Open Access
CC BY 4.0 · TH Open 2019; 03(02): e180-e189
DOI: 10.1055/s-0039-1692989
Original Article
Georg Thieme Verlag KG Stuttgart · New York

Potential Antimigraine Effects of Warfarin: An Exploration of Biological Mechanism with Survey of Patients

Benjamin Nilsson
1   Alberta Health Services, Edmonton, Alberta, Canada
2   Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
,
Valentina Back
2   Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
3   Cardiovascular Research Centre, University of Alberta, Edmonton, Alberta, Canada
,
Ran Wei
3   Cardiovascular Research Centre, University of Alberta, Edmonton, Alberta, Canada
4   Department of Pharmacology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada
,
Frances Plane
3   Cardiovascular Research Centre, University of Alberta, Edmonton, Alberta, Canada
4   Department of Pharmacology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada
,
Paul Jurasz*
2   Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
3   Cardiovascular Research Centre, University of Alberta, Edmonton, Alberta, Canada
4   Department of Pharmacology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada
5   Alberta Mazankowski Heart Institute, University of Alberta, Edmonton, Alberta, Canada
,
Tammy J. Bungard*
6   Department of Cardiology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada
› Author Affiliations

Funding This work was funded by grants from the Canadian Institutes of Health Research MOP-130289 (P.J.). We thank S. Simpson for assistance with survey.
Further Information

Publication History

01 April 2019

20 May 2019

Publication Date:
21 June 2019 (online)

Preview

Abstract

Case reports suggest a link between anticoagulant use and improved migraine symptoms, and a role for platelet-induced cerebral vasoconstriction in migraine pathobiology. Hence, we investigated the mechanism by which warfarin may affect migraine symptoms and whether there is a change in migraine symptomology in patients initiating oral anticoagulants, most commonly warfarin. The effects of warfarin on human platelet aggregation and secretion as well as platelet-induced rat cerebral artery vasoconstriction were studied. A survey of migraine and symptom change after starting or stopping oral anticoagulants was also conducted. Warfarin inhibited platelet aggregation and 5-hydroxytryptamine (5-HT) secretion in a concentration-dependent manner. Warfarin-inhibited platelet secretion products constricted middle cerebral arteries from male but not from female rats. For the survey, patient demographic information, migraine and medical history, and Migraine Disability Assessment Score (MIDAS) changes were collected. Out of 175 consenting, 40 respondents met the criteria for migraine and completed the survey. A total of 11 patients reported migraine symptom change, all coinciding with starting warfarin. Of those having symptom and MIDAS improvement, most were female with migraines with aura, whereas those worsening were male with fewer having migraine with aura. Of those reporting migraine symptom change with warfarin, female sex may be associated with improved MIDAS, and those experiencing an aura component are more likely to report a symptom change. Warfarin-mediated symptom improvement in females may occur due to inhibition of platelet 5-HT secretion and a lower sensitivity of female cerebral blood vessels to platelet-derived 5-HT-induced vasoconstriction.

* Co-senior authors.