It is widely accepted that borderline personality disorder (BPD) is associated with significant impairments in mentalization and theory of mind (ToM) which are considered as closely related concepts by many authors particularly in psychoanalytical circles. However, for understanding interpersonal difficulties in personality disorders, it is important to distinguish neuro-social cognitive impairment from the abnormal meta-social-cognitive style of patients.

The current systematic review aimed to conduct separate meta-analyses of ‘mentalization’ [reflective functioning (RF] and different aspects of ToM in BPD. A literature search was conducted to locate relevant articles published between January 1990 to July 2021. Random-effect meta-analyses were conducted in 34 studies involving 1448 individuals with BPD and 2006 healthy controls.

A very large impairment in RF was evident in BPD [d = 1.68, confidence interval (CI) = 1.17–2.19]. In contrast, ToM impairment was modest (d = 0.36, CI = 0.24–0.48). BPD patients underperformed healthy controls in ToM-reasoning (d = 0.44, CI = 0.32–0.56) but not ToM-decoding. Increased HyperToM (d = 0.60, CI = 0.41–0.79) and faux pas recognition (d = 0.62, CI = 0.35–0.90) errors in BPD compared to healthy controls were most robust ToM findings in this meta-analysis.

BPD is characterized by very severe deficits in RF and modest and selective abnormalities in ToM. Interpersonal problems and difficulties in processing social information in BPD can be best explained by patients' maldaptive meta-social cognitive style and top-down effects of these abnormalities rather than having a primary neuro-social cognitive deficit.

Obsessive-compulsive disorder (OCD) has been associated with cognitive deficits, particularly with executive functions. These findings support fronto-striatal dysfunction in OCD. However, it is not certain whether these findings are trait features of OCD. In recent years, a number of studies have investigated cognitive functions in unaffected relatives of OCD (OCDrel) but the findings of these studies are contradictory.

A systematic review in Pubmed and Scopus databases was performed until 18 March 2019, to locate the studies comparing cognitive functions of OCDrel with healthy controls and OCD patients (OCDpt). A random-effects meta-analysis was conducted.

Current meta-analysis included 16 studies including 527 OCDrel, 445 OCDpt and 639 healthy controls. Healthy controls overperformed OCDpt in all cognitive domains (d = 0.36–0.86). OCDrel underperformed healthy controls in inhibition (d = 0.58, CI = 0.29–0.86), planning (d = 0.45, CI = 0.28–0.63), decision-making (d = 0.58, CI = 0.19–0.98). OCDrel also had small-sized deficits in set-shifting (d = 0.37, CI = 0.04–0.69) and visual memory (d = 0.28, CI = 0.08–0.49). OCDpt underperformed OCDrel in visual memory (d = 0.45, CI = 0.22–0.67) and set-shifting (d = 0.23, CI = 0.04–0.42).

Current findings suggest that abnormalities in inhibition, planning/problem solving and reward-based decision-making are shared features of OCDrel and OCDpt and might be trait markers related to vulnerability for developing OCD. Visual memory and set-shifting deficits might potentially be biomarkers of incipient illness or subthreshold OCD presentation among OCDrel. Further exploration of cognitive heterogeneity in OCDrel and investigating the effects of the subtypes of OCD in probands on cognitive impairment in OCDrel are needed.

Previous findings indicated that schizophrenia patients might have a different personality structure from the general population on several dimensions of temperament and character. Some authors proposed that HA might be a marker of underlying genetic vulnerability to schizophrenia. Studies on high-risk subjects and first degree relatives of patients is essential to test the value of a measure as a marker of genetic vulnerability to a disease. Few studies tested the biopsychosocial model of personality on unaffected relatives of schizophrenia.

We compared the Temperament and Character (TCI) profiles of 94 first degree relatives of schizophrenia and 75 controls. We also investigated the relationship between schizotypy and TCI dimensions in the study sample.

The harm avoidance scores of the relatives of schizoprenia patients with schizotypal features were significantly higher. Self transcendence scores were also significantly higher among relatives with schizotypal features. In contrast, the relatives of the patients with schizophrenia who did not have schizotypal features had higher SD and C scores than the control group.

This finding is consistent with the previous findings which suggested harm avoidance as a vulnerability indicator of schizophrenia. Some character features like self transcendence might be also associated with schizotypal features.

Schizophrenia is associated with significant cognitive impairment. However, the pathophysiological mechanisms underlying cognitive dysfunction in schizophrenia remain unclear. Brain-derived neurotrophic factor (BDNF) and C-reactive protein (CRP) are among the most commonly investigated peripheral markers of cognition in schizophrenia.

A systematic review in PubMed and Scopus databases was performed until 31 January 2019 to assess the relationship between cognitive impairment, CRP and BDNF levels in schizophrenia. A random-effects meta-analysis was conducted.

Current meta-analysis included 21 studies including 2449 patients with schizophrenia-spectrum disorders. Overall, both BDNF [r = 0.12, confidence interval (CI) 0.04–0.19] and CRP (r = −0.13, CI 0.08–0.18) levels were very modestly but significantly related to cognitive functioning in schizophrenia (r = 0.12, CI 0.04–0.19). In meta-analyses of cognitive domains, BDNF levels were significantly associated with verbal memory (r = 0.16, CI 0.09–0.23), working memory (r = 0.14, CI 0.06–0.22), processing speed (r = 0.18, CI 0.10–0.26) and verbal fluency (r = 0.09, CI 0–0.18) performances. Elevated CRP levels were related to all cognitive domains (r = −0.09 to −0.13) except for fluency. Subgroup analyses suggested that the relationship between cognitive and BDNF levels were more pronounced in chronic samples.

Current findings suggest that cognitive impairment in schizophrenia is significantly related to elevated CRP and reduced BDNF levels in schizophrenia, particularly in chronic samples. However, small effect sizes of these correlations suggest that inflammation and decreased BDNF levels do not play a major role in cognitive dysfunction in most patients with schizophrenia. Further studies are needed to investigate the potential intermediating and confounding factors which can influence the level of relationship between inflammation, neurotrophic factors and cognition in schizophrenia.

Individuals with bipolar disorder (BD) have a higher prevalence of obesity and metabolic syndrome (MetS) compared with the general population. Obesity and MetS are associated with cognitive deficits and brain imaging abnormalities in the general population. Obesity and components of MetS might potentially associate with neuroimaging and neurocognitive findings in BD.

A literature search of studies investigating the association between obesity (and other components of MetS) and neurocognitive and neuroimaging findings in BD was conducted. In addition to a systematic review, a random-effects meta-analysis was conducted when sufficient data were available.

Twenty-three studies were included in the current systematic review. Overweight/obese patients were significantly associated with impaired neurocognition compared normal weight individuals with BD (d = 0.37). The most robust association between obesity and cognitive deficits in BD was observed in the cognitive subdomain of executive functions (d = 0.61). There was also evidence for a significant relationship between cognitive impairment in BD and other components of MetS including hypertension, dyslipidemia, and diabetes. Overweight/obese individuals with BD had more pronounced brain imaging abnormalities than normal weight individuals with BD.

Obesity and related cardiovascular risk factors significantly are associated with more severe cognitive and brain imaging abnormalities in BD. Medical co-morbidities can potentially contribute to functional decline observed in some patients throughout the course of BD.

Cognitive functioning in affective psychosis and schizoaffective disorder is much less studied compared with schizophrenia.

To quantitatively undertake a meta-analysis of the available data that directly compares cognitive functioning across schizophrenia, schizoaffective disorder and affective psychosis.

Following a thorough literature review, 31 studies that compared the performances of people with schizophrenia (1979 participants) with that of those with affective psychosis or schizoaffective disorder (1314 participants) were included. To determine the effect of demographic and clinical confounders, meta-regression and subgroup analyses were conducted.

In 6 of 12 cognitive domains, people with schizophrenia performed worse than people with schizoaffective disorder or affective psychosis. However, the between-group differences were small and the distribution of effect sizes showed substantial heterogeneity. The between-group differences were driven by a higher percentage of males, more severe negative symptoms and younger age at onset of illness in the schizophrenia samples.

Neuropsychological data do not provide evidence for categorical differences between schizophrenia and other groups. However, a subgroup of individuals with schizophrenia who have more severe negative symptoms may be cognitively more impaired than those with affective psychosis/schizoaffective disorder.