# Antiepileptic drugs induce subcritical dynamics in human cortical networks

## TL;DR

This study demonstrates that antiepileptic drugs induce subcritical dynamics in human cortical networks, supporting the branching process theory and providing insights into cortical excitability and epilepsy monitoring.

## Contribution

It provides causal evidence linking pharmacological reduction of network interactions to subcritical dynamics in human cortex, validating the branching process model.

## Key findings

- Cortical activity cascades decline with antiepileptic drugs
- Temporal correlations decrease as predicted by branching process theory
- Supports the causal relationship between network interactions and cortical activity

## Abstract

Cortical network functioning critically depends on finely tuned interactions to afford neuronal activity propagation over long distances while avoiding runaway excitation. This importance is highlighted by the pathological consequences and impaired performance resulting from aberrant network excitability in psychiatric and neurological diseases, such as epilepsy. Theory and experiment suggest that the control of activity propagation by network interactions can be adequately described by a branching process. This hypothesis is partially supported by strong evidence for balanced spatiotemporal dynamics observed in the cerebral cortex, however, evidence of a causal relationship between network interactions and cortex activity, as predicted by a branching process, is missing in humans. Here we test this cause-effect relationship by monitoring cortex activity under systematic pharmacological reduction of cortical network interactions with antiepileptic drugs. We report that cortical activity cascades, presented by the propagating patterns of epileptic spikes, as well as temporal correlations decline precisely as predicted for a branching process. Our results provide the missing link to the branching process theory of cortical network function with implications for understanding the foundations of cortical excitability and its monitoring in conditions like epilepsy.