Abstract

Experimental forced nocturnal awakenings increases next-day pain sensitivity and attenuates the degree to which affect modulates pain in healthy individuals. Naturalistic measures of sleep disruption have also linked to pain in patients with sickle cell disease. The aims of the present analysis were to examine interactions between nightly indices of naturalistic sleep disruption (nocturnal awakenings and minutes of wake after sleep onset(WASO)) and interactions between daily positive affect (PA) or negative affect (NA) and pain in patients with sickle cell disease. Individuals with sickle cell disease and daily pain (N=25, Mage=42.0) completed daily sleep diaries and reports of pain, PA, NA, and prescription opioid use. A total of 366 days were included in the analysis (M per participant=14.64). We examined whether sleep disruption variables moderated the relationship between affective variables (daily PA or NA) and pain using mixed models. Simple-slopes analyses were used to probe significant interactions. All models controlled for person-level opioid morphine milligram equivalents (MME, M=81.30). Daily PA (Bs> -0.16, ps<.002) and NA (Bs> 0.28, ps<.001) were associated with daily pain. Number of previous night awakenings moderated the effect of PA on daily pain (B=-0.15, p=.002), such that the association of low PA with elevated daily pain was stronger when nocturnal awakenings were more frequent. Awakenings did not moderate the effect of NA on pain. WASO predicted next-day pain in the PA model (B=0.004, p=.022), but not the NA model (p=.053), and did not interact with PA or NA to predict pain. These findings demonstrate that the elevation in pain observed under conditions of low PA is amplified following nights of disrupted sleep. This naturalistic study extends results from experimental studies to daily life and suggests that the effects of sleep, affect, and pain are better characterized through their interactions than their individual associations. Grant support from NINDS 3U54EB020404-05S1 JDE: NIDA T32DA007209, (PI = E. Stain, E. Weerts, G. Bigelow) CH, MS: NINDS T32NS070201, (PI = M. Smith). Experimental forced nocturnal awakenings increases next-day pain sensitivity and attenuates the degree to which affect modulates pain in healthy individuals. Naturalistic measures of sleep disruption have also linked to pain in patients with sickle cell disease. The aims of the present analysis were to examine interactions between nightly indices of naturalistic sleep disruption (nocturnal awakenings and minutes of wake after sleep onset(WASO)) and interactions between daily positive affect (PA) or negative affect (NA) and pain in patients with sickle cell disease. Individuals with sickle cell disease and daily pain (N=25, Mage=42.0) completed daily sleep diaries and reports of pain, PA, NA, and prescription opioid use. A total of 366 days were included in the analysis (M per participant=14.64). We examined whether sleep disruption variables moderated the relationship between affective variables (daily PA or NA) and pain using mixed models. Simple-slopes analyses were used to probe significant interactions. All models controlled for person-level opioid morphine milligram equivalents (MME, M=81.30). Daily PA (Bs> -0.16, ps<.002) and NA (Bs> 0.28, ps<.001) were associated with daily pain. Number of previous night awakenings moderated the effect of PA on daily pain (B=-0.15, p=.002), such that the association of low PA with elevated daily pain was stronger when nocturnal awakenings were more frequent. Awakenings did not moderate the effect of NA on pain. WASO predicted next-day pain in the PA model (B=0.004, p=.022), but not the NA model (p=.053), and did not interact with PA or NA to predict pain. These findings demonstrate that the elevation in pain observed under conditions of low PA is amplified following nights of disrupted sleep. This naturalistic study extends results from experimental studies to daily life and suggests that the effects of sleep, affect, and pain are better characterized through their interactions than their individual associations. Grant support from NINDS 3U54EB020404-05S1 JDE: NIDA T32DA007209, (PI = E. Stain, E. Weerts, G. Bigelow) CH, MS: NINDS T32NS070201, (PI = M. Smith).

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