Abstract

The following hypothesis is presented: A dysfunction of the hair cell cilia, either in the form of ciliary pathology or as a temporary loss of ciliary stiffness, both of which are documented, ought to lead to a partial decoupling of the involved hair cells from the tectorial membrane. Consequently, 1) energy transmission should be attenuated (= hearing loss), 2) the noise level at the hair cell input should be increased (= tinnitus) and, owing to the concomitant center-clipping of the signal waveform, 3) the input/output function should become steeper (= recruitment) and 4) the formant structure of speech should be largely destroyed (= relatively poor speech discrimination). The above signs and symptoms are characteristic of a number of acute cochlear disorders and would thus find a common explanation.

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