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Study Objectives: To evaluate non-rapid eye movement sleep instability (NREM), as measured by the cyclic alternating pattern (CAP), in a cohort of children with attention-deficit/hyperactivity disorder (ADHD) and normal controls., Design: Prospective study., Settings: Sleep laboratory., Participants: Twenty consecutive outpatients with ADHD (18 boys and 2 girls; age range 6-13 years, mean age 9.3 years) and 20 normal children matched for age and socioeconomic status underwent polysomnographic recordings for 2 consecutive nights in a standard laboratory setting. Sleep was visually scored for sleep macrostructure and CAP, according to standard criteria., Measurements and Results: Children with ADHD showed significantly reduced sleep duration and increased rate of stage shifts. All children with ADHD had an apnea-hypopnea index less than 1. Those with ADHD presented lower total CAP rates and lower CAP rates during sleep stage 2 than did normal controls. Moreover, in children with ADHD, we found a lower number of CAP sequences and a reduced total A1 index, mainly in light sleep (sleep stages 1 and 2). We did not find differences in A subtype percentages, but there was a longer duration of A1 subtypes in children with ADHD., Conclusions: Children with ADHD showed a lower CAP rate and a lower number of CAP sequences; this supports the hypothesis of the existence of a hypoarousal state in these patients.

Exposure to intermittent hypoxia, such as occurs in sleep-disordered breathing, is associated with oxidative stress, cognitive impairments, and increased neuronal apoptosis in brain regions involved in learning and memory. Apolipoprotein E (ApoE) has been implicated in neurodegenerative disorders, and in vitro studies suggest that one of the functions of ApoE may be to confer protection from oxidant stress-induced neuronal cell loss. Therefore, we hypothesized that ApoE-deficient (ApoE-/-) mice would display increased cognitive impairments following intermittent hypoxia. Twenty-four young adult male mice (ApoE-/-) and 24 wild-type littermates (ApoE +/+) were exposed to 14 days of normoxia (room air; n=12 per group) or intermittent hypoxia (5.7% O2 alternating with 21% O2 every 90 seconds, 12 daylight hours per day; n=12 per group). Behavioral testing consisting of a standard place-training reference memory task in the water maze revealed that ApoE+/+ and ApoE-/- mice exposed to intermittent hypoxia were found to require significantly longer times (latency) and distances (pathlength) to locate the hidden platform (P < .005), compared to mice exposed to room air. However, only intermittent hypoxia-exposed ApoE-/- mice were impaired on the final two days of training (P < .03), as well as on measures of spatial bias conducted 24 hours after completion of training (P < .02). Furthermore, increased prostaglandin E2 and malondiadehyde concentrations were present in hippocampal brain tissues following intermittent hypoxia but were significantly higher in ApoE-/- mice (P < .01). Thus, decreased ApoE function is associated with increased susceptibility to neurocognitive dysfunction in a rodent model of sleep-disordered breathing and may underlie the increased prevalence of Apolipoprotein E4 in patients with sleep-disordered breathing.