Benign paroxysmal positional vertigo
A canal-plugging mechanism produces dramatic positional nystagmus — and an SVV that is almost always normal.
Expected SVV signature
| Setting | SVV |
|---|---|
| Classical posterior canal BPPV | Normal (0–2°) |
| Active attack (head-tilted) | Brief tilt during the paroxysm — not a static finding |
| Multi-canal or recurrent BPPV | Usually still normal; rare reports of small persistent tilt |
| Post-canalith repositioning | Normal |
BPPV is a mechanical problem of the semicircular canals — displaced otoconia in the canal (canalolithiasis) or adherent to the cupula (cupulolithiasis). The utricle, the macula, and the central graviceptive pathways are not affected. Static SVV is therefore normal.
The rare exceptions
A persistent ipsilesional SVV tilt of more than 3° in a patient with otherwise classical BPPV should prompt a second look:
- BPPV plus a concurrent utricular insult. Otoconia detach from the utricular macula; the same event that displaces otoconia into the canal may have damaged the macula itself.
- BPPV plus vestibular neuritis. Post-neuritis BPPV is well described — the SVV tilt is from the neuritis, not the BPPV.
- Central positional vertigo. If the positional nystagmus is atypical (downbeating, sustained, non-fatiguing) and the SVV is tilted, posterior fossa imaging is warranted.
Why this matters clinically
BPPV is the commonest cause of vertigo and a frequent referral. A normal SVV is reassuring and consistent with the diagnosis. A grossly abnormal SVV in someone you have already labelled as BPPV is a red flag — the patient probably has additional vestibular pathology that the repositioning manoeuvre alone will not fix.
Companion findings
- Positive Dix–Hallpike (posterior canal) or supine roll test (horizontal canal)
- Up-beating torsional nystagmus on Dix–Hallpike for posterior canal BPPV
- Geotropic or apogeotropic horizontal nystagmus on roll test for horizontal canal BPPV
- Normal audiogram, normal caloric, normal VEMPs in pure BPPV