interplay between these factors remains unclear. This study examined the role of catastrophizing in moderating the relationship between sleep (insomnia symptoms & objective measures of sleep continuity) and clinical and laboratory pain. 127 women with TMD were recruited as part of a larger study evaluating interventions for sleep and catastrophizing on pain. Participants underwent baseline testing, including self-report measures (clinical pain, depression, anxiety, catastrophizing, insomnia-severity), laboratory pain testing measuring central sensitization (CS), actigraphy (14 days) and a one-night polysomnography (PSG). While objective measures of sleep continuity were not significantly correlated with self-report insomnia-severity, both were associated with clinical pain and CS, suggesting that they represent distinct but important contributors to pain. Catastrophizing was associated with clinical pain and CS. Self-report insomnia-severity interacted with catastrophizing in predicting both clinical pain and CS (p's<.05). Objective measures of sleep continuity: total sleep time (actigraphy; PSG), sleep-efficiency (actigraphy; PSG) and wake after sleep onset (WASO; actigraphy) interacted with catastrophizing in predicting CS (p's<.001), but not clinical pain. The same pattern of moderation emerged from all interactions: patients with more severe self-reported insomnia symptoms, shorter sleep time, low sleep-efficiency and greater WASO who also reported high catastrophizing demonstrated increased levels of CS. Depression, anxiety and age were controlled in all analyses. These findings suggest that among women with TMD the combination of high catastrophizing and poor sleep continuity is particularly important in understanding CS and clinical pain and emphasizes the need to target this group and provide interventions for both sleep and catastrophizing.

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