Summary
Abstract Background: Following surgical resection for intractable epilepsy caused by malformations of cortical development (MCDs), over 30% of children continue to have life-changing seizures. Mutations in genes of the mechanistic target of rapamycin (mTOR) pathway lead to these disorders that include focal cortical dysplasia (FCD), tuberous sclerosis complex and hemimegalencephaly. Therefore, there is a critical need to discover the specific mechanisms by which increased mTOR signaling leads to the development of epilepsy to develop specific therapies for children with MCDs. The central hypo
