Articles: neuralgia.
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Randomized Controlled Trial
Modulation of central pain mechanisms using high definition transcranial direct current stimulation: A double-blind, sham-controlled study.
The use of high-definition transcranial direct current stimulation (HD-tDCS) has shown analgesic effects in some chronic pain patients, but limited anti-nociceptive effects in healthy asymptomatic subjects. ⋯ HD-tDCS reduced the facilitation of TSP caused by tonic pain suggesting that efficacy of HD-tDCS might depend on the presence of sensitized central pain mechanisms.
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Studies have shown that the activation of microglia is the main mechanism of neuropathic pain. Kv1.3 channel is a novel therapeutic target for treating neuroinflammatory disorders due to its crucial role in subsets of microglial cells. As such, it may be involved in the processes of neuropathic pain, however, whether Kv1.3 plays a role in neuroinflammation following peripheral nerve injury is unclear. ⋯ Our research indicates that the Kv1.3 channel in the spinal cord contributes to neuropathic pain by promoting microglial M1 polarization and activating the NLRP3 inflammasome.
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Case Reports
Second-degree burn induced by high-concentration topical capsaicin with mobility sequelae: a case report.
High-concentration topical capsaicin is used as a second-line treatment for neuropathic pain. Transient, mild burning sensation and erythema are expected adverse drug reactions. ⋯ Nine months after the application, neuropathic pain still remained and the patient described mobility difficulties in daily activities, preventing her from returning to work. This report aims to raise the question of the benefit/risk ratio of high concentration topical capsaicin.
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To investigate the impact of early versus delayed surgery on sensory abnormalities in acute traumatic central cord syndrome (ATCCS). ⋯ Central hypersensitivity may be involved in the persistence of sensory symptoms in ATCCS, and this augmented central processing may commence in the early stage. Early surgical treatment may reverse dysfunction of endogenous pain modulation, thus reducing the risk of central sensitization and alleviating sensory symptoms.