The Clinical journal of pain
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Several independent pathophysiological mechanisms in both the peripheral and central nervous system are responsible for sensory symptoms as well as spontaneous and evoked pains in peripheral neuropathies: (1) Pathologic active or sensitized nociceptors can induce secondary changes in central processing, leading to spinal cord hyperexcitability that causes input from mechanoreceptive Abeta-fibers (light touching) to be perceived as pain. These patients characteristically have spontaneous pain, heat hyperalgesia, static mechanical allodynia, and and severe dynamic mechanical allodynia. (2) Nociceptor function may be selectively impaired within the allodynic skin. Pain and temperature sensation are profoundly impaired but light moving mechanical stimuli can often produce severe pain (dynamic mechanical allodynia). ⋯ A thorough analysis of sensory symptoms may, reveal the underlying mechanisms that are mainly active in a particular patient. The treatment of neuropathic pain is currently unsatisfactory. In the future, drugs will be developed that address specifically the relevant combination of mechanisms.
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Our knowledge about the pathogenesis of neuropathic pain has grown significantly during last two decades. Basic research with animal models of neuropathic pain and human clinical trials with neuropathic pain have accumulated solid evidence that a number of pathophysiologic and biochemical changes take place in the nervous system at a peripheral or central level as a result of the insult or disease. Many similarities between the pathophysiologic phenomena observed in some epilepsy models and neuropathic pain models justify the rationale for the use of anticonvulsant drugs in the symptomatic management of neuropathic pain disorders. ⋯ One small clinical trial with lamotrigine demonstrated improved pain control in TN. Evidence in support of the efficacy of anticonvulsant drugs in the treatment of neuropathic pain continues to evolve, and benefits have been clearly demonstrated in the case of GBP and CBZ. More advances in our understanding of the mechanisms underlying neuropathic pain syndromes should further our opportunities to establish the role of anticonvulsants in the treatment of neuropathic pain.
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Despite the availability of different pharmacologic agents for the treatment of various chronic neuropathic pain syndromes, complete symptom reduction and/or complete functional restoration is rarely achieved. New, safe, and effective treatments for chronic neuropathic pain, therefore, must be developed. One such agent, the lidocaine patch (Lidoderm, Endo Pharmaceuticals, Inc., Chadds Ford, PA), has been approved recently by the US Food and Drug Administration for the treatment of postherpetic neuralgia. ⋯ The Lidoderm patch is a topical agent and, consequently, insignificant serum levels are achieved even with chronic use. This fact enhances its safety. Recent studies have suggested that the lidocaine patch may be effective for chronic neuropathic pain conditions other than postherpetic neuralgia as well.
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Neuropathic pain is highly prevalent in patients with cancer and patients with AIDS, has profound effects on ability to function and quality of life, and is undertreated. Multiple obstacles to the adequate treatment of pain in patients with cancer and AIDS have been identified. Specific factors relevant to neuropathic pain, as well as the prevalence of substance abuse disorders in the AIDS population, contribute heavily to the undertreatment of pain in these patients. ⋯ The parallel objective of providing optimal analgesic treatment also requires an aggressive and systematic approach. The presence of comorbid substance abuse issues requires special considerations that ordinarily do not compromise analgesic approaches. This review summarized the neuropathic pain syndromes seen in cancer and in AIDS, presents principles of pain assessment, highlights treatment options, and addresses the issue of pain and chemical dependency.
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Studies on the psychosocial impact of neuropathic pain conditions, including postherpetic neuralgia, diabetic neuropathy, complex regional pain syndrome, post spinal cord injury, postamputation, and AIDS-related neuropathy, are reviewed. Although limited, data are consistent with the larger literature on chronic pain and indicate that neuropathic pain reduces quality of life, including mood and physical and social functioning. ⋯ Clinical trials of psychological interventions have not been reported, although some case series of successful treatment of neuropathic pain are reported, primarily in the area of biofeedback. Given the evidence indicating the broad impact of neuropathic pain on many areas of function, it is surprising that so few studies have investigated the impact of psychological interventions in these populations.