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Night-to-Night Changes in REM Sleep Are Associated With Symptom Severity in Children With Autism Spectrum Disorder: A
Jian Jiao1, Hang Zhang1, Xia Yang1
1Sleep Medicine Center, Mental Health Center, National Center for Mental Disorders, Sleep Research Laboratory, West China Hospital, Sichuan University, Chengdu, China.
None:
Sleep disturbances are highly prevalent in autism spectrum disorder (ASD), yet conventional single-night polysomnography (PSG) provides limited insight into dynamic sleep regulatory processes. Using the Synaptic Homeostasis Hypothesis as a conceptual framework, we quantified night-to-night changes (Δ; Night 2 - Night 1) in sleep architecture across two consecutive nights of home-based PSG and examined their association with ASD symptom severity. Seventy-nine children with ASD, stratified into mild ASD (M-ASD, n = 35) and moderate-to-severe ASD (MS-ASD, n = 44) subgroups using the Childhood Autism Rating Scale, and 30 typically developing controls (TDC) participated. Overall sleep-continuity changes were broadly comparable between ASD and TDC groups. However, sleep-architecture Δ measures showed a severity-related pattern: the M-ASD subgroup exhibited an overnight increase in rapid eye movement sleep percentage (ΔREM% = +2.6%, p = 0.002), whereas the MS-ASD subgroup showed no significant change (ΔREM% = -0.1%, p = 0.922). An adjusted pairwise comparison indicated a greater ΔREM% increase in M-ASD than in MS-ASD (adjusted mean difference = 3.4%, 95% CI: 1.2 to 5.6; Bonferroni-corrected p = 0.009). A similar exploratory difference was observed for NREM1%. ΔREM% was modestly and negatively associated with ASD symptom severity in correlation analysis (ρ = -0.234, p = 0.038) and age- and gender-adjusted regression analysis (β = -0.286, p = 0.016). Sensitivity analyses showed broadly consistent patterns, although severity-stratified overall effects were attenuated after FDR correction. These findings support further investigation of PSG-derived dynamic sleep measures as hypothesis-generating correlates of clinical heterogeneity in ASD.
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