Weber M, Birklein F, Neundörfer B, Schmelz M
Neurologische Klinik, Friedrich Alexander Universität Erlangen-Nürnberg, Universitätsstrasse 17, D-91054 Erlangen, Germany Institut für Physiologie und experimentelle Pathophysiologie, Friedrich Alexander Universität Erlangen-Nürnberg, Universitätsstrasse 17, D-91054 Erlangen, Germany.
Pain. 2001 Apr;91(3):251-257. doi: 10.1016/S0304-3959(00)00445-0.
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.
复杂性区域疼痛综合征（CRPS）具有多种临床特征，包括自发痛和痛觉过敏。外周伤害感受器神经肽释放增加被认为是引发营养改变、水肿、血管扩张和疼痛组合的一种可能的病理生理机制。为了验证CRPS中神经肽释放增加的情况，对患者和对照组进行了电诱导神经源性血管扩张和蛋白外渗评估。我们对10例急性且未经治疗的CRPS患者和10例匹配的健康对照进行了一项前瞻性研究。通过皮内微透析毛细血管进行强经皮电刺激引发神经源性炎症，同时能够测量蛋白外渗。使用激光多普勒扫描评估轴突反射性血管扩张。CRPS患者的轴突反射性血管扩张显著增加（相对于基线增加438±68%，而对照组为306±52%；P<0.05），经皮电刺激仅在患者中引发蛋白外渗（刺激前，0.28±0.03mg/ml；刺激期间，0.34±0.04mg/ml），而在健康对照组中刺激期间蛋白浓度稳步下降（刺激前，0.23±0.04mg/ml；刺激期间，0.18±0.04；P<0.001）。患者电诱导蛋白外渗的时间进程类似于应用外源性P物质（SP）后观察到的情况。我们得出结论，CRPS中神经源性炎症增强。我们的结果表明CRPS中神经肽的释放能力增加。
