Neu Daniel, Mairesse Olivier, Verbanck Paul, Le Bon Olivier
Brugmann University Hospital, Sleep Laboratory & Unit for Chronobiology U78, Université Libre de Bruxelles (U.L.B.), Brussels, Belgium; UNI, ULB Neurosciences Institute, Faculty of Medicine, Laboratory for Medical Psychology ULB312, Université Libre de Bruxelles (U.L.B.), Brussels, Belgium.
Brugmann University Hospital, Sleep Laboratory & Unit for Chronobiology U78, Université Libre de Bruxelles (U.L.B.), Brussels, Belgium; UNI, ULB Neurosciences Institute, Faculty of Medicine, Laboratory for Medical Psychology ULB312, Université Libre de Bruxelles (U.L.B.), Brussels, Belgium; Department of Experimental and Applied Psychology (EXTO), Vrije Universiteit Brussel (V.U.B.), Brussels, Belgium; Royal Military Academy, Department LIFE, Brussels, Belgium.
Clin Neurophysiol. 2015 Oct;126(10):1926-33. doi: 10.1016/j.clinph.2014.12.016. Epub 2015 Jan 10.
To investigate slow wave sleep (SWS) spectral power proportions in distinct clinical conditions sharing non-restorative sleep and fatigue complaints without excessive daytime sleepiness (EDS), namely the chronic fatigue syndrome (CFS) and primary insomnia (PI). Impaired sleep homeostasis has been suspected in both CFS and PI.
We compared perceived sleep quality, fatigue and sleepiness symptom-intensities, polysomnography (PSG) and SWS spectral power distributions of drug-free CFS and PI patients without comorbid sleep or mental disorders, with a good sleeper control group.
Higher fatigue without EDS and impaired perceived sleep quality were confirmed in both patient groups. PSG mainly differed in sleep fragmentation and SWS durations. Spectral analysis revealed a similar decrease in central ultra slow power (0.3-0.79Hz) proportion during SWS for both CFS and PI and an increase in frontal power proportions of faster frequencies during SWS in PI only. The latter was correlated to affective symptoms whereas lower central ultra slow power proportions were related to fatigue severity and sleep quality impairment.
In combination with normal (PI) or even increased SWS durations (CFS), we found consistent evidence for lower proportions of slow oscillations during SWS in PI and CFS.
Observing normal or increased SWS durations but lower proportions of ultra slow power, our findings suggest a possible quantitative compensation of altered homeostatic regulation.
研究在非恢复性睡眠和疲劳主诉但无过度日间嗜睡（EDS）的不同临床情况下，即慢性疲劳综合征（CFS）和原发性失眠（PI）中的慢波睡眠（SWS）频谱功率比例。CFS和PI均被怀疑存在睡眠稳态受损。
我们比较了无合并睡眠或精神障碍的无药物治疗的CFS和PI患者与良好睡眠者对照组的主观睡眠质量、疲劳和嗜睡症状强度、多导睡眠图（PSG）以及SWS频谱功率分布。
两个患者组均证实存在无EDS的较高疲劳以及受损的主观睡眠质量。PSG主要在睡眠片段化和SWS时长方面存在差异。频谱分析显示，CFS和PI在SWS期间中央超慢波功率（0.3 - 0.79Hz）比例均有类似下降，且仅PI在SWS期间更快频率的额叶功率比例增加。后者与情感症状相关，而较低的中央超慢波功率比例与疲劳严重程度和睡眠质量受损有关。
结合正常（PI）甚至增加的SWS时长（CFS），我们发现了PI和CFS在SWS期间慢振荡比例较低的一致证据。
观察到SWS时长正常或增加但超慢波功率比例较低，我们的研究结果提示了内稳态调节改变可能存在的定量补偿。
