Dataset Information

Adaptive frequency-based modeling of whole-brain oscillations: Predicting regional vulnerability and hazardousness rates.

ABSTRACT: Whole-brain computational modeling based on structural connectivity has shown great promise in successfully simulating fMRI BOLD signals with temporal coactivation patterns that are highly similar to empirical functional connectivity patterns during resting state. Importantly, previous studies have shown that spontaneous fluctuations in coactivation patterns of distributed brain regions have an inherent dynamic nature with regard to the frequency spectrum of intrinsic brain oscillations. In this modeling study, we introduced frequency dynamics into a system of coupled oscillators, where each oscillator represents the local mean-field model of a brain region. We first showed that the collective behavior of interacting oscillators reproduces previously shown features of brain dynamics. Second, we examined the effect of simulated lesions in gray matter by applying an in silico perturbation protocol to the brain model. We present a new approach to map the effects of vulnerability in brain networks and introduce a measure of regional hazardousness based on mapping of the degree of divergence in a feature space.

SUBMITTER: Kaboodvand N

PROVIDER: S-EPMC6779267 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Adaptive frequency-based modeling of whole-brain oscillations: Predicting regional vulnerability and hazardousness rates.

Kaboodvand Neda N van den Heuvel Martijn P MP Fransson Peter P

Network neuroscience (Cambridge, Mass.) 20190901 4

Whole-brain computational modeling based on structural connectivity has shown great promise in successfully simulating fMRI BOLD signals with temporal coactivation patterns that are highly similar to empirical functional connectivity patterns during resting state. Importantly, previous studies have shown that spontaneous fluctuations in coactivation patterns of distributed brain regions have an inherent dynamic nature with regard to the frequency spectrum of intrinsic brain oscillations. In this ...[more]

PMID: 31637340

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Project description:Focal cortical dysplasia (FCD) type II is a highly epileptogenic developmental malformation and a common cause of surgically treated drug-resistant epilepsy. While clinical observations suggest frequent occurrence in the frontal lobe, mechanisms for such propensity remain unexplored. Here, we hypothesized that cortex-wide spatial associations of FCD distribution with cortical cytoarchitecture, gene expression and organizational axes may offer complementary insights into processes that predispose given cortical regions to harbour FCD. We mapped the cortex-wide MRI distribution of FCDs in 337 patients collected from 13 sites worldwide. We then determined its associations with (i) cytoarchitectural features using histological atlases by Von Economo and Koskinas and BigBrain; (ii) whole-brain gene expression and spatiotemporal dynamics from prenatal to adulthood stages using the Allen Human Brain Atlas and PsychENCODE BrainSpan; and (iii) macroscale developmental axes of cortical organization. FCD lesions were preferentially located in the prefrontal and fronto-limbic cortices typified by low neuron density, large soma and thick grey matter. Transcriptomic associations with FCD distribution uncovered a prenatal component related to neuroglial proliferation and differentiation, likely accounting for the dysplastic makeup, and a postnatal component related to synaptogenesis and circuit organization, possibly contributing to circuit-level hyperexcitability. FCD distribution showed a strong association with the anterior region of the antero-posterior axis derived from heritability analysis of interregional structural covariance of cortical thickness, but not with structural and functional hierarchical axes. Reliability of all results was confirmed through resampling techniques. Multimodal associations with cytoarchitecture, gene expression and axes of cortical organization indicate that prenatal neurogenesis and postnatal synaptogenesis may be key points of developmental vulnerability of the frontal lobe to FCD. Concordant with a causal role of atypical neuroglial proliferation and growth, our results indicate that FCD-vulnerable cortices display properties indicative of earlier termination of neurogenesis and initiation of cell growth. They also suggest a potential contribution of aberrant postnatal synaptogenesis and circuit development to FCD epileptogenicity.

Dataset Information

Adaptive frequency-based modeling of whole-brain oscillations: Predicting regional vulnerability and hazardousness rates.

Publications

Adaptive frequency-based modeling of whole-brain oscillations: Predicting regional vulnerability and hazardousness rates.

Similar Datasets

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