Abstracts

Rationale: Myoclonic, absence and generalized tonic-clonic are the main seizure types in idiopathic generalized epilepsy (IGE). According to the predominant seizure type, IGEs are dividided in subsyndromes. The thalamo-cortical network is involved in the mechanisms behind all IGEs subsyndromes. The objective of this investigation was to detect cortical abnormalities in patients with IGE and to determine neuroanatomical differences in the cerebral cortex among patients with juvenile myoclonic epilepsy (JME), juvenile absence epilepsy (JAE) and idiopathic generalized epilepsy with generalized tonic-clonic only (GTCS). Methods: Volumetric (3D) T1 weighted images with 1 mm isotropic voxels were acquired in a 2 Tesla scanner using a spoiled gradient echo sequence. This sequence was used for the neuroimaging analysis. Cortical reconstruction and statistical analysis was performed with the Freesurfer image analysis suite (http://surfer.nmr.mgh.harvard.edu/). For the analysis, images were previously processed including motion correction, removal of non-brain tissue, automated Talairach transformation, intensity normalization, tessellation of the gray matter white matter boundary, automated topology correction, and surface deformation. After that, data processing included surface inflation, registration to a spherical atlas which utilized individual cortical folding patterns to match cortical geometry across subjects, parcellation of the cerebral cortex into units based on gyral and sulcal structure, and creation of a variety of surface based data including maps of curvature and sulcal depth. This method uses both intensity and continuity information from the entire three dimensional MR volume in segmentation and deformation procedures to produce representations of cortical thickness, calculated as the closest distance from the gray/white boundary to the gray/CSF boundary at each vertex on the tessellated surface. Statistical analysis was conducted using general linear model comparing patients groups to 20 controls (11 women, mean age 27±6 years, range 18-40). Comparisons were performed searching for differences in cortical thickness, folding pattern and sulcal depth. Results: We investigated 13 patients with JME (8 women, mean age 26±7 years, range 17-45), 9 patients with JAE (5 women, mean age 26±7 years, range 20-43) and 9 patients with GTCS (6 women, mean age 26±6 years, range 19-38). Surface-based analysis revealed small areas of abnormalities in all three groups of patients. However, JME group had more proeminent areas of cortical abnormalities located in the superior and inferior frontal gyrus (figure). The abnormalities detected were observed in the folding pattern and sulcal depth. Conclusions: Patients with IGE have subtle abnormalities in the cerebral cortex. JME showed more prominent abnormalities located at the frontal lobes. These findings support the participation of the cortex in IGE pathogenesis. There are distinct patterns of abnormalities in the IGE subsyndromes sugesting that, althought similar in clinical semiology they are different in the underlying mechanism.