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复杂性区域疼痛综合征(CRPS)的发病机制及临床特点

Mechanistic and clinical aspects of complex regional pain syndrome (CRPS).

作者信息

Baron Ralf

机构信息

Klinik für Neurologie, Christian-Albrechts-Universität Kiel, Niemannsweg 147, 24105 Kiel, Germany.

出版信息

Novartis Found Symp. 2004;261:220-33; discussion 233-8, 256-61.

PMID:15469053
Abstract

Complex regional pain syndromes (CRPS, reflex sympathetic dystrophy, causalgia) are painful disorders that develop after trauma affecting a limb with (I) or without (II) nerve injury. Clinical features are pain, impairment of motor function, swelling and autonomic abnormalities (changes in sweating and blood flow). Autonomic abnormalities. The maximal skin temperature difference between the affected and unaffected extremity that occurs during a controlled thermoregulation can be used as a diagnostic tool. SMP. Sympathetic outflow to the painful extremity was experimentally activated. The intensity as well as area of spontaneous pain and mechanical hyperalgesia increased considerably in patients that had been classified as having SMP by positive sympathetic blocks. A pathological interaction between sympathetic vasoconstrictor and afferent neurons within the affected skin is the likely explanation for SMP in CRPS patients. Motor abnormalities. Kinematic analysis of target reaching as well as grip force analysis showed a pathological sensorimotor integration located in the parietal cortex. Furthermore, MEG studies demonstrated a continuous inhibition of the primary motor cortex. Neurogenic inflammation. Some features of acute CRPS (vasodilatation, swelling, pain) indicate a localized inflammatory process. Transcutaneous electrical stimulation of nociceptive C-fibre provoked protein extravasation into the interstitial fluid (microdialysis) only in CRPS patients and not in controls.

摘要

复杂性区域疼痛综合征(CRPS,反射性交感神经营养不良,灼性神经痛)是在创伤后出现的疼痛性疾病,创伤累及肢体,可伴有(I型)或不伴有(II型)神经损伤。临床特征包括疼痛、运动功能障碍、肿胀和自主神经异常(出汗和血流变化)。自主神经异常。在可控体温调节过程中,患侧与未患侧肢体之间的最大皮肤温度差可作为一种诊断工具。交感神经维持性疼痛(SMP)。通过实验激活了向疼痛肢体的交感神经传出。在经阳性交感神经阻滞被归类为患有SMP的患者中,自发疼痛的强度和范围以及机械性痛觉过敏均显著增加。交感缩血管神经与患侧皮肤内传入神经元之间的病理性相互作用可能是CRPS患者SMP的原因。运动异常。对目标达成的运动学分析以及握力分析显示,顶叶皮质存在病理性感觉运动整合。此外,脑磁图研究表明初级运动皮质持续受到抑制。神经源性炎症。急性CRPS的一些特征(血管扩张、肿胀、疼痛)表明存在局部炎症过程。经皮电刺激伤害性C纤维仅在CRPS患者中引发蛋白质渗入间质液(微透析),而在对照组中未出现这种情况。

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