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Updated: Jun 30, 2026

Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats
Published on: January 21, 2020
Status of immune mediators in complex regional pain syndrome type I
Christian Schinkel1, Martin H Kirschner
1Berufsgenossenschaftliche Kliniken Bergmannsheil, Department of Surgery, Ruhr University Bochum, Buerkle-de-la-Camp-Pl.1, Bochum, Germany. christian.schinkel@ruhr-uni-bochum.de
Abstract:
Complex regional pain syndrome type I (CRPS-I) can affect an extremity after minor trauma or operation. The pathogenesis of this syndrome is unclear. It has clinical signs of severe local inflammation as a result of an exaggerated inflammatory response, but neurogenic dysregulation is also a contributor. Several studies investigated the role of inflammatory mediators and cytokines thus far; however, the results are heterogeneous and vary between different settings. This review summarizes recent study results that show a clear underlying inflammatory response at the local site, where systemic responses seem to be inconsistent. An induction of CRPS-like symptoms by application of neuroinflammatory mediators was shown recently. Local inflammation is involved in the pathophysiology of CRPS-I. We must expand our knowledge of pathophysiologic mechanisms, and we are still far away from using inflammatory markers in diagnosis and follow-up of CRPS-I.
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