The role of the ventromedial prefrontal cortex in self- and event-related schemata

The ventromedial prefrontal cortex (vmPFC) is one of the largest regions of the human brain. Its activity has been linked to a plethora of cognitive functions, such as self-referential cognition, mind wandering, memory recollection, and many more. Yet, we still lack an exhaustive understanding of the essence of its functional specialization, if any. The schema theory proposes that vmPFC’s overarching role lies in the activation of schematic knowledge in neocortex, which is then used by other brain regions, according to environmental demands. Therefore, the present thesis addresses the question of whether a vmPFC damage degrades schema-mediated cognition. In Chapter 1 I begin to investigate the role of vmPFC in imparting the memory advantage for self-referential information in memory. Whilst healthy and brain-damaged controls exhibit superior recall for self- (vs other-) related items, such advantage is proven absent in vmPFC patients, suggesting a degradation of the self-schema. In Chapter 2 I aim to clarify whether this lack of self-referential prioritization stems from vmPFC patients’ memory deficits, or from an impairment in self-knowledge itself. Whilst healthy and brain-damaged controls exhibit more consistent self- rather than other-referential ratings over time, vmPFC patients do not, again suggesting a disturbance of the self-schema. In Chapter 3 we investigate vmPFC’s involvement in activating (reinstatement) and using (instantiation) event-schemata, demonstrating that a vmPFC damage hinders schema reinstatement, wherein vmPFC patients reinstate incomplete, nebulous schemas. Finally, in Chapter 4 we model frontal and posterior cortical interactions in a hybrid Potts model of cortical dynamics, revealing a capacity of the frontal cortex to act as the source of predominant influence on latching dynamics. We interpret the result considering the schematic influence exerted from the frontal lobe on posterior brain regions observed in experimental practice. Finally, by modelling a frontal lesion, we reproduce event construction deficits of vmPFC damaged patients.