Elucidation of transphasic mechanisms (i.e., mechanisms that occur across illness phases) underlying negative symptoms could inform early intervention and prevention efforts and additionally identify treatment targets that could be effective regardless of illness stage. This study examined whether a key reinforcement learning behavioral pattern characterized by reduced difficulty learning from rewards that have been found to underlie negative symptoms in those with a schizophrenia diagnosis also contributes to negative symptoms in those at clinical high-risk (CHR) for psychosis.

CHR youth (n = 46) and 51 healthy controls (CN) completed an explicit reinforcement learning task with two phases. During the acquisition phase, participants learned to select between pairs of stimuli probabilistically reinforced with feedback indicating receipt of monetary gains or avoidance of losses. Following training, the transfer phase required participants to select between pairs of previously presented stimuli during the acquisition phase and novel stimuli without receiving feedback. These test phase pairings allowed for inferences about the contributions of prediction error and value representation mechanisms to reinforcement learning deficits.

In acquisition, CHR participants displayed impaired learning from gains specifically that were associated with greater negative symptom severity. Transfer performance indicated these acquisition deficits were largely driven by value representation deficits. In addition to negative symptoms, this profile of deficits was associated with a greater risk of conversion to psychosis and lower functioning.

Impairments in positive reinforcement learning, specifically effectively representing reward value, may be an important transphasic mechanism of negative symptoms and a marker of psychosis liability.

There is limited research in adolescent at risk for psychosis. The new criteria of Attenuated Psychosis Syndrome (APS) of Diagnostic and Statistical Manual of Mental Disorders- 5 (DSM-5) have not been validated.

The aims of this study were to: 1) characterize adolescent’s profile with APS (DSM-5 APS) compared to adolescents with early onset psychosis (EOP) and with other psychiatric disorders (non-APS); 2) to estimate their long-term risk of transition to psychosis and prognostic accuracy of DSM-5 APS.

243 adolescents, aged 12-17, were included (October 2012- July 2019) and dived in three sub-groups (110 DSM-5 APS, 31 EOP, 102 non-APS). All underwent a comprehensive assessment evaluating: sociodemographic characteristics, family and personal history of any DSM-5 psychiatric disorders, psychopathological assessment and level of functioning. An annual follow-up evaluation was carried out (up to 7 years) including a clinical interview to investigate DSM-5 criteria for transition to psychosis.

DSM-5 APS adolescents had on average higher comorbid disorders (2.3) and intermediate psychopathological and functioning profile between non-APS/EOP. The cumulative risk of transition at 1,2,3, 4-5 years was 13%, 17%, 24.2%, 26.8% and 26.8% in DSM-5 APS group, 0%, 0%, 3.2%, 3.2% and 3.2% in the non-APS. The 5-year prognostic accuracy of the DSM-5 APS in adolescent was adequate (Area Under the Curve=0.77) with high sensitivity (91.3%) and suboptimal specificity (63.2%).

The DSM-5 APS diagnosis can be used to detect help-seeking adolescents at risk of psychosis and predict their long-term outcomes, leading the way to new preventive approaches.

The authors declare that they do not have a significant financial interest, consultancy or other relationship with products, manufacturer(s) of products or providers of services related to this abstrac.

Prevalence and covariates of subclinical psychosis have gained increased interest in the context of early identification and treatment of persons at risk for psychosis.

We analysed 9829 adults representative of the general population within the canton of Zurich, Switzerland. Two psychosis syndromes, derived from the SCL-90-R, were applied: ‘schizotypal signs’ and ‘schizophrenia nuclear symptoms’.

Only a few subjects (13.2%) reported no schizotypal signs. While 33.2% of subjects indicated mild signs, only a small proportion (3.7%) reported severe signs. A very common outcome was no ‘schizophrenia nuclear symptoms’ (70.6%). Although 13.5% of the participants reported mild symptoms, severe nuclear symptoms were very rare (0.5%). Because these two syndromes were only moderately correlated (r = 0.43), we were able to establish sufficiently distinct symptom clusters. Schizotypal signs were more closely connected to distress than was schizophrenia nuclear symptoms, even though their distribution types were similar. Both syndromes were associated with several covariates, such as alcohol and tobacco use, being unmarried, low education level, psychopathological distress and low subjective well-being.

Subclinical psychosis symptoms are quite frequent in the general population but, for the most part, are not very pronounced. In particular, our data support the notion of a continuous Wald distribution of psychotic symptoms in the general population. Our findings have enabled us to confirm the usefulness of these syndromes as previously assessed in other independent community samples. Both can appropriately be associated with well-known risk factors of schizophrenia.