Analysis and Influence of Lidocaine on Evoked Otoacoustic Emissions from Tinnitus Sufferers
The discovery of otoacoustic emissions (Kemp, 1978) raised hope that some kind of tinnitus (that is, subjective sensations of sound without acoustical or electrical stimulation) could be attributed to mechanical hyperactivity in the inner ear. For this reason, the relation between tinnitus and spontaneous otoacoustic emissions (SOAEs) has been investigated by several authors (c.f. Wilson and Sutton, 1981, Hazell, 1984, Penner and Burns, 1987). Their findings of no affirmative relation between both phenomena could have been affected by two circumstances: First, a relation between otoacoustic emissions and tinnitus might only occur if both effects originate from roughly the same location within the auditory pathway. Therefore, only cases of “peripheral” (sensorineural) tinnitus should be considered if a reliable distinction between central and peripheral tinnitus can be made at all. Second, tinnitus is often associated with hearing impairment whereas otoacoustic emissions (OAEs) are rarely found in hearing-impaired subjects (Kemp, 1978). This fact might be due to attenuation in the middle ear (primarily for conductive hearing losses), the altered mechanical (back-)propagation in the basal turns of the cochlea and alterations in the “active” cochlea feedback mechanisms. In order to obtain information on these neuro-mechanical mechanisms even in hearing-impaired tinnitus sufferers in a reproducible way, we decided to record evoked otoacoustic emissions (EOAEs). In addition, we attempted to classify the probable origin of the tinnitus clinically and by the effect of lidocaine, a drug that prolongs the refractory period and hence reduces the activity of certain neurons: A subjective change in the perceived tinnitus after an infusion of lidocaine (2mg/kg body weight) indicates a peripheral (sensorineural) origin (Shulman and Seitz, 1981). In addition, a lidocaine effect on the EOAE would provide further evidence that OAEs in humans are generated by an active feedback mechanism which is controlled by neural activity. Last, a correlation between the lidocaine effect on EOAEs and tinnitus would help to clarify the origin of tinnitus.
KeywordsHearing Loss Acoustic Emission Stimulus Level Otoacoustic Emission Conductive Hearing Loss
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