ObjectiveTo review pharmacologic and nonpharmacologic strategies for treating sleep disturbances in children and adolescents with autism spectrum disorder (ASD) and to develop recommendations for addressing sleep disturbance in this population.MethodsThe guideline panel followed the American Academy of Neurology 2011 guideline development process, as amended. The systematic review included studies through December 2017. Recommendations were based on evidence, related evidence, principles of care, and inferences.Major recommendations (Level B)For children and adolescents with ASD and sleep disturbance, clinicians should assess for medications and coexisting conditions that could contribute to the sleep disturbance and should address identified issues. Clinicians should counsel parents regarding strategies for improved sleep habits with behavioral strategies as a first-line treatment approach for sleep disturbance either alone or in combination with pharmacologic or nutraceutical approaches. Clinicians should offer melatonin if behavioral strategies have not been helpful and contributing coexisting conditions and use of concomitant medications have been addressed, starting with a low dose. Clinicians should recommend using pharmaceutical-grade melatonin if available. Clinicians should counsel children, adolescents, and parents regarding potential adverse effects of melatonin use and the lack of long-term safety data. Clinicians should counsel that there is currently no evidence to support the routine use of weighted blankets or specialized mattress technology for improving disrupted sleep. If asked about weighted blankets, clinicians should counsel that the trial reported no serious adverse events with blanket use and that blankets could be a reasonable nonpharmacologic approach for some individuals.

Recent electrophysiological studies suggest that autism spectrum disorder is characterized by aberrant anatomical and functional neural circuitry. During normal brain development, pruning and synaptogenesis facilitate ongoing changes in both short- and long-range neural wiring. In developmental disorders such as autism, this process may be perturbed leading to abnormal neural connectivity. Careful analysis of electrophysiological connectivity patterns using EEG coherence may provide a way to probe the resulting differences in neurological function between people with and without autism. There is general consensus that EEG coherence patterns differ between individuals with and without autism spectrum disorders, however the exact nature of the differences and their clinical significance remain unclear. Here we review recent literature comparing EEG coherence patterns between patients with autism spectrum disorders or at high risk for autism and their non-autistic or low risk for autism peers.

Study Objectives: Polysomnographic investigation of sleep architecture in children presenting with pediatric acute-onset neuropsychiatric syndrome (PANS). Methods: Fifteen consecutive subjects meeting criteria for PANS (mean age = 7.2 y; range 3-10 y) underwent single-night full polysomnography (PSG) read by a pediatric neurologist. Results: Thirteen of 15 subjects (87%) had abnormalities detected with PSG. Twelve of 15 had evidence of rapid eye movement (REM) sleep motor disinhibition, as characterized by excessive movement, laughing, hand stereotypies, moaning, or the continuation of periodic limb movements during sleep (PLMS) into REM sleep. Conclusions: This study shows various forms of REM sleep motor disinhibition present in a population of children with PANS. Keywords: obsessive compulsive disorder, PANS, polysomnography, REM sleep behavior disorder Citation: Gaughan T, Buckley A, Hommer R, Grant P; Williams K, Leckman JF, Swedo SE. Rapid eye movement sleep abnormalities in children with pediatric acute-onset neuropsychiatric syndrome (PANS). J Clin Sleep Med 2016;12(7):1027-1032. I NTRO DUCTI O N Schenck et al.1 were the first to suggest that rapid eye movement (REM) sleep neurobehavioral disorders were a separate category of parasomnia in a 1986 case series of four males aged 67-72 y. Polysomnography (PSG) of these four subjects showed a loss of chin atonia and high limb-twitch activity among other REM sleep pathology, whereas videography showed various REM sleep behaviors including punching, kicking, and dream enactment.1 Since then, REM sleep behavior disorder (RBD) has been recognized across a wide range of ages, sometimes decades prior to the onset of other neurobehavioral changes and often heralding serious neurodegenerative conditions affecting synuclein.2 A recent retrospective study of patients showing REM sleep without atonia on PSG found a majority (73%) of patients had idiopathic RBD, defined as RBD in the absence of known neurological or sleep disorders.3 Recent reports suggest that clinical and subclinical forms of RBD occur in children and adolescents.4 Although pediatric RBD is considered to be a rare occurrence, its prevalence may be underestimated due to limited awareness, overlap with other parasomnias, and the requirement of nocturnal PSG for diagnosis.4,5 Additionally, it is unclear whether or not the adult clinical definitions should pertain to pediatric presentations due to a current lack of neuropathologic studies of childhood RBD.4 Differentiating RBD from other parasomnias in the younger population is significant clinically because of the potential to inform on neuropsychiatric state and therefore guide treatment choices, as evidenced in conditions such as narcolepsy where 60% of patients will have RBD. In adult psychiatric populations, RBD has been associated with the use of psychotropic medications and particularly with serotonin reuptake-blocking antidepressants.3,7 However, a recent study suggests that antidepressants cannot fully explain RBD symptomatology in their psychiat...

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