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Neurology 2001;57:1184-1190
© 2001 American Academy of Neurology


Articles

In vivo hippocampal glucose metabolism in mesial temporal lobe epilepsy

R. C. Knowlton, MD, K. D. Laxer, MD, G. Klein, PhD, S. Sawrie, PhD, G. Ende, PhD, R. A. Hawkins, MD PhD;, O. S. Aassar, MD, K. Soohoo, PhD, S. Wong, PhD and N. Barbaro, MD

From the Department of Neurology (Drs. Knowlton and Sawrie), University of Alabama at Birmingham; Department of Neurology (Dr. Laxer), Department of Radiology, Division of Nuclear Medicine (Drs. Hawkins and Aassar), Laboratory for Radiologic Informatics (Drs. Soohoo and Wong), Department of Neurosurgery (Dr. Barbaro), University of California, San Francisco; Lawrence Berkeley Laboratories (Dr. Klein), University of California, Berkeley; Central Institute of Mental Health (Dr. Ende), NMR Research in Psychiatry, Mannheim, Germany.

Address correspondence and reprint requests to Dr. Robert C. Knowlton, UAB Epilepsy Center, CIRC 312, 1719 6th Avenue South, Birmingham, AL 35294; e-mail: knowlton{at}uab.edu

Background: The appearance of decreased 2-[18F]fluoro-2-deoxy-D-glucose (FDG) uptake in the mesial temporal region in temporal lobe epilepsy may simply reflect loss of gray matter due to hippocampal atrophy. Increased partial volume effects due to atrophic hippocampi may further increase appearance of hypometabolism. Methods: The authors used a combination of MRI-PET coregistration, with MRI-based gray matter segmentation, and partial volume correction to improve the examination of hippocampal specific glucose uptake in FDG PET. The goal was to determine 1) if relative mesial temporal hypometabolism is an artifact of gray matter (hippocampal) atrophy, 2) whether hippocampal metabolism correlates with atrophy evaluated on MRI, and 3) if MRI-based partial volume correction influences measurement of hippocampal metabolic-volume relationships, including epilepsy lateralization. Results: Findings 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. Specifically, partial volume corrected hippocampal metabolism correlated strongly (r = 0.613, p < 0.001) with hippocampal volume. Without partial volume correction, a weaker, but still significant, correlation was present (r = 0.482, p < 0.001). Degree of asymmetry was consistently greater and provided higher sensitivity of lateralization with partial volume vs non–partial volume corrected metabolic measurements. Conclusions: Although, decreased metabolism may occur in the absence of neuronal cell loss, hippocampal atrophy and presumed degree of neuronal cell loss appears to be a primary factor involved in the cause of decreased metabolism in epileptogenic hippocampi. Partial volume correction is recommended for optimal interpretation of hippocampal structure and function relationships.




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