University of Tübingen, Department of Otolaryngology, Head and Neck Surgery, Tübingen Hearing Research Centre (THRC), Molecular Physiology of Hearing, Tübingen, Germany.
Prog Neurobiol. 2013 Dec;111:17-33. doi: 10.1016/j.pneurobio.2013.08.002. Epub 2013 Sep 6.
The prevalence of hearing problems in the Western world has, due to aging of the population, doubled over the past 30 years. Thereby, noise-induced hearing loss is an important factor that worsens over time in addition to age-related hearing loss. Hearing loss is usually measured as an elevation of a person's hearing thresholds, expressed in decibel (dB). However, recent animal studies have unraveled a type of permanent cochlear damage, without an elevation of hearing thresholds. This subtle damage is linked to a permanent and progressive degeneration of auditory fibers that occurs in association with damage of the inner hair cell synapse. Afferent neuronal degeneration has been suggested to be involved in hyperacusis (over sensitivity to sound) and tinnitus (a phantom sound percept). Hyperacusis and tinnitus are potentially devastating conditions that are still incurable. The main risk factors to develop tinnitus or hyperacusis are hearing loss, social stress and age. Both tinnitus and hyperacusis have been discussed in the context of a pathological increased response gain in subcortical brain regions as a reaction to deprivation of sensory input. Novel studies confirm the involvement of peripheral deafferentation for tinnitus and hyperacusis, but suggest that the disorder results from different brain responses to different degrees of deafferentation: while tinnitus may arise as a failure of the brain to adapt to deprived peripheral input, hyperacusis may result from an 'over-adaptive' increase in response gain. Moreover, moderate and high stress levels at the time of acoustic trauma have been suggested to play a pivotal role in the vulnerability of the cochlea to acoustic damage and therefore for the development of tinnitus and hyperacusis.
在过去的 30 年中，由于人口老龄化，西方世界听力问题的患病率增加了一倍。因此，除了与年龄相关的听力损失外，噪声引起的听力损失也是一个随时间恶化的重要因素。听力损失通常被测量为一个人听力阈值的升高，以分贝（dB）表示。然而，最近的动物研究揭示了一种没有听力阈值升高的永久性耳蜗损伤类型。这种微妙的损伤与听觉纤维的永久性和进行性退化有关，这种退化与内毛细胞突触的损伤有关。有人认为传入神经元退化与听觉过敏（对声音过度敏感）和耳鸣（一种幻听）有关。听觉过敏和耳鸣是潜在的破坏性疾病，目前仍无法治愈。发生耳鸣或听觉过敏的主要危险因素是听力损失、社会压力和年龄。耳鸣和听觉过敏都被认为是由于感觉输入剥夺引起的皮层下脑区病理性反应增益增加的结果。新的研究证实了外周去传入对耳鸣和听觉过敏的参与，但表明该疾病是由不同程度的去传入对大脑的不同反应引起的：虽然耳鸣可能是大脑无法适应剥夺外周输入的结果，但听觉过敏可能是由于反应增益的过度适应增加所致。此外，在声学创伤时的中度和高度应激水平被认为在耳蜗对声学损伤的易感性中起着关键作用，因此也是耳鸣和听觉过敏发展的关键因素。
