during clinical management.
https://thejns.org/doi/abs/10.3171/2016.9.JNS16503
KEY WORDS  superior semicircular canal dehiscence syndrome; superior semicircular canal; hearing loss; dizziness;
transtemporal repair; transmastoid approach; skull base

S
uperiorsemicircular canal dehiscence (SSCD) syn-
drome has been an increasingly recognized cause of
vestibular and/or auditory symptoms in both adults
and children since its initial description less than 2 decades
ago.60 Patients commonly present with vertigo, disequilib-
rium, conductive hyperacusis, autophony, conductive hear-
ing loss, pulsatile tinnitus, or aural fullness. Dizziness can
be associated with sound-induced (Tullio’s phenomenon)
or pressure-induced (Hennebert’s sign) triggers. These
symptoms are believed to result from the presence of a
pathological mobile “third window” into the labyrinth due
to deficiency in the osseous shell, which possibly results
in inadvertent hydroacoustic transmissions through the co-
chlea and labyrinth. The most common bony defect of the
superior canal is found over the arcuate eminence, with
rare cases involving the posteromedial limb of the superior
canal associated with the superior petrosal sinus. Symp-
toms vary widely from patient to patient, and diagnosis
is aided by audiometry, vestibular-evoked myogenic po-
tentials (VEMPs), and confirmatory findings on high-res-
olution CT (HRCT) scans. Operative intervention is indi-
cated for intractable or debilitating symptoms that persist
despite conservative management and vestibular sedation.
Surgical repair can be accomplished by reconstruction or
plugging of the bony defect or reinforcement of the round
window via a variety of operative approaches. We review
the etiology, pathophysiology, presentation, diagnosis, sur-
gical options, and outcomes in treatment of SSCD, with a
focus on potential pitfalls that may be encountered during
clinical management.
Epidemiology
The roof of the SSC is dehiscent in 0.5% and nearly de-
hiscent in another 1.4% of cadaveric temporal bone speci-
mens, localized to either the floor of the middle fossa or
between the SSC and the superior petrosal sinus.18,82 Near
dehiscence, established at a bone thickness of 0.1 mm or

ABBREVIATIONS  ECoG = electrocochleography; HRCT = high-resolution CT; ICP = intracranial pressure; SSC = superior semicircular canal; SSCD = superior semicircu-
lar canal dehiscence; VEMP = vestibular-evoked myogenic potential.
SUBMITTED  February 28, 2016.  ACCEPTED  September 7, 2016.
INCLUDE WHEN CITING  Published online January 13, 2017; DOI: 10.3171/2016.9.JNS16503.

1268 J Neurosurg  Volume 127 • December 2017 ©AANS, 2017


less in 1 study, compares to an average roof depth of 1 mm
in control adult specimens.18 Series in which HRCT was
used have estimated an incidence of SSCD of 3%–10% in
both adults and children, which may be an overestimate
given that even HRCT slices are thicker than the thickness
of some middle fossa floors.21,23,34,51,63,73,89 Superior semi-
circular canal dehiscence on one side is also associated
with contralateral thinning or dehiscence in one-third to
half of all cases on both cadaveric and radiological stud-
ies.18,74,92
Etiology
The SSC resides under the floor of the middle cranial
fossa, and is often denoted by the presence of a prominence
protruding into the floor known as the arcuate eminence.
In up to 15% of the population, no arcuate eminence is
discernible. In other patients, the arcuate eminence may
be rotated posteriorly from the position of the SSC.44 Both
congenital and acquired causes of SSCD have been pro-
posed.
During development, the covering of the SSC grows
from a diaphanous state to a robust trilaminar capsule be-
tween birth and 3 years of age.18 The SSC also protrudes
prominently into the middle fossa during gestation, com-
pared with a reduced prominent temporal bone location
in adults, which may lead to adhesion of the membranous
labyrinth to dura mater before complete ossification of the
bony labyrinth.78 A computer simulation model of inner-
ear ontogeny has attributed SSCD to a malpositioned
primitive otocyst and impaired migration of mesenchymal
cells to form the apical cap of the canal.82 Failure or inad-
equate osseous development may then manifest in overt
clinical symptoms following a second hit, such as minor
trauma, infection, inflammation, or chronic pressure from
CSF pulsations or the overlying temporal lobe.
The presence of SSCD in young children supports a
congenital etiology.73 An increasing prevalence of canal
dehiscence with age in temporal bone imaging series
suggests additional acquired factors.30,63 Frequent co-
occurrence with tegmen mastoideum and tympani bony
erosion and the incidence of bilateral SSCD can support
either acquired or congenital etiologies. Dehiscence in the
posterior semicircular canal and other locations has been
reported, but is much more rare.72
Chronic elevated intracranial pressure (ICP) has been
hypothesized to underlie co-occurrence of tegmen defects,
patulous internal auditory canal, and SSCD, because id-
iopathic intracranial hypertension is associated with teg-
men defects and CSF leakage.33,74 Indeed, up to 15% of
patients undergoing middle fossa craniotomy for repair of
spontaneous CSF otorrhea are noted to have dehiscence of
the SSC apex—higher than the reported prevalence in the
general population.5 Some patients with SSCD are also
observed to have higher rates of obstructive sleep apnea
and a higher body mass index, suggestive of a correlation
between elevated ICP and development of dehiscence.64,74
Several families with multiple members who have been
treated for SSCD have been reported.65 However, the con-
tribution of genes implicated in inner-ear development and
familial deafness syndromes, such as the homeobox genes
Superior semicircular canal dehiscence
HMX3 and POU3F4, Netrin1, cochlin (COCH), and the
solute carrier SLC26A4, to SSCD remains unclear.28,40,71
Pathophysiology
Superior semicircular canal dehiscence is hypoth-
esized to cause symptoms by creation of a mobile “third
window.” In normal conditions, the oval window, to which
the stapes footplate attaches, regulates sound input into
the inner ear, whereas the round window regulates sound
and mechanical energy release from the scala tympani of
the inner ear, among other functions. These 2 windows
typically direct forces associated with sound waves along
the spiral basilar membrane. In contrast, the membranous
vestibular labyrinth is insulated from sound or pressure
changes in the middle ear and CSF by a bony capsule, but
becomes sensitive to such changes if an osseous defect
occurs (Fig. 1A and B). Hence, addition of a nonphysi-
ological third window at the roof of the SSC results in
preferential hydroacoustic shunting toward the pathologi-
cal bony defect and away from the cochlear partition, to
produce symptoms of vertigo, conductive hyperacusis, or
conductive hearing loss. Transmission of ICP through the
vestibular system from the SSCD to the round window
also produces increased compliance of the inner ear, with
Hennebert’s sign, conductive hearing loss, and the percep-
tion of pulsatile tinnitus.
The concept of a third window has been conjectured to
result in stimuli-induced vertigo in chronic adhesive oti-
tis by disrupting the bony labyrinth.20 Similar phenomena
have been observed in dehiscence of posterior and hori-
zontal semicircular canals from various pathologies such
as cholesteatoma. Animal models, in which the bony apex
of the SSC is drilled while preserving the membranous
labyrinth, corroborate this hypothesis.8,16,42 Fenestration
of the bone overlying selected semicircular canals evokes
eye and head movements in the plane of the canal with
loud noises, producing a sound-induced vestibular activa-
tion known as the Tullio phenomenon.83 Removal of the
bony cap of the SSC in rodents also produces a signifi-
cant air-bone gap in response to clicks and a pattern of
auditory brain responses, consistent with SSCD findings
in patients.8 This underlying pathophysiology of an al-
tered pressure gradient between mobile window outlets
has prompted targeted treatment strategies, as discussed
below.
Clinical Presentation
Patients can present with vertigo, disequilibrium, os-
cillopsia, conductive hyperacusis, autophony, conductive
hearing loss, hearing distortion, gaze-evoked tinnitus,
and aural fullness or blockage.22,47,55,57,81,90,92 A quarter
of patients report an auditory sensation, described as a
“swishing,” associated with motion of the eyes or body,
particularly toward the affected ear. There is an enhanced
perception of bone-conducted sounds producing autopho-
ny of one’s own voice, neck creaking, chewing, and foot-
steps hitting the ground. As opposed to the autophony of
patulous eustachian tube, there is little or no autophony of
one’s breathing sounds. Less commonly, dysautonomia,
such as bradycardia and hypotension, may be triggered by
J Neurosurg  Volume 127 • December 2017 1269
W. L. Bi et al.

FIG. 1. Dehiscence of the SSC apical bony labyrinth introduces a mobile third window into the vestibular conduit, leading to
perturbation of the normal endolymph (A, arrows) to an aberrant state (B, counter arrows). Reconstruction of this osseous defect
can be accomplished through resurfacing or capping of the middle cranial fossa floor, including any adjacent tegmen defects (C;
illustrated with a layer of temporalis fascia overlaid by hydroxyapatite) or plugging of the dehiscence (D). Copyright Ryan Brewster.
Published with permission.

sound or pressure alteration of vestibulosympathetic re-
flexes.58 Unprovoked drop attacks have also been reported
in isolated cases, with amelioration following SSCD re-
pair.14 Symptoms vary widely from patient to patient.
Precipitating factors for the vertigo or oscillopsia in-
clude loud noise, or activities that produce changes in the
middle ear or ICP, such as lifting, straining, nose blowing,
Valsalva maneuvers, or pressure on the ear. Exercise and
exertion-induced vestibular symptoms have been associ-
ated with SSCD adjacent to the superior petrosal sinus in
particular.52 Antecedent head trauma or barotrauma may
be elicited in the history.
Diagnostic Evaluation
Differential diagnoses that often mimic SSCD syn-
drome include eustachian tube dilatory dysfunction,
patulous eustachian tube, otosclerosis, chronic otitis me-
dia, perilymph fistula, labyrinthitis, Ménière’s disease,
migraine-associated vertigo, and vestibular schwannoma,
establishing it as a great otological mimicker.92 Accurate
diagnosis relies on consistent symptoms, signs, audiomet-
ric and vestibular results, and imaging confirmation. In
particular, HRCT is increasingly found to overestimate
the true incidence of the clinical syndrome, because the
presence of bony dehiscence alone does not necessarily
indicate a pathological condition. Fortunately, the direc-
tion-specific physiology of semicircular canal biomechan-
ics produces several localizing signs that aid diagnosis.
Adjunctive testing, including provocative testing, audiom-
etry, electrocochleography (ECoG), and sound-induced
cervical VEMPs are necessary to confirm the clinical sig-
nificance of the radiology findings.10
Examination and Provocative Testing
Signs of SSCD syndrome can be induced with tones at
escalating frequencies and intensities, compression of the
tragus to increase external auditory canal pressure, jugu-
lar venous compression, and Valsalva maneuvers. Verti-
cal torsional eye movements produced by these stimuli
and observed with the patient wearing Frenzel lenses are
pathognomonic for SSCD syndrome.26 Nystagmus or ves-
tibular activation elicited by pressure changes at the ex-
ternal auditory canal, known as Hennebert’s sign, is also
classically associated with canal dehiscence but is not
diagnostic of it.39 Weber’s test typically lateralizes to the
symptomatic ear; this is attributed to a conductive hearing
loss or intralabyrinthine hearing loss.13
Audiometry Testing
Hearing loss may be conductive, sensorineural, or
mixed. Bone conduction is decreased and air conduction
is increased due to the presence of a mobile third window,
thereby producing the air-bone gap. Normal symmetri-
cal hearing helps eliminate retrocochlear pathologies as

1270 J Neurosurg  Volume 127 • December 2017

 Superior semicircular canal dehiscence

a cause of vertigo. Furthermore, the stapedial (or acous-

tic) reflex is typically preserved in SSCD, in contrast to
other causes of hearing loss such as otosclerosis, where it
is characteristically absent.59 Patients with predominantly
vestibular rather than auditory symptoms may still exhibit
some degree of hearing loss. Therefore, formal pure-tone
audiometry is frequently useful to establish a baseline, es-
pecially before planned operative interventions. After op-
erative repair of SSCD, the air-bone gap may partially or
completely resolve in long-term follow-up.43

Electrocochleography Testing
Electrocochleography offers an alternative periopera-
tive testing modality to assess SSCD pathological features
and repair. ECoG measurements reveal a significantly
higher cochlear summating potential/action potential ratio
in ears affected by SSCD, with improvement observed fol-
lowing operative repair.1,7 The ECoG measurement is not
specific to canal dehiscence because abnormal values are
also observed in other inner-ear conditions such as Mé-
nière’s disease and perilymphatic fistula. Isolated observa-
tion of intraoperative ECoG has also noted normalization
of the summating potential/action potential ratio immedi-
ately following canal occlusion.
Vestibular Evoked Myogenic Potential Testing
The VEMP assesses the response of postural muscles
that are under tonic control of the medial vestibulospi-
nal tract to vestibular activation. Auditory stimuli, such
as loud clicks, usually induce relaxation of the ipsilateral
sternocleidomastoid VEMP or orbicularis oculi VEMP,
which is measurable on electromyography. The pres-
ence of SSCD renders patients more sensitive to the au-
ditory stimulus and produces a vestibulocollic response,
in which the sternocleidomastoid muscle relaxes to ves-
tibular stimulation, at a lower (< 65 dB) threshold than in
control subjects on the affected side.87 Sternocleidomas-
toid VEMP has 80%–96% sensitivity and specificity in
confirming CT-proven SSCD, compared with > 90% for
orbicularis oculi VEMP; both may provide an appropriate
screening or confirmatory test in the diagnosis of SSCD
syndrome.92,94 The VEMP can also distinguish between
patients with near dehiscence, or thin bone, versus those
with true dehiscence over the SSC, both of whom can
present with similar symptoms.53 Following successful re-
pair of the dehiscence, the VEMP normalizes.13,88
FIG. 2. Temporal bone CT demonstrating illustrative case with (A) de-
hiscence of the SSC (arrow) and tegmen (arrowheads) on the left, and
with (B) intact middle cranial fossa floor on the right. Resurfacing of the
left middle fossa floor defects was performed with temporalis fascia and
hydroxyapatite bone cement (C).
techniques.32 An MRI study with a fast imaging employ-
ing steady-state acquisition (FIESTA) sequence demon-
strates 100% sensitivity and negative predictive value, but
96.5% specificity and 61% positive predictive value com-
pared with CT in evaluating SSCD, suggesting that MRI
might be adequate in excluding the diagnosis.15 Of note,
near dehiscence with extremely thin bone can produce
similar signs and symptoms as a fully dehiscent apical
cap, and may benefit from operative intervention.86 Most
importantly, imaging findings, as with all other diagnostic
adjuncts, should be interpreted against the background of
appropriate clinical symptoms and signs for a definitive
diagnosis of SSCD.
Management
Management after clinical diagnosis begins with avoid-
ance of provocative stimuli and vestibular sedation. It is
important to note that a majority of patients identified
with SSCD syndrome in the literature have not undergone

Imaging
A thin-cut HRCT scan, particularly in the coronal
plane, or an oblique cut directed to the plane of the semi-
circular canal, is confirmatory of the clinical diagnosis
(Fig. 2).9,12,49 However, even HRCT can produce false-
positive results if the canal roof is thinner than the image
resolution slice thickness, as might be expected given an
average SSC roof thickness of 1 mm in cadaveric stud-
ies.23,51,58,61,79 Osteoporosis can also lead to a false-positive
reading because of lack of calcium in the imaged bone. FIG. 3. Reformatted CT images perpendicular (A, Stenver’s plane) or
parallel (B, Pöschl’s plane) to the SSC may aid visualization of a bony
Reformatted images parallel (Pöschl’s plane) or perpen- dehiscence (arrows). Lines superimposed on an axial temporal bone
dicular (Stenver’s plane) to the SSC may aid visualization CT image indicate the plane of reconstruction for (C) Stenver and (D)
of a dehiscence (Fig. 3),9,29 as do novel 3D reconstruction Pöschl views.

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W. L. Bi et al.
surgical repair. Operative intervention is indicated for in-
tractable or debilitating symptoms. Surgical repair can be
accomplished through resurfacing of the SSC roof, plug-
ging of the osseous defect, or reinforcement of the round
or oval window to diminish the third window effect (Fig.
1C and D).
Canal Plugging
The original report of SSCD operative repair described
a middle fossa subtemporal extradural approach to ex-
pose the roof of the SSC and plug the defect with fascia,60
which has been subsequently expanded to muscle, bone
wax,56,70 and bone pâté.69 Given the risk of false-positive
CT diagnoses, the middle fossa approach allows en face
visualization and confirmation of the defect prior to op-
erative repair (either occlusion or resurfacing), and can be
further augmented by endoscopy in select cases.19
As an alternative, transmastoid occlusion of the SSC
appeals to otologists due to their ability to access large
areas of dehiscence via a familiar approach, the ability to
occlude the canal without manipulating the defect, and
the relatively lower invasiveness of a mastoidectomy com-
pared with a craniotomy.2,11,13,46,91 This can be achieved
with bone pâté or temporalis fascia placed within the
SSC, with > 90% postoperative improvement in vestibu-
lar and hearing symptoms.11 Some prefer the transmastoid
approach for repair of medially located SSCD adjacent
to the superior petrosal sinus.53,80 This surgical approach,
however, offers more limited visualization of the dehis-
cence and may be less favorable in the setting of a poorly
pneumatized temporal bone, low-lying temporal fossa, or
extensive concurrent tegmen defects. Concurrent plugging
of the defect, along with reconstruction or resurfacing of
the floor, is achievable through either a middle fossa or a
transmastoid approach.31,35,37
The choice of reconstructive material may also influ-
ence long-term outcome, although experience remains
limited. In an animal model of semicircular canal oc-
clusion, comparison of bone dust, bone wax, or muscle
revealed that the bone dust group had the best hearing
outcomes, with periosteal osteoneogenesis; the bone wax
group had the poorest hearing outcomes, with no osteo-
neogenesis observed but with the presence of perilym-
phatic inflammation.46
Canal Roof Resurfacing and Capping
Reconstruction or resurfacing of the dehiscent middle
fossa floor with fascia, perichondrium, cartilage,6 split-
thickness cortical bone, 59 bone substitute (e.g., hydroxy-
apatite or calcium phosphate),50,68 synthetic elastomer,38 or
a combination thereof, is a common alternative to canal
plugging. The use of hydroxyapatite cement for reconsti-
tuting the apical defect has also been termed capping.41,62
Notably, resurfacing allows for reconstruction of multiple
middle fossa floor defects, which is regularly encountered
in the setting of SSCD.
As with canal plugging, resurfacing can be accom-
plished via either a middle fossa or a transmastoid ap-
proach, with their respective strengths and limitations in
terms of ease of visualization, available surface area for
1272 J Neurosurg  Volume 127 • December 2017
reconstruction, and surgical corridor.6,27,80 Endoscopic as-
sistance provides another adjunct, based on surgeon pref-
erence.75
Analysis of select cases of recurrent SSCD symptoms
after use of an autologous temporal bone split-thickness
calvarial bone graft to resurface the middle fossa has
revealed resorption of the bone graft; this prompted the
conclusion that the entire temporal bone is abnormal in
patients with SSCD and that resurfacing using a calvarial
bone graft carries a higher risk of resorption.36 Concern
for graft resorption or migration as a mechanism of re-
surfacing failure over time prompts some surgeons to fa-
vor bone source substitute or silicone elastomer over au-
tologous grafts.38 Securing of the fascia-bone graft to the
calvaria with a small plate has also been performed, with
satisfactory results.24 Evolving appreciation of the biologi-
cal sequelae of reconstruction suggests that experience
from earlier resurfacing series may not be comparable to
contemporary results because of modifications to the tech-
nique.
Round Window Reinforcement
Several groups empirically investigated tissue graft
reinforcement of the round window, having observed
that patients who had undergone procedures to repair a
presumed perilymph fistula prior to the initial report of
SSCD, in retrospect may have had SSCD and may have
experienced significant benefit. The mechanism for why
it may help is uncertain, but it has been postulated that it
may be influencing the impedance of the inner-ear system,
perhaps reducing global hypercompliance and consequent
compression-related endolymph displacement.67,76,77 The
round window is directly accessible through a tympanic
membrane opening and can be reinforced with soft tis-
sue such as fascia, perichondrium, or muscle, gently filling
the round window niche after excoriating the mucosa, but
carefully preserving the membrane. Gelfoam or an autolo-
gous blood patch placed through a myringotomy can be
done as a trial in an office setting. All of these can also be
removed in the event of symptom worsening. Over-stiffen-
ing of the round window with bone wax or cartilage may
divert additional acoustic energy into the dehiscence and
cause a worsening of symptoms that can be reversed by
removal of the material.75 It appears that gentle reinforce-
ment of the round window may be beneficial—for reasons
to be determined—as opposed to severe dampening of the
round window, which exacerbates the condition, as may be
predicted from the “third window” model.67,75
There is a paucity of clinical data examining outcomes
following round window reinforcement for SSCD syn-
drome. Postoperative improvement in the full gamut of
SSCD-related symptoms has been reported, with the ex-
ception that conductive hearing loss does not improve.77
Although some advocate that round window occlusion
should be performed in patients whose primary symptom
is conductive hyperacusis,67 others suggest that both oval
and round window reinforcement may be beneficial for
that symptom.75
A concern is that the clinical outcome following round
window reinforcement may not be as durable as superior
canal plugging or resurfacing techniques; symptoms may

recur as the obliterated tissue atrophies. The minimally in-
vasive nature of this outpatient procedure, and its distinct
anatomical corridor compared with the middle fossa or
transmastoid approaches, allows for subsequent resurfac-
ing or plugging if symptoms fail to improve. Alternatively,
some practitioners use obliteration of the round window
in a diagnostic setting for patients with highly suspect
clinical findings, absent or equivocal CT evidence of de-
hiscence, but lowered thresholds with cervical VEMP or
increased amplitude with ocular VEMP; clinical improve-
ment may prompt subsequent transcranial repair or contin-
ued monitoring.77
Considerations in Bilateral SSCD
In the setting of bilateral SSCD, operative intervention
should address the symptomatic or more severely symp-
tomatic side first.54 The radiographic appearance of bi-
lateral SSCD is frequently detected and does not warrant
intervention in the absence of symptoms. Repair of SSCD
on one side can provoke or be followed by development
of contralateral symptoms attributable to the second canal
dehiscence, and patients must be counseled appropriately.4
Subsequent plugging of the second side is associated with
oscillopsia in half of the patients, but still provides satis-
factory relief of the primary debilitating symptoms. Bilat-
eral canal dehiscence is also associated with a prolonged
course of symptom recovery following unilateral canal
plugging, for which patients should be counseled.66
Considerations in Pediatric Patients
Experience with SSCD diagnosis and management in
children remains limited,47,52,93 although imaging series
suggest a 3%–10% incidence.21,73 Children present with a
varied constellation of hearing loss, vertigo, and disequi-
librium, with auditory symptoms typically occurring first.
Diagnosis of vestibular symptoms is more challenging in
younger children, and may manifest as delayed onset of
walking.47 The radiographic appearance of SSCD in chil-
dren younger than 3 years of age is consistent with normal
development, and should be handled with observation.
Conservative treatment is favored in children, including
the use of hearing aids, with operative intervention re-
served for intractable vestibular handicap.
Perioperative Considerations
Perioperative steroids are given variably across reports,
often for longer durations if signs of sensorineural hearing
loss, labyrinthine hypofunction, or facial paresis are de-
tected postoperatively.66,85 Early postoperative persistence
or slight decline in auditory and vestibular function may
be due to fluid, blood, or air at the surgical site, and may
be monitored. Preoperative and postoperative audiometry
and vestibular testing allow objective tracking of symp-
toms and outcomes, especially as experience with this dis-
ease entity accrues.
Outcomes
The majority of patients report improvement in pre-
senting symptoms following operative repair of SSCD,
regardless of the technique.6,11,25,37,41,57,62,66 Many studies
Superior semicircular canal dehiscence
cite a higher success rate with canal plugging compared
with resurfacing, 57 especially as a means to treat vestibular
imbalance; however, canal plugging demonstrates efficacy
equivalent to capping with hydroxyapatite, which is in es-
sence a reconstruction operation with nonmigratory mate-
rial.84 In a meta-analysis, all operative modalities achieved
equal success if auditory symptomatology was the pri-
mary indication for intervention. In addition to symptom
resolution, improvements in the VEMP threshold and air-
bone conduction gap are frequently observed following
successful repair of canal dehiscence.
Vestibular hypofunction3,58 and hearing loss60 are the
most feared complications following SSCD repair. Im-
pairment of the SSC function in isolation is common after
plugging.17 More global vestibular hypofunction is ob-
served in approximately one-third of patients in the early
postoperative period following middle fossa plugging,
with higher risk associated with an increased length of the
dehiscent area.3 This may result from intraoperative loss
or displacement of perilymph and redistribution of endo-
lymph into the horizontal and posterior canals by the plug
or during dural elevation over the dehiscent canal, during
which extra caution should be exerted. These symptoms
typically resolve over time as perioperative fluid resolves
and physiological vestibular compensation is attained,43
with 11% of patients demonstrating vestibular impairment
at 6 weeks postoperatively.3 Because of the concern for
compromise of SSC function, some surgeons favor resur-
facing over plugging strategies; capping with hydroxyapa-
tite may offer a suitable option of minimizing postopera-
tive vestibular side effects while providing high rates of
relief from preoperative vestibular handicap.
Significant hearing loss is uncommon after SSCD re-
pair, and does not correlate with either the plugging or re-
surfacing technique.48 In comparison, mild high-frequen-
cy sensorineural hearing loss, without change in speech
discrimination, has been observed in 25% of patients after
canal plugging via a middle fossa approach.85 Early meth-
ods emphasized full occlusion of the membranous supe-
rior canal during plugging, which might incur a higher
risk of postoperative hearing loss.60 Use of bone pâté for
plugging may be associated with a lower risk of hearing
impairment compared with other occlusive materials.2,45
Not surprisingly, the incidence of hearing loss rises in re-
vision procedures for SSCD, presumably due to adhesions
at the surgical site and injury to the membranous labyrinth
while separating the dura. Prior surgery on the cochlea or
stapes also increases the risk for hearing loss following
SSCD repair.48
Patients with bilateral SSCD, larger defects, and a his-
tory of migraines are more likely to experience a pro-
longed duration of symptoms following operative repair.66
Facial nerve dysfunction, CSF leakage, and other neu-
rological morbidities are rare after SSCD repair. On the
whole, quality of life measures and outcomes remain to be
clarified for patients with SSCD.
Conclusions
Over the past 2 decades, SSCD has been increasing-
ly recognized as a treatable cause of disequilibrium and
J Neurosurg  Volume 127 • December 2017 1273
W. L. Bi et al.
hearing loss. Its distinctive pathophysiology, arising from
the introduction of a mobile “third window” formed by
an unprotected membranous labyrinth at the apex of the
superior canal, accounts for characteristic symptoms, di-
agnostic signs, and treatment options. Regardless of the
approach, most patients experience alleviation of present-
ing symptoms following operative repair of the SSCD, al-
though risk of vestibular hypofunction and hearing loss
remain avenues for future improvement. The choice of op-
erative strategy ultimately depends on the surgeon’s expe-
rience and preference. A multidisciplinary approach to the
management of SSCD will continue to optimize outcomes
for this newly recognized disease entity.
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Disclosures
The authors report no conflict of interest concerning the materi-
als or methods used in this study or the findings specified in this
paper.
Author Contributions
Conception and design: Bi. Acquisition of data: Bi, Brewster.
Drafting the article: Bi. Critically revising the article: Dunn, Bi,
Poe, Vernick, Lee, Corrales. Reviewed submitted version of man-
uscript: Dunn, Bi, Brewster, Corrales. Approved the final version
of the manuscript on behalf of all authors: Dunn. Study supervi-
sion: Dunn, Bi.
Correspondence
Ian F. Dunn, Department of Neurosurgery, Brigham and Women’s
Hospital, 15 Francis St., Boston, MA 02115. email: idunn@
partners.org.