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Intradural artery dilation during experimentally induced migraine attacks

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@article{7070ba98e6c447e5844e79b52c8b39a4,
title = "Intradural artery dilation during experimentally induced migraine attacks",
abstract = "The middle meningeal artery is a proposed surrogate marker for activation of trigeminal nociceptors during migraine. Previous studies focused on the extracranial part of the artery; hence, vasoreactivity in the intradural arteries during migraine is unknown. Thirty-four patients with migraine without aura were given sildenafil on one day and calcitonin gene-related peptide on another in double-blind crossover fashion. Patients were scanned with 3.0 T MR angiography before drug administration and again 6 hours later during induced attacks of migraine. We measured circumference of the intradural segment of the middle meningeal artery before and during induced migraine attacks. The middle cerebral and superficial temporal arteries were also examined. Fourteen patients had attacks during the second scan after both study drugs and 11 had a migraine after either one or the other, resulting in a total of 39 attacks included in the final analysis. Mean circumference of the intradural middle meningeal artery at baseline was 3.18 mm with an increase of 0.11 mm during attacks (P = 0.005), corresponding to a relative dilation of 3.6{\%} [95{\%} CI: 1.4{\%}-5.7{\%}]. Middle cerebral artery dilated by 9.4{\%} [95{\%} CI: 7.1{\%}-11.7{\%}] and superficial temporal artery by 2.3{\%} [95{\%} CI: 0.2{\%}-4.4{\%}]. Our study shows that the intradural middle meningeal artery and the middle cerebral artery are dilated during migraine induced by calcitonin gene-related peptide as well as sildenafil. We propose that intradural vasculature is affected by migraine-driven activation of trigeminal afferents during migraine attacks.",
author = "Christensen, {Casper Emil} and Samaira Younis and Ulrich Lindberg and {de Koning}, Patrick and Daniel Tolnai and Paulson, {Olaf Bjarne} and {Wiberg Larsson}, {Henrik Bo} and Amin, {Faisal Mohammad} and Messoud Ashina",
year = "2020",
doi = "10.1097/j.pain.0000000000002008",
language = "English",
journal = "Pain",
issn = "0304-3959",
publisher = "Elsevier BV",

}

RIS

TY - JOUR

T1 - Intradural artery dilation during experimentally induced migraine attacks

AU - Christensen, Casper Emil

AU - Younis, Samaira

AU - Lindberg, Ulrich

AU - de Koning, Patrick

AU - Tolnai, Daniel

AU - Paulson, Olaf Bjarne

AU - Wiberg Larsson, Henrik Bo

AU - Amin, Faisal Mohammad

AU - Ashina, Messoud

PY - 2020

Y1 - 2020

N2 - The middle meningeal artery is a proposed surrogate marker for activation of trigeminal nociceptors during migraine. Previous studies focused on the extracranial part of the artery; hence, vasoreactivity in the intradural arteries during migraine is unknown. Thirty-four patients with migraine without aura were given sildenafil on one day and calcitonin gene-related peptide on another in double-blind crossover fashion. Patients were scanned with 3.0 T MR angiography before drug administration and again 6 hours later during induced attacks of migraine. We measured circumference of the intradural segment of the middle meningeal artery before and during induced migraine attacks. The middle cerebral and superficial temporal arteries were also examined. Fourteen patients had attacks during the second scan after both study drugs and 11 had a migraine after either one or the other, resulting in a total of 39 attacks included in the final analysis. Mean circumference of the intradural middle meningeal artery at baseline was 3.18 mm with an increase of 0.11 mm during attacks (P = 0.005), corresponding to a relative dilation of 3.6% [95% CI: 1.4%-5.7%]. Middle cerebral artery dilated by 9.4% [95% CI: 7.1%-11.7%] and superficial temporal artery by 2.3% [95% CI: 0.2%-4.4%]. Our study shows that the intradural middle meningeal artery and the middle cerebral artery are dilated during migraine induced by calcitonin gene-related peptide as well as sildenafil. We propose that intradural vasculature is affected by migraine-driven activation of trigeminal afferents during migraine attacks.

AB - The middle meningeal artery is a proposed surrogate marker for activation of trigeminal nociceptors during migraine. Previous studies focused on the extracranial part of the artery; hence, vasoreactivity in the intradural arteries during migraine is unknown. Thirty-four patients with migraine without aura were given sildenafil on one day and calcitonin gene-related peptide on another in double-blind crossover fashion. Patients were scanned with 3.0 T MR angiography before drug administration and again 6 hours later during induced attacks of migraine. We measured circumference of the intradural segment of the middle meningeal artery before and during induced migraine attacks. The middle cerebral and superficial temporal arteries were also examined. Fourteen patients had attacks during the second scan after both study drugs and 11 had a migraine after either one or the other, resulting in a total of 39 attacks included in the final analysis. Mean circumference of the intradural middle meningeal artery at baseline was 3.18 mm with an increase of 0.11 mm during attacks (P = 0.005), corresponding to a relative dilation of 3.6% [95% CI: 1.4%-5.7%]. Middle cerebral artery dilated by 9.4% [95% CI: 7.1%-11.7%] and superficial temporal artery by 2.3% [95% CI: 0.2%-4.4%]. Our study shows that the intradural middle meningeal artery and the middle cerebral artery are dilated during migraine induced by calcitonin gene-related peptide as well as sildenafil. We propose that intradural vasculature is affected by migraine-driven activation of trigeminal afferents during migraine attacks.

U2 - 10.1097/j.pain.0000000000002008

DO - 10.1097/j.pain.0000000000002008

M3 - Journal article

JO - Pain

JF - Pain

SN - 0304-3959

ER -

ID: 60567578