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Altered communication dynamics reflect cognitive deficits in temporal lobe epilepsy
Author(s) -
GirardiSchappo Mauricio,
Fadaie Fatemeh,
Lee Hyo Min,
Caldairou Benoit,
Sziklas Viviane,
Crane Joelle,
Bernhardt Boris C.,
Bernasconi Andrea,
Bernasconi Neda
Publication year - 2021
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/epi.16864
Subject(s) - temporal lobe , neuroscience , psychology , epilepsy , hippocampus , hippocampal formation , cognition , neocortex , thalamus , connectome , functional connectivity
Abstract Objective Although temporal lobe epilepsy (TLE) is recognized as a system‐level disorder, little work has investigated pathoconnectomics from a dynamic perspective. By leveraging computational simulations that quantify patterns of information flow across the connectome, we tested the hypothesis that network communication is abnormal in this condition, studied the interplay between hippocampal‐ and network‐level disease effects, and assessed associations with cognition. Methods We simulated signal spreading via a linear threshold model that temporally evolves on a structural graph derived from diffusion‐weighted magnetic resonance imaging (MRI), comparing a homogeneous group of 31 patients with histologically proven hippocampal sclerosis to 31 age‐ and sex‐matched healthy controls. We evaluated the modulatory effects of structural alterations of the neocortex and hippocampus on network dynamics. Furthermore, multivariate statistics addressed the relationship with cognitive parameters. Results We observed a slowing of in‐ and out‐spreading times across multiple areas bilaterally, indexing delayed information flow, with the strongest effects in ipsilateral frontotemporal regions, thalamus, and hippocampus. Effects were markedly reduced when controlling for hippocampal volume but not cortical thickness, underscoring the central role of the hippocampus in whole‐brain disease expression. Multivariate analysis associated slower spreading time in frontoparietal, limbic, default mode, and subcortical networks with impairment across tasks tapping into sensorimotor, executive, memory, and verbal abilities. Significance Moving beyond descriptions of static topology toward the formulation of brain dynamics, our work provides novel insight into structurally mediated network dysfunction and demonstrates that altered whole‐brain communication dynamics contribute to common cognitive difficulties in TLE.