Gracely Richard H, Lynch Sue A, Bennett Gary J
Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892 USA.
Pain. 1992 Nov;51(2):175-194. doi: 10.1016/0304-3959(92)90259-E.
We performed sensory assessments before and during diagnostic tourniquet-cuff and local anesthetic blocks in 4 patients diagnosed with reflex sympathetic dystrophy (RSD). All patients complained of mechano-allodynia; lightly touching the skin evoked an intense pain sensation. At detection levels, electrical stimuli were perceived as painful, suggesting that the mechano-allodynia was mediated by A beta low-threshold mechanoreceptor afferents. A beta-mediated allodynia was further supported by reaction time latencies to painful electrical stimuli at threshold for A-fiber activation and, in 1 patient, by differential cuff blocks which abolished A beta function and allodynia while thermal sensation (warm and cold) were preserved. Local anesthetic block of painful foci associated with previous trauma abolished mechano-allodynia, cold allodynia, and spontaneous pain in all patients and relieved the motor symptoms in 1 patient with tonic contractures of the toes. Tactile and thermal perception in the previously allodynic area was preserved. When the local anesthetic block waned, spontaneous pain, allodynia, and motor symptoms returned. We propose a model of neuropathic pain in which ongoing nociceptive afferent input from a peripheral focus dynamically maintains altered central processing that accounts for allodynia, spontaneous pain, and other sensory and motor abnormalities. Blocking the peripheral input causes the central processing to revert to normal, abolishing the symptoms for the duration of the block. The model accounts for sympathetically maintained (SMP) and sympathetically independent (SIP) pain. The peripheral input can be independent of sympathetic activity or driven completely or in part by activity in sympathetic efferents or by circulating catecholamines. The shared final common pathway may explain the common features of SMP and SIP.
我们对4例诊断为反射性交感神经营养不良（RSD）的患者在诊断性止血带袖带和局部麻醉阻滞前及过程中进行了感觉评估。所有患者均主诉机械性异常性疼痛；轻轻触摸皮肤会引发强烈的疼痛感。在检测水平上，电刺激被感知为疼痛，这表明机械性异常性疼痛是由Aβ低阈值机械感受器传入神经介导的。Aβ介导的异常性疼痛在A纤维激活阈值下对疼痛电刺激的反应时间潜伏期进一步得到支持，并且在1例患者中，通过差异袖带阻滞得到支持，该阻滞消除了Aβ功能和异常性疼痛，同时保留了热感觉（温暖和寒冷）。与先前创伤相关的疼痛病灶的局部麻醉阻滞消除了所有患者的机械性异常性疼痛、冷异常性疼痛和自发痛，并缓解了1例脚趾强直性挛缩患者的运动症状。先前存在异常性疼痛区域的触觉和热觉得以保留。当局部麻醉阻滞作用减弱时，自发痛、异常性疼痛和运动症状又会复发。我们提出了一种神经性疼痛模型，其中来自外周病灶的持续伤害性传入输入动态维持着改变的中枢处理过程，这解释了异常性疼痛、自发痛以及其他感觉和运动异常。阻断外周输入会使中枢处理恢复正常，在阻滞期间消除症状。该模型解释了交感神经维持性（SMP）和交感神经独立性（SIP）疼痛。外周输入可以独立于交感神经活动，或者完全或部分由交感神经传出活动或循环儿茶酚胺驱动。共同的最终共同通路可能解释了SMP和SIP的共同特征。
