Department of Psychiatry, University of Wisconsin - Madison, Madison, WI.
Department of Psychology, University of Wisconsin - Madison, Madison, WI.
Sleep. 2019 Jun 11;42(6). doi: 10.1093/sleep/zsz060.
To clarify whether hypersomnolence disorder is associated with a specific sleep phenotype and altered neurophysiological function in persons with and without hypersomnolence disorder and major depressive disorder (MDD).
Eighty-three unmedicated persons with and without hypersomnolence disorder and/or MDD underwent ad libitum high-density EEG polysomnography. Clinical and sleep architecture variables were compared between groups. Topographic patterns of slow-wave activity (SWA) relative to healthy controls were compared, with correlations between topographic SWA and daytime sleepiness assessed. Reductions in SWA in hypersomnolence disorder were mapped to specific cortical areas using source localization.
Regardless of the presence or absence of comorbid MDD, persons with hypersomnolence disorder had increased sleep duration relative to both controls and persons with MDD without hypersomnolence. Participants with hypersomnolence disorder also demonstrated reduced bilateral centroparietal low-frequency activity during nonrapid eye movement sleep relative to controls, a pattern not observed in persons with MDD but without hypersomnolence. SWA in these regions was negatively correlated with subjective measures of daytime sleepiness. Source localization demonstrated reductions in SWA in the supramarginal gyrus, somatosensory, and transverse temporal cortex in participants with hypersomnolence disorder.
Hypersomnolence disorder is characterized by increased sleep duration with normal sleep continuity, regardless of the presence or absence of comorbid depression. Reduced local SWA may be a specific neurophysiological finding in hypersomnolence disorder. Further research is warranted to elucidate the mechanisms through which these cortical changes are related to clinical complaints of daytime sleepiness.
阐明过度嗜睡障碍是否与特定的睡眠表型相关,并改变过度嗜睡障碍和伴有或不伴有重性抑郁障碍(MDD)的个体的神经生理功能。
83 名未经药物治疗的伴有或不伴有过度嗜睡障碍和/或 MDD 的个体接受了随意的高密度 EEG 多导睡眠图检查。比较了组间的临床和睡眠结构变量。比较了相对于健康对照的慢波活动(SWA)的地形模式,并评估了地形 SWA 与日间嗜睡之间的相关性。使用源定位将过度嗜睡障碍中的 SWA 减少映射到特定的皮质区域。
无论是否存在共病 MDD,伴有过度嗜睡障碍的个体与对照组和不伴有过度嗜睡障碍的 MDD 个体相比,睡眠时间均延长。与对照组相比,伴有过度嗜睡障碍的个体在非快速眼动睡眠期间还表现出双侧中央顶叶低频活动减少,而在不伴有 MDD 的个体中则没有观察到这种模式。这些区域的 SWA 与日间嗜睡的主观测量呈负相关。源定位显示,过度嗜睡障碍患者的额上回、体感和横颞皮质的 SWA 减少。
过度嗜睡障碍的特征是无论是否存在共病抑郁,睡眠时间延长且睡眠连续性正常。局部 SWA 减少可能是过度嗜睡障碍的一种特定神经生理发现。需要进一步研究阐明这些皮质变化与日间嗜睡临床症状相关的机制。