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Título

The impact of pharmacoresistant seizures on Gray Matter Atrophy in Generalized Genetic Epilepsy

Resumo

Introduction: Genetic generalized epilepsies (GGEs) correspond to 20-25% of all epilepsies. They are genetically determined disorders with subtle encephalic alterations affecting the white and gray matter (GM), as demonstrated by modern quantitative neuroimaging techniques. Alterations involving the thalamo-cortical connections are well described; however, few studies have investigated the impact of pharmacoresistant seizures on gray matter atrophy (GMA) in patients with GGEs.
Purpose: To investigate gray matter atrophy in Generalized Genetic Epilepsy (GGE) patients according to seizure control.
Methods: Fifty-six patients with GGE from UNICAMP’s Epilepsy Clinic were recruited: 33 Seizure-Persistent ([SZ-Persistent] patients with current seizures during the previous year of MRI acquisition, 21 women, median of 30 years); 23 Seizure-Free ([SZ-Free] free of any type of seizures for at least one year before MRI, 17 women, median 34 years), compared to 63 healthy controls (43 women, median 34 years) matched for age (p=0.51) and sex (p=0.83). High-resolution 3T T1-weighted scans were firstly segmented on CAT12/SPM12/MATLAB 2019 software (http://www.neuro.uni-jena.de/cat12-html/cat.html). Then, voxel-based morphometry (VBM) and surface-based morphometry (SBM) were performed to search for areas of gray matter volume and cortical thickness reduction with an ANOVA-test (between the SZ-Persistent group and SZ-Free groups compared to controls) on SPM12. We used age, sex and intracranial volume as covariates for the VBM analysis and sex and age for the SBM analysis. Clinical data were analyzed with SPSS20. The results from MRI analyses were reported with p <0.05, corrected for multiple comparisons.
Results: We identified cortical thickness atrophy only in the SZ-Persistent group, localized at the right precentral gyrus, while no alteration was observed in the SZ-Free. Regarding the analyses of cortical volume, we verified atrophy of the left thalamus in the SZ-Persistent group and the left precuneus region in the SZ-Free group.
Conclusion: As previously demonstrated in the literature, our results indicate that thalamo-frontal networks are vulnerable to persistent seizures in GGE, with significant gray matter atrophy. However, we also find that different degrees and locations of GM abnormalities are related to seizure control, which may have implications for the understanding of the physiopathology of the GGE.