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RESEARCH PRODUCT

Neurogenic Inflammation in Complex Regional Pain Syndrome (CRPS)

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This chapter explains symptoms and nature of neurogenic inflammation and its importance in posttraumatic complex regional pain syndrome (CRPS). Neurogenic inflammation regularly accompanies excitation of primary afferent nociceptors. It has two major components – plasma extravasation and vasodilatation. The most important mediators are the neuropeptides calcitonin gene-related peptide (CGRP) and substance P (SP). After peripheral trauma, immune reaction (e.g., cytokines) and the attempts of the tissue to regenerate (e.g., growth factors) sensitize nociceptors and thereby amplify neurogenic inflammation. This cascade of events has recently been demonstrated in rat models of CRPS employing distal tibial fractures and nerve transections. Clinical findings in these animals resemble clinical findings in CRPS, and these can be prevented by antineuropeptide treatment. Meanwhile, in CRPS patients, there is plenty of evidence that neurogenic inflammation contributes to clinical presentation. Increased cytokine production was demonstrated and facilitated neurogenic inflammation on the affected side. Surprisingly, there was moderately increased neurogenic inflammation in unaffected body regions also. This favors the possibility that CRPS patients have some genetic similarities. The importance of neurogenic inflammation in acute CRPS also has implications for pathophysiologically oriented treatment.