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In the present study we investigated sleep hygiene and actigraphically evaluated sleep in 74 medication-naïve children, aged 6–12 years, with rigorously diagnosed attention-deficit/hyperactivity disorder (ADHD) and chronic sleep onset insomnia (ADHD-SOI) and 23 ADHD controls without insomnia (ADHD-noSOI). Between-group differences were analysed for lights out (sleep log), actigraphically evaluated sleep onset, sleep latency, total sleep duration, actual sleep time and sleep hygiene as measured with the Children's Sleep Hygiene Scale. We found a significant difference ( P < 0.001) in mean (±SD) sleep onset between the ADHD-SOI group (21:49 ± 0:56 h) and ADHD-noSOI groups (20:41 ± 0:45 h). Sleep latency was significantly ( P < 0.001) longer in ADHD-SOI (00:53 ± 0:25 h) compared to ADHD-noSOI (00:26 ± 0:25 h). The difference in total sleep duration between ADHD-SOI (9:42 ± 0:44 h) and ADHD-noSOI (10:09 ± 0:43 h) was not significantly different ( P = 0.18). The group difference in actual sleep time was also not significant (8:43 ± 0:52 h in ADHD-SOI versus 9:13 ± 1:16 h; P = 0.40). There was no significant difference ( P = 0.17) in mean (±SD) total sleep hygiene score between the ADHD-SOI (56.4 ± 10.5) and ADHD-noSOI groups (53.0 ± 10.6). We conclude that there were differences in sleep onset and sleep latency in ADHD children with chronic SOI and those without insomnia; however, sleep hygiene practices were similar and did not relate to sleep characteristics. [ABSTRACT FROM AUTHOR]

Research has shown efficacy of melatonin treatment to advance sleep–wake rhythms in insomnia. In healthy adults, direction and magnitude of the phase shift depends on the timing of administration relative to the phase position of the circadian system. Therefore, in the present study we investigated whether in children with chronic sleep onset insomnia (SOI) efficacy of melatonin treatment in the early evening could be predicted from dim light melatonin onset (DLMO), a phase marker of the circadian system. We combined data of two previously published double blind, randomized, placebo-controlled trials in 110 participants, aged 6–12 years. Sleep was actigraphically estimated, and saliva collected, at baseline and in the third week of a 4-week treatment period with 5 mg melatonin or placebo at 18:00 or 19:00 hours. Primary outcome measures were pre- to post-treatment changes in dim light melatonin onset (ΔDLMO), sleep onset (ΔSO), sleep latency (ΔSL), and total sleep duration (ΔTSD). Melatonin advanced DLMO with +1:12 h (P < 0.001), SO with +0:42 h (P = 0.004), SL decreased with 25 min (P = 0.019), and TSD did not change significantly, as compared with placebo. In the melatonin-treated group, but not in the placebo-treated group, pretreatment DLMO was significantly related toΔDLMO [F(1, 29) = 7.28,P = 0.012] andΔSO [F(1, 25) = 7.72,P = 0.010]. The time interval between treatment administration and pretreatment DLMO (INT) was only significantly related toΔSO [F(1,26) = 5.40,P = 0.028]. The results suggest that in children with SOI, the efficacy of early evening melatonin to advance sleep onset and endogenous melatonin onset increases the later the pretreatment DLMO is. [ABSTRACT FROM AUTHOR]

The article focuses on the relation between sleep-related disorders and attention- deficit/hyperactivity disorder (ADHD). The comorbidity warrants close attention since sleep-related disorders impinge on the same functional domains as those impaired in ADHD, such as sustained attention, inhibition, and working memory. Hence, it has been alleged that sleep-related disorders might possibly lead to an aggravation or mimicry of the symptoms of ADHD. A second reason for the interest is that stimulants, the treatment of first choice for ADHD, are notorious for their deleterious effect on sleep.