Facilitated neurogenic inflammation in complex regional pain syndrome


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Abstract

Complex regional pain syndrome (CRPS) is characterized by a variety of clinical features including spontaneous pain and hyperalgesia. Increased neuropeptide release from peripheral nociceptors has been suggested as a possible pathophysiologic mechanism triggering the combination of trophic changes, edema, vasodilatation and pain. In order to verify the increased neuropeptide release in CRPS, electrically induced neurogenic vasodilatation and protein extravasation were evaluated in patients and controls. We performed a prospective study on 10 patients with acute and untreated CRPS and 10 matched healthy controls. Neurogenic inflammation was elicited by strong transcutaneous electrical stimulation via intradermal microdialysis capillaries which simultaneously enabled measurement of protein extravasation. Laser-Doppler scanning was used to assess axon reflex vasodilatation. Axon reflex vasodilatation was significantly increased in CRPS patients (438±68% of baseline vs. 306±52%; P<0.05) and transcutaneous electrical stimulation provoked protein extravasation only in the patients (before, 0.28±0.03 mg/ml; during stimulation, 0.34±0.04 mg/ml), whereas protein concentration steadily declined during stimulation in the healthy controls (before, 0.23±0.04 mg/ml; during stimulation, 0.18±0.04; P<0.001). The time course of electrically induced protein extravasation in the patients resembled the one observed following application of exogenous substance P (SP). We conclude that neurogenic inflammation is facilitated in CRPS. Our results suggest an increased releasability of neuropeptides in CRPS.

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