The journal of pain : official journal of the American Pain Society
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Bee venom (BV) acupuncture (BVA) involves injecting diluted BV into acupoints and is used for arthritis, pain, and rheumatoid diseases. The objective of this systematic review was to evaluate the evidence for the effectiveness of BVA in the treatment of musculoskeletal pain. Seventeen electronic databases were systematically searched up to September 2007 with no language restrictions. All randomized clinical trials (RCTs) of BVA for patients with musculoskeletal pain were considered for inclusion if they included placebo controls or were controlled against a comparator intervention. Methodology quality was assessed and, where possible, statistical pooling of data was performed. A total of 626 possibly relevant articles were identified, of which 11 RCTs met our inclusion criteria. Four RCTs that tested the effects of BVA plus classic acupuncture compared with saline injection plus classic acupuncture were included in the main meta-analysis. Pain was significantly lower with BVA plus classic acupuncture than with saline injection plus classic acupuncture (weighted mean difference: 100-mm visual analog scale, 14.0 mm, 95% CI = 9.5-18.6, P < .001, n = 112; heterogeneity: tau(2) = 0, chi(2) = 1.92, P = .59, I(2) = 0%). Our results provide suggestive evidence for the effectiveness of BVA in treating musculoskeletal pain. However, the total number of RCTs included in the analysis and the total sample size were too small to draw definitive conclusions. Future RCTs should assess larger patient samples for longer treatment periods and include appropriate controls. ⋯ Bee venom acupuncture involves injecting diluted BV into acupoints and is used for arthritis, pain, and rheumatoid diseases. A meta-analysis produced suggestive evidence for the effectiveness of BVA in musculoskeletal pain management. However, primary data were scarce. Future RCTs should assess larger patient samples for longer treatment periods and include appropriate controls.
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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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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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In the present study, a murine ex vivo somatosensory system preparation was used to determine the response characteristics of cutaneous sensory neurons staining positively for TRPV1 or TRPV2. TRPV1 immunostaining was found exclusively (11/11) in a specific set of mechanically insensitive unmyelinated (C) nociceptors that responded to heating of their receptive fields. No cutaneous C-fibers that responded to both mechanical and heat stimuli stained positively for TRPV1 (0/62). The relationship between TRPV2 and heat transduction characteristics was not as clear, as few unmyelinated or myelinated fibers that responded to heat contained TRPV2. TRPV2 was found most frequently in mechanically sensitive myelinated fibers, including both low threshold and high threshold mechanoreceptors (nociceptors). Although TRPV2 was found in only 1 of 6 myelinated polymodal nociceptors, it was found in a majority (10/16) of myelinated mechanical nociceptors. Thus, whereas the in vivo role of TRPV1 as a heat-sensitive channel in cutaneous sensory neurons is clearly defined, the role of TRPV2 in cutaneous neurons remains unknown. These results also suggest that TRPV1 may be essential for heat transduction in a specific subset of mechanically insensitive cutaneous nociceptors and that this subset may constitute a discrete heat input pathway for inflammation-induced thermal pain. ⋯ The distinct subset of murine cutaneous nociceptors containing TRPV1 has many attributes in common with mechanically insensitive C-fibers in humans that are believed to play a role in pathological pain states. Therefore, these murine fibers provide a clinically relevant animal model for further study of this group of cutaneous nociceptors.
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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.