Remodeling of brain morphology in temporal lobe epilepsy.

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info:eu-repo/semantics/altIdentifier/doi/10.1002/brb3.1825

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info:eu-repo/semantics/altIdentifier/pmid/32945137

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_3FA1440B13BD9

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info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/




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E. Roggenhofer et al., « Remodeling of brain morphology in temporal lobe epilepsy. », Serveur académique Lausannois, ID : 10.1002/brb3.1825


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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? 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. 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. 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.

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