The disorder
Pathophysiology & causes
BPPV is a mechanical disease: crystals that belong in the utricle end up in a semicircular canal, where they hijack the canal’s response to gravity. Two mechanisms — canalithiasis and cupulolithiasis — explain everything you see at the bedside.
Canalithiasis vs cupulolithiasis
Normally the otoconiasit on a membrane in the utricle and help sense gravity and movement. In BPPV some break loose and drift into a balance canal. Now, when the head moves, the loose crystals tug on the canal’s sensor and the brain is told the head is spinning when it is not — so the room seems to spin.
In canalithiasis — the commoner mechanism — otoconia float freely in the canal. A position change lets them fall under gravity, dragging endolymph and deflecting the cupula a moment later. That delay is the diagnostic latency; the brief, self-limiting nystagmus and its fatigability follow from the particles settling.1,3
In cupulolithiasis, otoconia adhere to the cupula itself, loading it so it stays gravity-sensitive. The result is a longer-lasting, non-fatiguing nystagmus that resists standard repositioning.2
The mechanism dictates the bedside signature and the treatment. Canalithiasis gives latent, transient, fatigable nystagmus and responds to repositioning that lets gravity walk the debris out of the canal. Cupulolithiasis gives persistent, low-latency, non-fatiguing nystagmus and must first be liberated from the cupula. The horizontal canal can convert between the two states, which is why the supine roll test can change between examinations.2
Which canal — and why the posterior dominates
The posterior canal accounts for 80–90% of BPPV because its orientation makes it the most gravity-dependent — debris naturally settles into it. The horizontal canal accounts for 5–15%, and the anterior (superior) canal for a rare 1–2%, where the presentation overlaps with central positional vertigo and demands care.1 Multi-canal and bilateral BPPV are uncommon but matter — they cluster after trauma and ear surgery and are more resistant to treatment.
Idiopathic and secondary causes
Most BPPV is idiopathic, especially in older adults, where age-related degeneration of the otolithic membrane lets otoconia detach — accounting for up to 50–70% of cases over 60. Secondary BPPV follows an identifiable insult:
- Head trauma (≈8–20%, more in younger patients) — often multi-canal, bilateral, and more refractory.
- Vestibular neuritis — BPPV emerges in recovery, usually posterior canal on the affected side.
- Ménière’s disease and post-surgical states (stapedectomy, labyrinthectomy, cochlear implant, schwannoma resection).
- Osteoporosis & low vitamin D — bone demineralisation impairs otoconial stability, raising incidence and recurrence; this links to the female and elderly predominance.4,5,6
- Prolonged bed rest / immobility — reduced head movement lets otoconia settle.
Key points
- BPPV is mechanical — displaced otoconia make a canal gravity-sensitive.
- Canalithiasis (free-floating) → latent, fatigable. Cupulolithiasis (cupula-bound) → persistent, non-fatiguing.
- Posterior canal dominates (80–90%) because it is most gravity-dependent.
- Idiopathic in most older adults; secondary after trauma, neuritis, surgery, and with osteoporosis/low vitamin D.