Abstracts

Rationale: Using surface based morphometry, our objective was to determine if the association between age and gray matter(GM) tissue thickness measured at high spatial resolution across the cortex differentiated the childhood absence epilepsy(CAE) and a healthy control group. Methods: The study included 24 CAE children, aged 5.5-15.8 years with IQ scores of 70 and above, and 37 age and gender matched normal children. High-resolution 3D MR images were obtained on a 1.5 Tesla scanner. After the 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 GM tissue were extracted. Cortical thickness at each point in the GM mantle is defined as the sum of the distances from this point to the GM/WM and GM/CSF 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. Group differences on age-cortical thickness association were considered the parameter of interest in the analysis. A general linear model was fitted at each reference cortical surface point with cortical thickness as the dependent variable, age, diagnosis, and their interaction as the predictors with sex as covariate. All statistical outcomes were corrected for multiple comparisons, using false discovery rate at p<0.05. Results: Regions of brain where children with CAE demonstrate statistically significant differences in local gray matter thickness and age association compared to healthy children are depicted in the figure. This figure plots cortical thickness distribution as a function of age for CAE and healthy groups for sample cortical locations where significant group differences were observed. From the developmental perspective, the CAE group did not demonstrate the normal age-related changes involving a decrease in cortical thickness in the left superior(including mesial surface), middle and inferior frontal lobe, somatosensory region, and superior temporal gyrus. Unlike the normal group, there also appeared to be an age-related thinning in the right posterior central gyrus and posterior part of the superior temporal gyrus, lingual gyrus, and paracentral gyrus. We observed cross-sectional pattern of abnormalities in age related changes in GM thickness with localized slowed thinning(prominently on the left hemisphere) and accelerated changes(on the right hemisphere). Conclusions: This first study on brain morphometry in children with absence seizures has important implications for advancing our understanding of brain development and of the comorbidities in CAE, as well as for revisiting the clinical notion that CAE is a benign disorder. Localization of increased cortical thickness in the superior temporal lobe, mainly the posterior part, is particularly interesting given the role of this brain region in language and evidence for both basic and higher level linguistic deficits in CAE children with average IQ scores.