Literature DB >> 9093668

Analysis of middle ear mechanics and application to diseased and reconstructed ears.

S N Merchant1, M E Ravicz, S Puria, S E Voss, K R Whittemore, W T Peake, J J Rosowski.   

Abstract

OBJECTIVE: To review current concepts of the mechanical processes of the human middle ear, and to apply them to practical issues in clinical otology and tympanoplasty surgery.
BACKGROUND: The wide range of conductive hearing losses associated with middle ear pathology and reconstruction cannot be adequately explained by simple models of middle ear function.
METHODS: Variables used to describe the system are sound pressure, volume velocity, and acoustic impedance. The relationship between specific middle ear structures and these variables is described such that inferences can be drawn regarding sound conduction in the normal, diseased, and reconstructed middle ear. RESULTS AND
CONCLUSIONS: Sound can be transmitted from the car canal to the cochlea via two mechanisms: the tympano-ossicular system (ossicular coupling) and direct acoustic stimulation of the oval and round windows (acoustic coupling). Acoustic coupling is negligibly small in normal ears, but can play a significant role in some diseased and reconstructed ears. In the normal ear, middle ear pressure gain (which is the result of ossicular coupling) is frequency-dependent and less than generally believed. The severity of conductive hearing loss due to middle-ear disease or after tympanoplasty surgery can be predicted by the degree to which ossicular coupling, acoustic coupling, and stapescochlear input impedance are altered. Hearing after type IV and V tympanoplasty is determined solely by acoustic coupling. The difference in magnitude between the oval- and round-window pressures is more important than the difference in phase in determining cochlear input. In tympanoplasty types I, II, and III, adequate middle-ear and round-window aeration is necessary and the tympanic membrane-ossicular configuration may be less crucial.

Entities:  

Mesh:

Year:  1997        PMID: 9093668

Source DB:  PubMed          Journal:  Am J Otol        ISSN: 0192-9763


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