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Background: Adults with schizophrenia experience a range of neurocognitive problems that affect their daily functioning. Evidence for the efficacy of cognitive remediation in schizophrenia has been established, but its implementation in under-resourced community-based settings is less well-studied. In recent years, interventions have also focused on the strategy-learning approach in favor of drill-and-practice. Moreover, there is an increasing recognition to address social cognition and negative symptoms alongside neurocognition. This study attempts to carry out cognitive remediation in a community mental health setting. The Neuropsychological and Educational Approach to Remediation (NEAR) is used as the cognitive remediation intervention. Neurocognitive and social cognitive games will be introduced during the computer-assisted cognitive exercises sessions. In addition, the instructional technique will foster the use of metacognition and cognitive strategies. Moreover, metamotivation training will be the focus of some bridging sessions to enhance motivation to engage in goal-directed learning behaviors. The aims of the study are to 1) investigate the effects of cognitive remediation on neurocognition, social cognition and functional outcomes of participants with schizophrenia/schizoaffective disorders in community mental health settings; and 2) explore the mediators for change (eg: metamotivation, metacognition and negative symptoms) in cognitive performance and functional outcomes. Methods: This randomized controlled trial will be conducted in three Singapore Anglican Community Services (SACS) centers, where standard psychiatric rehabilitation is delivered. Participants who are randomized to the experimental arm will receive cognitive remediation and psychiatric rehabilitation, while those randomized to the control arm will receive standard psychiatric rehabilitation only. Cognitive remediation is carried out three times a week for 12 weeks. It consists of computer-assisted cognitive exercises, as well as bridging groups to aid transfer of learning to daily living. Baseline, post-intervention and eight-week follow-up measurements will be collected. Group by time differences in cognitive performance, negative symptoms, metamotivation, metacognition, functioning and recovery will be analyzed across the three time points. Mediators for improvement in cognitive performance and functioning will also be explored. Discussion: Findings of this research will add to the body of knowledge about the key therapeutic ingredients within a strategy-based cognitive remediation program and improve its implementation within under-resourced community settings. Trial registration: This study has been registered with ClinicalTrials.gov (ID: NCT06286202). Date of registration: 29 February 2024. Date of last update: 21 May 2024. [ABSTRACT FROM AUTHOR]

Abstract Background Adults with schizophrenia experience a range of neurocognitive problems that affect their daily functioning. Evidence for the efficacy of cognitive remediation in schizophrenia has been established, but its implementation in under-resourced community-based settings is less well-studied. In recent years, interventions have also focused on the strategy-learning approach in favor of drill-and-practice. Moreover, there is an increasing recognition to address social cognition and negative symptoms alongside neurocognition. This study attempts to carry out cognitive remediation in a community mental health setting. The Neuropsychological and Educational Approach to Remediation (NEAR) is used as the cognitive remediation intervention. Neurocognitive and social cognitive games will be introduced during the computer-assisted cognitive exercises sessions. In addition, the instructional technique will foster the use of metacognition and cognitive strategies. Moreover, metamotivation training will be the focus of some bridging sessions to enhance motivation to engage in goal-directed learning behaviors. The aims of the study are to 1) investigate the effects of cognitive remediation on neurocognition, social cognition and functional outcomes of participants with schizophrenia/schizoaffective disorders in community mental health settings; and 2) explore the mediators for change (eg: metamotivation, metacognition and negative symptoms) in cognitive performance and functional outcomes. Methods This randomized controlled trial will be conducted in three Singapore Anglican Community Services (SACS) centers, where standard psychiatric rehabilitation is delivered. Participants who are randomized to the experimental arm will receive cognitive remediation and psychiatric rehabilitation, while those randomized to the control arm will receive standard psychiatric rehabilitation only. Cognitive remediation is carried out three times a week for 12 weeks. It consists of computer-assisted cognitive exercises, as well as bridging groups to aid transfer of learning to daily living. Baseline, post-intervention and eight-week follow-up measurements will be collected. Group by time differences in cognitive performance, negative symptoms, metamotivation, metacognition, functioning and recovery will be analyzed across the three time points. Mediators for improvement in cognitive performance and functioning will also be explored. Discussion Findings of this research will add to the body of knowledge about the key therapeutic ingredients within a strategy-based cognitive remediation program and improve its implementation within under-resourced community settings. Trial registration This study has been registered with ClinicalTrials.gov (ID: NCT06286202). Date of registration: 29 February 2024. Date of last update: 21 May 2024.

Abstract Purpose This study proposed and evaluated a theoretical model for exploring the relationships between neurocognition, self-defeatist beliefs, experiential negative symptoms, and social functioning in individuals with chronic schizophrenia. Method The study recruited 229 individuals given a diagnosis of schizophrenia and schizoaffective disorders from outpatient clinics and the day ward of a mental health hospital. After informed consent was obtained, the participants underwent assessments using the backward digit span, the digit symbol, and measures of self-defeatist beliefs, experiential negative symptoms, and social functioning. A structural equation model was applied to assess the fitness of the hypothesized model, with indices such as the goodness-of-fit index, comparative fit index, root mean square error of approximation, and standardized root mean square residual being used for model evaluation. Results The hypothesized model had an adequate fit. The study findings indicated that neurocognition might indirectly influence self-defeatist beliefs through its effect on experiential negative symptoms. Contrary to expectations, the study did not observe a direct influence of neurocognition, self-defeatist beliefs, or negative symptoms on social functioning. The revised model revealed the role of experiential negative symptoms in mediating the association between neurocognition and social functioning. However, self-defeatist beliefs did not significantly affect social functioning. Discussion Before modifying negative thoughts, enhancement of self-awareness ability can help improve negative symptoms and thereby improve the performance of social functions. Future research should develop a hierarchical program of negative symptoms, from cognition rehabilitation to enhancement of self-awareness, and end with modifying maladaptive beliefs.

Purpose: This study proposed and evaluated a theoretical model for exploring the relationships between neurocognition, self-defeatist beliefs, experiential negative symptoms, and social functioning in individuals with chronic schizophrenia. Method: The study recruited 229 individuals given a diagnosis of schizophrenia and schizoaffective disorders from outpatient clinics and the day ward of a mental health hospital. After informed consent was obtained, the participants underwent assessments using the backward digit span, the digit symbol, and measures of self-defeatist beliefs, experiential negative symptoms, and social functioning. A structural equation model was applied to assess the fitness of the hypothesized model, with indices such as the goodness-of-fit index, comparative fit index, root mean square error of approximation, and standardized root mean square residual being used for model evaluation. Results: The hypothesized model had an adequate fit. The study findings indicated that neurocognition might indirectly influence self-defeatist beliefs through its effect on experiential negative symptoms. Contrary to expectations, the study did not observe a direct influence of neurocognition, self-defeatist beliefs, or negative symptoms on social functioning. The revised model revealed the role of experiential negative symptoms in mediating the association between neurocognition and social functioning. However, self-defeatist beliefs did not significantly affect social functioning. Discussion: Before modifying negative thoughts, enhancement of self-awareness ability can help improve negative symptoms and thereby improve the performance of social functions. Future research should develop a hierarchical program of negative symptoms, from cognition rehabilitation to enhancement of self-awareness, and end with modifying maladaptive beliefs. [ABSTRACT FROM AUTHOR]

Abstract Background Few studies have focused on functional impairment in depressed patients during symptomatic remission. The exact relationship between cognitive performance and functional outcomes of patients with Major depressive disorder (MDD) remains unclear. Methods Participants diagnosed with MDD were included and interviewed at both baseline and follow-up. Cognitive function was assessed during acute episodes using the Cambridge Neuropsychological Test Automated Battery (CANTAB), which targeted attention (Rapid Visual Processing - RVP), visual memory (Pattern Recognition Memory - PRM), and executive function (Intra-Extra Dimensional Set Shift - IED). The 17-item Hamilton Depression Scale (HAMD) was used for symptom assessment. Participants were divided into two groups based on their SDSS (Social Disability Screening Schedule) scores, and the differences between their demographic information, HAMD scores, and baseline CANTAB test results were compared. Logistic regression analysis was used to identify cognitive predictors of social function during symptomatic remission. Results According to the SDSS score at follow-up, 103 patients were divided into the normal social function group (n = 81,78.6%) and the poor social function group (n = 22, 21.4%) during clinical remission. Participants with poorer social function performed worse in the visual memory (PRM) and executive function tests (IED) at the baseline. Logistic regression analysis suggested that performance on the PRM (95%CI = 0.31–0.93, p = 0.030) and IED (95%CI = 1.01–1.13, p = 0.014) tests, instead of less severe symptoms, significantly contributed to functional outcomes. Conclusion Better performance in visual memory and executive function during acute episodes may predict better social functional outcomes in individuals with MDD. A potential early intervention to improve social function in individuals with MDD could include the treatments for executive function and visual memory.

Background: Few studies have focused on functional impairment in depressed patients during symptomatic remission. The exact relationship between cognitive performance and functional outcomes of patients with Major depressive disorder (MDD) remains unclear. Methods: Participants diagnosed with MDD were included and interviewed at both baseline and follow-up. Cognitive function was assessed during acute episodes using the Cambridge Neuropsychological Test Automated Battery (CANTAB), which targeted attention (Rapid Visual Processing - RVP), visual memory (Pattern Recognition Memory - PRM), and executive function (Intra-Extra Dimensional Set Shift - IED). The 17-item Hamilton Depression Scale (HAMD) was used for symptom assessment. Participants were divided into two groups based on their SDSS (Social Disability Screening Schedule) scores, and the differences between their demographic information, HAMD scores, and baseline CANTAB test results were compared. Logistic regression analysis was used to identify cognitive predictors of social function during symptomatic remission. Results: According to the SDSS score at follow-up, 103 patients were divided into the normal social function group (n = 81,78.6%) and the poor social function group (n = 22, 21.4%) during clinical remission. Participants with poorer social function performed worse in the visual memory (PRM) and executive function tests (IED) at the baseline. Logistic regression analysis suggested that performance on the PRM (95%CI = 0.31–0.93, p = 0.030) and IED (95%CI = 1.01–1.13, p = 0.014) tests, instead of less severe symptoms, significantly contributed to functional outcomes. Conclusion: Better performance in visual memory and executive function during acute episodes may predict better social functional outcomes in individuals with MDD. A potential early intervention to improve social function in individuals with MDD could include the treatments for executive function and visual memory. [ABSTRACT FROM AUTHOR]

Abstract Background Research on the influence of neurocognitive factors on suicide risk, regardless of the diagnosis, is inconsistent. Recently, suicide risk studies propose applying a trans-diagnostic framework in line with the launch of the Research Domain Criteria Cognitive Systems model. In the present study, we highlight the extent of cognitive impairment using a standardized battery in a psychiatric sample stratified for different degrees of suicidal risk. We also differentiate in our sample various neurocognitive profiles associated with different levels of risk. Materials and methods We divided a sample of 106 subjects into three groups stratified by suicide risk level: Suicide Attempt (SA), Suicidal Ideation (SI), Patient Controls (PC) and Healthy Controls (HC). We conducted a multivariate Analysis of Variance (MANOVA) for each cognitive domain measured through the standardized battery MATRICS Consensus Cognitive Battery (MCCB). Results We found that the group of patients performed worse than the group of healthy controls on most domains; social cognition was impaired in the suicide risk groups compared both to HC and PC. Patients in the SA group performed worse than those in the SI group. Conclusion Social cognition impairment may play a crucial role in suicidality among individuals diagnosed with serious mental illness as it is involved in both SI and SA; noteworthy, it is more compromised in the SA group fitting as a marker of risk severity.

Abstract Background Impaired insight poses a challenge in the treatment of patients with schizophrenia because of its potential to jeopardize therapeutic engagement and medication adherence. This study explored how insight impairment, graded from none to extreme, is related to patient-reported mental health status, depression, and neurocognition in schizophrenia. Methods In a post hoc analysis of the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study (NCT00014001), insight was measured using the Positive and Negative Syndrome Scale (PANSS) Item G12 (lack of insight). Additional assessments for this analysis included the 12-Item Short-Form Health Survey (SF-12) Mental Component Summary (MCS), physician- and patient-reported Clinical Global Impression–Severity (CGI-S), MATRICS Consensus Cognitive Battery, and Calgary Depression Scale for Schizophrenia. Relationships between patient-reported outcomes and PANSS total and Item G12 ratings were evaluated. Results Among 1431 CATIE study participants in this analysis, increasingly impaired insight at baseline was significantly associated with better patient-reported quality of life (QoL), lower baseline depression, and greater divergence between physician- and patient-reported illness severity. Patients with more severely impaired insight reported milder illness compared with physician reports, particularly those with moderate-severe to extreme impairment (PANSS Item G12 rating ≥ 5), approximately 10% (138/1431) of CATIE participants. For the 90% of patients with PANSS Item G12 ratings

Abstract Background Patients with schizophrenia are unaware of their cognitive impairments. Misperception of cognitive impairment is an important factor associated with real-world functional outcomes in patients with schizophrenia. The patient’s family member plays a crucial role in detecting patients’ cognitive impairments when the patients are unaware of their own cognitive impairments. Previous studies have reported that not only the patient’s subjective rating, but also the patient’s family members’ rating of their cognitive impairment may not be precise. However, it is unclear why family ratings are inaccurate, and which factors impact family ratings. This study investigated whether family ratings differed significantly from the patients’ subjective ratings of the patients’ cognitive impairments and sought to determine the reason for the differences between the family ratings and the patients’ neurocognitive performances. We investigated the relationship between patients’ subjective ratings, family ratings for patients’ cognitive impairments, neuropsychological performance, and other aspects, including premorbid IQ and clinical symptoms. Method We evaluated 44 patients with schizophrenia for cognitive function using neuropsychological tests; in addition, both the patients and their families rated the patients’ cognitive impairments through questionnaires. We used the Mann–Whitney U test to examine whether the family ratings differed significantly from the patients’ self-reported ratings of their cognitive impairment. We conducted multiple regression analysis and structural equation modeling to determine why the patients’ subjective ratings and the family ratings were not definitively associated with the patients’ neurocognitive performances. We performed multiple regression analysis with a stepwise method with neurocognitive performance, premorbid IQ, positive symptoms, and negative symptoms as independent variables and family ratings of patients’ cognitive impairments as dependent variables. Results We found that the family ratings differed significantly from the patients’ subjective self-reported ratings of their cognitive impairments. Our results showed that the premorbid IQ of patients is the strongest predictor of family ratings. Furthermore, among the neurocognitive domains, only the processing speed of patients was associated with family ratings. Conclusions We found that the family ratings were not consistent with the patients’ subjective self-reported ratings and the family ratings were most affected by the patients’ premorbid intellectual abilities. These results suggest that the families’ current assessments of the patients’ current cognitive impairments were affected by the patients’ premorbid intellectual ability rather than the patients’ current neurocognitive performance. Patients’ processing speed predicted family ratings; however, family members' ratings were not related to verbal learning/memory, executive function, and language of patients. Therefore, our findings highlight that patients’ family ratings may differ from patients’ subjective ratings, results of performance-based neuropsychological tests, and clinician ratings.

Abstract Backgrounds Autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD) are neurodevelopmental disorders that exhibit within-disorder heterogeneity and cross-disorder phenotypic overlap, thus suggesting that the current disease categories may not fully represent the etiologic essence of the disorders, especially for highly comorbid neurodevelopmental disorders. In this study, we explored the subtypes of a combined sample of ASD and ADHD by integrating measurements of behavior, cognition and brain imaging. Methods A total of 164 participants, including 65 with ASD, 47 with ADHD, and 52 controls, were recruited. Unsupervised machine learning with an agglomerative hierarchical clustering algorithm was used to identify transdiagnostic symptom clusters. Neurocognition and brain structural connectivity measurements were used to assess symptom clusters. Mediation analysis was used to explore the relationship between transdiagnostic symptoms, neurocognition and brain structural connectivity. Results We identified three symptom clusters that did not fall within the diagnostic boundaries of DSM. External measurements from neurocognition and neuroimaging domains supported distinct profiles, including fine motor function, verbal fluency, and structural connectivity in the corpus callosum between these symptom clusters, highlighting possible biomarkers for ASD and ADHD. Additionally, fine motor function was shown to mediate the relationship between the corpus callosum and perseveration symptoms. Conclusions In this transdiagnostic study on ASD and ADHD, we identified three subtypes showing meaningful associations between symptoms, neurocognition and brain white matter structural connectivity. The fine motor function and structural connectivity of corpus callosum might be used as biomarkers for neurodevelopmental disorders with social skill symptoms. The results of this study highlighted the importance of precise phenotyping and further supported the effects of fine motor intervention on ASD and ADHD.

Abstract Background Ketamine has emerged as a rapid-acting antidepressant in treatment-resistant depression (TRD) increasingly used in non-research, clinical settings. Few studies, however, have examined neurocognitive effects of repeated racemic ketamine infusion treatments in patients with TRD. In an effort to identify potential effects after serial infusions, we conducted a retrospective chart review to identify statistically significant changes in cognition in patient undergoing serial intravenous infusions; concomitantly, we examined baseline cognition as potential predictor of anti-depressant potential. Methods Twenty-two patients with TRD were examined after they finished the induction phase of 8–10 repeated intravenous ketamine infusions and completed the assessments of their depressive symptoms (measured by the 16-item Quick Inventory of Depressive Symptomatology-Self Report Scale: QIDS-SR16) and cognitive function (measured by the Montreal Cognitive Assessment: MoCA) before the first and the last ketamine treatments. Results Repeated ketamine infusions administered through an escalating dose protocol with 8–10 infusion sessions produced a 47.2% reduction response in depression; there was no evidence of impairment as reflected in MoCA testing. There was a moderate association between baseline cognition and antidepressant response with a Pearson correlation of 0.453. Conclusion In this naturalistic sample of patients with TRD in our clinical service, repeated ketamine infusions significantly decreased depression symptoms without impairing cognitive performance. The baseline cognition may positively predict antidepressant responses of repeated ketamine treatment.

Background: Research on the influence of neurocognitive factors on suicide risk, regardless of the diagnosis, is inconsistent. Recently, suicide risk studies propose applying a trans-diagnostic framework in line with the launch of the Research Domain Criteria Cognitive Systems model. In the present study, we highlight the extent of cognitive impairment using a standardized battery in a psychiatric sample stratified for different degrees of suicidal risk. We also differentiate in our sample various neurocognitive profiles associated with different levels of risk. Materials and methods: We divided a sample of 106 subjects into three groups stratified by suicide risk level: Suicide Attempt (SA), Suicidal Ideation (SI), Patient Controls (PC) and Healthy Controls (HC). We conducted a multivariate Analysis of Variance (MANOVA) for each cognitive domain measured through the standardized battery MATRICS Consensus Cognitive Battery (MCCB). Results: We found that the group of patients performed worse than the group of healthy controls on most domains; social cognition was impaired in the suicide risk groups compared both to HC and PC. Patients in the SA group performed worse than those in the SI group. Conclusion: Social cognition impairment may play a crucial role in suicidality among individuals diagnosed with serious mental illness as it is involved in both SI and SA; noteworthy, it is more compromised in the SA group fitting as a marker of risk severity. [ABSTRACT FROM AUTHOR]

Background: Schizophrenia and related disorders are highly disabling and create substantial burdens for families, communities, and health care systems. Although pharmacological treatments can often lessen the psychotic symptoms that are a hallmark of schizophrenia, they do not lessen the social and cognitive deficits that create the greatest impediments to community engagement and functional recovery. This study builds on prior research on psychosocial rehabilitation by comparing the effectiveness of two treatments demonstrated as efficacious in improving social and community functioning, Cognitive Enhancement Therapy (CET) and a version of Social Skills Training (HOPES/SST). Methods: The study uses a randomized cluster design in which a pair of clinicians at community- and hospital-based mental service centers deliver either CET or HOPES to at least one group of 6-8 eligible clients for 12 months. Clinicians are trained and then supervised weekly, with ongoing process measurement of treatment fidelity, attendance, satisfaction, and retention, and use of other services. Measures administered at baseline and at 6 and 12 months while in treatment, and then at 18 and 24 months after treatment include social adjustment, quality of life, social skills, positive and negative symptoms, and neuro- and social cognition. We hypothesize that CET will be associated with greater improvements than SST in both the primary outcome of community functioning and the secondary outcomes of neuro- and social cognition and social skills. Secondarily, we hypothesize that more cognitive impairment at baseline and younger age will predict more benefit from CET compared to HOPES. Discussion: Resource shortages endemic in mental health services and exacerbated by the pandemic highlight the importance of identifying the most effective approach to improving social and community functioning. We aim to improve understanding of the impact of two efficacious psychosocial treatments and to improve clinicians' ability to refer to both treatments the individuals who are most likely to benefit from them. We expect the result to be programmatic improvements that improve the magnitude and durability of gains in community functioning. Trial registration: ClinicalTrial.gov NCT04321759, registered March 25, 2020. [ABSTRACT FROM AUTHOR]

Background: Impaired insight poses a challenge in the treatment of patients with schizophrenia because of its potential to jeopardize therapeutic engagement and medication adherence. This study explored how insight impairment, graded from none to extreme, is related to patient-reported mental health status, depression, and neurocognition in schizophrenia. Methods: In a post hoc analysis of the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study (NCT00014001), insight was measured using the Positive and Negative Syndrome Scale (PANSS) Item G12 (lack of insight). Additional assessments for this analysis included the 12-Item Short-Form Health Survey (SF-12) Mental Component Summary (MCS), physician- and patient-reported Clinical Global Impression–Severity (CGI-S), MATRICS Consensus Cognitive Battery, and Calgary Depression Scale for Schizophrenia. Relationships between patient-reported outcomes and PANSS total and Item G12 ratings were evaluated. Results: Among 1431 CATIE study participants in this analysis, increasingly impaired insight at baseline was significantly associated with better patient-reported quality of life (QoL), lower baseline depression, and greater divergence between physician- and patient-reported illness severity. Patients with more severely impaired insight reported milder illness compared with physician reports, particularly those with moderate-severe to extreme impairment (PANSS Item G12 rating ≥ 5), approximately 10% (138/1431) of CATIE participants. For the 90% of patients with PANSS Item G12 ratings < 5, patient-reported QoL decreased with increasing symptoms. SF-12 MCS scores were linearly related to baseline PANSS total score only in patients with PANSS total score < 90 (moderately ill or better), and better symptom scores were associated with higher QoL. No significant relationship between insight and neurocognition was observed. Conclusions: In the small subgroup (10%) of CATIE study patients with schizophrenia and PANSS Item G12 ratings ≥5, moderate-severe–severe/extreme insight impairment was associated with significantly more positive perception of QoL and illness severity by the patient versus the treating physician. This was not observed in the remaining 90% of patients with normal to moderately impaired insight, suggesting that poor insight as a threat to the validity of self-report is uncommon. [ABSTRACT FROM AUTHOR]

Background: The objectives of this study were to delineate whether delirium in older adults is associated with activation of the immune-inflammatory response system (IRS) as indicated by activation of M1, T helper (Th)1, and Th17 profiles, and/or by reduced activities of the compensatory immunoregulatory system (CIRS), including Th2 and T regulatory profiles. Methods: We recruited 65 older adult patients with a low energy impact hip fracture who underwent hip fracture operation. The CAM-ICU and the Delirium Rating Scale, Revised-98-Thai version (DRS-R-98) were assessed pre-operatively and 1, 2 and 3 days after surgery. Blood samples (day 1 and 2) post-surgery were assayed for cytokines/chemokines using a MultiPlex assay and the neutrophil/lymphocyte ratio. Results: We found that delirium and/or the DRS-R-98 score were associated with IRS activation as indicated by activated M1, Th1, Th17 and T cell growth profiles and by attenuated CIRS functions. The most important IRS biomarkers were CXCL8, interleukin (IL)-6, and tumor necrosis factor-α, and the most important CIRS biomarkers were IL-4 and soluble IL-1 receptor antagonist. We found that 42.5% of the variance in the actual changes in the DRS-R-98 score (averaged from day 1 to day 3) was explained by T cell growth factors, baseline DRS-R-98 scores and age. An increase in the NLR reflects overall IRS, M1, Th1, Th17, and Th2 activation. Conclusions: Post-hip surgery delirium is associated with activated IRS pathways and appears especially in patients with lowered CIRS functions. [ABSTRACT FROM AUTHOR]

Background: Patients with schizophrenia are unaware of their cognitive impairments. Misperception of cognitive impairment is an important factor associated with real-world functional outcomes in patients with schizophrenia. The patient's family member plays a crucial role in detecting patients' cognitive impairments when the patients are unaware of their own cognitive impairments. Previous studies have reported that not only the patient's subjective rating, but also the patient's family members' rating of their cognitive impairment may not be precise. However, it is unclear why family ratings are inaccurate, and which factors impact family ratings. This study investigated whether family ratings differed significantly from the patients' subjective ratings of the patients' cognitive impairments and sought to determine the reason for the differences between the family ratings and the patients' neurocognitive performances. We investigated the relationship between patients' subjective ratings, family ratings for patients' cognitive impairments, neuropsychological performance, and other aspects, including premorbid IQ and clinical symptoms. Method: We evaluated 44 patients with schizophrenia for cognitive function using neuropsychological tests; in addition, both the patients and their families rated the patients' cognitive impairments through questionnaires. We used the Mann–Whitney U test to examine whether the family ratings differed significantly from the patients' self-reported ratings of their cognitive impairment. We conducted multiple regression analysis and structural equation modeling to determine why the patients' subjective ratings and the family ratings were not definitively associated with the patients' neurocognitive performances. We performed multiple regression analysis with a stepwise method with neurocognitive performance, premorbid IQ, positive symptoms, and negative symptoms as independent variables and family ratings of patients' cognitive impairments as dependent variables. Results: We found that the family ratings differed significantly from the patients' subjective self-reported ratings of their cognitive impairments. Our results showed that the premorbid IQ of patients is the strongest predictor of family ratings. Furthermore, among the neurocognitive domains, only the processing speed of patients was associated with family ratings. Conclusions: We found that the family ratings were not consistent with the patients' subjective self-reported ratings and the family ratings were most affected by the patients' premorbid intellectual abilities. These results suggest that the families' current assessments of the patients' current cognitive impairments were affected by the patients' premorbid intellectual ability rather than the patients' current neurocognitive performance. Patients' processing speed predicted family ratings; however, family members' ratings were not related to verbal learning/memory, executive function, and language of patients. Therefore, our findings highlight that patients' family ratings may differ from patients' subjective ratings, results of performance-based neuropsychological tests, and clinician ratings. [ABSTRACT FROM AUTHOR]

Background: Ketamine has emerged as a rapid-acting antidepressant in treatment-resistant depression (TRD) increasingly used in non-research, clinical settings. Few studies, however, have examined neurocognitive effects of repeated racemic ketamine infusion treatments in patients with TRD. In an effort to identify potential effects after serial infusions, we conducted a retrospective chart review to identify statistically significant changes in cognition in patient undergoing serial intravenous infusions; concomitantly, we examined baseline cognition as potential predictor of anti-depressant potential. Methods: Twenty-two patients with TRD were examined after they finished the induction phase of 8–10 repeated intravenous ketamine infusions and completed the assessments of their depressive symptoms (measured by the 16-item Quick Inventory of Depressive Symptomatology-Self Report Scale: QIDS-SR16) and cognitive function (measured by the Montreal Cognitive Assessment: MoCA) before the first and the last ketamine treatments. Results: Repeated ketamine infusions administered through an escalating dose protocol with 8–10 infusion sessions produced a 47.2% reduction response in depression; there was no evidence of impairment as reflected in MoCA testing. There was a moderate association between baseline cognition and antidepressant response with a Pearson correlation of 0.453. Conclusion: In this naturalistic sample of patients with TRD in our clinical service, repeated ketamine infusions significantly decreased depression symptoms without impairing cognitive performance. The baseline cognition may positively predict antidepressant responses of repeated ketamine treatment. [ABSTRACT FROM AUTHOR]

Backgrounds: Autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD) are neurodevelopmental disorders that exhibit within-disorder heterogeneity and cross-disorder phenotypic overlap, thus suggesting that the current disease categories may not fully represent the etiologic essence of the disorders, especially for highly comorbid neurodevelopmental disorders. In this study, we explored the subtypes of a combined sample of ASD and ADHD by integrating measurements of behavior, cognition and brain imaging. Methods: A total of 164 participants, including 65 with ASD, 47 with ADHD, and 52 controls, were recruited. Unsupervised machine learning with an agglomerative hierarchical clustering algorithm was used to identify transdiagnostic symptom clusters. Neurocognition and brain structural connectivity measurements were used to assess symptom clusters. Mediation analysis was used to explore the relationship between transdiagnostic symptoms, neurocognition and brain structural connectivity. Results: We identified three symptom clusters that did not fall within the diagnostic boundaries of DSM. External measurements from neurocognition and neuroimaging domains supported distinct profiles, including fine motor function, verbal fluency, and structural connectivity in the corpus callosum between these symptom clusters, highlighting possible biomarkers for ASD and ADHD. Additionally, fine motor function was shown to mediate the relationship between the corpus callosum and perseveration symptoms. Conclusions: In this transdiagnostic study on ASD and ADHD, we identified three subtypes showing meaningful associations between symptoms, neurocognition and brain white matter structural connectivity. The fine motor function and structural connectivity of corpus callosum might be used as biomarkers for neurodevelopmental disorders with social skill symptoms. The results of this study highlighted the importance of precise phenotyping and further supported the effects of fine motor intervention on ASD and ADHD. [ABSTRACT FROM AUTHOR]

Abstract Background Accumulating evidence suggests that serum vascular endothelial growth factor (VEGF) in many neurobiological processes potentially contributes to the pathophysiology of psychiatric disorders, particularly cognitive decline. The purpose of this study was to explore the differences in neurocognition, social cognition and VEGF among remitted first-episode schizophrenic patients, non-remitters and normal control subjects. Moreover, we investigated the association between serum VEGF levels and cognitive functions. Method 65 remission (RS) and 45 nonremission patients (NRS) after first-episode schizophrenia, as well as 58 healthy controls (HC) were enrolled in this study. Social cognition was assessed using the Chinese Facial Emotion Test (CFET); neurocognition was measured with a test battery consisting of Hopkins Verbal Learning Test-Revised, Verbal Fluency Test, Trail Making Tests, Digit Span Tests (DST) and Stroop Tests. Blood samples were collected for VEGF measurements. Data was analyzed with SPSS 22.0 (Chicago, IL, USA). Results On nearly all neurocognitive tests (except for DST), RS performed significantly worse than HC but better than NRS (P RS > NRS). Conclusion Compared to HC, RS demonstrated poorer neurocognitive but intact social cognition functioning. These results indicate that VEGF levels decreased gradually with the severity of cognitive impairment in schizophrenia. VEGF may be involved in the pathological mechanism of cognitive performance in RS.

Abstract Background To measure the serum levels of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) in deficit schizophrenia (DS), in order to examine the association between these two neurotrophic factors (NFs) and cognitive performance. Methods A total of 109 male patients [51 DS and 58 non-deficit schizophrenia (NDS)] with schizophrenia and 40 sex and age matched healthy controls (HC) participated in this study. Processing speed, attention, executive function, and working memory of all subjects were assessed by means of a battery of classical neuropsychological tests. Serum BDNF and GDNF levels were measured simultaneously using a double-antibody sandwich enzyme-linked immunosorbent assay (ELISA). Results There were significant differences in the overall cognitive test scores between three groups (all p

Abstract Background Research suggests that young people with major depressive disorder (MDD) experience neurocognitive deficits and that these are associated with poorer functional and clinical outcomes. However, we are yet to understand how young people experience such difficulties. The aim of the current study was to explore the subjective experiences of neurocognitive functioning among young people with MDD. Methods Semi-structured qualitative interviews were conducted with 11 young people (aged 17–24 years) attending a specialist clinic for youth experiencing moderate-severe depression. Interview transcripts were analysed via Thematic Analysis to identify patterns and themes representing how young people with MDD subjectively experience neurocognitive deficits. Results Five main themes were identified: (1) experience of neurocognitive complaints; (2) relationship between neurocognitive complaints and depression; (3) impact on functioning; (4) strategies and supports; and (5) neurocognitive complaints and treatment. Overall, young people with MDD commonly experienced a range of subjective neurocognitive complaints. These appeared to have a bidirectional relationship with depressive symptomatology and significantly disrupted vocational, social and independent functioning, and aspects of psychological well-being including self-esteem. Neurocognitive difficulties represented an experiential barrier to psychological therapeutic engagement and were perceived as variably responsive to psychotropic medications, highlighting the need for targeted intervention. Discussion Neurocognitive difficulties are a common and pervasive experience for young people with MDD, with perceived impacts on depressive symptoms, attitudinal beliefs, everyday functioning and therapeutic engagement. Subjective neurocognitive complaints may therefore contribute to or exacerbate personal challenges faced by young people with MDD and thus, require early identification, consideration in psychological formulation, and treatment. Further research into the mechanisms of neurocognitive impairment in MDD is also needed.

Abstract Background Patients with anorexia nervosa (AN) experience difficulties in neurocognitive functioning in the acute phase of illness which might be related to clinical presentation, but also in the apparently remitted state after weight recovery. Among the most commonly reported persistent deficits is cognitive inflexibility, which can be interpreted as a vulnerability trait or a “neuropsychological scar” reflecting the detrimental effect of prolonged semi-starvation in patients with a long duration of illness. Studies of adolescent samples with a relatively short clinical course may enable avoiding the effect of prolonged illness and help to determine whether neuropsychological deficits are trait or state dependent. The aim of this study is to assess cognitive functioning in adolescents with AN before and after the inpatient treatment programme, including cognitive remediation therapy (CRT). Methods Forty-seven adolescent female inpatients with AN diagnosed according to DSM-5 and fifty healthy female adolescents matched for the education level and age were recruited. The patients underwent a multimodal treatment including a ten-week CRT. The standardized and cross-validated neuropsychological (Trail Making Test – TMT A and B, Color-Word Stroop Task – CWST, Ruff Figural Fluency Test – RFFT) and clinical measurements (Beck Depression Inventory – BDI, Eating Attitude Test – EAT-26, Yale-Brown Obsessive Compulsive Scale – Y-BOCS) were used to assess both clinical (in the acute phase and after partial weight recovery) and control subjects. Results Initially, AN patients performed significantly worse compared to the controls, but afterwards, inpatient treatment improvement was noted on all examined measures. In a few subtests (TMT, CWST) performance of AN patients after the programme was still significantly poorer than in HC. Conclusions Cognitive inflexibility in adolescent AN patients, as measured with TMT, CWST, and RFFT tends to improve after therapy. Nevertheless, a few neuropsychological subtests which did not show complete normalization may warrant attention in subsequent studies. Further research including control intervention is needed to conclude whether CRT intervention affects the outcome.

Abstract Background Evidence is accumulating that Cognitive Remediation Training (CRT) is effective for ameliorating cognitive deficits experienced by patients with schizophrenia and accompanying functional impairment. There has been no randomized controlled trial of CRT using a nationally representative population of forensic patients, despite the significant cognitive deficits frequently present within this group. Methods Sixty-five patients with schizophrenia or schizoaffective disorder were enrolled in a single blind randomized controlled trial of CRT versus treatment as usual (TAU); representing 94% of those eligible within a national forensic cohort. The primary outcome measure was the composite score of the MATRICS Consensus Cognitive Battery (MCCB). Secondary outcome measures included neurocognitive and social cognitive domains, symptoms, and ‘real world’ functioning. Patient satisfaction was examined using an exit interview. Participants were reassessed at 8 months follow up. All data were analyzed using an intention to treat design (ITT). Results For the primary outcome measure, the MCCB composite score, there were significant differences between those who participated in CRT and those receiving TAU at both end of treatment and 8 months follow up (Cohen’s d = 0.34. Significant improvements were observed in visual and working memory. Mediation analysis found that those who cognitively benefited from CRT had corresponding improved functioning, and more net positive therapeutic moves i.e. moves to units with lower security within the hospital. Ninety-six percent believed their cognitive gains positively affected their daily lives. Conclusions CRT may be an acceptable and efficacious intervention for forensic patients with schizophrenia or schizoaffective disorder. Trial registration ClinicalTrials.gov Identifier: NCT02360813. Trial registered Feb 4th 2015, last updated May 1st 2015.

Background: People with schizophrenia are ten times more likely to commit homicide than a member of the general population. The relationship between symptoms of schizophrenia and acts of violence is unclear. There has also been limited research on what determines the seriousness and form of violence, such as reactive or instrumental violence. Moral cognition may play a paradoxical role in acts of violence for people with schizophrenia. Thoughts which have moral content arising from psychotic symptoms may be a cause of serious violence. Method: We investigated if psychotic symptoms and moral cognitions at the time of a violent act were associated with acts of violence using a cross-sectional national forensic cohort (n = 55). We examined whether moral cognitions were associated with violence when controlling for neurocognition and violence proneness. We explored the association between all psychotic symptoms present at the time of the violent act, psychotic symptoms judged relevant to the violent act and moral cognitions present at that time. Using mediation analysis, we examined whether moral cognitions were the missing link between symptoms and the relevance of symptoms for violence. We also investigated if specific moral cognitions mediated the relationship between specific psychotic symptoms, the seriousness of violence (including homicide), and the form of violence. Results: Psychotic symptoms generally were not associated with the seriousness or form of violence. However, specific moral cognitions were associated with the seriousness and form of violence even when controlling for neurocognition and violence proneness. Specific moral cognitions were associated with specific psychotic symptoms present and relevant to violence. Moral cognitions mediated the relationship between the presence of specific psychotic symptoms and their relevance for violence, homicide, seriousness of violence, and the form of violence. Conclusions: Moral cognitions including the need to reduce suffering, responding to an act of injustice or betrayal, the desire to comply with authority, or the wish to punish impure or disgusting behaviour, may be a key mediator explaining the relationship between psychotic symptoms and acts of violence. Our findings may have important implications for risk assessment, treatment and violence prevention. [ABSTRACT FROM AUTHOR]

Background: Accumulating evidence suggests that serum vascular endothelial growth factor (VEGF) in many neurobiological processes potentially contributes to the pathophysiology of psychiatric disorders, particularly cognitive decline. The purpose of this study was to explore the differences in neurocognition, social cognition and VEGF among remitted first-episode schizophrenic patients, non-remitters and normal control subjects. Moreover, we investigated the association between serum VEGF levels and cognitive functions. Method: 65 remission (RS) and 45 nonremission patients (NRS) after first-episode schizophrenia, as well as 58 healthy controls (HC) were enrolled in this study. Social cognition was assessed using the Chinese Facial Emotion Test (CFET); neurocognition was measured with a test battery consisting of Hopkins Verbal Learning Test-Revised, Verbal Fluency Test, Trail Making Tests, Digit Span Tests (DST) and Stroop Tests. Blood samples were collected for VEGF measurements. Data was analyzed with SPSS 22.0 (Chicago, IL, USA). Results: On nearly all neurocognitive tests (except for DST), RS performed significantly worse than HC but better than NRS (P < 0.05). NRS, but not RS, exhibited markedly poorer social cognition than HC (except for Happiness and Surprise subscales of the CFET) (P < 0.05). VEGF levels showed a gradient change among three groups (HC > RS > NRS). Conclusion: Compared to HC, RS demonstrated poorer neurocognitive but intact social cognition functioning. These results indicate that VEGF levels decreased gradually with the severity of cognitive impairment in schizophrenia. VEGF may be involved in the pathological mechanism of cognitive performance in RS. [ABSTRACT FROM AUTHOR]

Abstract Background Using paradigms from game theory, researchers have reported abnormal decision-making in social context in patients with schizophrenia. However, less is known about the underpinnings of the impairment. This study aimed to test whether theory of mind (ToM) deficits and/or neurocognitive dysfunctions mediate impaired social decision-making in patients with schizophrenia. Methods We compared thirty-five patients with schizophrenia to thirty-eight matched healthy controls with regard to social decision-making using the mini Ultimatum Game (mini UG), a paradigm from game theory. Additionally, we assessed ToM using the Theory of Mind Picture Stories Task, a mental state attribution task, and assessed neurocognition using the Brief Assessment of Cognition in Schizophrenia. Mediation analyses were performed on the data. Results In contrast to the behavioral pattern of healthy controls in the mini UG, the patients with schizophrenia significantly accepted more disadvantageous offers and rejected more advantageous offers, and showed reduced sensitivity to the fairness-related context changes in the mini UG. Impaired ToM and neurocognition were also found in the patients. Mediation analyses indicated that ToM but not neurocognition partially mediated the group differences on the disadvantageous and advantageous offers in the mini UG. Conclusions Patients with schizophrenia exhibited impaired social decision-making. This impairment can be partly explained by their ToM deficits rather than neurocognitive deficits. However, the exact nature of the ToM deficits that mediate impaired social decision-making needs to be identified in future.

Background: Patients with anorexia nervosa (AN) experience difficulties in neurocognitive functioning in the acute phase of illness which might be related to clinical presentation, but also in the apparently remitted state after weight recovery. Among the most commonly reported persistent deficits is cognitive inflexibility, which can be interpreted as a vulnerability trait or a "neuropsychological scar" reflecting the detrimental effect of prolonged semi-starvation in patients with a long duration of illness. Studies of adolescent samples with a relatively short clinical course may enable avoiding the effect of prolonged illness and help to determine whether neuropsychological deficits are trait or state dependent. The aim of this study is to assess cognitive functioning in adolescents with AN before and after the inpatient treatment programme, including cognitive remediation therapy (CRT). Methods: Forty-seven adolescent female inpatients with AN diagnosed according to DSM-5 and fifty healthy female adolescents matched for the education level and age were recruited. The patients underwent a multimodal treatment including a ten-week CRT. The standardized and cross-validated neuropsychological (Trail Making Test – TMT A and B, Color-Word Stroop Task – CWST, Ruff Figural Fluency Test – RFFT) and clinical measurements (Beck Depression Inventory – BDI, Eating Attitude Test – EAT-26, Yale-Brown Obsessive Compulsive Scale – Y-BOCS) were used to assess both clinical (in the acute phase and after partial weight recovery) and control subjects. Results: Initially, AN patients performed significantly worse compared to the controls, but afterwards, inpatient treatment improvement was noted on all examined measures. In a few subtests (TMT, CWST) performance of AN patients after the programme was still significantly poorer than in HC. Conclusions: Cognitive inflexibility in adolescent AN patients, as measured with TMT, CWST, and RFFT tends to improve after therapy. Nevertheless, a few neuropsychological subtests which did not show complete normalization may warrant attention in subsequent studies. Further research including control intervention is needed to conclude whether CRT intervention affects the outcome. [ABSTRACT FROM AUTHOR]

Background: Evidence is accumulating that cognitive remediation therapy (CRT) is an effective intervention for patients with schizophrenia or schizoaffective disorder. To date there has been no randomised controlled trial (RCT) cohort study of cognitive remediation within a forensic hospital. The goal of this study is to examine the effectiveness of a trial of cognitive remediation for forensic mental health patients with schizophrenia or schizoaffective disorder. Methods: An estimated sixty patients will be enrolled in the study. Participants will be randomised to one of two conditions: CRT with treatment as usual (TAU), or TAU. CRT will consist of 42 individual sessions and 14 group sessions. The primary outcome measure for this study is change in cognitive functioning using the MATRICS Consensus Cognitive Battery (MCCB). Secondary outcomes include change in social and occupational functioning, disorganised symptoms, negative symptoms, violence, participation in psychosocial treatment and recovery. In addition to these effectiveness measures, we will examine patient satisfaction. Discussion: Cognitive difficulties experienced by schizophrenia spectrum patients are associated with general functioning, ability to benefit from psychosocial interventions and quality of life. Research into the treatment of cognitive difficulties within a forensic setting is therefore an important priority. The results of the proposed study will help answer the question whether cognitive remediation improves functional outcomes in forensic mental health patients with schizophrenia or schizoaffective disorder. Forensic mental health patients are detained for the dual purpose of receiving treatment and for public protection. There can be conflict between these two roles perhaps causing forensic services to have an increased length of stay compared to general psychiatric admissions. Ultimately a focus on emphasising cognition and general functioning over symptoms may decrease tension between the core responsibilities of forensic mental health services. [ABSTRACT FROM AUTHOR]

Background: Severe mental illnesses like schizophrenia and bipolar disorder are known to be diseases that to someextent, but not entirely can be understood genetically. The dominating hypothesis is that these disorders should be understood in a neurodevelopmental perspective where genes and environment as well as geneenvironment- interactions contribute to the risk of developing the disease. We aim to analyse the influences of genetic risk and environmental factors in a population of 520 7-year-old children with either 0, 1 or 2 parents diagnosed with schizophrenia spectrum psychosis or bipolar disorder on mental health and level of functioning. We hypothesize that a larger proportion of children growing up with an ill parent will display abnormal or delayed development, behavioural problems or psychiatric symptoms compared to the healthy controls. Methods/design: We are establishing a cohort of 5207 year old children and both their parents for a comprehensiveinvestigation with main outcome measures being neurocognition, behaviour, psychopathology and neuromotor development of the child. Parents and children are examined with a comprehensive battery of instruments and are asked for genetic material (saliva or blood) for genetic analyses. The participants arerecruited via Danish registers to ensure representativity. Data from registers concerning social status, birth complications, somatic illnesses and hospitalization are included in the database. Psychological and relational factors like emotional climate in the family, degree of stimulation and support in the home and attachment style are also investigated. Discussion: Data collection started January 1, 2013, and is successfully ongoing. By Aug 2015 424 families areincluded. About 20% of the invited families decline to participate, equal for all groups. [ABSTRACT FROM AUTHOR]

Background: There is a broad literature suggesting that cognitive difficulties are associated with violence across a variety of groups. Although neurocognitive and social cognitive deficits are core features of schizophrenia, evidence of a relationship between cognitive impairments and violence within this patient population has been mixed. Methods: We prospectively examined whether neurocognition and social cognition predicted inpatient violence amongst patients with schizophrenia and schizoaffective disorder (n = 89; 10 violent) over a 12 month period. Neurocognition and social cognition were assessed using the MATRICS Consensus Cognitive Battery (MCCB). Results: Using multivariate analysis neurocognition and social cognition variables could account for 34% of the variance in violent incidents after controlling for age and gender. Scores on a social cognitive reasoning task (MSCEIT) were significantly lower for the violent compared to nonviolent group and produced the largest effect size. Mediation analysis showed that the relationship between neurocognition and violence was completely mediated by each of the following variables independently: social cognition (MSCEIT), symptoms (PANSS Total Score), social functioning (SOFAS) and violence proneness (HCR-20 Total Score). There was no evidence of a serial pathway between neurocognition and multiple mediators and violence, and only social cognition and violence proneness operated in parallel as significant mediators accounting for 46% of the variance in violent incidents. There was also no evidence that neurocogniton mediated the relationship between any of these variables and violence. Conclusions: Of all the predictors examined, neurocognition was the only variable whose effects on violence consistently showed evidence of mediation. Neurocognition operates as a distal risk factor mediated through more proximal factors. Social cognition in contrast has a direct effect on violence independent of neurocognition, violence proneness and symptom severity. The neurocognitive impairment experienced by patients with schizophrenia spectrum disorders may create the foundation for the emergence of a range of risk factors for violence including deficits in social reasoning, symptoms, social functioning, and HCR-20 risk items, which in turn are causally related to violence. [ABSTRACT FROM AUTHOR]

Background: People with chronic psychosis often display theory of mind impairments that are not fully accounted for by other, more general neurocognitive deficits. In these patients, both theory of mind and neurocognitive deficits contribute to poor functioning, independently of psychotic symptoms. In young people with recent-onset psychosis, however, it is unclear the extent to which theory of mind impairment is independent of neurocognitive deficits. The primary aim of this study was to examine the evidence for specific theory of mind impairments in early psychosis. A secondary aim was to explore the relations between theory of mind, neurocognition, symptom severity, and functional outcomes. Methods: Twenty-three patients who were within two years of their first psychotic episode and 19 healthy controls completed theory of mind and neurocognitive batteries. Social functioning, quality of life, and symptom severity were also assessed in patients. Results: Patients demonstrated deficits in tasks assessing theory of mind and neurocognition relative to controls. Patients’ deficits in theory of mind were evident even after adjusting for their deficits in neurocognition. Neither theory of mind nor neurocognition predicted social functioning or quality of life in this early psychosis sample. Severity of negative symptoms, however, was a significant predictor of both outcomes. Conclusions: While a specific theory of mind impairment was evident in this early psychosis sample, severity of negative symptoms emerged as the best predictor of poor functional outcome. Further early psychosis research is needed to examine the longitudinal progression of theory of mind impairments – independent of neurocognitive deficits – and their impact on psychosocial function. [ABSTRACT FROM AUTHOR]

Background The purpose of this article was to conduct a review of the types of training offered to people with schizophrenia in order to help them develop strategies to cope with or compensate for neurocognitive or sociocognitive deficits. Methods We conducted a search of the literature using keywords such as "schizophrenia", "training", and "cognition" with the most popular databases of peer-reviewed journals. Results We reviewed 99 controlled studies in total (though nine did not have a control condition). We found that drill and practice training is used more often to retrain neurocognitive deficits while drill and strategy training is used more frequently in the context of sociocognitive remediation. Conclusions Hypotheses are suggested to better understand those results and future research is recommended to compare drill and strategy with drill and practice training for both social and neurocognitive deficits in schizophrenia. [ABSTRACT FROM AUTHOR]

Background: Evidence is accumulating that Cognitive Remediation Training (CRT) is effective for ameliorating cognitive deficits experienced by patients with schizophrenia and accompanying functional impairment. There has been no randomized controlled trial of CRT using a nationally representative population of forensic patients, despite the significant cognitive deficits frequently present within this group. Methods: Sixty-five patients with schizophrenia or schizoaffective disorder were enrolled in a single blind randomized controlled trial of CRT versus treatment as usual (TAU); representing 94% of those eligible within a national forensic cohort. The primary outcome measure was the composite score of the MATRICS Consensus Cognitive Battery (MCCB). Secondary outcome measures included neurocognitive and social cognitive domains, symptoms, and 'real world' functioning. Patient satisfaction was examined using an exit interview. Participants were reassessed at 8 months follow up. All data were analyzed using an intention to treat design (ITT). Results: For the primary outcome measure, the MCCB composite score, there were significant differences between those who participated in CRT and those receiving TAU at both end of treatment and 8 months follow up (Cohen's d = 0.34. Significant improvements were observed in visual and working memory. Mediation analysis found that those who cognitively benefited from CRT had corresponding improved functioning, and more net positive therapeutic moves i.e. moves to units with lower security within the hospital. Ninety-six percent believed their cognitive gains positively affected their daily lives. Conclusions: CRT may be an acceptable and efficacious intervention for forensic patients with schizophrenia or schizoaffective disorder. Trial registration: ClinicalTrials.gov Identifier: NCT02360813. Trial registered Feb 4th 2015, last updated May 1st 2015. [ABSTRACT FROM AUTHOR]

Background: Using paradigms from game theory, researchers have reported abnormal decision-making in social context in patients with schizophrenia. However, less is known about the underpinnings of the impairment. This study aimed to test whether theory of mind (ToM) deficits and/or neurocognitive dysfunctions mediate impaired social decision-making in patients with schizophrenia., Methods: We compared thirty-five patients with schizophrenia to thirty-eight matched healthy controls with regard to social decision-making using the mini Ultimatum Game (mini UG), a paradigm from game theory. Additionally, we assessed ToM using the Theory of Mind Picture Stories Task, a mental state attribution task, and assessed neurocognition using the Brief Assessment of Cognition in Schizophrenia. Mediation analyses were performed on the data., Results: In contrast to the behavioral pattern of healthy controls in the mini UG, the patients with schizophrenia significantly accepted more disadvantageous offers and rejected more advantageous offers, and showed reduced sensitivity to the fairness-related context changes in the mini UG. Impaired ToM and neurocognition were also found in the patients. Mediation analyses indicated that ToM but not neurocognition partially mediated the group differences on the disadvantageous and advantageous offers in the mini UG., Conclusions: Patients with schizophrenia exhibited impaired social decision-making. This impairment can be partly explained by their ToM deficits rather than neurocognitive deficits. However, the exact nature of the ToM deficits that mediate impaired social decision-making needs to be identified in future.