Articles: neuralgia.
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Br J Health Psychol · Nov 2016
The devil in the corner: A mixed-methods study of metaphor use by those with spinal cord injury-specific neuropathic pain.
Metaphorical expressions of persistent pain play an influential role in the modulation of pain. This may be particularly distressing for those with physical disabilities such as spinal cord injury (SCI). Neuropathic pain (NP) after SCI is often described using metaphorical expressions such as burning and electricity. This study explored the use of metaphors by those with NP after SCI. ⋯ This study highlights the power of metaphor in eliciting understanding of NP after SCI from others, whilst demonstrating the challenge of communicating NP. Cognitive treatment that incorporates image-based techniques with acceptance and mindfulness-based therapies may encourage adaptive responses to, and interpretation of, pain. This may subsequently reduce pain-related distress and catastrophizing. Statement of contribution What is already known on this subject? Neuropathic pain is often described with metaphorical language such as burning and crushing. For those with physical limitations, metaphor use may induce or exacerbate psychological distress. However, for those with spinal cord injuries, metaphor use has received little attention. What does this study add? Metaphor use is common in those with spinal cord injury, with differences across gender and age. Core metaphors used conceptualized pain as an attacker or likened pain to heat and burning. Such language may have benefits in terms of improved understanding and increased empathy, but may be reflective of catastrophic thinking.
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Neuropathic pain is a common side-effect of chemotherapy. Although precise mechanisms are unclear, oxidative stress and mitochondrial damage are involved. We investigated whether the mitochondria targeted antioxidant, MitoVitE, provided better protection against paclitaxel-induced mitochondrial damage in rat dorsal root ganglion (DRG) cells, than a non-targeted form of vitamin E, Trolox. We also determined whether MitoVitE, compared with duloxetine, could limit paclitaxel-induced mechanical hypersensitivity in rats. ⋯ Paclitaxel affected mitochondrial function and glutathione in DRG cells, which was abrogated by MitoVitE but not Trolox, without decreasing cancer cell cytotoxicity. In rats, paclitaxel-induced mechanical hypersensitivity was ameliorated by MitoVitE treatment to an extent similar to duloxetine. These data confirm mitochondria as a mechanistic target for paclitaxel-induced damage and suggest mitochondria targeted antioxidants as future therapeutic strategies.
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Neuropathic pain afflicts millions of people, and the development of an effective treatment for this intractable pain is an urgent issue. Recent evidence has implicated microglia in neuropathic pain. The present study showed that the DNAX-activating protein of 12 kDa (DAP12) and its associated "triggering receptor expressed on myeloid cells 2" (TREM2) were predominantly expressed by microglia in the dorsal horn after spinal nerve injury, revealing a role for TREM2/DAP12 signaling in neuropathic pain. ⋯ The agonistic antibody induced proinflammatory responses and neuropathic pain was not observed in Dap12-deficient mice. Together, these results suggest that TREM2/DAP12-mediated signals in microglia exacerbate nerve injury-induced neuropathic pain by inducing proinflammatory cytokine secretion from microglia. Suppression of DAP12-mediated signals could be a therapeutic target for neuropathic pain.
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Chemotherapy-induced peripheral neuropathy (CIPN), characterized by pain and numbness in hands and feet, is a common side effect of cancer treatment. In most patients, symptoms of CIPN subside after treatment completion. However, in a substantial subgroup, CIPN persists long into survivorship. ⋯ Paclitaxel increased DRG IL-10 receptor expression and this effect requires CD8+ T cells. In conclusion, we identified a novel mechanism for resolution of CIPN that requires CD8+ T cells and endogenous IL-10. We propose that CD8+ T cells increase DRG IL-10 receptor expression and that IL-10 suppresses the abnormal paclitaxel-induced spontaneous discharges by DRG neurons to promote recovery from CIPN.