Eaton-Peabody Laboratories, Massachusetts Eye and Ear, Boston, Massachusetts.
Department of Information Technology, Ghent University, Ghent, Belgium.
J Neurophysiol. 2021 Apr 1;125(4):1213-1222. doi: 10.1152/jn.00620.2020. Epub 2021 Mar 3.
Permanent threshold elevation after noise exposure or aging is caused by loss of sensory cells; however, animal studies show that hair cell loss is often preceded by degeneration of the synapses between sensory cells and auditory nerve fibers. Silencing these neurons is likely to degrade auditory processing and may contribute to difficulties understanding speech in noisy backgrounds. Reduction of suprathreshold ABR amplitudes can be used to quantify synaptopathy in inbred mice. However, ABR amplitudes are highly variable in humans, and thus more challenging to use. Since noise-induced neuropathy preferentially targets fibers with high thresholds and low spontaneous rate and because phase locking to temporal envelopes is particularly strong in these fibers, measuring envelope following responses (EFRs) might be a more robust measure of cochlear synaptopathy. A recent auditory model further suggests that modulation of carrier tones with rectangular envelopes should be less sensitive to cochlear amplifier dysfunction and, therefore, a better metric of cochlear neural damage than sinusoidal amplitude modulation. In this study, we measure performance scores on a variety of difficult word-recognition tasks among listeners with normal audiograms and assess correlations with EFR magnitudes to rectangular versus sinusoidal modulation. Higher harmonics of EFR magnitudes evoked by a rectangular-envelope stimulus were significantly correlated with word scores, whereas those evoked by sinusoidally modulated tones did not. These results support previous reports that individual differences in synaptopathy may be a source of speech recognition variability despite the presence of normal thresholds at standard audiometric frequencies. Recent studies suggest that millions of people may be at risk of permanent impairment from cochlear synaptopathy, the age-related and noise-induced degeneration of neural connections in the inner ear. This study examines electrophysiological responses to stimuli designed to improve detection of neural damage in subjects with normal hearing sensitivity. The resultant correlations with word recognition performance are consistent with a contribution of cochlear neural damage to deficits in hearing in noise abilities.
暴露于噪声或衰老后的永久性阈移是由感觉细胞的损失引起的；然而，动物研究表明，毛细胞的损失通常发生在感觉细胞和听神经纤维之间的突触退化之前。使这些神经元沉默可能会降低听觉处理能力，并可能导致在嘈杂背景下理解言语的困难。降低阈上 ABR 幅度可用于量化近交系小鼠的突触病。然而，ABR 幅度在人类中高度可变，因此更具挑战性。由于噪声诱导的神经病优先靶向具有高阈值、低自发率的纤维，并且这些纤维对时间包络的相位锁定特别强，因此测量包络跟随反应（EFR）可能是耳蜗突触病的更可靠测量方法。最近的听觉模型进一步表明，用矩形包络调制载波音应该对耳蜗放大器功能障碍不太敏感，因此比正弦幅度调制更能衡量耳蜗神经损伤。在这项研究中，我们在具有正常听力图的听众中测量了各种困难的单词识别任务的表现得分，并评估了与 EFR 幅度对矩形与正弦调制的相关性。由矩形包络刺激引起的 EFR 幅度的高次谐波与单词得分显著相关，而由正弦调制音引起的 EFR 幅度则没有。这些结果支持先前的报告，即尽管在标准听力频率下存在正常阈值，但突触病的个体差异可能是言语识别变异性的一个来源。最近的研究表明，数以百万计的人可能面临耳蜗突触病（内耳神经连接的年龄相关性和噪声诱导性退化）永久性损害的风险。本研究检查了对旨在提高正常听力敏感度受试者中神经损伤检测的刺激的电生理反应。与单词识别性能的相关性与耳蜗神经损伤对噪声能力听力下降的贡献一致。
