Pain
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Serotonin is critically involved in neuropathic pain. However, its role is far from being understood owing to the number of cellular targets and receptor subtypes involved. In a rat model of neuropathic pain evoked by chronic constriction injury (CCI) of the sciatic nerve, we studied the role of 5-HT(2B) receptor in dorsal root ganglia (DRG) and the sciatic nerve. ⋯ In the latter structure, it was biphasic, consisting of a transient early increase (23-fold), 2 days after the surgery and before the neuropathic pain emergence, followed by a steady (5-fold) increase, that remained constant until pain disappeared. In DRG and sciatic nerve, 5-HT(2B) receptors were immunolocalized on sensory neurons and infiltrating macrophages. Our data reveal a relationship between serotonin, immunocytes, and neuropathic pain development, and demonstrate a critical role of 5-HT(2B) receptors in blood-derived macrophages.
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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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Sleep disturbance and pain catastrophizing are important mediators of the chronic pain experience. To date, these factors have not been considered concurrently despite compelling theoretical rationale to do so. In the present study, we examined whether pain catastrophizing not only has direct effects on clinical pain and pain-related interference, but also indirect effects through its association with sleep disturbance. ⋯ Prospective studies are needed to examine lagged associations between these constructs. These findings have important theoretical and clinical implications. Critically, interventions that reduce pain catastrophizing may concurrently improve sleep and clinical pain.
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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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A number of pharmacologic treatments examined in recent randomized clinical trials (RCTs) have failed to show statistically significant superiority to placebo in conditions in which their efficacy had previously been demonstrated. Assuming the validity of previous evidence of efficacy and the comparability of the patients and outcome measures in these studies, such results may be a consequence of limitations in the ability of these RCTs to demonstrate the benefits of efficacious analgesic treatments vs placebo ("assay sensitivity"). ⋯ On the basis of this meeting and subsequent discussions, the authors recommend consideration of a number of patient, study design, study site, and outcome measurement factors that have the potential to affect the assay sensitivity of RCTs of chronic pain treatments. Increased attention to and research on methodological aspects of clinical trials and their relationships with assay sensitivity have the potential to provide the foundation for an evidence-based approach to the design of analgesic clinical trials and expedite the identification of analgesic treatments with improved efficacy and safety.