title: Medial temporal lobe neuronal damage in temporal and extratemporal lesional epilepsy.
abstract: OBJECTIVE
  To assess the extent of medial temporal lobe (TL) abnormalities of the neuronal marker N-acetylaspartate (NAA) in TL and extra-TL lesional partial epilepsy, and to determine whether decreases in NAA are related to lesion location, to lesion pathology, or to the seizures themselves.
  
  
  METHODS
  The authors studied 19 patients with intractable partial epilepsy and an isolated structural cerebral lesion (10 TL, 9 extra-TL; 10 cortical dysplasia [CD], 9 non-CD lesions). Proton MRS imaging was used to determine the average relative resonance intensity of NAA for the TL regions of the left and right hemispheres. Values less than two SDs below the mean of normal control subjects were considered abnormal.
  
  
  RESULTS
  Fourteen patients (74%) had abnormally low NAA relative to creatine (NAA/Cr) in at least one TL. Three-way analysis of variance (ANOVA; lesion pathology, lesion location, side of NAA/Cr decrease) showed that ipsilateral NAA/Cr was lower than contralateral (p = 0. 04). Three-way ANOVA (lesion location, generalized tonic-clonic seizures, side of NAA/Cr decrease) showed that generalized tonic-clonic seizures were associated with lower TL NAA/Cr (p = 0. 02). Lesion location and pathology showed no main effect on the NAA-to-Cr ratio in either analysis (p > 0.05). Linear regression analyses between seizure duration and NAA/Cr decrease was not significant.
  
  
  CONCLUSIONS
  The authors demonstrated abnormally low TL NAA/Cr in the majority of patients with structural cerebral lesions. This abnormality did not differ with lesion location or pathology. They propose that the altered function of neuronal networks by an isolated structural cerebral lesion results in remote "functional dual pathology."
authors.affiliation: Department of Neurology and Neurosurgery & Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec, Canada.
authors.forename: S P
authors.initials: SP
authors.lastname: Miller
authors.forename: L M
authors.initials: LM
authors.lastname: Li
authors.forename: F
authors.initials: F
authors.lastname: Cendes
authors.forename: E
authors.initials: E
authors.lastname: Tasch
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: D000200:Action Potentials / Q000502:physiology; D000293:Adolescent; D000328:Adult; D000704:Analysis of Variance; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D001932:Brain Neoplasms / Q000473:pathology; D002648:Child; D003401:Creatine / Q000378:metabolism; D004569:Electroencephalography / Q000379:methods; D004828:Epilepsies, Partial / Q000150:complications / Q000378:metabolism* / Q000473:pathology*; D004833:Epilepsy, Temporal Lobe / Q000150:complications / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D018303:Ganglioglioma / Q000473:pathology; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D006801:Humans; D016014:Linear Models; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D009837:Oligodendroglioma / Q000473:pathology; D012640:Seizures / Q000209:etiology; D013702:Temporal Lobe / Q000378:metabolism / Q000473:pathology*
chemical_list: D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine