Current pain and headache reports
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Complex regional pain syndrome (CRPS) is clinically characterized by pain, abnormal regulation of blood flow and sweating, edema of skin and subcutaneous tissues, active and passive movement disorders, and trophic changes. It is classified as type I (reflex sympathetic dystrophy) and type II (causalgia). ⋯ This situation changed when a proposal to redefine neuropathic pain states was recently published, which resulted in an exclusion of CRPS from neuropathic pain disorders. We analyzed the strength of the scientific evidence that supports the neuropathic nature of complex regional pain syndromes.
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Central neuropathic pain is common in multiple sclerosis (MS), and its prevalence increases with physical disability. Sufficient evidence links dysesthetic pain, trigeminal neuralgia, Lhermitte's sign, and painful tonics spasms to plaque formation in the spinal cord and brain, whereas the association with headache and back pain remains unclear. ⋯ Because of unique characteristics of MS-related trigeminal neuralgia, ganglion and root level neuroablative procedures are worth considering before microvascular decompression. Overall, the lack of controlled clinical trials, together with our limited understanding of the pathophysiological mechanisms involved, form a hindrance to a systematic and rational management of MS-related pain.
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Despite ongoing efforts, neither effective treatments nor mechanistic understanding of the pathogenesis of human neuropathic pain exists. Genetic association studies may point to the novel molecules that mediate neuropathic pain, facilitating its understanding and management. ⋯ This article summarizes and discusses current strategies to optimize population-based association studies of human neuropathic pain focusing on principles of measuring neuropathic pain phenotypes and genotyping techniques. We also consider advantages and challenges of study designs and statistical analyses.
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Curr Pain Headache Rep · Jun 2010
ReviewSpinal cord mechanisms of chronic pain and clinical implications.
Chronic pain is a prevalent and challenging problem for most medical practitioners. Because of the complex pathologic mechanisms involved in chronic pain, optimal treatment is still under development. The spinal cord is an important gateway for peripheral pain signals transmitted to the brain. ⋯ These events induce multiple inflammatory and neuropathic processes in the spinal cord dorsal horn, and trigger modification and plasticity of local neural circuits. As a result, ongoing noxious signals to the brain are amplified and prolonged, a phenomenon known as central sensitization. In this review, the molecular events associated with central sensitization, as well as their clinical implications, are discussed.
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Curr Pain Headache Rep · Apr 2010
ReviewThe effect of morphine on glial cells as a potential therapeutic target for pharmacological development of analgesic drugs.
Opioids have played a critical role in achieving pain relief in both modern and ancient medicine. Yet, their clinical use can be limited secondary to unwanted side effects such as tolerance, dependence, reward, and behavioral changes. Identification of glial-mediated mechanisms inducing opioid side effects include cytokine receptors, kappa-opioid receptors, N-methyl-D-aspartate receptors, and the recently elucidated Toll-like receptors. Newer agents targeting these receptors such as AV411, MK-801, AV333, and SLC022, and older agents used outside the United States or for other disease conditions, such as minocycline, pentoxifylline, and UV50488H, all show varied but promising profiles for providing significant relief from opioid side effects, while simultaneously potentiating opioid analgesia.