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学術論文

Remodeling of brain morphology in temporal lobe epilepsy

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Draganski,  Bogdan
Département des Neurosciences Cliniques, Laboratoire de Recherche en Neuroimagerie (LREN), Centre hospitalier universitaire vaudois, Lausanne, Switzerland;
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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引用

Roggenhofer, E., Muller, S., Santarnecchi, E., Melie‐Garcia, L., Wiest, R., Kherif, F., & Draganski, B. (2020). Remodeling of brain morphology in temporal lobe epilepsy. Brain and Behavior, 10(11):. doi:10.1002/brb3.1825.


引用: https://hdl.handle.net/21.11116/0000-0007-17F9-7
要旨

Background: Mesial temporal lobe epilepsy (TLE) is one of the most widespread neurological network disorders. Computational anatomy MRI studies demonstrate a robust pattern of cortical volume loss. Most statistical analyses provide information about localization of significant focal differences in a segregationist way. Multivariate Bayesian modeling provides a framework allowing inferences about inter-regional dependencies. We adopt this approach to answer following questions: Which structures within a pattern of dynamic epilepsy-associated brain anatomy reorganization best predict TLE pathology. Do these structures differ between TLE subtypes?
Methods: We acquire clinical and MRI data from TLE patients with and without hippocampus sclerosis (n = 128) additional to healthy volunteers (n = 120). MRI data were analyzed in the computational anatomy framework of SPM12 using classical mass-univariate analysis followed by multivariate Bayesian modeling.
Results: After obtaining TLE-associated brain anatomy pattern, we estimate predictive power for disease and TLE subtypes using Bayesian model selection and comparison. We show that ipsilateral para-/hippocampal regions contribute most to disease-related differences between TLE and healthy controls independent of TLE laterality and subtype. Prefrontal cortical changes are more discriminative for left-sided TLE, whereas thalamus and temporal pole for right-sided TLE. The presence of hippocampus sclerosis was linked to stronger involvement of thalamus and temporal lobe regions; frontoparietal involvement was predominant in absence of sclerosis.
Conclusions: Our topology inferences on brain anatomy demonstrate a differential contribution of structures within limbic and extralimbic circuits linked to main effects of TLE and hippocampal sclerosis. We interpret our results as evidence for TLE-related spatial modulation of anatomical networks.