Abstract
AbstractTraumatic brain injury is a devastating injury to the brain that can have permanent or fatal effects, leading to life-long deficits or death. Among these effects is psychosis and schizophrenia, sometimes reported in the population of TBI sufferers. Here we evaluate a possible mechanism of post-traumatic psychosis, shedding light on the anomalous nature of psychosis as over-activity and brain injury as destruction. Using a multiscale model of the brain to relate molecular pathology to connectomic and macroscopic features of the brain, we identify cell lysis and membrane deformation as a possible mechanism for psychosis after injury. We also evaluate the reorganisation of functional networks and cortical activation post-injury, and find the features of a simulated brain under traumatic injury correlate with recorded results on the schizophrenic functional connectome. This provides a possible mechanism for post-traumatic psychosis, as well as a proof-of-principle of advanced multiscale modelling methods in computational psychiatry and neuromedicine. It also elaborates on the relationship between structure and function in the brain, information processing, and the delicate regulation of activity in healthy brains.
Publisher
Cold Spring Harbor Laboratory