Nofzinger Eric A, Buysse Daniel J, Germain Anne, Price Julie C, Miewald Jean M, Kupfer David J
Western Psychiatric Institute and Clinic, Sleep Neuroimaging Research Program, Department of Psychiatry, University of Pittsburgh School of Medicine, 3811 O'Hara St., Pittsburgh, PA 15213-2593, USA.
Am J Psychiatry. 2004 Nov;161(11):2126-8. doi: 10.1176/appi.ajp.161.11.2126.
The authors investigated the neurobiological basis of poor sleep and daytime fatigue in insomnia.
[(18)F]Fluorodeoxyglucose positron emission tomography was used to assess regional cerebral glucose metabolism of seven patients with insomnia and 20 healthy subjects.
Compared with healthy subjects, patients with insomnia showed greater global cerebral glucose metabolism during sleep and while awake, a smaller decline in relative metabolism from waking to sleep states in wake-promoting regions, and reduced relative metabolism in the prefrontal cortex while awake.
Subjectively disturbed sleep in patients with insomnia is associated with greater brain metabolism. The inability to fall asleep may be related to a failure of arousal mechanisms to decline in activity from waking to sleep states. Further, daytime fatigue may reflect decreased activity in the prefrontal cortex resulting from inefficient sleep.
作者研究了失眠患者睡眠不佳和日间疲劳的神经生物学基础。
采用[18F]氟脱氧葡萄糖正电子发射断层扫描技术评估7名失眠患者和20名健康受试者的局部脑葡萄糖代谢情况。
与健康受试者相比,失眠患者在睡眠和清醒时均表现出更高的全脑葡萄糖代谢,促醒区域从清醒到睡眠状态的相对代谢下降较小,且清醒时前额叶皮质的相对代谢降低。
失眠患者主观睡眠障碍与大脑代谢增加有关。无法入睡可能与唤醒机制在从清醒到睡眠状态时活动未能下降有关。此外,日间疲劳可能反映了因睡眠效率低下导致的前额叶皮质活动减少。