Ample evidence suggests that sleep and pain are related. However, many questions remain about the direction of causality in their association, as well as mechanisms that may account for their association. The prevailing view has generally been that they are reciprocally related. The present review critically examines the recent prospective and experimental literature (2005-present) in an attempt to update the field on emergent themes pertaining to the directionality and mechanisms of the association of sleep and pain. A key trend emerging from population-based longitudinal studies is that sleep impairments reliably predict new incidents and exacerbations of chronic pain. Microlongitudinal studies employing deep subjective and objective assessments of pain and sleep support the notion that sleep impairments are a stronger, more reliable predictor of pain than pain is of sleep impairments. Recent experimental studies suggest that sleep disturbance may impair key processes that contribute to the development and maintenance of chronic pain, including endogenous pain inhibition and joint pain. Several biopsychosocial targets for future mechanistic research on sleep and pain are discussed, including dopamine and opioid systems, positive and negative affect, and sociodemographic factors.Perspective-This critical review examines the recent prospective and experimental research (2005-present) on the association of sleep and pain in an attempt to identify trends suggestive of directionality and potential mechanisms. An update on this literature is needed to guide future clinical efforts to develop and augment treatments for chronic sleep disturbance and chronic pain.

Psychological treatment has emerged as a common component of a multidimensional and interdisciplinary plan of pain care for many persons with persistent pain. Treatments are informed by a biopsychosocial model of pain and a long history of psychological research that has identified the central role of behavioral, cognitive, and emotional factors that are believed to contribute to the perpetuation, if not the development, of chronic pain and pain-related disability and emotional distress. Empirically supported self-regulatory, behavioral, cognitive-behavioral, and acceptance and commitment interventions are reviewed, and current and future interventions are highlighted. Important issues related to individual differences and disparities in the experience of pain and pain treatment are discussed. In particular, race and ethnicity are considered, and special considerations for the management of pain in children and older adults are discussed.

This study tested the effects of aging and race on responses to noxious stimuli using a wide range of stimulus modalities. The participants were 53 non-Hispanic Blacks and 138 non-Hispanic White adults, ages 45 to 76. The participants completed a single 3-hour sensory testing session where responses to thermal, mechanical, and cold stimuli were assessed. The results suggest that there are selected age differences, with the older group less sensitive to warm and painful heat stimuli than middle-aged participants, particularly at the knee. This site effect supports the hypothesis that the greatest decrement in pain sensitivity associated with aging occurs in the lower extremities. In addition, there were several instances where age and race effects were compounded, resulting in greater race differences in pain sensitivity among the older participants. Overall, the data suggest that previously reported race differences in pain sensitivity emerged in our older samples, and this study contributes new findings in that these differences may increase with age in non-Hispanic Blacks for temporal summation and both heat and cold immersion tolerance. We have added to the aging and pain literature by reporting several small to moderate differences in responses to heat stimuli between middle and older age adults.

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Objective To identify psychological profiles in persons with knee osteoarthritis (OA) and to determine the relationship between these profiles and specific pain and sensory characteristics, including temporal summation and conditioned pain modulation. Methods Individuals with knee OA (n = 194) completed psychological, health, and sensory assessments. Hierarchical cluster analysis was used to derive psychological profiles that were compared across several clinical pain/disability and experimental pain responses. Results Cluster 1 had high optimism with low negative affect, pain vigilance, anger, and depression, along with the lowest self-reported pain/disability and the lowest sensitivity to mechanical, pressure, and thermal pain (P < 0.01 for all). Cluster 2 had low positive affect with high somatic reactivity, while cluster 3 showed high pain vigilance with low optimism. Clusters 2 and 3 had intermediate levels of self-reported pain/disability and cluster 3 experienced central sensitization to mechanical stimuli. Participants in cluster 3 also displayed significant pain facilitation (P < 0.05). Cluster 4 exhibited the highest pain vigilance, reactivity, negative affect, anger, and depression. These individuals experienced the highest self-reported pain/disability, including widespread pain (P < 0.001 for all). Cluster 4 was most sensitive to mechanical, pressure, and thermal stimuli, and showed significant central sensitization to mechanical and thermal stimuli (P < 0.001 for all). Conclusion Our findings demonstrate the existence of homogeneous psychological profiles displaying unique sets of clinical and somatosensory characteristics. Multidisciplinary treatment approaches consistent with the biopsychosocial model of pain should provide significant advantages if targeted to profiles such as those in our OA sample.