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ObjectivesMindfulness-based interventions (MBIs) have emerged as promising prophylactic episodic migraine treatments. The present study investigated biopsychosocial predictors and outcomes associated with formal, daily-life meditation practice in migraine patients undergoing MBI, and whether augmented mindfulness mechanistically underlies change.MethodsSecondary analyses of clinical trial comparing data 12-week mindfulness-based stress reduction (MBSR+; n = 50) to stress management for headache (SMH; n = 48) were conducted.ResultsPre-treatment mesocorticolimbic system functioning (i.e., greater resting state ventromedial prefrontal cortex-right nucleus accumbens [vmPFC-rNAC] functional connectivity) positively predicted meditation practice duration over MBSR+ (r = .58, p = .001), and moderated change in headache frequency from pre to post-treatment (b = -12.60, p = .02) such that patients with greater vmPFC-rNAC connectivity showed greater reductions in headache frequency. Patients who meditated more showed greater increases in mindfulness (b = .52, p = .02) and reductions in the helplessness facet of pain catastrophizing (b = -.13, p = .01), but not headache frequency, severity or impact. Augmented mindfulness mediated reductions in headache impact resulting from MBSR+, but not headache frequency.ConclusionsMesocorticolimbic system function is implicated in motivated behavior, and thus could be a target of augmentative interventions designed to enhance meditation practice engagement. Meditation practice appears to benefit pain-related cognitions, but not clinical pain, while mindfulness emerges as a mechanism of MBIs on headache impact, but not frequency. Further research is needed to investigate the day-to-day effects of meditation practice on pain, and continue to characterize the specific mechanisms of MBIs on headache outcomes.

Formal training in mindfulness-based practices promotes reduced experimental and clinical pain, which may be driven by reduced emotional pain reactivity and undergirded by alterations in the default mode network (DMN), implicated in mind-wandering and self-referential processing. Recent results published in this journal suggest that mindfulness, defined here as the day-to-day tendency to maintain a non-reactive mental state in the absence of training, associates with lower pain reactivity, greater heat-pain thresholds, and resting-state DMN functional connectivity (FC) in healthy adults in a similar manner to trained mindfulness. The extent to which these findings extend to chronic pain samples and replicate in healthy samples is unknown. Using data from healthy adults (n = 36) and episodic migraine patients (n = 98) and replicating previously published methods, we observed no significant association between mindfulness and heat-pain threshold (r = -0.05, p = .80), pain intensity (r = -.02, p = .89) or unpleasantness (r = .02, p = .89), or pain catastrophizing (PC; r = .30, p = .08) in healthy controls, or between mindfulness and headache frequency (r = -.11, p = .26), severity (r = .03, p = .77), impact (r = -.17, p = .10) or PC (r = -0.09, p = .36) in patients. There was no association between DMN connectivity and mindfulness in either sample when probed via seed-based FC analyses. In post-hoc whole brain exploratory analyses, a meta-analytically derived DMN node (i.e., posterior cingulate cortex; PCC) showed connectivity with regions unassociated with pain processing as a function of mindfulness, such that healthy adults higher in mindfulness showed greater PCC-cerebellum FC. Collectively, these findings suggest that the relationship between mindfulness and DMN-FC may be nuanced or lacking in robustness, and cast doubt on mindfulness as a clinically meaningful protective factor in migraine.PerspectiveThis study tested relationships between mindfulness and pain, pain reactivity and default mode connectivity in healthy adults and migraine patients. Findings cast doubt on mindfulness as an individual difference marker of the ability to cope with pain in healthy adults, and as a protective factor in episodic migraine.

Existing data demonstrate reduced delta power during sleep in patients with depression and chronic pain. However, there has been little examination of the relationship between delta power and pain-reports, or pain-catastrophizing. We recruited female participants (n = 111) with insomnia and temporomandibular disorder, and measured nocturnal and daytime measures of pain and pain catastrophizing, and calculated relative nocturnal delta (0.5-4 Hz) power during sleep. We fit linear regression models, and further examined the moderating effect of depressive symptom severity. Lower relative delta power across the whole night was significantly associated with greater nocturnal pain (B = -20.276, P = .025, R

Approximately 2.7 million individuals in the United States had an opioid use disorder (OUD) in 2020. Chronic pain may exacerbate opioid withdrawal severity, yet most research on opioid withdrawal has not collected data on chronic pain status. Moreover, there is limited evidence that women tend to experience greater opioid withdrawal severity than men, but large, confirmatory studies on this topic have not been published. The goal of this study was to examine the roles of chronic pain and gender on opioid withdrawal severity using a large, multi-site database.Data were collected from N = 1252 individuals with OUD entering eight residential addiction treatment facilities. Demographic, drug use behaviors, and chronic pain status were collected at treatment intake, and self-reported opioid withdrawal and craving were measured at intake and 1-3 days, 4-6 days, and 7-9 days after intake. Regression analyses were used to predict withdrawal and craving severity at intake and across the four timepoints.At intake, withdrawal was higher in persons who were older, had greater SUD severity, women, had chronic pain, and used 1 substance (p-values ≤.007) and craving was higher in persons with greater SUD severity (p .001) and women (p = .033). Withdrawal remained higher in women and persons with chronic pain across timepoints but decreased at a similar rate relative to comparators.Women and persons with chronic pain would benefit from earlier engagement in treatment and may require a more intensive strategy to mitigate opioid withdrawal in early treatment.

Objectives: Osteoarthritis, a chronic degenerative joint disorder, is characterized by joint pain. Emerging research demonstrates that a significant number of patients evidence central sensitization (CS), a hyper-excitability in nociceptive pathways, which is known to amplify and maintain clinical pain. The clinical correlates of CS in OA, however, are poorly understood. Insomnia is prevalent in older adults with OA and recent experiments suggest associations between poor sleep and measures of CS. Catastrophizing, a potent predictor of pain outcomes has also been associated with CS, but few studies have investigated possible interactions between catastrophizing, sleep and CS. Methods: We conducted a case controlled study of 4 well characterized groups of adults with insomnia and/or knee osteoarthritis. A total of 208 participants completed multimodal sleep assessments (questionnaire, diary, actigraphy, polysmnography) and extensive evaluation of pain using clinical measures and quantitative sensory testing to evaluate associations between CS, catastrophizing and insomnia. Descriptive characterization of each measure is presented, with specific focus on sleep efficiency and CS. Results: The KOA-Insomnia group demonstrated the greatest degree of CS compared to controls. In the overall sample, we found that catastrophizing moderated the relationship between sleep efficiency and CS. Specifically those with low sleep efficiency and high catastrophizing scores reported increased levels of CS. In addition, CS was significantly associated with increased clinical pain. Conclusions: These findings highlight the importance of assessing sleep efficiency, CS and catastrophizing in chronic pain patients and have important clinical implications for treatment planning.