The Clinical journal of pain
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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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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.
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Herpes zoster is a common and painful disease that is caused by reactivation of the varicella-zoster virus. Herpes zoster pain that persists after healing of the acute infection is termed postherpetic neuralgia (PHN), a chronic pain syndrome that is often refractory to all treatment. The prevalence of PHN is expected to increase substantially in the coming decades, because the incidence of herpes zoster and the risk of PHN will both increase as the population ages. Although the results of recent studies provide a basis for improved treatment of patients with PHN, as many as half of all PHN patients do not obtain relief of their pain. Research on the development of improved treatments is continuing, but it has not been generally recognized that an equally important goal should be the design of interventions to prevent PHN. The prevention of PHN would lead to major reductions in disability, suffering, and the use of health care resources. ⋯ This treatment approach would be expected to reduce the risk of PHN in herpes zoster patients by attenuating acute pain and thereby preventing the initiation of central mechanisms of chronic pain.
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The clinical approach to complex regional pain syndrome (CRPS) is complicated by a lack of precision diagnostically, and a lack of evidence-based information for treatment. The vagaries of diagnosis were somewhat improved by the Orlando Conference (1993), where a consensus panel of experts developed a new taxonomy and criteria. Unfortunately the criteria can be based entirely on subjective grounds (patient history), and as such provides a very sensitive but not very specific device. ⋯ Once the diagnosis is made it is necessary to proceed in a pragmatic empirical way, following the best guidelines available. The guidelines should be considered a "rough sketch" and the key to clinical success will be flexibility, a vast fund of the available knowledge, patience, and compassion. To allow the deficiencies in the science to paralyze the clinical process is therapeutic nihilism, and not acceptable.
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The objective was to report on the possibility of allergic reaction to the components of a spinal cord stimulator. ⋯ There exists a possibility that a patient may experience an allergic reaction to spinal cord stimulator components. Recognition of such contact sensitivity is important for physicians implanting such devices. Patients may be misdiagnosed as having infections, which can delay appropriate management; definitive diagnosis can be confirmed with a patch test. Treatment consists of removal of such devices.