Pain
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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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The shared-representation model of empathy suggests that vicarious pain processes rely partly on the activation of brain systems underlying self-pain in the observer. Here, we tested the hypothesis that self-pain may be facilitated by the vicarious priming of neural systems underlying pain perception. Pictures illustrating painful agents applied to the hand or the foot (sensory information), or painful facial expressions (emotional information) were shown to 43 participants to test the effects of vicarious pain on the nociceptive flexion reflex (NFR) of the lower limb and pain intensity and unpleasantness produced by transcutaneous electrical stimulation applied over the sural nerve. ⋯ In contrast, the change in perceived shock-pain intensity was negatively correlated with empathic traits. This dissociation implies that low-level vicarious priming processes underlying pain facilitation may be downregulated at higher pain-processing stages in individuals reporting higher levels of empathy. We speculate that this process contributes to reducing self-other assimilation and is necessary to adopt higher-order empathic responses and altruistic behaviors.
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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.