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Mediators of Inflammation
Volume 11 (2002), Issue 1, Pages 47-51
http://dx.doi.org/10.1080/09629350210307

Evidence for local inflammation in complex regional pain syndrome type 1

1Pain Treatment Centre, Department of Anesthesiology, Erasmus Medical Centre, P.O. Box 2040, Rotterdam 3000 CA , The Netherlands
2Department of Physiotherapy, Erasmus Medical Centre, Rotterdam, The Netherlands

Copyright © 2002 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background: The pathophysiology of complex regional pain syndrome type 1 (CRPS 1) is still a matter of debate. Peripheral afferent, efferent and central mechanisms are supposed. Based on clinical signs and symptoms (e.g. oedema, local temperature changes and chronic pain) local inflammation is suspected.

Aim: To determine the involvement of neuropetides, cytokines and eicosanoids as locally formed mediators of inflammation.

Methods: In this study, nine patients with proven CRPS 1 were included. Disease activity and impairment was determined by means of a Visual Analogue Scale, the McGill Pain Questionnaire, the difference in volume and temperature between involved and uninvolved extremities, and the reduction in active range of motion of the involved extremity. Venous blood was sampled from and suction blisters made on the involved and uninvolved extremities for measurement of cytokines interleukin (IL)-6, IL-1β and tumour necrosis factor-α (TNF-α), the neuropetides NPY and CRGP, and prostaglandin E2.

Results: The patients included in this study did have a moderate to serious disease activity and impairment. In plasma, no changes of mediators of inflammation were observed. In blister fluid, however, significantly higher levels of IL-6 and TNF-α in the involved extremity were observed in comparison with the uninvolved extremity.

Conclusions: This is the first time that involvement of mediators of inflammation in CRPS 1 has been so clearly and directly demonstrated. This observation opens new approaches for the succesful use and development of immunosuppressives in CRPS 1.