Kay Daniel B, Karim Helmet T, Soehner Adriane M, Hasler Brant P, Wilckens Kristine A, James Jeffrey A, Aizenstein Howard J, Price Julie C, Rosario Bedda L, Kupfer David J, Germain Anne, Hall Martica H, Franzen Peter L, Nofzinger Eric A, Buysse Daniel J
Department of Psychiatry, Sleep and Chronobiology Center, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA.
Sleep. 2016 Oct 1;39(10):1779-1794. doi: 10.5665/sleep.6154.
The neurobiological mechanisms of insomnia may involve altered patterns of activation across sleep-wake states in brain regions associated with cognition, self-referential processes, affect, and sleep-wake promotion. The objective of this study was to compare relative regional cerebral metabolic rate for glucose (rCMR) in these brain regions across wake and nonrapid eye movement (NREM) sleep states in patients with primary insomnia (PI) and good sleeper controls (GS).
Participants included 44 PI and 40 GS matched for age (mean = 37 y old, range 21-60), sex, and race. We conducted [F]fluoro-2-deoxy-D-glucose positron emission tomography scans in PI and GS during both morning wakefulness and NREM sleep at night. Repeated measures analysis of variance was used to test for group (PI vs. GS) by state (wake vs. NREM sleep) interactions in relative rCMR.
Significant group-by-state interactions in relative rCMR were found in the precuneus/posterior cingulate cortex, left middle frontal gyrus, left inferior/superior parietal lobules, left lingual/fusiform/occipital gyri, and right lingual gyrus. All clusters were significant at P < 0.05.
Insomnia was characterized by regional alterations in relative glucose metabolism across NREM sleep and wakefulness. Significant group-by-state interactions in relative rCMR suggest that insomnia is associated with impaired disengagement of brain regions involved in cognition (left frontoparietal), self-referential processes (precuneus/posterior cingulate), and affect (left middle frontal, fusiform/lingual gyri) during NREM sleep, or alternatively, to impaired engagement of these regions during wakefulness.
失眠的神经生物学机制可能涉及与认知、自我参照过程、情感及睡眠-觉醒促进相关的脑区在睡眠-觉醒状态下激活模式的改变。本研究的目的是比较原发性失眠(PI)患者和良好睡眠者对照组(GS)在清醒和非快速眼动(NREM)睡眠状态下这些脑区的相对局部脑葡萄糖代谢率(rCMR)。
参与者包括44名PI患者和40名在年龄(平均37岁,范围21 - 60岁)、性别和种族上匹配的GS对照者。我们在早晨清醒和夜间NREM睡眠期间对PI患者和GS对照者进行了[F]氟代-2-脱氧-D-葡萄糖正电子发射断层扫描。采用重复测量方差分析来检验相对rCMR中状态(清醒与NREM睡眠)与组(PI与GS)之间的交互作用。
在前楔叶/后扣带回皮质、左侧额中回、左侧顶下小叶/顶上小叶、左侧舌回/梭状回/枕回以及右侧舌回中发现了相对rCMR的显著组×状态交互作用。所有聚类在P < 0.05时具有显著性。
失眠的特征是在NREM睡眠和清醒状态下相对葡萄糖代谢存在局部改变。相对rCMR的显著组×状态交互作用表明,失眠与NREM睡眠期间参与认知(左侧额顶叶)、自我参照过程(前楔叶/后扣带回)和情感(左侧额中回、梭状回/舌回)的脑区脱离受损有关,或者在清醒时这些区域的参与受损有关。