Articles: neuropathic-pain.
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Comparative Study
Comparison of the analgesic effects of pulse radiofrequency and cryoablation in rabbits with mental nerve neuropathic pain.
After mental nerve injury, several sensory disorders may occur. The alterations in sensation may differ from mild paresthesia to complete anesthesia, or neuropathic pain. Neuropathic pain is a difficult clinical condition to manage. The aim of this study was to compare the analgesic effects of pulsed radiofrequency (PRF) and cryoablation in an experimental mental nerve neuropathic pain model in rabbits. ⋯ Both PRF and cryoablation therapies are successful in the treatment of experimentally induced mental nerve neuropathic pain in rabbits.
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Anesthesia and analgesia · May 2018
Neural Invasion Spreads Macrophage-Related Allodynia via Neural Root in Pancreatic Cancer.
Neural invasion (N-inv) induces the neural damage and pain in pancreatic cancer (PCa). Benign nerve injury evokes allodynia through neuroinflammation in the neural root, which might be seen in PCa. Macrophages have the potential to release excitatory cytokines after nerve injury and so may play a role in the generation of chronic neuropathic pain. The aim of this study is to represent N-inv-induced allodynia in patients with PCa and to characterize allodynia-related neuroinflammation as macrophage accumulation on dorsal root ganglion (DRG) in the N-inv animal model (N-inv model). ⋯ The present study first showed that the N-inv-induced allodynia was spread in patients with PCa and in the N-inv model. Allodynia was related to the amount of macrophages at DRG in the N-inv model. The neuroinflammation may be a target for researching the N-inv-induced pain mechanism and developing novel analgesics.
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Elevated N-methyl-D-aspartate receptor (NMDAR) activity is linked to central sensitization and chronic pain. However, NMDAR antagonists display limited therapeutic potential because of their adverse side effects. Novel approaches targeting the NR2B-PSD95-nNOS complex to disrupt signaling pathways downstream of NMDARs show efficacy in preclinical pain models. ⋯ Finally, TAT-GESV (i.t.) did not induce NMDAR-mediated motor ataxia in the rotarod test and did not alter basal nociceptive thresholds in the radiant heat tail-flick test. These observations support the hypothesis that antiallodynic efficacy of an nNOS-NOS1AP disruptor may result, at least in part, from blockade of p38 MAPK-mediated downstream effects. Our studies demonstrate, for the first time, that disrupting nNOS-NOS1AP protein-protein interactions attenuates mechanistically distinct forms of neuropathic pain without unwanted motor ataxic effects of NMDAR antagonists.
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Neuropathic pain (NP) is an increasingly common chronic pain state and a major health burden, affecting approximately 7% to 10% of the general population. Emerging evidence suggests that genetic factors could partially explain individual susceptibility to NP and the estimated heritability in twins is 37%. The aim of this study was to systematically review and summarize the studies in humans that have investigated the influence of genetic factors associated with NP. ⋯ These findings demonstrate an important and specific contribution of genetic factors to the risk of developing NP. However, large-scale replication studies are required to validate these candidate genes. Our review also highlights the need for genome-wide association studies with consistent case definition to elucidate the genetic architecture underpinning NP.