Manchester Centre for Audiology and Deafness, School of Health Sciences, University of Manchester, Manchester, M13 9PL, United Kingdom.
Manchester Centre for Audiology and Deafness, School of Health Sciences, University of Manchester, Manchester, M13 9PL, United Kingdom; Department of Psychology, Lancaster University, Lancaster, LA1 4YF, United Kingdom.
Neuroscience. 2019 May 21;407:192-199. doi: 10.1016/j.neuroscience.2019.03.017. Epub 2019 Mar 16.
The occurrence of tinnitus is associated with hearing loss and neuroplastic changes in the brain, but disentangling correlation and causation has remained difficult in both human and animal studies. Here we use earplugs to cause a period of monaural deprivation to induce a temporary, fully reversible tinnitus sensation, to test whether differences in subcortical changes in neural response gain, as reflected through changes in acoustic reflex thresholds (ARTs), could explain the occurrence of tinnitus. Forty-four subjects with normal hearing wore an earplug in one ear for either 4 (n = 27) or 7 days (n = 17). Thirty subjects reported tinnitus at the end of the deprivation period. ARTs were measured before the earplug period and immediately after taking the earplug out. At the end of the earplug period, ARTs in the plugged ear were decreased by 5.9 ± 1.1 dB in the tinnitus-positive group, and by 6.3 ± 1.1 dB in the tinnitus-negative group. In the control ear, ARTs were increased by 1.3 ± 0.8 dB in the tinnitus-positive group, and by 1.6 ± 2.0 dB in the tinnitus-negative group. There were no significant differences between the groups with 4 and 7 days of auditory deprivation. Our results suggest that either the subcortical neurophysiological changes underlying the ART reductions might not be related to the occurrence of tinnitus, or that they might be a necessary component of the generation of tinnitus, but with additional changes at a higher level of auditory processing required to give rise to tinnitus. This article is part of a Special Issue entitled: Hearing Loss, Tinnitus, Hyperacusis, Central Gain.
耳鸣的发生与听力损失和大脑的神经可塑性变化有关,但在人类和动物研究中,要理清相关性和因果关系一直很困难。在这里,我们使用耳塞来引起单侧听觉剥夺,以诱导暂时的、完全可逆的耳鸣感觉,来测试亚皮质神经反应增益变化(通过听反射阈值的变化反映)是否可以解释耳鸣的发生。44 名听力正常的受试者在一只耳朵中佩戴耳塞,时间分别为 4 天(n=27)或 7 天(n=17)。在剥夺期结束时,30 名受试者报告出现耳鸣。在耳塞期之前和取出耳塞后立即测量听反射阈值。在耳塞期结束时,在有耳鸣的阳性组中,耳塞耳的听反射阈值下降了 5.9±1.1dB,在无耳鸣的阴性组中下降了 6.3±1.1dB。在对照耳中,在有耳鸣的阳性组中听反射阈值增加了 1.3±0.8dB,在无耳鸣的阴性组中增加了 1.6±2.0dB。在听觉剥夺 4 天和 7 天的组之间没有显著差异。我们的结果表明,ART 降低所涉及的亚皮质神经生理变化可能与耳鸣的发生无关,或者它们可能是耳鸣产生的必要组成部分,但需要在更高水平的听觉处理中发生额外的变化才能引起耳鸣。本文是一个特刊的一部分,主题为:听力损失、耳鸣、听觉过敏、中枢增益。