Relations of genetic and environmental factors in the etiology of epilepsy

Authors

  • Dr Ruth Ottman,

    Corresponding author
    1. G. H. Sergievsky Center and Epidemiology Division, School of Public Health, Columbia University, New York Stare Psychiatric Institute, New York, NY
    2. Epidemiology of Brain Disorders Research Department, New York Stare Psychiatric Institute, New York, NY
    • G. H. Sergievsky center, Columbia University, 630 W. 168th Street, New York, NY 10032
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  • John F. Annegers,

    1. School of Public Health, University of Texas Health Sciences Center at Houston, Houston, TX
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  • Neil Risch,

    1. Department of Genetics, Stanford University School of Medicine, Stanford, CA
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  • W. Allen Hauser,

    1. G. H. Sergievsky Center and Epidemiology Division, School of Public Health, Columbia University, New York Stare Psychiatric Institute, New York, NY
    2. Department of Neurology, Columbia University, New York Stare Psychiatric Institute, New York, NY
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  • Mervyn Susser

    1. G. H. Sergievsky Center and Epidemiology Division, School of Public Health, Columbia University, New York Stare Psychiatric Institute, New York, NY
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Abstract

We assessed the relations of genetic and environmental factors in the etiology of epilepsy. The study population comprised 9,705 first-degree relatives of 1,951 adults with epilepsy ascertained from voluntary organizations. We calculated standardized morbidity ratios for specific etiologies of epilepsy in the relatives of probands with the same etiologies, using population incidence rates from Rochester, MN, as the reference. Relatives of probands with idiopathic/cryptogenic epilepsy had increased risk for idiopathic/cryptogenic epilepsy and for epilepsy associated with neurological deficit presumed present at birth (cerebral palsy or mental retardation) but not for symptomatic epilepsy associated with postnatal central nervous system insults. Relatives of probands with neurodeficits had increased risks for idiopathic/ cryptogenic epilepsy. Risk for epilepsy was not increased among relatives of probands with postnatal symptomatic epilepsy. The degree of increased risk of idiopathic/cryptogenic epilepsy in relatives of probands with idiopathiclcryptogenic epilepsy diminished with increasing age of the relatives; risk was not increased at age 35 or older. These findings support the possibility of a shared genetic susceptibility to epilepsy and cerebral palsy, and suggest that the genetic contributions to postnatal symptomatic epilepsy are minimal.

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