A 58-year-old woman presents with brief episodes of intense rotatory vertigo lasting 20–40 seconds triggered by rolling over in bed and looking up. She denies hearing loss, tinnitus, or aural fullness. The Dix-Hallpike maneuver on the right side reproduces short-latency (2–5 second), geotropic up-beating torsional nystagmus lasting

Question

A 58-year-old woman presents with brief episodes of intense rotatory vertigo lasting 20–40 seconds triggered by rolling over in bed and looking up. She denies hearing loss, tinnitus, or aural fullness. The Dix-Hallpike maneuver on the right side reproduces short-latency (2–5 second), geotropic up-beating torsional nystagmus lasting <60 seconds with fatigability on repeat testing. Pure-tone audiometry is completely normal with symmetric thresholds. The clinical findings shown in the diagram at **A** are consistent with right posterior canal BPPV. Which of the following BEST describes the pathophysiological mechanism underlying this patient's vertigo?

Accepted Answer

A. Migration of dislodged otoconia (calcium carbonate crystals) from the utricle into the posterior semicircular canal, causing gravity-dependent endolymph flow and cupular deflection. ## Why option 1 is correct

The pathophysiology of BPPV, particularly posterior canal involvement (85–90% of cases), is **canalolithiasis** — dislodged otoconia (calcium carbonate crystals) from the macula of the utricle migrate into a semicircular canal. Gravity-dependent movement of this otoconial debris produces abnormal endolymph flow and inappropriate cupular deflection, triggering the characteristic brief, positional vertigo with nystagmus. The normal audiogram and absence of hearing loss, tinnitus, and aural fullness exclude inner ear pathology affecting the cochlea, confirming a purely vestibular (mechanical) etiology. This mechanism is the diagnostic hallmark of BPPV as described in Dhingra ENT and the AAO-HNS guideline.

## Why each distractor is wrong

- **Option 2 (Vestibular nerve inflammation)**: This describes vestibular neuritis, which presents with persistent vertigo, not brief positional episodes. Fatigability and short latency are hallmarks of canalolithiasis, not inflammation.
- **Option 3 (Hair cell degeneration in ampulla)**: While hair cell loss occurs in sensorineural hearing loss and some vestibular disorders, it does not explain the mechanical, gravity-dependent, brief, fatigable positional vertigo characteristic of BPPV. Audiometry would also show hearing loss.
- **Option 4 (Saccular calcium deposition migrating to horizontal canal)**: Otoconia originate from the **utricle** (not saccule), and this option incorrectly specifies the horizontal canal when the clinical findings (Dix-Hallpike positive, up-beating nystagmus) are diagnostic of **posterior canal** BPPV.

**High-Yield:** BPPV = canalolithiasis (otoconia migration from utricle) → brief, fatigable, positional vertigo with preserved hearing; posterior canal most common (85–90%); Epley maneuver is first-line curative treatment.

[cite: Dhingra ENT 7e Ch 20; AAO-HNS BPPV guideline 2017]

Answer

B. Abnormal calcium deposition in the saccule with subsequent migration into the horizontal semicircular canal

Answer

C. Degeneration of hair cells in the ampulla of the posterior semicircular canal with loss of vestibular transduction

Answer

D. Inflammation of the vestibular nerve with secondary endolymphatic hydrops and cupular dysfunction

Explanation

Why option 1 is correct

Why each distractor is wrong

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