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In vivo hippocampal metabolic dysfunction in human temporal lobe epilepsy
Robert C Knowlton1, Bassel Abou-Khalil, Stephen M Sawrie
1UAB Epilepsy Center, Department of Neurology, University of Alabama at Birmingham School of Medicine, 35294-0021, USA. knowlton@uab.edu
Archives of Neurology
|December 10, 2002
Summary
Mesial temporal lobe epilepsy shows distinct hippocampal metabolic disturbances. Fludeoxyguclose F 18 PET and proton MRI reveal different biochemical dysfunctions, not correlating with each other.
Area of Science:
- Neuroscience
- Medical Imaging
- Epilepsy Research
Background:
- The precise nature of functional metabolic abnormalities in mesial temporal lobe epilepsy (MTLE) is not fully understood.
- Investigating these disturbances is crucial for understanding epilepsy pathophysiology.
Purpose of the Study:
- To compare in vivo hippocampal metabolic measures in MTLE using fludeoxyglucose F 18 positron emission tomography (PET) and proton magnetic resonance spectroscopic imaging (MRSI).
- To explore the relationship between N-acetylaspartate (NAA) levels and glucose metabolism derangements in MTLE.
Main Methods:
- Utilized fludeoxyglucose F 18 PET to obtain a glucose uptake metabolic index by normalizing hippocampal glucose metabolism to whole brain counts.
- Employed high-field (4.1 T) proton MRSI to measure the creatinine/NAA ratio in predominantly hippocampal voxels.
- Performed direct comparisons and correlation analyses between PET and MRSI measures.
Main Results:
- The ipsilateral hippocampal glucose metabolic index was normal, while the contralateral index was borderline elevated.
- The ipsilateral hippocampal creatinine/NAA ratio was significantly elevated, indicating reduced NAA, while the contralateral ratio was normal.
- No significant correlation was found between hippocampal glucose metabolism and creatinine/NAA measures, nor between asymmetry measures.
Conclusions:
- Hippocampal metabolic disturbances in MTLE, as assessed by fludeoxyglucose F 18 PET and proton MRSI, indicate different underlying biochemical dysfunction mechanisms.
- The lack of correlation suggests that varying degrees of cellular energy metabolism impairment differentially affect glucose utilization and NAA biosynthesis.