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Children with autism spectrum disorder (ASD) often have comorbid sleep problems, but our understanding of how sleep dysregulation influences development is still emerging. For children with ASD and sleep dysregulation, previous studies document elevated rates of aggression, repetitive behaviors, emotional outbursts, and attention difficulties (e.g., Goldman et al., 2011). The present study aims to inform a potential physiological indicator/mechanism through which sleep dysregulation may influence daytime behaviors like attention and emotion/arousal modulation. Specifically, this study assesses the associations between sleep dysregulation and electrodermal activity (EDA), an index of sympathetic arousal.
For this study, eight children (mean age of 6.38 years, SD = 2.45) contributed over 57,000 minutes of sleep-wake data and 6,000 minutes of EDA data across five nights and the corresponding treatment days. All children attended a center-based applied behavior analysis program from 08:00 and 17:00 for up to 9 hours per day. Children wore an actigraph to index their wake-sleep patterns for five consecutive 24-hour periods and an Empatica E4 multi-sensor to capture EDA during in-center treatment hours. Child sleep was classified as regulated (n = 4) or dysregulated (n = 4; Figure 1). Children in the regulated group slept more hours per night with less variability across nights (M = 9.39, SD = 1.38) than children in the dysregulated group (M = 6.61, SD = 2.90). EDA signal decomposition provided phasic and tonic indices of sympathetic arousal. For each minute, phasic indices included the number of skin conductance responses (SCR), peak SCR amplitude, and average SCR amplitude.
To assess the associations between sleep dysregulation and daily EDA patterns, a series of ANOVAs were conducted across the regulated and dysregulated sleep groups. In the morning, regulated and dysregulated EDA profiles were comparable. However, in the afternoon children in the dysregulated group had fewer SCRs and tended to have lower SCR amplitude (Table 1). These findings are consistent with the two-process model of sleep which highlights the afternoon (i.e., 14:00-16:00) as a key intersection between circadian and homeostatic sleep pressures (Borbély, 1982). This suggests that children with dysregulated sleep may be able to modulate arousal in the morning; however, in the afternoon homeostatic pressure may contribute to lower attention and arousal modulation, which in turn may impact learning and daytime behavior presentations.
Implications for these findings are two-fold. First, for children with ASD, sleep dysregulation does not appear to influence sympathetic arousal globally, but rather follows a cyclical pattern. Specifically, children are less aroused when homeostatic pressures are high and circadian pressures are low (around 14:00-16:00). SCRs reflect sympathetic arousal to environmental stimuli, and in the context of treatment are associated with attention and emotional responses. Second, from a physiological perspective, the findings of this study best support the use of morning treatment hours for children with ASD and sleep dysregulation. Notably, this is a pilot/feasibility study and replication is needed before clinical recommendations can be made. However, the richness of this physiological study provides a valuable starting point for future work.