Methods: Using baseline data from the ongoing SPIN Opioid randomized controlled trial (R01DA054311; PI: McCrae), participants with insomnia, chronic pain, and taking prescribed opioids for their pain (N = 23, x̄ age = 54) completed ~14 days of baseline electronic sleep diaries assessing sleep onset latency (SOL), wake after sleep onset (WASO), pain intensity (0–100), and trauma-related symptoms by asking how much the participant was bothered by their histories of stressful life experiences (bSLE) (0-4). Linear mixed models examined the effects of person-centered daily sleep factors, bSLE, and their interaction on pain intensity.
Results: A significant predictor of pain included the WASO × bSLE interaction (b = −0.03, p = .032), indicating that the association between WASO and pain was stronger at lower levels of trauma-related symptoms and attenuated at higher levels. Main effects of WASO (p = .101) and bSLE (p = .061) were not significant. In the SOL model, bSLE was significantly associated with pain (b = 2.04, p = .049), whereas SOL was not (p = .078). The SOL × bSLE was not significant (p = .114). Random intercepts were included to account for between-person variability in pain, and an autoregressive (AR1) covariance structure was specified to model within-person temporal dependence across days.
Conclusions and Implications: Sleep characteristics demonstrated differential associations with pain at the within-person (daily) level. WASO interacted with daily trauma-related symptoms such that the association between WASO and pain was attenuated at higher levels of trauma-related symptoms, indicating a conditional relationship between WASO and pain. In contrast, SOL was not significantly associated with pain, though it trended toward a positive association, whereas daily trauma-related symptoms were significantly associated with increased pain, suggesting that trauma-related symptoms may represent a more consistent driver of pain at the daily level. Both sleep disturbances and trauma-related symptoms are implicated in central sensitization but may operate through partially distinct mechanisms. Trauma-related processes may engage top-down emotional pathways that amplify fear–pain responses and influence sleep initiation, whereas sleep fragmentation may disrupt physiological mechanisms involved in pain inhibition, contributing to increased pain sensitivity. These findings highlight the importance of developing integrated sleep and trauma-focused interventions for pain reduction. Implications for social work practice include emphasizing non-pharmacological, trauma-informed care for individuals with co-occurring sleep disturbance, trauma-related symptoms, and chronic pain.
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