Articles: hyperalgesia.
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The traditional specificity theory of pain perception holds that pain involves a direct transmission system from somatic receptors to the brain. The amount of pain perceived, moreover, is assumed to be directly proportional to the extent of injury. Recent research, however, indicates far more complex mechanisms. ⋯ It is clear from the material presented that the perception of pain does not simply involve a moment-to-moment analysis of afferent noxious input, but rather involves a dynamic process that is influenced by the effects of past experiences. Sensory stimuli act on neural systems that have been modified by past inputs, and the behavioral output is significantly influenced by the "memory" of these prior events. An increased understanding of the central changes induced by peripheral injury or noxious stimulation should lead to new and improved clinical treatment for the relief and prevention of pathological pain.
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Neuropathic pains associated with an injury of the peripheral or central nervous system are among the most difficult to treat. One of the reasons for the therapeutic difficulties in these patients is that the pharmacological treatments are used in a uniform fashion whatever the clinical picture, while these syndromes are in fact highly heterogenous. The patients can express various combinations of painful symptoms--spontaneous (continuous and/or paroxysmal) and evoked (allodynia and/or hyperalgesia). ⋯ Such data emphasize the necessity of a thorough evaluation of patients presenting with neuropathic pains, notably by using quantitative sensory testing. Following recent advances in the understanding of the pathophysiological mechanisms underlying these painful syndromes, through experimental studies in animals, a "mechanism-based" classification and treatment of neuropathic pains can be envisaged. The main goal for clinicians is to propose new methods and strategies for identifying pathophysiological mechanisms in patients in order to validate such an approach in the clinical context.
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Ann. N. Y. Acad. Sci. · Mar 2001
ReviewSpinal cord neuroplasticity following repeated opioid exposure and its relation to pathological pain.
Convincing evidence has accumulated that indicates neuroplastic changes within the spinal cord in response to repeated exposure to opioids. Such neuroplastic changes occur at both cellular and intracellular levels. It has been generally acknowledged that the activation of N-methyl-D-aspartate (NMDA) receptors plays a pivotal role in the development of neuroplastic changes following repeated opioid exposure. ⋯ Interestingly, similar cellular and intracellular changes occur in the spinal cord following peripheral nerve injury. These findings indicate that interactions exist in the spinal cord neural structures between two seemingly unrelated conditions-chronic opioid exposure and a pathological pain state. These observations may help understand mechanisms of chemical intolerance and multiple chemical sensitivity as well as have significant clinical implications in pain management with opioid analgesics.