Cognitive impairment (CI) is one of the most prevalent and burdensome consequences of COVID-19 infection, which can persist up to months or even years after remission of the infection. Current guidelines on post-COVID CI are based on available knowledge on treatments used for improving CI in other conditions. The current review aims to provide an updated overview of the existing evidence on the efficacy of treatments for post-COVID CI.

A systematic literature search was conducted for studies published up to December 2023 using three databases (PubMed–Scopus–ProQuest). Controlled and noncontrolled trials, cohort studies, case series, and reports testing interventions on subjects with CI following COVID-19 infection were included.

After screening 7790 articles, 29 studies were included. Multidisciplinary approaches, particularly those combining cognitive remediation interventions, physical exercise, and dietary and sleep support, may improve CI and address the different needs of individuals with post-COVID-19 condition. Cognitive remediation interventions can provide a safe, cost-effective option and may be tailored to deficits in specific cognitive domains. Noninvasive brain stimulation techniques and hyperbaric oxygen therapy showed mixed and preliminary results. Evidence for other interventions, including pharmacological ones, remains sparse. Challenges in interpreting existing evidence include heterogeneity in study designs, assessment tools, and recruitment criteria; lack of long-term follow-up; and under-characterization of samples in relation to confounding factors.

Further research, grounded on shared definitions of the post-COVID condition and on the accurate assessment of COVID-related CI, in well-defined study samples and with longer follow-ups, is crucial to address this significant unmet need.

The potential involvement of the immune and inflammatory systems has been extensively studied in mood disorders (MDs). Despite these findings and despite the fact that the pathogenetic role of altered immunologic and metabolic profiles in MDs is being confirmed in many current studies, there is still a lack of consensus about it, due to controversial results.

The present study aimed to appraise peripheral metabolic parameters (blood glucose, lipoproteins, triglycerides, uric acid, blood urea nitroge [BUN], transaminases and others9 and plasma/serum levels of essential nutrients (vitamin D, B12, folate and homocysteine) in a group of inpatients affected by MDs, as compared with healthy controls.

Methods. Ten ml of venous blood was drawn from fasting subjects. The metabolic parameters and vitamins were measured according to common clinical-chemistry methods.Comparisons for continuous variables were performed by the Student’s t-test for variables that follow a normal distribution, and by the Wilcoxon-Mann-Whitney test for variables not normally distributed. The correlations between biological markers were explored by calculating the Pearson’s correlation coefficient or Spearman rank correlation.

Most patients showed loer circulating vitamin D levels, in respect to both control subjects (P< .0001) and the normative cut-off values. This finding was paralleled by increased serum homocysteine concentrations i (P<.0001), indicating an imbalance in their methionine metabolism. Homocysteine levels were negatively correlated with vitamin D, vitamin B12 and folate in control subjects, but not in patients. In addition, patients displayed higher blood glucose and lower BUN than controls, indicating an impaired protein-to-carbohydrate metabolism and/or altered nutritional/dietary status.

We provide herein further support to the notion that MD patients are a population where vitamin deficits, dysmetabolism and/or dietary defects are common feature, and, s such, they might be more vulnerable to a variety of somatic illnesses than the general population. This cross-sectional investigation, albeit preliminary, might contribute to improve the characterization and the monitoring of the clinical status of mood disorder patients, as well as to identify new molecular targets for more tailored treatments ad of more pointed health-care intervention,

None Declared

This work aims to provide an updated overview of the eating disorders (EDs) which are a widespread pathology nowadays. Informations related to the clinical-nosographic characteristics, an in-depth analysis about systemic-relational theories and historical evolution are provided. In addition, current informations about epidemiological data, recovery, treatment related implications, new neuroscientific theories and risk factors are shown. Given the complexity of these disorders, the lack of resources and the the increasing demands for treatment, the main object is related to the construction of a questionnaire to manage the waiting lists.

Building a waiting list management model for EDs, Study and compare advantages and disadvantages of the source allocation ethical models (utilitarianism, prioritarianism, egalitarianism), Analyze EDs leading experts (doctors, dietitians, psychologists, psychiatrists) and EDs patients positioning with respect to priority treatment factors. Promote constructive dialog between EDs experts from different backgrounds and EDs patients.

In order to know the various treatment alternatives available, the different levels and reference structures are illustrated. In addition, it is also suggested different reasoning based on the ethical models of egalitarianism, utilitarianism and prioritarianism in order to build a waiting list management model, which is the maximum goal of this work. This model needs to be supported by a series of validated tools such as the clinical interview and self-administered questionnaires to investigate psychopathological aspects and psychiatric symptoms. Going into more details, a questionnaire is proposed to the EDs leading experts, so that they can provide their own priority factors list and related thoughts in order to build “the most ethical” waiting list.

It is expected that both patients and clinicians tend to give priority to patients with greater psychophysical severity, not exclusively on the basis of physical parameters. Further hypothesis related to clinicians lead us believe that they tend to use utilitarian logics, in compliance with the demonstrated efficacy of early intervention. An evaluation that could lead to a disagreement between experts and patients is related to prioritize patients in the initial phase of the disease, which could be supported by clinicians, but not by patients, probably in connection with their personal experiences. In fact, this favoritism could have a negative impact on the care of the most serious cases who risk to be left to themselves.

This work aims to encourage a constructive dialogue between experts and patients with EDs in order to build a functional intervention model which should be “the most ethical as possible” in order to save the greatest number of lives in respect of mental suffering.

None Declared

The conceptualization of negative symptoms (NS) in schizophrenia is still controversial. Recent confirmatory factor-analytic studies suggested that the bi-dimensional model (motivational deficit [MAP] and expressive deficit [EXP]) may not capture the complexity of NS structure, which could be better defined by a five-factor (five NS domains) or a hierarchical model (five NS domains as first-order factors, and MAP and EXP, as second-order factors). A validation of these models is needed to define the structure of NS. To evaluate the validity and temporal stability of the five-factor or the hierarchical structure of the brief negative symptom scale (BNSS) in individuals with schizophrenia (SCZ), exploring associations between these models with cognition, social cognition, functional capacity, and functioning at baseline and at 4 years follow-up.

Clinical variables were assessed using state-of-the-art tools in 612 SCZ at two-time points. The validity of the five-factor and the hierarchical models was analyzed through structural equation models.

The two models had both a good fit and showed a similar pattern of associations with external validators at the two-time points, with minor variations. The five-factor solution had a slightly better fit. The associations with external validators favored the five-factor structure.

Our findings suggest that both five-factor and hierarchical models provide a valid conceptualization of NS in relation to external variables and that five-factor solution provides the best balance between parsimony and granularity to summarize the BNSS structure. This finding has important implications for the study of pathophysiological mechanisms and the development of new treatments.

Diagnostic criteria are not always useful to discriminate major depression with anxious distress (ADS-D; Diagnostic and Statistical Manual for Mental Disorders, version-5 [DSM-5] criteria) from mixed depression (Koukopoulos’ criteria; KMX-D). So, clinicians need alternative tools to improve their diagnostic ability and to choose the most appropriate treatment. The aim of the present study is to identify socio-demographic and clinical features that discriminate patients with ADS-D from those with KMX-D.

Two hundred and forty-one consecutive outpatients with unipolar (51%) and bipolar (49%) disorder, fulfilling DSM-5 criteria for a current major depressive episode (MDE) and with a 21-item Hamilton Depression Rating Scale score ≥ 14, were recruited and treated in a prospective observational study.

Ten percent of patients met criteria for KMX-D, 22% ADS-D, and 37% for both. Irritable premorbid temperament, mixed depression polarity at onset, mixed depression recurrence, and a high number of mania symptoms at intake were typical features of patients with KMX-D. Depressive polarity at onset, a low number of mania symptoms at intake, and generalized anxiety disorder comorbidity were typical features of patients with ADS-D. Multinomial logistic regression confirmed that higher rate of irritable temperament and higher Young Mania Rating Scale total score differentiated patients with KMX-D from patients with pure MDE.

Our findings suggest some clinical features that could help differentiate between ADS-D and KMX-D in patients meeting both conditions and to select the appropriate treatment. However, the small sample size may have limited the power to detect differences between the groups. Further research is needed to confirm the results of present study.

The structure of negative symptoms of schizophrenia is still a matter of controversy. Although a two-dimensional model (comprising the expressive deficit dimension and the motivation and pleasure dimension) has gained a large consensus, it has been questioned by recent investigations.

To investigate the latent structure of negative symptoms and its stability over time in people with schizophrenia using network analysis.

Negative symptoms were assessed in 612 people with schizophrenia using the Brief Negative Symptom Scale (BNSS) at baseline and at 4-year follow-up. A network invariance analysis was conducted to investigate changes in the network structure and strength of connections between the two time points.

The network analysis carried out at baseline and follow-up, supported by community detection analysis, indicated that the BNSS's items aggregate to form four or five distinct domains (avolition/asociality, anhedonia, blunted affect and alogia). The network invariance test indicated that the network structure remained unchanged over time (network invariance test score 0.13; P = 0.169), although its overall strength decreased (6.28 at baseline, 5.79 at follow-up; global strength invariance test score 0.48; P = 0.016).

The results lend support to a four- or five-factor model of negative symptoms and indicate overall stability over time. These data have implications for the study of pathophysiological mechanisms and the development of targeted treatments for negative symptoms.

Negative symptoms represent a fundamental aspect of schizophrenia: they have a substantial impact on patients’ real-life functioning and do not respond satisfactorily to currently available treatments. Therefore, a better understanding of the pathophysiological mechanisms underlying these symptoms could favor the development of new treatments.

To date, the most validated pathophysiological hypothesis indicates an association between the Motivational domain (consisting of avolition, anhedonia and asociality) and alterations in the neuronal circuits involved in motivation. The Expressive Deficit domain (consisting of blunted affect and alogia) would be subtended by widespread alterations of cortical connectivity and associated with impaired neurocognition, social cognition, and the presence of neurological soft signs.

The aim of the present study is to examine the neurobiological correlates of the two domains of negative symptoms, starting from the brain areas that have been most commonly found in the literature to be associated with negative symptoms.

Resting-state (rs) fMRI data were acquired in 62 subjects with schizophrenia (SZ) and 46 healthy controls (HC). The two negative symptom domains were assessed using the Brief Negative Symptom Scale. In addition, the following assessment tools were used: the Positive and Negative Syndrome Scale for the assessment of positive symptoms and disorganization, the Calgary Depression Scale for Schizophrenia for depression and the St. Hans Rating Scale for extrapyramidal symptoms. The study of the possible relationships between rs-brain activity and the negative symptoms domains was conducted through partial correlations, checking for possible confounding factors (positive, depressive, extrapyramidal symptoms and disorganization).

The SZ, compared to the HC, showed higher rs-brain activity of the right inferior parietal lobule and of the right temporoparietal junction and lower rs-brain activity of the right dorsolateral prefrontal cortex, bilateral anterior dorsal cingulate cortex, bilateral ventral caudate and bilateral dorsal caudate. Furthermore, in the group of patients, the rs-brain activity of the left ventral caudate showed a moderate negative correlation with the Expressive deficit domain (r = -0.401; p = 0.003), but not with the Motivational domain.

The results of the present study, in line with the literature, demonstrated how the two domains of negative symptomatology are subtended by different pathophysiological mechanisms. Given the role played by the ventral caudate in neurocognitive processes, these results are in line with the hypothesis that Expressive deficit may have a common etiopathogenesis with cognitive deficits. A better understanding of the neurobiology of negative symptoms could foster the development of innovative treatment strategies targeting the two negative symptom domains.

None Declared

Negative symptoms (NS) represent a heterogeneous construct of schizophrenia, whose conceptualization is still to be clarified. In the last decade, the conceptualization model that has received the most support from the literature has described 2 NS domains: the expressive deficit (EXP), which includes blunted affect and alogia, and the motivational deficit (MAP), which includes avolition, asociality, and anhedonia. However, different confirmatory factor-analytic studies suggest that the bi-dimensional model may not capture the complexity of this construct, which could be better defined by a 5-factor model (5 individual negative symptoms) or a hierarchical model (5 individual negative symptoms as first-order factors, and the 2 domains, MAP and EXP domains, as second-order factors). However, to our knowledge, no study has investigated associations between negative symptom models with social cognition and functional capacity, which are largely documented to correlate with negative symptoms, nor the associations with external validators over time, looking at the potential stability of negative symptom models validity through the course of the illness.

In the light of this observations, we investigated, the external validity of the five-factor model and the hierarchical model of the BNSS in subjects with schizophrenia, looking at associations with cognition, social cognition, functioning and functional capacity at baseline and at four years follow-up.

NS were assessed in 612 subjects with schizophrenia using the Brief Negative Symptom Scale at the baseline and after 4-year follow-up. State of the art assessment instruments were used to assess cognitive and functioning related variables. Structural equation models (SEM) that included the NS models and 4 external variables were used to our aim.

According to recent multicenter studies, our results confirmed the validity of the 5-factor- and the hierarchical-model of negative symptoms. In particular, these 2 models proved to be equivalent in terms of fit to the data at baseline and follow-up. As regard to the relationship of the two BNSS models with external variables, we found that there was a similar pattern of associations at the two time points despite minor variations.

The five factor and the hierarchical models provide an optimal conceptualization of negative symptoms in relation to external variables. The similar pattern of associations with external variables of the two models at the two time points despite minor variations, suggests that the simple and widely used 5-factor solution provides the best balance between parsimony and granularity to summarize BNSS structure. This data is of important relevance with consequent implications in the study of pathophysiological mechanisms and the development of targeted treatments for NS.

None Declared

In recent years the increasing presence of refugees and asylum seekers displaced from their country of origin, determined significant social, economic, humanitarian and public health implications in host nations. Advancing the knowledge on factors contributing to these implications, could foster the implementation of new public-health plans for these population. As a matter of fact, to date, the rates of mental disorders in these population are uncertain due to the high variability of methods used in the studies on topic, and of risk and protective factors analyzed. The most replicated finding is the high prevalence of Post-Traumatic Stress Disorder (PTSD) and depression in refugees and asylum seekers as compared to the population of host countries.

The aim of the present study was to investigate the needs for mental health prevention, care and rehabilitation of adult refugees and asylum seekers in Italy, performing a multidisciplinary evaluation of migrants who were guests in two refugees’ centers in Campania (Salerno and Avellino).

The Mini-International Neuropsychiatric Interview (MINI) was assessed in 303 migrants, in order to evaluate the presence or not of a psychiatric diagnosis. Analysis of variance (ANOVA) was used to investigate differences between migrants with a mental disorder vs migrants without a mental disorder in terms of cognitive functions, depressive and anxiety symptoms, traumatic events and pre-migration risk factors. Person’s correlation was performed to investigate relationships between the Hopkins Symptom Checklist-25 (HSCL-t25) psychopathological index with all the other above-mentioned variables. Logistic regression was used to evaluate factors associated to the presence of a current mental disorder.

At least one mental disorder was found in 90 subjects (29.7% of the sample). Most prevalent diagnoses were major depressive disorder, lifetime panic disorder, PTSD, and generalized anxiety disorder. People with at least one psychiatric illness showed impaired global (F=6.62; p=.011) and social (F=8.22; p=.004) cognition, higher trauma levels (F=70.59; p<.0001) and more severe anxiety and depressive symptoms (F=61.84; p<.0001) compared to healthy migrants. Only trauma levels significantly correlated with HSCL-t25 psychopathological index. Trauma levels, global cognition, occupation, and migration status were associated to the presence of a current mental disorder.

The results of the present study demonstrated that almost 1/3 of the guests of refugee centers in Campania have a mental disorder. The identification of risk factors associated to the onset of mental disorder and to severity of psychopathology in refugees and asylum seekers, may contribute to plan preventive and early psychiatric care in this population.

None Declared

Negative symptoms (NS) represent an unmet need of treatment in schizophrenia (SCZ). As a result, these symptoms pose a significant burden on patients, their families, and the health care system. In the last decade, the conceptualization model that has received the most support from the literature has described 2 domains of NS: the expressive deficit (EXP), which includes blunted affect and alogia, and the motivational deficit (MAP), which includes avolition, asociality, and anhedonia. However, different confirmatory factor-analytic studies suggest that the bi-dimensional model may not capture the complexity of this construct, which could be better defined by the 5-factor model. To date no study exploiting innovative tools and state of the art assessment instruments has yet been conducted to evaluate the NS structure stability over time.

The aim of this study was to investigate the stability of the latent structure of NS in subjects with SCZ.

NS were assessed in 612 subjects with SCZ using the Brief Negative Symptom Scale (BNSS) at the baseline and after 4-year follow-up. A network invariance analysis was conducted for the data collected longitudinally.

Results showed that the BNSS’ items aggregated to form 5 distinct domains (avolition, asociality, blunted affect, alogia and anhedonia). The result of the network invariance test indicated that the network structure remained unchanged over time (network invariance test = 0.13; p = 0.169) while its overall strength decreased significantly (6.28 baseline, 5.79 at follow-up; global strength invariance test = 0.48; p = 0.016).

The results of this study show how the construct of NS can be better explained by the 5 individual negative symptoms and that this model is almost stable over time. Therefore the 2-dimensional model may be insufficient to describe the characteristics of NS. This data is of important relevance with consequent implications in the study of pathophysiological mechanisms and the development of targeted treatments for NS.

None Declared

In patients with schizophrenia, numerous studies have shown a relationship between negative symptoms and cognitive deficits (both neurocognition and social cognition deficits) and a similar impact of these domains on different clinical features such as onset, course and prognostic relevance. However, this relationship is still today subject of scientific debate.

The aim of the present study is to conduct a systematic review of the literature on data concerning the relationships between neurocognition and social cognition deficits and the two different domains of negative symptoms ̶ avolition-apathy and expressive deficit.

A systematic review of the literature was carried out following PRISMA guidelines and examining articles in English published in the last fifteen years (2007 - March 2022) using three different databases (Pubmed, Scopus and PsychINFO). The included studies involved subjects with one of the following diagnoses: high risk of psychosis, first episode of psychosis, or chronic schizophrenia. Other inclusion criteria of the reviewed studies included: evaluation of at least one neurocognitive or social cognition domain and at least one negative symptom using standardized scales; analysis of the relationship between at least one neurocognitive or social cognition domain and a negative symptom.

Databases search produced 8497 results. After title and abstract screening, 395 articles were selected, of which 103 met inclusion criteria. The analysis of retrieved data is still ongoing. Preliminary evidence highlighted: a correlation between social cognition and negative symptoms, in particular with the “expressive deficit” domain; a positive correlation between the severity of negative symptoms and that of neurocognitive deficits (in particular with the “processing speed” domain); an association of verbal working memory deficits with alogia and anhedonia.

The study of the relationship between negative symptoms, neurocognitive deficits and social cognition could contribute to the understanding of the aetiology of psychotic disorders and therefore to the identification of therapies for the improvement of overall functioning and quality of life. The studies analysed so far show some interesting associations between cognition and negative symptoms, but the presence of often inconsistent results, partially attributable to the different conceptualizations of the various domains of negative symptoms adopted, hinders the generalization of the results.

None Declared

After coronavirus disease 2019 (COVID-19) infection, many individuals reported neurological and psychiatric sequelae, including cognitive impairment, even several months after the acute infection.

The present study aims to provide a critical overview of the literature on the relationships between post-acute COVID-19 infection and cognitive impairment, highlighting limitations and confounding factors.

A systematic search of articles published from January 1st, 2020, to July 1st, 2022 was performed in Pubmed/Medline. We followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.

Only studies using validated instruments for the assessment of cognitive impairment were included. Out of 5478 screened records, 72 studies met inclusion criteria. Time of patients’ assessment varied from 4 weeks to 12 months after the infection. The available evidence revealed the presence of impairment in executive functions, attention and memory in subjects recovered from COVID-19. However, several limitations of the literature reviewed should be highlighted: most studies were performed on small samples, not stratified by severity of disease and age, used a cross-sectional or a short-term longitudinal design, and provided a limited assessment of the different cognitive domains. Few studies investigated neurobiological correlates of cognitive deficits in individuals recovered from COVID-19.

Based on the literature reviewed, it is difficult, to date, to draw conclusions about the relationships between COVID-19 infection and cognitive impairment. Therefore, further studies with an adequate methodological design are needed in order to better understand these relationships, identify neurobiological correlates of COVID-related cognitive deficits and evaluate their course over time. Enhancing the knowledge on this topic could favor the development of effective therapeutic strategies for cognitive deficits in individuals recovered from COVID-19.

None Declared

The neurobiological underpinnings of negative symptoms in schizophrenia remain unclear. Previous studies have revealed that in schizophrenia, the anticipatory component of the hedonic experience (anticipatory anhedonia, failure to anticipate reward or pleasurable experiences) is more markedly impaired than the consummatory aspect of pleasure (consummatory anhedonia, in the moment experience of pleasure during pleasurable situations). Several neuroimaging focused on reward prediction deficit have shown dysfunctions in the neuronal circuits that sustain these processes in patients, but findings have not been consistent.

The current study aimed at investigating the impairment of reward anticipation in subjects with schizophrenia (SCZ) during the “Monetary Incentive Delay task” (MID task), employing the topographic analysis of event-related potentials (ERPs) with EEG recordings. Furthermore, the associations with negative symptoms and anticipatory and consummatory hedonic experience were investigated.

EEG data were recorded in thirty SCZ and twenty-three matched HC, during the MID task in which reward and loss cues (incentive cues of positive and negative value) of different magnitude, as well as neutral cues were presented. Anticipation and experience of pleasure were measured by the Temporal Experience of Pleasure Scale (TEPS), while negative symptom dimensions by the Schedule for the Deficit Syndrome (SDS). For the EEG data analysis, the topographic analysis of variance (TANOVA) that uses the global field power of difference maps was used to evaluate between-group differences in scalp topography. Correlation analyses between hedonic experience, negative symptoms and ERPs were performed.

The TANOVA interaction effect (group x cue) was significant in the time window between 140.6 and 195.3 msec after cue presentation (p<.05). Post-hoc analysis showed that significant differences in topography were observed for the reward condition (p=.0006) but not for the loss one (p=.6732) between SCZ and HC. Finally, a significant correlation (p<.01) between t-maps values obtained in the same time-frame and the anticipation of pleasure scores was detected, while no significant correlations were found with the experience of pleasure scores or the severity negative symptom.

SCZ are unable to integrate the incentive magnitude and reward value of future events in the context of their ongoing task. Topographic abnormalities in ERP could be traced already during early stages of reward processing and were associated with anticipation of pleasure, but not with the experience of pleasure or the avolition, suggesting that these constructs might be partially separate.

None Declared

Different electrophysiological (EEG) indices have been investigated as possible biomarkers of schizophrenia. However, these indices have a very limited use in clinical practice, as their associations with clinical and functional outcomes remain unclear. This study aimed to investigate the associations of multiple EEG markers with clinical variables and functional outcomes in subjects with schizophrenia (SCZs).

Resting-state EEGs (frequency bands and microstates) and auditory event-related potentials (MMN-P3a and N100-P3b) were recorded in 113 SCZs and 57 healthy controls (HCs) at baseline. Illness- and functioning-related variables were assessed both at baseline and at 4-year follow-up in 61 SCZs. We generated a machine-learning classifier for each EEG parameter (frequency bands, microstates, N100-P300 task, and MMN-P3a task) to identify potential markers discriminating SCZs from HCs, and a global classifier. Associations of the classifiers’ decision scores with illness- and functioning-related variables at baseline and follow-up were then investigated.

The global classifier discriminated SCZs from HCs with an accuracy of 75.4% and its decision scores significantly correlated with negative symptoms, depression, neurocognition, and real-life functioning at 4-year follow-up.

These results suggest that a combination of multiple EEG alterations is associated with poor functional outcomes and its clinical and cognitive determinants in SCZs. These findings need replication, possibly looking at different illness stages in order to implement EEG as a possible tool for the prediction of poor functional outcome.

Impairment in a wide range of cognitive abilities has been consistently reported in individuals with schizophrenia. Both neurocognitive and social cognitive deficits are thought to underlie severe functional disabilities associated with schizophrenia. Despite the key role in schizophrenia outcome, cognition is still poorly assessed in both research and clinical settings.

In this guidance paper, we provide a systematic review of the scientific literature and elaborate several recommendations for the assessment of cognitive functions in schizophrenia both in research settings and in real-world clinical practice.

Expert consensus and systematic reviews provided guidance for the optimal assessment of cognitive functions in schizophrenia. Based on the reviewed evidence, we recommend a comprehensive and systematic assessment of neurocognitive and social cognitive domains in schizophrenia, in all phases of the disorder, as well as in subjects at risk to develop psychosis. This European Psychiatric Association guidance recommends not only the use of observer reports but also self-reports and interview-based cognitive assessment tools. The guidance also provides a systematic review of the state of the art of assessment in the first episode of psychosis patients and in individuals at risk for psychosis.

The comprehensive review of the evidence and the recommendations might contribute to advance the field, allowing a better cognitive assessment, and avoiding overlaps with other psychopathological dimensions. The dissemination of this guidance paper may promote the development of shared guidelines concerning the assessment of cognitive functions in schizophrenia, with the purpose to improve the quality of care and to obtain recovery.

Although cognitive impairment is a core symptom of schizophrenia related to poorer outcomes in different functional domains, it still remains a major therapeutic challenge. To date, no comprehensive treatment guidelines for cognitive impairment in schizophrenia are implemented.

The aim of the present guidance paper is to provide a comprehensive meta-review of the current available evidence-based treatments for cognitive impairment in schizophrenia. The guidance is structured into three sections: pharmacological treatment, psychosocial interventions, and somatic treatments.

Based on the reviewed evidence, this European Psychiatric Association guidance recommends an appropriate pharmacological management as a fundamental starting point in the treatment of cognitive impairment in schizophrenia. In particular, second-generation antipsychotics are recommended for their favorable cognitive profile compared to first-generation antipsychotics, although no clear superiority of a single second-generation antipsychotic has currently been found. Anticholinergic and benzodiazepine burdens should be kept to a minimum, considering the negative impact on cognitive functioning. Among psychosocial interventions, cognitive remediation and physical exercise are recommended for the treatment of cognitive impairment in schizophrenia. Noninvasive brain stimulation techniques could be taken into account as add-on therapy.

Overall, there is definitive progress in the field, but further research is needed to develop specific treatments for cognitive impairment in schizophrenia. The dissemination of this guidance paper may promote the development of shared guidelines concerning the treatment of cognitive functions in schizophrenia, with the purpose to improve the quality of care and to achieve recovery in this population.

Honoraria, advisory board, or consulting fees from Angelini, Astra Zeneca, Bristol-Myers Squibb, Gedeon Richter Bulgaria, Innova-Pharma, Janssen Pharmaceuticals, Lundbeck, Otsuka, Pfizer, and Pierre Fabre, for services not related to this abstract