The pathophysiological basis of Meniere's disease is endolymphatic hydrops. The most accepted mechanism by which endolymphatic sac dysfunction leads to episodic attacks involves:

• A Rupture of Reissner's membrane allowing endolymph (high K+) to mix with perilymph, causing K+ intoxication of VIII nerve terminals (hair cells and cochlear nerve), explaining the acute onset of vertigo, hearing loss, and tinnitus ✓
• B Inflammatory infiltration of the spiral ligament causing permanent hair cell destruction
• C Autoimmune attack on myelin of the vestibulocochlear nerve at the IAC
• D Perilymphatic fistula formation from the round window into the subarachnoid space

Explanation

In Meniere's disease, impaired endolymphatic sac resorption leads to progressive accumulation of endolymph (hydrops). Episodic attacks are triggered by rupture of the Reissner's membrane (roof of the cochlear duct), allowing endolymph with its abnormally high K+ concentration (~150 mEq/L) to flood into the scala vestibuli (perilymph, normally low K+). This K+ intoxication depolarizes cochlear nerve endings and hair cells, causing the triad of episodic vertigo, fluctuating SNHL (low-frequency), and tinnitus. The Reissner's membrane repairs itself, restoring ion balance and ending the acute attack.

Reference: Dhingra Diseases of Ear, Nose and Throat, 7th ed.

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Written and medically reviewed by the StethoPrep medical team.