Sleep, Pain Catastrophizing, and Central Sensitization in Knee Osteoarthritis Patients With and Without Insomnia.

OBJECTIVE: Osteoarthritis (OA), a chronic degenerative joint disorder, is characterized by joint pain. Emerging research demonstrates that a significant number of patients evidence central sensitization (CS), a hyperexcitability 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-control study of 4 well-characterized groups of adults with insomnia and/or knee OA. A total of 208 participants completed multimodal sleep assessments (questionnaire, diary, actigraphy, and polysomnography) 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 knee OA-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. CONCLUSION: These findings highlight the importance of assessing sleep efficiency, CS, and catastrophizing in chronic pain patients and have important clinical implications for treatment planning.

Circadian rest/activity rhythms in knee osteoarthritis with insomnia: a study of osteoarthritis patients and pain-free controls with insomnia or normal sleep.

Aberrant circadian rest/activity rhythms (RARs) may promote poor aging-related health outcomes. Osteoarthritis and chronic insomnia are common age-related conditions, but the circadian RARs of each group have not been well characterized or compared. We evaluated actigraphic RARs in individuals with: (1) knee osteoarthritis (KOA) only; (2) chronic insomnia only; (3) KOA + insomnia; and (4) pain-free good sleepers. Compared to participants with KOA only, those with KOA + insomnia had less robust RARs. There were no differences between other groups. Further research is needed to evaluate whether aberrant RARs contribute to arthritis symptoms and insomnia in KOA, and whether strengthening RARs ameliorates arthritis symptoms.

Changes in pain catastrophizing predict later changes in fibromyalgia clinical and experimental pain report: cross-lagged panel analyses of dispositional and situational catastrophizing.

INTRODUCTION: Fibromyalgia (FM), characterized by wide-spread diffuse pain and sensory abnormalities, is associated with elevated indices of distress and pain-related catastrophizing compared to both pain-free samples and those with chronic pain conditions. Catastrophizing is a pervasive negative mental set, and is a strong predictor of negative pain-related outcomes such as clinical pain intensity, and physical disability. Situational catastrophizing, measured in the context of experimentally-induced pain, is strongly related to enhanced pain sensitivity, a core aspect of the pathophysiology of fibromyalgia. However, little is known regarding the temporal course of the association between catastrophizing and pain-related "outcomes". Most studies involve only static assessments of pain and catastrophizing at a single time point, which provides little insight into the direction of the observed associations. We sought to investigate the temporal relationships between catastrophizing and indices of both clinical pain (substudy 1) and experimentally-induced pain (substudy 2) in a larger randomized controlled longitudinal trial. METHODS: Fifty-seven patients with FM completed catastrophizing, depression, and pain questionnaires as well as laboratory cold pressor pain testing at baseline, post-intervention and three month follow-up during a lifestyle physical activity study. Cross-lagged panel analyses were used to address these temporal relationships. RESULTS: In substudy 1, analyses revealed that pre-to-post changes in dispositional catastrophizing ratings prospectively accounted for unique variance in subsequent post-to-follow-up changes in clinical pain ratings (p = 0.005), while pre-to-post changes in pain ratings did not account for unique variance in post-to-follow-up changes in catastrophizing ratings. An identical pattern was observed experimentally in substudy 2, with pre-to-post changes in situational catastrophizing ratings prospectively accounting for unique variance in subsequent post-to-follow-up changes in experimental pain ratings (p = 0.014), while pre-to-post changes in pain ratings did not account for unique variance in post-to-follow-up changes in catastrophizing ratings. Specifically, initial alterations in catastrophizing were associated with subsequent alterations in clinical and experimentally induced pain. Controlling for levels of depression did not affect the results. CONCLUSIONS: These findings provide empirical evidence that catastrophizing processes might precede and contribute to subsequent alterations in the pain experience for FM patients. TRIAL REGISTRATION: clinicaltrials.gov: NCT00383084.