Bao Xiaoyu, Feng Xueji, Huang Haiyun, Li Man, Chen Di, Wang Zijian, Li Jiahong, Huang Qiyun, Cai Yuexin, Li Yuanqing
School of Automation Science and Engineering, South China University of Technology, Guangzhou, 510641, China; Research Center for Brain Machine Intelligence, Pazhou Lab, Guangzhou, 510005, China.
School of Artificial Intelligence, South China Normal University, Foshan, 528225, China; Research Center for Brain Machine Intelligence, Pazhou Lab, Guangzhou, 510005, China.
Sleep Med. 2025 Jul;131:106519. doi: 10.1016/j.sleep.2025.106519. Epub 2025 Apr 15.
Tinnitus, which affects 12-30 % of the population, is associated with sleep disturbances and daytime dysfunction, yet the neural mechanisms that link wake-up states remain unclear. This study investigated electroencephalographic (EEG) characteristics of 51 tinnitus patients and 51 controls across wakefulness (eyes-open, eyes-closed, mental arithmetic) and sleep stages (N1, N2, N3, REM) to clarify day-night pathological mechanisms. The key findings showed persistent hyperarousal in tinnitus: wakefulness revealed enhanced gamma power (30-45 Hz) in eyes-closed and task states, while sleep demonstrated elevated gamma/beta power across all stages accompanied by reduced delta/theta power in deep sleep (N2/N3).). An analysis of sleep structure indicates impaired stability in maintaining the N2 stage among tinnitus patients, corroborating a reduction in N3 duration and an increased proportion of the N2 stage. From the wake states to the sleep stages, group × state interactions for the delta/theta power suggest an impaired state regulation capacity in tinnitus patients. Correlation clustering further revealed aberrant integration of wake-related gamma/beta activity into non-rapid eye movement sleep, indicating neuroplastic overgeneralization of wake hyperarousal into sleep. These results extend the so-called loss-of-inhibition theory to sleep, proposing that deficient low-frequency oscillations fail to suppress hyperarousal, impairing sleep-dependent neuroplasticity, and perpetuating daytime symptoms. Furthermore, this study establishes sleep as a critical therapeutic target to interrupt the 24-h dysfunctional cycle of tinnitus.
耳鸣影响着12%至30%的人群，与睡眠障碍和日间功能障碍相关，但连接清醒状态的神经机制仍不清楚。本研究调查了51名耳鸣患者和51名对照者在清醒（睁眼、闭眼、心算）和睡眠阶段（N1、N2、N3、快速眼动）的脑电图（EEG）特征，以阐明昼夜病理机制。关键发现显示耳鸣患者存在持续的高觉醒状态：在清醒状态下，闭眼和任务状态时γ功率（30 - 45赫兹）增强，而在睡眠中，所有阶段的γ/β功率均升高，同时深度睡眠（N2/N3）时的δ/θ功率降低。睡眠结构分析表明耳鸣患者在维持N2阶段的稳定性受损，证实了N3持续时间缩短和N2阶段比例增加。从清醒状态到睡眠阶段，δ/θ功率的组×状态交互作用表明耳鸣患者的状态调节能力受损。相关性聚类进一步揭示了与清醒相关的γ/β活动异常整合到非快速眼动睡眠中，表明清醒时的高觉醒状态过度泛化到睡眠中。这些结果将所谓的抑制缺失理论扩展到睡眠领域，提出低频振荡不足无法抑制高觉醒状态，损害了依赖睡眠的神经可塑性，并使日间症状持续存在。此外，本研究将睡眠确立为中断耳鸣24小时功能障碍周期的关键治疗靶点。
