Production mechanisms and propagation times for tone -burst evoked OAEs in the guinea pig

Measures of cochlear delay made on the basilar membrane or inferred from auditory nerve recordings represent delays to a single cochlear location. Otoacoustic emissions (OAEs) provide an alternative, non-invasive means of examining cochlear mechanics with OAE delays representing a global cochlear response. Cochlear delays are typically calculated from the phase gradient; an alternative measure of group delay that has not been examined previously for OAEs and can be made directly in the time domain is to use amplitude modulation (AM). Here, OAEs were measured in response to AM stimuli, the OAE extracted using a nonlinear extraction paradigm with a 6 dB stimulus level ratio. AM stimuli had carrier frequencies of 4, 9, and 18 kHz and modulation rates of 86 or 172 Hz with stimuli presented over the range 40 to 90 dB pSPL. It was found that approximately 50% of the OAEs had waveform morphologies similar to the evoking stimulus, allowing for a direct calculation of group delay; the other 50% had distorted morphologies. The possibility of a two-component interaction as a source of this distortion was examined using inverse Fourier analysis and time-domain windowing of the OAE spectrum in response to tone burst stimuli. It was found that stimulus frequency OAEs in the guinea pig arise from a stimulus level-dependent mix of linear-reflection and nonlinear-distortion mechanisms, with a linear-reflection mechanism dominating at low and moderate stimulus levels and a nonlinear-distortion mechanism dominating at higher levels. Group delays were calculated for AM-evoked OAEs for those OAEs that retained morphologies similar to the evoking stimuli. Group delays for SFOAEs evoked by 18 kHz stimuli at low levels were consistent with a round-trip delay based on comparison with basilar membrane phase-gradient estimates of delay. At higher levels the SFOAE delays diverged from BM delays, decreasing rapidly as stimulus level increased. The divergence of OAE and BM delays with increasing stimulus level is presumably a product of a basal-ward shift in the excitation pattern on the basilar membrane with increasing stimulus level, as well as the contribution of a nonlinear distortion mechanism, which does not yield physiological estimates of delay.