Posterior integration and thalamo-frontotemporal broadcasting are impaired in disorders of consciousness

The study of the brain’s static and dynamical activity is opening a valuable source of assistance for the clinical assessment of patients with disorders of consciousness. For example, glucose uptake and dysfunctional spread of naturalistic and synthetic stimuli has proven useful to characterize hampered consciousness. However, understanding of the mechanisms behind loss of consciousness following brain injury is still missing. Here, we study the propagation of endogenous and in-silico exogenous perturbations in patients with disorders of consciousness, based upon directed and causal interactions estimated from resting-state fMRI. We found that patients with disorders of consciousness suffer decreased capacity for neural propagation and responsiveness to events, and that this can be related to glucose metabolism as measured with [ 18 F]FDG-PET. In particular, we show that loss of consciousness is related to the malfunctioning of two neural circuits: the posterior cortical regions failing to convey information, in conjunction with reduced broadcasting of information from subcortical, temporal, parietal and frontal regions. These results seed light on the mechanisms behind disorders of consciousness, triangulating network function with basic measures of brain integrity and behavior. Highlights Propagation of neural events and network responses are disrupted in patients with DoC. Loss of consciousness is related to the malfunctioning of two neural circuits. Posterior cortical regions lack to integrate information in altered consciousness. Breakdown of information broadcasting of subcortical cortical areas in DoC. Loss of network responses in DoC patients is related to glucose metabolism.