title: Human epilepsies: interaction of genetic and acquired factors.
abstract: Epilepsies, once regarded as due to demoniacal possession, can have both genetic and acquired causes, with interaction of these factors in many cases. To date, nearly all the genes discovered to be involved in human epilepsies encode subunits of ion channels, both voltage-gated and ligand-gated. Established acquired causes include serious brain trauma, stroke, tumours and infective lesions. Thus, in terms of exploring the neurobiology of "nature and nurture" in disease, the epilepsies are an excellent paradigm. Here, we review the evidence and discuss the possibility that ion channels are a common biological substrate for both genetic and acquired epilepsies. This review is part of the INMED/TINS special issue "Nature and nurture in brain development and neurological disorders", based on presentations at the annual INMED/TINS symposium (http://inmednet.com/).
authors.affiliation: Department of Medicine and Epilepsy Research Centre, University of Melbourne, Austin Health, Heidelberg West, VIC 3081, Australia. Electronic address: s.berkovic@unimelb.edu.au.
authors.forename: Samuel F
authors.initials: SF
authors.lastname: Berkovic
authors.affiliation: Department of Genetic Medicine, Women's and Children's Hospital and School of Molecular and Biomedical Sciences, University of Adelaide, North Adelaide, SA 5006, Australia.
authors.forename: John C
authors.initials: JC
authors.lastname: Mulley
authors.affiliation: Department of Medicine and Epilepsy Research Centre, University of Melbourne, Austin Health, Heidelberg West, VIC 3081, Australia.
authors.forename: Ingrid E
authors.initials: IE
authors.lastname: Scheffer
authors.affiliation: Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, VIC 3010, Australia.
authors.forename: Steven
authors.initials: S
authors.lastname: Petrou
mesh_terms: D001932:Brain Neoplasms / Q000150:complications / Q000235:genetics; D004777:Environment; D004827:Epilepsy / Q000209:etiology* / Q000235:genetics* / Q000503:physiopathology; D006801:Humans; D000860:Hypoxia / Q000150:complications / Q000235:genetics; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D020521:Stroke / Q000150:complications / Q000235:genetics
chemical_list: D007473:Ion Channels