0215 The Role of Adverse Childhood Experiences in the Relationship Between Experimental Sleep Disruption and Pain in Healthy Young Adults

Abstract Introduction Adverse Childhood Experiences (ACEs) increase risk for insomnia and chronic pain, but it remains unknown whether ACEs influence the relationship between sleep and pain. We examined whether experimental sleep disturbances alter suprathreshold heat pain as a function of ACEs. Methods Following baseline, 68 healthy, pain-free, good sleepers (M Age = 30.5; 66.2% female) were randomly assigned in a parallel arm experiment to: Sleep Continuity Disruption [SCD (n = 24)]; Sleep Fragmentation [SF (n = 22)] or Undisturbed Sleep [US ( n = 22)] for two nights. SCD involved 8-hourly forced awakenings (7, 20-mins. and 1, 60-min). SF involved auditory and vibrotactile stimulation to induce microarousals (~42/hr.) The morning following the second sleep condition, participants completed PET neuroimaging, during which we administered suprathreshold heat pain to the ventral forearm for 45-minutes. Pain intensity was rated each minute. Thermode temperature was preset, individually tailored at baseline to yield moderate pain (40/100). Results None of the conditions differed on baseline sleep continuity and architecture (p > .05). SCD demonstrated significantly reduced TST (~45%), N3 and REM mins compared to US (p < .001). SF demonstrated a two-fold increase in the arousal index and N1 mins compared to US and SCD (p<.001), but TST and continuity were preserved. At baseline, all conditions achieved comparable pain40 ratings with no differences by ACEs (p = .69). The prevalence of reporting at least one ACE did not differ across conditions (SCD = 60.0%, SF = 50.0%, US = 55.6%; p = .83). Among participants without ACEs, multilevel models controlling for pain40 temperature, yielded a significant group X time interaction, such that pain intensity increased in SCD compared to US (p < .05). Participants with ACEs, however exhibited an opposite pattern. SCD reported lower pain intensity (p = .06) and no sleep condition X time interaction (p = .22). There were no alterations in pain in SF compared to controls, regardless of ACEs (p > .52). Conclusion ACEs may influence the effects of sleep disruption on suprathreshold pain. The presence of at least one ACE conferred resilience to the hyperalgesic effects of SCD on pain sensitivity. Support (if any) NIH/NHLBI 1U01 HL150568 (MTS)