European journal of pain : EJP
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Aberrations of cardiovascular regulation and dysfunction of endogenous pain modulation have been reported in fibromyalgia (FM) patients. This study aimed at investigating the interactions between cardiovascular regulation and pain perception during static muscle contractions. Seventeen FM patients and 17 healthy controls performed a standardised static contraction (m. quadriceps femoris dx) until exhaustion. ⋯ In conclusion, no indication of an attenuated cardiovascular response to exercise was found in our FM patients. The more pronounced HR increase in patients during contraction was most likely due to deconditioning. No exercise related change in PPTs was seen in either group, most likely due to insufficient exercise intensity, but the contraction induced pain was more pronounced in the FM patients.
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Persistent non-cancer pain is a common reason for consultation in primary care but treatment options, including non-opioid analgesics, are limited, and neither strong evidence nor established guidelines address when and how primary care doctors should prescribe opioid analgesics for persistent non-cancer pain. The aim of this study was to investigate associations between doctors' prescribing patterns for persistent non-cancer pain in primary care and their personal and practice characteristics and beliefs about appropriateness and risks of opioids. A pilot survey sampled beliefs concerning the need for and risks of opioid prescribing for persistent non-cancer pain among volunteers from primary care practices and postgraduate educational events, using a self-report questionnaire, and related these beliefs to their reported opioid prescribing. ⋯ Both prescribers and non-prescribers expressed concern about the risks of opioids. In addition, most primary care doctors were dissatisfied with their training on pain; few had prescribing guidelines; and neither training nor guidelines influenced prescribing. In conclusion, whether or not GPs prescribe opioids for persistent non-cancer pain is mainly determined by their personal beliefs about appropriateness of opioids for this problem.
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Using immunohistochemical methods we determined the presence of SP- and CGRP-immunopositive nerve fibers in the hip joint of patients with femoral neck fracture (controls, group 1), painful osteoarthritis (group 2), and painless failed total hip arthroplasties (group 3). Immunoreactive nerve fibers were found in the soft tissue of the fossa acetabuli as well as in the subintimal part of the synovial layer in the hip joint capsule of groups 1 and 2. In the capsule of controls the innervation density had a median of 5.7fibers/cm(2) for CGRP-ir and 3.2fibers/cm(2) for SP-ir afferents. ⋯ This is supported by the fact, that patients with loosened total hip arthroplasties, where we failed to detect SP- and CGRP-immunoreactive fibers, did not feel pain. The upregulation of SP- and CGRP-positive neurons in response to arthritic stages suggests a mechanism involving neuropeptides in the maintenance of a painful degenerative joint disease and in mediating noxious stimuli from the periphery. Furthermore, these findings help to explain clinical observations, such as effectiveness of local therapy to control hip pain with intraarticular injection, synovectomy and denervation procedures.
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Several reviews of randomized controlled trials (RCTs) have shown the efficacy of mu-opioids in reducing spontaneous neuropathic pain (NP). However, relatively little is known about their specific efficacy for evoked pain, which is a significant problem for many patients with NP. The present systematic review assesses the efficacy of opioid agonists for the treatment of evoked NP based upon published RCTs. We searched articles in any language using the MEDLINE database (1966 to December 2004), the Cochrane Central Register of Controlled Trials (4th quarter, 2004) and the reference lists of retrieved papers, employing search terms for RCTs, opioids and NP. Only RCTs in which opioid agonists were given to treat NP of any etiology, and evoked pain was assessed were included. Data were extracted by two independent investigators. Nine articles met inclusion criteria and were classified as short-term (less than 24h; n=7) or intermediate-term trials (4 weeks; n=2). Although the scarcity of retrieved data precluded formal meta-analysis of short-term trials, we found that the intensity of dynamic mechanical allodynia was significantly attenuated by opioids relative to placebo in all studies. In contrast, no consistent effects on the magnitude of static allodynia, the threshold for mechanical allodynia or the threshold or magnitude of heat allodynia were found. The threshold and magnitude of cold-induced allodynia generally responded positively to opioid treatments in patients with peripheral pain syndromes, but not central pain syndromes. Evoked pain was studied in only two intermediate-term trials, in both of which oxycodone was significantly superior to placebo. The results of the two trials were combinable for a meta-analysis that showed an overall 24 points difference in endpoint pain intensities between patients given opioids and those treated with placebo (95% CI -33 to -15; p<0.00001). ⋯ short-term studies show that opioids can reduce the intensity of dynamic mechanical allodynia and perhaps of cold allodynia in peripheral NP. Insufficient evidence precludes drawing conclusions regarding the effect of opioids on other forms of evoked NP. A meta-analysis of intermediate-term studies demonstrates the efficacy of opioids over placebo for evoked NP. These findings are clinically relevant because dynamic mechanical allodynia and cold allodynia are the most prevalent types of evoked pain in NP.