The Clinical journal of pain
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There have been considerable advances in our understanding of the pathophysiology of neuropathic pain. There is still a lack of consensus about the optimal therapeutic strategy of such conditions, however. Drugs are generally selected on the basis of their established efficacy in randomized controlled studies in etiologically based groups of patients. ⋯ More specific therapeutic strategies based on precise quantified assessment of the various components of neuropathic pain are now increasingly used and may provide insight regarding the effects of treatments of particular symptoms (e.g., allodynia, hyperalgesia). In some cases, such assessment may also help to analyze the mechanisms involved in pain, thus allowing selection of treatment on a more rational basis. A mechanism-based approach seems promising for clinical research studies, although its application in current management remains challenging.
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Research on the pathophysiology of chronic pain has begun to challenge the traditional diagnostic and treatment paradigms for the patient with neuropathic pain. The heterogeneous nature of neuropathic pain indicates that more than one anatomic lesion is most likely responsible for the clinical presentation of a particular syndrome. Numerous pharmacologic agents that have shown improved efficacy in the treatment of neuropathic pain have been developed over the past decade. For the practicing clinician, an important concern is whether the current paradigm for classification of neuropathic pain syndromes is comprehensive enough to address this rapidly expanding body of knowledge.
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Although pain is always intense and unpleasant, the capacity to experience this sensation is, under normal circumstances, fundamental to the preservation of bodily integrity. Clinically, however, after injury to peripheral tissue or directly to the nervous system, spontaneous and evoked pain manifest that serve no physiologic function, are crippling to patients, and are difficult to treat. ⋯ This spinal neuronal plasticity is shown to be a key contributor to pathologic pain hypersensitivity. The potential for the molecular mechanisms responsible for the spinal plasticity in revealing new targets for future treatment is also discussed.
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Acute mechanical, thermal, and chemically induced pains in the skin are signalled by a set of specific nociceptive afferents, which encode the magnitude of the perceived pain by their discharge intensity. After tissue injury or inflammation, a number of changes in the properties of the primary afferent occur parallel to profound changes in the central nervous system. ⋯ Collectively, these changes are the basis for the many forms of hyperalgesia that can present clinically as incident pain. Knowledge of the various types of hyperalgesia and their underlying mechanisms is required for better treatment of this challenging aspect of chronic pain.