ENT Department and German Center for Vertigo and Balance Disorders (IFB), University Hospital Munich, Marchioninistr.15, 81377, Munich, Germany,
J Assoc Res Otolaryngol. 2014 Feb;15(1):57-72. doi: 10.1007/s10162-013-0424-x. Epub 2013 Nov 20.
Loud low-frequency sounds can induce temporary oscillatory changes in cochlear sensitivity, which have been termed the 'bounce' phenomenon. The origin of these sensitivity changes has been attributed to slow fluctuations in cochlear homeostasis, causing changes in the operating points of the outer hair cell mechano-electrical and electro-mechanical transducers. Here, we acquired three objective and subjective measures resulting in a comprehensive dataset of the bounce phenomenon in each of 22 normal-hearing human subjects. We analysed the level and phase of cubic and quadratic distortion product otoacoustic emissions and the auditory thresholds before and after presentation of a low-frequency stimulus (30 Hz sine wave, 120 dB SPL, 90 s) as a function of time. In addition, the perceived loudness of temporary, tinnitus-like sensations occurring in all subjects after cessation of the low-frequency stimulus was tracked over time. The majority of the subjects (70 %) showed a significant, biphasic change of quadratic, but not cubic, distortion product otoacoustic emissions of about 3-4 dB. Eighty-six percent of the tested subjects showed significant alterations of hearing thresholds after low-frequency stimulation. Four different types of threshold changes were observed, namely monophasic desensitisations (the majority of cases), monophasic sensitisations, biphasic alterations with initial sensitisation and biphasic alterations with initial desensitisation. The similar duration of the three bounce phenomenon measures indicates a common origin. The current findings are consistent with the hypothesis that slow oscillations of homeostatic control mechanisms and associated operating point shifts within the cochlea are the source of the bounce phenomenon.
大强度低频声音可以引起耳蜗敏感性的暂时振荡变化，这种现象被称为“弹回”现象。这些敏感性变化的起源归因于耳蜗内稳态的缓慢波动，导致外毛细胞机械电和机电换能器的工作点发生变化。在这里，我们获得了三个客观和主观的测量结果，为 22 名正常听力人类受试者的弹回现象综合数据集。我们分析了三次和二次失真产物耳声发射的幅度和相位，以及低频刺激（30 Hz 正弦波，120 dB SPL，90 s）前后的听觉阈值，作为时间的函数。此外，我们还跟踪了所有受试者在低频刺激停止后暂时出现的耳鸣样感觉的感知响度随时间的变化。大多数受试者（70%）表现出二次失真产物耳声发射的显著双相变化，幅度约为 3-4 dB，但三次失真产物耳声发射没有变化。86%的受测受试者在低频刺激后听力阈值发生显著变化。观察到四种不同类型的阈值变化，即单相脱敏（大多数情况）、单相致敏、初始致敏的双相变化和初始脱敏的双相变化。三种弹回现象测量结果的相似持续时间表明它们具有共同的起源。目前的发现与假设一致，即稳态控制机制的缓慢振荡和耳蜗内相关工作点的变化是弹回现象的来源。
