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机构地区:[1]第四军医大学西京医院麻醉科,陕西西安710032
出 处:《现代生物医学进展》2012年第22期4376-4379,4383,共5页Progress in Modern Biomedicine
基 金:国家自然科学基金面上项目(30872434)
摘 要: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。Neural damage to the PNS provokes maladaptive responses in nociceptive pathways that drive spontaneous pain and sensory amplification.Multiple mechanisms are responsible for neuropathic pain,including changes in ion channels that lead to ectopic activity,synaptic facilitation,and central sensitization caused by loss of inhibition at multiple levels of the neuraxis.In addition,neuronal cell apoptosis and aberrant synaptic connectivity provide the structural basis for persistently altered processing of both nociceptive and innocuous afferent input.What's more,neural damage provokes vigorous and highly organized neuro-immune interactions that play a key role in initiating many cellular mechanisms that underlie persistent neuropathic pain.It is necessary to understand the underlying mechanisms of neuropathic pain by neural damage to the PNS,and it will guide us in the searching of treatment target and give solid theoretic foundation for our treatment strategy.
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