  Focal epilepsy is a devastating neurological disorder that affects an
overwhelming number of patients worldwide, many of whom prove resistant to
medication. The efficacy of current innovative technologies for the treatment
of these patients has been stalled by the lack of accurate and effective
methods to fuse multimodal neuroimaging data to map anatomical targets driving
seizure dynamics. Here we propose a parsimonious model that explains how
large-scale anatomical networks and shared genetic constraints shape
inter-regional communication in focal epilepsy. In extensive ECoG recordings
acquired from a group of patients with medically refractory focal-onset
epilepsy, we find that ictal and preictal functional brain network dynamics can
be accurately predicted from features of brain anatomy and geometry, patterns
of white matter connectivity, and constraints complicit in patterns of gene
coexpression, 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 most
prevalent in high frequency ictal dynamics and low frequency preictal dynamics.
Finally, we find that ictal dynamics are better predicted by white matter
features and more poorly predicted by geometry and genetic constraints than
preictal dynamics, suggesting that the functional brain network dynamics
manifest in seizures rely on - and may directly propagate along - underlying
white matter structure that is largely conserved across humans. Broadly, our
work offers insights into the generic architectural principles of the human
brain that impact seizure dynamics, and could be extended to further our
understanding, models, and predictions of subject-level pathology and response
to intervention.
