Rossi G, Solero P, Rolando M, Olina M
Institute of Audiology, University of Turin, Italy.
ORL J Otorhinolaryngol Relat Spec. 1991;53(1):15-8. doi: 10.1159/000276177.
The recovery time of temporary threshold shift after 1-kHz tone bursts delayed evoked otoacoustic emissions (DEOE) after the same stimulus were studied after auditory fatigue (AF) with a pure tone (0.75 kHz, 10 min, 95 dB HL) in 20 normal-hearing subjects aged 19-23 years. Close similarities were observed in the two experimental conditions. Since DEOE are transmitted to the outer ear via structures independent of the fibers of the afferent acoustic pathway and their synapses, it may be supposed that changes in the motile activity of the outer hair cells caused by AF could be partly responsible for their production and could constitute an active intracochlear mechanism taking part in this phenomenon. It may also be supposed that the effects of this active mechanism could be superimposed on those produced by a passive intracochlear mechanism consisting of the traveling wave induced in the basilar membrane by the perilymph owing to the movements of the stapes.
对20名年龄在19 - 23岁的听力正常受试者施加纯音(0.75kHz,10分钟,95dB HL)造成听觉疲劳(AF)后,研究了1kHz短音诱发的瞬态阈移恢复时间以及相同刺激后的延迟诱发耳声发射(DEOE)。在两种实验条件下观察到了密切的相似性。由于DEOE是通过独立于传入听觉通路纤维及其突触的结构传输到外耳的,因此可以推测,AF引起的外毛细胞运动活性变化可能部分导致了它们的产生,并且可能构成参与这一现象的一种活跃的耳蜗内机制。还可以推测,这种活跃机制的作用可能叠加在由镫骨运动引起的外淋巴在基底膜上诱发的行波所构成的被动耳蜗内机制的作用之上。