Articles: neuralgia.
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Curr Pain Headache Rep · Dec 2024
ReviewIs Chronic Tendon Pain Caused by Neuropathy? Exciting Breakthroughs may Direct Potential Treatment.
Tendinopathy significantly impacts the quality of life and imposes a high economic burden, accounting for a large proportion of sports and musculoskeletal injuries. Traditionally considered a collagen-related inflammatory disorder, emerging evidence suggests a critical role of neuropathic processes in chronic tendon pain. ⋯ Chronic tendon pain may be predominantly neuropathic, driven by pathologic neuronal ingrowth from paratenon into the tendon proper. Interventions that accurately target and disrupt these nerve pathways could revolutionize the treatment of tendinopathy. Further research is required to validate these findings and refine treatment modalities to ensure safety and efficacy.
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Neuropathic pain (NP) is a widespread public health problem that existing therapeutic treatments cannot manage adequately; therefore, novel treatment strategies are urgently required. G-protein-coupled receptors are important for intracellular signal transduction, and widely participate in physiological and pathological processes, including pain perception. ⋯ Here we reviewed the advantages of Group I mGluRs negative allosteric modulators (NAMs) over orthosteric site antagonists based on allosteric modulation mechanism, and the challenges and opportunities of Group I mGluRs NAMs in NP treatment. This article aims to elucidate the advantages and future development potential of Group I mGluRs NAMs in the treatment of NP.
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Curr Pain Headache Rep · Nov 2024
ReviewAdvances in the Treatment of Neuropathic Pain by Sympathetic Regulation.
To explore the mechanism and therapeutic effect of sympathetic nerve regulation on neuropathic pain. ⋯ A comprehensive search was conducted in the PubMed and CNKI libraries, using the following keywords: stele ganglion block, neuropathic pain, sympathetic nerve block, sympathetic chemical destruction, and sympathetic radiofrequency thermocoagulation. We selected and critically reviewed research articles published in English that were related to sympathetic modulation in the treatment of neuropathic pain. The collected literature will be classified according to content and reviewed in combination with experimental results and clinical cases. Neuropathic pain was effectively treated with sympathetic regulation technology. Its mechanism includes the inhibition of sympathetic nerve activity, regulation of the inflammatory response, and inhibition of pain transmission, which greatly alleviates neuropathic pain in patients. Stellate ganglion blocks, thoracic and lumbar sympathectomies, chemical destruction, and radiofrequency thermocoagulation have been widely used to treat neuropathic pain. Sympathetic regulation can effectively relieve pain symptoms and improve the patient's quality of life by inhibiting sympathetic nerve activity, reducing the production and release of pain-related mediators, and inhibiting pain transmission. CT-guided radiofrequency thermocoagulation of the thoracic and lumbar sympathetic nerves is effective and durable, with few complications, and is recommended as a treatment for intractable neuropathic pain.
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Review Meta Analysis
Are combined conservative interventions effective in reducing pain, disability and/or global rating of pain in people with sciatica with known neuropathic pain mechanisms?
National Clinical Guidelines recommend an integrated combination of conservative management strategies for sciatica. However, the efficacy of such combinations have not been established. The purpose of this systemic review with meta-analysis was to determine the efficacy of combined conservative (non-pharmacological) compared to single interventions for people with sciatica with a confirmed neuropathic mechanism. ⋯ There are few studies that have combined conservative (non-pharmacological) interventions for the management of sciatica with a neuropathic component pain mechanism, as recommended by National Clinical Guidelines. This review indicates that combining conservative (no-pharmacological) management strategies appeared more effective than single interventions for the outcomes of low back pain in the short and long term, and for disability in the short term, but not for leg pain at any time point. The overall low certainty of evidence, suggests that future studies with more robust methodologies are needed.
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Understanding the mechanisms that underpin the transition from acute to chronic pain is critical for the development of more effective and targeted treatments. There is growing interest in the contribution of glial cells to this process, with cross-sectional preclinical studies demonstrating specific changes in these cell types capturing targeted timepoints from the acute phase and the chronic phase. In vivo longitudinal assessment of the development and evolution of these changes in experimental animals and humans has presented a significant challenge. ⋯ These advances now permit tracking of glial changes over time and provide the ability to relate these changes to pain-relevant symptomology, comorbid psychiatric conditions, and treatment outcomes at both a group and an individual level. In this article, we summarize evidence for gliosis in the transition from acute to chronic pain and provide an overview of the specific radiotracers available to measure this process, highlighting their potential, particularly when combined with ex vivo / in vitro techniques, to understand the pathophysiology of chronic neuropathic pain. These complementary investigations can be used to bridge the existing gap in the field concerning the contribution of gliosis to neuropathic pain and identify potential targets for interventions.