Positron emission tomography (PET) of glucose metabolism is often applied f
or the localization of epileptogenic brain regions, but hypometabolic areas
are often larger than or can miss epileptogenic cortex in nonlesional neoc
ortical epilepsy. The present study is a three-dimensional brain surface an
alysis designed to demonstrate the functional relation between glucose PET
abnormalities and epileptogenic cortical regions. Twelve young patients (me
an age, 10.8 years) with intractable epilepsy of neocortical origin underwe
nt chronic intracranial electroencephalographic monitoring. The exact locat
ion of the subdural electrodes was determined on high-resolution three-dime
nsional reconstructed magnetic resonance imaging scan volumes. The electrod
es were classified according to their locations over cortical areas, which
were defined as hypometabolic, normometabolic, or at the border between hyp
ometabolic and normal cortex (metabolic "border zones") based on interictal
glucose PET. Electrodes with seizure onset were located over metabolic bor
der zones significantly more frequently than over hypometabolic or normomet
abolic regions. Seizure spread electrodes also more frequently overlay meta
bolic 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 occu
rs in the surrounding cortex. This feature of hypometabolic cortex is remar
kably similar to that of structural brain lesions surrounded by epileptogen
ic cortex. Cortical areas bordering hypometabolic regions can be highly epi
leptogenic and should be carefully assessed in presurgical evaluations.