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Superior Canal Dehiscence

Wayne T Shaia, MD, Consulting Staff, Department of Otology/Neurotology, Medical College of Virginia
Jack M Kartush, MD, Clinical Professor, Department of Otolaryngology, Wayne State University; Director of Otology, Neurotology, and Skull Base Surgery, Providence Hospital; President, Michigan Ear Institute; President, American NeuroMonitoring

Updated: Sep 2, 2009

Introduction

Background

Superior canal dehiscence syndrome (SCDS) is a newly described condition in which vestibular symptoms are elicited by sound or pressure secondary to a dehiscent superior semicircular canal. More than 70 years have passed since Tullio and Hennebert described their findings of sound-induced and pressure-induced vestibular activation.

Since then, the Tullio phenomenon, wherein vestibular symptoms are induced by loud sounds, has been associated with syphilis, perilymphatic fistula, congenital deafness, Ménière disease, head trauma, Lyme disease, cholesteatomas with labyrinthine fistula, and fenestration operations. The Hennebert sign of vestibular symptoms due to changes in external auditory canal pressure is frequently found in conjunction with the Tullio phenomenon (as in perilymphatic fistula, syphilis, Ménière disease).

In 2000, Minor found a series of patients with positive Tullio and Hennebert signs.1 He was the first to relate these positive findings directly to an anatomical defect of the superior semicircular canal that was detected with high-resolution computed tomography (HRCT; see Image 1). Minor theorized that, when the bone over the canal becomes thin or dehiscent, it acts as an additional window for the vestibular system, allowing pressure and noise changes to induce vestibular activity. SCDS, as it has become known, is now recognized and treated by otolaryngologists and neurootologists throughout the world.

Coronal high-resolution computed tomography scan ...

Coronal high-resolution computed tomography scan (1-mm sections) that demonstrates the presence of the superior semicircular canal (figure A, black arrow). As the scan is followed posteriorly (figures B, C, D), the bony dehiscence over the superior canal (black arrow) becomes more apparent.


Pathophysiology

The cochleovestibular system has 2 functional windows. The oval window, which houses the footplate of the stapes, allows sound to enter the inner ear (vestibule) and to be carried via hydroacoustic waves through the perilymph. This allows the mechanical wave to be transduced into neural activity, and, thus, sound is perceived.

The function of the round window is more controversial. It is thought to have several roles. Its first role is thought to involve the release of sound and mechanical energy from the scala tympani. Another proposed role is its participation in the secretion and absorption of substances in the inner ear. The round window may also play a role as a defense mechanism of the inner ear.

These 2 windows of the inner ear work together to regulate hearing and balance. When a dehiscence in the superior semicircular canal is created, a third-window effect is thought to take place. As a result, endolymph within the labyrinthine system continues to move in relation to sound or pressure, which causes an activation of the vestibular system. The intracranial pressure transmission to the round window may also result in increased compliance of the inner ear from stretching of the round window membrane. This pressure transmission may also result in a frank round window (or oval window) fistula.

Frequency

United States

The true incidence of persons with symptomatic SCDS is currently unknown. One study of 1000 cadaveric temporal bones revealed that a dehiscence of bone that overlies the superior canal was present in approximately 0.5% of temporal bone specimens. In an additional 1.4% of the specimens, the bone was markedly thin (≤ 0.1 mm) compared with the normal bone.

Race

SCDS has no racial bias.

Sex

SCDS appears to affect males and females equally.

Age

In 2000, Minor reported that, in his original series of 17 patients, the median age at diagnosis was 40 years (range, 27-70 y).1

Clinical

History

Patients with superior canal dehiscence syndrome (SCDS) usually present with symptoms of sound- or pressure-induced dizziness. Chronic imbalance is another symptom of SCDS. The patient's symptoms may be re-created when sound or pressure is presented to the affected ear. Patients often control these symptoms with strict avoidance of noisy environments. In addition, some patients may hear a swishing noise when they move their eyes in a certain direction. This gaze-evoked tinnitus can be found in almost 25% of patients with SCDS. Hyperacusis is defined as an unusual sensitivity to normal everyday sounds. Although not specific, this condition is found in a high percentage of patients with SCDS.

Physical

After a general head and neck examination is performed, a detailed neurootological examination should be performed in all patients with vertigo. Other, more common, causes of vertigo and imbalance must be eliminated before SCDS can be diagnosed.

  • Gait test: Determine whether the patient staggers or is off-balance with gait. Typically, patients with SCDS demonstrate a normal gait pattern.
  • Oculomotor examination: All patients must be assessed for an intranuclear ophthalmoplegia and other signs of multiple sclerosis. In addition, gaze-dependent nystagmus must be eliminated as a cause of the imbalance. Nystagmus of peripheral (ie, labyrinthine) origin is usually unidirectional. Nystagmus of central origin (ie, brainstem) is usually bidirectional. Patients with SCDS do not typically demonstrate nystagmus upon routine examination. Nystagmus can be induced with loud sounds or with a pressure fistula test.
  • Romberg test: This test is used to evaluate peripheral sensation, dorsal column function, and midline cerebellar function. The results of this test are usually abnormal in patients with a central pathologic condition. Patients with SCDS demonstrate normal Romberg test results.
  • Fukuda test: Patients who undergo this test are asked to step in place for 20-30 seconds with their eyes closed. Rotation of the patient may indicate a unilateral loss of vestibular function. The results of this nonspecific test are typically normal in patients with SCDS.
  • Dix-Hallpike maneuver: The Dix-Hallpike maneuver is performed by laying a patient back suddenly with the patient's head turned to one side. The test results are considered abnormal (or positive) if the examiner sees geotropic or ageotropic rotatory nystagmus that typically lasts less than 60 seconds. An abnormal or positive Dix-Hallpike examination result is most likely due to benign paroxysmal positional vertigo (see the eMedicine article Benign Paroxysmal Positional Vertigo). Patients with SCDS do not typically have positive Dix-Hallpike test results.
  • Head-shake test: The patient wears Frenzel lenses, and the examiner shakes the patient's head at approximately 1 Hz in the horizontal plane for 20 seconds. After the shaking is stopped, the eyes are observed for nystagmus. This test can reveal latent nystagmus and indicate which labyrinth is malfunctioning. In this test, the fast phase of nystagmus is directed toward the normal (or better-performing) labyrinth. The results of this nonspecific test may be abnormal in patients with SCDS.
  • Head-thrust test: The patient is asked to gaze steadily at a target in the room while the examiner briskly moves the patient's head from side to side. If the patient's eyes remain fixed on the target, the test result is normal. When the eyes make a compensatory movement after the head is stopped to reacquire the target (a refixation saccade), the test results are abnormal. This test can indicate if the output of one or both labyrinths is depressed. This is usually not a typical finding in SCDS.
  • Visual dynamic acuity test: Before and during vigorous vertical shaking, followed by horizontal head shaking, the patient is asked to read the smallest visible line on the Snellen eye chart. A normal result is the ability to maintain acuity within 2 lines of the acuity at rest. An abnormal visual acuity test suggests bilateral vestibulopathy, which is most commonly observed in ototoxicity. The dynamic visual acuity test results are normal in patients with SCDS.
  • Fistula test: The fistula test is designed to elicit symptoms and signs of an abnormal connection between the labyrinth and the surrounding structures. This is usually performed while the patient wears Frenzel lenses. Pressure can be applied to the patient's ear by pushing the tragus over the ear canal or with the use of a Bruening otoscope. If vertiginous symptoms are elicited or if nystagmus is seen the patient has positive fistula test results. In SCDS, the superior canal can be thought of as a fistula with connection to the middle cranial fossa. With SCDS, the direction of the nystagmus, as a result of pressure applied to the ear, results in vertical-torsional nystagmus with slow waves directed away from the labyrinth suspected of being dehiscent. Other tests, such as the pinched nostril test, can demonstrate similar findings, whereas a Valsalva maneuver produces nystagmus in the opposite direction.
  • Eye movements evoked by sound are found in most patients with SCDS. These sound-induced eye movements are typically found at frequencies of 500-2000 Hz, with an intensity of 100-110 dB. The eye movements are typically vertical and torsional, away from the side of the stimulus.
  • A Barany noise box can also be used to help elicit the noise-induced vertigo (Tullio phenomenon). This commercially available box simply makes a loud (100 dB) noise. When the box is slowly moved towards the patient's symptomatic ear, the vertiginous symptoms may be re-created.

Causes

An embryological etiology of SCDS has been proposed; this theory involves a postnatal failure of bone formation over the superior semicircular canal. Tsunoda and Terasaki, with the use of a computer simulation model, determined that the cause of bony dehiscence of the superior semicircular canal was due to a malpositioned primitive otocyst.2 When this otocyst lies too close to the developing brain, the migratory patterns of the loose reticular cells are altered. These mesenchymal cells are thought to be necessary for completion of the bony development of the labyrinthine structures. This region may be left with incomplete or thin bony development over the superior semicircular canal.

Differential Diagnoses

Benign Paroxysmal Positional Vertigo
Inner Ear, Ototoxicity
Inner Ear, Evaluation of Dizziness
Inner Ear, Perilymphatic Fistula
Inner Ear, Labyrinthitis
Middle Ear, Otosclerosis
Inner Ear, Meniere Disease, Medical Treatment
Migraine-Associated Vertigo

Other Problems to Be Considered

Multiple sclerosis
Syphilis

Workup

Laboratory Studies

No specific laboratory studies confirm the diagnosis of superior canal dehiscence syndrome (SCDS). Laboratory tests may be obtained to rule out other pathological causes of vertigo (ie, multiple sclerosis, syphilis).

Imaging Studies

  • Imaging studies are critical in the diagnosis of SCDS. A high-resolution computed tomography (HRCT) scan of the temporal bones without contrast is required to make a definitive diagnosis. Views that are oblique to the temporal bone must be obtained with a HRCT scan in order to properly see the superior semicircular canal. Image 1 displays the typical findings in a patient with SCDS.
  • Magnetic resonance imaging (MRI) cannot be used to confirm the diagnosis of SCDS; however, it may be of benefit in ruling out a retrocochlear process.

Other Tests

Audiometric testing

Comprehensive audiometric evaluation is indicated in any patient with vestibular symptoms. In a patient with SCDS, key factors may be revealed. One key is the presence of normal symmetrical hearing, which helps eliminate a retrocochlear process as a cause of vertigo.

Patients with SCDS may have conductive hearing loss. The air-bone gaps are typically greatest at frequencies below 1 kHz.

The conductive hearing loss is believed to be due to the third mobile window of the superior semicircular canal dehiscence, resulting in elevation of thresholds of air-conduction sounds and a reduction of thresholds for bone-conduction sounds.

Acoustic reflex testing is preserved in a patient with SCDS as a cause of conductive hearing loss, as opposed to a loss of the reflex with other conductive or mixed hearing loss conditions such as otosclerosis.

Electronystagmography testing

 Routine electronystagmography (ENG) testing reveals no objective or pathognomonic signs of SCDS. All patients with suspicion of the disorder should undergo ENG to further eliminate other potential causes.

Video-oculography can be valuable in recording the vertical and torsional eye movements specific to SCDS.

Caloric test results are usually unaffected in patients with SCDS; however, when the dehiscence is large (>0.5 mm), reduced caloric test results may be demonstrated on the affected side.

Vestibular evoked myogenic potentials

 Vestibular evoked myogenic potentials (VEMPs) have recently been suggested to help with the diagnosis of SCDS. The inferior vestibular nerve innervates the saccule, which has some sound sensitivity. The inferior vestibular nerve has its main input to the lateral vestibular nucleus (Deiter nucleus), where the 2 main postural tracts originate. The medial vestibulospinal tract is responsible for postural control of the neck, whereas the lateral vestibulospinal tract is dedicated to the lower trunk and limbs.

For the most part, sound-evoked VEMPs are considered completely unilateral. This test is performed by placing electrodes on the sternocleidomastoid neck muscle. Patients hold their head up unsupported, using only their anterior neck muscles. Patients are instructed to tense the muscle during acoustic stimulation and to relax after the stimulation stops. Loud clicks or tone bursts (95-100 dB nHL) are repeatedly presented to each ear.3 If the neck muscles are activated at this level, a VEMP is produced.

In patients with SCDS, a response at very low thresholds (<65 dB) can be noted to produce a VEMP on the affected side. This is thought to occur secondary to the hypercompliance of the vestibular system on the affected sided secondary to the third-window effect. A low-threshold VEMP raises the suspicion of SCDS

Vibration-induced nystagmus

Most recently, patients with known SCDS underwent a series of cranial vibratory tests. A 100 Hz oscillator was placed against the cranium at different places for 10-15 seconds. Nystagmus was digitally recorded by infrared video oculography. All patients demonstrated distinct torsional vibration-induced nystagmus that was especially prominent with suboccipital vibration. Vibration of the suboccipital region and the demonstration of torsional nystagmus is an emerging technique for the diagnosis of SCDS.4

Treatment

Surgical Care

Surgical correction of superior canal dehiscence syndrome (SCDS) is reserved for patients with severe disabling symptoms. The treatment options for patients with SCDS are still expanding, with new innovative methods under development.

  • Middle fossa craniotomy and repair of fistula: In this procedure, patients undergo a middle cranial fossa craniotomy on the affected side. The temporal lobe is gently retracted. Upon elevation of the dura, care is required to avoid stretching the greater superficial petrosal nerve, which could injure the facial nerve. The region of the superior semicircular canal is located with identification of the arcuate eminence. A dehiscence of the superior semicircular canal can be covered with bone wax, bone cement, or fascia, or the canal can be ablated with wax or bone cement. Current evidence suggests that ablation gives better long-term results.
  • Transmastoid superior canal occlusion: In this approach, a mastoidectomy is performed and the superior semicircular canal is identified near the ossicular heads. The superior semicircular canal is then ablated with a combination of tissue and fascia. Brantberg et al performed a superior canal–plugging procedure via a transmastoid approach in 2 patients.5 Postoperatively, sound- and pressure-induced symptoms and nystagmus were resolved in response to offending stimuli. Although this approach can be effective, the risk of sensorineural hearing loss increases with this procedure because of limited exposure versus middle fossa craniotomy.
  • Minimally invasive approach via transcanal oval and round window reinforcement
    • The optimal surgical treatment of superior canal dehiscence syndrome has yet to be determined. Rather than directly addressing the dehiscent canal via a middle fossa craniotomy, Kartush (2002) suggested that dampening the inner ear's sensitivity by reinforcing the oval and round windows may alleviate symptoms in some patients.6 The concept is to reduce the effects of a third window at the superior semicircular canal by reinforcing the other 2 natural windows. By dampening the hypercompliance of the inner ear at the oval and round windows, rather than intracranially, the risks of craniotomy, which include death, stroke, cranial palsies, and cerebrospinal fluid leaks, are avoided.
    • Symptoms resolved in 2 patients with SCDS treated with transcanal reinforcement of the oval and round windows. If such a minimally invasive procedure proves helpful, middle fossa craniotomy with resurfacing of the canal could then be reserved for patients with persistent symptoms.
    • Under local anesthesia, a transcanal approach to the middle ear is performed with elevation of the tympanic membrane. Small amounts of fascia are harvested from a postauricular incision and are used to reinforce both the oval and round windows. The postoperative risk of hearing loss and facial nerve injury is minimal. This procedure can be performed on an outpatient basis.
  • Gianoli and Soileau have advocated a combination approach.7 In this technique, the superior canal defect is repaired via the middle fossa approach with concomitant reinforcement of the oval and round windows. The authors claim improved outcomes over middle fossa repair alone, reporting a resolution of vertigo in 24 cases with a 5-year follow-up period.

Consultations

Consultation with an otologist or neurootologist should be obtained in any patient with symptoms that coincide with superior canal dehiscence.

Follow-up

Further Outpatient Care

Patients are monitored based on the intervention and the severity and complexity of the patient's symptoms. Patients who undergo a craniotomy for repair should expect to stay in the hospital for 1-7 days (median 2 d). They may experience imbalance for approximately one month postoperatively.

Prognosis

  • The success rate in the treatment of superior canal dehiscence is quite high. In 2005, a study looked at 20 patients with severe symptoms who underwent surgical repair of their superior canal dehiscence through a middle fossa approach (Gianoli, 2005).7 Canal plugging was performed in 9 patients and a resurfacing technique was performed in 11 patients.
  • Complete resolution of all vestibular symptoms and signs was achieved in 8 of the 9 patients after the canal was plugged. A lower but still significant number of patients with a resurfacing procedure (7 of the 11) had resolution of their vestibular complaints. A total of 15 of the 20 patients (75%) of the patients had resolution of their symptoms after surgical plugging or resurfacing of their dehiscent canal.

Miscellaneous

Medicolegal Pitfalls

  • An estimated 8 million patients annually present to their physician offices with vertigo. Although the identification of superior canal dehiscence syndrome (SCDS) is increasing, SCDS accounts for only a small number of patients with vertiginous symptoms. Thus, the elimination of other, more common, causes of vertigo is necessary before SCDS can be diagnosed.
  • As the recognition of this entity increases, the realization that patients can present with varying degrees of vertigo and hearing loss is becoming apparent. Audiometric testing may reveal a substantial unilateral conductive hearing loss with a narrowing of the air-bone gap at 2000 Hz (Carhart notch), typically associated only with otosclerosis. The noise-induced symptoms may be absent. This clinical presentation is similar to that of otosclerosis, and, consequently, the otologist may recommend surgical correction via stapedectomy. Intraoperative finding of a mobile stapes should raise the suspicion to the otologist of the possibility of SCDS. In addition, patients with persistent air-bone gaps after uneventful stapedectomy may have an unrecognized dehiscence of their superior semicircular canal.
  • In order to prevent unnecessary middle ear exploration, acoustic reflex testing must be performed in all patients with a conductive hearing loss. Acoustic reflexes may be present in early otosclerosis, while reflexes are always present in cases of SCDS. VEMP testing results may be abnormal in SCDS, whereas HRCT is the criterion standard for the diagnosis of SCDS.

Multimedia

Coronal high-resolution computed tomography scan ...

Media file 1: Coronal high-resolution computed tomography scan (1-mm sections) that demonstrates the presence of the superior semicircular canal (figure A, black arrow). As the scan is followed posteriorly (figures B, C, D), the bony dehiscence over the superior canal (black arrow) becomes more apparent.

References

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  2. Tsunoda A, Terasaki O. Dehiscence of the bony roof of the superior semicircular canal in the middle cranial fossa. J Laryngol Otol. Jul 2002;116(7):514-8. [Medline].

  3. Brantberg K, Verrecchia L. Testing vestibular-evoked myogenic potentials with 90-dB clicks is effective in the diagnosis of superior canal dehiscence syndrome. Audiol Neurootol. Sep 2009;14(1):54-8. [Medline].

  4. White JA, Hughes GB, Ruggieri PN. Vibration-induced nystagmus as an office procedure for the diagnosis of superior semicircular canal dehiscence. Otol Neurotol. Oct 2007;28(7):911-6. [Medline].

  5. Brantberg K, Bergenius J, Mendel L, Witt H, Tribukait A, Ygge J. Symptoms, findings and treatment in patients with dehiscence of the superior semicircular canal. Acta Otolaryngol. Jan 2001;121(1):68-75. [Medline].

  6. Kartush JK. Superior Canal Dehiscence Syndrome symptoms resolved by reinforcement of the oval and round windows. Unpublished data. 2002.

  7. Gianoli GJ, Soileau JS. The dehiscent middle fossa: prevalence, manifestations, associated findings and results of 24 surgical explorations for superior semicircular canal dehiscence. Publication pending: presented as triologic thesis, 2005.

  8. Banerjee A, Whyte A, Atlas MD. Superior canal dehiscence: review of a new condition. Clin Otolaryngol. 2005;Feb 30(1):9-15. [Medline].

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Keywords

superior canal dehiscence, Hennebert sign, Hennebert's sign, Tullio phenomenon, Tullio's phenomenon, sound-induced vertigo, pressure-induced vertigo, vertigo, dizziness, chronic imbalance, hyperacusis, SCDS, superior canal dehiscence syndrome, vestibular evoked myogenic potentials, VEMPs, hearing loss, dehiscent superior semicircular canal, vestibular symptoms, syphilis, perilymphatic fistula, congenital deafness, Ménière disease, head trauma, Lyme disease, cholesteatomas with labyrinthine fistula, fenestration operations, malpositioned primitive otocyst

Contributor Information and Disclosures

Author

Wayne T Shaia, MD, Consulting Staff, Department of Otology/Neurotology, Medical College of Virginia
Disclosure: Nothing to disclose.

Coauthor(s)

Jack M Kartush, MD, Clinical Professor, Department of Otolaryngology, Wayne State University; Director of Otology, Neurotology, and Skull Base Surgery, Providence Hospital; President, Michigan Ear Institute; President, American NeuroMonitoring
Jack M Kartush, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Neurotology Society, and American Otological Society
Disclosure: Nothing to disclose.

Medical Editor

Robert A Battista, MD, FACS, Assistant Professor of Otolaryngology, Northwestern University Medical School; Physician, Ear Institute of Chicago, LLC
Robert A Battista, MD, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Neurotology Society, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gerard J Gianoli, MD, Clinical Associate Professor, Department of Otolaryngology-Head and Neck Surgery, Tulane University School of Medicine; Vice President, The Ear and Balance Institute; Chief Executive Officer, Ponchartrain Surgery Center
Gerard J Gianoli, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Neurotology Society, American Otological Society, Society of University Otolaryngologists-Head and Neck Surgeons, and Triological Society
Disclosure: Nothing to disclose.

CME Editor

Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation unstricted gift unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo  Consulting; Medvoy Ownership interest Management position

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