Ever since Pliny the Elder coined the term tinnitus, the perception of sound in the absence of an external sound source has remained enigmatic. Traditional theories assume that tinnitus is triggered by cochlear damage, but many tinnitus patients present with a normal audiogram, i.e., with no direct signs of cochlear damage. Here, we report that in human subjects with tinnitus and a normal audiogram, auditory brainstem responses show a significantly reduced amplitude of the wave I potential (generated by primary auditory nerve fibers) but normal amplitudes of the more centrally generated wave V. This provides direct physiological evidence of "hidden hearing loss" that manifests as reduced neural output from the cochlea, and consequent renormalization of neuronal response magnitude within the brainstem. Employing an established computational model, we demonstrate how tinnitus could arise from a homeostatic response of neurons in the central auditory system to reduced auditory nerve input in the absence of elevated hearing thresholds.
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机译：自从老普林尼（Pliny the Elder）创造了“耳鸣”一词以来，在没有外部声源的情况下，对声音的感知一直是令人迷惑的。传统理论认为耳鸣是由耳蜗损伤引起的，但是许多耳鸣患者表现出正常的听力图，即没有耳蜗损伤的直接迹象。在这里，我们报告说，在具有耳鸣和正常听力图的人类受试者中，听觉脑干反应显示出I波（由初级听觉神经纤维产生）的振幅显着降低，但更集中产生的V波的振幅却正常。 “隐性听力损失”的生理学证据，表现为耳蜗神经输出减少，从而导致脑干内神经元反应幅度重新恢复正常。利用建立的计算模型，我们证明了在不提高听力阈值的情况下，中枢听觉系统中神经元对减少听觉神经输入的稳态反应如何引起耳鸣。
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