Articles: neuropathic-pain.
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Frontiers in pharmacology · Jan 2019
Sigma-1 Receptor Inhibition Reduces Neuropathic Pain Induced by Partial Sciatic Nerve Transection in Mice by Opioid-Dependent and -Independent Mechanisms.
Sigma-1 (σ1) receptor antagonists are promising tools for neuropathic pain treatment, but it is unknown whether σ1 receptor inhibition ameliorates the neuropathic signs induced by nerve transection, in which the pathophysiological mechanisms and response to drug treatment differ from other neuropathic pain models. In addition, σ1 antagonism ameliorates inflammatory pain through modulation of the endogenous opioid system, but it is unknown whether this occurs during neuropathic pain. We investigated the effect of σ1 inhibition on the painful hypersensitivity associated with the spared nerve injury (SNI) model in mice. ⋯ The repeated administration of S1RA twice a day during 10 days reduced SNI-induced cold, mechanical, and heat hypersensitivity without inducing analgesic tolerance during treatment. These effects were observed up to 12 h after the last administration, when S1RA was undetectable in plasma or brain, indicating long-lasting pharmacodynamic effects. These data suggest that σ1 antagonism may have therapeutic value for the treatment of neuropathic pain induced by the transection of peripheral nerves.
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Journal of pain research · Jan 2019
The efficacy of pregabalin for the management of acute and chronic postoperative pain in thoracotomy: a meta-analysis with trial sequential analysis of randomized-controlled trials.
Pregabalin is commonly used as an analgesic for neuropathic pain. But pregabalin as an adjunct to a multimodal analgesic regimen - although standard clinical protocol in some settings - has remained controversial. This meta-analysis was conducted to identify the efficacy of pregabalin for management of postoperative pain in thoracotomy. ⋯ Pregabalin can prevent postoperative pain in thoracotomy and decrease incidence of neuropathic pain and morphine consumption. Pregabalin may be a valuable asset in management of acute and persistent postoperative pain in thoracotomy.
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Ann Phys Rehabil Med · Jan 2019
Virtual reality for spinal cord injury-associated neuropathic pain: Systematic review.
Treatment of spinal cord injury (SCI)-associated neuropathic pain is challenging, with limited efficacy and no definitive options, and SCI patients often show resistance to pharmacologic treatment. Virtual reality (VR) therapy is a non-invasive, non-pharmacologic alternative with minimal adverse effects. ⋯ VR therapy could reduce SCI-associated neuropathic pain, although the clinical significance of this analgesic effect is unclear. Clinical trials evaluating VR therapy as standalone and/or adjunct therapy for neuropathic pain in SCI patients are warranted.
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Review
The Etiological Contribution of GABAergic Plasticity to the Pathogenesis of Neuropathic Pain.
Neuropathic pain developing after peripheral or central nerve injury is the result of pathological changes generated through complex mechanisms. Disruption in the homeostasis of excitatory and inhibitory neurons within the central nervous system is a crucial factor in the formation of hyperalgesia or allodynia occurring with neuropathic pain. The central GABAergic pathway has received attention for its extensive distribution and function in neural circuits, including the generation and development of neuropathic pain. ⋯ In this review, we describe possible mechanisms associated with GABAergic plasticity, such as central sensitization and GABAergic interneuron apoptosis, and the epigenetic etiologies of GABAergic plasticity in neuropathic pain. Moreover, we summarize potential therapeutic targets of GABAergic plasticity that may allow for successful relief of hyperalgesia from nerve injury. Finally, we compare the effects of the GABAergic system in neuropathic pain to other types of chronic pain to understand the contribution of GABAergic plasticity to neuropathic pain.
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Chronic pain is a significant unmet medical problem. Current research regarding sodium channel function in pathological pain is advancing with the hope that it will enable the development of isoform-specific sodium channel blockers, a promising treatment for chronic pain. Before advancements in the pharmacological field, an elucidation of the roles of Nav1.7 and Nav1.8 in the pathophysiology of pain states is required. ⋯ Research concerning the genetic links of Nav1.7 and Nav1.8 in acquired neuropathic and inflammatory pain states from the scientific literature in this field is reported. The role of Nav1.7 and Nav1.8 in the generation and maintenance of abnormal neuronal electrogenesis and hyperexcitability highlights the importance of these channels in the development of pathological pain. However, further research in this area is required to fully elucidate the roles of Nav1.7 and Nav1.8 in the pathophysiology of pain for the development of subtype-specific sodium channel blockers.