Stroke · 2018 · 33 citations · 14 references
Life SciencesNeurologyNeuroscienceCerebrovascular SurgeryClinical NeuroscienceNeurocritical CareAcute Ischemic StrokeCerebrovascular DiseaseHeadache DisordersStrokeInfarct Core MismatchInfarct Size AssessmentInfarct Size QuantificationMigraine AssociationMigraine AuraMigraine HistoryMigraine Without AuraPerfusion Computed Tomography
Background and Purpose— Cerebral hyperexcitability in migraine experiencers might sensitize brain tissue to ischemia. We investigated whether a personal history of migraine is associated with vulnerability to brain ischemia in humans. Methods— Multicenter cohort study of patients with acute ischemic stroke who underwent a brain computed tomography perfusion and were scheduled to undergo reperfusion therapy. In a case–control design, we compared the proportion of subjects with no-mismatch, the volume of penumbra salvaged, as well as the final infarct size in a group of patients with migraine and a group of patients with no history of migraine. Results— We included 61 patients with migraine (34 [55.7%] men; mean age, 52.2±15.1 years; migraine without aura/migraine with aura, 44/17) and 61 patients with no history of migraine. The proportion of no-mismatch among migraineurs was significantly higher than among nonmigraineurs (17 [27.9%] versus 7 [11.5%]; P =0.039) and was more prominent among patients with migraine with aura (6 [35.3%]; P =0.030) while it was nonsignificantly increased in patients with migraine without aura (11 [25.0%]; P =0.114). Migraine, especially migraine with aura, was independently associated with a no-mismatch pattern (odds ratio, 2.65; 95% CI, 0.95–7.41 for migraine; odds ratio, 5.54; 95% CI, 1.28–23.99 for migraine with aura), and there was a linear decrease of the proportion of patients with migraine with aura with increasing quartiles of mismatch volumes. Patients with migraine with aura had also smaller volumes of salvaged penumbra (9.8±41.2 mL) compared with patients with migraine without aura (36.4±54.1 mL) and patients with no migraine (45.1±55.0 mL; P =0.056). Conversely, there was no difference in final infarct size among the 3 migraine subgroups ( P =0.312). Conclusions— Migraine is likely to increase individual vulnerability to ischemic stroke during the process of acute brain ischemia and might represent, therefore, a potential new therapeutic target against occurrence and progression of the ischemic damage.
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