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Focal epilepsy is a devastating neurological disorder that affects anoverwhelming number of patients worldwide, many of whom prove resistant tomedication. The efficacy of current innovative technologies for the treatmentof these patients has been stalled by the lack of accurate and effectivemethods to fuse multimodal neuroimaging data to map anatomical targets drivingseizure dynamics. Here we propose a parsimonious model that explains howlarge-scale anatomical networks and shared genetic constraints shapeinter-regional communication in focal epilepsy. In extensive ECoG recordingsacquired from a group of patients with medically refractory focal-onsetepilepsy, we find that ictal and preictal functional brain network dynamics canbe accurately predicted from features of brain anatomy and geometry, patternsof white matter connectivity, and constraints complicit in patterns of genecoexpression, all of which are conserved across healthy adult populations.Moreover, we uncover evidence that markers of non-conserved architecture,potentially driven by idiosyncratic pathology of single subjects, are mostprevalent in high frequency ictal dynamics and low frequency preictal dynamics.Finally, we find that ictal dynamics are better predicted by white matterfeatures and more poorly predicted by geometry and genetic constraints thanpreictal dynamics, suggesting that the functional brain network dynamicsmanifest in seizures rely on - and may directly propagate along - underlyingwhite matter structure that is largely conserved across humans. Broadly, ourwork offers insights into the generic architectural principles of the humanbrain that impact seizure dynamics, and could be extended to further ourunderstanding, models, and predictions of subject-level pathology and responseto intervention.

Genetic and Neuroanatomical Support for Functional Brain Network Dynamics in Epilepsy