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Review
. 2023 Apr 11;100(15):716-726.
doi: 10.1212/WNL.0000000000201699. Epub 2022 Dec 15.

Microembolism and Other Links Between Migraine and Stroke: Clinical and Pathophysiologic Update

Simona Sacco  1 , Andrea M Harriott  1 , Cenk Ayata  1 , Raffaele Ornello  1 , Rodrigo Bagur  1 , Amado Jimenez-Ruiz  1 , Luciano A Sposato  2
Affiliations
Review

Microembolism and Other Links Between Migraine and Stroke: Clinical and Pathophysiologic Update

Simona Sacco et al. Neurology. .

Abstract

Migraine and stroke are highly prevalent diseases with a high effect on quality of life, with multiple epidemiologic, pathophysiologic, clinical, and prognostic areas of overlap. Migraine is a risk factor for stroke. This risk is explained by common risk factors, migraine-specific mechanisms, and non-migraine-specific mechanisms that have a relevant role in patients with migraine with aura (e.g., atrial fibrillation and paradoxical embolism through a patent foramen ovale). Another important link between migraine aura and ischemic stroke is cardiac embolism. Cardioembolism is the most frequent cause of ischemic stroke, and increasing evidence suggests that microembolism, predominantly but not exclusively originating in the heart, is a contributing mechanism to the development of migraine aura. In this review, we discuss epidemiologic aspects of the association between migraine and ischemic stroke, the clinical presentation of ischemic strokes in patients with migraine, and the differentiation between migrainous and nonmigrainous infarctions. After that, we review migraine-specific and non-migraine-specific stroke mechanisms. We then review updated preclinical and clinical data on microembolism as a cause of migraine aura. In the last section, we summarize knowledge gaps and important areas to explore in future research. The review includes a clinical vignette with a discussion of the most relevant topics addressed.

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Conflict of interest statement

S. Sacco reports personal fees as speaker or advisor from Abbott, Allergan-AbbVie, AstraZeneca, Eli Lilly, Lundbeck, Novartis, NovoNordisk, Pfizer, and Teva; research grants from Allergan, Novartis, and Uriach; nonfinancial support from Abbott, Allergan, Bayer, Bristol-Myers Squibb, Daiichi Sankyo, Eli Lilly, Lundbeck, Medtronic, Novartis, Pfizer, Starmed, and Teva; and fees for CME/education from Medscape and Neurodiem Ology Medical Education; she is a member of the editorial boards of Neurology®, Stroke, European Stroke Journal, International Journal of Stroke, and the Journal of Headache and Pain; she is chief section editor for the section Headache and Neurogenic Pain in Frontiers of Neurology. A.M. Harriott and C. Ayata report no disclosures relevant to the manuscript. R. Ornello reports personal fees from Novartis, Teva, and Eli Lilly and nonfinancial support from Novartis, Teva, and Allergan-AbbVie; he is a member of the junior editorial board of the Journal of Headache and Pain and is associate editor for the Headache and Neurogenic Pain section of Frontiers in Neurology. R. Bagur and A. Jimenez-Ruiz report no disclosures relevant to the manuscript. L.A. Sposato reports speaker and consulting honoraria (Boehringer Ingelheim, Pfizer, Bayer, and Gore); consulting honoraria (Daiichi Sankyo); editorial board member (Neurology, Stroke, and JAHA); coeditor, Neurocardiology Section of Stroke; and associate editor, JAHA. Go to Neurology.org/N for full disclosures.

Figures

Figure 1
Figure 1. MRI (Clinical Vignette)
(A) Diffusion-weighted imaging sequence showing restricted diffusion in the right subcortical frontal lobe. (B) Corresponding hyperintense lesion on fluid-attenuated inversion recovery sequence.
Figure 2
Figure 2. Potential Mechanisms of Migrainous and Nonmigrainous Infarctions in Patients With Migraine
MA = migraine with aura.
Figure 3
Figure 3. Interplay Between Susceptibility to Cortical Spreading Depolarization and the Effect of Microembolization
Neuronal excitability, possibly led by genetic factors, together with the size of microemboli and duration of cardioembolism, may lead to different consequences of spreading depolarization–related spreading depression of neuronal activity. Those consequences span from migraine auras, in which altered neuronal activity and hypoperfusion are not linked to cell death, to ischemic infarction in which cell death occurs. Created with BioRender.com.
See this image and copyright information in PMC

Comment in

References

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