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与睡眠良好者相比,延迟睡眠期障碍者的内源性昼夜温度周期长度(tau)。

The endogenous circadian temperature period length (tau) in delayed sleep phase disorder compared to good sleepers.

机构信息

Flinders University of South Australia, Adelaide, SA, Australia.

出版信息

J Sleep Res. 2013 Dec;22(6):617-24. doi: 10.1111/jsr.12072. Epub 2013 Jul 31.

DOI:10.1111/jsr.12072
PMID:23899423
Abstract

The currently assumed aetiology for delayed sleep phase disorder (DSPD) is a delay of the circadian system. Clinicians have sought to use bright light therapy, exogenous melatonin or chronotherapy to correct the disorder. However, these treatments have achieved unreliable outcomes for DSPD patients and, as such, one suggestion has been that the disorder may be caused by a longer than normal circadian rhythm period length (i.e. tau). The present study investigated this premise using a 78-h ultradian, ultra-short sleep-wake cycle. This constant bedrest routine was used to simulate a series of 1-h long 'days' by alternating 20-min sleep opportunities and 40 min of enforced wakefulness. Thirteen participants were recruited for the study including, six people diagnosed with DSPD according to the International Classification of Sleep Disorders-2 [mean age = 22.0, standard deviation (SD) = 3.3] and seven good sleepers (mean age = 23.1, SD = 3.9) with normal sleep timing. The DSPD participants' core temperature rhythm tau (mean = 24 h 54 min, SD = 23 min) was significantly longer (t = -2.33, P = 0.04, Cohen's d = 1.91) than the good sleepers' (mean 24 h 29 min, SD = 16 min). The temperature rhythm of the DSPD participants delayed more rapidly (i.e. >25 min day(-1) ) than the good sleepers'. These findings provide an explanation for the difficulty that DSPD patients have in phase advancing to a more conventional sleep time and their frequent relapse following treatment. The outcomes of this study support a vigorous and continued application of chronobiological and behavioural therapies to entrain DSPD patients to their desired earlier sleep times.

摘要

目前认为,睡眠时相延迟障碍(DSPD)的病因是昼夜节律系统的延迟。临床医生试图使用亮光疗法、外源性褪黑素或时间疗法来纠正这种障碍。然而,这些治疗方法对 DSPD 患者的疗效并不可靠,因此有人提出,这种障碍可能是由于昼夜节律周期长度(即 tau)长于正常。本研究使用了一个 78 小时的超短睡眠-觉醒周期来验证这一前提。这种固定卧床休息的常规作息用于模拟一系列 1 小时长的“白天”,通过交替 20 分钟的睡眠时间和 40 分钟的强制清醒。本研究招募了 13 名参与者,包括 6 名根据国际睡眠障碍分类-2 诊断为 DSPD 的人(平均年龄 22.0,标准差 3.3)和 7 名睡眠良好的人(平均年龄 23.1,标准差 3.9),他们的睡眠时间正常。DSPD 参与者的核心体温节律 tau(平均值 24 小时 54 分钟,标准差 23 分钟)明显长于睡眠良好者(平均值 24 小时 29 分钟,标准差 16 分钟)(t=-2.33,P=0.04,Cohen's d=1.91)。DSPD 参与者的体温节律延迟速度更快(即>25 分钟/天),而睡眠良好者的体温节律延迟速度较慢。这些发现为 DSPD 患者难以提前相位到更传统的睡眠时间以及治疗后经常复发提供了解释。本研究的结果支持大力和持续应用生物节律和行为疗法,使 DSPD 患者的睡眠时间提前到他们期望的时间。

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