Abstract

Abstract Introduction Functional Abdominal Pain Disorders (FAPD), in which chronic abdominal pain occurs independently of organic pathology, are common in adolescents. FAPD can lead to significant impairment in daytime function and may overlap with sleep disorders. Though several studies have explored the nature of sleep disturbances experienced by adolescents with FAPD, none have characterized differences in sleep architecture in this population. Methods Adolescents (age 11-18 years) with FAPD and age/gender-matched controls were prospectively recruited to undergo polysomnography (PSG). PSG was performed according to AASM guidelines, scored by a registered sleep technologist, and interpreted by a board-certified sleep physician. 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. Comparisons between groups were made using Wilcoxon rank sum tests or t-tests for non-normal and normal data, respectively. Results A total of 41 subjects were recruited (FAPD n=21, control n=20). The FAPD group had a greater arousal index and a lower percentage of NREM 3 sleep when compared to the control group (FAPD arousals: mean=10.08/min ± 4.89 min, control arousals mean=7.31/min ± 3.61/min, p = 0.046), FAPD NREM 3: mean=20.13% ± 5.47%, control NREM 3: mean=24.77% ± 6.94%, p =0.023). 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). Conclusion This study demonstrates significant differences in sleep architecture of adolescents with FAPD compared to their peers. In particular, decreased proportions of NREM 3 sleep and lower Delta power are indicative of diminished slow wave sleep (SWS). 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. Further research is indicated. Support (if any) This research is supported by the Cincinnati Children’s Research Foundation and the Summer Medical Student Respiratory Research Fellowship program at Cincinnati Children’s.

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