Multi-scale structural alterations of the thalamus and basal ganglia in focal epilepsy as demonstrated by 7T MRI
Roy A.M. HaastiD, Benoît TestudiD, Julia MakhalovaiD, Hugo DaryiD, Alexandre Cabane, Arnaud Le TroteriD, Jean‐Philippe RanjevaiD, Fabrice BartoloméiiD, Maxime GuyeiD
Abstract
Focal epilepsy is characterized by repeated spontaneous seizures that originate from cortical epileptogenic zone networks (EZN). More recently, analysis of intracerebral recordings showed that subcortical structures, and in particular the thalamus, play an important role in facilitating and/or propagating epileptic activity. This supports previously reported structural alterations of these structures. Nonetheless, between-patient differences in EZN (e.g., temporal vs. non-temporal lobe epilepsy) as well as other clinical features (e.g., number of epileptogenic regions) might impact the magnitude as well as spatial distribution of subcortical structural changes. Here we used 7 Tesla MRI T1 data to provide a comprehensive description of subcortical morphological (volume, tissue deformation, and shape) and longitudinal relaxation (T1) changes in focal epilepsy patients to evaluate the impact of the EZN and patient-specific clinical features. Our results showed widespread morphometric and T1 changes. Focusing on the thalamus, atrophy varied across nuclei but appeared most prominent for the TLE group and the ipsilateral side, while shortening of T1 was observed for the lateral thalamus, in particular. Multivariate analyses across thalamic nuclei and basal ganglia showed that volume acted as the dominant discriminator between patients and controls, while (posterolateral) thalamic T1 measures looked promising to further differentiate patients based on EZN. In particular, the observed differences in T1 changes between thalamic nuclei indicated differential involvement of thalamic nuclei based on EZN. Finally, the number of epileptogenic regions was found to best explain the observed variability between patients. To conclude, this work revealed multi-scale subcortical alterations in focal epilepsy as well as their dependence on several clinical characteristics. Our results provide a basis for further, in-depth investigations using (quantitative) MRI and SEEG data and warrant further personalization of intervention strategies, such as deep brain stimulation, for treating focal epilepsy patients.
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