[Physiopathology and clinical aspects of Menière's disease]

The most prominent changes in temporal bone histopathology of Menière's disease are hydrops-like extensions of the endolymphatic spaces. The endolymphatic hydrops seems to be the consequence of a diminished function or complete atrophy of the endolymphatic sac. The etiology or pathomechanism of perisaccular fibrosis or saccular degeneration is unknown. But as a consequence of experimental datas obtained by animal studies the pathogenesis of the endolymphatic hydrops can be explained by osmotic active forces which develope within the endolymphatic spaces after blockage of the endolymphatic aqueduct or sac: An increasing concentration of osmotic active endolymphatic components cause an influx of water from the perilymphatic (extracellular) environment so that the limiting membranes of the endolymphatic space have to extend (e.g. Reissner's membrane, saccular membrane). At any topographic location of the endolymphatic spaces these membranes can rupture followed by intermixing of potassium-rich endolymph with sodium rich perilymph. This leads to an acute or chronic intoxication of those sensory nerve elements which have close contact to perilymphatic fluid. The hypothesis of an osmotic induced accumulation of "water' during endolymphatic hydrops is supported by sometime striking results of the glycerol test. Nevertheless, the pathogenesis and etiology of Menière's disease remains obscure, as indicated by the diverging spectrum of the different conservative or surgical therapeutic methods in use.