  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.
