Hogan Sarah E, Delgado Gisela M, Hall Martica H, Nimgaonkar Vishwajit L, Germain Anne, Buysse Daniel J, Wilckens Kristine A
University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
St. Luke's Warren Campus, Phillipsburg, New Jersey.
J Clin Sleep Med. 2020 Sep 15;16(9):1445-1454. doi: 10.5664/jcsm.8568.
High-frequency electroencephalographic activity (> 16 Hz activity) is often elevated during nonrapid eye movement sleep among individuals with insomnia, in line with the hyperarousal theory of insomnia. Evidence regarding sleep depth marked by slow-wave activity (< 4 Hz) is more mixed. Distinguishing subcomponents of slow-wave activity (slow-oscillation [< 1 Hz] or delta activity [1-4 Hz)]) may be critical in understanding these discrepancies, given that these oscillations have different neural generators and are functionally distinct. Here we tested the effects of insomnia diagnosis and insomnia treatment on nonrapid eye movement electroencephalography in older adults, distinguishing slow-oscillation and delta power.
In 93 older adults with insomnia and 71 good sleeper control participants (mean ages 68 years), effects of insomnia and cognitive behavioral therapy for insomnia (insomnia group only) on electroencephalographic spectral power were analyzed. Main effects and interactions with nonrapid eye movement period were assessed for the following frequency bands: slow-oscillation (0.5-1 Hz), delta (1-4 Hz), theta (4-8 Hz), alpha (8-12 Hz), sigma (12-16 Hz), and beta (16-32 Hz).
Slow-oscillation absolute and relative power were lower in the insomnia group compared with controls. There were no group differences in delta power. Insomnia was also associated with elevated 4-32 Hz absolute and relative power. After cognitive behavioral therapy for insomnia, absolute sigma and beta activity decreased.
Deficits in slow-wave activity in insomnia are specific to the slow-oscillation. Elevated high frequency activity is reduced for sigma and beta power following cognitive behavioral therapy for insomnia . These findings inform the pathophysiology of insomnia, including the mechanisms underlying cognitive behavioral therapy for insomnia in older adults.
根据失眠的高觉醒理论，失眠患者在非快速眼动睡眠期间高频脑电图活动（>16Hz活动）通常会升高。关于以慢波活动（<4Hz）为标志的睡眠深度的证据则更为复杂。鉴于这些振荡具有不同的神经发生器且功能不同，区分慢波活动的子成分（慢振荡[<1Hz]或δ活动[1-4Hz]）对于理解这些差异可能至关重要。在此，我们测试了失眠诊断和失眠治疗对老年人非快速眼动脑电图的影响，区分了慢振荡和δ功率。
在93名患有失眠的老年人和71名睡眠良好的对照参与者（平均年龄68岁）中，分析了失眠和失眠认知行为疗法（仅失眠组）对脑电图频谱功率的影响。评估了以下频段的主效应以及与非快速眼动期的相互作用：慢振荡（0.5-1Hz）、δ（1-4Hz）、θ（4-8Hz）、α（8-12Hz）、σ（12-16Hz）和β（16-32Hz）。
与对照组相比，失眠组的慢振荡绝对功率和相对功率较低。两组在δ功率上没有差异。失眠还与4-32Hz的绝对功率和相对功率升高有关。经过失眠认知行为疗法后，绝对σ和β活动降低。
失眠患者慢波活动的缺陷特定于慢振荡。失眠认知行为疗法后，高频活动升高的σ和β功率降低。这些发现为失眠的病理生理学提供了信息，包括老年人失眠认知行为疗法的潜在机制。
