Drug-induced changes in cerebral glucose consumption in bifrontal epilepsy

Purpose: Positron emission tomography (PET) using F-18-radiolabeled deoxygl ucose (F-18-FDG) is a sensitive procedure for detection of epileptogenic fo ci. Although alterations in glucose consumption are not restricted to the a rea of seizure generation itself, the magnitude and extent of cerebral meta bolic disturbances induced by epileptic discharges can be detected. Despite two decades of epilepsy research using F-18- FDG-PET, little is known abou t the metabolic changes during therapy of focal epilepsy. We report on a ch ild with frontal epilepsy with severe glucose hypometabolism that was nearl y completely normalized during drug therapy. Methods: Interictal F-18-FDG-PET was performed at the onset of epilepsy and after optimized drug therapy in a 5-year-old boy with behavioral abnormali ties and repetitive seizures of frontal origin with bifrontal interictal EE G slowing for 8 weeks. Both scans were anatomically matched; initial and in tratherapeutic glucose metabolism were compared. Results: In accordance with the epileptogenic focus as identified by EEG an d ictal/interictal perfusion single-photon emission tomography (SPECT), bif rontal hypometabolism was depicted by F-18-FDG-PET. Magnetic resonance imag ing (MRI) was unremarkable. After dual-drug therapy (valproate, carbamazepi ne), the boy became seizure free, and his initial behavioral deficits disap peared. A control PET study after 3 months of therapy showed restored gluco se consumption; the frontal EEG slowing was normalized. Conclusions: This case demonstrates that reduction of glucose metabolism in epileptogenic foci may be a result of reversible neuronal dysfunction that correlates with the electroclinical follow-up.