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Long-term Risk of Epilepsy in Subarachnoid Hemorrhage Survivors With Positive Family History: A Population-Based
Juho Tapio Paavola1, Jenna Jokimäki2, Terhi Johanna Huttunen2
1From the Neurosurgery of NeuroCenter (J.T.P., T.J.H., T.K., O.-P.K., J.E.J., R.K., A.E.L., J.H.), Kuopio University Hospital; Institute of Clinical Medicine (J.T.P., J.J., T.J.H., T.K., O.-P.K., M.L., J.E.J., A.E.L., J.H.), Faculty of Health Sciences, University of Eastern Finland, Kuopio; Department of Neurosurgery (M.U.Z.F.), Oulu University Hospital; Research Unit of Clinical Medicine (M.U.Z.F.), University of Oulu; Neurointensive Care Unit (M.L.), Kuopio University Hospital; Epilepsy Center (R.K.), Neuro Center, Kuopio University Hospital, Member of the European Reference Network EpiCARE; and Department of Clinical Radiology (A.E.L.), Kuopio University Hospital, Finland. juho.paavola@pshyvinvointialue.fi.
Background And Objectives:
Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating form of stroke affecting the working-age population, where epilepsy is a common complication and major prognostic factor for increased morbidity in aSAH survivors. The objective of this analysis was to assess whether epilepsy in first-degree relatives is a risk of developing epilepsy after aSAH.
Methods:
We used a region-specific database that includes all cases of unruptured and ruptured saccular intracranial aneurysm admitted to Kuopio University Hospital from its defined Eastern Finnish catchment population. We also retrieved data from Finnish national health registries for prescription drug purchases and reimbursement, hospital discharge, and cause of death and linked them to patients with aSAH, their first-degree relatives, and population controls matched 3:1 by age, sex, and birth municipality. Cox regression modeling and Kaplan-Meier survival curves were used for analysis.
Results:
We examined data for 760 consecutive 12-month survivors of aSAH, born in 1950 or after, with a first aSAH from January 1, 1995, to December 31, 2018. Of the 760 patients (median age, 47 years; 53% female; median follow-up, 11 years), 111 (15%) developed epilepsy at a median of 7 months (interquartile range, 2-14 months) after admission for aSAH. Of the 2,240 population controls and 4,653 first-degree relatives of patients with aSAH, 23 (0.9%) and 80 (1.7%), respectively, developed epilepsy during the follow-up period. Among 79 patients with epilepsy in first-degree relatives, 22 (28%) developed epilepsy after aSAH; by contrast, among 683 patients with no epilepsy in first-degree relatives, 89 (13%) developed epilepsy after aSAH. Having at least 1 relative with epilepsy was an independent risk factor of epilepsy after aSAH (hazard ratio, 2.44; 95% CI 1.51-3.95). Cumulative 1-year rates by first-degree relationship were 40% with 1 or more children with epilepsy, 38% with 1 or more affected parents, 5% with 1 or more affected siblings, and 10% with no relatives with epilepsy.
Discussion:
Patients who developed epilepsy after aSAH were significantly more likely to have first-degree relatives with epilepsy than those who did not develop epilepsy after the aSAH.
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