Sleep Spindles and K-Complexes: EEG Markers of Poor Sleep in Autism?

Thursday, May 17, 2012
Sheraton Hall (Sheraton Centre Toronto)
11:00 AM
S. M. Duplan1, M. Chicoine2, C. Berthiaume3, E. Chevrier4, L. Mottron5,6,7,8,9 and R. Godbout4,10,11, (1)Sleep Laboratory and Clinic, Hôpital Rivière-des-Prairies, Montréal, QC, Canada, (2)Hôpital Rivière-des-Prairies, Montréal, QC, Canada, (3)Hopital Riviere-des-Prairies, Montreal, QC, Canada, (4)Sleep Laboratory & Clinic, Hôpital Rivière-des-Prairies, Montréal, QC, Canada, (5)Autism Excellence Center, Hôpital Rivière-des-Prairies, Montréal, QC, Canada, (6)Psychiatry, Université de Montréal, Montréal, QC, Canada, (7)Centre d'excellence en Troubles envahissants du développement de l'Université de Montréal (CETEDUM), Montreal, QC, Canada, (8)Centre d'excellence en Troubles envahissants du développement de l’Université de Montréal (CETEDUM), Montreal, QC, Canada, (9)Psychiatry, University of Montreal, Montréal, QC, Canada, (10)Psychiatry, Universite de Montreal, Montreal, QC, Canada, (11)7070 Boul. Perras, Sleep Laboratory & Clinic, Montreal, QC, Canada
Background: Sleep recording of adults with Autism Spectrum Disorders (ASD) show signs of poor sleep, including long latencies to sleep onset and frequent nocturnal awakenings. Sleep spindles and K-complexes are EEG phasic events thought to reflect sleep protective mechanisms that inhibit the processing of potentially arousing stimuli. 

Objectives: To evaluate sleep protective mechanisms in children and adult autistics through the quantification and scalp distribution of EEG sleep spindles and K-complexes.  

Methods: Twenty-nine individuals with ASD (16 adults: 14 M, 2 F, 22.1 ± 1.3 years; 13 boys, 10.7 ± 1.9 years) with normal IQ and a comparison group of 31 typically developed participants (TD; 18 adults: 17 M, 1 F, 21.1 ± 1.0 years; 13 boys, 9.8 ± 2.2 years) were recorded for two consecutive nights in a sleep laboratory. Sleep spindles were recorded in children and adults using a central (C3) and a frontal (Fp1) electrode and visually identified as bursts of EEG activity at 12-14 Hz, lasting 0.5 to 2.0 seconds. K-complexes were scored in adults only, using a 14-electrodes montage and defined as negative-going biphasic waves with sharp onset and smoother offset, lasting 0.5 to 1.5 seconds, with an amplitude of at least 75 µV. Spectral analysis of the EEG 2 seconds before and 2 seconds after K-complexes was performed and spectral power was calculated for delta (0.5-3.5 Hz), theta (4.0-7.5 Hz), alpha (8.0-12.5 Hz) and beta (13.0-30.0 Hz) frequency bands.  

Results: Sleep spindles in adults were less in the ASD group than in the TD group at the central (C3), not the frontal (Fp1) electrode. No differences were found in children. K-complexes were significantly less in the adult ASD group compared to the TSD group at the parietal and occipital recording sites. Spectral analysis of the EEG showed, however, that K-complexes were followed in both group by an increase in delta activity.  

Conclusions: These data suggest that cortical sleep protective mechanisms are impaired in autism, particularly in centro-posterior regions. The fact that EEG delta activity was increased in both groups following K-complexes suggests that the problem do not reside in the capacity per se of EEG events to keep the brain asleep but rather their topographical distribution. More electrodes need to be analyzed in children in order to test the hypothesis of an atypical developmental course.  

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