Abstract
Complex regional pain syndrome (CRPS) is clinically characterized by pain, abnormal regulation of blood flow and sweating, edema of skin and subcutaneous tissues, active and passive movement disorders, and trophic changes of skin, appendages of skin, and subcutaneous tissues. It is classified into type I (reflex sympathetic dystrophy) and II (causalgia). CRPS patients exhibit changes that occur in the somatosensory (SI) systems processing noxious, tactile, and thermal information, in sympathetic systems innervating skin (blood vessels, sweat glands), and in the somatomotor system. This indicates that the central representations of these systems are changed and that CRPS is a systemic disease involving these neuronal systems. CRPS patients also demonstrate peripheral changes, such as edema, signs of inflammation, sympathetic–afferent coupling (as a basis for sympathetically maintained pain), and trophic changes, which cannot be explained by but also not be seen independently of the central changes. Therefore, CRPS cannot be reduced to one system or to one mechanism only. This view is based on clinical observations and experimentation on humans and animals. The key future question to be asked in research is: What is the organizing principle leading to this complex syndrome? The changed view of pathophysiological interactions that we have acquired in the past years will shift the focus of our research efforts, will bring about a diagnostic reclassification and redefinition of CRPS, and finally will have bearings on novel therapeutic approaches.
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