PURPOSE: Evidence suggests that while the high prevalence of obstructive sleep apnea (OSA) in children with Down syndrome (DS) likely contributes to sleep fragmentation, their poor sleep is only partly attributable to the presence of OSA. We hypothesized that a sleep phenotype exists for DS, which would be independent of OSA and evident across childhood. METHODS: This is a retrospective study of sleep architecture in children with DS together with matched controls. All subjects underwent baseline polysomnography between January 1985 and January 2013. Case-control pairs were compared according to age group. RESULTS: Sleep characteristics were compared in 130 DS subjects aged 0-17.8 years (median 5.8 years) and 130 matched controls. Body mass index z-scores were similar between cases and controls. Compared to controls, children with DS had a lower sleep efficiency and higher percentage of slow-wave sleep at 2-6.9, 7-11.9, and 12-17.9 years (p <0.05 for all) as well as reduced rapid-eye movement (REM) sleep percentage, significant at 7-11.9 years (p <0.05). Children with DS exhibited increased N1 sleep at 2-6.9 years but decreased N1 sleep at 12-17.9 years compared to controls (p <0.05 for both). CONCLUSIONS: Children with DS exhibit altered sleep architecture when compared to non-DS children of similar age and OSA severity. Notably, reduced REM sleep and increased slow-wave sleep was seen independent of OSA in children with DS over 2 years. Amounts of both REM and non-REM sleep may have important implications for learning, memory, and behavior, all the more significant in this population with baseline neurocognitive impairment.
PURPOSE: Evidence suggests that while the high prevalence of obstructive sleep apnea (OSA) in children with Down syndrome (DS) likely contributes to sleep fragmentation, their poor sleep is only partly attributable to the presence of OSA. We hypothesized that a sleep phenotype exists for DS, which would be independent of OSA and evident across childhood. METHODS: This is a retrospective study of sleep architecture in children with DS together with matched controls. All subjects underwent baseline polysomnography between January 1985 and January 2013. Case-control pairs were compared according to age group. RESULTS: Sleep characteristics were compared in 130 DS subjects aged 0-17.8 years (median 5.8 years) and 130 matched controls. Body mass index z-scores were similar between cases and controls. Compared to controls, children with DS had a lower sleep efficiency and higher percentage of slow-wave sleep at 2-6.9, 7-11.9, and 12-17.9 years (p <0.05 for all) as well as reduced rapid-eye movement (REM) sleep percentage, significant at 7-11.9 years (p <0.05). Children with DS exhibited increased N1 sleep at 2-6.9 years but decreased N1 sleep at 12-17.9 years compared to controls (p <0.05 for both). CONCLUSIONS:Children with DS exhibit altered sleep architecture when compared to non-DS children of similar age and OSA severity. Notably, reduced REM sleep and increased slow-wave sleep was seen independent of OSA in children with DS over 2 years. Amounts of both REM and non-REM sleep may have important implications for learning, memory, and behavior, all the more significant in this population with baseline neurocognitive impairment.
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