Abstract
BackgroundThe general consensus on the role of hearing loss in generating tinnitus is not relevant in tinnitus patients with normal hearing thresholds. One source of tinnitus may be related to damage to outer hair cells (OHC) of the cochlea. If the OHC of the human cochlea are to be involved in the generation of tinnitus, testing of Otoacoustic emissions (OAE) could provide a reliable means of recording OHC dysfunction. We investigated the role of OHC and cochlear efferent system in tinnitus development in normal hearing ears through studying of Distortion Product Otoacoustic Emissions (DPOAE) and Transient Evoked Otoacoustic Emissions (TEOAE) amplitudes, contralateral suppression amplitudes and suppression value in 15 normal hearing tinnitus patients and 15 control subjects.ResultsMean f2 DPOAE amplitudes and contralateral suppression were significantly lower in tinnitus group compared to controls for all frequencies from 1001 to 6348 Hz. Suppression values of DPOAEs revealed lower but not significant difference between tinnitus and control groups for all frequencies except 1587 and 6348 Hz. TEOAE amplitudes and contralateral suppression were significantly lower in tinnitus groups for all frequencies from 1000 to 4000 Hz compared to the control group. Suppression value of TEOAEs revealed no significant difference between the two groups for all frequencies except 3000 and 4000 Hz were significantly lower in the tinnitus group compared to the control group.ConclusionsNormal hearing manifested by pure tone audiometry in non-vascular tinnitus sufferers does not exclude OHC and/or cochlear efferent pathology.
Highlights
The general consensus on the role of hearing loss in generating tinnitus is not relevant in tinnitus patients with normal hearing thresholds
Evidence indicates that changes in the cochlea can be detected by otoacoustic emissions (OAEs), contralateral suppression, and suppression value testing even before the occurrence of considerable changes in the patient’s audiogram [5]
The OAEs are produced by the outer hair cells (OHCs) of the cochlea as a result of nonlinear active
Summary
The general consensus on the role of hearing loss in generating tinnitus is not relevant in tinnitus patients with normal hearing thresholds. One source of tinnitus may be related to damage to outer hair cells (OHC) of the cochlea. We investigated the role of OHC and cochlear efferent system in tinnitus development in normal hearing ears through studying of Distortion Product Otoacoustic Emissions (DPOAE) and Transient Evoked Otoacoustic Emissions (TEOAE) amplitudes, contralateral suppression amplitudes and suppression value in 15 normal hearing tinnitus patients and 15 control subjects. Jastreboff considers that tinnitus usually starts in the cochlea and generates abnormal activity. The absence of audiometric hearing loss challenges the cochlear theories of tinnitus generation in normal hearing tinnitus patients [2]. The OAEs are produced by the outer hair cells (OHCs) of the cochlea as a result of nonlinear active Evidence indicates that changes in the cochlea can be detected by otoacoustic emissions (OAEs), contralateral suppression, and suppression value testing even before the occurrence of considerable changes in the patient’s audiogram [5].
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