Child Autism & Insomnia
Insomnia & Autism
Studies have suggested that sleep problems are associated with autistic behaviors and that between 50-80% of children with ASD suffer from insomnia, much more than typically developing children.
Most of the sleep complaints are difficulty in falling asleep (=sleep onset) but also maintaining sleep due to irregular awakenings, both contributing to a shortened night sleep. People affected by ASD already have numerous difficulties engaging in social interaction, and lack of sleep can make this even worse by causing daytime impairments such as increased hyperactivity and irritability, greater anxiety and higher sensory sensitivity.
Studies report that reduced amount of sleep - total sleep time (TST) is related to more severe ASD symptoms such as impaired social communication, increased restricted and repetitive behaviors and reduced IQ score.
Beyond negative effect on child daytime behavior and functioning, sleep disruption in the ASD child affects overall family sleep, health and well-being and is associated with maternal depression and family disorganization.
It was found that improvement in the duration of longest sleep episode (LSE) (the longest uninterrupted sleep period during the night) led to a significant improvement in daytime behavior in ASD children and was associated with a significant improvement in quality of life of the parents.
Etiology of insomnia in children with ASD
Many factors may play a role in insomnia in ASD children with genetic, environmental, immunological and neurological factors thought to have a key role.
A growing body of evidence indicates abnormal melatonin secretion and circadian rhythmicity in children with neurodevelopmental disorders, specifically ASD, which may be the cause of insomnia.
Insomnia treatment goals
In line with DSM 5, when treating insomnia in children with ASD we should evaluate the child sleep according to the following treatment goals:
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Total sleep time (TST) within the acceptable range recommended by the national sleep foundation (NSF)
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Sleep onset latency (SOL) < 30 minutes
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Longest (uninterrupted) sleep episode (LSE)>6 hours
In addition to the above sleep outcomes, when evaluating treatment success, a clinician should also evaluate the improvement in the child’s behavior and parents’ satisfaction from child sleep.
For a useful tool to evaluate treatment success click here
Sleep duration recommendation by the National Sleep Foundation:
Current insomnia treatment in children with ASD
Current practices recommend parent-directed sleep hygiene interventions including establishing bedtime routines as first-line treatment for pediatric insomnia in ASD, however, the response rate is only about 25%.
Pharmacotherapy is often provided when sleep hygiene intervention fails. Physicians often prescribe off-label drugs (e.g., antihistamines, a-adrenergic agonists [clonidine], antidepressants, antipsychotics) for their sedative side effects without proven safety, efficacy, or dosing regimen.
Melatonin replacement therapy to address this deficiency in the endogenous sleep-regulating hormone has been shown to improve sleep and restore the daily sleep-wake cycle. However, unlicensed melatonin preparations or food supplements are also used, despite considerable concerns over the quality, efficacy and potential safety hazards. Moreover, as melatonin has a very short half-life (40 minutes), immediate release preparations may improve only sleep initiation but do not affect sleep maintenance and cause early awakenings.
The USA National Sleep Foundation has developed a consensus statement where it has summarized the profile of the ideal pharmacological therapy for pediatric insomnia. One such therapy should be able to positively affect sleep parameters, be easy to administer, dose adjustable, have good safety profile, sustainable benefits and will not impair sleep architecture.
In ASD and Smith Magenis Syndrome (SMS) children who suffer from insomnia, Slenyto® is the only approved pharmacotherapy. It isa prolonged-release melatonin (PRM) formulation, designed to mimic the endogenous profile by releasing melatonin throughout the night, helping to improve both sleep initiation and sleep maintenance without early awakenings.
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