Abstracts

Rationale: Epilepsies are conditions of functionally and anatomically connected networks [1]. So far, studies of abnormal networks in epilepsies were based on analysis of groups of patients. However, there is significant interindividual variation in the clinical characteristics of epilepsies [2]. The aim of this study is to investigate the overlap of individual functional and structural networks in patients with pharmacoresistant focal epilepsies. Methods: We selected 25 patients (age range 19-56 years, 44% male) submitted to concomitant EEG and functional MRI (EEG-fMRI) and diagnosis of pharmacoresistant focal epilepsies followed at Unicamp. All patients had the epileptogenic zone defined according to extensive pre-surgical evaluation. Patients underwent 20-48 minutes echo-planar imaging sequences in a 3T MRI. EEG was acquired using 64 MRI-compatible electrodes. EEG-fMRI was analyzed with SPM12. Interictal epileptiform discharges were visually identified and used to define blood oxygen level depended (BOLD) changes (interictal-related functional changes) (p < 0.001, minimum of 20 contiguous voxels). The evaluation of the individual structural brain changes looking for gray matter (GM) atrophy was performed by voxel based morphometry (VBM) technique with SPM8. T1-weighted volumetric images of 150 healthy subjects (age range 19-69 years, 41% male) were used as control and compared to the same type of image of each patient (two-sample T-tests, p < 0.001, minimum of 20 contiguous voxels). We evaluated the co-localization of structural and functional abnormalities through the co-registration of maps of each patient using SPM12 software. Results: 84% of patients (21/25) had interictal-related BOLD changes and 92 % (23/25) had GM atrophy including areas outside the epileptogenic zone. Eighteen patients had both interictal-related functional abnormalities and a network of GM atrophy. The co-registration of individual maps showed that 47% (9/19) of patients had overlap of the functional and structural abnormalities, which varied from 0.01% to 2.85% of the areas of the functional maps (figure1). Conclusions: The present work showed no significant overlap of the GM atrophy outside the epileptogenic zone and the interictal-related functional changes in individuals with pharmacoresistant epilepsies. One hypothesis for the diffuse network of GM atrophy in patients with pharmacoresistant epilepsies is that the occurrence of frequent interictal epileptiform discharges might contribute to the GM damage [1,2].  Therefore, the network of GM atrophy should be individually concordant with the functional abnormalities associated with the interictal discharges. We demonstrated, however, the absence of significant overlap in areas of GM atrophy and interictal-related functional abnormalities in individual analysis. This data corroborates the complex interactions between functional and structural networks in focal epilepsies.References: [1] Spencer SS, Epilepsia 43(3):219–227, 2002; [2] Laufs H, Curr Opin Neurol 25(2):194-200, 2012.  Funding: This study was funded by São Paulo Research Foundation - FAPESP (2016/10812-0).