Articles: neuralgia.
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J. Korean Med. Sci. · Aug 2015
Mechanical Antiallodynic Effect of Intrathecal Nefopam in a Rat Neuropathic Pain Model.
Nefopam has a pharmacologic profile distinct from that of opioids or other anti-inflammatory drugs. Several recent studies demonstrate that nefopam has a mechanism of action similar to those of anti-depressants and anticonvulsants for treating neuropathic pain. The present study investigates the mechanical antiallodynic effect of nefopam using immunohistochemical study and western blot analysis in a rat neuropathic pain model. ⋯ The N10 and N100 groups showed improved mechanical allodynic threshold, reduced CD11b and GFAP expression, and attenuated ERK 1/2 and CREB in the affected L5 spinal cord. In conclusion, intrathecal nefopam reduced mechanical allodynia in a rat neuropathic pain model. Its mechanical antiallodynic effect is associated with inhibition of glial activation and suppression of the transcription factors' mitogen-activated protein kinases in the spinal cord.
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The most common surgical options for trigeminal neuralgia (TN) are microvascular decompression (MVD) and gamma knife surgery (GKS). Currently, there is no definitive consensus as to which of the 2 options is more effective at providing immediate and long-lasting pain relief. This study seeks to better evaluate the differences between these 2 options in terms of rates of complete pain relief and pain-free recurrence. ⋯ MVD may be a more effective intervention than GKS because of the higher rates of initial pain-free outcomes and long-term pain-free outcomes, and lower rates pain-free recurrences.
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Neuropathic pain is a common complication of treatment with the anti-neoplastic drug paclitaxel. Animal studies suggest neuroinflammation and transient receptor potential channels TRPA1 and TRPV4 are involved in the pathogenesis of pain in this condition. However, how neuroinflammation and TRPA1 and TRPV4 are linked to cause pain in paclitaxel-treated animals is not known. ⋯ These results suggest that paclitaxel activation of TLR-4 to cause release of TNF-α from satellite glial cells increases the expression of TRPA1 and TRPV4 in DRG neurons to cause neuropathic pain.