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The study of the brain's dynamical activity is opening a window to help the clinical assessment of patients with disorders of consciousness. For example, glucose uptake and the 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 data, fitted to a linear model of activity propagation. 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 severe reduction of glucose metabolism as measured with [18F]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 shed light on the mechanisms behind disorders of consciousness, triangulating network function with basic measures of brain integrity and behavior. [ABSTRACT FROM AUTHOR]

Susceptibility to motion sickness varies greatly across individuals. However, the neural mechanisms underlying this susceptibility remain largely unclear. To address this gap, the current study aimed to identify the neural correlates of motion sickness susceptibility using multimodal MRI. First, we compared resting‐state functional connectivity between healthy individuals who were highly susceptible to motion sickness (N = 36) and age/sex‐matched controls who showed low susceptibility (N = 36). Seed‐based analysis revealed between‐group differences in functional connectivity of core vestibular regions in the left posterior Sylvian fissure. A data‐driven approach using intrinsic connectivity contrast found greater network centrality of the left intraparietal sulcus in high‐ rather than in low‐susceptible individuals. Moreover, exploratory structural connectivity analysis uncovered an association between motion sickness susceptibility and white matter integrity in the left inferior fronto‐occipital fasciculus. Taken together, our data indicate left parietal involvement in motion sickness susceptibility. [ABSTRACT FROM AUTHOR]