Search PubMed⌕ Search

PubMed · 7391356

An improved WKB calculation for a two-dimensional cochlear model.

Abstract

The finite difference calculations of Neely [E.D. thesis, California Institute of Technology, Pasadena, CA (1977)] and the WKB solution of Steele and Taber [J. Acoust. Soc. Am. 65, 1001-1006 (1979)] generally agree, except in the "phase plateau" region, where both are irregular. In the present work, an improvement in the accuracy of the WKB procedure is gained by using a closed-form integral which gives the phase and damping functions in the short wavelength region. The present results agree qualitatively with the preceding but show a smooth variation with frequency and distance along the cochlea.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

C R Steele, C E Miller. 1980. An improved WKB calculation for a two-dimensional cochlear model.. https://doi.org/10.1121/1.384640

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

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.

Cochlea↗