ObjectiveTo identify the association between brain vascular changes and cortical volumes on MRI and late-onset epilepsy.MethodsIn 1993-1995, 1,920 participants (median age 62.7, 59.9% female) in the community-based Atherosclerosis Risk in Communities (ARIC) Study underwent MRI, and white matter hyperintensities were measured. In addition, in 2011-2013, 1,964 ARIC participants (median age 72.4, 61.1% female) underwent MRI, and cortical volumes and white matter hyperintensities were measured. We identified cases of late-onset epilepsy (starting at age 60 or later) from ARIC hospitalization records and Medicare claims data. Using the 1993-1995 MRI, we evaluated the association between white matter hyperintensities and subsequent epilepsy using survival analysis. We used the 2011-2013 MRI to conduct cross-sectional logistic regression to examine the association of cortical volumes and white matter hyperintensities with late-onset epilepsy. All models were adjusted for demographics, hypertension, diabetes, smoking, and APOE ϵ4 allele status.ResultsNinety-seven ARIC participants developed epilepsy after having an MRI in 1993-1995 (incidence 3.34 per 1,000 person-years). The degree of white matter hyperintensities measured at ages 49-72 years was associated with the risk of late-onset epilepsy (hazard ratio 1.27 per age-adjusted SD, 95% confidence interval [CI] 1.06-1.54). Lower cortical volume scores were associated cross-sectionally with higher odds of late-onset epilepsy (odds ratio 1.87, 95% CI 1.16-3.02) per age-adjusted SD.ConclusionsThis study demonstrates associations between earlier-life white matter hyperintensities on MRI and later-life incident epilepsy, and between cortical volumes measured later in life and late-onset epilepsy. These findings may help illuminate the causes of late-onset epilepsy.
|State||Published - Feb 26 2019|
Bibliographical noteFunding Information:
The Atherosclerosis Risk in Communities study has been funded in whole or in part by federal funds from the National Heart, Lung, and Blood Institute, NIH, Department of Health and Human Services, under contract nos. HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I, and HHSN268201700005I. Neurocognitive data are collected by U01 HL096812, HL096814, HL096899, HL096902, and HL096917, with previous brain MRI examinations funded by R01-HL70825.
E. Johnson reports no disclosures. G. Krauss is a consultant and investigator for Eisai Laboratory and SK Bios and an investigator for UCB Pharma. A. Lee reports no disclosures. A. Schneider is supported by the NIH/NINDS via an administrative supplement to award R25NS065729. A. Kucharska-Newton and J. Huang report no disclosures. C. Jack receives research funding from the NIH and the Alexander Family Alzheimer Disease Research Professorship of the Mayo Foundation Family. R. Gottesman serves as Asso-ciateEditorforNeurology®and receives research support from the NIH. Go to Neurology.org/N for full disclosures.
© 2019 American Academy of Neurology.
ASJC Scopus subject areas
- Clinical Neurology