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Attention-deficit/hyperactivity disorder (ADHD) is one of the most common psychiatric disorders in childhood. Around 25-50% of these children suffered from some kind of sleep disorder especially with chronic form of insomnia. Nowadays, we know that there is a noticeable relationship between ADHD and sleep disorders and by improving these children's sleep, not only the daily functions of them improve, but also the symptoms of ADHD maybe become better. This research evaluates the effects of melatonin on improvement of Sleep quality in children with ADHD whom received Ritalin
Method
Participants included 22 children suffered ADHD and concomitant sleep problems patients who underwent melatonin prescription and placebo at night in two sequencial periods. The effects of the melatonin were compared with placebo on the sleep problem improvements in each one.
Results
Although sleep onset, total sleep time and sleep quality advanced with melatonin, wake up time and the time to go to bed had not significant difference between the melatonin and placebo group. In addition, there were significant effects on attention, hyper activity index and impulsivity of the patients in the melatonin group.
Conclusion
Melatonin advanced circadian rhythms of sleep-wake and not only enhanced total time asleep in children with ADHD and chronic sleep onset insomnia, but also can improve the quality of life of these patients.
The principal classes of glia in the mature brain are astrocytes, microglia and oligodendrocytes. According to the Benington-Heller hypothesis, astrocytic glycogen, which acts as a reserve glucose store for neurons, is depleted during wakefulness and restored during non-rapid-eye-movement (NREM) sleep. Cerebral microglia and oligodendrocytes cells secrete a number of substances in vitro known to influence sleep or brain activity in sleep. As sleep deprivation is associated with an increase in markers of cellular stress, it has been proposed that substances secreted by microglia may play a central role in sleep regulation. An important future area of investigation is to determine the anatomic locations where glial cells exert their effects on sleep and/or brain activity. Glia is dispersed widely in subcortical and cortical brain areas including regions known to trigger sleep and wakefulness. Astrocytic adenosine is likely to be a key mediator of sleep behavior and brain activity.
This chapter describes the recent progress on the molecular mechanism of prostaglandin (PG) D2-induced sleep, basic and clinical studies on the roles of PGD2 in physiological sleep regulation, and current and emerging roles of adenosine in regulating sleep. There are two distinct types of PGD synthase (PGDS), one being lipocalin-type PGDS (L-PGDS) and the other, hematopoietic PGDS (H-PGDS). When PGD2 is infused into the subarachnoid space of the basal forebrain of wild-type mice, the region in which DP1 receptors are most abundant, the extracellular adenosine concentration increases in a dose-dependent manner. This increase is absent in DP1 receptor knockout (KO) mice, indicating that the increase in adenosine in the subarachnoid space depends on DP1 receptors. Adenosine deaminase, an enzyme that catabolizes adenosine to inosine, is predominantly localized in the tuberomammilary nucleus (TMN) of the brain.
This chapter discusses traditional metabolic genes that contribute to sleep regulation as well as candidate genes that may govern the systems independently. Inadequate sleep simultaneously modulates the level of multiple hormones that govern metabolism. In general, with sleep deprivation, the following hormones are decreased: insulin, growth hormone (GH), growth hormone releasing hormone (GHRH), and leptin levels. Even though starvation appears to confer fewer detrimental effects with extended waking than sleep deprivation, this response may come with consequences of its own. There are increasing number of proteins that affect sleep and metabolism, but are not classical metabolic genes. One class of genes that links metabolism and sleep is the circadian rhythm genes. It is interesting to note how often the effect of sleep deprivation invokes a starvation-like response from the body and how a starvation or a starvation-like state results in decreased sleep.
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