Alessandro Pezzini1, Giorgio Busto2, Marialuisa Zedde2, Massimo Gamba2, Andrea Zini2, Loris Poli2, Filomena Caria2, Valeria De Giuli2, Anna Maria Simone2, Rosario Pascarella2, Alessandro Padovani2, Marina Padroni2, Roberto Gasparotti2, Stefano Colagrande2, Enrico Fainardi2. 1. From the Dipartimento di Scienze Cliniche e Sperimentali, Clinica Neurologica (A.P., L.P., F.C., V.D.G., A.P.) and Sezione di Neuroradiologia, Dipartimento di Specialità Medico-Chirurgiche, Scienze Radiologiche e Sanità Pubblica (R.G.), Università degli Studi di Brescia, Italia; Dipartimento di Scienze Biomediche, Sperimentali e Cliniche, Struttura Operativa Dipartimentale di Radiodiagnostica 2 (G.B., S.C.) and Dipartimento di Scienze Biomediche, Sperimentali e Cliniche, Struttura Operativa Dipartimentale di Neuroradiologia (E.F.), Università degli Studi di Firenze, Azienda Ospedaliero-Universitaria Careggi, Italia; Unità di Neurologia, Stroke Unit (M.Z.) and Unità di Neuroradiologia (R.P.), Arcispedale Santa Maria Nuova - IRCCS, Reggio Emilia, Italia; Stroke Unit, Neurologia Vascolare, Spedali Civili di Brescia, Italia (M.G.); Stroke Unit, Clinica Neurologica, Nuovo Ospedale Civile S. Agostino Estense, AUSL Modena, Italia (A.Z., A.M.S.); and Unità di Neurologia, Dipartimento di Scienze Biologiche, Psichiatriche e Psicologiche, Università di Ferrara, Italia (M.P.). alessandro.pezzini@unibs.it. 2. From the Dipartimento di Scienze Cliniche e Sperimentali, Clinica Neurologica (A.P., L.P., F.C., V.D.G., A.P.) and Sezione di Neuroradiologia, Dipartimento di Specialità Medico-Chirurgiche, Scienze Radiologiche e Sanità Pubblica (R.G.), Università degli Studi di Brescia, Italia; Dipartimento di Scienze Biomediche, Sperimentali e Cliniche, Struttura Operativa Dipartimentale di Radiodiagnostica 2 (G.B., S.C.) and Dipartimento di Scienze Biomediche, Sperimentali e Cliniche, Struttura Operativa Dipartimentale di Neuroradiologia (E.F.), Università degli Studi di Firenze, Azienda Ospedaliero-Universitaria Careggi, Italia; Unità di Neurologia, Stroke Unit (M.Z.) and Unità di Neuroradiologia (R.P.), Arcispedale Santa Maria Nuova - IRCCS, Reggio Emilia, Italia; Stroke Unit, Neurologia Vascolare, Spedali Civili di Brescia, Italia (M.G.); Stroke Unit, Clinica Neurologica, Nuovo Ospedale Civile S. Agostino Estense, AUSL Modena, Italia (A.Z., A.M.S.); and Unità di Neurologia, Dipartimento di Scienze Biologiche, Psichiatriche e Psicologiche, Università di Ferrara, Italia (M.P.).
Abstract
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.
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.
Authors: Nicoletta Brunelli; Claudia Altamura; Carlo A Mallio; Gianguido Lo Vullo; Marilena Marcosano; Marcel Bach-Pages; Bruno Beomonte Zobel; Carlo Cosimo Quattrocchi; Fabrizio Vernieri Journal: Int J Environ Res Public Health Date: 2022-07-14 Impact factor: 4.614