Abstracts

Rationale: Decreased cortical thickness (CT) and increased sulcal depth (SD), proceeds in a posterior-anterior direction and then from frontal to temporal lobe[1, 2] in late childhood and adolescence. This study determined if CT and SD in focal epilepsy (FE) youth under 10.5 years (Y-FE) differed from younger healthy controls (Y-HC) in parietal and occipital regions but in frontal and temporal regions in FE patients above age 10.5 (O-FE) compared to older controls (O-HC). We determined if seizure variables, a perinatal marker (birth weight)[3, 4], and/or a clinical marker (family history of epilepsy)[5] predicted these findings. Methods: High-resolution 3D MR images were obtained on 26Y-FE, 17O-FE, 22Y-HC, and 24O-HC in a 1.5 Tesla scanner. After removal of non-brain tissue from MR images, image voxels were classified into different tissue types. Cortical surface representations at the geometric center of the 3D gray matter (GM) tissue were extracted. Cortical thickness at each point in the cortical GM mantle was defined as the sum of the distances from this point to the GM/white matter and GM/cerebrospinal-fluid tissue boundaries following a flow field, which guarantees a one-to-one, symmetric and continuous correspondence between the two tissue boundaries. A surface-based spatial normalization technique was used to match anatomically homologous cortical features across subjects before performing cross-subject comparison. Parents provided seizure variable, birth weight, and family history of epilepsy information (Table 1). General linear models were used with CT and SD as dependent variables and group (FE, HC), age group (<=10.5 years, >10.5 years), and group x age-group interaction term as independent variables. In regions with a significant interaction term, birth weight, age of seizure onset, seizure frequency, family history of seizures were added as additional predictors in the model. Results: There was a significant interaction of group x age-group in middle (F (1,85) 4.51, p<.04) and inferior occipital (F(1,83) 4.41, p<.04) regional CT and in precuneus (F(1,82) 9.47, p<.003) and middle occipital (F(1,83) 4.86, p<.04) regional SD. The O-FE group had significantly thinner middle occipital cortex (p<.05) and shallower SD (p<.03) as well as thinner inferior occipital cortex than the O-HC group (p<.02), thinner middle (p<.005) and inferior occipital cortex (p<.002) than the Y-FE group, and deeper precuneus SD than the O-HC (p<.03) and Y-FE groups (p<.0002). There were no significant CT and SD differences between the Y-HC and O-HC in these regions. Birth weight, not seizure and family history variables, reduced the significance of the precuneus SD (p<.006) and the middle and inferior occipital SD, and CT findings were no longer significant. Conclusions: Exaggerated cortical pruning is found in O-FE precuenus, middle occipital, and inferior occipital regions, and might reflect perinatal but not seizure and familial epilepsy variables.