Evidence for a vascular factor in migraine

TY - JOUR

T1 - Evidence for a vascular factor in migraine

AU - Asghar, Mohammad S

AU - Hansen, Adam E

AU - Amin, Faisal Mohammad

AU - van der Geest, R J

AU - Koning, Patrick van der

AU - Larsson, Henrik B W

AU - Olesen, Jes

AU - Ashina, Messoud

N1 - Copyright © 2010 American Neurological Association.

PY - 2011/3

Y1 - 2011/3

N2 - 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 nonheadache 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.

AB - 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 nonheadache 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.

U2 - 10.1002/ana.22292

DO - 10.1002/ana.22292

M3 - Journal article

C2 - 21416486

SN - 0364-5134

VL - 69

SP - 635

EP - 645

JO - Annals of Neurology

JF - Annals of Neurology

IS - 4

ER -