Module 10 · Disease pages

BPPV

Positional vertigo with a normal vHIT
Clinical vignette
A 64-year-old woman describes brief spinning vertigo whenever she rolls over in bed or tips her head back to look up. Each spell lasts about 20 seconds. There is no hearing loss and no spontaneous symptoms. The Dix-Hallpike manoeuvre to the right reproduces brief up-beat torsional nystagmus with vertigo, settling after 15 seconds. Her vHIT, performed the next day, is entirely normal.
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What it is

Benign paroxysmal positional vertigo (BPPV) is the commonest cause of vertigo in adults. Otoconia (calcium carbonate crystals) detach from the utricular macula and migrate into one of the semicircular canals, most often the posterior canal. Once dislodged, these particles drift within the endolymph during head position changes, deflecting the cupula and triggering brief episodes of vertigo with characteristic positional nystagmus.

Why this chapter exists

BPPV is included in a vHIT atlas precisely because the test is normal. Recognising the normal pattern in a patient with positional vertigo confirms that you're dealing with a canalith problem rather than canal nerve loss — and it rules out the differential diagnoses that vHIT could detect (acute neuritis with positional features, schwannoma, central positional vertigo).

Six-canal vHIT in pure BPPV
0100200R latg=0.950100200L latg=0.940100200R antg=0.890100200L antg=0.880100200R postg=0.860100200L postg=0.87
All six canals within normal range. No corrective saccades. Pure BPPV does not affect VOR gain because the canal nerve and sensory epithelium remain healthy — the disorder is mechanical, not neural.

The diagnostic logic

BPPV is a clinical diagnosis based on the history (brief positional vertigo, less than a minute per spell, triggered by head position changes) and positional manoeuvres (Dix-Hallpike for posterior and anterior canals; supine roll test for lateral canal). vHIT is not required for diagnosis but is useful in two scenarios:

  • When the history is ambiguous and you want to rule out an acute vestibular lesion. A normal vHIT is reassuring evidence against neuritis, schwannoma, or other peripheral pathology.
  • When a patient with established BPPV develops new continuous symptoms. A new vHIT abnormality after months of stable BPPV suggests a second pathology, not a worsening of the BPPV.

BPPV after vestibular neuritis

A small but clinically important subset of patients develop BPPV in the weeks after acute vestibular neuritis. The proposed mechanism is detachment of utricular otoconia during the inflammatory insult to the labyrinth. In this scenario the vHIT will reflect the underlying neuritis pattern (reduced lateral and anterior canal gain on the affected side) while the superimposed positional vertigo reflects the canalith. The two diagnoses coexist; don't let an abnormal vHIT in such a patient distract you from doing Dix-Hallpike.

Key teaching points

  • vHIT is normal in pure BPPV — the lesion is mechanical (loose otoconia), not neural.
  • The role of vHIT in suspected BPPV is to exclude other peripheral lesions, not to diagnose BPPV itself.
  • New BPPV after neuritis is common; expect to see both findings on testing.
  • Persistent positional nystagmus without fatigability + normal vHIT + abnormal central oculomotor signs = central positional vertigo until imaging proves otherwise.

References

  1. Halmagyi GM, Chen L, MacDougall HG, Weber KP, McGarvie LA, Curthoys IS. The video head impulse test. Frontiers in Neurology 2017;8:258. doi:10.3389/fneur.2017.00258
  2. MacDougall HG, McGarvie LA, Halmagyi GM, Curthoys IS, Weber KP. The video head impulse test (vHIT) detects vertical semicircular canal dysfunction. PLoS One 2013;8:e61488. doi:10.1371/journal.pone.0061488
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