Articles: neuralgia.
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Decreased Gamma-aminobutyric acid (GABA)-ergic phasic inhibitory transmission in the spinal cord is thought to be responsible for the development of neuropathic pain. However, the role of GABAergic tonic current in substantia gelatinosa (SG) neurons in neuropathic pain remains to be fully elucidated. In this study, we assessed GABAergic tonic currents of SG neurons in a sciatic nerve chronic constriction injury (CCI) mouse. ⋯ A reduction in the expression the δ subunit of the GABAAreceptor and diminished GABAergic tonic current in SG neurons were observed after CCI in mice. GABAergic tonic current plays a key role in neuropathic pain. The GABAAreceptor δ subunit may be a therapeutic target in neuropathic pain. WHAT DOES THIS STUDY ADD?: In spinal SG neurons, GABAergic inhibitory transmission operates through both phasic and tonic currents, but physiological role is largely unknown. In this study, we report dysregulation of GABAAreceptor δ subunit-mediated tonic current in SG neurons may result in spinal disinhibition resulting in neuropathic pain in CCI mice.
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Curr Pain Headache Rep · Nov 2016
ReviewReview of Recent Advances in Peripheral Nerve Stimulation (PNS).
Peripheral nerve stimulation (PNS) for the treatment of chronic pain has become an increasingly important field in the arena of neuromodulation, given the ongoing advances in electrical neuromodulation technology since 1999 permitting minimally invasive approaches using an percutaneous approach as opposed to implantable systems. Our review aims to provide clinicians with the recent advances and studies in the field, with specific emphasis on clinical data and indications that have been accumulated over the last several years. In addition, we aim to address key basic science studies to further emphasize the importance of translational research outcomes driving clinical management.
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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.