Schwartzman Robert J, Alexander Guillermo M, Grothusen John
Drexel University College of Medicine, Department of Neurology, 245 N. 15 Street, MS 423 Philadelphia, PA 19102, USA.
Expert Rev Neurother. 2006 May;6(5):669-81. doi: 10.1586/14737175.6.5.669.
Complex regional pain syndrome (CRPS) most often follows injury to peripheral nerves or their endings in soft tissue. A combination of prostanoids, kinins and cytokines cause peripheral nociceptive sensitization. In time, the Mg(2+) block of the N-methyl-D-aspartate receptor is removed, pain transmission neurons (PTN) are altered by an influx of Ca(2+) that activates kinases for excitation and phosphatases for depression, activity-dependent plasticity that alters the firing of PTN. In time, these neurons undergo central sensitization that lead to a major physiological change of the autonomic, pain and motor systems. The role of the immune system and the sickness response is becoming clearer as microglia are activated following injury and can induce central sensitization while astrocytes may maintain the process.
复杂性区域疼痛综合征（CRPS）最常继发于周围神经或其在软组织中的末梢损伤。前列腺素、激肽和细胞因子共同作用导致外周伤害性致敏。随着时间推移，N-甲基-D-天冬氨酸受体的镁离子阻滞被解除，疼痛传递神经元（PTN）因钙离子内流而发生改变，钙离子内流激活激酶以促进兴奋，激活磷酸酶以抑制兴奋，这是一种依赖活动的可塑性变化，改变了PTN的放电。随着时间推移，这些神经元会发生中枢致敏，导致自主神经系统、疼痛系统和运动系统发生重大生理变化。随着损伤后小胶质细胞被激活，免疫系统和疾病反应的作用变得越来越清晰，小胶质细胞可诱导中枢致敏，而星形胶质细胞可能维持这一过程。
