Articles: neuralgia.
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Cochrane Db Syst Rev · Oct 2015
Review Meta AnalysisOral nonsteroidal anti-inflammatory drugs for neuropathic pain.
Although often considered to be lacking adequate evidence, nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used in the management of neuropathic pain. Previous surveys found 18% to 47% of affected people reported using NSAIDs specifically for their neuropathic pain, although possibly not in the United Kingdom (UK). ⋯ There is no evidence to support or refute the use of oral NSAIDs to treat neuropathic pain conditions.
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It is estimated that 23 million Germans suffer from chronic pain. A recent survey has revealed that 30 % of chronic pain patients are dissatisfied with their pain management. Furthermore, five million Germans suffer from neuropathic pain, 20 % of whom are inadequately treated. ⋯ Besides well-established therapeutic agents and current -therapeutic standards, it discusses specific options based on guidelines (where available). Current knowledge on peri- and postoperative pain management is briefly outlined. This article addresses: ▸ The fundamentals of the classification and neurophysiology of pain; ▸ Standards for pain documentation in children and adults; ▸ General standards for pharmaceutical pain management; ▸ Current specific treatment options for postherpetic neuralgia, leg ulcers, and -pyoderma gangrenosum in conjunction with the expanded WHO analgesic -ladder.
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We have previously demonstrated that activation of the spinal sigma-1 receptor (Sig-1R) plays an important role in the development of mechanical allodynia (MA) via secondary activation of the N-methyl-d-aspartate (NMDA) receptor. Sig-1Rs have been shown to localize to astrocytes, and blockade of Sig-1Rs inhibits the pathologic activation of astrocytes in neuropathic mice. However, the mechanism by which Sig-1R activation in astrocytes modulates NMDA receptors in neurons is currently unknown. d-serine, synthesized from l-serine by serine racemase (Srr) in astrocytes, is an endogenous co-agonist for the NMDA receptor glycine site and can control NMDA receptor activity. ⋯ Finally, BD-1047 administration inhibited the development of MA and this inhibition was reversed by intrathecal treatment with exogenous d-serine. These findings demonstrate for the first time that the activation of Sig-1Rs increases the expression of Srr and d-serine in astrocytes. The increased production of d-serine induced by CCI ultimately affects dorsal horn neurons that are involved in the development of MA in neuropathic mice.
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Chronic widespread pain (CWP) has complex aetiology and forms part of the fibromyalgia syndrome. Recent evidence suggests a higher frequency of neuropathic pain features in those with CWP than previously thought. The aim of this study was to determine the prevalence of neuropathic pain features in individuals with CWP and to estimate the influence of genetic and environmental factors on neuropathic pain in CWP. ⋯ Bivariate analysis of the 2 pain traits revealed that genetic predisposition to neuropathic pain is shared with that for CWP. This is the first study to provide formal heritability estimates for neuropathic pain in CWP. The findings suggest that at least some of the genetic factors underlying the development of neuropathic pain and CWP are the same.
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Neuropathic pain is defined as pain arising as a direct consequence of a lesion or a disease affecting the somatosensory system and it affects around 1 in 4 diabetic patients in the UK. The purpose of this genome-wide association study (GWAS) was to identify genetic contributors to this disorder. Cases of neuropathic pain were defined as diabetic patients with a multiple prescription history of at least one of five drugs specifically indicated for the treatment of neuropathic pain. ⋯ We found a cluster in the Chr1p35.1 (ZSCAN20-TLR12P) with a lowest P value of 2.74 × 10(- 7) at rs71647933 in females and a cluster in the Chr8p23.1, next to HMGB1P46 with a lowest P value of 8.02 × 10(- 7) at rs6986153 in males. Sex-specific narrow sense heritability was higher in males (30.0%) than in females (14.7%). This GWAS on diabetic neuropathic pain provides evidence for the sex-specific involvement of Chr1p35.1 (ZSCAN20-TLR12P) and Chr8p23.1 (HMGB1P46) with the disorder, indicating the need for further research.