Abstracts

Measurement of tissue glutamate using 1H spectroscopic imaging has the potential to identify abnormalities in epilepsy. As glutamate functions both as the major excitatory neurotransmitter and a critical metabolite for energy generation, determining the concentration of glutamate in epilepsy is of interest for both lateralization and pathophysiology. We have performed glutamate spectroscopic imaging in the human hippocampus, comparing n=12 controls with n=9 patients with unilateral temporal lobe epilepsy. Glutamate spectroscopic imaging was performed on a whole body 4T (Varian Inova) MR system using a J-suppressed adiabatic refocusing sequence. An inversion recovery was used to minimize contributions from macromolecules. The plane of study was angulated along the planum temporale, TR/TE 2000/37, voxel 1.44cc, acquisition time 34min. Quantitative T1 based tissue segmentation was performed to correct for CSF contamination of spectral voxels. Analysis was performed using a linear components model, fitting NAA, creatine (Cr), choline, glutamate (Glu), aspartate and glutamine. Quantification was performed in reference to CSF measured in the ambient cistern. N=12 controls and n=9 unilateral hippocampal epilepsy patients were studied. In voxels located within the body of the hippocampus, NAA was significantly different between patients and controls. As expected, Cr/NAA is significantly increased in both the ipsilateral and contralateral hippocampus compared to control. Glutamate was reduced in the ipsilateral hippocampus, but was not significantly different from control in the contralateral hippocampus. Creatine concentrations and the Glu/NAA ratio was not significantly different in patients relative to controls. We have used a J-suppressed adiabatic sequence to perform glutamate spectroscopic imaging in patients with hippocampal epilepsy. In this group of patients, the ipsilateral hippocampal tissue glutamate is lower than that seen in control. The Glu/NAA ratio was not significantly different between control and epilepsy patients, ipsi- or contralateral. Thus as both NAA and glutamate are low in patients, this may reflect metabolic injury in the seizure focus.[table1] (Supported by NIH RO1-NS40550 and PO1 NS39092.)