Superior Canal Dehiscence Explained: Symptoms, Causes, and How Doctors Confirm the Diagnosis

Superior canal dehiscence is a tiny bony opening over the superior semicircular canal of the inner ear that creates a “third window,” letting sound and pressure abnormally move inner-ear fluids and trigger dizziness, hearing distortion, and startling sensitivity to internal sounds—like hearing your eyeballs move. ^[1]

In a typical ear, sound energy enters primarily through two “windows” (oval and round). When a defect opens in the bone over the superior semicircular canal, a third pathway for energy is created. That extra window shunts acoustic and pressure energy into the balance organs. The result is a signature cluster of symptoms:

• Sound- or pressure-induced vertigo and nystagmus (for example, from loud speakers, coughing, sneezing, straining, or pressure changes).
• Bone-conduction hyperacusis (hearing internal sounds unusually loudly)—footsteps, heartbeat, chewing, your own voice echoing, and in striking cases hearing eye movements across the orbit.
• Pulsatile tinnitus, ear fullness, or autophony.
• A conductive hearing loss pattern on the audiogram that looks like a middle-ear problem but with a normal eardrum exam and normal middle-ear reflexes. ^[1]

These features reflect classic “third-window” physiology: energy leaks away from the cochlea (mimicking a conductive loss) and abnormally stimulates the canal (provoking dizziness and eye-movement responses) when sound or pressure reaches the ear. ^[2]

Superior canal dehiscence was formally described in 1998, when patients with sound- or pressure-triggered vertigo and a characteristic eye-movement pattern were found to have a focal bony defect over the superior canal on high-resolution computed tomography; plugging or resurfacing the canal improved symptoms. That first description turned scattered, puzzling complaints into a coherent syndrome with effective treatment options. ^[1]

Since then, consensus diagnostic criteria have been published: a combination of typical symptoms, physiologic test abnormalities, and high-resolution images confirming the dehiscence. Using all three prevents over-diagnosis from imaging alone because small “near-dehiscences” and imaging artifacts can appear in people without symptoms. ^[2]

Superior canal dehiscence can present from childhood through late adulthood but is most commonly recognized in mid-life. Many people recall a “trigger” (an upper respiratory infection, heavy lifting, barotrauma), but others have gradual onset. Anatomical predisposition—thin bone over the canal—appears important; some patients have bilateral defects, although one ear is usually more symptomatic. As with many vestibular disorders, diagnosis often takes time because early symptoms can be dismissed as anxiety or migraine until the pattern becomes clear. ^[1]

• Dizziness or vertigo induced by loud sound (concerts, vacuum, blender) or pressure (coughing, sneezing, straining).
• Hearing internal sounds too loudly: heartbeat, footstep thuds, chewing, jaw clicks, ocular movement “squeaks” during eye tracking, your own voice echoing.
• Pulsatile tinnitus or ear fullness that changes with posture or pressure.
• Sensitivity to low-frequency sound and a “plugged ear” sensation with normal ear drum exam. ^[1]

• Perilymphatic fistula and enlarged vestibular aqueduct can mimic the third-window picture; imaging and physiologic testing help separate them. ^[3]
• Middle-ear disorders such as otosclerosis, ossicular discontinuity, or chronic otitis media create a true conductive loss, but typically show abnormal tympanometry or absent stapedial reflexes—unlike many superior canal dehiscence cases where these are intact despite an air–bone gap. ^[3]
• Vestibular migraine can cause sound sensitivity and dizziness but lacks the characteristic physiologic and imaging signature of superior canal dehiscence. Clinical testing distinguishes them. ^[1]

Many people show a low-frequency air–bone gap on the hearing test, which looks like middle-ear conductive hearing loss—but tympanometry and reflexes are often normal. That paradox is a hallmark of a third-window lesion. ^[3]

Vestibular evoked myogenic potentials measure how the balance organs respond to sound. In superior canal dehiscence, these responses are abnormally easy to evoke and abnormally large, because sound energy is shunted to the canal. Two complementary recordings are common:

• Cervical vestibular evoked myogenic potentials (from the neck muscles) often show lower-than-normal thresholds to sound and may have large amplitudes.
• Ocular vestibular evoked myogenic potentials (from the extra-ocular muscles beneath the eye) often show large amplitudes on the affected side.

Contemporary reviews detail how reduced thresholds and elevated amplitudes strongly support the diagnosis, especially when paired with the right symptoms and imaging. ^[4]

Clinicians may observe nystagmus in the plane of the superior canal when sound or pressure is applied (a modern echo of the classic Tullio and Hennebert signs). This physiologic signature links the symptom to the canal itself. ^[1]

High-resolution computed tomography of the temporal bone is the traditional standard for seeing the bony opening. Thin-slice images with reconstructions in Pöschl (parallel to the canal) and Stenver (perpendicular to the canal) planes help avoid false positives and make the dehiscence clear. Experienced radiologists also rely on high-quality coronal multiplanar reformats. ^[5]

Magnetic resonance imaging with special reformations is improving and may help in some centers, but computed tomography remains the most widely accepted anatomic test; magnetic resonance imaging cannot yet replace computed tomography everywhere. (Emerging studies are exploring magnetic resonance imaging in Pöschl and Stenver planes, but practice is evolving.) ^[6]

Important caution: Imaging alone does not equal disease. Small “dehiscences” or very thin bone can be found in asymptomatic people; diagnosis requires the triad: compatible symptoms, abnormal physiologic testing, and a computed tomography that truly shows the defect. ^[2]

The Bárány Society’s consensus criteria require:

1. At least one typical symptom of a third-window lesion (for example, sound- or pressure-induced vertigo, pulsatile tinnitus, autophony, or bone-conduction hyperacusis);
2. Objective physiological evidence of third-window mechanics (for example, abnormally low cervical vestibular evoked myogenic potential thresholds or abnormally high ocular vestibular evoked myogenic potential amplitudes, or sound- or pressure-induced eye movements in the plane of the superior canal); and
3. High-resolution imaging demonstrating dehiscence of bone over the superior semicircular canal.

Applying all three elements reduces misdiagnosis and guides appropriate care. ^[2]

Not everyone needs an operation. Many people choose activity modification—avoiding very loud environments, heavy straining, or Valsalva maneuvers; using hearing protection strategically; and treating coexisting problems like migraine or temporomandibular disorders that amplify sensitivity. A specialist can help personalize these steps while the diagnostic work-up proceeds. ^[1]

If symptoms are disabling and the triad of criteria is met, surgical repair targets the root cause: the “third window.” Two time-tested strategies are used to plug and/or resurface the superior canal, preventing abnormal fluid motion:

• Middle cranial fossa approach (through a small opening above the ear) allows direct visualization of the canal roof for plugging and resurfacing the defect.
• Transmastoid approach (through the mastoid bone behind the ear) allows canal plugging in many cases with less brain retraction.

In experienced hands, most appropriately selected patients improve, often dramatically, in sound-induced dizziness, hyperacusis to internal sounds, and pulsatile tinnitus. Reported series across two decades describe high rates of symptom relief and quality-of-life gains; as with any operation, outcomes vary with anatomy and surgeon experience. ^[1]

Expected short-term dizziness is common as the brain adapts; hearing is usually preserved, but sensorineural or conductive changes and balance symptoms can occur. Serious complications are uncommon in expert centers but can include hearing loss, cerebrospinal fluid leak, and facial nerve injury; discussion of risks is individualized. ^[1]

A striking feature of superior canal dehiscence is the air–bone gap at low frequencies on the hearing test even though the ear drum, middle-ear pressure, and stapedial reflexes are normal. The third window allows acoustic energy to escape the cochlea into the balance system, reducing the apparent efficiency of air conduction while making bone conduction seem unusually good. Recognizing this paradox prevents unnecessary middle-ear surgery. ^[3]

1. History and physical examination focused on sound- and pressure-induced symptoms; bedside pressure or sound testing may provoke characteristic eye movements in the canal’s plane. ^[1]
2. Audiometry with tympanometry and acoustic reflexes to detect the third-window pattern (air–bone gap with intact reflexes). ^[3]
3. Vestibular evoked myogenic potentials (cervical and ocular) looking for low thresholds or high amplitudes on the affected side. ^[4]
4. High-resolution temporal-bone computed tomography with targeted planes (Pöschl and Stenver) to visualize the bony opening. ^[5]
5. Shared decision-making about observation versus surgery, tailored to how much symptoms limit daily life and to test results that support a true third-window lesion per consensus criteria. ^[2]

Why do loud sounds make me dizzy?

The “third window” lets sound energy push on the balance canals. The superior canal is most affected, so loud sounds or pressure make the eyes move in that canal’s plane, causing vertigo or a sense of motion. ^[1]

Can I really hear my eyeballs move?

Yes—some people perceive a scratch or crunch with eye movements because internal bone-conducted sounds are abnormally amplified through the third window. It is bizarre but well documented in this syndrome. ^[1]

Is magnetic resonance imaging enough, or do I need computed tomography?

Magnetic resonance imaging techniques are improving, but high-resolution computed tomography with dedicated planes remains the most established way to see the tiny bony defect. Many centers still rely on computed tomography to confirm anatomy even when magnetic resonance imaging suggests a dehiscence. ^[5]

What exactly do vestibular evoked myogenic potentials show?

They show how easily sound can stimulate vestibular organs. In superior canal dehiscence, thresholds are lower and amplitudes larger because the third window “supercharges” the canal’s sensitivity to sound. ^[4]

Will surgery cure me?

Most well-selected patients improve substantially, especially for sound- and pressure-induced dizziness and for bone-conduction hyperacusis. Some symptoms may persist or recur, and small risks exist, so decisions are individualized with an experienced team. ^[1]

• Superior canal dehiscence produces sound- and pressure-induced vertigo, bone-conduction hyperacusis, and pulsatile tinnitus through a tiny “third window” in the inner ear. ^[1]
• Diagnosis is a triad: typical symptoms, physiologic evidence (audiogram pattern, vestibular evoked myogenic potentials, sound- or pressure-evoked eye movements), and high-resolution computed tomography in targeted planes showing the bony opening. Do not rely on imaging alone. ^[2]
• Surgical plugging or resurfacing of the superior canal helps many people when symptoms are disabling and tests align; observation and trigger avoidance are reasonable for milder cases. ^[1]

Educational information only; not a substitute for personal medical advice. If you have sound-triggered dizziness or new hearing changes, seek evaluation by an ear, nose, and throat specialist or a neurotologist.