The search for noise-induced cochlear synaptopathy in humans: Mission impossible?
The search for noise-induced cochlear synaptopathy in humans: Mission impossible?
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DOI：
10.1016/j.heares.2019.02.016
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发表时间：
2019-06-01
期刊：
影响因子：
2.8
通讯作者：
Canlon, Barbara
中科院分区：
文献类型：
--
作者：
Bramhall, Naomi;Beach, Elizabeth Francis;Canlon, Barbara
动物研究表明，即使外毛细胞完好无损且没有临床相关的永久性阈值移位，噪声暴露也会永久性地损害内毛细胞和听神经纤维之间的突触。突触病破坏耳蜗和中枢听觉系统之间的传入连接，预计会损害嘈杂环境中的言语理解，并可能导致耳鸣和/或听觉亢进。虽然耳蜗突触病已经在许多实验动物模型中得到证实，但突触病只能通过死后颞骨分析来证实，因此很难在活人身上进行研究。各种非侵入性的方法已经被用来确定噪音诱导的突触病变是否发生在人类身上，但结果是相互矛盾的。本文的总体目标是综合现有的关于噪声诱发的突触病在人类听觉系统中的功能影响的数据。文章的第一部分总结了为支持和反对人类噪声诱发的突触病变提供证据的研究。第二部分提供了不同研究结果的潜在解释。最后一节概述了诊断人类突触病变的建议方法，目的是提高研究的一致性。(C) 2019 Elsevier B.V.版权所有
Animal studies demonstrate that noise exposure can permanently damage the synapses between inner hair cells and auditory nerve fibers, even when outer hair cells are intact and there is no clinically relevant permanent threshold shift. Synaptopathy disrupts the afferent connection between the cochlea and the central auditory system and is predicted to impair speech understanding in noisy environments and potentially result in tinnitus and/or hyperacusis. While cochlear synaptopathy has been demonstrated in numerous experimental animal models, synaptopathy can only be confirmed through post-mortem temporal bone analysis, making it difficult to study in living humans. A variety of non-invasive measures have been used to determine whether noise-induced synaptopathy occurs in humans, but the results are conflicting. The overall objective of this article is to synthesize the existing data on the functional impact of noise-induced synaptopathy in the human auditory system. The first section of the article summarizes the studies that provide evidence for and against noise-induced synaptopathy in humans. The second section offers potential explanations for the differing results between studies. The final section outlines suggested methodologies for diagnosing synaptopathy in humans with the aim of improving consistency across studies. (C) 2019 Elsevier B.V. All rights reserved.