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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tuberous sclerosis complex is an autosomal dominant disorder characterized by abnormal cellular differentiation and proliferation, as well as abnormal neuronal migration. It is a disease affecting multiple organ systems and typically has brain involvement, causing severe disabilities. This article reviews the literature of the commonly associated neuropsychiatric complications, including mental retardation, autism-like features, and other behavior problems, which are discussed in the context of the neuropathology and epilepsy observed in tuberous sclerosis complex. The potential pathogenesis of neuropsychiatric problems is explored, including links to the genetics, neuropathology, neurotrophins, and epilepsy factors associated with tuberous sclerosis complex. Treatment of neuropsychiatric symptoms, including autism-like features, attention deficits, and sleep disorders, is also discussed.
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PMID:Neuropsychiatric problems in tuberous sclerosis complex. 1516 88

Autism is a developmental disability characterized by severe deficits in social interaction and communication, and the presence of repetitive-ritualistic behaviors. Sleep problems are frequently reported by parents of children with autism with prevalence estimates of 44-83% for sleep disorders in this population. To better understand sleep in autism, we surveyed sleep problems in 210 children with autism using a Likert-based questionnaire for parent report. The most frequently reported sleep problems included difficulty in falling asleep, restless sleep, not falling asleep in own bed, and frequent wakenings. Least frequently reported sleep problems were sleep walking, morning headaches, crying during sleep, apnea, and nightmares. When surveys were divided into mental retardation (MR)/not MR categories, no significant differences were identified in frequencies of reported sleep problems except for waking at night which occurred much more frequently in the MR group. There was also no difference in sleep problems related to age of the child other than nocturnal enuresis. An association was noted between certain medical problems and sleep problems. Vision problems, upper respiratory problems, and runny nose were associated with decreased nighttime sleep. Vision problems, poor appetite, and poor growth were associated with increased nighttime waking. Poor appetite and poor growth were associated with decreased willingness to fall asleep. This study confirms a high prevalence of sleep problems reported by parents of children with autism and points to the need for more systematic research as an initial step in developing treatment strategies.
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PMID:Sleep problems in children with autism. 1533 62

The purpose of this review article is to describe the clinical data linking autism with sleep and epilepsy and to discuss the impact of treating sleep disorders in children with autism either with or without coexisting epileptic seizures. Studies are presented to support the view that sleep is abnormal in individuals with autistic spectrum disorders. Epilepsy and sleep have reciprocal relationships, with sleep facilitating seizures and seizures adversely affecting sleep architecture. The hypothesis put forth is that identifying and treating sleep disorders, which are potentially caused by or contributed to by autism, may impact favorably on seizure control and on daytime behavior. The article concludes with some practical suggestions for the evaluation and treatment of sleep disorders in this population of children with autism.
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PMID:Sleep disorders, epilepsy, and autism. 1536 68

Cognitive plasticity, a developmental trait that promotes acquisition of complex skills such as language or playing musical instruments, diminishes substantially during puberty. The loss of plasticity has been attributed to surge of sex steroids during adolescence, but the phenomenon remains poorly understood. We hypothesize that pineal involution during puberty may contribute to plasticity decay. The pineal gland produces melatonin, the level of which declines dramatically during onset of puberty. Emerging evidence suggest that melatonin may modulate cognitive plasticity, independent of the effects of sex steroids, and low sex steroids and high melatonin may be simultaneously required to maintain cognitive plasticity. Potential mechanisms by which melatonin may modulate plasticity are examined within the sleep and hippocampal long-term potentiation frameworks. Implications for psychiatric conditions that involve sleep disorders and learning dysfunctions such as schizophrenia and autism are discussed, and the potential adaptive roles of postprandial and postcoital sleep are explored. From the Darwinian perspective, development and reproductive maturity may represent distinct phases that require tailored cognitive strategies to maximize fitness. While cognitive flexibility and susceptibility to new skills may be paramount during development, reduced cognitive flexibility and increased cognitive determinism may enable more efficient responses to stimuli during adulthood. Thus, cognitive plasticity and cognitive determinism may represent trade-off adaptations and different dimensions of intelligence. The decline of plasticity and emergence of puberty during the second decade may be relics of prehistoric times when the human lifespan was short and the environment was relatively simple and static. Today, when the environment is more complex and dynamic, and humans are living far longer, the early obsolescence of plasticity during puberty may represent a Darwinian inefficiency exposed by evolutionary displacement. Regulation of plasticity may be a systemic phenomenon, as exemplified by the association of learning disability with allergic conditions, a form of immune plasticity dysfunction. Ramifications for other plastic functions that decline during puberty such as wound healing and hyaline cartilage regeneration are explored. Like the plasticity of immunity and cognition, the plasticity of hyaline cartilage during youth may enable hosts to respond to ecologic opportunities and generate the optimally adapted adult phenotype. Pineal involution may represent a potential target for therapeutic extension or restoration of plasticity after puberty. Extending plasticity may have far-reaching consequences for human evolution.
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PMID:Pineal attrition, loss of cognitive plasticity, and onset of puberty during the teen years: is it a modern maladaptation exposed by evolutionary displacement? 1550 60

A growing body of evidence indicates that people with autism frequently experience sleep disorders and exhibit atypical sleep architecture. In order to establish whether sleep disorders truly belong to the autism spectrum disorder (ASD) phenotype, we conducted a subjective and objective study of sleep in a group of high-functioning adults with ASD but without sleep complaints, psychiatric disorders or neurological comorbidity. We compared the subjective data of 27 ASD participants with those of 78 healthy controls matched for chronological age and gender. Subjective measures of sleep in the clinical group were compatible with insomnia and/or a tolerable phase advance of the sleep-wake cycle. Subjective data were confirmed by objective laboratory sleep recordings in a subset of 16 patients and 16 controls. Persons with autism presented with a longer sleep latency (P < 0.04), more frequent nocturnal awakenings (P < 0.03), lower sleep efficiency (P < 0.03), increased duration of stage 1 sleep (P < 0.02), decreased non-REM sleep (stages 2 + 3 + 4, P < 0.04) and slow-wave sleep (stages 3 + 4, P < 0.05), fewer stage 2 EEG sleep spindles (P < 0.004), and a lower number of rapid eye movements during REM sleep (P < 0.006) than did control participants. On clinical scales, the scores of persons with ASD on the Beck Depression Inventory were similar to those of persons without, but their trait anxiety scores on the Spielberger Anxiety Scale were higher (P < 0.02). The state anxiety scores of the Spielberger scale and cortisol levels were the same in the two groups. Objective total sleep time correlated negatively with the Social (-0.52, P < 0.05) and Communication (-0.54, P < 0.02) scales of the Autism Diagnostic Interview-Revised. The sleep of clinical subgroups (10 with high-functioning autism, six with Asperger syndrome) did not differ, except for the presence of fewer EEG sleep spindles in the Asperger syndrome subgroup (P < 0.05). In conclusion, these findings indicate that atypicalities of sleep constitute a salient feature of the adult ASD phenotype and this should be further investigated in younger patients. Moreover, the results are consistent with an atypical organization of neural networks subserving the macro- and microstructure of sleep in ASD. We are furthering this research with quantified analysis of sleep EEG.
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PMID:Atypical sleep architecture and the autism phenotype. 1570 9

Developmental disorders such as mental retardation, language disorders, autistic disorders, learning disorders, attention deficit/hyperactivity syndrome and conduct disorders are an important part of our daily practice in child neurology. Early diagnosis and early or timely intervention in these kinds of developmental disorders were stressed and family support in child-rearing was emphasized in this symposium. In addition to the above, sleep disorders in developmental disorders were discussed.
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PMID:[Early diagnosis and early intervention in children with developmental disorders: introductory remarks]. 1577 24

Sleep disorders can affect daytime functioning in a variety of neurologic conditions, including autism spectrum disorder. This report describes improvements in sleep, social communication, attention, repetitive behaviors, and hypersensitivity after adenotonsillectomy for obstructive sleep apnea in a 5-year-old female with an autism spectrum disorder. Improvements were documented via pre- and postsurgical measures of parent report, polysomnography, validated sleep and behavior scales, and the Autism Diagnostic Observation Schedule. Identification and treatment of sleep disorders, including obstructive sleep apnea, may improve daytime behavior in children with autism spectrum disorders.
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PMID:Impact of treating sleep apnea in a child with autism spectrum disorder. 1663 13

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.
J Autism Dev Disord 2006 Aug
PMID:An open-label study of controlled-release melatonin in treatment of sleep disorders in children with autism. 1689 3

This study examined sleep patterns, sleep problems, and their correlates in children with autism spectrum disorders (ASD). Subjects consisted of 167 ASD children, including 108 with autistic disorder, 27 with Asperger's syndrome, and 32 with other diagnoses of ASD. Mean age was 8.8 years (SD = 4.2), 86% were boys. Parents completed a self-administered child sleep questionnaire. Results showed that average night sleep duration was 8.9 h (SD = 1.8), 16% of children shared a bed with parent. About 86% of children had at least one sleep problem almost every day, including 54% with bedtime resistance, 56% with insomnia, 53% with parasomnias, 25% with sleep disordered breathing, 45% with morning rise problems, and 31% with daytime sleepiness. Multivariate logistic regression analyses indicated that younger age, hypersensitivity, co-sleeping, epilepsy, attention-deficit/hyperactivity disorder (ADHD), asthma, bedtime ritual, medication use, and family history of sleep problems were related to sleep problems. Comorbid epilepsy, insomnia, and parasomnias were associated with increased risk for daytime sleepiness. Results suggest that both dyssomnias and parasomnias are very prevalent in children with ASD. Although multiple child and family factors are associated with sleep problems, other comorbid disorders of autism may play a major role.
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PMID:Sleep disturbances and correlates of children with autism spectrum disorders. 1700 27

Pediatric sleep disorders are common, affecting approximately 25% to 40% of children and adolescents. Although there are several different types of sleep disorders that affect youth, each disorder can have a significant impact on daytime functioning and development, including learning, growth, behavior, and emotion regulation. Researchers are only beginning to uncover the interaction between sleep and psychiatric disorders in children and adolescents, including depression, attention-deficit/hyperactivity disorder, and autism. This article reviews normal sleep and sleep disorders in children and adolescents, the assessment of sleep in pediatric populations, common pediatric sleep disorders, and sleep in children who have common psychiatric disorders.
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PMID:Sleep and sleep disorders in children and adolescents. 1711 82


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