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Robert C. Knowlton, MD; Bassel Abou-Khalil, MD; Stephen M. Sawrie, PhD; Roy C. Martin, PhD; R. Edward Faught, MD; Ruben I. Kuzniecky, MD

Arch Neurol. 2002;59:1882-1886.

Background  The nature of functional metabolic disturbances in mesial temporal lobe epilepsy remains unclear.

Objectives  To compare in vivo measures of hippocampal metabolic abnormalities in mesial temporal lobe epilepsy, as acquired with fludeoxyglucose F 18 positron emission tomography and proton magnetic resonance spectroscopic imaging, and to determine the relationship between N-acetylaspartate (NAA) disturbances and well-established derangements of glucose metabolism.

Design  Measures of hippocampal glucose metabolism from fludeoxyglucose F 18 positron emission tomography were normalized to whole brain counts to provide a glucose uptake metabolic index. Proton magnetic resonance spectroscopic imaging was performed at 4.1 T, and measures of creatinine/NAA ratio were made from mostly hippocampal-only voxels. Direct comparisons and correlation analysis of measures were performed.

Setting  Presurgical evaluations for treatment of intractable epilepsy.

Patients  Twenty-nine patients between July 1994 and June 1996 who were candidates for anterior-medial temporal lobectomy at the epilepsy centers of the University of Alabama at Birmingham and Vanderbilt University schools of medicine were studied.

Results  The mean ipsilateral hippocampal glucose metabolic index (0.85) was normal, while the contralateral metabolic index (0.95) was nearly significant for an abnormally elevated measure. The mean ipsilateral hippocampal creatinine/NAA (1.26) was abnormally elevated; the mean contralateral creatinine/NAA (0.88) was normal. Hippocampal glucose and creatinine/NAA measures did not correlate; asymmetry measures also did not correlate.

Conclusions  Hippocampal metabolic disturbances in mesial temporal lobe epilepsy as measured by fludeoxyglucose F 18 positron emission tomography vs proton magnetic resonance spectroscopic imaging reflect different mechanisms of biochemical dysfunction. This lack of correlation is hypothesized to reflect a differential effect of varying degrees of disturbed cellular energy metabolism on mechanisms of glucose use and biosynthesis of NAA.

From the UAB Epilepsy Center, Department of Neurology, University of Alabama at Birmingham School of Medicine (Drs Knowlton, Sawrie, Martin, Faught, and Kuzniecky); and Department of Neurology, Vanderbilt University School of Medicine, Nashville, Tenn (Dr Abou-Khalil).

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