Pain
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Controlled Clinical Trial
Conditioned pain modulation predicts duloxetine efficacy in painful diabetic neuropathy.
This study aims to individualize the selection of drugs for neuropathic pain by examining the potential coupling of a given drug's mechanism of action with the patient's pain modulation pattern. The latter is assessed by the conditioned pain modulation (CPM) and temporal summation (TS) protocols. We hypothesized that patients with a malfunctioning pain modulation pattern, such as less efficient CPM, would benefit more from drugs augmenting descending inhibitory pain control than would patients with a normal modulation pattern of efficient CPM. ⋯ No predictive role was found for TS. In conclusion, the coupling of CPM and duloxetine efficacy highlights the importance of pain pathophysiology in the clinical decision-making process. This evaluative approach promotes personalized pain therapy.
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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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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.