Bennett G J
Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892.
Muscle Nerve. 1993 Oct;16(10):1040-8. doi: 10.1002/mus.880161007.
Recent work has succeeded in producing models of painful peripheral neuropathies in laboratory animals. There is evidence that the animals experience both abnormal spontaneous pain and abnormal evoked pains (allodynia and hyperalgesia). Experimental analyses of these models have demonstrated potential pathophysiologic mechanisms in both the peripheral and central nervous systems; it is likely that the model neuropathic pain syndromes are due to several different mechanisms. One line of evidence suggests that these pain states gradually become centralized due to an excitotoxic effect on spinal cord dorsal horn inhibitory interneurons. The role of the sympathetic nervous system appears to vary, depending on the type of nerve injury and the temporal evolution of the syndrome. There is evidence indicating that the abnormality of cutaneous temperature regulation that often accompanies painful peripheral neuropathy is not necessarily due to the activity of sympathetic vasomotor efferents.
最近的研究成功地在实验动物身上制造出了疼痛性周围神经病变的模型。有证据表明,这些动物会经历异常的自发痛和异常的诱发性疼痛(痛觉过敏和超敏反应)。对这些模型的实验分析已经证明了外周和中枢神经系统中潜在的病理生理机制;很可能模型中的神经性疼痛综合征是由几种不同的机制引起的。有一系列证据表明,由于对脊髓背角抑制性中间神经元的兴奋性毒性作用,这些疼痛状态会逐渐向中枢发展。交感神经系统的作用似乎有所不同,这取决于神经损伤的类型和综合征的时间演变。有证据表明,疼痛性周围神经病变常伴随的皮肤温度调节异常不一定是由于交感血管运动传出神经的活动所致。