Many of the theories attempting to explain the pathogenic physiology of Meniere's disease rest almost wholly upon anatomic observations. In general, however, the symptomatology of this disease is more complex than the observed anatomical changes warrant, with the result that the theories are elaborate extensions beyond the anatomical facts. It is known that the labyrinth gives evidence of outward displacement of Reissner's membrane and bulging of all walls of the saccule and utricle. 1-7 These changes in the gross anatomy of the labyrinth have suggested a disturbance of endolymphatic and perilymphatic humoral production, circulation, or absorption. Most recently, and again on anatomical evidence, Lawrence and McCabe 7 suggest that the periodicity of symptoms may be related to intermittent rupture and repair of Reissner's membrane, with subsequent contamination of endolymph by perilymph and resultant chemical alteration of endolymph; the latter being known to be high in K+ and the perilymph in
No takes yet. Share an insight, caveat, or question.
Litton et al. (1961) studied this question.