The journal of pain : official journal of the American Pain Society
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Recent developments in cognitive behavioral theory emphasize the role of "psychological flexibility" in adaptive functioning. Psychological flexibility includes processes of acceptance, mindfulness, values, and cognitive defusion. The present study was intended to investigate aspects of psychological flexibility in relation to the functioning of patients with chronic pain. Two hundred sixty patients seeking treatment for chronic pain completed a battery of measures, including an expanded version of an instrument assessing responses to pain that reflect both psychological flexibility and traditionally conceived "pain management strategies" (ie, pacing, relaxation, positive self-statements). Initial psychometric evaluation of the expanded instrument yielded 2 reliable subscales, as hypothesized. Both subscales were correlated with measures of emotional functioning and psychosocial disability, although psychological flexibility achieved larger correlations and was correlated with additional measures of physical functioning, health care use, and work status. Regression analyses indicated that, after pain and patient background variables were statistically controlled, psychological flexibility accounted for significant variance in eight separate measures of functioning while pain management strategies accounted for significant variance in none. These results may call for a shift in our approaches to chronic pain in line with developments taking place in broader areas of behavioral and cognitive therapy. ⋯ This study includes development of an instrument for assessing coping, consisting of traditionally conceived coping strategies and a process that may be unfamiliar to most readers, termed "psychological flexibility." Results demonstrated that this process, a blend of acceptance, values-based action, mindfulness, and cognitive defusion, is significantly related to patient functioning with chronic pain.
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The current study examined the utility of a biopsychosocial model of chronic pain, and the associations between specific pain-related beliefs, coping, and social support and both mental health and pain interference, in persons with Spinal Cord Injury (SCI) and pain. A total of 157 patients completed surveys assessing physical and psychological functioning, as well as psychosocial, demographic, and injury-related variables. Greater catastrophizing and pain-related beliefs (eg, the belief that pain signals damage) were related with increased pain interference and poorer mental health, while coping styles (eg, resting, asking for assistance) were related only with pain interference. Alternatively, greater perceived social support was related with better mental health. The findings are consistent with a biopsychosocial model, implicating the need to consider the impact of process and clinical variables on adjustment to chronic pain in persons with SCI. ⋯ This article identifies several psychosocial variables, including coping, catastrophizing, pain-related beliefs, and social support that are related to adjustment in persons with SCI and pain. These results have implications for interventions designed to treat pain interference in persons with SCI.
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All data obtained in experimental animal pain models support the role of nerve growth factor (NGF) as a putative candidate intervening in the pathogenesis of chronic pain, including chronic daily headache (CDH). Few studies have been carried out to establish its role in maintaining pain states in humans. The present study was aimed at investigating cerebrospinal fluid (CSF) levels of NGF and brain-derived neurotrophic factor (BDNF), both measured by sensitive immunoassay, in 20 chronic migraine (CM) patients and 20 patients affected by primary fibromyalgia syndrome (PFMS), compared with those of 20 age-matched control subjects. Significantly higher levels of both neurotrophins and glutamate were found. A significantly positive correlation emerged between CSF values of BDNF and those of NGF (r = .61, P < .001; r = .53, P < .01) and glutamate (r = .44, P < .02; r = .51, P < .01) in CM and PFMS patients, respectively. These findings suggest the possibility of a NGF-mediated up-regulation of BDNF involved in the pathophysiological events underlying long-term neuroplastic changes in persistent chronic painful conditions, such as CM and fibromyalgia. NGF might indirectly exert its effect through enhancing glutamatergic transmission via BDNF. The above mechanisms could account for sustained central sensitization in both chronic pain states. ⋯ This article presents findings of higher NGF and BDNF levels correlated to increased glutamate levels in the CSF of both chronic migraine and fibromyalgia patients. This opens new insights into the pathogenic mechanisms of chronic pain and offers clinicians new therapeutic perspectives targeting the above mechanisms in both painful disorders.
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This study examined coping predictors of laboratory-induced pain tolerance, intensity, and unpleasantness among 244 healthy children and adolescents (50.8% female; mean age, 12.73 +/- 2.98 years; range, 8-18 years). Participants were exposed to separate 4-trial blocks of pressure and thermal (heat) pain stimuli, as well as 1 trial of cold pain stimuli. Strategies for coping with pain were measured using the Pain Coping Questionnaire (PCQ). Linear regression analyses were conducted to examine the associations between the 8 PCQ subscales and pain responses (pain tolerance, intensity, and unpleasantness) to all 3 pain tasks, controlling for age and sex. We found that internalizing/catastrophizing predicted higher pain intensity across the 3 pain tasks and higher cold pain unpleasantness; seeking emotional support predicted lower pressure pain tolerance; positive self-statements predicted lower pressure pain intensity and lower cold pain intensity and unpleasantness; and behavioral distraction predicted higher pressure pain tolerance and lower heat pain unpleasantness. These results suggest that in healthy children, internalizing/catastrophizing, and seeking emotional support may be conceptualized as pain-prone coping strategies, and positive self-statements and behavioral distraction as pain-resistant coping strategies within the context of laboratory pain. ⋯ These results support investigation of interventions with children that aim to reduce acute pain responses by modifying coping to reduce seeking of emotional support and catastrophizing and enhance the use of positive self statements and behavioral distraction.
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Chronic muscle pain is a major clinical problem that is often associated with fatigue. Conversely, chronic fatigue conditions are commonly associated with muscle pain. We tested the hypothesis that muscle fatigue enhances hyperalgesia associated with injection of acidic saline into muscle. We evaluated mechanical sensitivity of the paw (von Frey) in mice after 2 intramuscular injections of saline (20 microL; pH 4, pH 5, pH 6, pH 7.2) in a fatigue and a control group. To induce fatigue, mice were run for 2 h/day for 2 days prior to the first injection and 2 h/day for 2 days prior to the second injection. Muscle lactate, pCO(2), pO(2), creatinine kinase, phosphate, and histology were examined after the fatigue task and compared to a control group. Grip force was significantly decreased after 2 h of running indicating fatigue. The fatigue task did not induce muscle damage as there was no difference in muscle lactate, pCO(2), pO(2), creatinine kinase, phosphate, or histology. The fatigue task altered the dose-response relationship to intramuscular acidic saline injections. Mechanical hyperalgesia was observed in both fatigue and control groups after intramuscular injection of pH 4.0, but only the fatigue group after injection of pH 5. Neither the fatigue nor the control group developed hyperalgesia in response to intramuscular injection of pH 6 or pH 7.2. In conclusion, fatigue modified the susceptibility of mice to acid injection of pH 5.0 to result in mechanical hyperalgesia after 2 injections of pH 5.0. The fatigue task did not produce measurable changes in the muscle tissue suggesting a central mechanism mediating the enhancement of hyperalgesia. ⋯ These data therefore show that muscle fatigue can enhance the likelihood that one develops pain to a mild insult. Clinically, this could relate to the development of pain from such conditions as repetitive strain injury, and may relate to the interrelationship between chronic pain and fatigue.