Metabolic and electrophysiological alterations in subtypes of temporal lobe epilepsy: a combined proton magnetic resonance spectroscopic imaging and depth electrodes study.

Maxime Guye, Yann Le Fur, Sylviane Confort-Gouny, Jean-Philippe Ranjeva, Fabrice Bartolomei, Jean Régis, Charles A Raybaud, Patrick Chauvel, Patrick J Cozzone
Author Information
  1. Maxime Guye: Service de Neurophysiologie Clinique and Laboratoire de Neurophysiologie et Neuropsychologie, EMI-U INSERM 9926, Marseille, France. mguye@ion.ucl.ac.uk

Abstract

PURPOSE: This study compared the metabolic regional alterations, characterized by proton magnetic spectroscopic imaging ((1)H-MRSI), with electrophysiological abnormalities recorded by using depth electrodes and with structural lesions, in patients with several subtypes of temporal lobe epilepsy (TLE).
METHODS: Twenty-five subjects were investigated, including 15 controls and 10 patients with drug-resistant unilateral TLE, nine of whom had structural abnormalities identified by MRI. All patients underwent noninvasive presurgical evaluation and then stereoelectroencephalography (SEEG). We performed an original metabolic exploration combining two (1)H-MRS imaging acquisitions associated with two single-voxel acquisitions (temporal poles) to map the most informative regions of interest (ROIs) including mesial and neocortical localizations. The N-acetyl aspartate/(choline+creatine) ratio was chosen as a metabolic index. SEEG analysis allowed the classification of each ROI as electrically normal or abnormal (i.e., involved in ictal and/or interictal discharges). Groups were compared by using a nonparametric Mann-Whitney U test.
RESULTS: N-Acetyl aspartate/(choline+creatine) was significantly lower in all regions involved in SEEG electrophysiological epileptic abnormalities than in controls (p < 0.05). In contrast, the regions without any electrophysiological abnormalities were not metabolically different from those in controls (p > 0.05) except in one ROI. No differences between the metabolic profiles of epileptogenic and irritative zones were found. The metabolic alterations included, but also extended beyond, the lesions. The presence of metabolic abnormalities in mesial structures was not specific for the mesial subtype and generally extended outside the mesial structures.
CONCLUSIONS: These results indicate that metabolic abnormalities are linked to ictal and interictal epileptiform activities rather than to structural alterations in TLE.

MeSH Term

Adolescent
Adult
Amygdala
Aspartic Acid
Choline
Electrodes, Implanted
Electroencephalography
Epilepsy, Temporal Lobe
Female
Hippocampus
Humans
Limbic System
Magnetic Resonance Imaging
Magnetic Resonance Spectroscopy
Male
Middle Aged
Neocortex
Phosphocreatine
Temporal Lobe
Ureohydrolases
Videotape Recording

Chemicals

Phosphocreatine
Aspartic Acid
N-acetylaspartate
Ureohydrolases
creatinase
Choline