REM Sleep EEG Activity and Clinical Correlates in Adults With Autism.

We tested the hypothesis of an atypical scalp distribution of electroencephalography (EEG) activity during Rapid Eye Movement (REM) sleep in young autistic adults. EEG spectral activity and ratios along the anteroposterior axis and across hemispheres were compared in 16 neurotypical (NT) young adults and 17 individuals with autism spectrum disorder (ASD). EEG spectral power was lower in the ASD group over the bilateral central and right parietal (beta activity) as well as bilateral occipital (beta, theta, and total activity) recording sites. The NT group displayed a significant posterior polarity of intra-hemispheric EEG activity while EEG activity was more evenly or anteriorly distributed in ASD participants. No significant inter-hemispheric EEG lateralization was found. Correlations between EEG distribution and ASD symptoms using the Autism Diagnostic Interview-Revised (ADI-R) showed that a higher posterior ratio was associated with a better ADI-R score on communication skills, whereas a higher anterior ratio was related to more restricted interests and repetitive behaviors. EEG activity thus appears to be atypically distributed over the scalp surface in young adults with autism during REM sleep within cerebral hemispheres, and this correlates with some ASD symptoms. These suggests the existence in autism of a common substrate between some of the symptoms of ASD and an atypical organization and/or functioning of the thalamo-cortical loop during REM sleep.

Atypical sleep architecture and the autism phenotype.

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.

EEG spectral analysis of wakefulness and REM sleep in high functioning autistic spectrum disorders.

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.

Relationship between poor sleep and daytime cognitive performance in young adults with autism.

Poor sleep is a common feature in autism even though patients themselves do not necessarily complain. The impact of poor sleep on daytime cognitive functioning in autism is not well-known and we therefore investigated whether sleep in autism correlates with daytime cognitive performance. A battery of non-verbal tasks was administered, in the morning after a second night of sleep in the laboratory, to 17 young adults with autism and normal intelligence, and 14 typically developed individuals matched for age and IQ; none of the participants complained about sleep problems. Two dimensions of attention (sustained and selective) and 4 types of memory (working, declarative, sensory-motor and cognitive procedural) were tested. Individuals with autism showed clear signs of poor sleep. Their performance differed from the controls in response speed but not in accuracy. Signs of poor sleep in the autism group were significantly correlated with either normal performance (selective attention and declarative memory) or performance inferior to that of the controls (sensory-motor and cognitive procedural memories). Both groups presented a significant negative correlation between slow-wave sleep (SWS) and learning a sensory-motor procedural memory task. Only control participants showed a positive association between SWS duration and number of figures recalled on the declarative memory task. Correlation patterns differed between groups when sleep spindles were considered: they were negatively associated with number of trials needed to learn the sensory-motor procedural memory task in autism and with reaction time and number of errors on selective attention in the controls. Correlation between rapid eye movements (REMs) in REM sleep and cognitive procedural memory was not significant. We conclude that some signs reflecting the presence of poor sleep in adults with high-functioning autism correlate with various aspects of motor output on non-verbal performance tasks. The question is raised whether poor sleep in non-complaining persons with autism should be treated.

Enhanced connectivity between visual cortex and other regions of the brain in autism: a REM sleep EEG coherence study.

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.

Hemispheric lateralization of the EEG during wakefulness and REM sleep in young healthy adults.

EEG recordings confirm hemispheric lateralization of brain activity during cognitive tasks. The aim of the present study was to investigate spontaneous EEG lateralization under two conditions, waking and REM sleep. Bilateral monopolar EEG was recorded in eight participants using a 12-electrode montage, before the night (5 min eyes closed) and during REM sleep. Spectral analysis (0.75-19.75 Hz) revealed left prefrontal lateralization on total spectrum amplitude power and right occipital lateralization in Delta activity during waking. In contrast, during REM sleep, right frontal lateralization in Theta and Beta activities and right lateralization in occipital Delta activity was observed. These results suggest that spontaneous EEG activities generated during waking and REM sleep are supported in part by a common thalamo-cortical neural network (right occipital Delta dominance) while additional, possibly neuro-cognitive factors modulate waking left prefrontal dominance and REM sleep right frontal dominance.