Articles: hyperalgesia.
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Animal models of neuropathic pain have significantly advanced our knowledge of abnormalities in central pain processing mechanisms in chronic pain disorders. New neuroimaging techniques using functional magnetic resonance imaging and positron emission tomography scanning are beginning to provide insight into cortical participation in the processing of pain. Irritable bowel syndrome (IBS) is one of the most common gastrointestinal disorders seen by physicians. ⋯ Patients with IBS also have many extraintestinal symptoms consistent with a central hyperalgesic state. Recent studies suggest that patients with IBS may also have cutaneous hyperalgesia similar to that seen in other chronic pain disorders such as fibromyalgia. This suggests that abnormalities of central nociceptive processing are present in IBS.
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Review
Peripheral and central sensitization in musculoskeletal pain disorders: an experimental approach.
This report provides a brief introduction to the manifestations of peripheral and central sensitization involved in musculoskeletal pain disorders. It has become increasingly evident that muscle hyperalgesia, referred pain, referred hyperalgesia, and widespread hyperalgesia play an important role in chronic musculoskeletal pain. A better understanding of the involved basic mechanisms and better methods to assess muscle pain in the clinic may provide new possibilities for designing rational therapies and for targeting the pharmacologic intervention optimally. ⋯ Quantitative sensory testing provides the possibility to evaluate these manifestations in a standardized way in patients with musculoskeletal pain or in healthy volunteers (eg, experimentally induced referred pain can be used to assess the potential involvement of central sensitization in musculoskeletal pain conditions). Central sensitization may play a role in the persistence, amplification, and spread of pain. Interventions should take this aspect into consideration.
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While it may be convenient to categorize neuropathic pain syndromes on the basis of anatomical distribution or disease state (e.g., diabetic neuropathy, radiculopathy, postherpetic neuralgia), the treatment of neuropathic pain, alone, should also consider the signs and symptoms and the underlying putative mechanisms that may then be inferred from each individual's signs and symptoms. A diagnosis-based approach to treatment may not effectively relieve a patient's pain or improve his or her quality of life, the ultimate goal of treatment. Although research that supports a symptom- and mechanism-based approach to treating neuropathic pain is ongoing and dynamic, the preclinical and clinical data available thus far form an initial rational framework within which we may attempt to target putative pain mechanisms.
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Neuropathic pain represents a series of relatively uncommon chronic pain conditions, caused by lesions or dysfunctions of peripheral or central afferent pathways in the nervous system. The symptoms and signs of neuropathic pain can all be explained by a neuronal hyperexcitability at the site of the nerve lesion, which subsequently and in a dynamic fashion recruits more central sites. The manifestations of such neuronal hyperexcitability are therefore rather similar, irrespective of the causes or sites of the lesions. ⋯ Our understanding of the mechanisms underlying neuronal hyperexcitability has increased dramatically within the last decade, and accordingly, it has been suggested that pain be classified according to a mechanism-based approach. The challenge for an improved understanding of neuropathic pain--which is the key for better treatment--lies in elucidating the relationships between symptoms, signs, aetiology, anatomical lesions, and underlying mechanisms. At present, this is not a trivial task.
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This review addresses the issue of how axotomy of peripheral nerve fibers leads to pain and hyperalgesia. The point of axotomy (the nerve injury site), the dorsal root ganglia, and the dorsal horn of the spinal cord are candidate sites for generation of the pain signal that is likely to be critical for maintaining the neuropathic pain state. This review considers neuropathic pain from a "systems" perspective, tracing concepts of neuropathic pain from the work of Henry Head to the present. ⋯ These abnormalities in the intact nociceptor, which arise in the context of Wallerian degeneration, probably play a role in creating or maintaining the abnormal pain state. These considerations probably also apply to the understanding of pain arising in other neuropathies. The findings relative to the "intact" nociceptor provide a rationale by which to understand how therapies distal to the nerve injury site may diminish pain.