0911 Characterization of Sleep Architecture and Other Sleep Biomarkers in Adolescents with Functional Abdominal Pain

Abstract Introduction Functional Abdominal Pain Disorders (FAPD) are associated with significant functional disability and sleep disturbances. To date, no studies have characterized differences in sleep architecture and sleep spindles, the representation of the thalamic gating function of sensory information to the cortex during Non-Rapid Eye Movement (NREM) sleep, in pediatric FAPD. We aimed to examine sleep architecture and sleep spindles in adolescents with FAPD compared to healthy controls. Methods Adolescents (age 11-18 years) with FAPD and age/gender-matched controls underwent polysomnography (PSG) according to AASM guidelines. The first four hours of artifact-free NREM sleep were analyzed using fast Fourier transformation with Welch tapered windows of 1024 samples (and 50% overlap) averaged over 30-second epochs. Total power was calculated for very low (0.3 – 1 Hz), delta (1 – 4 Hz), theta (4 – 8 Hz), and alpha (8-12 Hz) frequencies. Sleep spindles were characterized using the YASA python package / A7 algorithm with selections confirmed against gold standard (manual scoring). Results Of 41 subjects (FAPD=21, control=20), the FAPD group had greater arousal index and lower %NREM3 sleep when compared to controls (FAPD arousals: mean=10.08/min ± 4.89 min, control arousals mean=7.31/min ± 3.61/min, p = 0.046, FAPD NREM3: mean=20.13% ± 5.47%, control NREM3: mean=24.77% ± 6.94%, p =0.02). Delta power was significantly lower in the FAPD group compared to controls (FAPD Delta mean=488.67 μV2 ± 282.82 μV2, control Delta mean=1193.14 μV2 ± 663.89 μV2, p < 0.001). During NREM2 sleep, the FAPD group had significantly greater spindle density over frontal head regions than controls (FAPD: 2.80/min ±1.39/min, control: 1.86/min ±1.35/min, p = 0.04). Conclusion Children with FAPD have greater sleep spindle density, higher arousal indices, decreased proportions of NREM3 sleep and lower Delta power, indicative of diminished slow wave sleep (SWS) compared to healthy peers. Reductions in SWS may be indicative of common neurotransmitter pathways shared between sleep and chronic pain syndromes, or secondary to sleep disruption associated with pain. Future studies can assess the impact of these changes on GI symptoms and psychological functioning in this population. Support (if any)