The journal of pain : official journal of the American Pain Society
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Multidisciplinary treatment programs for chronic pain typically emphasize the importance of decreasing maladaptive and encouraging adaptive coping responses. The Chronic Pain Coping Inventory (CPCI), developed to assess coping strategies targeted for change in multidisciplinary pain treatment, is a 64-item instrument that contains 8 subscales: Guarding, Resting, Asking for Assistance, Relaxation, Task Persistence, Exercising/Stretching, Coping Self-Statements, and Seeking Social Support. A previous validation study with 210 patients in a Canadian academic hospital setting supported an 8-factor structure for the CPCI. The current study was undertaken to validate the CPCI among 564 veterans with a more extended history of chronic pain. Patients completed the study questionnaires before multidisciplinary treatment. A confirmatory factor analysis was used to examine the factor structure of the 64-item CPCI. A series of hierarchical multiple regression analyses were performed with depression, pain interference, general activity level, disability, and pain severity as the criterion variables and the 8 CPCI factors as the predictor variables, controlling for pain severity and demographic variables. The confirmatory factor analysis results strongly supported an 8-factor model, and the regression analyses supported the predictive validity of the CPCI scales, as indicated by their association with measures of patient adjustment to chronic pain. ⋯ This article validated the 8-factor structure of the CPCI by using a confirmatory factor analysis and a series of linear regressions. The results support the applicability and utility of the CPCI in a heterogeneous population of veterans with severe chronic pain treated in a tertiary teaching hospital. The CPCI provides an important clinical and research tool for the assessment of behavioral pain coping strategies that might have an impact on patient outcomes.
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The zinc finger transcription factor Egr1 is critical for coupling extracellular signals to changes in cellular gene expression. Expression of Egr1, as well as other immediate early genes, is up-regulated in response to a number of noxious stimuli. Activity-dependent activation of Egr1 has been reported in forebrain regions, including the anterior cingulate cortex (ACC), after peripheral injury. However, no study has reported a direct contribution of Egr1 to behavioral nociceptive responses. Here, we use Egr1 knockout mice to show that Egr1 is selectively required for behavioral responses to persistent inflammatory pain. Behavioral responses to peripheral inflammation were significantly reduced in Egr1 knockout mice, whereas responses to acute noxious stimuli were normal. In addition, inflammation triggered an up-regulation of Egr1 expression in the ACC of wild-type mice. Last, synaptic potentiation induced by theta (theta) burst stimulation in the ACC was significantly reduced or blocked in Egr1 knockout mice. Our study suggests that the transcription factor Egr1 plays a selective role in nociceptive behavioral responses to persistent inflammatory pain but not to acute noxious stimuli. ⋯ Chronic pain diminishes the quality of life. Here, we show that the immediate early gene Egr1 plays a role in chronic inflammatory, but not acute, pain. Egr1 knockout mice showed reduced nociceptive behaviors to persistent inflammatory pain and inflammation increased Egr1 expression in the anterior cingulate cortex of wild-type mice.