Shir Yoram, Seltzer Ze'ev
Department of Anesthesiology and Pain Clinic, Hadassah University Hospital, JerusalemIsrael Physiology Branch, Faculty of Dental Medicine, Hebrew University of Jerusalem Israel.
Pain. 1991 Jun;45(3):309-320. doi: 10.1016/0304-3959(91)90056-4.
In a previous report we presented a novel behavioral model of neuropathic pain disorders, produced in rat by a unilateral ligation of about half of the sciatic nerve. The model is characterized by rapid onset of behaviors suggesting spontaneous pain and disordered responses to non-noxious and noxious stimuli. These include reduced withdrawal thresholds to repetitive touch in the partially deafferented skin ('touched-evoked hyperesthesia'), touch-evoked allodynia, reduced withdrawal thresholds to noxious thermal stimuli and exaggerated responses to noxious heat and mechanical stimuli ('thermal hyperalgesia'). Some of these disorders are seen at mirror image sites on the hind limb opposite the lesion. These disorder start within hours after partial nerve injury, last many months and are very similar to causalgia in humans following partial nerve injury. Since sympathetic efferent activity is known to aggravate causalgia in humans and sympathectomy is known to relieve it, we studied the effect of changing sympathetic outflow in the rat model. Reversible sympathectomy was carried out using guanethidine injected intraperitoneally in 3 experiments, each at a different time in relation to the partial nerve injury. We found that: (1) sympathectomy performed several months postoperatively alleviated the sensory disorders bilaterally; (2) sympathectomy prior to nerve injury partially prevented the appearance of thermal hyperalgesia but did not affect hyperesthesia to repetitive touch; and (3) sympathectomy at the time of nerve injury aggravated the sensory disorders during the first few days. As maintenance and production of the sensory disorders in this animal model depended on sympathetic nervous outflow, we conclude that the rats were suffering from a syndrome analogous to sympathetically maintained causalgia in man.
在之前的一份报告中，我们介绍了一种神经性疼痛障碍的新型行为模型，该模型通过对大鼠坐骨神经约一半进行单侧结扎产生。该模型的特点是行为迅速出现，提示自发疼痛以及对非伤害性和伤害性刺激的反应紊乱。这些包括在部分去传入神经的皮肤中对重复触摸的退缩阈值降低（“触摸诱发的感觉过敏”）、触摸诱发的痛觉过敏、对伤害性热刺激的退缩阈值降低以及对伤害性热和机械刺激的夸张反应（“热痛觉过敏”）。其中一些障碍在损伤对侧后肢的镜像部位可见。这些障碍在部分神经损伤后数小时内开始，持续数月，与人类部分神经损伤后的灼性神经痛非常相似。由于已知交感传出活动会加重人类的灼性神经痛，而交感神经切除术已知可缓解该症状，我们研究了改变大鼠模型中交感神经流出的影响。在3个实验中，通过腹腔注射胍乙啶进行可逆性交感神经切除术，每个实验在与部分神经损伤相关的不同时间进行。我们发现：（1）术后数月进行的交感神经切除术双侧缓解了感觉障碍；（2）神经损伤前进行的交感神经切除术部分预防了热痛觉过敏的出现，但不影响对重复触摸的感觉过敏；（3）神经损伤时进行的交感神经切除术在最初几天加重了感觉障碍。由于该动物模型中感觉障碍的维持和产生依赖于交感神经流出，我们得出结论，大鼠患有类似于人类交感神经维持性灼性神经痛的综合征。
