A growing body of evidence indicates that people with autism frequently experi ence sleep disorders and exhibit atypical sleep architecture. In order to establ ish whether sleep disorders truly belong to the autism spectrum disorder (ASD) p henotype, we conducted a subjective and objective study of sleep in a group of h igh-functioning adults with ASD but without sleep complaints, psychiatric disor ders or neurological comorbidity. We compared the subjective data of 27 ASD part icipants with those of 78 healthy controls matched for chronological age and gen der. Subjective measures of sleep in the clinical group were compatible with ins omnia 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 patie nts 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 m ovements during MEM sleep (P < 0.006) than did control participants. On clinical scales, the scores of persons with ASD on the Beck Depression Inventory were si milar to those of persons without, but their trait anxiety scores on the Spielbe rger Anxiety Scale were higher (P < 0.02). The state anxiety scores of the Spiel berger scale and cortisol levels were the same in the two groups. Objective tota l sleep time correlated negatively with the Social (-0.52, P < 0.05) and Commun ication (-0.54, P < 0.02) scales of the Autism Diagnostic Interview-Revised. T he sleep of clinical subgroups (10 with high-functioning autism, six with Asper ger syndrome) did not differ, except for the presence of fewer EEG sleep spindle s in the Asperger syndrome subgroup (P < 0.05). In conclusion, these findings in dicate 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 su bserving the macro-and microstructure of sleep in ASD. We are furthering this r esearch with quantified araalysis of sleep EEG. A growing body of evidence that that with autism often experi ence sleep disorders and exhibit atypical sleep architecture. In order to establ ish whether sleep disorders truly belongs to the autism spectrum disorder (ASD) p henotype, we conducted a subjective and objective study of sleep in a group of h igh-functioning adults with ASD but without sleep complaints, psychiatric disor ders or neurological comorbidity. We compared the subjective measures of 27 ASD part icipants with those of 78 healthy controls matched for chronological age and gen der. of sleep in the clinical group were compatible with ins omnia 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 <0.004), and a lower number of rapid eye m ovements during MEM sleep (P <0.006) than did control participants. On clinical scales, the scores of persons with ASD on the Beck Depression Inventory were si milar to those of persons without, but their trait anxiety scores on the Spielbeger Anxiety Scale were higher (P <0.02). The state anxiety scores of the Spiel berger scale and cortisol levels were the same in the two groups. Objective tota l 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. T he sleep of clinical subgroups (10 with high-functioning autism, six with Asperger syndrome) did not differ , except for the presence of fewer EEG sleep spindle s in the Asperger syndrome subgroup (P <0.05). In conclusion, these findings in dicate 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 su bserving the macro-and microstructure of sleep in ASD We are furthering this r esearch with quantified araalysis of sleep EEG.