偏头痛病生机制三叉神经血管通路的解剖及
2016-12-1 来源:不详 浏览次数:次中文翻译
科学证据支持偏头痛的病理生理涉及到遗传易感人群这些方面的遗传变化:脑兴奋性、颅内血管扩张、三叉神经血管通路的反复激活和敏感化,以及随之发生的结构和功能改变。
?脑兴奋性改变的证据见于临床和临床前研究中感觉性先兆、发作期和发作间期对视觉、听觉和嗅觉刺激的过度敏感,以及下行抑制性疼痛通路的活性降低。
?支持三叉神经血管系统活化和敏感化的资料包括在偏头痛发作过程中进展发生的头部和全身皮肤异常疼痛。
?结构和功能改变包括皮层下脑白质损伤、参与感觉信息整合的皮层区增厚、皮层扩展性抑制导致的皮层神经可塑性改变。
因而,我们回顾了近期关于三叉神经血管通路及其被皮层扩展性抑制活化的解剖学资料,对偏头痛性畏光、脑干/丘脑/皮层调控三叉神经血管通路的神经基础有了新的理解。
英文原文
Migrainepathophysiology:anatomyofthetrigeminovascularpathwayandassociatedneurologicalsymptoms,corticalspreadingdepression,sensitization,andmodulationofpain.
NosedaR,BursteinR.
Abstract
Scientificevidencesupportsthenotionthatmigrainepathophysiologyinvolvesinheritedalterationofbrainexcitability,intracranialarterialdilatation,recurrentactivation,andsensitizationofthetrigeminovascularpathway,andconsequentialstructuralandfunctionalchangesingeneticallysusceptibleindividuals.Evidenceofalteredbrainexcitabilityemergedfromclinicalandpreclinicalinvestigationofsensoryauras,ictalandinterictalhypersensitivitytovisual,auditory,andolfactorystimulation,andreducedactivationofdescendinginhibitorypainpathways.Datasupportingtheactivationandsensitizationofthetrigeminovascularsystemincludetheprogressivedevelopmentofcephalicandwhole-bodycutaneousallodyniaduringamigraineattack.Inaddition,structuralandfunctionalalterationsincludethepresenceofsubcorticalwhitematerlesions,thickeningofcorticalareasinvolvedinprocessingsensoryinformation,andcorticalneuroplasticchangesinducedbycorticalspreadingdepression.Here,wereviewrecentanatomicaldataonthetrigeminovascularpathwayanditsactivationbycorticalspreadingdepression,anovelunderstandingoftheneuralsubstrateofmigraine-typephotophobia,andmodulationofthetrigeminovascularpathwaybythebrainstem,hypothalamusandcortex.
文章来源:Pain.Dec;Suppl1:S44-53.
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