## Why option 1 is right Meniere disease results from endolymphatic hydrops—excess endolymph that distends the membranous labyrinth. The cochlear duct's apex (low-frequency region) has greater compliance and is affected first by this distension. Repeated pressure increases cause rupture of Reissner's membrane, allowing potassium-rich endolymph to mix with perilymph and damage low-frequency hair cells preferentially. This produces the characteristic low-frequency rising (ascending) sensorineural hearing loss pattern seen on audiometry, which is a cardinal diagnostic feature of Meniere disease. As the disease progresses and hydrops worsens, hearing loss eventually flattens and extends to mid and high frequencies. The pattern marked **B** (low-frequency rising SNHL at 250–1000 Hz) directly reflects this pathophysiology. ## Why each distractor is wrong - **Option 2**: While endolymph–perilymph mixing does occur, the differential susceptibility is not based on potassium toxicity selectivity. The low-frequency involvement is anatomic (apex affected first by hydrops), not due to preferential high-frequency resistance to potassium. - **Option 3**: Stria vascularis fibrosis is a feature of age-related hearing loss and occurs diffusely, not selectively in the basal turn. It does not explain the early low-frequency pattern in Meniere disease, which is driven by hydrops, not metabolic degeneration. - **Option 4**: Acoustic trauma from head movements during vertigo is not a recognized mechanism of hearing loss in Meniere disease. The hearing loss is sensorineural and related to endolymphatic distension and membrane rupture, not mechanical trauma. **High-Yield:** Meniere disease = endolymphatic hydrops → apex (low-frequency region) affected first → low-frequency rising SNHL is the hallmark early audiometric pattern. [cite: Dhingra ENT 7e Ch 16; AAO-HNS 2015 & Bárány Society 2015 diagnostic criteria]
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