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Correlation of Hippocampal Neuronal Density and FDG‐PET in Mesial Temporal Lobe Epilepsy
Author(s) -
Foldvary N.,
Lee N.,
Hanson M. W.,
Coleman R. E.,
Hulette C. M.,
Friedman A. H.,
Bej M. D.,
Radtke R. A.
Publication year - 1999
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1999.tb01984.x
Subject(s) - subiculum , hippocampal sclerosis , ictal , hippocampal formation , temporal lobe , positron emission tomography , pathology , hippocampus , epilepsy , medicine , neuroscience , psychology , dentate gyrus
Summary:Purpose: Interictal [ 18 F]fluorodeoxyglucose (FDG) positron emission tomography (PET) reveals regional hypometabolism in 60–80% of patients with mesial temporal lobe epilepsy (MTLE). The extent of hypometabolism generally extends beyond the epileptogenic zone. The pathophysiology underlying this widespread change is unknown. This study evaluated the relation between hippocampal neuronal loss and hypometabolism in patients with MTLE. Methods: Forty‐three patients with MTLE after anterior temporal lobectomy were included. Pathology demonstrated mesial temporal sclerosis (n = 41) or endfolium sclerosis (n = 2). Interictal FDG‐PET scans were graded by visual analysis on a scale ranging from normal (grade 1) to severe (grade 5) hypometabolism. Neuronal counting was performed in the subiculum, hippocampal subfields, and dentate granular cell layer (DG). Neuronal density of patients was compared with that of seven autopsy controls. Data were compared by using Student's t tests and Kruskal‐Wallis one‐way analysis of variance (ANOVA). Results: Significant neuronal loss in CA1 through CA4 and DG was found in patients compared with controls. Neuronal density in the subiculum, CA1, CA4, and DG did not correlate with severity of hypometabolism. However, patients with abnormal FDG‐PET had higher neuronal density in CA2 and CA3 versus patients with normal studies. Conclusions: This study supports a previous observation that degree of FDG‐PET hypometabolism does not parallel severity of hippocampal neuronal loss in MTLE.