The relation between sleep and pain sensitization in pediatric sickle cell disease.

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Title: The relation between sleep and pain sensitization in pediatric sickle cell disease.
Authors: Kell, Parker A (AUTHOR), Morris, Matthew C (AUTHOR), Wilde, Zachary C (AUTHOR), Golden, Andrea P (AUTHOR), Dickens, Harrison (AUTHOR), Williams-Kirkwood, Wynette (AUTHOR), Ford, Hannah A (AUTHOR), Karlson, Cynthia W (AUTHOR)
Source: Journal of Pediatric Psychology. Feb2026, Vol. 51 Issue 2, p134-143. 10p.
Subjects: Sleep, Sickle cell anemia, Pain measurement, Chronic pain, Nociceptors, Hyperalgesia
Abstract: Objective Sickle cell disease (SCD) is an inherited blood disorder characterized by acute pain crises and heightened chronic pain prevalence. Approximately 30%–40% of pediatric patients with SCD have chronic pain, contributing to poorer psychosocial outcomes. Central sensitization (central nervous system hyperexcitability) may heighten chronic SCD pain, yet few investigations have examined factors related to central sensitization in pediatric SCD. Sleep has been identified as a modifiable factor that may influence central sensitization and contribute to pain outcomes in both chronic pain-free and clinical populations. Methods Our study examined the role of sleep in relation to central sensitization in 55 participants (26 girls: mean age = 16.43 years) with severe SCD genotypes (hemoglobin Type SS n  = 54, Type S beta-zero thalassemia n  = 1). Mean-level and within-person variability sleep indices were measured at home over 7 days using wrist actigraphy and daily sleep diaries. To measure central sensitization, participants completed one session of quantitative sensory testing. Conditioned pain modulation (CPM) (n  = 34) assessed endogenous pain inhibition, and temporal summation (n  = 39) assessed pain facilitation. Multilevel models assessed pain ratings for each task. Results When controlling for age, sex assigned at birth, and task unpleasantness, lower actigraphy-derived sleep efficiency was associated with worse pain inhibition during CPM. Sleep was unrelated to pain facilitation during temporal summation. Conclusions Findings provide further evidence linking poor sleep to increased pain via impaired pain inhibition but may be best captured using objective sleep measures in pediatric SCD. Interventions aimed at improving sleep efficiency may have downstream effects on clinical pain in this population. [ABSTRACT FROM AUTHOR]
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Database: Psychology and Behavioral Sciences Collection
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