Abstract
ObjectivesTo evaluate sleep consolidation and circadian activity rhythms in infants and toddlers with Down syndrome (DS) under light and socially entrained conditions within a familiar setting. Given previous human and animal data suggesting intact circadian regulation of melatonin across the day and night, it was hypothesized that behavioral indices of circadian rhythmicity would likewise be intact in the sample with DS. MethodsA cross-sectional study of 66 infants and young children with DS, aged 5–67 months, and 43 typically developing age-matched controls. Sleep and measures of circadian robustness or timing were quantified using continuous in-home actigraphy recordings performed over seven days. Circadian robustness was quantified via time series analysis of rest-activity patterns. Phase markers of circadian timing were calculated alongside these values. Sleep efficiency was also estimated based on the actigraphy recordings. ResultsThis study provided further evidence that general sleep quality is poor in infants and toddlers with DS, a population that has sleep apnea prevalence as high as 50% during the preschool years. Despite poor sleep quality, circadian rhythm and phase were preserved in children with DS and displayed similar developmental trajectories in cross-sectional comparisons with a typically developing (TD) cohort. In line with past work, lower sleep efficiency scores were quantified in the group with DS relative to TD children. Infants born with DS exhibited the worst sleep fragmentation; however, in both groups, sleep efficiency and consolidation increased across age. Three circadian phase markers showed that 35% of the recruitment sample with DS was phase-advanced to an earlier morning schedule, suggesting significant within-group variability in the timing of their daily activity rhythms. ConclusionsCircadian rhythms of wake and sleep are robust in children born with DS. The present results suggest that sleep fragmentation and any resultant cognitive deficits are likely not confounded by corresponding deficits in circadian rhythms.
Highlights
Down syndrome (DS) emerges out of the biological sequelae produced by an extra copy of all or part of human chromosome 21 (Hsa21; trisomy-21) [1]
Non-Parametric Circadian Rhythm Analyses (NPCRA)-intradaily variability (IV) and NPCRAeIS values bore a strong relation to age, but did not distinguish children born with DS from those with a typical genetic background (p > 0.70 and 0.13, respectively; Tables 1 and 2)
The cross-sectional data suggest that children with DS see a remarkable conservation in the development of their circadian rhythms that parallel the developmental course seen in children from a typical genetic background
Summary
Down syndrome (DS) emerges out of the biological sequelae produced by an extra copy of all or part of human chromosome 21 (Hsa; trisomy-21) [1]. In addition to well-documented functional strengths, individuals with this condition face many challenges throughout their lifespan. Soft tissue crowding of the pharynx and palate ensues, which is exacerbated by a posterior displacement of the tongue, enlarged tonsils and adenoids, and medially displaced tonsils that occlude the back of the throat [5e7]. These craniofacial features narrow airflow passage through the upper respiratory tract and, together with decreased pharyngeal muscle tone and airway collapse, result in obstructive sleep apnea syndrome (OSAS) and sleep fragmentation in the majority of individuals with DS [8e13]
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