Sleep in Autism Spectrum Disorders

Veatch, Olivia J.; Maxwell-Horn, Angela; Malow, Beth A.

doi:10.1007/s40675-015-0012-1

Cited by 81 publications

(54 citation statements)

References 115 publications

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“…Sleep disturbance is common in individuals with ASD and may be associated with exacerbation of problematic daytime behavior. [420][421][422][423][424][425][426][427] Problems with initiating and maintaining sleep are reported for 50% to 80% of children with ASD. 428 Children who are later diagnosed with ASD are reported to have had sleep problems by 30 months of age.…”

Section: Sleep Problemsmentioning

confidence: 99%

Identification, Evaluation, and Management of Children With Autism Spectrum Disorder

2020

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Autism spectrum disorder (ASD) is a common neurodevelopmental disorder with reported prevalence in the United States of 1 in 59 children (approximately 1.7%). Core deficits are identified in 2 domains: social communication/interaction and restrictive, repetitive patterns of behavior. Children and youth with ASD have service needs in behavioral, educational, health, leisure, family support, and other areas. Standardized screening for ASD at 18 and 24 months of age with ongoing developmental surveillance continues to be recommended in primary care (although it may be performed in other settings), because ASD is common, can be diagnosed as young as 18 months of age, and has evidenced-based interventions that may improve function. More accurate and culturally sensitive screening approaches are needed. Primary care providers should be familiar with the diagnostic criteria for ASD, appropriate etiologic evaluation, and co-occurring medical and behavioral conditions (such as disorders of sleep and feeding, gastrointestinal tract symptoms, obesity, seizures, attention-deficit/hyperactivity disorder, anxiety, and wandering) that affect the child' s function and quality of life. There is an increasing evidence base to support behavioral and other interventions to address specific skills and symptoms. Shared decision making calls for collaboration with families in evaluation and choice of interventions. This single clinical report updates the 2007 American Academy of Pediatrics clinical reports on the evaluation and treatment of ASD in one publication with an online table of contents and section view available through the American Academy of Pediatrics Gateway to help the reader identify topic areas within the report.

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Section: Sleep Problemsmentioning

confidence: 99%

Identification, Evaluation, and Management of Children With Autism Spectrum Disorder

2020

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“…It is possible that ASD symptoms drive disturbed sleep or that expression of ASD symptoms with comorbid sleep disturbances are modified by convergent genetic risk factors (Hu et al, ; Pagan et al, ; Veatch, Goldman, Adkins, & Malow, ; Veatch, Maxwell‐Horn, & Malow, ; Yang et al, ). Defining the relationship of disturbed sleep to ASD symptom severity in large databases with extensive phenotypic and genetic data available is a necessary step toward generating hypotheses about how short sleep duration may affect ASD, and moving toward more effective approaches to mitigate these symptoms.…”

Section: Introductionmentioning

confidence: 99%

Shorter sleep duration is associated with social impairment and comorbidities in ASD

et al. 2017

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Sleep disturbance, particularly insomnia, is common in children with autism spectrum disorders (ASD). Furthermore, disturbed sleep affects core symptoms and other related comorbidities. Understanding the causes and consequences of sleep disturbances in children with ASD is an important step toward mitigating these symptoms. To better understand the connection between sleep duration and ASD severity, we analyzed ASD-related symptoms using the Autism Diagnostic Interview-Revised (ADI-R), Autism Diagnostic Observation Schedule (ADOS), IQ scores, and parent reports of the average amount of time slept per night that were available in the medical histories of 2,714 children with ASD in the Simons Simplex Collection (SSC). The mean (SD) sleep duration was 555 minutes. Sleep duration and severity of core ASD symptoms were negatively correlated, and sleep duration and IQ scores were positively correlated. Regression results indicated that more severe social impairment, primarily a failure to develop peer relationships, is the core symptom most strongly associated with short sleep duration. Furthermore, increased severity for numerous maladaptive behaviors assessed on the Child Behavior Checklist, as well as reports of attention deficit disorder, depressive disorder, and obsessive compulsive disorder were associated with short sleep duration. Severity scores for social/communication impairment and restricted and repetitive behaviors (RRB) were increased, and IQ scores were decreased, for children reported to sleep ≤420 minutes per night (lower 5th percentile) compared to children sleeping ≥660 minutes (upper 95th percentile). Our results indicate that reduced amounts of sleep are related to more severe symptoms in children with ASD. Autism Res 2017. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. Autism Res 2017, 10: 1221-1238. © 2017 International Society for Autism Research, Wiley Periodicals, Inc.

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“…38 The PSQI data presented here revealed significant concerns with nighttime awakenings as well as difficulty in initiating sleep, similar to that observed in children with ASD. 39 A previous 24-hour sleep study in a small subset of patients with PTLS with ASD also documented multiple nocturnal awakenings and mixed sleep apnea characterized by significant oxygen desaturation and hypercapnia, further supporting the diagnosis of a form of sleep dyssomnia. 11 Further analysis is warranted to elucidate whether circadian deficits are causal to sleep phenotype manifestations in these disorders.…”

Section: Discussionmentioning

confidence: 66%

RAI1 Overexpression Promotes Altered Circadian Gene Expression and Dyssomnia in Potocki–Lupski Syndrome

et al. 2017

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( ) encodes a dosage-sensitive gene that when haploinsufficient results in Smith-Magenis syndrome (SMS) and when overexpressed results in Potocki-Lupski syndrome (PTLS). Phenotypic and molecular evidence illustrates that haploinsufficiency of disrupts circadian rhythm through the dysregulation of the master circadian regulator, ( , and other core circadian components, contributing to prominent sleep disturbances in SMS. However, the phenotypic and molecular characterization of sleep features in PTLS has not been elucidated. Using the Pittsburgh Sleep Quality Index (PSQI), caregivers of 15 school-aged children with PTLS reported difficulties in initiating sleep. Indeed, more than 70% of individuals manifested moderate to severe sleep latency, as defined by the PSQI. Moreover, these individuals manifested difficulties in sleep maintenance, with middle of the night and early morning awakenings. When assessing daytime sleepiness through the Epworth Sleepiness Scale, approximately 21% of the individuals manifested excessive daytime somnolence. This indicates that mild dyssomnia characterizes the majority of the sleep phenotype, with occasionally problematic daytime somnolence, a phenotype different than that expressed by individuals with SMS, where daytime sleepiness is a chronic problem. Gene expression analysis of the core circadian machinery in the hypothalamus of the PTLS mouse model ( -Tg) found significant dysregulation of the transcriptional activators, and , and the transcriptional repressors, and , during both light and dark phases. These findings suggest a partial loss of circadian entrainment typically evoked by environmental photic cues. Examination of circadian clock gene expression in the Tg mouse heart, liver, and kidney found unchanged expression of and most of its downstream targets during both light and dark phases, suggesting an asynchronized circadian rhythm. Furthermore, examination of circadian gene expression in synchronized PTLS lymphoblasts revealed reduced transcripts of the Period ( ) family and normal expression of . The finding that central circadian gene expression was altered while many peripheral circadian components were intact suggests a tissue-specific circadian uncoupling of the circadian machinery due to overexpression. Overall, our results demonstrate that overexpression of results in sleep deficiencies in individuals with PTLS due to a lack of properly regulated circadian machinery gene expression and highlight the importance of evaluating sleep concerns in individuals with PTLS.

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Sleep in Autism Spectrum Disorders

Cited by 81 publications

References 115 publications

Identification, Evaluation, and Management of Children With Autism Spectrum Disorder

Identification, Evaluation, and Management of Children With Autism Spectrum Disorder

Shorter sleep duration is associated with social impairment and comorbidities in ASD

RAI1 Overexpression Promotes Altered Circadian Gene Expression and Dyssomnia in Potocki–Lupski Syndrome

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