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Status of immune mediators in complex regional pain syndrome type I

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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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Authors and Affiliations

  1. Berufsgenossenschaftliche Kliniken Bergmannsheil, Department of Surgery, Ruhr University Bochum, Buerkle-de-la-Camp-Pl.1, 44789, Bochum, Germany

    Christian Schinkel

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  1. Christian Schinkel
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  2. Martin H. Kirschner
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Correspondence to Christian Schinkel.

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Schinkel, C., Kirschner, M.H. Status of immune mediators in complex regional pain syndrome type I. Current Science Inc 12, 182–185 (2008). https://doi.org/10.1007/s11916-008-0032-3

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