Abstracts

Rationale: In clinical practice, children with Rolandic epilepsy may display language impairment. Epileptiform discharges have been associated with disturbed functionality of the language network. However, whether abnormalities in cortical morphology exist and may explain the language impairment has not been investigated. The aim of this study is to compare the cortical thickness and language performance of children with Rolandic epilepsy with healthy controls. Methods: This is a cross-sectional study of children with Rolandic epilepsy.Structural T1-weighted MRI (1 mm iso, 3 Tesla) and the Clinical Evaluation of Language Fundamentals (CELF-4, Dutch edition) language test were performed in 21 children with typical Rolandic epilepsy confirmed by EEG (age, mean SD: 135 24 months) and 21 age-matched controls (125 20 months). The Freesurfer image analysis software package was used to measure cortical thickness and to perform linear regression with CELF language metrics and age. Cortical regions of abnormal thickness were identified using uncorrected trends of p<0.01 and subsequent correction for multiple comparison.Results: On the CELF-4, children with Rolandic epilepsy (core language score: 92.2 18.8) performed lower than the norm score (100) and significantly worse than healthy controls (106.2 9.3) (p=0.03). A trend of cortical thinning was found in the supramarginal cortex in Rolandic epilepsy compared to controls (p=0.08). In children with Rolandic epilepsy, the cortical thickness decreased significantly with age in the left postcentral gyrus, middle temporal lobe, pars triangularis, superiorfrontal cortex, inferior parietal cortex, superiorparietal cortex and lateral occipital cortex (p<0.01) (Fig 1). Furthermore, the cortical thickness increased significantly with decreasing language score in the left lingual cortex for children with Rolandic epilepsy (p=0.012) (Fig 2), but not for controls.Conclusions: For the first time, abnormal cortical morphology was identified in children with Rolandic epilepsy relative to age-matched healthy controls. The observed cortical thinning was localized in language mediating brain regions in the left hemisphere. The region in the left lingual cortex (associated with word recognition) that appeared thicker at lower language score may indicate a compensation mechanism. These observations suggest that Rolandic epilepsy cannot be merely considered as a benign condition in children. A large population with Rolandic epilepsy and more detailed analysis of language performance is needed to further strengthen these findings.