Superior semicircular canal dehiscence
A third window changes the conductive picture, the VEMP, and the vestibular reflexes — but usually leaves SVV close to normal.
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Superior canal dehiscence is a third-window disorder, and SVV's role here is to tell you what is not happening. Static SVV is usually normal, and that normality is part of the diagnosis.
The dehiscence is a defect in the bone over the superior semicircular canal, opening an abnormal pathway between the labyrinth and the middle cranial fossa. The mechanical consequence is exaggerated motion signal from the affected canal — manifest as the Tullio phenomenon, autophony, and conductive hyperacusis.
Critically, the utricular macula is mechanically and functionally intact in SCD. There is no hair cell damage, no afferent loss, no graviceptive asymmetry. The static SVV stays within ±2°.
Compare with vestibular neuritis on the same side. Neuritis: SVV tilted, oVEMP reduced or absent. SCD: SVV normal, oVEMP augmented with lowered threshold. These two combinations cleanly discriminate.
Some series report subtle utricular asymmetry on dynamic SVV in SCD. The clinical relevance is small — augmented oVEMP with lowered threshold is the more useful and more sensitive sign.
After surgical plugging or resurfacing of the dehiscent canal, transient utricular insult can produce a small new ipsiversive SVV tilt of three to six degrees, decaying over six to twelve weeks. This is a useful post-operative tracking variable.
Expected SVV signature
| Feature | Finding |
|---|---|
| Magnitude | Typically 0–2° (within or just outside normal) |
| Direction | Variable; small ipsilesional tilt when present |
| Sound/pressure-evoked tilt | SVV can shift transiently with Tullio stimuli (research finding) |
| Asymmetry | Subtle utricular asymmetry on dynamic SVV in some series |
SCD is a third-window disorder: a defect in the bone over the superior semicircular canal opens an abnormal pathway between the labyrinth and the middle cranial fossa. The dominant effects are on the affected canal (Tullio phenomenon, low-frequency conductive hyperacusis, augmented oVEMP) — utricular function is usually preserved, and so is the static SVV.
Why SVV is normal in SCD (and why that’s useful)
SCD does not destroy hair cells or vestibular afferents. It opens an extra pressure-release path that exaggerates motion signals from the superior canal. The utricular macula is mechanically and functionally intact, and the tonic graviceptive signal feeding the SVV remains balanced. A near-normal SVV in a patient with augmented oVEMP amplitudes and lowered oVEMP thresholds is a textbook SCD pattern.
Compare with vestibular neuritis on the same side: there the oVEMP is reduced or absent, and the SVV is grossly tilted. The combination of these two findings discriminates the two conditions confidently[2].
Surgical considerations
Plugging or resurfacing the dehiscent canal damps the third window but can transiently impair canal function on that side. A new ipsilesional SVV tilt of 3–6° in the days after surgery is a marker of intra-operative utricular insult or vestibular nerve irritation. Most cases compensate by 6–12 weeks.
Companion findings
- Conductive hyperacusis — autophony, hearing the eyes move, hearing footsteps
- Low-frequency conductive hearing loss with normal acoustic reflexes (the classic third-window air–bone gap)
- Tullio phenomenon and Hennebert sign — vertigo provoked by sound or pressure
- Augmented oVEMP amplitude and lowered oVEMP thresholds (the most sensitive single test)
- HRCT with reformats in the plane of the superior canal — diagnostic