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Does the “Reticular Lamina Nonlinearity” Contribute to the Basal DPOAE Source?
Author(s) -
Arturo Moleti,
Renata Sisto
Publication year - 2020
Publication title -
journal of the association for research in otolaryngology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.498
H-Index - 72
eISSN - 1525-3961
pISSN - 1438-7573
DOI - 10.1007/s10162-020-00771-2
Subject(s) - nonlinear system , basilar membrane , physics , acoustics , otoacoustic emission , cochlea , hearing loss , anatomy , biology , medicine , quantum mechanics , audiology
The spatial extent of the cochlear region that actually contributes to the DPOAE signal measured in the ear canal may be evaluated experimentally using interference tones or computed numerically using nonlinear cochlear models. A nonlinear transmission-line cochlear model is used in this study to evaluate whether the recently reported nonlinear behavior of the reticular lamina (RL) over a wide basal region may be associated with generation of a significant distortion product otoacoustic emission (DPOAE) component. A two-degrees-of-freedom 1-D nonlinear model was used as discussed by Sisto et al. (2019), in which each local element consists of two coupled oscillators, roughly representing the basilar membrane (BM) and the RL. In this model, the RL shows a strongly nonlinear response over a wide region basal to the characteristic place, whereas the BM response is linear outside the narrow peak region. Such a model may be considered as that using the minimal number of degrees of freedom necessary to separately predict the motion of the BM and RL, while preserving important cochlear symmetries, such as the zero-crossing invariance of the impulse response. In the numerical simulations, the RL nonlinearity generates indeed a large intracochlear distortion product source, extended down to very basal cochlear regions. Nevertheless, due to the weak and indirect coupling between the RL motion and the differential fluid pressure in the basal part of the traveling wave path, no significant contribution from this mechanism is predicted by the model to the generation of the DPOAE signal that is eventually measured in the ear canal.

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