Background Children with Down syndrome (DS) are at increased risk of obstructive sleep disordered breathing (SDB), which is associated with sleep disruption affecting daytime functioning. We examined the effects of treatment of SDB on sleep and daytime functioning in children with DS. Methods Children with DS and SDB (n=34) completed a baseline and follow-up study which included 7 days of actigraphy in conjunction with a parental sleep diary. Parents also completed a number of questionnaires assessing sleep, behaviour, daytime functioning and quality of life (QOL). All children had overnight polysomnography (PSG) at baseline and 24 had PSG at follow-up. Results 15 children (44%) were treated. At baseline the treated group had more severe SDB at baseline compared to the untreated group: obstructive apnoea hypopnoea index (OAHI) 29.3 ± 38.2 events/h vs 3.3 ± 5.2 events/h (p<0.01). Actigraphy showed no significant differences in total sleep time or sleep efficiency from baseline to follow up in either the treated or untreated group. Wake after sleep onset increased at follow-up in the untreated group (p<0.01). The sleep disturbance (p<0.01) and total problems (p<0.05) scales on the OSA-18 and the SDB subscale on the Pediatric Sleep Problem Survey Instrument (p<0.01) improved in the treated children. No changes were seen in any of the measures in the untreated children. Conclusions Treatment of SDB improves QOL, despite treatment having no demonstrable impacts on actigraphic sleep measures. In contrast despite having less severe SDB children who were untreated had no improvements in QOL and increased sleep disruption.
Introduction Conventional sleep macro-architecture measures of sleep disruption have not been associated with the adverse neurocognitive sequelae of sleep disordered breathing (SDB). Sleep spindles protecting the sleeping brain from external sensory stimuli and can serve as markers of sleep integrity. We investigated the relationship between sleep spindles and sleep fragmentation and neurocognition across the spectrum of SDB in children. Methods Children 3-12y referred for clinical assessment of SDB and age matched control children from the community were recruited. Sleep spindles were identified manually during N2 and N3 sleep. Spindle activity was characterised as spindle number, spindle density (number of spindles/ h) and spindle intensity (spindle density x average spindle duration). The Stanford-Binet Intelligence Scales measured global intellectual ability and the NeuroPSYchological assessment (NEPSY-II) measured language, attention, visuospatial ability and sensorimotor skills. Results Children were grouped into control, Primary Snoring, Mild OSA and Moderate/severe OSA, N=10/ group. All measures of spindle activity were lower in the SDB groups compared to the Control children and this reached statistical significance for Mild OSA (p<0.05 for all). Spindle activity was not correlated with any measure of the Stanford-Binet. Overall, all measures of spindle activity were positively correlated with the Design Copy and the Inhibition Naming combined scale score and negatively correlated with Auditory Attention subscales of the NEPSY-II. Conclusion The reduced spindle activity observed in the children with SDB, particularly Mild OSA, indicates that sleep micro-architecture is disrupted and that this disruption may underpin the negative effects of SDB on attention, learning and memory.
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