College of Education, Psychology, and Social Work.
J Consult Clin Psychol. 2019 Jan;87(1):16-32. doi: 10.1037/ccp0000357. Epub 2018 Nov 15.
To systematically investigate whether cognitive "insomnia" processes are implicated in adolescent Delayed Sleep-Wake Phase Disorder (DSWPD) and to examine whether these processes are responsive to chronobiological treatment.
Sixty-three adolescents (M = 15.8 ± 2.2 years, 63.5% f) diagnosed with DSWPD and 40 good sleeping adolescents (M = 15.9 ± 2.4 years, 75% f) completed baseline measures of sleep, daytime functioning and cognitive "insomnia" processes (i.e., repetitive negative thinking, physiological hyperarousal, distress, sleep-related attention and monitoring, sleep misperception). Sixty DSWPD adolescents (M = 15.9 ± 2.2 y, 63% f) entered a treatment trial and received 3 weeks of light therapy. Sleep, daytime functioning, and insomnia were measured again post-treatment and at 3-month follow-up.
Adolescents with DSWPD had significantly later sleep timing (d = 0.99-1.50), longer sleep latency (d = 1.14), and shorter total sleep time (d = 0.85) on school nights, compared with the good sleeping adolescents. There was evidence of cognitive "insomnia" symptoms, with the DSWPD group reporting more repetitive negative thinking (d = 0.70-1.02), trait hyperarousal (d = 0.55), distress (d = 2.19), sleep associated monitoring (d = 0.76), and sleep onset misperception (d = 1.29). Across treatment and follow-up, adolescents with DSWPD reported advanced sleep timing (d = 0.54-0.62), reduced sleep latency (d = 0.53), increased total sleep time (d = 0.49), and improved daytime functioning (d = 0.46-1.00). Repetitive negative thinking (d = 0.64-0.96), physiological arousal (d = 0.69), distress (d = 0.87), and sleep onset misperception (d = 0.37) also showed improvement.
Cognitive "insomnia" processes may be implicated in the development and maintenance of DSWPD in adolescents. Many of these processes are amendable to chronobiological treatment; however, residual symptoms may place adolescents at risk of poor treatment outcome or relapse. (PsycINFO Database Record (c) 2018 APA, all rights reserved).
系统地调查认知“失眠”过程是否与青少年延迟睡眠-觉醒时相延迟障碍(DSWPD)有关,并研究这些过程是否对生物节律治疗有反应。
63 名被诊断为 DSWPD 的青少年(M=15.8±2.2 岁,63.5%女性)和 40 名睡眠良好的青少年(M=15.9±2.4 岁,75%女性)完成了睡眠、日间功能和认知“失眠”过程(即,重复性消极思维、生理过度唤醒、苦恼、与睡眠相关的注意和监测、睡眠错觉)的基线测量。60 名 DSWPD 青少年(M=15.9±2.2 岁,63%女性)进入了一项治疗试验,并接受了 3 周的光照治疗。治疗后和 3 个月随访时再次测量睡眠、日间功能和失眠情况。
与睡眠良好的青少年相比,DSWPD 青少年在上学日的睡眠开始时间(d=0.99-1.50)、睡眠潜伏期(d=1.14)和总睡眠时间(d=0.85)明显更晚。有证据表明存在认知“失眠”症状,DSWPD 组报告的重复性消极思维(d=0.70-1.02)、特质性过度唤醒(d=0.55)、苦恼(d=2.19)、与睡眠相关的监测(d=0.76)和入睡错觉(d=1.29)更多。在治疗和随访过程中,DSWPD 青少年报告的入睡时间提前(d=0.54-0.62)、睡眠潜伏期缩短(d=0.53)、总睡眠时间增加(d=0.49)和日间功能改善(d=0.46-1.00)。重复性消极思维(d=0.64-0.96)、生理唤醒(d=0.69)、苦恼(d=0.87)和入睡错觉(d=0.37)也有所改善。
认知“失眠”过程可能与青少年 DSWPD 的发生和维持有关。这些过程中的许多都可以通过生物节律治疗来改善;然而,残留的症状可能使青少年面临治疗效果不佳或复发的风险。