title: Correlation of hippocampal glucose oxidation capacity and interictal FDG-PET in temporal lobe epilepsy.
abstract: OBJECTIVE
  Interictal [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) demonstrates temporal hypometabolism in the epileptogenic zone of 60-90% of patients with temporal lobe epilepsy. The pathophysiology of this finding is still unknown. Several studies failed to show a correlation between hippocampal FDG-PET hypometabolism and neuronal cell loss. Because FDG is metabolized by hexokinase bound to the outer mitochondrial membrane, we correlated the glucose-oxidation capacity of hippocampal subfields obtained after surgical resection with the corresponding hippocampal presurgical FDG-PET activity.
  
  
  METHODS
  In 16 patients with electrophysiologically confirmed temporal lobe epilepsy, we used high-resolution respirometry to determine the basal and maximal glucose-oxidation rates in 400-microm-thick hippocampal subfields obtained after dissection of human hippocampal slices into the CA1 and CA3 pyramidal subfields and the dentate gyrus.
  
  
  RESULTS
  We observed a correlation of the FDG-PET activity with the maximal glucose-oxidation rate of the CA3 pyramidal subfields (rp = 0.7, p = 0.003) but not for the regions CA1 and dentate gyrus. In accordance with previous studies, no correlation of the FDG-PET to the neuronal cell density of CA1, CA3, and dentate gyrus was found.
  
  
  CONCLUSIONS
  The interictal hippocampal FDG-PET hypometabolism in patients with temporal lobe epilepsy is correlated to the glucose-oxidation capacity of the CA3 hippocampal subfield as result of impaired oxidative metabolism.
authors.affiliation: Department of Neurology II, University of Magdeburg Medical Center, Magdeburg, Germany. vielhaber@medizin.uni-magdeburg.de
authors.forename: Stefan
authors.initials: S
authors.lastname: Vielhaber
authors.forename: Joachim H
authors.initials: JH
authors.lastname: Von Oertzen
authors.forename: Alexei F
authors.initials: AF
authors.lastname: Kudin
authors.forename: Ariel
authors.initials: A
authors.lastname: Schoenfeld
authors.forename: Christian
authors.initials: C
authors.lastname: Menzel
authors.forename: Hans-Juergen
authors.initials: HJ
authors.lastname: Biersack
authors.forename: Thomas
authors.initials: T
authors.lastname: Kral
authors.forename: Christian E
authors.initials: CE
authors.lastname: Elger
authors.forename: Wolfram S
authors.initials: WS
authors.lastname: Kunz
mesh_terms: D000293:Adolescent; D000328:Adult; D017209:Apoptosis / Q000502:physiology; D001786:Blood Glucose / Q000378:metabolism*; D004734:Energy Metabolism / Q000502:physiology*; D004833:Epilepsy, Temporal Lobe / Q000000981:diagnostic imaging* / Q000473:pathology / Q000601:surgery; D005260:Female; D019788:Fluorodeoxyglucose F18; D006593:Hexokinase / Q000502:physiology; D006624:Hippocampus / Q000000981:diagnostic imaging / Q000473:pathology / Q000601:surgery; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D012598:Sclerosis / Q000000981:diagnostic imaging / Q000473:pathology / Q000601:surgery; D014055:Tomography, Emission-Computed
chemical_list: D001786:Blood Glucose; D019788:Fluorodeoxyglucose F18; D006593:Hexokinase