PubMed · 4846718
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P Allaire, S Raynor, M Billone. 1974. Cochlear partition stiffness--a composite beam model.. https://doi.org/10.1121/1.1914693
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The propagation of inhomogeneous, weakly nonlinear waves is considered in a cochlear model having two degrees of freedom that represent the transverse motions of the tectorial and basilar membranes within the organ of Corti. It is assumed that nonlinearity arises from the saturation of outer hair cell active force generation. I use multiple scale asymptotics and treat nonlinearity as a correction to a linear hydroelastic wave. The resulting theory is used to explain experimentally observed features of the response of the cochlear partition to a pure tone, including: the amplification of the response in a healthy cochlea vs a dead one; the less than linear growth rate of the response to increasing sound pressure level; and the amount of distortion to be expected at high and low frequencies at basal and apical locations, respectively. I also show that the outer hair cell nonlinearity generates retrograde waves.
The cochlea is organized tonotopically: each frequency between 20 Hz and 20 kHz has its own location on the basilar membrane. In addition the cochlea has a large dynamic range (sound intensity). Active movements of the outer hair cells of the sensory organ of Corti play a crucial part in determining hearing acuity and frequency selectivity. Long-known properties such as combination tones and more recent observations like spontaneous and evoked otoacoustic emissions (the cochlea as sound source) fit in the same concept of a cochlea acting as a non-linear fine-tuned amplifier. Most sensorineural losses in people with diminished hearing are caused by injury to the hair cells, e.g. by medicines. Damage of outer hair cells impairs the cochlear amplifier, leading to loss of sensitivity to soft sounds and loss of frequency selectivity. Damage to the inner hair cells has much the same effect as conductive hearing loss. Tinnitus is not caused by otoacoustic emissions, but probably by denervation hypersensitivity following loss of cochlear input.