Articles: neuralgia.
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Neuropathic pain is responsible for a significant amount of the morbidity associated with generalized and focal peripheral neuropathies. It is a consequence of alterations in neuronal function, chemistry, and structure that occur secondary to nerve injury. These manifestations of neuronal plasticity occur in the peripheral nerve, spinal cord, and brain. ⋯ These include antidepressants, first- and second-generation anticonvulsants, antiarrhythmic agents, topical agents, N-methyl-D-aspartate receptor antagonists, and opioid analgesics. The use of these adjuvant analgesics, either alone or in combination, should result in the alleviation of neuropathic pain in most patients. Recent advances in the understanding of pain mechanisms at multiple central nervous system levels should pave the way toward more effective treatment modalities.
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Despite significant improvements in our ability to treat neuropathic pain, we are far from the situation of being able to guarantee pain relief. The next few years promise to see the introduction of novel pharmacologic entities that show potential in the field of neuropathic pain treatment. ⋯ However, not every product of our improved knowledge will manifest as a new drug treatment for neuropathic pain. Despite evidence of efficacy, some drugs will fail to reach commercialization due to the lack of investment in their clinical development.
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Neuropathic pain is caused by functional abnormalities of structural lesions in the peripheral or central nervous system, and occurs without peripheral nociceptor stimulation. Many common diseases, such as postherpetic neuralgia, trigeminal neuralgia, diabetic neuropathy, spinal cord injury, cancer, stroke, and degenerative neurological diseases may produce neuropathic pain. Recently, theories have been proposed that state there are specific cellular and molecular changes that affect membrane excitability and induce new gene expression after nerve injury, thereby allowing for enhanced responses to future stimulation. ⋯ Since it has been established that intense noxious stimulation produces a sensitization of central nervous neurons, it may be possible to direct treatments not only at the site of peripheral nerve injury, but also at the target of central changes. In order to provide better pain control, the mechanism-based approach in treating neuropathic pain should be familiar to physicians. In the future, it is hoped that a combination of new pharmacotherapeutic developments, careful clinical trials, and an increased understanding of the contribution and mechanisms of neuroplasticity will lead to an improvement in the results of clinical treatments and prevention of neuropathic pain.
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The appropriateness and utility of considering fibromyalgia syndrome (FM) and other syndromes without anatomically localized pathology of the nervous system as neuropathic pain syndromes is uncertain. In this afterword, a synthesis of the information presented in these proceedings and opinion as to how FM relates to classical neuropathic pain syndromes is provided.
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The fibromyalgia syndrome (FM) seems an unlikely candidate for classification as a neuropathic pain. The disorder is diagnosed based on a compatible history and the presence of multiple areas of musculoskeletal tenderness. A consistent pathology in either the peripheral or central nervous system (CNS) has not been demonstrated in patients with FM, and they are not at higher risk for diseases of the CNS such as multiple sclerosis or of the peripheral nervous system such as peripheral neuropathy. ⋯ Requiring demonstrable pathology in the nervous system in the definition of neuropathic pain is the traditional approach. The expansion of the definition to require only enduring nervous system dysfunction is less palatable because it opens the classification to many disorders of uncertain etiology, including complex regional pain syndrome. As it is uncertain which of the many different chronic pain syndromes include an enduring component of central sensitization, restricting the term "neuropathic pain" to those disorders with a primary etiology clearly related to the peripheral or CNS is prudent and consistent with clinical practice.