Individual differences in pain sensitivity are associated with cognitive network functional connectivity following one night of experimental sleep disruption. Issue 3 (16th October 2019)

• Record Type: Journal Article
• Authors: Letzen, Janelle E.; Remeniuk, Bethany; Smith, Michael T.; Irwin, Michael R.; Finan, Patrick H.; Seminowicz, David A.
• Is Part Of: Human brain mapping. Volume 41:Issue 3(2020)
• Page Start: 581
• Page End: 593
• Publication Date: 2019-10-16
• Subjects: default mode network -- executive control network -- neuroimaging -- pain sensitivity -- sleep disruption; Brain mapping -- Periodicals; 611.81
• DOI: 10.1002/hbm.24824
• Languages: English
• ISSNs: 1065-9471

Abstract

Abstract: Previous work suggests that sleep disruption can contribute to poor pain modulation. Here, we used experimental sleep disruption to examine the relationship between sleep disruption‐induced pain sensitivity and functional connectivity (FC) of cognitive networks contributing to pain modulation. Nineteen healthy individuals underwent two counterbalanced experimental sleep conditions for one night each: uninterrupted sleep versus sleep disruption. Following each condition, participants completed functional MRI including a simple motor task and a noxious thermal stimulation task. Pain ratings and stimulus temperatures from the latter task were combined to calculate a pain sensitivity change score following sleep disruption. This change score was used as a predictor of simple motor task FC changes using bilateral executive control networks (RECN, LECN) and the default mode network (DMN) masks as seed regions of interest (ROIs). Increased pain sensitivity after sleep disruption was positively associated with increased RECN FC to ROIs within the DMN and LECN ( F (4, 14) = 25.28, pFDR = 0.05). However, this pain sensitivity change score did not predict FC changes using LECN and DMN masks as seeds ( pFDR > 0.05). Given that only RECN FC was associated with sleep loss‐induced hyperalgesia, findings suggest that cognitive networks only partially contribute to the sleep‐pain dyad.