Acute unilateral vestibulopathy / vestibular neuritis
The cleanest example of a peripheral SVV pattern: large, ipsiversive, and decaying over weeks.
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Vestibular neuritis is the most informative SVV diagnosis. It presents acutely, the pattern is stereotyped, and the test directly probes the structure most likely to be involved.
Picture the typical patient: 40s, viral prodrome two weeks ago, now 36 hours of continuous vertigo and nausea. Spontaneous horizontal-torsional nystagmus beating away from the affected side. Positive head impulse test toward the affected side. No hearing loss.
The SVV in this setting tilts ipsilesionally — toward the affected side — typically five to ten degrees, with low trial-to-trial variability. The patient sets the line precisely, but tilted.
Why? The lesion is in the vestibular nerve, on one side. The utricular afferents on that side are silenced. The vestibular nuclei receive an asymmetric input — full tone from the intact side, none from the affected side. That asymmetry tilts the central estimate of vertical toward the lesion.
The superior division of the vestibular nerve carries utricular afferents along with the anterior and lateral canal afferents. Most cases of vestibular neuritis affect this division. The inferior division — saccular and posterior canal — is involved in only about 10 to 15 percent of cases.
That anatomy explains an important pattern: in isolated inferior-division neuritis, the SVV is normal. The patient has spontaneous vertigo and posterior-canal nystagmus, but the utricle is spared.
Combining SVV with VEMP gives you a clean dissociation: SVV and oVEMP probe the superior division; cVEMP probes the inferior. The four-cell table you can build from these tests partitions every case of acute vestibulopathy by anatomical sub-territory.
Time course. The acute tilt — five to ten degrees — decays over weeks. By three months, central compensation has rebalanced the static signal in most patients. The static SVV may be entirely normal even though the lesion persists.
This is where dynamic SVV becomes useful. A normal static SVV at three months does not exclude residual asymmetry; the underlying peripheral lesion does not heal — the brain learns to ignore it.
Expected SVV signature
| Feature | Acute (days 0–7) | Chronic (months) |
|---|---|---|
| Direction | Ipsilesional | Often normalised |
| Magnitude | 5–10° (sometimes >10°) | 0–3° |
| OTR triad | Often partial | Resolved |
| Variability | Low — precise but tilted | Low |
The superior division of the vestibular nerve is involved in ~85% of cases[11], which is why utricular afferents — and therefore SVV — are nearly always affected. Inferior-division neuritis (cVEMP abnormal, SVV usually normal) is a useful subtype to recognise.
Time course
The SVV tilt decays exponentially over weeks as central compensation rebalances the tonic asymmetry. By 3 months the static SVV has typically normalised even though the head impulse test and caloric weakness persist — this is why dynamic SVV (eccentric rotation) is useful in chronic UVL to confirm residual otolithic asymmetry.
Companion findings
- Spontaneous horizontal-torsional nystagmus beating away from the affected ear
- Positive head impulse test toward the affected side (in superior-division neuritis)
- Caloric weakness on the affected side
- Abnormal oVEMP on the affected side (utricular); cVEMP usually preserved in superior-division neuritis