Articles: neuralgia.
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Neuropathic pain is a widespread clinical issue caused by somatosensory nervous system damage, affecting numerous individuals. It poses considerable economic and public health challenges, and managing it can be challenging due to unclear underlying mechanisms. Nevertheless, emerging evidence suggests that neurogenic inflammation and neuroinflammation play a role in developing pain patterns. ⋯ However, our limited knowledge of miRNA targets hinders a complete grasp of miRNA's functions. Meanwhile, exploring exosomal miRNA, a recently uncovered role, has significantly advanced our comprehension of neuropathic pain's pathophysiology in recent times. In this review, we present a comprehensive overview of the latest miRNA studies and explore the possible ways miRNAs might play a role in the development of neuropathic pain.
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Observational Study
The Impact of Dorsal Root Ganglion Stimulation on Pain Levels and Functionality in Patients With Chronic Postsurgical Knee Pain.
Chronic postsurgical pain is a considerable source of disabling neuropathic pain. Rates of knee replacement surgeries are increasing, and many patients report chronic postsurgical pain in their wake. When conventional therapies prove ineffective, neuromodulation options such as dorsal root ganglion stimulation (DRGS) may be used. However, little is known about the effect of DRGS on improvements in quantitative functional outcome parameters. ⋯ Both subjective-based questionnaire and quantitative examination-based variables were in broad agreement on the value of DRGS in improving functionality and chronic postsurgical pain in the knee. Although this finding is limited by the small sample size, this intervention may have utility in the many cases in which pain becomes problematic after orthopedic knee surgery.
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Postgraduate medicine · Jan 2024
Obstructive sleep apnea increases the risk of herpes zoster and postherpetic neuralgia.
Diseases associated with chronic pain are typically a major source of stress for patients; and have been linked to herpes zoster (HZ) development. Here, we investigated whether obstructive sleep apnea (OSA) is a potential stressor that increases the risk of HZ and postherpetic neuralgia (PHN) in affected individuals. ⋯ OSA increases the risk of not only HZ but also PHN. Therefore, patients with OSA should be aware of the potential effect of the disease on their stress levels, as well as the increased risk of developing HZ and PHN.
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Neuropathic pain is caused by injury or disease of the somatosensory system, and its course is usually chronic. Several studies have been dedicated to investigating neuropathic pain-related targets; however, little attention has been paid to the persistent alterations that these targets, some of which may be crucial to the pathophysiology of neuropathic pain. The present study aimed to identify potential targets that may play a crucial role in neuropathic pain and validate their long-term impact. ⋯ In vivo experiments showed that sustained suppression of spinal NHE1 expression by siRNA-loaded nanoparticles resulted in delayed hyperalgesia in naïve and SNL model rats, whereas amiloride-induced transient suppression of NHE1 expression yielded no significant changes in pain sensitivity. We identified Slc9a1, which encodes NHE1, as a key gene in neuropathic pain. Utilizing the sustained release properties of nanoparticles enabled us to elucidate the chronic role of decreased NHE1 expression, establishing its significance in the mechanisms of neuropathic pain.
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Randomized Controlled Trial Multicenter Study
The effect of lacosamide in peripheral neuropathic pain: A randomized, double-blind, placebo-controlled, phenotype-stratified trial.
Neuropathic pain is common and difficult to treat. The sodium channel blocker lacosamide is efficacious in animal models of pain, but its effect on neuropathic pain in humans is inconclusive. ⋯ Treatment of neuropathic pain is often a trial and error process. Little is known about which patient benefit from which kind of medication. The sodium channel blocker lacosamide shows variable effect on neuropathic pain. Pain sensory phenotype, as defined by quantitative sensory testing, did not predict response to treatment with lacosamide.