Social cognition includes a range of cognitive processes that help individuals to understand how others think and feel. There is emerging evidence that social cognitive deficits may represent a transdiagnostic issue, potentially serving as a marker of neurological abnormality. We performed an electronic database search in order to identify published, peer-reviewed meta-analyses that compared facial emotion recognition or theory of mind task performance between individuals meeting clinical criteria for a psychiatric, neurological or developmental condition against healthy controls. We identified 31 meta-analyses eligible for inclusion that examined performance across relevant tasks among 30 different clinical populations. The results suggest that social cognitive deficits appear to be a core cognitive phenotype of many clinical conditions. Across the clinical groups, deficits in social cognitive domains were broadly similar in magnitude to those previously reported for more established aspects of cognition, such as memory and executive function. There is a need to clarify the 'real world' impact of these deficits, and to develop effective transdiagnostic interventions for those individuals that are adversely affected.

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Background Anxiety and depression are leading causes of disability worldwide, yet individuals are often unable to access appropriate treatment. There is a need to develop effective interventions that can be delivered remotely. Previous research has suggested that emotional processing biases are a potential target for intervention, and these may be altered through brief training programs. Methods We report two experimental medicine studies of emotional bias training in two samples: individuals from the general population (n = 522) and individuals currently taking antidepressants to treat anxiety or depression (n = 212). Participants, recruited online, completed four sessions of EBT from their own home. Mental health and cognitive functioning outcomes were assessed at baseline, immediately post-training, and at 2-week follow-up. Results In both studies, our intervention successfully trained participants to perceive ambiguous social information more positively. This persisted at a 2-week follow-up. There was no clear evidence that this change in emotional processing transferred to improvements in symptoms in the primary analyses. However, in both studies, there was weak evidence for improved quality of life following EBT amongst individuals with more depressive symptoms at baseline. No clear evidence of transfer effects was observed for self-reported daily stress, anhedonia or depressive symptoms. Exploratory analyses suggested that younger participants reported greater treatment gains. Conclusions These studies demonstrate the effectiveness of delivering a multi-session online training program to promote lasting cognitive changes. Given the inconsistent evidence for transfer effects, EBT requires further development before it can be considered as a treatment for anxiety and depression.

BackgroundIt remains unclear whether the lack of clinical trial success and drug approval for cognitive impairment associated with schizophrenia (CIAS) is due to compounds being ineffective, or whether trial methodology itself has been a limiting factor in successfully demonstrating the efficacy of these agents. Schizophrenia is a heterogeneous disorder and whilst cognitive deficits are a core feature, the profile and degree of neuropsychological impairment can vary across patients. Though most individuals with schizophrenia exhibit some general cognitive impairment compared to antecedent expectations, such as premorbid intelligence, up to a quarter display cognitive performance in the ‘normal’ range. This may pose a problem for pro-cognitive drug trials in this population given that it potentially inflates baseline scores and reduces the scope to see improvement between treatment and placebo groups. In order to examine this potential issue, we investigated participant-level trajectories of cognitive performance among patients with schizophrenia enrolled in a multi-national, phase II clinical trial.MethodsWe conducted a post-hoc analysis of existing trial data from 463 patients with schizophrenia who participated in a randomized, double-blind, placebo-controlled trial. Patients met established diagnosis for schizophrenia (DSM-5), were clinically stable (non-acute) and had no more than moderate severity ratings on the Positive and Negative Syndrome Scale (PANSS). During the trial, participants completed two different neurocognitive test batteries, the Cambridge Neuropsychological Test Automated Battery (CANTAB) and the MATRICS Consensus Cognitive Battery (MCCB), at 4 separate time points (screening, baseline, week 6 & week 12). Participant data were pooled across placebo and treatment groups to explore trajectories of cognitive performance, at the participant-level, across the course of the study.ResultsLinear mixed model analyses revealed that participants who performed within the ‘normal range’ at screening on cognitive tasks as measured by CANTAB, continued to perform well at baseline, week 6 and week 12, showing no significant change in their performance. By contrast, participants who performed below the normal range at screening, showed a significant improvement in their test performance across the remainder of the study. When compared in the context of MCCB, those participants who performed a standard deviation (SD) above the MCCB normative mean at screening, were also the participants who performed within the normal range on CANTAB. Approximately 25% of the overall sample were performing within a clinically normal cognitive range at screening.DiscussionSubstantial variability was evident in cognitive performance among the current sample of patients with schizophrenia. We identified a subsample of patients whose performance fell within a clinically normal range. Cognitive improvement was observed only in those who exhibited a deficit at screening, bringing into question whether the inclusion of unimp...

There are currently no regulatory approved pharmacological treatments for cognitive impairment associated with schizophrenia (CIAS). One possibility is that trial methodology itself is hindering their development. Emerging evidence suggests that patients with schizophrenia may show limited benefit from pro-cognitive interventions if they already exhibit intact cognitive performance, relative to normative thresholds. The aim of this report was to examine the extent to which objectively assessed cognitive performance has been used as an eligibility and/or stratification criterion in CIAS pharmacotherapy trials. On 16th January 2019, we conducted a systematic search of studies listed on ClinicalTrials.gov to identify randomized, double-blind, placebo-controlled, add-on pharmacotherapy trials conducted in patients with a diagnosis of schizophrenia, in which a paper-and-pencil or computerized cognitive task (or battery) was specified as a primary outcome measure. Of the 87 trials that met our inclusion criteria, 10 (11.5%) required the presence of an objectively assessed cognitive deficit as part of their patient eligibility criteria. No studies reported stratifying patients according to the presence or degree of cognitive impairment they exhibited. These results suggest that the vast majority of CIAS trials may have been underpowered due to the inclusion of cognitively “normal” patients. Purposive screening for cognitive impairment could increase CIAS trial success.