ABSTRACT
AIM: To evaluate the prevalence and types of sleep problems and their correlations with melatonin content and behavior in Attention-Deficit Hyperactivity Disorder (ADHD) children. METHOD: Sleep in ADHD children and typically developing children (TD) aged 6-14 was assessed by the Sleep Disorders Scale for Children (SDSC) and actigraphy, salivary melatonin quantified by ELISA, and behavior was analyzed using the Strengths and Difficulties Questionnaire. RESULTS: ADHD children showed a higher frequency of sleep disturbances, higher sleep latency, and lower sleep efficiency than in the TD group. The ADHD group presented lower melatonin nocturnal content compared to the TD group. Disorders of Initiating and Maintaining Sleep (DIMS) was moderately associated with nocturnal melatonin. The total behavior difficulties were correlated with Disorders of Initiating and Maintaining Sleep (DIMS), Sleep/Wake Transition Disorders (SWTD), Disorders of Excessive Somnolence (DES), Sleep Hyperhidrosis (SHY) and Total SDSC Score. The behavior was the only determinant of the total SDSC score (R2 = 0.499; p < 0.002). CONCLUSION: This study provides, for the first time, evidence that among the frequent sleep disturbances in ADHD, the disorders in initiating and maintaining sleep are associated with the low levels of melatonin found in this population. Additionally, these, along with other sleep disturbances, are linked to behavioral problems in ADHD.
ABSTRACT
BACKGROUND: The alterations in neurological and neuroendocrine functions observed in the autism spectrum disorder (ASD) involves environmentally dependent dysregulation of neurodevelopment, in interaction with multiple coding gene defects. Disturbed sleep-wake patterns, as well as abnormal melatonin and glucocorticoid secretion, show the relevance of an underlying impairment of the circadian timing system to the behavioral phenotype of ASD. Thus, understanding the mechanisms involved in the circadian dysregulation in ASD could help to identify early biomarkers to improve the diagnosis and therapeutics as well as providing a significant impact on the lifelong prognosis. OBJECTIVE: In this review, we discuss the organization of the circadian timing system and explore the connection between neuroanatomic, molecular, and neuroendocrine responses of ASD and its clinical manifestations. Here we propose interconnections between circadian dysregulation, inflammatory baseline and behavioral changes in ASD. Taking into account, the high relevancy of melatonin in orchestrating both circadian timing and the maintenance of physiological immune quiescence, we raise the hypothesis that melatonin or analogs should be considered as a pharmacological approach to suppress inflammation and circadian misalignment in ASD patients. STRATEGY: This review provides a comprehensive update on the state-of-art of studies related to inflammatory states and ASD with a special focus on the relationship with melatonin and clock genes. The hypothesis raised above was analyzed according to the published data. CONCLUSION: Current evidence supports the existence of associations between ASD to circadian dysregulation, behavior problems, increased inflammatory levels of cytokines, sleep disorders, as well as reduced circadian neuroendocrine responses. Indeed, major effects may be related to a low melatonin rhythm. We propose that maintaining the proper rhythm of the circadian timing system may be helpful to improve the health and to cope with several behavioral changes observed in ASD subjects.
