Pain medicine : the official journal of the American Academy of Pain Medicine
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To review mechanisms that might contribute to sensory disturbances and sympathetically-maintained pain in complex regional pain syndrome (CRPS). ⋯ Sympathetic neural activity might contribute to pain and sensory disturbances in CRPS by feeding into nociceptive circuits at the site of injury or elsewhere in the CRPS-affected limb, within the dorsal horn, or via thalamo-cortical projections.
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Complex regional pain syndrome-type I (CRPS-I; reflex sympathetic dystrophy) is a chronic pain condition that usually follows a deep-tissue injury such as fracture or sprain. The cause of the pain is unknown. We have developed an animal model (chronic post-ischemia pain) that creates CRPS-I-like symptomatology. ⋯ These data, and a large body of clinical evidence, suggest that in at least a subset of CRPS-I patients, the fundamental cause of the abnormal pain sensations is ischemia and inflammation due to microvascular pathology in deep tissues, leading to a combination of inflammatory and neuropathic pain processes. Moreover, we suggest a unifying idea that relates the pathogenesis of CRPS-I to that of CRPS-II. Lastly, our hypothesis suggests that the role of the sympathetic nervous system in CRPS-I is a factor that is not fundamentally causative, but may have an important contributory role in early-stage disease.
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The current diagnostic criteria for complex regional pain syndrome (CRPS), codified by the International Association for the Study of Pain's taxonomy committee, and newer statistically derived criteria (the "Budapest" criteria), are both deliberately based on bedside testing. Designing criteria that are accessible to any clinician, not requiring any special equipment or training, is very important for clinical diagnosis. ⋯ Fortunately, with some new technologies and new approaches to old technologies, significant improvements can be made not only in terms of quantification, but also in allowing significant objectification of the diagnostic data. We will initiate a discussion of some of these potentially useful approaches.
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Complex regional pain syndrome (CRPS) patients exhibit multiorgan pathology and inflammatory changes after limb trauma. The objective of this study was to identify how neuro-cutaneous signaling is facilitated after fracture and examine how this altered signaling contributes to the development of CRPS-like changes in the injured limb. ⋯ Collectively, these data suggest that neuro-cutaneous signaling is up-regulated and can mediate inflammatory changes observed in the hindpaw skin of the fracture rat model and in human CRPS skin. Future translational and clinical studies mapping these inflammatory changes may identify novel therapeutic targets for preventing post-traumatic pain from transitioning into chronic CRPS.