Abstract

Objective. This review aims to examine neurocognitive deficits in individuals at clinical high risk (CHR) for psychosis, focusing on comparisons with healthy controls (HCs), differences between CHR individuals who transition to psychosis (CHR-T) and those who do not (CHR-NT), the relationship between cognition, symptoms, and functioning, and longitudinal trajectories of cognitive performance.

Methods. A systematic search of PubMed identified studies published between January 1998 and November 2024. Inclusion criteria required studies to assess neurocognitive performance in CHR individuals using validated criteria, compare CHR individuals to HCs or CHR subgroups (CHR-T/CHR-NT), and evaluate cognitive domains. The findings were analyzed to highlight the most affected cognitive domains and to explore longitudinal patterns of change.

Results. CHR individuals exhibited widespread neurocognitive impairments, with verbal memory, processing speed, and executive functions most consistently affected compared to HCs. CHR-T individuals demonstrated greater baseline deficits and progressive reductions in cognitive performance over time, particularly in verbal memory and processing speed, while CHR-NT showed stability or improvement. Neurocognitive deficits were linked to symptom severity and poorer functional outcomes, with CHR-NT improvements associated with reduced symptoms. Longitudinal analyses highlighted heterogeneous trajectories, underscoring the importance of identifying early cognitive markers of transition risk.

Conclusions. Neurocognitive deficits are central to psychosis risk, with distinct trajectories differentiating CHR-T from CHR-NT individuals. These findings emphasize the need for targeted interventions and integration of neurocognitive assessments in clinical practice to enhance prediction and prevention efforts.

INTRODUCTION

Deficits in neurocognition are a core feature of schizophrenia but are also consistently reported among individuals at clinical high risk (CHR) of psychosis1-3. The CHR criteria include: attenuated psychotic symptoms (APS), representing mild positive symptoms; brief and limited intermittent psychotic symptoms (BLIPS), characterized by transient, non-serious psychotic symptoms lasting part of the day, and lasted for a maximum period of one week after which spontaneously went to remission; and genetic risk and deterioration syndrome (GRD), including patients with family history of psychosis or schizotypal personality disorder, with additional decline in functioning4. Validated assessment scales, such as the Comprehensive Assessment of At-Risk Mental States (CAARMS)5 and the Structured Interview for Psychosis-Risk Syndromes (SIPS)6, enable early detection of vulnerability and risk stratification for psychosis in CHR individuals.

Longitudinal studies show that not all individuals identified as CHR will develop a first episode of psychosis. Cumulative transition rates are approximately 18% at 6 months, 22% at 1 year, 29% at 2 years, and 36% at 3 years1. This suggests that the only presence of attenuated symptoms is not sufficient to predict clinical outcome.

In recent decades, there has been an increasing focus on neurocognition as a central aspect of understanding risk mechanisms and designing targeted preventive interventions. Emerging early in the prodromal stages, these deficits have been identified as markers of vulnerability and potential endophenotypes, playing a central role in predicting the transition to psychosis and contributing to significant impairments in social and role functioning1-3.

Numerous studies have shown that CHR individuals have significant neurocognitive deficits compared to healthy controls (HCs), although these deficits are less pronounced than those observed in patients with first-episode psychosis (FEP)2,3,7. Alterations in domains such as processing speed, verbal memory, and executive functioning often emerge in the prodromal stages of the illness, suggesting that these deficits may serve as early markers of vulnerability2,8 and providing valuable targets for early intervention. In particular, processing speed has emerged as one of the most impaired domains in CHR, consistently identified as a robust predictor of transition to psychosis3.

In CHR individuals, deficits in processing speed, in particular, may hinder the ability to process complex social information and respond appropriately to environmental stimuli, compromising the development of essential social skills in critical life stages such as adolescence and early adulthood. In addition, deficits in attention and working memory can impair the ability to keep attention on prolonged tasks and retain new information, further impairing academic and occupational functioning8. These difficulties in maintaining social relationships and academic or work performance often persist into adult life, despite whether the individual transitions to psychosis8.

Another central issue concerns the interaction between neurocognition and clinical symptoms. Negative symptoms, such as social withdrawal and reduced motivation, can amplify the impact of neurocognitive deficits on functioning, contributing to impairment9. Attenuated positive symptoms (e.g., ideas of reference or unusual perceptions) may disrupt processes such as verbal learning or problem solving, indicating that cognitive domains may be differentially affected by distinct symptom domains10.

Recent literature has shown that neurocognitive changes in CHR individuals are characterized by significant variability. While some studies suggest stability of deficits over time, others report declines in specific domains such as processing speed or visual memory, often associated with a subsequent transition to psychosis (CHR-T)2,11,12. Conversely, there is evidence of neurocognitive improvements in subgroups of CHR who do not transition to psychosis (CHR-NT), suggesting the presence of resilience or compensatory mechanisms12,13. This variability might reflect the phenotypic diversity of CHR populations and the complexity of interactions between neurocognition, clinical symptoms, and functional outcomes.

These inconsistencies highlight the need for further research to elucidate the longitudinal trajectories of cognitive deficits and their predictive role in both the transition to psychosis and the remission of prodromal symptoms.

The aim of the present review is four-fold: (1) to summarize findings on neurocognitive deficits in CHR individuals compared to HCs; (2) to examine differences in cognitive profiles between CHR-T and CHR-NT groups basing on existing literature; (3) to explore the relationship between neurocognitive performance, clinical symptoms, and functional outcomes; and (4) to review evidence on longitudinal changes in specific cognitive processes.

MATERIALS AND METHODS

Literature search, screening and selection process

Two independent authors (A.C., C.M.) conducted a review of the scientific literature published in the last 26 years (1 January 1998–19 November 2024). The research was restricted to those articles published from 1998 onward, because this is the year in which the first prospective studies with subjects meeting validated CHR criteria have been published14.

The PubMed database was searched using the following key terms: (‘at risk mental state’ OR ‘ultra high risk’ OR ‘UHR’ OR ‘clinical high risk’ OR ‘psychosis risk’ OR ‘prodrome’ OR ‘psychosis’ OR ‘basic symptoms’) AND (‘neurocognitive’ OR ‘cognitive’) AND (‘retest’ OR ‘longitudinal’ OR ‘change’ OR ‘follow-up’ OR ‘course’).

This qualitative review was executed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standard, including evaluation of bias (confounding, overlapping data, publication bias)15.

Identified articles were initially screened by title and abstract to assess their potential for inclusion. Subsequently, the full text of relevant papers was reviewed to determine eligibility. Additionally, a manual search of the reference lists of the included articles was conducted to identify further relevant studies.

A.C. prepared a form to define the data to extract. A.C. and C.M. independently extracted data, and C.M. checked for the correctness and completeness of extracted data.

Several variables have been extracted from the evaluated articles: author, year of publication, sample characteristics (e.g. number of subjects, task used for CHR assessment, follow-up period) and details of neurocognitive measures (e.g. task used, domain).

Eligibility criteria

These are the inclusion criteria for the studies in the present review: (a) original articles, to be published in English; (b) presence of CHR subjects, according to international standard criteria, as defined by validated scales including the CAARMS5 and SIPS6; (c) inclusion of comparison group of HCs or comparison of CHR-T and CHR-NT groups; (d) administered the same cognitive test at both assessments and reported the test scores.

Studies were excluded if they: (a) were unpublished studies, reviews, conference abstracts or case reports; (b) had overlapping samples on the same cognitive measure; (c) only examined cognitive performance in FEP, schizophrenia or bipolar disorder samples (no CHR sample); (d) included intervention therapies to improve cognition between assessments.

Neurocognitive domains and task analysed

Individual tasks that were analysed included Trail Making Test A (TMT-A)16,17 and B (TMT-B)18, Brief Assessment of Cognition Scale (BACS) symbol coding19,20, semantic fluency20-24, letter fluency20-22,24, Continuous Performance Task – Identical Pairs (CPT-IP)25,26, Rey Auditory Verbal Learning Test (RAVLT) immediate recall27,28, Hopkins Verbal Learning Test-Revised (HVLT-R)29, California Verbal Learning Test (CVLT) immediate recall30-32, Wechsler Adult Intelligence Scale (WAIS) block design33,34, digit symbol and digit span33,35,36. For consistency of interpretations, task outcome measures were categorised into neurocognitive domains based on the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) criteria37. These included: (a) processing speed, (b) attention/vigilance, (c) verbal learning and memory, (d) visuospatial ability, (e) executive functioning and (f) working memory (Tab. I).

RESULTS

Our search produced 20,707 results. After screening, the results were reduced to 123 articles relevant to the subject. As described in Figure 1, by applying the proposed criteria, the final number of publications deemed eligible for this review is 17.

Table II shows the characteristics of the included studies.

Neurocognitive performance in CHR individuals compared to HCs

CHR individuals consistently demonstrate neurocognitive deficits across several domains compared to HCs. Verbal memory impairments were one of the most reported deficits (9 out of 17 studies), with studies highlighting reduced immediate and delayed recall in CHR individuals compared to HCs38-40. Tasks such as the CVLT and HVLT-R consistently identified these deficits.

Visual memory was similarly impaired in CHR individuals, with delayed recall being particularly affected40,41. Additionally, processing speed emerged as one of the most affected domains (11 out of 17 studies), with CHR individuals performing worse on the TMT-A and WAIS-Digit Symbol41,42.

Deficits in executive functions were evident in 10 out of 17 studies. Tasks such as the WCST and TMT-B revealed impairments in cognitive flexibility and problem-solving, with higher perseverative errors among CHR individuals compared to HCs38,43,44. In verbal fluency, both phonemic and semantic fluency tasks showed reduced performance in CHR individuals, as noted in studies by Lee et al.39, Hedges et al.42, and Zhang et al.40

As for the severity of neurocognitive deficits, Barbato et al.43 reported milder impairments in attention and working memory compared to the more severe deficits observed by Tor et al.41.

In summary, the findings converge to suggest that CHR individuals exhibit widespread deficits in neurocognitive functioning, particularly in verbal and visual memory, processing speed, executive functions, and verbal fluency, with their performance lying intermediate between HCs and individuals with FEP.

Differences between CHR-T and CHR-NT

Significant neurocognitive differences between CHR-T and CHR-NT individuals were observed across studies. Verbal memory was consistently identified as a domain where CHR-T individuals performed worse at baseline. Tests like the HVLT-R and CVLT showed that CHR-T individuals had lower immediate and delayed recall scores compared to CHR-NT39,40,45. Similarly, deficits in executive functions, particularly in cognitive flexibility and problem-solving, were noted, with higher perseverative errors on the WCST and slower performance on the TMT-B42-44.

Processing speed also emerged as a key distinguishing factor, with CHR-T individuals showing poorer performance on tests like the DSST and TMT-A compared to CHR-NT41,42. Studies highlighted that these deficits were present even before the onset of psychosis, suggesting their potential role as early markers of transition40,43.

Working memory impairments were another domain of divergence. CHR-T individuals scored lower on tasks such as the Digit Span Backward and N-back, indicating difficulties in maintaining and manipulating information41,43,45.

Longitudinally, decline in cognitive performance was observed primarily in CHR-T individuals. Studies documented worsening in verbal memory, processing speed, and executive functions over time in this group. Woodberry et al.38 reported significant decline in verbal learning and memory, while Zhang et al.40 highlighted progressive impairments in processing speed performance. This decline has not been shown in CHR-NT individuals, whose cognitive performance tended to remain stable or even improve42,43.

Overall, CHR-T individuals exhibited more pronounced baseline deficits and specific longitudinal declines in neurocognitive domains as compared to CHR-NT, highlighting the predictive value of these impairments for psychosis transition.

Relationships between neurocognition, symptoms, and functioning

The relationship between neurocognitive performance, symptom severity, and functional outcomes was a central focus in 10 out 17 studies. Verbal memory deficits were closely linked to higher levels of APS, with tests like HVLT-R and CVLT showing significant associations between poorer memory and more severe clinical presentations43,44. Executive function impairments, measured through tasks like WCST and TMT-B, were similarly associated with worse social and role functioning40,42.

Negative symptoms, such as reduced motivation and social withdrawal, appeared to amplify the impact of cognitive deficits on functional outcomes. Tor et al.41 found that decline in processing speed and working memory was strongly correlated with worsening negative symptoms. Similarly, Hedges et al.42 reported that impairments in verbal memory and processing speed were linked to reduced occupational functioning, even after controlling for positive symptoms.

Cognitive improvements in CHR-NT individuals were often accompanied by reductions in symptom severity. Jahshan et al.46 observed correlations between improvements in positive symptoms (SIPS Positive) and better global cognition.

Conversely, impairment of neurocognitive performance in CHR-T subjects appeared to be associated with symptom progression and functional impairment. Zhang et al.40 reported that worsening in verbal memory and executive functions corresponded to increased symptom severity and social impairment over time.

In summary, neurocognitive performance plays a central role in shaping both clinical symptoms and functional outcomes in CHR individuals. While improvements are possible in CHR-NT, the progressive decline observed in CHR-T highlights the importance of early intervention targeting cognitive and clinical domains.

Longitudinal trajectories of neurocognitive performance

Longitudinal studies, with follow-up periods ranging from 6 to 157 months, investigating the trajectories of neurocognitive performance in CHR individuals, revealed distinct patterns of stability, improvement, or decline. Some studies suggested that CHR individuals as a group might experience overall stability, with variability depending on transition status. Metzler et al.47 found that CHR individuals, including both converters and non-converters, generally improved in verbal memory and processing speed over 12 months.

Impairments in cognitive performance have been observed primarily in CHR-T individuals, with significant worsening in key domains such as verbal memory, processing speed, and executive functions over time. For instance, Woodberry et al.38 reported significant declines in verbal learning and memory among converters over a one-year follow-up; Zhang et al.40 highlighted progressive impairments in processing speed, verbal learning and executive functions, while Tor et al.41 observed reductions in processing speed and working memory.

These reductions of neurocognitive performance have not been shown in CHR-NT individuals, typically demonstrating stable or improving cognitive performance over time. Barbato et al.43 reported significant gains in attention (CPT), processing speed (TMT-A), and executive functions (WCST) after six months, while verbal memory and fluency remained stable.

In summary, the longitudinal data highlight that CHR-NT individuals often stabilize or improve cognitively, while CHR-T individuals experience progressive declines, particularly in verbal memory, executive functions, and processing speed.

DISCUSSION

For the purpose of our paper, we had four aims.

First, as for the comparison between CHR individuals and HCs, this review confirms that individuals at CHR for psychosis exhibit widespread neurocognitive impairments across several domains when compared to HCs. The most consistently affected domains include verbal memory, processing speed, executive functions, and verbal fluency, with CHR individuals performing at an intermediate level between HCs and those with FEP. These findings align with established literature identifying neurocognitive deficits as a hallmark of psychosis risk1,2. Specifically, verbal memory deficits, assessed through tasks like the HVLT-R and CVLT, were among the most robust markers, observed across multiple studies. Processing speed, measured via the TMT-A and WAIS-Digit Symbol, emerged as another highly affected domain, with impairments consistently reported in CHR groups compared to HCs.

Regarding the issue of the difference between CHR-T and CHR-NT individuals, this review highlights key differences in neurocognitive performance. CHR-T individuals not only exhibited greater baseline impairments in verbal memory, processing speed, and executive functions but also experienced progressive declines in these domains over time. For instance, longitudinal studies revealed worsening CVLT performance in CHR-T, whereas CHR-NT individuals demonstrated cognitive stability or even improvement, particularly in attention and processing speed40,42,43. These findings underscore the prognostic value of neurocognitive performance and support the neurodevelopmental model of psychosis, which posits that cognitive deterioration reflects ongoing neurobiological changes preceding illness onset2.

We explored the relationship between neurocognitive performance, clinical symptoms, and functional outcomes to better understand the interplay between these factors. Deficits in verbal memory and executive functions were closely linked to greater severity of APS and poorer functional outcomes, consistent with previous findings emphasizing the bidirectional relationship between cognitive and clinical trajectories1,44. This interaction may reflect underlying neurobiological mechanisms, whereby cognitive impairments exacerbate the functional burden of symptoms, creating a feedback loop that accelerates clinical deterioration. Conversely, improvements in neurocognitive performance among CHR-NT individuals were frequently associated with reductions in symptom severity, further underscoring the dynamic interplay between cognition and clinical outcomes.

Lastly, we analyzed longitudinal trajectories of neurocognitive changes to assess patterns of stability, improvement, or decline over time in CHR populations. While cognitive performance remained stable or even improved in CHR-NT individuals, CHR-T individuals experienced significant reductions in verbal memory, processing speed, and executive functions over time. Interestingly, the present findings contrast with those of Bora and Murray’s2 systematic review and meta-analysis, which highlighted a general stability of cognitive deficits in CHR individuals over time. One notable difference lies in the domain of verbal fluency: while Bora and Murray2 reported more pronounced improvements in verbal fluency among HCs compared to CHR individuals, our review found that verbal fluency deficits persisted, particularly in CHR-T individuals. This discrepancy may stem from methodological differences. Specifically, only 5 out of the 25 studies included in Bora and Murray’s analysis examined cognitive performance separately in CHR-T and CHR-NT individuals. By not distinguishing between these subgroups, the inclusion of CHR-NT participants—who often demonstrate cognitive stability or improvement—may have influenced their findings and obscured the more pronounced declines observed in CHR-T individuals. Additionally, Bora and Murray2 aggregated task-level performance into global domain scores, which could further mask nuanced trajectories in specific cognitive functions.

In summary, the findings of this review reinforce the centrality of neurocognition in understanding psychosis risk. They emphasize the heterogeneity of trajectories among CHR individuals, with CHR-T and CHR-NT following distinct cognitive paths. Moreover, the alignment and divergence with prior meta-analytic data highlight the need for further longitudinal studies to disentangle the complex relationships between neurocognition, clinical symptoms, and functional outcomes in this population.

Clinical implications

The different cognitive trajectories observed between CHR-T and CHR-NT individuals have significant implications for both understanding psychosis and clinical practice. The impairments observed in verbal memory, processing speed, and executive functions in CHR-T provide strong support for models emphasizing progressive neurobiological deterioration during the prodromal phase. These findings align with evidence suggesting that processes such as synaptic pruning, neurobiological inflammation, or other neurodevelopmental changes may underlie the cognitive decline associated with the transition to psychosis2. In contrast, the stability or improvement observed in CHR-NT may reflect resilience mechanisms, potentially mediated by neuroplasticity or adaptive compensatory processes.

Clinically, these findings underline the importance of integrating neurocognitive assessments into CHR monitoring protocols. Verbal memory and processing speed, in particular, have emerged as robust markers of psychosis risk and could be used to stratify individuals based on their likelihood of transitioning.

Additionally, the relationship between cognitive improvements and symptom reduction suggests that cognitive remediation therapies could be promising for CHR populations, particularly interventions targeting deficits in verbal memory and executive functions. These approaches could be integrated with psychosocial interventions to promote functional recovery and reduce the symptom burden.

Finally, the persistence of cognitive deficits in CHR-NT individuals highlights the importance of long-term follow-up and continuous support. While these individuals may not transition to psychosis, their cognitive deficits may still have significant implications for academic, occupational, and social functioning. Interventions targeting these deficits could therefore be crucial in promoting recovery and improving quality of life in this subgroup

Strengths and limitations

This review has some strengths: first, the inclusion of studies that examine both baseline deficits and longitudinal changes, providing a comprehensive overview of neurocognitive trajectories in CHR individuals; second, the selection of studies that employed validated scales, such as CAARMS5 and SIPS6, ensures a rigorous identification of CHR populations; third, the focus on multiple cognitive domains, including verbal memory, processing speed, executive functions, and verbal fluency, allows for a detailed understanding of specific deficits and their predictive value for psychosis transition.

In spite of these strengths, some limitations should be acknowledged. First, the review was conducted on a single database; second, the heterogeneity of CHR populations, including sample sizes and follow-up durations, may have contributed to variability in the findings. Furthermore, the relatively small number of longitudinal studies, particularly those with extended follow-up periods, limits the ability to fully capture progressive or improving cognitive trajectories. While cross-sectional comparisons provide valuable insights, they cannot comprehensively depict the dynamic nature of neurocognitive changes. Additionally, most studies did not control for potential confounding factors such as socioeconomic status or comorbid conditions, which may influence cognitive outcomes. These limitations highlight the need for more standardized methodologies and larger, more diverse samples in future research.

Future directions

Future research should address three key areas to enhance the understanding and management of psychosis risk in CHR individuals. First, longitudinal studies with extended follow-up periods are needed to clarify long-term cognitive trajectories. These should include monitoring cognitive decline in CHR-T, particularly after transitioning to psychosis, as well as analyzing improvements in CHR-NT, which could provide valuable insights into resilience mechanisms.

Second, it is essential to further investigate the effectiveness of targeted interventions, such as cognitive remediation therapies and pharmacological approaches, in improving specific cognitive performances and reducing psychosis risk. Future studies should focus on identifying optimized interventions tailored to particular cognitive domains or population subgroups, thereby contributing to the development of personalized treatment strategies.

Finally, greater integration of data from multimodal markers, including neuroimaging, genetic profiles, and neurocognitive assessments, could enhance the accuracy of risk prediction models. Neuroimaging techniques, such as functional MRI (fMRI) and diffusion tensor imaging (DTI), may serve as complementary tools to enrich our understanding of the brain changes associated with cognitive decline and clinical progression.

CONCLUSIONS

This review points to the central role of neurocognitive disorders in understanding the risk of psychosis. CHR individuals exhibit diffuse neurocognitive deficits, with verbal memory, processing speed, and executive functions emerging as critical domains. While CHR-NT individuals often demonstrate cognitive stability or improvement, CHR-T individuals follow a trajectory of progressive decline, underscoring the need for early identification and intervention. These findings highlight the importance of integrating neurocognitive assessments into clinical protocols and the application of more targeted preventive interventions.

Conflict of interest statement

The authors declare no conflict of interest.

Funding

None.

Authors contributions

A.C.: methodology, investigation, writing - original draft; C.M.: methodology, investigation, validation, writing-review and editing, supervision; C.B.: conceptualization, validation, writing-review and editing, supervision; P.R.: conceptualization, validation, writing-review and editing, supervision.

Figures and tables

FIGURE 1. Flowchart showing the study selection procedure.

Neurocognitive Domains Tasks
Processing speed Trail Making Test A (TMT-A)Brief Assessment of Cognition Scale (BACS) symbol codingSemantic fluencyLetter fluency
Executive functioning Trail Making Test B (TMT-B)
Working memory WAIS I/R/III digit span
Attention/vigilance Continuous Performance Task - Identical Pairs I/II (CPT-IP)
Verbal learning and memory Rey Auditory Verbal Learning Test (RAVLT)Hopkins Verbal Learning Test-Revised (HVLT-R)California Verbal Learning Test I/II (CVLT)
Visuospatial ability Wechsler Adult Intelligence Scale R/III (WAIS) block design
TABLE I. Neurocognitive domains and individual tasks.
Study Sample Sample size, N FUP (mo) CHR assessment Tasks analysed
HC CHR CHR-NT CHR-T
Wood et al. (2007) 49 Personal Assessment and Crisis Evaluation Clinic, Australia 17 16 9 7 12 SIPS TMT-A, letter fluency, WAIS-R block design, TMT-B, WAIS-R digit span
Becker et al. (2010) 46 Academic Medical Centre, The Netherlands 17 41 24 17 18 SIPS Semantic fluency, letter fluency, CVLT
Jahsan et al. (2010) 47 Cognitive Assessment and Risk Evaluation, USA 29 46 - - 36 SIPS WAIS-III block design
Barbato et al. (2013) 43 PREDICT Study, USA - - 72 9 6 SIPS TMT-A, semantic fluency, CPT-IP, RAVLT, TMT-B
Woodberry et al. (2013) 38 FACT Study, USA 32 53 43 10 12 SIPS CPT-IP-II, CVLT-II, TMT-B
Lee et al. (2014) 39 Seoul Youth Clinic, South Korea - - 61 14 24 SIPS TMT-A, semantic fluency, letter fluency, K-CVLT, TMT-B, WAIS-K digit span
Metzler et al. (2015) 48 ZInEP, Switzerland 60 12 - - 12 SIPS TMT-A, semantic fluency, letter fluency, RAVLT, TMT-B, WAIS digit span
Liu et al. (2015) 49 SOPRES Study, Taiwan 137 53 35 18 12 SIPS TMT-A, semantic fluency, WAIS-III block design, TMT-B, WAIS-III digit span
Shin et al. (2016) 50 Seoul Youth Clinic, South Korea 28 47 - - 24 SIPS TMT-A, semantic fluency, letter fluency, TMT-B, WAIS-K digit span
Lam et al. (2018) 51 Longitudinal Youth At-Risk Study, Singapore 384 173 156 17 24 CAARMS Semantic fluency, BACS symbol coding, semantic fluency, CPT-IP
Addington et al. (2019) 13 North American Prodrome Longitudinal Study 2, USA 143 366 278 88 24 SIPS TMT-A, BACS symbol coding
Allott et al. (2019) 12 Personal Assessment and Crisis Evaluation Clinic 1994-2000, Australia 49 31 - - 157 SIPS TMT-A, RAVLT, TMT-B, WAIS-R digit span
Fujioka et al. (2020) 52 IN-STEP Study, Japan 21 3 - - 37 SIPS BACS-J symbol coding, semantic fluency, letter fluency
Hedges et al. (2022) 42 EU-GEI High Risk study 60 316 256 60 36 CAARMS WAIS-III, RAVLT, letter fluency, semantic fluency
Carrion et al. (2024) 44 NAPLS, USA 278 345 - - 24 SIPS TMT-A, BACS symbol coding, CPT-IP, WMS- Spatial Span, Letter-number Span, HVLT
Tor et al. (2024) 41 The Child and Adolescent Psychosis Risk Syndrome study, Spain 76 98 74 24 18 SIPS WISC-IV, WAIS-III, WMS-III, TMT-A, CPT-IP, WCST, TMT-B
Zang et al., (2024) 40 Shanghai At Risk for Psychosis extended program, China 774 794 447 114 24 SIPS TMT-A, BACS symbol coding, semantic fluency, CPT-IP, WMS-IIISpatial Span, HVLT-R
HC Healthy controls; CHR Clinical high-risk; FUP follow-up period; SIPS Structured Interview for Prodromal Syndromes; CAARMS Comprehensive Assessment of At-Risk Mental States; TMT Trail making test; WAIS Weschler Adult Intelligence Scale; D-KEFS Delis-Kaplan Executive Function System; CVLT California Verbal Learning Test; CPT-IP Continuous Performance Test – Identical Pairs; HVLT-R Hopkins Verbal Learning Test-Revised; RAVLT Rey Auditory Verbal Learning Test; BACS Brief Assessment of Cognition Scale.
TABLE II. Dataset: characteristics of included studies.

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Anna Carluccio - Department of Neuroscience Rita Levi Montalcini, University of Turin, Turin, Italy

Cristiana Montemagni - Department of Neuroscience Rita Levi Montalcini, University of Turin, Turin, Italy

Claudio Brasso - Department of Neuroscience Rita Levi Montalcini, University of Turin, Turin, Italy

Paola Rocca - Department of Neuroscience Rita Levi Montalcini, University of Turin, Turin, Italy

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Carluccio, A., Montemagni, C. ., Brasso, C., & Rocca, P. (2025). Neurocognitive deficits and trajectories in individuals at clinical high risk for psychosis. Italian Journal of Psychiatry, 11(2). https://doi.org/10.36180/2421-4469-2025-864
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