BASAL COCHLEAR LESIONS RESULT IN INCREASED AMPLITUDE OF OTOACOUSTIC EMISSIONS

We have measured the changes in transient otoacoustic emissions (TEOAE s) and distortion product otoacoustic emissions (DPOAEs) during and af ter ototoxic amikacin treatment in an animal (chinchilla) model. TEOAE and DPOAE were recorded from 6 adult chinchillas over a 6-week time c ourse starting just before a 5-day or 7-day treatment period with amik acin sulphate (400 mg/kg/day, i.m.). After final recordings, cochlear morphology was assessed by scanning electron microscopy. Generally, bo th DPOAE and TEOAE amplitudes change during and after treatment in a s ystematic fashion. High-frequency components change first, followed by lower-frequency components. We note that there is often a long latenc y to the onset of changes in otoacoustic emissions (OAE), and that the se changes can continue for weeks after treatment. Most importantly we report that when the basal region of the cochlea is damaged in the fr equency region above the OAE recording bandwidth (0.6-6 kHz for TEOAE; 1-6.7 kHz for DPOAE), we often find an increase in OAE amplitudes. Mo re specifically, we note that as a cochlear lesion progresses apically , there is often a transient increase in a frequency-specific OAE befo re it reduces or is lost. Our results suggest that the increase in OAE amplitudes precedes the expression of detectable cochlear pathology.