Reduced 'Sleep Pressure' Contributes To Insomnia In Autism

Disturbances in sleep homeostasis, manifested as reduced pressure to sleep after being awake for a longer period, contribute to insomnia in young children with autism-spectrum disorder (ASD), researchers from Israel report.

"Sleep pressure is building up during the day as a function of prior wakefulness until sleep onset," said Dr. Ayelet Arazi of Ben Gurion University of the Negev, in Beer-Sheva.

"Hence, children who fall asleep later at night should develop larger sleep pressure compared with children who fall asleep earlier," she told Reuters Health by email. "Our results show the opposite, indicating a disruption in the homeostatic mechanism of sleep in children with autism."

Sleep disturbances are about twice as common in children with ASD as in typically developing children, and poor sleep in these children is associated with increased sensory sensitivities and increased aberrant behaviors. Polysomnographic (PSG) studies have yielded mixed results regarding abnormalities in sleep architecture in children with ASD.

Dr. Arazi and colleagues quantified slow-wave activity (SWA, a measure of sleep pressure) and traditional sleep staging in 29 children with ASD and 23 typically developing controls. They examined whether individual differences in SWA explained differences in the severity of sleep disturbances as observed in the sleep laboratory and as reported by parents.

Compared with controls, children with ASD spent significantly less time in bed and had significantly shorter total sleep time. Sleep efficiency, percentage of wake after sleep onset, sleep latency and arousal index did not differ between children with ASD and controls.

Children with ASD exhibited significantly weaker SWA power, compared with controls, especially during the first two hours of sleep, the researchers report in Sleep.

Children with ASD also had a significantly larger percentage of N2 (light sleep associated with increases in brainwave frequency) and a significantly lower percentage of N3 (deep sleep associated with slower delta waves) during the first half of the sleep period, as well as a lower percentage of REM sleep during the second half of the sleep period.

There were significant negative correlations between SWA power and bedtime resistance and total sleep disturbances (as reported by parents) and the absolute time that children fell asleep in the lab.

"These results suggest that weaker SWA power in children with ASD at the beginning of the night can partially explain individual problems of initiating sleep, resulting in late sleep onset," the authors say.

"Revealing a disruption in the homeostatic sleep regulation in children with autism opens the door to a variety of clinical interventions," Dr. Arazi said. "Several treatments have been proven to increase slow-waves in patients with insomnia, ranging from mild intervention such as increased exercise and cognitive behavioral treatment (CBT) to pharmacological treatment with specific sleep medications. Further clinical studies should examine the efficacy of these treatments for children with autism."
—Will Boggs, MD



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