4.7 Article

Multi-scale structural alterations of the thalamus and basal ganglia in focal epilepsy using 7T MRI

Journal

HUMAN BRAIN MAPPING
Volume 44, Issue 13, Pages 4754-4771

Publisher

WILEY
DOI: 10.1002/hbm.26414

Keywords

focal epilepsy; subcortical gray matter; multivariate analysis; T-1; volume; shape; deformation

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This study used 7T MRI T-1 data to describe subcortical morphological and longitudinal relaxation changes in focal epilepsy patients and evaluated the influence of clinical characteristics. Results showed variable levels of atrophy across thalamic nuclei, with the most prominent changes in the temporal lobe epilepsy group. T-1 measures in the thalamus appeared to differentiate patients based on epileptogenic zone localization.
Focal epilepsy is characterized by repeated spontaneous seizures that originate from cortical epileptogenic zone networks (EZN). Analysis of intracerebral recordings showed that subcortical structures, and in particular the thalamus, play an important role in seizure dynamics as well, supporting their structural alterations reported in the neuroimaging literature. Nonetheless, between-patient differences in EZN localization (e.g., temporal vs. non-temporal lobe epilepsy) as well as extension (i.e., number of epileptogenic regions) might impact the magnitude as well as spatial distribution of subcortical structural changes. Here we used 7 Tesla MRI T-1 data to provide an unprecedented description of subcortical morphological (volume, tissue deformation, and shape) and longitudinal relaxation (T-1) changes in focal epilepsy patients and evaluate the impact of the EZN and other patient-specific clinical features. Our results showed variable levels of atrophy across thalamic nuclei that appeared most prominent in the temporal lobe epilepsy group and the side ipsilateral to the EZN, while shortening of T-1 was especially observed for the lateral thalamus. Multivariate analyses across thalamic nuclei and basal ganglia showed that volume acted as the dominant discriminator between patients and controls, while (posterolateral) thalamic T-1 measures looked promising to further differentiate patients based on EZN localization. In particular, the observed differences in T-1 changes between thalamic nuclei indicated differential involvement based on EZN localization. Finally, EZN extension 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.

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