[Medical treatment of Meniere's disease].
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Sixty-six patients with Meniere's disease were studied for possible general immunologic abnormalities. The disease was bilateral in 20 cases, causing active symptoms in 49. Thirty-six healthy control subjects were also studied. Immune activity was assessed by quantitative measurement of the circulating immune complexes, serum immunoglobulin assay, and acetate electrophoresis, and by an autoantibody screen to a battery of ten general tissue antigens. Thirty-six (54.5%) of the 66 patients with Meniere's disease were found to have significantly raised circulating immune complex levels compared with one (2.9%) of the 36 controls. A statistically significant increased incidence of autoantibodies was also found in the Meniere's group.
Pure tone audiograms of 300 patients with Meniere's disease and 400 patients without Meniere's disease were compared for prevalence of a high-frequency peak configuration. Prevalence rate of 42% for a peak audiogram was observed in ears diagnosed with Meniere's disease compared with 6% for patients with cochlear hearing loss not attributed to Meniere's disease, and 7% for normal hearing patients. Prevalence of the peak audiogram in patients with Meniere's disease was significantly greater than either of the patient groups without Meniere's disease. Prevalence of peak audiogram was affected by duration and bilaterality of Meniere's disease, but not by the degree of hearing loss. A classification system is proposed for describing the peak audiogram based on the severity of the peak configuration and the degree of hearing loss.
PURPOSE OF REVIEW: Meniere's disease is characterized by the triad of fluctuating hearing loss, episodic vertigo, and tinnitus and by endolymphatic hydrops found on post-mortem examination. The cause of Meniere's disease remains unclear. Numerous factors play a role in the development of hydrops and in the pathogenesis of related cochleovestibular dysfunction. This review highlights recent advances in the understanding of the pathophysiology of symptom development in Meniere's disease by detailing the role of genetics, autoimmunity, endolymphatic fluid homeostasis, excitotoxicity, oxidative stress, and cellular apoptosis. Emphasis is placed on reviewing the newly described animal models that exhibit endolymphatic hydrops. RECENT FINDINGS: Recent evidence suggests that hearing loss might be explained in part by apoptosis of spiral ganglion neurons and that hydrops could represent an epiphenomenon rather than an initiating factor. In addition, the accepted guinea pig model described by Kimura has certain limitations. An animal model that would supplement and in some cases replace the surgically induced model is currently being sought. SUMMARY: These recent advances have expanded our understanding and will allow for the development of targeted therapeutic interventions aimed at preventing the progression oochleovestibular deterioration.
We examined the sera of patients with Meniere's disease for the presence of antibodies against 8 inner ear antigens by enzyme-linked immunosorbent assay (ELISA). One hundred eight patients with Meniere's disease and 28 control subjects were studied. The antibodies against chicken type II collagen, bovine type II collagen, the cyanogen bromide cleaved peptide 11 (CB11) of each, type IX and XI collagens, C-Raf, and tubulin were measured by ELISA. The sensitivity of each antigen was between 37% and 60% individually, and was 91% when all 8 inner ear antigens were combined. These results showed that 91% of Meniere's disease sera have antibody activities to 1 or more of these inner ear antigens. The results suggest that performing ELISA for these 8 inner ear antigens was useful as a diagnostic tool for Meniere's disease. Further study is required for elucidating the role of these antigens in the pathogenesis of Meniere's disease, which might eventually result in better therapy.
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