title: Drug-induced changes in cerebral glucose consumption in bifrontal epilepsy.
abstract: OBJECTIVE
  Positron emission tomography (PET) using 18F-radiolabeled deoxyglucose (18F-FDG) is a sensitive procedure for detection of epileptogenic foci. Although alterations in glucose consumption are not restricted to the area of seizure generation itself, the magnitude and extent of cerebral metabolic disturbances induced by epileptic discharges can be detected. Despite two decades of epilepsy research using 18F-FDG-PET, little is known about the metabolic changes during therapy of focal epilepsy. We report on a child with frontal epilepsy with severe glucose hypometabolism that was nearly completely normalized during drug therapy.
  
  
  METHODS
  Interictal 18F-FDG-PET was performed at the onset of epilepsy and after optimized drug therapy in a 5-year-old boy with behavioral abnormalities and repetitive seizures of frontal origin with bifrontal interictal EEG slowing for 8 weeks. Both scans were anatomically matched; initial and intratherapeutic glucose metabolism were compared.
  
  
  RESULTS
  In accordance with the epileptogenic focus as identified by EEG and ictal/interictal perfusion single-photon emission tomography (SPECT), bifrontal hypometabolism was depicted by 18F-FDG-PET. Magnetic resonance imaging (MRI) was unremarkable. After dual-drug therapy (valproate, carbamazepine), the boy became seizure free, and his initial behavioral deficits disappeared. A control PET study after 3 months of therapy showed restored glucose 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.
authors.affiliation: Department of Nuclear Medicine, University of Münster, Münster, Germany. matheja@uni-muenster.de
authors.forename: P
authors.initials: P
authors.lastname: Matheja
authors.forename: M
authors.initials: M
authors.lastname: Weckesser
authors.forename: O
authors.initials: O
authors.lastname: Debus
authors.forename: J
authors.initials: J
authors.lastname: Löttgen
authors.forename: G
authors.initials: G
authors.lastname: Schuierer
authors.forename: O
authors.initials: O
authors.lastname: Schober
authors.forename: G
authors.initials: G
authors.lastname: Kurlemann
mesh_terms: D000927:Anticonvulsants / Q000494:pharmacology* / Q000627:therapeutic use*; D002220:Carbamazepine / Q000494:pharmacology / Q000627:therapeutic use; D002540:Cerebral Cortex / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000378:metabolism*; D002675:Child, Preschool; D003545:Cysteine / Q000031:analogs & derivatives; D004569:Electroencephalography / Q000706:statistics & numerical data*; D004828:Epilepsies, Partial / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000378:metabolism; D017034:Epilepsy, Frontal Lobe / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000378:metabolism*; D019788:Fluorodeoxyglucose F18; D007839:Functional Laterality / Q000502:physiology; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D015609:Organotechnetium Compounds; D019275:Radiopharmaceuticals; D014055:Tomography, Emission-Computed; D015899:Tomography, Emission-Computed, Single-Photon; D014635:Valproic Acid / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000927:Anticonvulsants; D015609:Organotechnetium Compounds; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; D002220:Carbamazepine; D014635:Valproic Acid; C059659:technetium Tc 99m bicisate; D005947:Glucose; D003545:Cysteine