Unraveling neural and behavioral mechanisms of cognitive self-attenuation and alienation

The present thesis aimed at investigating behavioral and neural underpinnings of the mechanisms related to the different aspects of self-monitoring. The first aim was to study functional connectivity alterations related to the mechanisms accounting for the alienation in psychotic patients and those at high-risk to develop it. The second aim was to extend the fundamental knowledge of whether higher-level cognitive processes beyond sensorimotor involvement are subject to attenuation and whether it is affected in psychotic patients with thought insertion.

In Part I of the thesis, I have studied whether the neural mechanisms (PH-network) accounting for the presence hallucination (PH), the experience that someone is here when no one is around, could also be relevant to understand alienation experienced in psychotic patients. In Study 1, I have investigated psychotic patients with passivity experiences where one's own actions, thoughts and emotions are perceived as not self-generated and caused by an external entity. In Study 2, individuals with 22q11 deletion syndrome who are at high-risk for psychosis development were investigated. In both populations, reduced functional connectivity between fronto-temporal connections within the PH-network was revealed. Taken together, these studies show that PH-network is affected not only when psychosis manifests but also in individuals prone to develop psychosis. The current findings strengthen the relevance of PH mechanisms to explain the occurrence of psychotic symptoms, specifically the alienation, and potentially could provide a biomarker for the disease development.

In Part II of the thesis, I have investigated self-attenuation, an important aspect for the sense of agency, during the cognitive function of numerosity estimations in healthy individuals and psychotic patients with thought insertion. In Study 3, a novel fMRI task was designed, allowing a controlled comparison of numerosity estimations for self and externally generated words in healthy volunteers. For the first time, self-attenuation during cognitive function beyond sensorimotor processing was reported. It was linked to the functional network involving intraparietal sulcus (key numerosity region) and extended areas more generally associated with attenuation processes. This work was continued in Study 4, where psychotic patients with thought insertion were studied. I showed that cognitive self-attenuation during numerosity estimations can be observed in patients with thought insertion and is related to altered executive functioning. Importantly, increased functional connectivity within the network related to attenuation processing during numerosity estimations was found in patients with thought insertion suggesting insufficient attenuation at the neural level. Lastly, I found the association between the altered functional connectivity within the PH-network and cognitive self-attenuation, providing a link between two different aspects related to