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Association of acetazolamide infusion with headache and cranial artery dilation in healthy volunteers

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@article{45a67d5e83ac40839e98ba28c640aba9,
title = "Association of acetazolamide infusion with headache and cranial artery dilation in healthy volunteers",
abstract = "The carbonic anhydrase inhibitor acetazolamide causes extracellular acidosis and dilatation of cerebral arterioles. In this study, we tested the hypothesis that acetazolamide also may induce headache and dilatation of cranial arteries. In a randomized double-blind crossover study design, 12 young healthy women were allocated to injection of 1 g acetazolamide or placebo on 2 separate days. We recorded headache on a verbal rating scale from 0 to 10 during an immediate phase (0-90 minutes) and a delayed phase (2-12 hours). The circumference of cranial arteries was measured using 3T high-resolution magnetic resonance angiography 30 and 60 minutes after injection. Acetazolamide provoked immediate headache in 9 participants compared to 3 participants after placebo (P=.031). Eleven participants reported headache in the delayed phase after acetazolamide, compared with 4 after placebo (P=.016). The area under the curve for headache was increased after acetazolamide compared to placebo in the delayed phase (2-12 h) (P=.005). Compared to placebo, arterial circumference increased after acetazolamide in the basilar artery (P=.002) as well as the cerebral (P=.003), cavernous (P=.002), and cervical (P=.005) parts of the internal carotid artery, but no other extracranial arteries changed after acetazolamide. In conclusion, acetazolamide caused immediate and delayed headache as well as dilatation of intracranial arteries in healthy volunteers. It is possible that extracellular acidosis induced by acetazolamide causes sensitization of cephalic perivascular nociceptors, which, in combination with vasodilatation, leads to delayed headache.",
author = "Arngrim, {Nanna Bj{\o}rkbom} and Schytz, {Henrik Winther} and Asghar, {Mohammed Sohail} and Amin, {Faisal Mohammad} and Anders Hougaard and Larsen, {Vibeke Andr{\'e}e} and {de Koning}, {Patrick J H} and Larsson, {Henrik Bo Wiberg} and Jes Olesen and Messoud Ashina",
note = "Copyright {\textcopyright} 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.",
year = "2014",
month = aug,
doi = "10.1016/j.pain.2014.05.019",
language = "English",
volume = "155",
pages = "1649--58",
journal = "Pain",
issn = "0304-3959",
publisher = "Elsevier BV",
number = "8",

}

RIS

TY - JOUR

T1 - Association of acetazolamide infusion with headache and cranial artery dilation in healthy volunteers

AU - Arngrim, Nanna Bjørkbom

AU - Schytz, Henrik Winther

AU - Asghar, Mohammed Sohail

AU - Amin, Faisal Mohammad

AU - Hougaard, Anders

AU - Larsen, Vibeke Andrée

AU - de Koning, Patrick J H

AU - Larsson, Henrik Bo Wiberg

AU - Olesen, Jes

AU - Ashina, Messoud

N1 - Copyright © 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

PY - 2014/8

Y1 - 2014/8

N2 - The carbonic anhydrase inhibitor acetazolamide causes extracellular acidosis and dilatation of cerebral arterioles. In this study, we tested the hypothesis that acetazolamide also may induce headache and dilatation of cranial arteries. In a randomized double-blind crossover study design, 12 young healthy women were allocated to injection of 1 g acetazolamide or placebo on 2 separate days. We recorded headache on a verbal rating scale from 0 to 10 during an immediate phase (0-90 minutes) and a delayed phase (2-12 hours). The circumference of cranial arteries was measured using 3T high-resolution magnetic resonance angiography 30 and 60 minutes after injection. Acetazolamide provoked immediate headache in 9 participants compared to 3 participants after placebo (P=.031). Eleven participants reported headache in the delayed phase after acetazolamide, compared with 4 after placebo (P=.016). The area under the curve for headache was increased after acetazolamide compared to placebo in the delayed phase (2-12 h) (P=.005). Compared to placebo, arterial circumference increased after acetazolamide in the basilar artery (P=.002) as well as the cerebral (P=.003), cavernous (P=.002), and cervical (P=.005) parts of the internal carotid artery, but no other extracranial arteries changed after acetazolamide. In conclusion, acetazolamide caused immediate and delayed headache as well as dilatation of intracranial arteries in healthy volunteers. It is possible that extracellular acidosis induced by acetazolamide causes sensitization of cephalic perivascular nociceptors, which, in combination with vasodilatation, leads to delayed headache.

AB - The carbonic anhydrase inhibitor acetazolamide causes extracellular acidosis and dilatation of cerebral arterioles. In this study, we tested the hypothesis that acetazolamide also may induce headache and dilatation of cranial arteries. In a randomized double-blind crossover study design, 12 young healthy women were allocated to injection of 1 g acetazolamide or placebo on 2 separate days. We recorded headache on a verbal rating scale from 0 to 10 during an immediate phase (0-90 minutes) and a delayed phase (2-12 hours). The circumference of cranial arteries was measured using 3T high-resolution magnetic resonance angiography 30 and 60 minutes after injection. Acetazolamide provoked immediate headache in 9 participants compared to 3 participants after placebo (P=.031). Eleven participants reported headache in the delayed phase after acetazolamide, compared with 4 after placebo (P=.016). The area under the curve for headache was increased after acetazolamide compared to placebo in the delayed phase (2-12 h) (P=.005). Compared to placebo, arterial circumference increased after acetazolamide in the basilar artery (P=.002) as well as the cerebral (P=.003), cavernous (P=.002), and cervical (P=.005) parts of the internal carotid artery, but no other extracranial arteries changed after acetazolamide. In conclusion, acetazolamide caused immediate and delayed headache as well as dilatation of intracranial arteries in healthy volunteers. It is possible that extracellular acidosis induced by acetazolamide causes sensitization of cephalic perivascular nociceptors, which, in combination with vasodilatation, leads to delayed headache.

U2 - 10.1016/j.pain.2014.05.019

DO - 10.1016/j.pain.2014.05.019

M3 - Journal article

C2 - 24861583

VL - 155

SP - 1649

EP - 1658

JO - Pain

JF - Pain

SN - 0304-3959

IS - 8

ER -

ID: 44991680