Articles: neuralgia.
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Curr Pain Headache Rep · May 2021
ReviewRepetitive Transcranial Magnetic Stimulation for Treating Chronic Neuropathic Pain: a Systematic Review.
Given pharmacological interventions' limited efficacy and abundance of its adverse effects, the repetitive transcranial magnetic stimulation (rTMS) is considered a viable non-invasive option for managing chronic neuropathic pain of different origins with promising outcomes. PURPOSE OF REVIEW: The provision of a systematic review of current literature on rTMS for managing chronic neuropathic pain of different origins, and assess its efficacy and outcomes, highlighting the need for standard protocols for utilizing rTMS. RECENT Variable stimulation modalities were trialed targeting the M1, DLPFC, and somatosensory cortices S1 and S2. ⋯ The lack of standard methods for rTMS, stimulatory parameters, and target stimulation site precludes concluding the optimal modality for stimulation. The practical algorithm by Lefaucheur and Nguyen (Neurophysiol Clin. 49(4):301-7, 2019) can guide setting standardized algorithms for rTMS. Defining optimal stimulation sites, frequencies, and pulses to maximize patient's pain relief and minimize required rTMS sessions requires further research.
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Leriche syndrome is an aortoiliac occlusive disease caused by atherosclerotic occlusion. We report a case of Leriche syndrome with a fracture that was suspected as complex regional pain syndrome (CRPS), as the post-traumatic pain gradually worsened in the form of excruciating neuropathic pain. ⋯ A chip fracture in a region with insufficient blood flow could manifest as excruciating neuropathic pain in Leriche syndrome.
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Chronic pain continues to present a large burden to the US healthcare system. Neuropathic pain, a common class of chronic pain, remains particularly difficult to treat despite extensive research efforts. Current pharmacologic regimens exert limited efficacy and wide, potentially dangerous side effect profiles. This review provides a comprehensive, preclinical evaluation of the literature regarding the role of flavonoids in the treatment of neuropathic pain. ⋯ Flavonoids are naturally occurring compounds, found in plants and various dietary sources, which may have potential benefit in neuropathic pain. Numerous animal-model studies have demonstrated this benefit, including reversal of hyperalgesia and allodynia. Flavonoids have also exhibited an anti-inflammatory effect relevant to neuropathic pain, as evidenced by the reduction in multiple pro-inflammatory mediators, such as TNF-α, NF-κB, IL-1β, and IL-6. Flavonoids represent a potentially new treatment modality for neuropathic pain in preclinical models, though human clinical evidence is yet to be explored at this time.
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Randomized Controlled Trial
Efficacy of Pulsed Radiofrequency or Short-Term Spinal Cord Stimulation for Acute/Subacute Zoster-Related Pain: A Randomized, Double-Blinded, Controlled Trial.
Postherpetic neuralgia (PHN) is the final stage of varicella zoster infection and a severe refractory neuropathic pain. Hence preventing transition of herpes zoster-related pain to PHN is a very important therapeutic principle for patients at an early stage, especially for older patients.Both pulsed radiofrequency (PRF) and short-term spinal cord stimulation (stSCS) have been proven to be effective to relieve acute/subacute zoster-related pain. However, which treatment could achieve better analgesic effects remains unclear. ⋯ PRF and stSCS are both effective and safe therapeutic alternatives for patients with acute/subacute zoster-related pain, however, stSCS could achieve more pain relief and improvement of life quality compared with PRF.
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Neuropathic pain remains an undertreated condition and there is a medical need to develop effective treatments. Accumulating evidence indicates that posttranscriptional regulation of gene expression is involved in neuropathic pain; however, RNA processing is not clearly investigated. Our study investigated the role of HuR, an RNA binding protein, in promoting neuropathic pain and trauma-induced microglia activation in the spared nerve injury mouse model. ⋯ An anti-HuR ASO inhibited the activation of spinal microglia by reducing the levels of proinflammatory cytokines, inducible nitric oxide synthase, the activation of nuclear factor-κB (NF-κB), and suppressed the spared nerve injury-induced overphosphorylation of spinal p38, ERK1/2 and c-Jun-N-terminal kinase (JNK)-1. In addition, HuR silencing increased the expression of the anti-inflammatory cytokine IL-10, promoting the shift of microglial M1 to M2 phenotype. Targeting HuR by i.n. anti-HuR ASO might represent a noninvasive promising perspective for neuropathic pain management by its powerful inhibition of microglia-mediated spinal neuroinflammation and promotion of an anti-inflammatory and neuroprotectant response.