title: [Electrocochleographic analysis of the suppression of tinnitus by electrical promontory stimulation and changes in compound action potentials].
abstract: We performed Electrical Promontory Stimulation (EPS) for the suppression of tinnitus in 52 patients and measured Compound Action Potentials (CAP) using electrocochleography before and after EPS. We examined the relation between residual inhibition and CAP. The purpose of this study was to investigate the origin and mechanism of suppression of tinnitus. Tinnitus was suppressed in 27 patients (52%) after EPS. In the group of patients in which we suppressed tinnitus, the CAP amplitudes increased from 3.0 +/- 1.5 microV to 3.2 +/- 1.6 microV (p < 0.05), the loudness of tinnitus was reduced from 7.3 +/- 4.7 dBSL to 5.6 +/- 5.1 dBSL (p < 0.05) and the CAP latencies did not exhibit remarkable change. In the group of patients in which we did not suppress tinnitus, the CAP amplitudes, latencies and the loudness of tinnitus did not change remarkably. These data indicate that EPS affects auditory nerve fibers directly. It was reported that EPS is effective for tinnitus of peripheral origin and not for that of central origin and, that in tinnitus of peripheral origin, the spontaneous discharges of the auditory nerve increase in number. It is hypothesized that EPS affects auditory nerve fibers and suppresses tinnitus by synchronizing these spontaneous discharges. Side effects of EPS were cough and discomfort of the throat, nose, lips and oral cavity. These effects were observed only during electrical stimulation and there were no permanent side effects. In conclusion, EPS affects auditory nerve fibers directly, is effective for tinnitus of peripheral origin and is not associated with serious complications.
mesh_terms: D000200:Action Potentials; D000328:Adult; D000368:Aged; D001300:Audiometry, Evoked Response; D004432:Ear, Middle / Q000502:physiology; D004599:Electric Stimulation Therapy; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D014012:Tinnitus / Q000503:physiopathology / Q000628:therapy*; D000159:Vestibulocochlear Nerve / Q000502:physiology