Neurocognitive profiles in treatment-resistant bipolar I and bipolar II disorder depression

Background The literature on the neuropsychological profiles in Bipolar disorder (BD) depression is sparse. The aims of the study were to assess the neurocognitive profiles in treatment-resistant, acutely admitted BD depression inpatients, to compare the neurocognitive functioning in patients with BD I and II, and to identify the demographic and clinical illness characteristics associated with cognitive functioning. Methods Acutely admitted BD I (n = 19) and BD II (n = 32) inpatients who fulfilled the DSM-IV-TR criteria for a major depressive episode were tested with the MATRICS Consensus Cognitive Battery (MCCB), the Wechsler Abbreviated Scale of Intelligence, the National Adult Reading Test, and a battery of clinical measures. Results Neurocognitive impairments were evident in the BD I and BD II depression inpatients within all MCCB domains. The numerical scores on all MCCB-measures were lower in the BD I group than in the BD II group, with a significant difference on one of the measures, category fluency. 68.4% of the BD I patients had clinically significant impairment (>1.5 SD below normal mean) in two or more domains compared to 37.5% of the BD II patients (p = 0.045). A significant reduction in IQ from the premorbid to the current level was seen in BD I but not BD II patients. Higher age was associated with greater neurocognitive deficits compared to age-adjusted published norms. Conclusions A high proportion of patients with therapy-resistant BD I or II depression exhibited global neurocognitive impairments with clinically significant severity. The cognitive impairments were more common in BD I compared to BD II patients, particularly processing speed. These findings suggest that clinicians should be aware of the severe neurocognitive dysfunction in treatment-resistant bipolar depression, particularly in BD I.publishedVersio

Social cognitive heterogeneity in schizophrenia: A cluster analysis

This study examined social cognitive heterogeneity in Norwegian sample of individuals with schizophrenia (n = 82). They were assessed with three social cognitive tests: Emotion in Biological Motion (emotion processing), Relationships Across Domains (social perception), and Movie for the Assessment of Social Cognition (theory of mind). Hierarchical and k-means cluster analyses using standardized scores on these three tests provided two clusters. The first cluster (68 %) had mild social cognitive impairments (2 standard deviations below healthy comparison participants). Validity of the two social cognitive subgroups was indicated by significant differences in functioning, symptom load and nonsocial cognition. Our study shows that social cognitive tests can be used for clinical and cognitive subtyping. This is of potential relevance for treatment

Neurocognitive decrements are present in intellectually superior schizophrenia

Data suggest that individuals with schizophrenia (SZ) and superior intelligence can present without specific neurocognitive deficits. However, neurocognitive decrements, defined as worse cognition than expected, have been reported in practically all SZ cases. This study investigated if neurocognitive decrements are present in intellectually superior SZ by comparing the neuropsychological profile of SZ cases with IQ-matched healthy controls (HC) across intellectual levels. Participants with SZ and HCs were stratified into three IQ-groups; intellectually low (IQ 80–95; SZ n = 65 and HC n = 13), intellectually normal (IQ = 100–115; SZ n = 111 and HC n = 115), and intellectually superior (IQ = 120; SZ n = 20 and HC n = 50). A repeated measures multivariate analysis of co-variance compared performance on eight selected neuropsychological tests across IQ-strata and diagnostic group. Differences in clinical characteristics and social functioning in SZ across IQ-strata were investigated with multivariate and univariate analyses of variance. Intellectually superior SZ participants scored within normal limits, but had neurocognitive decrements compared to superior HCs. Decrements were of the same magnitude as in the low and normal IQ-strata. Levels of functional impairments and clinical characteristics in participants with SZ did not differ significantly across IQ-strata. Results indicate that neurocognitive decrements are present in intellectually superior SZ to the same extent as in intellectually low and intellectually normal SZ, supporting the notion that SZ is a neurocognitive disorder. Similar levels of social functional deficits and clinical symptoms suggest similar disease processes in SZ across intellectual level

Reading Emotions from Body Movement: A Generalized Impairment in Schizophrenia

Body language reading is a social cognitive process with importance for successful maneuvering of social situations. In this study, we investigated body language reading as assessed with human point-light displays in participants with a diagnosis of schizophrenia (n = 84) compared to healthy control participants (n = 84), aiming to answer three questions: (1) whether persons with a diagnosis of schizophrenia have poorer body language reading abilities than healthy persons; (2) whether some emotions are easier to read from body language than others, and if this is the same for individuals with schizophrenia and healthy individuals, and (3) whether there are sex differences in body language reading in participants with schizophrenia and healthy participants. A fourth research aim concerned associations of body language reading with symptoms and functioning in participants with schizophrenia. Scores on the body language reading measure was first standardized using a separate sample of healthy control participants (n = 101). Further results showed that persons with schizophrenia had impaired body language reading ability compared to healthy persons. A significant effect of emotion indicated that some emotions (happiness, neutral) were easier to recognize and this was so for both individuals with schizophrenia and healthy individuals. There were no sex differences for either diagnostic group. Body language reading ability was not associated with symptoms or functioning. In conclusion; schizophrenia was characterized by a global impairment in body language reading that was present for all emotions and across sex

Theory of mind in women with borderline personality disorder or schizophrenia: differences in overall ability and error patterns

Although borderline personality disorder (BPD) and schizophrenia (SZ) are notably different mental disorders, they share problems in social cognition—or understanding the feelings, intentions and thoughts of other people. To date no studies have directly compared the social cognitive abilities of individuals with these two disorders. In this study, the social cognitive subdomain theory of mind was investigated in women with BPD (n = 25), women with SZ (n = 25) and healthy women (n = 25). An ecologically valid video-based measure (Movie for the Assessment of Social Cognition) was used. For the overall score, women with SZ performed markedly below both healthy women and women with BPD, whereas women with BPD did not perform significantly different compared to the healthy control group. A statistically significant error type × group interaction effect indicated that the groups differed with respect to kind of errors. Whereas women with BPD made mostly overmentalizing errors, women with SZ in addition committed undermentalizing errors. Our study suggests different magnitude and pattern of social cognitive problems in BPD and SZ

Emotion perception, non-social cognition and symptoms as predictors of theory of mind in schizophrenia

Background: Theory of mind (ToM) can be divided into cognitive and affective ToM, and a distinction can be made between overmentalizing and undermentalizing errors. Research has shown that ToM in schizophrenia is associated with non-social and social cognition, and with clinical symptoms. In this study, we investigate cognitive and clinical predictors of different ToM processes. Methods: Ninety-one individuals with schizophrenia participated. ToM was measured with the Movie for the Assessment of Social Cognition (MASC) yielding six scores (total ToM, cognitive ToM, affective ToM, overmentalizing errors, undermentalizing errors and no mentalizing errors). Neurocognition was indexed by a composite score based on the non-social cognitive tests in the MATRICS Consensus Cognitive Battery (MCCB). Emotion perception was measured with Emotion in Biological Motion (EmoBio), a point-light walker task. Clinical symptoms were assessed with the Positive and Negative Syndrome Scale (PANSS). Seventy-one healthy control (HC) participants completed the MASC. Results: Individuals with schizophrenia showed large impairments compared to HC for all MASC scores, except overmentalizing errors. Hierarchical regression analyses with the six different MASC scores as dependent variables revealed that MCCB was a significant predictor of all MASC scores, explaining 8–18% of the variance. EmoBio increased the explained variance significantly, to 17–28%, except for overmentalizing errors. PANSS excited symptoms increased explained variance for total ToM, affective ToM and no mentalizing errors. Discussion: Both social and non-social cognition were significant predictors of ToM. Overmentalizing was only predicted by non-social cognition. Excited symptoms contributed to overall and affective ToM, and to no mentalizing errors

The factor structure of social cognition in schizophrenia: Weak evidence for separable domains

This study examined the factor structure of social cognition in a Norwegian sample of individuals diagnosed with schizophrenia (n = 83). Eight variables from three social cognitive tests from three theoretical domains were included: emotion processing, social perception and theory of mind. Factor analysis with maximum likelihood extraction and oblique rotation resulted in two factors using Kaiser's criterion. Although the two-factor model had better fit than a unifactorial model, it did not represent the data well. Two social cognitive variables did not load on either factor. The two extracted factors did not correspond to an expected distinction between low and high level of processing or between affective and cognitive processes. A non-negligible number of nonredundant residuals between observed and computed correlations suggested poor model fit. In conclusion, this study failed to identify separable dimensions of social cognition in spite of including measures from different theoretical domains

Neurocognitive profiles in treatment-resistant bipolar I and bipolar II disorder depression

Background The literature on the neuropsychological profiles in Bipolar disorder (BD) depression is sparse. The aims of the study were to assess the neurocognitive profiles in treatment-resistant, acutely admitted BD depression inpatients, to compare the neurocognitive functioning in patients with BD I and II, and to identify the demographic and clinical illness characteristics associated with cognitive functioning. Methods Acutely admitted BD I (n = 19) and BD II (n = 32) inpatients who fulfilled the DSM-IV-TR criteria for a major depressive episode were tested with the MATRICS Consensus Cognitive Battery (MCCB), the Wechsler Abbreviated Scale of Intelligence, the National Adult Reading Test, and a battery of clinical measures. Results Neurocognitive impairments were evident in the BD I and BD II depression inpatients within all MCCB domains. The numerical scores on all MCCB-measures were lower in the BD I group than in the BD II group, with a significant difference on one of the measures, category fluency. 68.4% of the BD I patients had clinically significant impairment (>1.5 SD below normal mean) in two or more domains compared to 37.5% of the BD II patients (p = 0.045). A significant reduction in IQ from the premorbid to the current level was seen in BD I but not BD II patients. Higher age was associated with greater neurocognitive deficits compared to age-adjusted published norms. Conclusions A high proportion of patients with therapy-resistant BD I or II depression exhibited global neurocognitive impairments with clinically significant severity. The cognitive impairments were more common in BD I compared to BD II patients, particularly processing speed. These findings suggest that clinicians should be aware of the severe neurocognitive dysfunction in treatment-resistant bipolar depression, particularly in BD I

A randomized controlled trial of training of affect recognition (TAR) in schizophrenia shows lasting effects for theory of mind

Schizophrenia is characterized by social cognitive impairments that predict functioning. Social cognitive training aims to target these impairments. Although it can improve the targeted social cognitive domain, it is unclear if the training generalizes to non-targeted domains and to functioning, with lasting effects. This randomized controlled trial examined the effect of a targeted facial affect recognition training program, Training of Affect Recognition (TAR), in persons with schizophrenia. Individuals with schizophrenia were randomized to receive treatment as usual and TAR (n = 24) or treatment as usual (n = 24) after assessments with a comprehensive protocol at baseline (T1). Participants were reassessed immediately after the intervention period (T2: after 8 weeks) and at 3-month follow-up (T3). The protocol included tests of social cognition (facial or body affect recognition, theory of mind), nonsocial cognition (Matrics Consensus Cognitive Battery), clinical symptoms (Positive and Negative Syndrome Scale, Calgary Depression Scale for Schizophrenia), functioning (self-reported, social or nonsocial functional capacity), self-esteem, self-efficacy and insight. Linear mixed models yielded a significant group × time interaction effect for a non-targeted social cognitive domain (theory of mind) and a trend-level effect for social functional capacity with the intervention group performing better over time. No beneficial effects on nonsocial cognition, other measures of functioning, clinical symptoms, or self-esteem/self-efficacy appeared for the TAR program. This study provides evidence for transfer and durability effects of facial affect recognition training to theory of mind, but also highlights the need for additional treatments to achieve functional benefits

GWAS meta-analysis reveals novel loci and genetic correlates for general cognitive function: a report form the COGENT consortium

The complex nature of human cognition has resulted in cognitive genomics lagging behind many other fields in terms of gene discovery using genome-wide association study (GWAS) methods. In an attempt to overcome these barriers, the current study utilized GWAS meta-analysis to examine the association of common genetic variation (~8M single-nucleotide polymorphisms (SNP) with minor allele frequency ⩾1%) to general cognitive function in a sample of 35 298 healthy individuals of European ancestry across 24 cohorts in the Cognitive Genomics Consortium (COGENT). In addition, we utilized individual SNP lookups and polygenic score analyses to identify genetic overlap with other relevant neurobehavioral phenotypes. Our primary GWAS meta-analysis identified two novel SNP loci (top SNPs: rs76114856 in the CENPO gene on chromosome 2 and rs6669072 near LOC105378853 on chromosome 1) associated with cognitive performance at the genome-wide significance level (P<5 × 10^−8). Gene-based analysis identified an additional three Bonferroni-corrected significant loci at chromosomes 17q21.31, 17p13.1 and 1p13.3. Altogether, common variation across the genome resulted in a conservatively estimated SNP heritability of 21.5% (s.e.=0.01%) for general cognitive function. Integration with prior GWAS of cognitive performance and educational attainment yielded several additional significant loci. Finally, we found robust polygenic correlations between cognitive performance and educational attainment, several psychiatric disorders, birth length/weight and smoking behavior, as well as a novel genetic association to the personality trait of openness. These data provide new insight into the genetics of neurocognitive function with relevance to understanding the pathophysiology of neuropsychiatric illness