Pain
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The current study examined the relationship between pain-related fear, physical performance, and pain-related interference in the context of experimentally induced pain to the lower back. Thirty healthy participants completed a test of maximal trunk strength before and after induction of delayed-onset muscle soreness (DOMS) to the trunk extensors. Pain-related fear (Tampa Scale of Kinesiophobia and Pain Anxiety Symptom Scale) was assessed prior to DOMS induction, and measures of current pain and pain-related interference with life activities were obtained 1 day after DOMS induction. ⋯ Current pain intensity and anthropometric factors did not contribute significantly to these outcome measures. To our knowledge, this is the first study to identify the impact of pain-related fear on physical performance among a healthy group of individuals following experimental acute low back injury. The findings extend previous research on psychological variables and simulated injury, and suggest that pain-related fear may be an important vulnerability factor in development of disability following acute pain experience.
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Platinum-based anticancer drugs cause neurotoxicity. In particular, oxaliplatin produces early-developing, painful, and cold-exacerbated paresthesias. However, the mechanism underlying these bothersome and dose-limiting adverse effects is unknown. ⋯ Administration of cisplatin evoked mechanical allodynia, an effect that was reduced in TRPA1-deficient mice. TRPA1 is therefore required for oxaliplatin-evoked mechanical and cold hypersensitivity, and contributes to cisplatin-evoked mechanical allodynia. Channel activation is most likely caused by glutathione-sensitive molecules, including reactive oxygen species and their byproducts, which are generated after tissue exposure to platinum-based drugs from cells surrounding nociceptive nerve terminals.
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Lidocaine applied systemically or locally attenuates neuropathic pain in patients. Here we tested the hypothesis that ectopic activity in injured afferent A- or C-fibers is suppressed by lidocaine. In rats the sural nerve (skin nerve) or lateral gastrocnemius-soleus nerve (muscle nerve) was crushed. ⋯ Intravenous application of lidocaine depressed ongoing ectopic activity in A- and C-fibers dose-dependently. Responses to heat or mechanical stimulation of the injured nerve were not suppressed at the highest concentrations of lidocaine. The results support the hypothesis that decrease of neuropathic pain following local or systemic application of a local anesthetic is related to decrease of ectopic ongoing activity in injured afferent nerve fibers.