Abstracts

RATIONALE: Decreased [italic]N[/italic]-acetyl aspartate (NAA) measured by proton magnetic resonance spectroscopy (¹H-MRS) has been reported in epileptogenic brain regions. This finding is commonly interpreted as a sign of neuronal loss or dysfunction. In our previous study (Ann Neurol 2000;48:88-96), 2-deoxy-2-[¹⁸F]fluoro-D-glucose (FDG) positron emission tomography (PET), a technique widely used to define epileptogenic regions, showed that the cortical region [underline]bordering[/underline] hypometabolic cortex corresponded to the site of seizure onset measured by intracranial EEG, rather than cortex within the hypometabolic area. In the present study, we measured NAA concentrations within and bordering hypometabolic regions on FDG-PET by using ¹H-MRS imaging (¹H-MRSI), and compared these values to NAA concentrations measured in surrounding gray and underlying white matter.
METHODS: Multi-voxel ¹H-MRSI (chemical-shift imaging) and FDG-PET scans were performed in 6 children (4 boys and 2 girls, mean age: 6.8[plusminus]4.2 years) with medically intractable non-lesional extratemporal lobe epilepsy. The extent of glucose hypometabolism on PET was identified objectively by marking cortical regions with greater than 10% hypometabolism compared to the contralateral homologous cortex. FDG-PET images with [dsquote]marked[dsquote] hypometabolic cortex were coregistered to the MRI. After coregistration, voxels on MRSI were classified as corresponding to the hypometabolic zone, metabolic borderzone (voxels located at the border of marked hypometabolic cortex), surrounding gray matter (voxels outside the borderzone), and underlying white matter. NAA concentrations in contralateral homologous voxels were also measured to calculate an asymmetry index (AI) of NAA for each group of voxels.
RESULTS: Fifteen hypometabolic areas were detected in the 6 children. All 15 metabolic borderzone regions showed lower NAA than the homologous contralateral region (greater than 10% asymmetry). In contrast, only two hypometabolic zone regions showed decreased NAA. Four surrounding gray matter regions and one underlying white matter region also showed decreased NAA. The mean NAA concentration was significantly reduced in the metabolic borderzone (mean AI: -18.75%) as compared to the hypometabolic zone (mean AI: -5.84%), surrounding gray matter (mean AI: -6.69%) and underlying white matter (mean AI: -4.68%) (p[lt]0.0001; ANOVA). Mean NAA concentrations in the latter three regions did not differ significantly from each other.
CONCLUSIONS: In non-lesional extratemporal lobe epilepsy patients with focal FDG hypometabolism, ¹H-MRSI showed greatest reduction of NAA in voxels bordering the hypometabolic brain region. Such metabolic borderzone areas were found to be most epileptogenic in our previous studies. The results suggest that FDG-PET hypometabolism and decreased NAA reflect different physiological processes and provide complementary information regarding the extent of cortical dysfunction in neocortical epilepsy. ¹H-MRSI may assist to delineate the epileptogenic zone for successful epilepsy surgery in conjunction with other localization techniques.
[Supported by: This grant was supported in part by NIH Grant NS 34488.]