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Introduction: Chronic pain is highly prevalent in US military Veterans. Non-opioid and non-pharmacologic treatments are recommended when clinically appropriate, but research on the mechanisms underlying benefits of these treatments is lacking. Here, we examined the role of sleep in the effects of three non-pharmacologic pain treatments in Veterans. Specifically, we investigated whether treatment effects on sleep predicted treatment effects on pain occurring later, or vice versa. Methods: Veterans enrolled in a randomized controlled trial were invited to participate in this supplementary sleep study. A total of 174 Veterans were randomized to one of three 8-session, in-person, group-based pain treatments: hypnosis, mindfulness meditation, or education control. Measurements included self-reported sleep disturbance, pain intensity, and pain catastrophizing; sleep duration was assessed with actigraphy. Sleep and pain measurements were obtained at baseline, posttreatment, and 3-month posttreatment follow-up. Results: At baseline, average pain intensity was moderate (mean ± SD: 5.7 ± 1.7 on the 0-10 Numeric Rating Scale), pain catastrophizing was just below the clinically relevant threshold (mean ± SD: 28.6 ± 12.2 on the Pain Catastrophizing Scale), and subjective sleep disturbance exceeded the US population average (mean ± SD: 58.5 ± 8.1 on the Patient Reported Outcomes Measurement Information System Sleep Disturbance - Short Form). By contrast, objective sleep duration was consistent with the recommended daily sleep amount of 7-8 h for adults (mean ± SD: 8.3 ± 1.4 h). Across treatment conditions, pain intensity, pain catastrophizing, and subjective sleep disturbance were significantly less at posttreatment and 3-month follow-up than at baseline (p < 0.001). Actigraphic sleep duration did not differ significantly as a function of time. There was a high degree of covariation among the measures of pain intensity, pain catastrophizing, and sleep disturbance (p < 0.05). However, self-reported sleep disturbance was not significantly correlated with actigraphic sleep duration (|r| <= 0.13, p > 0.05). Sleep and pain variables observed at prior assessments predicted these same variables at subsequent assessments. There was no significant evidence that changes in pain preceded changes in sleep or that changes in sleep preceded changes in pain (all p > 0.05). Discussion: For this study's Veterans, treatment-related changes in sleep and pain appeared to occur in parallel. The concomitant changes in sleep and pain suggest that therapies improving pain in Veterans may yield attendant benefits for the treatment of sleep, and possibly vice versa.
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Neurobehavioral task performance is modulated by the circadian and homeostatic processes of sleep/wake regulation. Biomathematical modeling of the temporal dynamics of these processes and their interaction allows for prospective prediction of performance impairment in shift-workers and provides a basis for fatigue risk management in 24/7 operations. It has been reported, however, that the impact of the circadian rhythm-and in particular its timing-is inherently task-dependent, which would have profound implications for our understanding of the temporal dynamics of neurobehavioral functioning and the accuracy of biomathematical model predictions. We investigated this issue in a laboratory study designed to unambiguously dissociate the influences of the circadian and homeostatic processes on neurobehavioral performance, as measured during a constant routine protocol preceded by three days on either a simulated night shift or a simulated day shift schedule. Neurobehavioral functions were measured every 2 h using three functionally distinct assays: a digit symbol substitution test, a psychomotor vigilance test, and the Karolinska Sleepiness Scale. After dissociating the circadian and homeostatic influences and accounting for inter-individual variability, peak circadian performance occurred in the late biological afternoon (in the "wake maintenance zone") for all three neurobehavioral assays. Our results are incongruent with the idea of inherent task-dependent differences in the endogenous circadian impact on performance. Rather, our results suggest that neurobehavioral functions are under top-down circadian control, consistent with the way they are accounted for in extant biomathematical models.
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INTRODUCTION: Veterans with chronic pain frequently report comorbid disruptions in sleep and psychological dysfunction. The purpose of this study was to investigate whether psychological function variables mediate the sleep-pain relationship. Knowledge regarding such contributing factors can inform the development and optimization of treatments for sleep disturbances and pain. MATERIALS AND METHODS: In an IRB-approved, registered clinical trial, we collected objective sleep data from U.S. military Veterans with chronic pain (N = 184, ages 23-81) using wrist actigraphy for 7 days and self-reported survey data assessing sleep quality, pain intensity, and psychological function (depression, anxiety, post-traumatic stress disorder, and pain catastrophizing). We investigated the associations between objectively measured and self-reported sleep quality and self-reported pain intensity. In addition, using parallel mediation analyses, we examined whether psychological function variables mediated these associations. RESULTS: Actigraphy showed suboptimal sleep duration (less than 7 hours) and sleep fragmentation for most participants. Self-reported poor sleep quality and pain intensity were significantly correlated. Pain catastrophizing was found to mediate the association between self-reported sleep quality and pain intensity. CONCLUSIONS: Sleep disturbances in this sample of Veterans with chronic pain included insufficient sleep, fragmented sleep, and perceived poor sleep quality. Analyses suggest that poor perceived sleep quality and pain intensity are mediated via pain catastrophizing. The finding highlights the potential importance of pain catastrophizing in Veterans with chronic pain. Future longitudinal research is needed to determine the extent to which treatments that reduce pain catastrophizing might also improve both sleep and pain outcomes.
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In shift work settings and on-call operations, workers may be at risk of sleep inertia when called to action immediately after awakening from sleep. However, individuals may differ substantially in their susceptibility to sleep inertia. We investigated this using data from a laboratory study in which 20 healthy young adults were each exposed to 36 h of total sleep deprivation, preceded by a baseline sleep period and followed by a recovery sleep period, on three separate occasions. In the week prior to each laboratory session and on the corresponding baseline night in the laboratory, participants either extended their sleep period to 12 h/day or restricted it to 6 h/day. During periods of wakefulness in the laboratory, starting right after scheduled awakening, participants completed neurobehavioral tests every 2 h. Testing included the Karolinska Sleepiness Scale to measure subjective sleepiness, for which the data were analyzed with nonlinear mixed-effects regression to quantify sleep inertia. This revealed considerable interindividual differences in the magnitude of sleep inertia, which were highly stable within individuals after both baseline and recovery sleep periods, regardless of study condition. Our results demonstrate that interindividual differences in subjective sleepiness due to sleep inertia are substantial and constitute a trait.
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Total sleep deprivation (TSD) and time-on-task (TOT), especially in combination, increase cognitive instability and cause performance impairment. There are large inter-individual differences in TSD and TOT effects which, in part, have a genetic basis. Here, we show that the dopamine receptor D2 C957T genetic polymorphism predicts the magnitude of the TOT effect on a psychomotor vigilance test (PVT) during 38 h of TSD. This finding indicates that dopamine availability in the striatum, where the dopamine receptor D2 is most prevalent, influences the TOT effect, suggesting a role for dopaminergic pathways in sustained attention deficits during sleep loss.