Autism is a neurodevelopemental disorder characterized by atypical connectivity between brain regions. People with autism are known to have sleep disorders and the purpose of this study was to analyze brain connectivity before and after a night of sleep using EEG coherence analysis. Nine adults with autism (21.1 ± 4.0 years) and 20 control participants (20.8 ± 4.2 years) were recorded for two consecutive nights in a sleep laboratory, using a 22-electrode montage. Every participant had a normal IQ and none were taking medication. Wake EEG was recorded for 5 min at bedtime and just before final rise time in the morning, while lying in bed with eyes closed. EEG coherence values were compared with a multivariate repeated measures design using Group × Moment × Frequency band factors for each electrode separately, followed by post hoc tests. In the evening, the autistic group displayed more Alpha coherence than controls within the left visual area (P3-O1: p = 0.049; T5-O1: p = 0.03 and T5-P3: p = 0.014). In the morning more Alpha coherence in the autistic group within the left visual area was also measured (T5-O1: p = 0.009 and T5-P3: p = 0.015) as well as more Delta coherence at the T5-O1 electrode pair (p = .027). Moreover, morning recordings showed less Delta coherence within the right frontal area, (Fp2-F8: p = 0.037; F4-F8: p = 0.011) and between left and right hemispheres (F3-F4: p = 0.019; F7-F8: p = 0.003). A previous study performed during REM sleep (Léveillé et al., 2010) found a greater intrahemispheric EEG coherence in autistic participants compared to controls between the left visual cortex and regions either close to or distant from it. The present results are in the same direction, upon both evening and morning wake recordings, suggesting that sleep per se is not responsible for these signs of overconnectivity. The present results also revealed a morning specific lower EEG coherence values for slow frequencies in the right frontal area in participants with autism compared to controls, suggesting that sleep per se could be responsible for these signs of underconnectivity. Canadian Institute for Health Research; "Fonds de recherche du Québec – Santé".

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.

Objective: The aim of this study was to investigate the involvement of temporo-occipital regions in the pathophysiology of autistic spectrum disorders (ASD) by using REM sleep and waking EEG.Methods: The EEG recordings of 9 persons with ASD and 8 control participants were recorded using a 12-electrode montage. Spectral analysis (0.75-19.75 Hz) was performed on EEG activity recorded upon two activated states: REM sleep and wakefulness.Results: During REM sleep, persons with ASD showed a selective, significantly lower absolute beta (13.0-19.75 Hz) spectral amplitude over the primary (O-1, O-2) and associative (T-5, T-6) cortical visual areas compared to controls. Persons with ASD showed significantly higher absolute theta (4.0-7.75 Hz) spectral amplitude over the left frontal pole region (Fp1) compared to controls during evening wakefulness, but not during morning wakefulness.Significance: The results of waking EEG are consistent with previously reported observations of neuropsychological signs of frontal atypicalities in ASD; results from REM sleep are the first EEG evidence to support the hypothesis of abnormal visuoperceptual functioning in ASD. Altogether, these results point toward atypical thalamo-cortical mechanisms subserving the neural processing of information in ASD. (C) 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.