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偏头痛的血管因素证据。

Evidence for a vascular factor in migraine.

机构信息

Danish Headache Center and Department of Neurology, Glostrup Hospital, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.

出版信息

Ann Neurol. 2011 Apr;69(4):635-45. doi: 10.1002/ana.22292. Epub 2011 Mar 17.

DOI:10.1002/ana.22292
PMID:21416486
Abstract

OBJECTIVE

It has been suggested that migraine is caused by neural dysfunction without involvement of vasodilatation. Because dismissal of vascular mechanisms seemed premature, we examined diameter of extra- and intracranial vessels in migraine without aura patients.

METHODS

A novel high-resolution direct magnetic resonance angiography imaging technique was used to measure arterial circumference of the extracranial middle meningeal artery (MMA) and the intracranial middle cerebral artery (MCA). Data were obtained at baseline, during migraine attack, and after treatment with the migraine abortive drug sumatriptan (a 5-hydroxytryptamine agonist).

RESULTS

We found dilatation of both MMA and MCA during migraine attack (p = 0.001). Sumatriptan administration caused amelioration of headache (p < 0.001) and contraction of MMA (p < 0.001), but MCA remained unchanged (p = 0.16). Exploratory analysis revealed that in migraine attacks with half-sided headache, there was only dilatation on the headache side of MMA of 12.49% (95% confidence interval [CI], 4.16-20.83%) and of MCA of 12.88% (95% CI, 3.49-22.27%) and no dilatation on the non headache side of MMA (95% CI, -4.27 to 11.53%) and MCA (95% CI, -6.7 to 14.28%). In double-sided headache we found bilateral vasodilatation of both MMA and MCA (p < 0.001).

INTERPRETATION

These data show that migraine without aura is associated with dilatation of extra- and intracerebral arteries and that the headache location is associated with the location of the vasodilatation. Furthermore, contraction of extracerebral and not intracerebral arteries is associated with amelioration of headache. Collectively, these data suggest that vasodilatation and perivascular release of vasoactive substances is an integral mechanism of migraine pathophysiology.

摘要

目的

有人认为偏头痛是由神经功能障碍引起的,与血管扩张无关。由于排除血管机制似乎还为时过早,我们检查了无先兆偏头痛患者的颅外和颅内血管直径。

方法

使用一种新颖的高分辨率直接磁共振血管造影成像技术测量颅外脑膜中动脉(MMA)和颅内大脑中动脉(MCA)的动脉周长。在基线、偏头痛发作期间和偏头痛发作缓解药物舒马曲坦(5-羟色胺激动剂)治疗后获得数据。

结果

我们发现偏头痛发作期间 MMA 和 MCA 均扩张(p = 0.001)。舒马曲坦给药可改善头痛(p < 0.001)并收缩 MMA(p < 0.001),但 MCA 无变化(p = 0.16)。探索性分析显示,在偏头痛单侧头痛发作中,MMA 头痛侧扩张 12.49%(95%置信区间 [CI],4.16-20.83%),MCA 扩张 12.88%(95% CI,3.49-22.27%),而 MMA 非头痛侧无扩张(95% CI,-4.27 至 11.53%)和 MCA(95% CI,-6.7 至 14.28%)。在双侧头痛中,我们发现 MMA 和 MCA 双侧扩张(p < 0.001)。

结论

这些数据表明无先兆偏头痛与颅外和颅内动脉扩张有关,头痛部位与血管扩张部位有关。此外,颅外血管收缩而不是颅内血管收缩与头痛缓解有关。综上所述,这些数据表明血管扩张和血管活性物质的血管周围释放是偏头痛病理生理学的一个完整机制。

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