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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Functional interregional neural coupling was measured as EEG coherence during REM sleep, a state of endogenous cortical activation, in 9 adult autistic individuals (21.1±4.0 years) and 13 typically developed controls (21.5±4.3 years) monitored for two consecutive nights in a sleep laboratory. Spectral analysis was performed on 60 s of artefact-free EEG samples distributed equally throughout the first four REM sleep periods of the second night. EEG coherence was calculated for six frequency bands (delta, theta, alpha, sigma, beta, and total spectrum) using a 22-electrode montage. The magnitude of coherence function was computed for intra- and interhemispheric pairs of recording sites. Results were compared by Multivariate Analysis of Variance (MANOVA). Each time the autistic group showed a greater EEG coherence than the controls; it involved intrahemispheric communication among the left visual cortex (O1) and other regions either close to or distant from the occipital cortex. In contrast, lower coherence values involved frontal electrodes in the right hemisphere. No significant differences between groups were found for interhemispheric EEG coherence. These results show that the analysis of EEG coherence during REM sleep can disclose patterns of cortical connectivity that can be reduced or increased in adults with autism compared to typically developed individuals, depending of the cortical areas studied. Superior coherence involving visual perceptual areas in autism is consistent with an enhanced role of perception in autistic brain organization.

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