Migraine with aura and risk of silent brain infarcts and white matter hyperintensities: an MRI study

Garcı́a-Dorado, David; Garde, Ellen; Blaabjerg, Morten; Nielsen, Helle Hvilsted; Krøigård, Thomas; Østergaard, Kamilla; Møller, Harald Settergren; Hjelmborg, Jacob; Madsen, Camilla Gøbel; Iversen, Pernille; Kyvik, Kirsten Ohm; Siebner, Hartwig R.; Ashina, Messoud

doi:10.1093/brain/aww099

Cited by 81 publications

(63 citation statements)

References 23 publications

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“…The studies demonstrated that topical cortical application of ET‐1 potently elicits CSD‐like changes in cortical activity. Subsequent studies showed that the cause of CSD elicitation is most likely vasoconstrictive ischemia leading to areas of micronecrosis and not a direct neuronal effect of ET‐1 . This is in line with the general observation that CSD can be induced by various forms of cortical damage, including cortical infarction .…”

Section: Discussionsupporting

confidence: 67%

“…The likely reason for this is that circulating ET‐1 would have to cross the blood‐brain barrier (BBB) to exert the effects observed in the animals, and ET‐1 passage through the BBB is very limited . In addition, spontaneous aura attacks are not induced by this mechanism since migraine attacks with aura are not generally associated with the vascular cerebral damage …”

Section: Discussionmentioning

confidence: 99%

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Intravenous Endothelin‐1 Infusion Does Not Induce Aura or Headache in Migraine Patients With Aura

et al. 2020

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Objective To investigate whether intravenously infused provokes migraine aura and migraine headache in migraine patients with aura. Background Migraine with aura has been associated with endothelial dysfunction and increased stroke risk. The initiating mechanism of migraine aura symptoms is not known. Experimental provocation of migraine headache using vasoactive peptides has provided tremendous advances in the understanding of migraine pathophysiology but substances that can induce migraine aura have not been identified. Endothelin‐1 (ET‐1), an endogenous, potent vasoconstrictor peptide released from the vascular endothelium, has been proposed to trigger migraine aura. This hypothesis is based on reports of increased plasma ET‐1 levels early during the migraine attacks and the observation that ET‐1 applied to the cortical surface potently induces the cortical spreading depolarization, the underlying electrophysiological phenomenon of migraine aura, in animals. Further, endothelial damage due to, for example, carotid puncture and vascular pathology is known to trigger aura episodes. Methods We investigated whether intravascular ET‐1 would provoke migraine aura in patients. Using a two‐way crossover, randomized, placebo‐controlled, double‐blind design, we infused high‐dose (8 ng/kg/minutes for 20 minutes) intravenous ET‐1 in patients with migraine with typical aura. The primary end‐point was the difference in incidence of migraine aura between ET‐1 and placebo. Experiments were carried out at a public tertiary headache center (Danish Headache Center, Rigshospitalet Glostrup, Denmark). Results Fourteen patients received intravenous ET‐1. No patients reported migraine aura symptoms or migraine headache during or up to 24 hours following the ET‐1 infusion. Four patients reported mild to moderate headache only on the ET‐1 day, 3 patients reported moderate headache on the placebo day, and 1 patient reported mild headache on both days. No serious adverse events occurred during or after infusion. Conclusions Provocation of migraine aura by procedures or conditions involving vascular irritation is unlikely to be mediated by ET‐1.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Intravenous Endothelin‐1 Infusion Does Not Induce Aura or Headache in Migraine Patients With Aura

et al. 2020

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“…Therefore, despite some of the limitations, our findings are more comprehensive and clinically relevant. Furthermore, our finding is in line with the recent report that MA is not associated with silent stroke on MRI (average age 48) in a well‐designed MRI image study . Additionally, risk of ischemic stroke was not higher in migraineurs (MA and MO) after adjusting for a comprehensive lists of cardiovascular risk factors in a large population‐based Swedish twin study (mean age at the time of enrollment 45.3) .…”

Section: Discussionsupporting

confidence: 90%

Migraine Age of Onset and Association With Ischemic Stroke in Late Life: 20 Years Follow‐Up in ARIC

et al. 2019

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Background and Purpose To evaluate the association between cumulative exposure to migraine and incidence of ischemic stroke in the Atherosclerosis Risk in Communities (ARIC) study. Methods In this ongoing, prospective longitudinal community‐based cohort, participants were interviewed to ascertain migraine history at the third visit (1993–1995), followed for ischemic stroke incidence over 20 years. We performed a post hoc analysis to evaluate the association between the age of migraine onset and ischemic stroke. Results We identified 447 migraineurs with aura (MA) and 1128 migraineurs without aura (MO) among 11,592 black and white participants. There was an association between the age of MA onset ≥50 years old (average duration = 4.75 years) and ischemic stroke when compared to no headache group (multivariable adjusted HR = 2.17, 95% CI [1.39–3.39], P < .001). MA onset <50 years old (average duration = 28.17 years) was not associated with stroke (multivariable adjusted HR = 1.31, 95% CI [0.86–2.02], P = .212). These results were consistent with our logistic regression model. MO was not associated with increased stroke regardless of the age of onset. The absolute risk for stroke in migraine with aura is 37/447 (8.27%) and migraine without aura is 48/1128 (4.25%). Conclusion As compared to the no headache participants, increased stroke risk in late life was observed in participants with late onset of MA. In this cohort, longer cumulative exposure to migraine with visual aura, as would be expected with early onset of migraine, was not associated with increased risk of ischemic stroke in late life. This study underscores the importance of the age of onset of MA in assessing stroke risk in older migraineurs.

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“…In contrast, researchers have argued that it is the deep white matter lesions on MRI and not SBIs that produces the dizziness and headache of non-specific cause (13,14) . Further, Gaist et al, in a recent study, have reported the lack of evidence of an association between the white matter hyperintensities, SBIs, and migraine with aura (5) .…”

Section: Discussionmentioning

confidence: 96%

“…Despite being asymptomatic, the occurrence of SBIs have been associated with the development of certain nonspecific neurological symptoms such as dizziness, forgetfulness, age, and hypertension, as reported by Hougaku et al (4) . Even though several studies have been conducted on association of migraine and SBI (5) , there is lacuna in studies exploring the association of other non-specific neurological symptoms in patients diagnosed with SBI. Therefore, this study examines the patients with non-specific neurological symptoms for the presence of SBIs and is believed to be the first Indian study to assess the role of these symptoms in diagnosing SBIs.…”

Section: Introductionmentioning

confidence: 99%

Silent Brain Infarcts in Patients with Non-Specific Neurological Symptoms: 1-Year Cross-Sectional Study

Pakalapati¹

2018

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Migraine with aura and risk of silent brain infarcts and white matter hyperintensities: an MRI study

Cited by 81 publications

References 23 publications

Intravenous Endothelin‐1 Infusion Does Not Induce Aura or Headache in Migraine Patients With Aura

Intravenous Endothelin‐1 Infusion Does Not Induce Aura or Headache in Migraine Patients With Aura

Migraine Age of Onset and Association With Ischemic Stroke in Late Life: 20 Years Follow‐Up in ARIC

Silent Brain Infarcts in Patients with Non-Specific Neurological Symptoms: 1-Year Cross-Sectional Study

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