Pain
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Review Meta Analysis Comparative Study
Pain perception in athletes compared to normally active controls: a systematic review with meta-analysis.
This study systematically reviewed differences in pain perception between athletes and normally active controls. We screened MEDLINE, Sport-Discus, EMBASE, Web of Science, PsycINFO, PSYNDEX, and the citations of original studies and systematic reviews. All studies on experimentally induced pain that compared pain perception between athletes and normally active controls were eligible. ⋯ After exclusion of studies with high risk of bias, differences between groups in pain threshold were not significant any longer. Our data suggest that regular physical activity is associated with specific alterations in pain perception. Psychological and biological factors that may be responsible for these alterations are discussed.
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One might expect that injury compensation would leave injured parties better off than they would otherwise have been, yet many believe that compensation does more harm than good. This study systematically reviews the evidence on this "compensation hypothesis" in relation to compensable whiplash injuries. PubMed, CINAHL, EMBASE, PEDro, PsycInfo, CCTR, Lexis, and EconLit were searched from the date of their inception to April 2010 to locate longitudinal studies, published in English, comparing the health outcomes of adults exposed/not exposed to compensation-related factors. ⋯ Irrespective of the compensation-related factor involved and the health outcome measured, the quality of these studies was similar to studies that did not find a significant negative association: most took some measures to address selection bias, confounding, and measurement bias, and none resolved the potential for reverse causality bias that arises in the relationship between compensation-related factors and health. Unless ambiguous causal pathways are addressed, one cannot draw conclusions from statistical associations, regardless of their statistical significance and the extent of measures to address other sources of bias. Consequently, there is no clear evidence to support the idea that compensation and its related processes lead to worse health.
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Multicenter Study
Demographic and medical parameters in the development of complex regional pain syndrome type 1 (CRPS1): prospective study on 596 patients with a fracture.
Limited data are available on the incidence of complex regional pain syndrome type 1 (CRPS1) and on demographic and medical risk factors for the development of CRPS1. The objective of this study was to investigate the incidence of CRPS1 in patients with a fracture using 3 sets of diagnostic criteria and to evaluate the association between demographic/medical factors and the development of CRPS1 diagnosed with the Harden and Bruehl criteria. A prospective multicenter cohort study of 596 patients (ages 18 years and older) with a single fracture of the wrist, scaphoid, ankle, or metatarsal V, recruited patients from the emergency rooms of 3 Dutch hospitals. ⋯ At baseline, patients with CRPS1 had significantly more pain than patients without CRPS1 (P<.001). The incidence of the diagnosis of CRPS1 after a single fracture depends to a large extent on the diagnostic criteria used. After a fracture, 7% of the patients developed CRPS1 and none of the patients were free of symptoms at 1-year follow-up.
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Injuries can induce adaptations in pain processing that result in amplification of signaling. One mechanism may be analogous to long-term potentiation and involve the atypical protein kinase C, PKMζ. The possible contribution of PKMζ-dependent and independent amplification mechanisms to experimental neuropathic pain was explored in rats with spinal nerve ligation (SNL) injury. ⋯ Thus, PKMζ-dependent amplification contributes to nerve injury-induced aversiveness within the rACC. Moreover, unlike mechanisms maintaining memory, the consequences of PKMζ inhibition within the rACC are not permanent in neuropathic pain, possibly reflecting the re-establishment of amplification mechanisms by ongoing activity of injured nerves. In the spinal cord, however, both PKMζ-dependent and independent mechanisms contribute to amplification of evoked responses, but apparently not spontaneous pain.