In vivo hippocampal glucose metabolism in mesial temporal lobe epilepsy

Citation
Rc. Knowlton et al., In vivo hippocampal glucose metabolism in mesial temporal lobe epilepsy, NEUROLOGY, 57(7), 2001, pp. 1184-1190
Citations number
35
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
57
Issue
7
Year of publication
2001
Pages
1184 - 1190
Database
ISI
SICI code
0028-3878(20011009)57:7<1184:IVHGMI>2.0.ZU;2-B
Abstract
Background: The appearance of decreased 2-[F-18]fluoro-2-deoxy-D-glucose (F DG) uptake in the mesial temporal region in temporal lobe epilepsy may simp ly reflect loss of gray matter due to hippocampal atrophy. Increased partia l volume effects due to atrophic hippocampi may further increase appearance of hypometabolism. Methods: The authors used a combination of MRI-PET core gistration, with MRI-based gray matter segmentation, and partial volume cor rection to improve the examination of hippocampal specific glucose uptake i n FDG PET. The goal was to determine 1) if relative mesial temporal hypomet abolism is an artifact of gray matter (hippocampal) atrophy, 2) whether hip pocampal metabolism correlates with atrophy evaluated on MRI, and 3) if MRI -based partial volume correction influences measurement of hippocampal meta bolic-volume relationships, including epilepsy lateralization. Results: Fin dings showed that ipsilateral hippocampi of mesial temporal lobe epilepsy ( MTLE) are relatively hypometabolic per unit of gray matter volume, and that hippocampal metabolism directly correlates with hippocampal volume. Specif ically, partial volume corrected hippocampal metabolism correlated strongly (r = 0.613, p < 0.001) with hippocampal volume. Without partial volume cor rection, a weaker, but still significant, correlation was present (r = 0.48 2, p < 0.001). Degree of asymmetry was consistently greater and provided hi gher sensitivity of lateralization with partial volume vs non-partial volum e corrected metabolic measurements. Conclusions: Although, decreased metabo lism may occur in the absence of neuronal cell loss, hippocampal atrophy an d presumed degree of neuronal cell loss appears to be a primary factor invo lved in the cause of decreased metabolism in epileptogenic hippocampi. Part ial volume correction is recommended for optimal interpretation of hippocam pal structure and function relationships.