Brai(2)n, TRI & Department of Neurosurgery, University Hospital Antwerp, Belgium.
Hear Res. 2013 Feb;296:141-8. doi: 10.1016/j.heares.2012.10.003. Epub 2012 Oct 23.
Animal research has shown that loss of normal acoustic stimulation can increase spontaneous firing in the central auditory system and induce cortical map plasticity. Enriched acoustic environment after noise trauma prevents map plasticity and abolishes neural signs of tinnitus. In humans, the tinnitus spectrum overlaps with the area of hearing loss. Based on these findings it can be hypothesized that stimulating the auditory system by presenting music compensating specifically for the hearing loss might also suppress chronic tinnitus. To verify this hypothesis, a study was conducted in three groups of tinnitus patients. One group listened just to unmodified music (i.e. active control group), one group listened to music spectrally tailored to compensate for their hearing loss, and a third group received music tailored to overcompensate for their hearing loss, associated with one (in presbycusis) or two notches (in audiometric dip) at the edge of hearing loss. Our data indicate that applying overcompensation to the hearing loss worsens the patients' tinnitus loudness, the tinnitus annoyance and their depressive feelings. No significant effects were obtained for the control group or for the compensation group. These clinical findings were associated with an increase in current density within the left dorsal anterior cingulate cortex in the alpha2 frequency band and within the left pregenual anterior cingulate cortex in beta1 and beta2 frequency band. In addition, a region of interest analysis also demonstrated an associated increase in gamma band activity in the auditory cortex after overcompensation in comparison to baseline measurements. This was, however, not the case for the control or the compensation groups. In conclusion, music therapy compensating for hearing loss is not beneficial in suppressing tinnitus, and overcompensating hearing loss actually worsens tinnitus, both clinically and electrophysiologically.
动物研究表明，正常声刺激的丧失会增加中枢听觉系统的自发放电，并诱导皮质图的可塑性。噪声损伤后的丰富声环境可防止图谱可塑性，并消除耳鸣的神经迹象。在人类中，耳鸣频谱与听力损失区域重叠。基于这些发现，可以假设通过呈现专门补偿听力损失的音乐来刺激听觉系统也可能抑制慢性耳鸣。为了验证这一假设，对三组耳鸣患者进行了研究。一组仅听未经修改的音乐（即主动对照组），一组听频谱上专门补偿听力损失的音乐，第三组听补偿听力损失的音乐，与听力损失边缘的一个（在老年性聋中）或两个凹口（在听力下降时）相关联。我们的数据表明，对听力损失进行过度补偿会使患者的耳鸣响度、耳鸣烦恼和抑郁感恶化。对照组或补偿组未获得显著效果。这些临床发现与左背侧前扣带回皮质在 alpha2 频带和左前扣带回皮质在 beta1 和 beta2 频带中的电流密度增加有关。此外，兴趣区域分析还表明，与基线测量相比，过度补偿后听觉皮层的伽马频带活动也会增加。然而，对照组或补偿组并非如此。总之，补偿听力损失的音乐疗法并不能抑制耳鸣，而且过度补偿听力损失实际上会使耳鸣在临床和电生理上都恶化。
