Abstracts

Rationale: It has been demonstrated that MRS is a useful and sensitive technique for identification of hippocampal pathology in patients with temporal lobe epilepsy, particularly when associated with structural changes such as mesial temporal sclerosis. However, its role in patients with normal structural studies is still controversial. Most studies have been retrospective and included small numbers of patients with normal 1.5 or 3 T MRI, but the utility of 1H-MRS in idiopathic localization-related temporal lobe epilepsy has not been prospectively studied with a high magnetic field (7T) MRI. The purpose of this study is to determine whether N-acetylaspartate (NAA) is decreased and glutamate (Glu) is increased on the side of seizure onset in patients with cryptogenic (normal MRI) localization-related temporal lobe epilepsy. Methods: 1H spectroscopy data were acquired on a 7.0 Tesla head only Agilent MRI using the LASER localization sequence (TE = 38 ms), from a 2.7x1.3x1.3 cm3 voxel in the left and right hippocampi of three subjects. Levels of NAA, choline (Cho), Myo-inositol (Myo), taurine (Tau), and Glu were measured using the fitMAN software (v1.7) and normalized to creatine (Cr). Lateralization of epileptogenic focus was determined by clinical assessment, interictal and ictal video-EEG recordings, and neuropsychological evaluation. PET data was included when available. Metabolite levels were compared between ipsilateral and contralateral hippocampi using a t-test. Results: Figure 1 shows all metabolite ratios in patients (ipsilateral to seizure onset hemisphere in blue, contralateral side in red). In this preliminary study, there were no significant differences in metabolite levels between the ipsilateral and contralateral side. Conclusions: The identification of metabolic abnormalities not seen with conventional/standard MRI, will allow a better surgical selection of patients with temporal lobe epilepsy. Better identification of the epileptogenic focus will improve outcomes from seizure surgery. Recruitment of additional subjects is needed to confirm these findings. Funding for this project was provided by the Ontario Brain Institute Epilepsy Discovery Project.