title: In vivo hippocampal metabolic dysfunction in human temporal lobe epilepsy.
abstract: BACKGROUND
  The nature of functional metabolic disturbances in mesial temporal lobe epilepsy remains unclear.
  
  
  OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  METHODS
  Presurgical evaluations for treatment of intractable epilepsy.
  
  
  METHODS
  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.
authors.affiliation: UAB Epilepsy Center, Department of Neurology, University of Alabama at Birmingham School of Medicine, 35294-0021, USA. knowlton@uab.edu
authors.forename: Robert C
authors.initials: RC
authors.lastname: Knowlton
authors.forename: Bassel
authors.initials: B
authors.lastname: Abou-Khalil
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Sawrie
authors.forename: Roy C
authors.initials: RC
authors.lastname: Martin
authors.forename: R Edward
authors.initials: RE
authors.lastname: Faught
authors.forename: Ruben I
authors.initials: RI
authors.lastname: Kuzniecky
mesh_terms: D000293:Adolescent; D000328:Adult; D004833:Epilepsy, Temporal Lobe / Q000378:metabolism* / Q000473:pathology; D005260:Female; D019788:Fluorodeoxyglucose F18; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods / Q000706:statistics & numerical data; D008297:Male; D008875:Middle Aged; D014055:Tomography, Emission-Computed / Q000379:methods / Q000706:statistics & numerical data
chemical_list: D019788:Fluorodeoxyglucose F18