Jerome Mawet1, Katharina Eikermann-Haerter1, Kwang-Yeol Park1, Johanna Helenius1, Ali Daneshmand1, Lea Pearlman1, Ross Avery1, Andrea Negro1, Murat Velioglu1, Ethem Murat Arsava1, Hakan Ay2, Cenk Ayata2. 1. From the Neurovascular Research Laboratory, Department of Radiology (J.M., K.E.-H., A.D., L.P., A.N., C.A.), Martinos Center for Biomedical Imaging and Stroke Service (K.-Y.P., J.H., R.A., M.V., E.M.A., H.A.), and Stroke Service and Neuroscience Intensive Care Unit, Department of Neurology (C.A.), Massachusetts General Hospital, Harvard Medical School, Charlestown; and Emergency Headache Center (J.M.), Lariboisière Hospital, APHP, DHU Neurovasc Sorbonne Paris-Cité, Paris, France. 2. From the Neurovascular Research Laboratory, Department of Radiology (J.M., K.E.-H., A.D., L.P., A.N., C.A.), Martinos Center for Biomedical Imaging and Stroke Service (K.-Y.P., J.H., R.A., M.V., E.M.A., H.A.), and Stroke Service and Neuroscience Intensive Care Unit, Department of Neurology (C.A.), Massachusetts General Hospital, Harvard Medical School, Charlestown; and Emergency Headache Center (J.M.), Lariboisière Hospital, APHP, DHU Neurovasc Sorbonne Paris-Cité, Paris, France. cayata@mgh.harvard.edu hay@mgh.harvard.edu.
Abstract
OBJECTIVE: Migraine, particularly with aura, is a risk factor for ischemic stroke. Recent data in migraine mutant mice suggest that cerebral hyperexcitability associated with migraine accelerates recruitment of ischemic penumbra into the core, resulting in faster infarct growth compared with wild type. We hypothesized that individuals with a history of migraine are more likely to exhibit increased recruitment of ischemic tissue into the infarct in acute stroke. METHODS: In this retrospective case-control study, we identified participants with reliably documented migraine history, measured lesion volumes on diffusion-weighted and perfusion-weighted MRI obtained within 72 hours of symptom onset, calculated the proportion of ischemic tissue on perfusion-weighted imaging (PWI) hyperintense on diffusion-weighted imaging (DWI), and compared the proportion of patients with no-mismatch pattern defined as DWI lesion >83% of PWI lesion. RESULTS: Migraineurs (n = 45) were younger, more often female, less likely to have vascular risk factors, and more often had cervical artery dissection, but otherwise did not differ from controls (n = 27). A significantly larger proportion of migraineurs had no-mismatch pattern, indicating that the entire perfusion defect was recruited into the infarct by the time of MRI (22% vs 4% of migraineurs and controls, respectively; p = 0.044). The difference was even more prominent in migraineurs with aura (36% vs 4%, p = 0.019). The association between migraine and no-mismatch pattern persisted after adjustment for time to MRI (p = 0.041). CONCLUSIONS: This case-control study supports the hypothesis that a history of migraine, particularly with aura, is associated with a no-mismatch pattern during acute ischemic stroke, consistent with data obtained in migraine mutant mice.
OBJECTIVE:Migraine, particularly with aura, is a risk factor for ischemic stroke. Recent data in migraine mutant mice suggest that cerebral hyperexcitability associated with migraine accelerates recruitment of ischemic penumbra into the core, resulting in faster infarct growth compared with wild type. We hypothesized that individuals with a history of migraine are more likely to exhibit increased recruitment of ischemic tissue into the infarct in acute stroke. METHODS: In this retrospective case-control study, we identified participants with reliably documented migraine history, measured lesion volumes on diffusion-weighted and perfusion-weighted MRI obtained within 72 hours of symptom onset, calculated the proportion of ischemic tissue on perfusion-weighted imaging (PWI) hyperintense on diffusion-weighted imaging (DWI), and compared the proportion of patients with no-mismatch pattern defined as DWI lesion >83% of PWI lesion. RESULTS:Migraineurs (n = 45) were younger, more often female, less likely to have vascular risk factors, and more often had cervical artery dissection, but otherwise did not differ from controls (n = 27). A significantly larger proportion of migraineurs had no-mismatch pattern, indicating that the entire perfusion defect was recruited into the infarct by the time of MRI (22% vs 4% of migraineurs and controls, respectively; p = 0.044). The difference was even more prominent in migraineurs with aura (36% vs 4%, p = 0.019). The association between migraine and no-mismatch pattern persisted after adjustment for time to MRI (p = 0.041). CONCLUSIONS: This case-control study supports the hypothesis that a history of migraine, particularly with aura, is associated with a no-mismatch pattern during acute ischemic stroke, consistent with data obtained in migraine mutant mice.
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