Articles: neuralgia.
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Our aim was to investigate the differences in pressure sensitivity over musculoskeletal and nerve symptomatic and distant areas between individuals with plantar heel pain and healthy subjects and to determine the relationship between sensitivity to pressure pain, foot pain, and fascia thickness. Thirty-five patients with unilateral chronic plantar heel pain and 35 matched healthy controls participated. Pressure pain thresholds (PPTs) were assessed bilaterally over several nerve trunks (median, radial, ulnar, common peroneal, tibial, and sural nerve trunks) and musculoskeletal structures (calcaneus, medial gastrocnemius, tibialis anterior, and second metacarpal) by an assessor blinded to the subject's condition. ⋯ This study found widespread pressure pain hypersensitivity over both nerve trunks and musculoskeletal structures in individuals with unilateral chronic plantar heel pain, suggesting the presence of a central altered central nociceptive pain processing. Pressure hypersensitivity over nerve trunks on the lower extremity was associated with higher pain intensity and related disability. PERSPECTIVES: This study found widespread pressure hypersensitivity over both nerve trunks and musculoskeletal structures in individuals with unilateral chronic plantar heel pain, as a manifestation of a centrally altered central nociceptive pain processing.
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To explore the role and potential mechanism of miR-212-3p in neuropathic pain regulation. ⋯ The expression of miR-212a-3p attenuates neuropathic pain by targeting NaV1.3.
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The most common neurological complication in patients receiving successful combination antiretroviral therapy (cART) is peripheral neuropathic pain. Data show that distal symmetric polyneuropathy (DSP) also develops along with murine acquired immunodeficiency syndrome (MAIDS) after infection with the LP-BM5 murine retrovirus mixture. Links between cannabinoid receptor 2 (CB2R) and peripheral neuropathy have been established in animal models using nerve transection, chemotherapy-induced pain, and various other stimuli. ⋯ Infection-induced macrophage activation and T-cell infiltration into the DRG and LSC were observed at 12 wk p.i., but this neuroinflammation was not affected by treatment with any CB2R agonist. Activation of JAK/STAT3 has been shown to contribute to development of neuropathic pain in the LSC and pretreatment of primary murine microglia (2 h) with JWH015-, JWH133-, or Gp1a-blocked IFN-gamma-induced phosphorylation of STAT1 and STAT3. Taken together, these data show that CB2R agonists demonstrate acute, but not long-term, antiallodynic effects on retrovirus infection-induced neuropathic pain.
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Frontiers in neurology · Jan 2019
Intra-Venous Lidocaine to Relieve Neuropathic Pain: A Systematic Review and Meta-Analysis.
Background: The prevalence of neuropathic pain is estimated to be between 7 and 10% in the general population. The efficacy of intravenous (IV) lidocaine has been studied by numerous clinical trials on patients with neuropathic pain. The aim of this systematic review and meta-analysis was to evaluate the efficacy of IV lidocaine compared with a placebo for neuropathic pain and secondly to assess the safety of its administration. ⋯ IV infusions of the drug are associated with an increased risk of side effects compared to a placebo. However, the risk of serious adverse events is negligible. Further, well-designed RCTs evaluating the effects of various dosages and infusion periods of IV lidocaine are required to provide clear guidelines on its clinical use.