Long-term effectiveness of controlled-release melatonin in 25 children, aged 2.6-9.6 years with autism without other coexistent pathologies was evaluated openly. Sleep patterns were studied using Children's Sleep Habits Questionnaire (CSHQ) and sleep diaries at baseline, after 1-3-6 months melatonin treatment and 1 month after discontinuation. Sleep diary and CSHQ showed a more problematic sleep in autistic children compared with controls. During treatment sleep patterns of all children improved. After discontinuation 16 children returned to pre-treatment score, readministration of melatonin was again effective. Treatment gains were maintained at 12 and 24-month follow-ups. No adverse side effects were reported. In conclusion, controlled-release melatonin may provide an effective and well-tolerated treatment for autistic children with chronic sleep disorders.

This study investigated sleep of children with autism and developmental regression and the possible relationship with epilepsy and epileptiform abnormalities. Participants were 104 children with autism (70 non-regressed, 34 regressed) and 162 typically developing children (TD). Results suggested that the regressed group had higher incidence of circadian rhythm disorders than non-regressed children. The regressed group showed higher Children's Sleep Habits Questionnaire Bedtime Resistance, Sleep Onset Delay, Sleep Duration and Night-Wakings scores. Epilepsy and frequent epileptiform EEG abnormalities were more frequent in regressed children. Past sleep disorders and a history of developmental regression were significantly associated with sleep disorders. This study is an initial step in better understanding sleep problems in regressed children with autism, further studies are necessary to better investigate these aspects.

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Summary The purpose of the present investigation was to characterize and compare traditional sleep architecture and non‐rapid eye movement (NREM) sleep microstructure in a well‐defined cohort of children with regressive and non‐regressive autism, and in typically developing children (TD). We hypothesized that children with regressive autism would demonstrate a greater degree of sleep disruption either at a macrostructural or microstructural level and a more problematic sleep as reported by parents. Twenty‐two children with non‐regressive autism, 18 with regressive autism without comorbid pathologies and 12 with TD, aged 5–10 years, underwent standard overnight multi‐channel polysomnographic evaluation. Parents completed a structured questionnaire (Childrens’ Sleep Habits Questionnaire—CSHQ). The initial hypothesis, that regressed children have more disrupted sleep, was supported by our findings that they scored significantly higher on CSHQ, particularly on bedtime resistance, sleep onset delay, sleep duration and night wakings CSHQ subdomains than non‐regressed peers, and both scored more than typically developing controls. Regressive subjects had significantly less efficient sleep, less total sleep time, prolonged sleep latency, prolonged REM latency and more time awake after sleep onset than non‐regressive children and the TD group. Regressive children showed lower cyclic alternating pattern (CAP) rates and A1 index in light sleep than non‐regressive and TD children. Our findings suggest that, even though no particular differences in sleep architecture were found between the two groups of children with autism, those who experienced regression showed more sleep disorders and a disruption of sleep either from a macro‐ or from a microstructural viewpoint.

The authors describe an Italian child with guanidinoacetate methyltransferase deficiency, neurologic regression, movement disorders, and epilepsy during the first year of life. Brain MRI showed pallidal and periaqueductal alterations. In vivo 1H-MRS showed brain creatine depletion. The assessment of guanidinoacetic acid concentration in biologic fluids confirmed the diagnosis. Clinical, biochemical, and neuroradiologic improvement followed creatine supplementation.