Reissner’s Membrane in Aging, Menière’s Disease, and Profound Sensorineural Deafness

ORL ◽  
1990 ◽  
Vol 52 (5) ◽  
pp. 273-280 ◽  
Author(s):  
Mario L. Quijano ◽  
Robert S. Kimura ◽  
Karen B. Fowler
1980 ◽  
Vol 89 (4) ◽  
pp. 335-341 ◽  
Author(s):  
Arndt J. Duvall ◽  
Peter A. Santi ◽  
Margaret J. Hukee

Stria edema, and in some cases atrophy, follows osmotic agents, loop-inhibiting diuretics, acoustic trauma, and rupture of Reissner's membrane. All have in common an imbalance of fluid and electrolytes in the cochlear duct. The glycerol test causes temporary improvement in hearing in Menière's disease. Glycerol causes stria edema and collapse of Reissner's membrane in the chinchilla. Stria edema, as well as stria atrophy, are found in Menière's disease. Metabolic manipulation of the stria might be the best approach in the search for successful treatment of Menière's disease.


1976 ◽  
Vol 85 (6) ◽  
pp. 791-801 ◽  
Author(s):  
Robert S. Kimura ◽  
Carol Y. Ota ◽  
Harold F. Schuknecht ◽  
Tadahiko Takahashi

Electron microscopic study of the cochleas of an individual with bilateral Ménière's disease revealed the presence of many abnormal sensory cells in the apical regions of the cochleas. The pathological alterations were greater in the left ear with the greater hearing loss. There were some giant cilia, fusion of cilia, and loss of cilia. The outer hair cells contained diffuse cuticular bodies near or basal to the nuclei. Many outer hair cells were retracted away from the reticular membrane. The population of the nerve endings appeared normal. The inner hair cells of the apical turns appeared essentially normal. The spiral ganglia were normal in number and morphology at the apical turns, and a majority of their cell bodies were of the unmyelinated or partly myelinated types. The stria vascularis showed atrophy; however, the magnitude of this change was consistent with that known to occur in the aging ear. In the distended areas Reissner's membrane showed areas devoid of mesothelial cells, as well as atrophic epithelial cells. The blood vessels were no different from other human cochlear vessels. These abnormalities seen in the stereocilia, the outer hair cells, and Reissner's membrane are a matter of fact. We must admit, however, that not enough electron microscopic studies have been performed on ears from aging individuals or ears with other pathologies to state that these changes are unique to Ménière's disease. Furthermore, there is currently insufficient knowledge to predict whether these changes affect auditory function.


2004 ◽  
Vol 130 (1) ◽  
pp. 113-119 ◽  
Author(s):  
Sebahattin Cureoglu ◽  
Patricia A. Schachern ◽  
Saurav Paul ◽  
Michael M. Paparella ◽  
Rajesh K. Singh

1983 ◽  
Vol 91 (1) ◽  
pp. 61-67 ◽  
Author(s):  
Herve J. Koskas ◽  
Fred H. Linthicum ◽  
William F. House

Whether or not attacks of Meniere's disease are related to ruptures in the membranous labyrinth is still a point of contention. To help clarify this point, we used light microscopy to study the membranous labyrinth in 14 temporal bones with hydrops from patients with Meniere's disease, four bones with hydrops from patients without Meniere's disease, and 11 normal bones. Findings suggest that ruptures are specific to bones with hydrops from patients with Meniere's disease and that they occur more frequently in Reissner's membrane than in the vestibular membranes.


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