Barata, Vera A.Lavoie, SuzieGawęda, ŁukaszLi, EmilySass, Louis A.Koren, DannyMcGorry, Patrick D.Jack, Bradley N.Parnas, JosefPolari, AndreaAllott, KellyHartmann, Jessica A.Krcmar, MarijaRasmussen, Andreas R.Whitford, Thomas J.Wannan, Cassandra M.J.Nelson, Barnaby2026-09-162026-09-161039-8562PubMed:40464568https://hdl.handle.net/1885/733815475Introduction: We previously proposed a neurophenomenological model of schizophrenia, linking basic self-disturbance with neural deficits of source monitoring and aberrant salience. Baseline comparisons in ultra-high risk (UHR) and first-episode psychosis (FEP) samples indicated a relationship between basic self-disturbance and source monitoring deficits, but not aberrant salience. The current paper reports on the 12-month follow-up results in the UHR group (n = 43), focusing on the association between baseline variables and clinical outcomes. Methods: One-way ANOVA compared UHR-remitters (n = 18), UHR-persistent/transitioned to psychosis cases (n = 25) and FEP (n = 38) groups on baseline clinical and neuro-measures. Logistic regression assessed the baseline variables’ predictive power for UHR outcomes. Results: Higher baseline self-disturbance scores (EASE total) were found in the UHR persistence/transition and FEP groups compared to the UHR-remission group, and predicted worse UHR clinical outcomes. Source monitoring deficits were higher in FEP individuals compared to those with UHR persistence/transition. Conclusion: High levels of basic self-disturbance may be a useful predictor marker of poor prognosis in UHR patients.The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by a Brain and Behavior Research Foundation (BBRF) Independent Investigator Award [23199] to BN.6enPublisher Copyright: © The Royal Australian and New Zealand College of Psychiatrists 2025. This article is distributed under the terms of the Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).neurocognitionphenomenologyprodromepsychosisschizophrenia202510.1177/10398562251346619105007630947