Kortekaas Minke C, Niehof Sjoerd P, Stolker Robert J, Huygen Frank J P M
Department of Anesthesiology, Center for Pain Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands.
Pain Pract. 2016 Sep;16(7):905-14. doi: 10.1111/papr.12403. Epub 2015 Nov 7.
Complex regional pain syndrome (CRPS) is characterized by continuous pain, disproportional to the initial trauma. It usually spreads to the distal parts of the affected limb. Besides continuing pain, a mix of sensory, sudo- and vasomotor disturbances, motor dysfunction, and trophic changes is responsible for physical complaints. Vasomotor disturbance is characterized by changes in skin temperature and color. In CRPS patients with a cold extremity, a decrease in blood flow can cause decreased tissue saturation and tissue acidosis, resulting in ischemic pain. The pathophysiology of vasomotor disturbances is not completely understood. Temperature asymmetry is generally assumed as a result of disturbance in the sympathetic nervous system. Vasodilating drugs and sympathetic blockade have been cornerstones of therapy in cold CRPS for years. However, only a limited part of these patients improve on this kind of therapies. Research has shown a pivotal role for inflammation in the pathophysiology of CRPS. Inflammation can result in endothelial dysfunction. Endothelial function plays an important role in the local regulation of vascular tone. Endothelial dysfunction could be another mechanism responsible for the vasomotor disturbances in cold CRPS. An important goal in the treatment of cold-type CRPS is the restoration of a normal blood flow. Consequently it is important to distinguish the underlying pathophysiological mechanisms of vasomotor disturbances. A disturbance of the sympathetic nervous system may require another type of treatment than inflammation-induced endothelial dysfunction. Diagnostic tools to distinguish these underlying pathophysiological mechanisms of vasomotor disturbances would enable a mechanism-based treatment and improve clinical outcome.
复杂性区域疼痛综合征（CRPS）的特征是持续性疼痛，与初始创伤不成比例。它通常会蔓延至受影响肢体的远端部位。除了持续性疼痛外，感觉、出汗和血管舒缩功能障碍、运动功能障碍以及营养改变等多种因素共同导致了身体不适。血管舒缩功能障碍的特征是皮肤温度和颜色的变化。在患有肢体发冷的CRPS患者中，血流减少会导致组织饱和度降低和组织酸中毒，从而引起缺血性疼痛。血管舒缩功能障碍的病理生理学尚未完全明确。一般认为温度不对称是交感神经系统紊乱的结果。多年来，血管扩张药物和交感神经阻滞一直是治疗冷型CRPS的基石。然而，只有有限一部分此类患者通过这种治疗方法得到改善。研究表明，炎症在CRPS的病理生理学中起关键作用。炎症可导致内皮功能障碍。内皮功能在局部血管张力调节中起重要作用。内皮功能障碍可能是冷型CRPS血管舒缩功能障碍的另一种机制。治疗冷型CRPS的一个重要目标是恢复正常血流。因此，区分血管舒缩功能障碍的潜在病理生理机制非常重要。交感神经系统紊乱可能需要与炎症诱导的内皮功能障碍不同类型的治疗方法。区分血管舒缩功能障碍这些潜在病理生理机制的诊断工具将有助于进行基于机制的治疗并改善临床结果。
