A NOVEL BEHAVIORAL-MODEL OF NEUROPATHIC PAIN DISORDERS PRODUCED IN RATS BY PARTIAL SCIATIC-NERVE INJURY
A NOVEL BEHAVIORAL-MODEL OF NEUROPATHIC PAIN DISORDERS PRODUCED IN RATS BY PARTIAL SCIATIC-NERVE INJURY
复制标题
DOI：
10.1016/0304-3959(90)91074-s
复制
发表时间：
1990-11-01
期刊：
影响因子：
7.4
通讯作者：
SHIR, Y
中科院分区：
文献类型：
--
作者：
SELTZER, Z;DUBNER, R;SHIR, Y
部分神经损伤是人类血管样疼痛障碍的主要原因。我们在这里提出了一种新的动物模型，这种情况。在大鼠中，我们单侧结扎了大腿上方大约一半的坐骨神经。在手术后的几个小时内，以及此后的几个月，大鼠出现了同侧后爪的守卫行为，并经常舔它，这表明自发性疼痛的可能性。足底表面的脚均匀hyperesthetic无害和有害的刺激。所有大鼠均未发生自切。有一个急剧下降，在撤回阈值双边响应于重复的Von Frey毛发刺激在足底侧。在手术侧一系列这样的刺激后，轻触引起厌恶反应，提示触摸异常性疼痛。CO_2激光热脉冲引起的退缩阈值明显降低。阈上伤害性热脉冲引起单侧夸大的反应，表明热痛觉过敏。针刺引起这种夸张的反应双边（机械痛觉过敏）。在一份配套报告中，我们表明，这些异常严重依赖于交感神经外流。基于类似症状的立即发作和长期持续，例如触摸诱发的异常性疼痛和痛觉过敏，以及对侧现象与某些患有头痛的人的“镜像”疼痛的相似性，我们认为这种制剂可以作为由部分神经损伤触发并由交感神经活动维持的Cajorgiform综合征的模型。
Partial nerve injury is the main cause of causalgiform pain disorders in humans. We present here a novel animal model of this condition. In rats we unilaterally ligated about half of the sciatic nerve high in the thigh. Within a few hours after the operation, and for several months thereafter, the rats developed guarding behavior of the ipsilateral hind paw and licked it often, suggesting the possibility of spontaneous pain. The plantar surface of the foot was evenly hyperesthetic to non-noxious and noxious stimuli. None of the rats autotomized. There was a sharp decrease in the withdrawal thresholds bilaterally in response to repetitive Von Frey hair stimulation at the plantar side. After a series of such stimuli in the operated side, light touch elicited aversive responses, suggesting allodynia to touch. The withdrawal thresholds to CO2 laser heat pulses were markedly lowered bilaterally. Suprathreshold noxious heat pulses elicited exaggerated responses unilaterally, suggesting thermal hyperalgesia. Pin-prick evoked such exaggerated responses bilaterally (mechanical hyperalgesia). In a companion report, we show that these abnormalities critically depend on the sympathetic outflow. Based on the immediate onset and long-lasting perpetuation of similar symptoms, such as touch-evoked allodynia and hyperalgesia, and the resemblance of the contralateral phenomena to ''mirrow image'' pains in some humans with causalgia, we suggest that this preparation may serve as a model for syndromes of the causalgiform variety that are triggered by partial nerve injury and maintained by sympathetic activity.