title: Is epileptogenic cortex truly hypometabolic on interictal positron emission tomography?
abstract: Positron emission tomography (PET) of glucose metabolism is often applied for the localization of epileptogenic brain regions, but hypometabolic areas are often larger than or can miss epileptogenic cortex in nonlesional neocortical epilepsy. The present study is a three-dimensional brain surface analysis designed to demonstrate the functional relation between glucose PET abnormalities and epileptogenic cortical regions. Twelve young patients (mean age, 10.8 years) with intractable epilepsy of neocortical origin underwent chronic intracranial electroencephalographic monitoring. The exact location of the subdural electrodes was determined on high-resolution three-dimensional reconstructed magnetic resonance imaging scan volumes. The electrodes were classified according to their locations over cortical areas, which were defined as hypometabolic, normometabolic, or at the border between hypometabolic and normal cortex (metabolic "border zones") based on interictal glucose PET. Electrodes with seizure onset were located over metabolic border zones significantly more frequently than over hypometabolic or normometabolic regions. Seizure spread electrodes also more frequently overlay metabolic border zones than hypometabolic regions. These findings suggest that cortical areas with hypometabolism should be interpreted as regions mostly not involved in seizure activity, although epileptic activity commonly occurs in the surrounding cortex. This feature of hypometabolic cortex is remarkably similar to that of structural brain lesions surrounded by epileptogenic cortex. Cortical areas bordering hypometabolic regions can be highly epileptogenic and should be carefully assessed in presurgical evaluations.
authors.affiliation: Department of Pediatrics, Children's Hospital of Michigan, Detroit Medical Center, Wayne State University School of Medicine, USA.
authors.forename: C
authors.initials: C
authors.lastname: Juhász
authors.forename: D C
authors.initials: DC
authors.lastname: Chugani
authors.forename: O
authors.initials: O
authors.lastname: Muzik
authors.forename: C
authors.initials: C
authors.lastname: Watson
authors.forename: J
authors.initials: J
authors.lastname: Shah
authors.forename: A
authors.initials: A
authors.lastname: Shah
authors.forename: H T
authors.initials: HT
authors.lastname: Chugani
mesh_terms: D001928:Brain Diseases, Metabolic / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology*; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology*; D002648:Child; D004569:Electroencephalography; D004734:Energy Metabolism / Q000502:physiology; D004827:Epilepsy / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D014055:Tomography, Emission-Computed
chemical_list: D005947:Glucose