A 45-year-old man has dozens of brief attacks of rotatory vertigo each day, each lasting only a few seconds, precipitated by turning his head or changing position. Between attacks he is asymptomatic. A therapeutic trial of carbamazepine markedly reduces the attacks. The most likely underlying mechanism is:
- A Endolymphatic hydrops with rupture of Reissner's membrane
- B Autoimmune inflammation of the vestibular ganglion
- C Canalolithiasis of the posterior semicircular canal
- D Neurovascular compression of the eighth cranial nerve causing ectopic firing ✓
Explanation
Very brief (seconds), high-frequency attacks of vertigo provoked by head movement, with a dramatic response to carbamazepine, define vestibular paroxysmia. The mechanism is neurovascular compression of the eighth cranial nerve, analogous to trigeminal neuralgia, producing ectopic discharges. Canalolithiasis causes longer positional episodes with characteristic nystagmus and does not respond to carbamazepine. Endolymphatic hydrops produces attacks lasting 20 minutes to hours with auditory symptoms. Autoimmune vestibulopathy causes progressive, not paroxysmal, dysfunction.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.