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PubMed · 2329095

Cochlear preprocessing in analog models, in digital models and in human inner ear.

E Zwicker·W Peisl
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Abstract

Data of spontaneous, delayed, and simultaneously evoked otoacoustic emissions produced in human subjects are compared with data produced in an analog and in a digital wave-parameter realization of our model. The high probability of the frequency distance of the emission's extreme values at 0.4 Bark, corresponding to a local distance of 0.5 mm along the basilar membrane is found also in the models. The influence of the lateral feedback coupling in the models on the frequency selectivity and on the appearance of emissions show the high quality of simulating human peripheral signal processing by the models.

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CochleaEar, InnerHumansMembrane PotentialsModels, NeurologicalReaction TimeJournal ArticleResearch Support, Non-U.S. Gov't

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BibTeXRIS

E Zwicker, W Peisl. 1990. Cochlear preprocessing in analog models, in digital models and in human inner ear.. https://doi.org/10.1016/0378-5955(90)90081-y

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A model of peripherally developing hearing loss and tinnitus based on the role of hypoxia and ischemia.

The incidence of sensorineural hearing loss often caused by direct damage to the cochlear hair cells is by far more frequent and more serious than disorders affecting the external ear or the middle ear. Mechanisms that are discussed to be relevant for the genesis of tinnitus and acquired hearing impairment are hair cell loss, signal transduction disturbances in the region of the outer and inner hair cells and the spiral ganglion, impairment of cochlear blood flow, mechanical disturbance, and hypoxia and ischemia. The present model surveys the possible cellular and molecular biological causes of peripherally developing hearing loss and tinnitus. In particular, the paper discusses the roles of hypoxia and ischemia in the cochlea and in the etiology of the neurosensory types of tinnitus. Peripheral origins of hearing disturbances and tinnitus may be: (a) damage to the stereocilia and the tip links, (b) dysfunction of potassium channels or (c) modification of the glutamate release. Moreover, the hypoxia inducible factor-1 may have an important role to play as a key transcription factor in the cells' adaptation to hypoxia and ischemia. An impairment of the cochlear blood flow may be induced by the expression of target genes like nitrogen monoxide synthase and endothelin-1 resulting in tinnitus. The paper discusses consequences resulting from the present model for the medical treatment of peripherally developing tinnitus and hearing loss.

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