Articles: neuralgia.
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Bortezomib is a mainstay of therapy for multiple myeloma, frequently complicated by painful neuropathy. The objective of this study was to describe clinical, electrophysiological, and pathological changes of bortezomib-induced peripheral neuropathy (BiPN) in detail and to correlate pathological changes with pain descriptors. Clinical data, nerve conduction studies, and lower leg skin biopsies were collected from 22 BiPN patients. ⋯ Finally, significant correlations between UDNFD of PGP9.5 versus the evaluative Pain Rating Index (PRI) and number of words count (NWC) of the MPQ, and significant inverse correlations between SENFD/UDNFD of CGRP versus the sensory-discriminative MPQ PRI/NWC were found. BiPN is a sensory neuropathy, in which neuropathic pain is the most striking clinical finding. Bortezomib-induced neuropathic pain may be driven by sprouting of parasympathetic fibers in the upper dermis and impaired regeneration of CGRP fibers in the subepidermal layer.
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Autonomic dysreflexia (AD) and neuropathic pain occur after severe injury to higher levels of the spinal cord. Mechanisms underlying these problems have rarely been integrated in proposed models of spinal cord injury (SCI). Several parallels suggest significant overlap of these mechanisms, although the relationships between sympathetic function (dysregulated in AD) and nociceptive function (dysregulated in neuropathic pain) are complex. ⋯ In addition, numerous nociceptors become hyperexcitable, hypersensitive to chemicals associated with injury and inflammation, and spontaneously active, greatly amplifying sensory input to sensitized spinal circuits. As discussed with the aid of a preliminary functional model, these effects are likely to have mutually reinforcing relationships with each other, and with consequences of SCI-induced interruption of descending excitatory and inhibitory influences on spinal circuits, with SCI-induced inflammation in the spinal cord and in DRGs, and with activity in sympathetic fibers within DRGs that promotes local inflammation and spontaneous activity in sensory neurons. This model suggests that interventions selectively targeting hyperactivity in C-nociceptors might be useful for treating chronic pain and AD after high SCI.
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Background: Clinical studies have shown that applying pulsed radiofrequency (PRF) to the neural stem could relieve neuropathic pain (NP), albeit through an unclear analgesic mechanism. And animal experiments have indicated that calcitonin gene-related peptide (CGRP) expressed in the dorsal root ganglion (DRG) is involved in generating and maintaining NP. In this case, it is uncertain whether PRF plays an analgesic role by affecting CGRP expression in DRG. ⋯ Meanwhile, the CGRP content of Group D gradually dropped over time, from 76.4 pg/mg (Day 0) to 57.5 pg/mg (Day 14). Conclusions: In this study, we found that, after sciatic nerve ligation, rats exhibited apparent hyperalgesia and allodynia, and CGRP mRNA and CGRP contents in the L4-L6 DRG increased significantly. Through lowering CGRP expression in the DRG, PRF treatment might relieve the pain behaviors of NP.
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Several guidelines for neuropathic pain management and various effective drugs are available; however, neuropathic pain remains undertreated. This retrospective study aimed to evaluate the efficacy of topical capsaicin 8% in peripheral neuropathic pain in a routine clinical setting. ⋯ This study suggests that topical capsaicin 8% reduces peripheral neuropathic pain as well as treatment pain area.
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Protein kinase M ζ is well known for its role in maintaining memory and pain. Previously, we revealed that the activation of protein kinase M ζ in the anterior cingulate cortex plays a role in sustaining neuropathic pain. ⋯ We also reveal that the inhibition of protein kinase M ζ through zeta inhibitory peptide treatment is enough to reduce mechanical allodynia responses in mice with one-month-old nerve injuries. However, the zeta inhibitory peptide treatment was only effective for a limited time.