Devor M
J Auton Nerv Syst. 1983 Mar-Apr;7(3-4):371-84. doi: 10.1016/0165-1838(83)90090-5.
In contrast to sensory endings in skin, muscle, etc., afferents in the mid-course of intact nerves are normally incapable of generating impulses upon slow or prolonged depolarization. However, after various types of nerve injury, including complete nerve section and local demyelination, an ectopic pacemaker capability develops. One peculiarity of such abnormal differentiated sites is chemosensitivity to alpha-adrenergic agonists and to sympathetic efferents discharge. Such ectopic chemosensitivity may well be involved in the etiology of paraesthesias and pain in reflex sympathetic dystrophies including causalgia. Specifically, it is proposed that the fundamental cause of these conditions is the development of abnormal electrogenic membrane properties in the region of demyelination and sprout outgrowth. These abnormal properties presumably include the appearance of excess inward current conductances and ectopic alpha-adrenergic receptors. Catecholamines released from sympathetic efferents in the area of injury locally depolarize damaged sensory fibers, and because of the abnormal electrogenic properties of these fibers, an abnormal afferent discharge is generated.
与皮肤、肌肉等部位的感觉末梢不同，完整神经中段的传入神经在缓慢或长时间去极化时通常无法产生冲动。然而，在包括完全性神经切断和局部脱髓鞘在内的各种类型的神经损伤后，会产生异位起搏能力。这种异常分化部位的一个特点是对α-肾上腺素能激动剂和交感传出神经放电具有化学敏感性。这种异位化学敏感性很可能参与了包括灼性神经痛在内的反射性交感神经营养不良中感觉异常和疼痛的病因。具体而言，有人提出这些病症的根本原因是脱髓鞘和芽生生长区域出现异常的电发生膜特性。这些异常特性可能包括过量内向电流电导和异位α-肾上腺素能受体的出现。损伤区域交感传出神经释放的儿茶酚胺使受损的感觉纤维局部去极化，并且由于这些纤维的异常电发生特性，会产生异常的传入放电。
