Abstract

Objective: 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. Method: 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. Results: 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. Conclusions: Cognitive “insomnia” processes may be implicated in the develop- ment and maintenance of DSWPD in adolescents. Many of these processes are amendable to chrono- biological treatment; however, residual symptoms may place adolescents at risk of poor treatment outcome or relapse.