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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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 objective of this article was to review the positive scientific data on antidepressants and opioids, which are largely confined to randomized controlled trials in two neuropathic pain conditions that have proved to be good models for clinical investigation. These two disorders are postherpetic neuralgia and painful diabetic neuropathy. ⋯ First-line therapy for neuropathic pain may be either an older generation antidepressant such as amitriptyline or nortriptyline or the anticonvulsant gabapentin. For refractory cases, chronic opioid therapy may be the only avenue of relief, and evidence is accumulating that this approach is safe if proper guidelines are observed.