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延迟诱发耳声发射(DEOE)仅仅是耳蜗内主动机制的结果吗?

Are delayed evoked oto-acoustic emissions (DEOE) solely the outcome of an active intracochlear mechanism?

作者信息

Rossi G, Solero P, Rolando M, Olina M

机构信息

Institute of Audiology, University of Turin, Italy.

出版信息

Scand Audiol. 1989;18(2):99-104. doi: 10.3109/01050398909070729.

Abstract

Post-mumps and post-measles hearing losses are a result of the destruction of Corti's organ. Both the basilar and the Reissner membranes are unimpaired. In 11 subjects with post-mumps (8 cases) and post-measles (3 cases) unilateral anacusis, DEOE with a mean amplitude lower than that of the contralateral normal ear with the same sensation level were observed with 0.5, 1 and 2 kHz tone-bursts and air conduction stimulation. These findings lend credit to the view that DEOE could in part be produced by a passive intracochlear mechanism, probably a consequence of the basilar membrane travelling wave induced by the displacement of the perilymph. In a normal ear, this passive mechanism could be superimposed by an active mechanism linked to the contractile activity of the outer hair cells (OHC) which modulates and increases the travelling wave depth.

摘要

腮腺炎和麻疹后听力损失是柯蒂氏器遭到破坏的结果。基底膜和赖斯纳膜均未受损。在11例患有腮腺炎后(8例)和麻疹后(3例)单侧全聋的受试者中,通过0.5、1和2千赫短纯音及气导刺激观察到,畸变产物耳声发射(DEOE)的平均振幅低于具有相同感觉级的对侧正常耳。这些发现支持了这样一种观点,即DEOE可能部分由耳蜗内的被动机制产生,这可能是外淋巴移位引起基底膜行波的结果。在正常耳中,这种被动机制可能会被与外毛细胞(OHC)收缩活动相关的主动机制叠加,后者可调节并增加行波深度。

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