Articles: neuralgia.
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If the patient with hand pain remains without significant relief and without recovery of function after appropriate pharmaceutical and physical modality treatments, it is appropriate to consider a surgical approach to the pain. Categories of pain amenable to a surgical approach are pain caused by nerve compression, pain caused by a neuroma, and joint pain of neural origin. ⋯ Painful neuroma must be resected to stop the pain generator. For a painful joint, the biomechanics of that joint must first be stable before denervation.
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J Vasc Interv Radiol · Feb 2016
Cryoneurolysis in Patients with Refractory Chronic Peripheral Neuropathic Pain.
To evaluate the safety and efficacy of cryoneurolysis in patients with refractory peripheral neuropathic pain. ⋯ Cryoneurolysis caused a significant decrease in self-reported pain scores in patients with chronic refractory neuropathic pain, with moderately long-term relief. Cryoneurolysis is an additional therapy that can alleviate severe chronic neuropathic pain.
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Neuroscience bulletin · Feb 2016
Upregulation of Chemokine CXCL12 in the Dorsal Root Ganglia and Spinal Cord Contributes to the Development and Maintenance of Neuropathic Pain Following Spared Nerve Injury in Rats.
Emerging evidence indicates that CXCL12/CXCR4 signaling is involved in chronic pain. However, few studies have systemically assessed its role in direct nerve injury-induced neuropathic pain and the underlying mechanism. Here, we determined that spared nerve injury (SNI) increased the expression of CXCL12 and its cognate receptor CXCR4 in lumbar 5 dorsal root ganglia (DRG) neurons and satellite glial cells. ⋯ The mechanical hypersensitivity induced in naïve rats by i.t. CXCL12 was alleviated by pretreatment with the MEK inhibitor PD98059. Collectively, our results revealed that TNF-α might mediate the upregulation of CXCL12 in the DRG and spinal cord following SNI, and that CXCL12/CXCR4 signaling via ERK activation contributes to the development and maintenance of neuropathic pain.
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T-type channels are important contributors to the initiation and the maintenance of chronic pain states. Blocking T-type channels is therefore a possible therapeutic strategy for relieving pain. Here, we report the Cav3.2 T-type channel blocking action of a previously reported small organic molecule, KYS-05090S. ⋯ Its antinociceptive effect was not observed when delivered to Cav3.2 null-mice revealing a Cav3.2-dependent mechanism. KYS-05090S also reduced neuropathic pain in a model of partial sciatic nerve injury. Those results indicate that KYS-05090S mediates a potent analgesic effect in inflammatory and neuropathic pain through T-type channel modulation, suggesting that its scaffold could be explored as a new class of analgesic compounds.
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Targeting peripheral neuropathic pain at its origin may prevent the development of hypersensitivity. Recently we showed this can be mediated by opioid receptors at the injured nerve trunk. Here, we searched for the most relevant peripheral site to block transient receptor potential vanilloid 1 (TRPV1), and investigated analgesic interactions between TRPV1 and opioids in neuropathy. ⋯ Together, the identification of the primary action site in damaged nerves is crucial for effective pain control. Contrary to opioids, the TRPV1 blockade in the injured nerve peripheral terminals, rather than at the nerve trunk, appears promising against heat pain. Opioid/TRPV1 antagonist combinations at both locations partially reduced neuropathy-triggered heat and mechanical pain.