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Animal models have been used to investigate the cause\u2013effect relationships between aberrant cortical structure and epilepsy. In this article, we discuss three such models: (1) the Eker rat model of tuberous sclerosis, in which a gene mutation gives rise to cortical disorganization and cytologically abnormal cellular elements; (2) the p35 knockout mouse, in which the genetic dysfunction gives rise to compromised cortical organization and lamination, but in which the cellular elements appear normal; and (3) the methylazoxymethanol\u2010exposed rat, in which time\u2010specific chemical DNA disruption leads to abnormal patterns of cell formation and migration, resulting in heterotopic neuronal clusters. Integrating data from studies of these animal models with related clinical observations, we propose that the neuropathologic features of these cortical dysplastic lesions are insufficient to determine the seizure\u2010initiating process. Rather, it is their interaction with a more subtly disrupted cortical \u201csurround\u201d that constitutes the circuitry underlying epileptiform activities as well as seizure propensity and ictogenesis.<\/jats:p>","DOI":"10.1111\/j.1528-1167.2012.03473.x","type":"journal-article","created":{"date-parts":[[2012,5,21]],"date-time":"2012-05-21T20:20:45Z","timestamp":1337631645000},"page":"35-44","source":"Crossref","is-referenced-by-count":28,"title":["Are developmental dysplastic lesions epileptogenic?"],"prefix":"10.1111","volume":"53","author":[{"given":"Philip A.","family":"Schwartzkroin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. 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