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Correlation of Hippocampal Glucose Oxidation Capacity and Interictal FDG‐PET in Temporal Lobe Epilepsy
Author(s) -
Vielhaber Stefan,
Von Oertzen Joachim H.,
Kudin Alexei F.,
Schoenfeld Ariel,
Menzel Christian,
Biersack HansJuergen,
Kral Thomas,
Elger Christian E.,
Kunz Wolfram S.
Publication year - 2003
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1046/j.1528-1157.2003.38102.x
Subject(s) - hippocampal formation , dentate gyrus , ictal , temporal lobe , epilepsy , hippocampus , neuroscience , positron emission tomography , chemistry , endocrinology , medicine , pathology , psychology
Summary:  Purpose: Interictal [ 18 F]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‐μm‐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 (r p = 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.

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