Calcitonin gene-related peptide triggers migraine-like attacks in patients with migraine with aura

Calcitonin gene-related peptide triggers migraine-like attacks in patients with migraine with aura
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DOI:
10.1177/0333102410368444
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发表时间:
2010-10-01
期刊:
影响因子:
4.9
通讯作者:
Ashina, Messoud
Ashina, Messoud
中科院分区:
医学2区
文献类型:
--
作者:
Hansen, Jakob Moller;Hauge, Anne Werner;Ashina, Messoud

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简介:降钙素基因相关肽(CGRP)是偏头痛发病的关键分子。无先兆偏头痛(MO)患者静脉注射CGRP可引发延迟性偏头痛样发作。与MO患者相比,在先前的研究中,家族性偏瘫性偏头痛(FHM)患者与对照组相比没有报告更多的偏头痛样发作。CGRP是否会引发伴有先兆的典型(非偏瘫)偏头痛患者的偏头痛尚不清楚。在本研究中,我们检测了CGRP输注对MA患者和健康对照者的偏头痛诱导作用。方法:14例典型先兆偏头痛患者和11名健康志愿者连续静脉滴注1.5 μ g/min CGRP,持续20分钟。头痛和其他偏头痛症状在1小时内每10分钟评分一次,此后每小时自记录一次,直至注射后13小时。结果:CGRP输注引起的MA患者延迟性头痛发生率(14 / 12)明显高于对照组(11 / 2)(p = 0.001)。此外,与对照组(0%,11人中0人)相比,更多的MA患者(57%,14人中8人)符合CGRP后实验性诱发偏头痛发作的标准(P = 0.003)。4例患者(28%)报告CGRP输注后出现先兆症状。结论:CGRP在MA患者中引发无先兆偏头痛样发作。它还在28%的患者中引发了典型的先兆。这些数据表明,MA和MO患者引发偏头痛的神经生物学途径相似,并提示MA/MO和FHM之间存在差异。
Introduction: Calcitonin gene-related peptide (CGRP) is a key molecule in migraine pathogenesis. Intravenous CGRP infusion triggers delayed migraine-like attacks in patients with migraine without aura (MO). In contrast to patients with MO, in prior studies patients with familial hemiplegic migraine (FHM) did not report more migraine-like attacks compared to controls. Whether CGRP triggers migraine in patients with typical (non-hemiplegic) migraine with aura is (MA) unknown. In the present study we examined the migraine inducing effect of CGRP infusion in patients suffering from MA and healthy controls.Methods: Fourteen patients suffering exclusively from migraine with typical aura (MA) and 11 healthy volunteers received a continuous intravenous infusion of 1.5 mu g/min CGRP over 20 minutes. Headache and other migraine symptoms were scored every 10 minutes for one hour and self recorded hourly thereafter and until 13 hours post-infusion.Results: CGRP infusion induced significantly more delayed headaches in MA patients (12 out of 14) than in controls (2 out of 11) (p = 0.001). Furthermore, significantly more MA patients (57%; 8 out of 14) fulfilled criteria for an experimentally induced migraine attack after CGRP than controls (0%; 0 out of 11) (P = 0.003). Four patients (28%) reported aura symptoms after CGRP infusion.Conclusion: CGRP triggered migraine-like attacks without aura in patients suffering exclusively from MA. It also triggered a typical aura in 28% of the patients. These data indicate similar neurobiological pathways responsible for triggering migraine headache in MA and MO patients, and suggest differences between MA/MO and FHM.