Articles: neuropathic-pain.
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Brachial plexus avulsion injuries result in permanent motor and sensory deficits, leading to debilitating symptoms. We report the case of a 25-year-old man with chronic pain following right-sided C5-T1 nerve root avulsion without evidence of peripheral nerve injury. ⋯ These results agree with data suggesting collateral sprouting of sensory nerves occurs following a brachial plexus injury. Further study is needed if we are to understand the mechanisms of the peripheral nerve stimulator as a treatment option.
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Glia (i.e., astrocyte and microglia) activation in the central nervous system plays a critical role in developing neuropathic pain. Microglia can be activated into proinflammatory (M1) and anti-inflammatory (M2) phenotypes. Switching microglial polarization from M1 to M2 phenotypes represents a novel therapeutic strategy for neuropathic pain. Curcumin has been widely used for its anti-inflammatory and immunomodulatory effects. This study investigated effects of curcumin on astrocyte activation and microglia polarization in the cuneate nucleus (CN) and development of neuropathic pain behavior after chronic constriction injury (CCI) of the median nerve. ⋯ In our findings, curcumin switches microglial phenotypes from M1 to M2 by suppressing astrocytic activation, reducing proinflammatory cytokine release, promoting anti-inflammatory cytokine production, and contributing to relief of neuropathic pain.
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Peripheral nerve injuries remain a major medical problem worldwide and are associated with multiple causes, including gunshot wounds (GSWs), which are the second most common cause of brachial plexus injuries in peacetime and the main, or only, cause reported in wartime studies. The ulnar nerve (UN) is one of the most affected nerves. Peripheral nerve trauma may cause intense neuropathic pain, which is very difficult to control. Particularly UN gunshot injuries may impact individual daily life, as injuries to this nerve result in both sensory and motor deficits within the hand. We evaluated the improvement of neuropathic pain after surgical treatment in a consecutive series of 20 patients with UN injury due to GSWs. ⋯ Surgery is an effective treatment for neuropathic pain from GSWs. Early isolated external neurolysis is associated with better pain management and functional outcomes postoperatively.
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Clinically, neuropathic pain is a severe side effect of oxaliplatin chemotherapy, which usually leads to dose reduction or cessation of treatment. Due to the unawareness of detailed mechanisms of oxaliplatin-induced neuropathic pain, it is difficult to develop an effective therapy and limits its clinical use. ⋯ These findings suggest that reduction of SIRT1-mediated epigenetic upregulation of Nav1.7 in the DRG contributes to the development of oxaliplatin-induced neuropathic pain in rats. The intrathecal drug delivery treatment of activating SIRT1 might be a novel therapeutic option for oxaliplatin-induced neuropathic pain.
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MMG22 is a bivalent ligand containing MOR agonist and mGluR5 antagonist pharmacophores connected by a 22-atom linker. Intrathecal (i.t.) administration of MMG22 to inflamed mice has been reported to produce fmol-range antinociception in the reversal of LPS-induced hyperalgesia. MMG22 reduced hyperalgesia in the spared nerve injury (SNI) model of neuropathic pain at 10 days after injury but not at 30 days after injury, perhaps related to the inflammation that occurs early after injury but subsequently subsides. ⋯ We propose that MMG22 induces the formation of a MOR-mGluR5 heteromer through selective interaction with the upregulated NR2B subunit of activated NMDAR, in view of the 4600-fold reduction of i.t. MMG22 antinociception by the selective NR2B antagonist, Ro25-6981. A possible explanation for the substantially reduced potency for MMG22 in the SNI model is discussed.