title: Interaction between akt1-positive neurons and age at surgery is associated with surgical outcome in children with isolated focal cortical dysplasia.
abstract: To identify pathologic characteristics that are associated with outcome, we performed a retrospective analysis of the clinical, radiologic, and pathologic features of 44 children with isolated focal cortical dysplasia (FCD) after epilepsy surgery. Based on the International League Against Epilepsy Classification, 16 patients had FCD Type I and 28 subjects had FCD Type II. A significantly higher percentage of subjects with FCD Type IIb versus Types I and IIa were seizure-free after surgery. Akt (also known as protein kinase B) is the main downstream target of phosphatidylinositol 3'-kinase and has been implicated in epilepsy pathogenesis. Semiquantitative analysis of cortical gliosis and quantitation of Akt1-immunoreactive neurons indicated that individuals with FCD Type II were more likely to have diffuse astrogliosis and higher counts of Akt1-positive neurons versus those with FCD Type I. A logistic regression model, including Akt1-positive neurons, age at surgery, and the interaction of these factors, was significantly associated with seizure-free outcome. This study provides evidence that astrogliosis and overexpression of neuronal Akt1 protein may be important factors in the pathogenesis of FCD and suggests that the pathogenesis of FCD Type I may differ from that of FCD Type II in children.
authors: Divisions of Pathology and Laboratory Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. lili.miles@cchmc.org
authors: Lili
authors: L
authors: Miles
authors: Hansel M
authors: HM
authors: Greiner
authors: Michael V
authors: MV
authors: Miles
authors: Francesco T
authors: FT
authors: Mangano
authors: Paul S
authors: PS
authors: Horn
authors: James L
authors: JL
authors: Leach
authors: Joo H
authors: JH
authors: Seo
authors: Ki H
authors: KH
authors: Lee
mesh_terms: D000293:Adolescent; D000375:Aging; D001927:Brain Diseases / Q000145:classification / Q000000981:diagnostic imaging / Q000209:etiology / Q000473:pathology*; D002452:Cell Count; D002540:Cerebral Cortex / Q000000981:diagnostic imaging / Q000473:pathology*; D002648:Child; D002675:Child, Preschool; D004827:Epilepsy / Q000601:surgery; D005260:Female; D019788:Fluorodeoxyglucose F18; D005500:Follow-Up Studies; D005904:Glial Fibrillary Acidic Protein; D006801:Humans; D007223:Infant; D008279:Magnetic Resonance Imaging; D008297:Male; D054220:Malformations of Cortical Development / Q000145:classification / Q000000981:diagnostic imaging / Q000209:etiology / Q000473:pathology*; D065703:Malformations of Cortical Development, Group I; D009474:Neurons / Q000378:metabolism*; D049268:Positron-Emission Tomography; D011183:Postoperative Complications / Q000209:etiology / Q000473:pathology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D012189:Retrospective Studies; D018709:Statistics, Nonparametric
chemical_list: D005904:Glial Fibrillary Acidic Protein; D019788:Fluorodeoxyglucose F18; C494918:AKT1 protein, human; D051057:Proto-Oncogene Proteins c-akt