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逆行性血管扩张与偏头痛发病机制。

Antidromic vasodilatation and the migraine mechanism.

机构信息

Headache Centre, Careggi University Hospital, Department of Preclinical and Clinical Pharmacology, University of Florence, Florence, Italy.

出版信息

J Headache Pain. 2012 Mar;13(2):103-11. doi: 10.1007/s10194-011-0408-3. Epub 2011 Dec 27.

Abstract

Despite the fact that an unprecedented series of new discoveries in neurochemistry, neuroimaging, genetics and clinical pharmacology accumulated over the last 20 years has significantly increased our current knowledge, the underlying mechanism of the migraine headache remains elusive. The present review article addresses, from early evidence that emerged at the end of the nineteenth century, the role of 'antidromic vasodilatation' as part of the more general phenomenon, currently defined as neurogenic inflammation, in the unique type of pain reported by patients suffering from migraine headaches. The present paper describes distinctive orthodromic and antidromic properties of a subset of somatosensory neurons, the vascular- and neurobiology of peptides contained in these neurons, and the clinical-pharmacological data obtained in recent investigations using provocation tests in experimental animals and human beings. Altogether, previous and recent data underscore that antidromic vasodilatation, originating from the activation of peptidergic somatosensory neurons, cannot yet be discarded as a major contributing mechanism of the throbbing head pain and hyperalgesia of migraine.

摘要

尽管过去 20 年来神经化学、神经影像学、遗传学和临床药理学领域前所未有的一系列新发现极大地增加了我们目前的知识,但偏头痛的潜在机制仍然难以捉摸。本文从 19 世纪末出现的早期证据出发,探讨了“逆行性血管扩张”作为更普遍现象(目前定义为神经源性炎症)的一部分,在偏头痛患者报告的独特类型疼痛中的作用。本文描述了感觉神经元子集的独特顺行和逆行特性、这些神经元中包含的肽的血管和神经生物学,以及最近在实验动物和人类中使用激发试验进行的临床药理学研究中获得的数据。总之,过去和最近的数据表明,起源于肽能感觉神经元激活的逆行性血管扩张,仍不能被排除为搏动性头痛和偏头痛的痛觉过敏的主要发病机制。

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