Meningeal contribution to migraine pain: A magnetic resonance angiography study

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Meningeal contribution to migraine pain : A magnetic resonance angiography study. / Khan, Sabrina; Amin, Faisal Mohammad; Christensen, Casper Emil; Ghanizada, Hashmat; Younis, Samaira; Olinger, Anne Christine Rye; De Koning, Patrick J.H.; Larsson, Henrik B.W.; Ashina, Messoud.

I: Brain, Bind 142, Nr. 1, 2019, s. 93-102.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Khan, S, Amin, FM, Christensen, CE, Ghanizada, H, Younis, S, Olinger, ACR, De Koning, PJH, Larsson, HBW & Ashina, M 2019, 'Meningeal contribution to migraine pain: A magnetic resonance angiography study', Brain, bind 142, nr. 1, s. 93-102. https://doi.org/10.1093/brain/awy300

APA

Khan, S., Amin, F. M., Christensen, C. E., Ghanizada, H., Younis, S., Olinger, A. C. R., De Koning, P. J. H., Larsson, H. B. W., & Ashina, M. (2019). Meningeal contribution to migraine pain: A magnetic resonance angiography study. Brain, 142(1), 93-102. https://doi.org/10.1093/brain/awy300

Vancouver

Khan S, Amin FM, Christensen CE, Ghanizada H, Younis S, Olinger ACR o.a. Meningeal contribution to migraine pain: A magnetic resonance angiography study. Brain. 2019;142(1):93-102. https://doi.org/10.1093/brain/awy300

Author

Khan, Sabrina ; Amin, Faisal Mohammad ; Christensen, Casper Emil ; Ghanizada, Hashmat ; Younis, Samaira ; Olinger, Anne Christine Rye ; De Koning, Patrick J.H. ; Larsson, Henrik B.W. ; Ashina, Messoud. / Meningeal contribution to migraine pain : A magnetic resonance angiography study. I: Brain. 2019 ; Bind 142, Nr. 1. s. 93-102.

Bibtex

@article{a2a2bccd27674b7f93641c7bf279270e,
title = "Meningeal contribution to migraine pain: A magnetic resonance angiography study",
abstract = "The origin of migraine pain is unknown but possibly implicates the dura mater, which is pain sensitive in proximity to the meningeal arteries. Therefore, subtle changes in vessel calibre on the head pain side could reflect activation of dural perivascular nociceptors that leads to migraine headache. To test this hypothesis, we measured circumference changes of cranial arteries in patients with cilostazol-induced unilateral migraine without aura using 3 T high resolution magnetic resonance angiography. The middle meningeal artery was of key interest, as it is the main supply of the dura mater. We also measured the superficial temporal and external carotid arteries as additional extracranial segments, and the middle cerebral, the cerebral and cavernous parts of the internal carotid (ICAcerebral and ICAcavernous), and the basilar arteries as intracranial arterial segments. Magnetic resonance angiography scans were performed at baseline, migraine onset, after sumatriptan, and ≥27 h after migraine onset. Thirty patients underwent magnetic resonance angiography scans, of which 26 patients developed unilateral attacks of migraine without aura and were included in the final analysis. Eleven patients treated their migraine with sumatriptan while the remaining 15 patients did not treat their attacks with analgesics or triptans. At migraine onset, only the middle meningeal artery exhibited greater circumference increase on the pain side (0.24 ± 0.37 mm) compared to the non-pain side (0.06 ± 0.38 mm) (P = 0.002). None of the remaining arteries revealed any pain-side specific changes in circumference (P > 0.05), but exhibited bilateral dilation. Sumatriptan constricted all extracerebral arteries (P < 0.05). In the late phase of migraine, we found sustained bilateral dilation of the middle meningeal artery. In conclusion, onset of migraine is associated with increase in middle meningeal artery circumference specific to the head pain side. Our findings suggest that vasodilation of the middle meningeal artery may be a surrogate marker for activation of dural perivascular nociceptors, indicating a meningeal site of migraine headache.",
keywords = "dura mater, headache, inflammation, perivascular, trigeminal",
author = "Sabrina Khan and Amin, {Faisal Mohammad} and Christensen, {Casper Emil} and Hashmat Ghanizada and Samaira Younis and Olinger, {Anne Christine Rye} and {De Koning}, {Patrick J.H.} and Larsson, {Henrik B.W.} and Messoud Ashina",
year = "2019",
doi = "10.1093/brain/awy300",
language = "English",
volume = "142",
pages = "93--102",
journal = "Brain",
issn = "0006-8950",
publisher = "Oxford University Press",
number = "1",

}

RIS

TY - JOUR

T1 - Meningeal contribution to migraine pain

T2 - A magnetic resonance angiography study

AU - Khan, Sabrina

AU - Amin, Faisal Mohammad

AU - Christensen, Casper Emil

AU - Ghanizada, Hashmat

AU - Younis, Samaira

AU - Olinger, Anne Christine Rye

AU - De Koning, Patrick J.H.

AU - Larsson, Henrik B.W.

AU - Ashina, Messoud

PY - 2019

Y1 - 2019

N2 - The origin of migraine pain is unknown but possibly implicates the dura mater, which is pain sensitive in proximity to the meningeal arteries. Therefore, subtle changes in vessel calibre on the head pain side could reflect activation of dural perivascular nociceptors that leads to migraine headache. To test this hypothesis, we measured circumference changes of cranial arteries in patients with cilostazol-induced unilateral migraine without aura using 3 T high resolution magnetic resonance angiography. The middle meningeal artery was of key interest, as it is the main supply of the dura mater. We also measured the superficial temporal and external carotid arteries as additional extracranial segments, and the middle cerebral, the cerebral and cavernous parts of the internal carotid (ICAcerebral and ICAcavernous), and the basilar arteries as intracranial arterial segments. Magnetic resonance angiography scans were performed at baseline, migraine onset, after sumatriptan, and ≥27 h after migraine onset. Thirty patients underwent magnetic resonance angiography scans, of which 26 patients developed unilateral attacks of migraine without aura and were included in the final analysis. Eleven patients treated their migraine with sumatriptan while the remaining 15 patients did not treat their attacks with analgesics or triptans. At migraine onset, only the middle meningeal artery exhibited greater circumference increase on the pain side (0.24 ± 0.37 mm) compared to the non-pain side (0.06 ± 0.38 mm) (P = 0.002). None of the remaining arteries revealed any pain-side specific changes in circumference (P > 0.05), but exhibited bilateral dilation. Sumatriptan constricted all extracerebral arteries (P < 0.05). In the late phase of migraine, we found sustained bilateral dilation of the middle meningeal artery. In conclusion, onset of migraine is associated with increase in middle meningeal artery circumference specific to the head pain side. Our findings suggest that vasodilation of the middle meningeal artery may be a surrogate marker for activation of dural perivascular nociceptors, indicating a meningeal site of migraine headache.

AB - The origin of migraine pain is unknown but possibly implicates the dura mater, which is pain sensitive in proximity to the meningeal arteries. Therefore, subtle changes in vessel calibre on the head pain side could reflect activation of dural perivascular nociceptors that leads to migraine headache. To test this hypothesis, we measured circumference changes of cranial arteries in patients with cilostazol-induced unilateral migraine without aura using 3 T high resolution magnetic resonance angiography. The middle meningeal artery was of key interest, as it is the main supply of the dura mater. We also measured the superficial temporal and external carotid arteries as additional extracranial segments, and the middle cerebral, the cerebral and cavernous parts of the internal carotid (ICAcerebral and ICAcavernous), and the basilar arteries as intracranial arterial segments. Magnetic resonance angiography scans were performed at baseline, migraine onset, after sumatriptan, and ≥27 h after migraine onset. Thirty patients underwent magnetic resonance angiography scans, of which 26 patients developed unilateral attacks of migraine without aura and were included in the final analysis. Eleven patients treated their migraine with sumatriptan while the remaining 15 patients did not treat their attacks with analgesics or triptans. At migraine onset, only the middle meningeal artery exhibited greater circumference increase on the pain side (0.24 ± 0.37 mm) compared to the non-pain side (0.06 ± 0.38 mm) (P = 0.002). None of the remaining arteries revealed any pain-side specific changes in circumference (P > 0.05), but exhibited bilateral dilation. Sumatriptan constricted all extracerebral arteries (P < 0.05). In the late phase of migraine, we found sustained bilateral dilation of the middle meningeal artery. In conclusion, onset of migraine is associated with increase in middle meningeal artery circumference specific to the head pain side. Our findings suggest that vasodilation of the middle meningeal artery may be a surrogate marker for activation of dural perivascular nociceptors, indicating a meningeal site of migraine headache.

KW - dura mater

KW - headache

KW - inflammation

KW - perivascular

KW - trigeminal

U2 - 10.1093/brain/awy300

DO - 10.1093/brain/awy300

M3 - Journal article

C2 - 30590467

AN - SCOPUS:85059281938

VL - 142

SP - 93

EP - 102

JO - Brain

JF - Brain

SN - 0006-8950

IS - 1

ER -

ID: 230246785