Sounds originating from within the inner ear, known as otoacoustic emissions (OAEs), are widely exploited in clinical practice but the mechanisms underlying their generation are not entirely clear. Here we present simulation results and theoretical considerations based on a hydrodynamic model of the human inner ear. Simulations show that, if the cochlear amplifier (CA) gain is a smooth function of position within the active cochlea, filtering performed by a middle ear with an irregular, i.e., nonsmooth, forward transfer function suffices to produce irregular and long-lasting residual oscillations of cochlear basilar membrane (BM) at selected frequencies. Feeding back to the middle ear through hydrodynamic coupling afforded by the cochlear fluid, these oscillations are detected as transient evoked OAEs in the ear canal. If, in addition, the CA gain profile is affected by irregularities, residual BM oscillations are even more irregular and tend to evolve towards self-sustaining oscillations at the loci of gain irregularities. Correspondingly, the spectrum of transient evoked OAEs exhibits sharp peaks. If both the CA gain and the middle-ear forward transfer function are smooth, residual BM oscillations have regular waveforms and extinguish rapidly. In this case no emissions are produced. Finally, and paradoxically albeit consistent with observations, simulating localized damage to the CA results in self-sustaining BM oscillations at the characteristic frequencies (CFs) of the sites adjacent to the damage region, accompanied by generation of spontaneous OAEs. Under these conditions, stimulusfrequency OAEs, with typical modulation patterns, are also observed for inputs near hearing threshold. This approach can be exploited to provide novel diagnostic tools and a better understanding of key phenomena relevant for hearing science.
There is a long-lasting question of how distortion products (DPs) arising from nonlinear amplification processes in the cochlea are transmitted from their generation sites to the stapes. Two hypotheses have been proposed: (1) the slow-wave hypothesis whereby transmission is via the transverse pressure difference across the cochlear partition and (2) the fast-wave hypothesis proposing transmission via longitudinal compression waves. Ren with co-workers have addressed this topic experimentally by measuring the spatial vibration pattern of the basilar membrane (BM) in response to two tones of frequency f(1) and f(2). They interpreted the observed negative phase slopes of the stationary BM vibrations at the cubic distortion frequency f(DP) = 2f(1) - f(2) as evidence for the fast-wave hypothesis. Here, using a physically based model, it is shown that their phase data is actually in accordance with the slow-wave hypothesis. The analysis is based on a frequency-domain formulation of the two-dimensional motion equation of a nonlinear hydrodynamic cochlea model. Application of the analysis to their experimental data suggests that the measurement sites of negative phase slope were located at or apical to the DP generation sites. Therefore, current experimental and theoretical evidence supports the slow-wave hypothesis. Nevertheless, the analysis does not allow rejection of the fast-wave hypothesis.
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