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外周神经损伤可引起对神经系统的一种适应不良反应,其产生神经病理性痛的主要特点为痛觉增敏和异常疼痛。目前文献报道多种机制涉及此反应,包括离子通道改变引起的异常放电、突触易化、多种轴突水平抑制作用缺失导致的中枢敏化、神经元细胞的凋亡以及异常的突触连接等结构的改变,另外神经损伤引起的神经免疫之间的相互作用在神经病理性痛的持续性发展中发挥着不可替代的作用。了解外周神经损伤引起的神经病理性的发病机制将对我们寻找治疗靶点和治疗策略提供坚实的理论基础。
Peripheral nerve injury can cause an adverse reaction to the nervous system, and the main hallmarks of its neuropathic pain are hyperalgesia and allodynia. It is reported in the literature that various mechanisms are involved in this reaction, including abnormal discharge caused by ion channel changes, synapse facilitation, central sensitization caused by the lack of inhibition of multiple axonal levels, apoptosis of neuronal cells, and abnormal synaptic connections And other structural changes, in addition to nerve damage caused by neuroimmunity between the interaction in the sustained development of neuropathic pain play an irreplaceable role. Understanding the pathogenesis of neuropathies caused by peripheral nerve injury will provide a solid theoretical basis for our search for therapeutic targets and therapeutic strategies.