The journal of pain : official journal of the American Pain Society
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Little is known about cognitive and behavioral factors that influence older adults' adjustment to chronic pain. The objective of this study was to investigate the relationship of self-efficacy for managing pain to reports of pain intensity, pain-related disability, depressive symptoms, and pain coping strategy use among 140 retirement community residents (88% female; age mean = 81.7, range 66-99 years) with chronic pain. The 8-item Arthritis Self-Efficacy Scale, modified to specify pain rather than arthritis, demonstrated good psychometric characteristics (Cronbach alpha = .89, minimal floor and ceiling effects, and validity) in this sample. Controlling for age, gender, and pain intensity, self-efficacy was associated significantly and negatively with pain-related disability and depressive symptoms (P values < .001), and positively with use of pain coping strategies previously found to be associated with better outcomes (task persistence, exercise/stretch, coping self-statements, activity pacing; P values < .05). Self-efficacy for managing pain appears to be important in the adjustment of older adults with pain. Research is needed to determine whether interventions designed to increase self-efficacy improve quality of life and prevent functional declines in this population. ⋯ Among retirement community residents (mean age of 82 years) with chronic pain, higher self-efficacy for managing pain is associated with less disability and depression and with the use of pain coping strategies related to better adjustment. This suggests the potential value of interventions to increase self-efficacy in this population.
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Previous studies have shown that chemokines might play a role in the pathology of chronic pain. The purpose of this study was to provide an immunohistochemical description of the distribution of CX3CL1 (fractalkine) and its receptor CX3CR1 in the rat spinal cord in a model of inflammatory pain induced by unilateral intraplantar complete Freund's adjuvant (CFA) and in a model of neuropathic pain induced by L5 spinal nerve ligation (modified Chung model or mSNL). In naïve rats, CX3CL1 is found in the cytoplasm of neurons as shown by colocalization of CX3XL1 and NeuN. Similar distribution of CX3CL1 was observed after CFA, whereas after mSNL, CX3CL1 was not only observed in neurons but also found in astrocytes, as shown by colocalization of CX3CL1 and GFAP. Weak immunoreactivity for the CX3CL1 receptor, CX3CR1, was found in microglia in the spinal cord of either naïve rats or rats with inflammation. However, after spinal nerve injury, CX3CR1-LI was upregulated in microglia throughout the dorsal horn. ⋯ This study shows that spinal nerve injury, but not peripheral inflammation, induces the expression of a chemokine, CX3CL1 (fractalkine), in astrocytes and upregulates CX3CR1 in microglia in the spinal cord. This selective regulation of CX3CL1 and its receptor, CX3CR1, suggests that these chemokines may represent new targets for the treatment of neuropathic pain.