title: Spatial extent of neuronal metabolic dysfunction measured by proton MR spectroscopic imaging in patients with localization-related epilepsy.
abstract: OBJECTIVE
  To assess the spatial extent of the decrease in the neuronal marker N-acetyl-aspartate (NAA) relative to creatine (Cr) in patients with localization-related epilepsy, and to assess clinical differences between patients with and without widespread NAA/Cr reduction.
  
  
  METHODS
  We studied 51 patients with localization-related epilepsy. Patients were divided into three groups according to the EEG investigation: (a) temporal lobe epilepsy (TLE, n = 21), (b) extratemporal lobe epilepsy (extra-TLE, n = 20), and (c) multilobar epilepsy (patients with a wider epileptogenic zone, n = 10). We acquired proton magnetic resonance (MR) spectrocopic imaging (1H-MRSI) of temporal and frontocentroparietal regions in separate examinations for both patients and controls. NAA/Cr values 2 standard deviations below the mean of normal controls were considered abnormal.
  
  
  RESULTS
  Twenty-three (45%) patients including 12 with TLE had normal MR imaging including volumetric studies of the hippocampus. Forty-nine (96%) patients had low NAA/Cr, indicating neuronal dysfunction in either temporal and/or extratemporal 1H-MRSIs; 38% of patients with TLE and 50% of patients with extra-TLE also had NAA/Cr reduction outside the clinical and EEG-defined primary epileptogenic area. The NAA/Cr reduction was more often widespread in the multilobar group [six (60%) of 10] than in temporal or extratemporal groups [five (31%) of 16]. Nonparametric tests of (a) seizure duration, (b) seizure frequency, and (c) lifetime estimated seizures showed no statistically significant difference (p > 0.05) for TLE and extra-TLE patients with or without NAA/Cr reduction outside the seizure focus.
  
  
  CONCLUSIONS
  Of patients with localization-related epilepsy, 40-50% have neuronal metabolic dysfunction that extends beyond the epileptogenic zone defined by clinical-EEG and/or the structural abnormality defined by MRI.
authors.affiliation: Department of Neurology and Neurosurgery & the Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec, Canada.
authors.forename: L M
authors.initials: LM
authors.lastname: Li
authors.forename: F
authors.initials: F
authors.lastname: Cendes
authors.forename: F
authors.initials: F
authors.lastname: Andermann
authors.forename: F
authors.initials: F
authors.lastname: Dubeau
authors.forename: D L
authors.initials: DL
authors.lastname: Arnold
mesh_terms: D000293:Adolescent; D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D002648:Child; D003401:Creatine / Q000378:metabolism*; D004569:Electroencephalography / Q000706:statistics & numerical data; D004828:Epilepsies, Partial / Q000175:diagnosis* / Q000378:metabolism*; D004833:Epilepsy, Temporal Lobe / Q000175:diagnosis / Q000378:metabolism; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006624:Hippocampus / Q000378:metabolism*; D006801:Humans; D009682:Magnetic Resonance Spectroscopy / Q000706:statistics & numerical data; D008875:Middle Aged; D017966:Pyramidal Cells / Q000378:metabolism
chemical_list: D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine