摘要
目的:病理学研究证实神经源性炎症在偏头痛中确实存在,围绕偏头痛中神经源性炎症的相关内容加深认识对指导临床工作颇有意义。资料来源:应用计算机检索PUBMED1995-01/2005-12期间的相关文章,检索词为“migraine,neurogenicinflammation”,并限定文章语言种类为English。资料选择:对资料进行初审,并查看每篇文献后的引文。纳入标准:文章所述内容应与偏头痛的神经源性炎症研究相关。排除标准:重复研究或Meta分析类文章。资料提炼:共收集到97篇相关文献,29篇文献符合纳入标准,排除的68篇文献为内容陈旧或重复。符合纳入标准的29篇文献中,17篇涉及神经肽,6篇涉及炎症相关因子,1篇涉及皮层扩布性抑制,2篇涉及5-羟色胺,2篇涉及内皮素,1篇涉及γ-氨基丁酸。资料综合:三叉神经血管学说在偏头痛发病机制中占主导地位,神经源性炎症是其中的关键环节,而以往的病理学研究也证实了神经源性炎症在偏头痛中确实存在。降钙素基因相关肽、P物质和神经激肽A等神经肽的释放及其所导致的神经源性炎症被认为是偏头痛的病理生理基础;β-转化生长因子、白介素8、组胺等炎症因子的释放及血小板激活的增加也参与其中。动物实验结果表明,皮层扩布性抑制和内皮素对大鼠硬脑膜神经源性炎症起重要作用;5-羟色胺1B/1D受体激动剂、丙戊酸是通过各自不同的机制阻滞硬脑膜内的神经源性炎症。但少数临床和动物实验的研究结果却表明,神经源性炎症并不是偏头痛的主要因素。结论:偏头痛的发作是多因素作用的结果,是当某一诱发因素启动时,体内神经-血管及诸多生化因子共同参与的连锁反应。目前认为神经源性炎症是偏头痛的基本病理过程,在这一过程中也有诸多因素的参与。
OBJECTIVE： Neurogenic inflammation has been confirmed to exist in migraine by pathological research; therefore, it is necessary to deepen the understanding of related content on neurogenic inflammation in migraine, which is meaningful to guide the clinical research.
DATA SOURCES： A computer-based online search of PUBMED database was undertaken to identify related articles published in English between January 1995 and December 2005 with the key words of ＂migraine, neurogenic inflammation＂.
STUDY SELECTION： The data were examined firstly, and the quotations of every article were looked over. Inclusive criteria： Articles correlated with the neurogenic inflammation involved in migraine. Exclusive criteria： Repeated search or Meta analytic articles.
DATA EXTRACTION： Among the 97 collected articles, 29 ones were consistent with the inclusive criteria and 69 ones were out of date or repetitive. In the 29 inclusive articles, 17 ones involved in neuropeptide, 6 involved in inflammatory related factors, 1 related to cortical spreading depression, 2 involved in serotonin, 2 involved in endothelin and 1 involved in gamma-aminobutyric acid.
DATA SYNTHESIS： The trigeminovascular theory is dominant in the pathogenesis of migraine, and neurogenic inflammation is the key element of it. Previous research has confirmed that neurogenic inflammation exist in migraine. Release of neuropeptide, mainly calcitonin gene-related peptide, .substance P and neurokinin A and the following neurogenic inflammation are proposed to be the pathophysiogical foundation. Release of inflammatory factors such as 13-transforming growth factor, interleukin-8, histamine and so on and increased activated platelet also participate in this course. Animal experiments have shown that cortical spreading depression and endothelin play important roles in rat dural neurogenic inflammation; 5-hydroxytryptamine1B/1D receptor agonist and valproic acid block dural neurogenic inflammation by different mechanism. However, a few clinical and animal experiments show that neurogenic inflammation is not the major element in migraine.
CONCLUSION： Migraine is the complex result of multiple factor, which is a chain reaction of collective participation of internal nerve-vessel and many biochemical factors after a certain causative factor triggers a migraine attack. Now neurogenin inflammation is considered as the basic pathological process of migraine accompanying participation of many other factors.
出处
《中国临床康复》
CSCD
北大核心
2006年第42期118-120,共3页
Chinese Journal of Clinical Rehabilitation
作者简介
郭丽，女，1973年生，山东省泰安市人，汉族，天津中医学院在读博士．主要从事神经系统疾病方面的研究。
