Campbell James N, Raja Srinivasa N, Meyer Richard A, Mackinnon Susan E
Department of Neurosurgery, Johns Hopkins University, Baltimore, MD 21205 U.S.A. Department of Anesthesiology and Critical Care Medicine,Johns Hopkins University, Baltimore, MD 21205 U.S.A. Applied Physics Laboratory, School of Medicine, Johns Hopkins University, Baltimore, MD 21205 U.S.A. Division of Plastic Surgery, University of Toronto, TorontoCanada.
Pain. 1988 Jan;32(1):89-94. doi: 10.1016/0304-3959(88)90027-9.
Pain to light touching of the skin is a hallmark sign of causalgia. The purpose of this study was to determine whether myelinated or unmyelinated afferent fibers signal this hyperalgesia. Sensory testing was performed in 17 patients with long-standing hyperalgesia after nerve injury. The patients underwent a differential ischemic block of nerve function of the involved area. At a time when touch sensation in adjacent normal skin was eliminated, but when sensibility to warming and cooling stimuli was unaffected, the hyperalgesia to mechanical stimuli was abolished in 15 of the subjects. In 2 of these 15 patients, a differential local anesthetic block of the injured nerve was performed proximal to the site of injury. When temperature sensibility was absent, but when touch sensation was intact, hyperalgesia was present. In a third study, latency measurements in response to 400 micron stepped displacement stimuli were made in two patients who had hyperalgesia on the foot. The mean latency for detection of pain in the hyperalgesic region was 414 +/- 18 msec, compared to 458 +/- 16 msec for the detection of touch to the same stimuli applied to the opposite normal foot. These 3 lines of evidence indicate that myelinated primary afferents, perhaps A beta fibers, signal the hyperalgesic pain in causalgia. These fibers may be sensitized A beta nociceptors or low-threshold mechanoreceptors.
皮肤受到轻触即疼痛是灼性神经痛的一个标志性体征。本研究的目的是确定有髓或无髓传入纤维是否传递这种痛觉过敏。对17例神经损伤后长期存在痛觉过敏的患者进行了感觉测试。患者接受了受累区域神经功能的选择性缺血性阻滞。当相邻正常皮肤的触觉消失，但对温热和冷刺激的感觉不受影响时，15名受试者对机械刺激的痛觉过敏消失。在这15名患者中的2例，在损伤部位近端对受伤神经进行了选择性局部麻醉阻滞。当温度感觉缺失但触觉完好时，痛觉过敏仍然存在。在第三项研究中，对两名足部有痛觉过敏的患者进行了对400微米阶梯位移刺激的潜伏期测量。痛觉过敏区域检测疼痛的平均潜伏期为414±18毫秒，而对同一刺激施加于对侧正常足部的触觉检测平均潜伏期为458±16毫秒。这三条证据表明，有髓初级传入纤维，可能是Aβ纤维，传递灼性神经痛中的痛觉过敏疼痛。这些纤维可能是致敏的Aβ伤害感受器或低阈值机械感受器。
