The journal of pain : official journal of the American Pain Society
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Cognitive and behavioral pain-coping strategies, particularly catastrophizing, are important determinants of the pain experience. Most studies of pain-coping are performed in samples of treatment-seeking patients with longstanding pain complaints. Individual differences in pain-coping styles may also significantly affect day-to-day pain and quality of life in nonclinical samples, though this has rarely been investigated. In particular, headache pain is common in the general population, and little is known about how pain-related coping affects pain and quality of life among headache sufferers from a nonclinical setting. In this study, 202 generally healthy subjects were divided into 2 groups, those who reported problem headaches and pain-free control subjects. Reports of pain-related catastrophizing and the use of active pain-coping strategies did not differ between the groups, but differential associations between pain-coping strategies and emotional functioning were observed. Specifically, within the headache group only, those reporting higher levels of pain catastrophizing and lower levels of active pain-coping showed the highest level of depressive symptoms. Further, higher catastrophizing was associated with greater headache pain and pain-related interference. These findings suggest that catastrophizing has little influence on emotional functioning in those without ongoing pain complaints and highlight the importance of coping in modulating the consequences of pain on day-to-day functioning, even in samples from nonclinical settings. Moreover, these findings indirectly suggest that interventions that increase adaptive coping and decrease catastrophizing may help to buffer some of the deleterious functional consequences of headache pain. ⋯ This study adds to a growing literature that conceptualizes catastrophizing as a diathesis, or risk factor, for deleterious pain-related consequences. These data suggest that catastrophizing may require the presence of a pain condition before its detrimental effects are exerted.
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The purpose of the present study was to test a hypothetical model of the relationships between perceived social support, coping responses to pain, pain intensity, depressed mood, and functional disability (functional status and functional impairment) in a population of patients with chronic pain in a Spanish Clinical Pain Unit. It was postulated that social support and pain coping responses both independently influence reported pain intensity, depressed mood, and functional disability. Analyses were performed by Structural Equation Modelling. The results indicated that satisfaction with social support is significantly associated with a depressed mood and pain intensity, but not with functional disability. Although this effect is independent of the use of active coping responses by patients, there is a modest but significant relationship between social support and passive coping strategies, indicating that higher levels of perceived social support are related to less passive pain coping strategies. The findings underscore the potential importance of psychosocial factors in adjustment to chronic pain and provide support for a biopsychosocial model of pain. ⋯ This article tested a hypothetical model of the relationships between social support, pain coping, and chronic pain adjustment by using Structural Equation Modelling. The results indicate that perceived social support and pain coping are independent predictors of chronic pain adjustment, providing support for a biopsychosocial model of pain.
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Peripheral nerve injury has been associated with changes in the modulatory action of noradrenergic pathways on nociceptive traffic through the spinal cord. Thus, the purpose of this study was to assess whether endogenous noradrenergic descending inhibition, acting via spinal alpha(2)-receptors, is altered after peripheral nerve damage. We investigated the effects of spinal administration of a selective alpha(2)-adrenoceptor antagonist, atipamezole, on the evoked activity of deep dorsal horn neurons in animals with selective spinal nerve ligation (SNL) compared with a sham-operated group. Intrathecal administration of atipamezole (1, 10, and 100 microg) did not produce any significant effects on the electrically evoked neuronal responses in either animal group, with the exception of a small but significant enhancement of the postdischarge in the sham control group only. Similarly, no significant effects were observed with the heat-evoked neuronal responses in either group. Interestingly, atipamezole significantly increased the evoked responses of neurons to low-intensity mechanical stimuli in the sham control group but was without effect in the SNL group. Thus, our findings suggest that peripheral nerve injury can result in the suppression of noradrenergic spinal alpha(2)-adrenoceptor-mediated inhibition of spinal dorsal horn neuronal activity evoked by low-intensity mechanical stimuli. ⋯ These results suggest that a tonically active noradrenergic inhibition of mechanically evoked spinal dorsal horn neuronal responses is lost after nerve injury. This shift in the balance of noradrenergic controls may be one of the many underlying mechanisms by which behavioral symptoms of hypersensitivity develop after nerve damage.
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Comparative Study
Memory for pain? A comparison of nonexperiential estimates and patients' reports of the quality and intensity of postoperative pain.
Prior research has questioned the extent to which postoperative retrospective ratings of acute pain actually reflect memory of that pain. To investigate this issue, pain ratings provided by patients who had undergone vascular surgery were compared with estimates of this pain provided by 2 groups of healthy, nonpatient participants with no personal experience of the surgery. Patient participants rated postoperative pain while actually experiencing it and again 4 to 6 weeks after surgery. Nonpatient groups read either a comprehensive information leaflet describing postoperative pain after vascular surgery, or a short general information leaflet about the surgery and provided 2 estimates of the likely nature of the pain, 4 to 6 weeks apart. Compared with patients, both nonpatient groups overestimated pain severity, and nonpatients provided with the comprehensive information leaflet were less consistent in their estimates compared with the other 2 groups. However, qualitative descriptions of the pain provided by the 3 groups shared many similarities. Our findings highlight limitations of inferring pain memory accuracy by comparing ratings given while in pain with those provided retrospectively and demonstrate the need to consider the phenomenological awareness accompanying recollections of prior pain events to advance our understanding of memory for pain. ⋯ The observed similarities between pain ratings made by individuals who have experienced a particular pain and estimates made by those without personal experience question whether retrospective pain ratings can be assumed to reflect memory of that pain. The need to adopt new approaches to assess memory for pain is highlighted.