Articles: neuralgia.
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Cell. Mol. Neurobiol. · Aug 2020
ReviewRegional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury.
Spinal cord injury (SCI) causes maladaptive changes to nociceptive synaptic circuits within the injured spinal cord. Changes also occur at remote regions including the brain stem, limbic system, cortex, and dorsal root ganglia. These maladaptive nociceptive synaptic circuits frequently cause neuronal hyperexcitability in the entire nervous system and enhance nociceptive transmission, resulting in chronic central neuropathic pain following SCI. ⋯ Current literature describes regional studies of electrophysiological or neurochemical mechanisms for enhanced nociceptive transmission post-SCI, but few studies report the electrophysiological, neurochemical, and neuroanatomical changes across the entire nervous system following a regional SCI. We, along with others, have continuously described the enhanced nociceptive transmission in the spinal dorsal horn, brain stem, thalamus, and cortex in SCI-induced chronic central neuropathic pain condition, respectively. Thus, this review summarizes the current understanding of SCI-induced neuronal hyperexcitability and maladaptive nociceptive transmission in the entire nervous system that contributes to chronic central neuropathic pain.
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Peripheral neuralgia is a common cause of chronic pain. Treatment might be challenging, and the condition can be resistant to commonly used treatment modalities for chronic pain. We present five cases of peripheral neuralgia who were successfully treated using wireless peripheral nerve stimulation. ⋯ We present five patients with peripheral neuralgias resistant to other treatment modalities who received excellent pain relief following implantation of a peripheral nerve stimulator.
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Gabapentinoids are commonly prescribed for the treatment of neuropathic pain but are not recommended for the primary treatment of carpal tunnel syndrome (CTS). We sought (1) to investigate the preoperative use of gabapentinoids for the treatment of CTS and (2) to determine whether preoperative exposure is associated with persistent gabapentinoid and opioid use after carpal tunnel release. ⋯ Prognostic II.
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This study was performed to characterize the effect of microRNA-101 (miR-101) on the pain hypersensitivity in CCI rat models with the involvement of mitogen-activated protein kinase phosphatase 1 (MKP-1) in spinal cord microglial cells. The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) in the developed CCI models were determined to assess the hypersensitivity of rats to mechanical stimulation and thermal pain. To assess inflammation, the levels of interleukin (IL)-1β, IL-6 and tumour necrosis factor-α (TNF-α) in the spinal dorsal horns of CCI rats and lipopolysaccharide (LPS)-activated microglial cells were examined. miR-101 and MKP-1 gain- and loss-of-function experiments were conducted in in vivo and in vitro settings to examine the roles of miR-101 and MKP-1 in CCI hypersensitivity and inflammation. ⋯ MiR-101 was shown to target MKP-1, inhibiting its expression. Moreover, miR-101 promoted pain hypersensitivity in CCI rat models by inhibiting MKP-1 expression and activating the mitogen-activated protein kinase (MAPK) signalling pathway. Taken together, miR-101 could potentially promote hypersensitivity and inflammatory response of microglial cells and aggravate neuropathic pain in CCI rat models by inhibiting MKP-1 in the MAPK signalling pathway.
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Brain Behav. Immun. · Aug 2020
S100A9 plays a pivotal role in a mouse model of herpetic neuralgia via TLR4/TNF pathway.
Herpetic neuralgia is a painful condition following herpes zoster disease, which results from Varicella-zoster virus reactivation in the dorsal or trigeminal sensory ganglia. Nevertheless, the pathophysiological mechanisms involved in herpetic neuralgia are not well understood. Recently, we identified, that neuroimmune-glia interactions in the sensory ganglion is a critical mechanism for the development of herpetic neuralgia. ⋯ Functionally, genetic or pharmacological inhibition of S100A9 impairs the development of HSV-1 infection-induced mechanical pain hypersensitivity. Finally, we found that the pronociceptive role of S100A9 in herpetic neuralgia depends on the TLR4/TNF pathway. These results unraveled previously unknown mechanisms involved in the pathophysiology of herpetic neuralgia and indicate that S100A9 might be an important target for novel therapies aiming acute herpetic neuralgia.