Early and late contingent negative variation (CNV) reflect different aspects of deficits in schizophrenia.

Abnormal reward processing and psychomotor slowing are well-known in schizophrenia (SZ). As a slow frontocentral potential, contingent negative variation (CNV) is associated with anticipatory attention, motivation and motor planning. The present study aims to evaluate the early and late amplitude and latencies of CNV in patients with SZ compared to healthy controls during a reward processing task and to show its association with clinical symptoms. We recruited 21 patients with SZ and 22 healthy controls to compare early and late CNV amplitude and latency values during a Monetary Incentive Delay (MID) Task between groups. Patients' symptom severity, levels of negative symptoms and depressive symptoms were assessed. Clinical features of the patients were further examined for their relation with CNV components. In conclusion, we found decreased early CNV amplitudes in SZ during the reward condition. They also displayed diminished and shortened late CNV responses for incentive cues, specifically at the central location. Furthermore, early CNV amplitudes exhibited a significant correlation with positive symptoms. Both CNV latencies were linked with medication dosage and the behavioural outcomes of the MID task. We revealed that early and late CNV exhibit different functions in neurophysiology and correspond to various facets of the deficits observed in patients. Our findings also emphasized that slow cortical potentials are indicative of deficient motivational processes as well as impaired reaction preparation in SZ. To gain a deeper understanding of the cognitive and motor impairments associated with psychosis, future studies must compare the effects of CNV in the early and late phases.

Reduced Reward Processing in Schizophrenia: A Comprehensive EEG Event-Related Oscillation Study.

It is well known that abnormal reward processing is a characteristic feature of various psychopathologies including schizophrenia (SZ). Reduced reward anticipation has been suggested as a core symptom of SZ. The present study aims to evaluate the event-related oscillations (EROs) delta, theta, alpha, beta, and gamma in patients with SZ during the Monetary Incentive Delay (MID) task, which elicits the neural activity of reward processing. Twenty-one patients with SZ and twenty-two demographically matched healthy controls were included in the study. EROs were compared between groups and correlation analyses were conducted to determine a possible relationship between clinical scores and ERO values. Compared with healthy controls, the SZ group had reduced (1) delta and theta amplitudes in the reward condition (2) total beta and non-incentive cue-related beta amplitudes, and (3) incentive cue-related frontal gamma amplitudes. These reductions can be interpreted as impaired dopaminergic neurotransmission and disrupted cognitive functioning in the reward processing of SZ. In contrast, SZ patients showed higher incentive cue-related theta and occipital gamma amplitudes compared to controls. These increments may reflect negative symptoms in SZ. Moreover, theta amplitudes showed a negative correlation with Calgary Depression Scale for Schizophrenia scores and a positive correlation with attentional impulsivity. This is the first study showing the impairments of SZ patients in EROs from delta to gamma frequency bands compared with healthy controls during reward anticipation. Being the first comprehensive study, our results can be interpreted as providing evidence for disrupted brain dynamics in the reward processing of SZ studied by EROs. It may become possible to help patients' wellness by improving our understanding of reward processing in schizophrenia and developing innovative rehabilitation treatments based on these findings.

Abnormal Structural Network Communication Reflects Cognitive Deficits in Schizophrenia.

Schizophrenia has long been thought to be a disconnection syndrome and several previous studies have reported widespread abnormalities in white matter tracts in individuals with schizophrenia. Furthermore, reductions in structural connectivity may also impair communication between anatomically unconnected pairs of brain regions, potentially impacting global signal traffic in the brain. Therefore, we used different communication models to examine direct and indirect structural connections (polysynaptic) communication in large-scale brain networks in schizophrenia. Diffusion-weighted magnetic resonance imaging scans were acquired from 62 patients diagnosed with schizophrenia and 35 controls. In this study, we used five network communication models including, shortest paths, navigation, diffusion, search information and communicability to examine polysynaptic communication in large-scale brain networks in schizophrenia. We showed less efficient communication between spatially widespread brain regions particulary encompassing cortico-subcortical basal ganglia network in schizophrenia group relative to controls. Then, we also examined whether reduced communication efficiency was related to clinical symptoms in schizophrenia group. Among different measures of communication efficiency, only navigation efficiency was associated with global cognitive impairment across multiple cognitive domains including verbal learning, processing speed, executive functions and working memory, in individuals with schizophrenia. We did not find any association between communication efficiency measures and positive or negative symptoms within the schizophrenia group. Our findings are important for improving our mechanistic understanding of neurobiological process underlying cognitive symptoms in schizophrenia.

Negative symptoms are associated with modularity and thalamic connectivity in schizophrenia.

Negative symptoms, including avolition, anhedonia, asociality, blunted affect and alogia are associated with poor long-term outcome and functioning. However, treatment options for negative symptoms are limited and neurobiological mechanisms underlying negative symptoms in schizophrenia are still poorly understood. Diffusion-weighted magnetic resonance imaging scans were acquired from 64 patients diagnosed with schizophrenia and 35 controls. Global and regional network properties and rich club organization were investigated using graph analytical methods. We found that the schizophrenia group had higher modularity, clustering coefficient and characteristic path length, and lower rich connections compared to controls, suggesting highly connected nodes within modules but less integrated with nodes in other modules in schizophrenia. We also found a lower nodal degree in the left thalamus and left putamen in schizophrenia relative to the control group. Importantly, higher modularity was associated with greater negative symptoms but not with cognitive deficits in patients diagnosed with schizophrenia suggesting an alteration in modularity might be specific to overall negative symptoms. The nodal degree of the left thalamus was associated with both negative and cognitive symptoms. Our findings are important for improving our understanding of abnormal white-matter network topology underlying negative symptoms in schizophrenia.

Deficits in Analytic and Common-Sense Reasoning in Schizophrenia.

ABSTRACT: Human rationality has a dual nature including analytic and common-sense thinking. Symptoms of schizophrenia have been suggested to be related to deficits in these aspects of logical reasoning. However, empirical studies investigating logical reasoning errors in schizophrenia and their clinical and neurocognitive correlates are scarce. Formal thought disorder and theory of mind (ToM) might be particularly important for understanding logical reasoning errors in schizophrenia. The current study compared the performances of 80 patients with schizophrenia with those of 49 healthy controls on syllogistic and counterfactual reasoning tasks and investigated clinical, neuropsychological, and social cognitive correlates of logical reasoning in schizophrenia. Patients with schizophrenia were impaired in both analytic and common-sense thinking. ToM impairment was a significant predictor of analytic reasoning abilities in schizophrenia. Executive functions and verbal memory were also significantly associated with analytic reasoning in schizophrenia. Further studies investigating logical reasoning errors in the early phases of the illness are needed.

Social Cognition in Opioid Use Disorder.

Background: Opioid use disorder (OUD) is associated with significant functional impairment and neurocognitive dysfunction, but only a handful of studies have investigated social cognitive abilities in this condition. This study aimed to investigate facial emotion recognition accuracy/biases and two different aspects of theory of mind (ToM) (ToM-decoding vs ToM-reasoning) in people with recovered OUD. Methods: The participants included 32 people with recovered OUD who were on Buprenorphine + Naloxone (B/N) maintenance treatment and 32 healthy controls. In addition to neurocognitive tasks, both groups were assessed by a facial emotion recognition task, the faux pas recognition task, and the reading the mind from the eyes task. Results: In comparison to healthy controls, people on B/N maintenance treatment showed deficits in facial emotion recognition (d = 1.32) and both aspects of ToM (d = 0.87-1.21). In analyses of individual emotions, people on B/N maintenance treatment had decreased accuracy in recognition of anger and fear and had a bias to identify other emotions as sad. The duration of opioid use was robustly associated with difficulties in the recognition of anger. Conclusion: People in B/N maintenance treatment have significant difficulties in recognizing the emotions and mental states of others. Deficits in social cognition might be important for understanding the difficulties in interpersonal and social functioning in people with OUD.

Evaluating the tendencies of community practitioners who actively practice in child and adolescent psychiatry to diagnose and treat DSM-5 attenuated psychotic syndrome.

The detection of individuals at clinical ultra-high risk for psychosis (CHR-P) may be a key limiting step for early interventions, and there is some uncertainty regarding the true clinical reliability of the CHR-P states. The aim of this study was to explore how practitioners who were in the direct treatment of children with psychiatric disorders [child psychiatry specialists/trainees (n = 227, n = 131), adult psychiatrists (n = 27), and child neurologists (n = 2)] perceive the DSM-5-Attenuated Psychosis Syndrome (DSM-5-APS), and their clinical routine practice in the treatment of it. Three vignettes describing fictional cases presented with symptoms of either DSM-5-Schizophrenia, DSM-5-APS, and no psychotic symptoms were created. We asked these practitioners to apply a DSM-5 diagnosis and to choose appropriate treatment(s) for these vignettes. Of the responders, 43% correctly diagnosed the APS vignette, whereas 37.4% mentioned that it had a full-blown psychotic episode. Regarding the therapeutic approach for the APS vignette, 72.1% of all practitioners chose a psychopharmacological intervention and 32% individual psychotherapy. This study showed that the diagnostic inter-rater reliability of the DSM-5-APS among child/adolescent mental health practitioners was consistent with the results from the DSM-5 field trials (Kappa = 0.46). Moreover, almost three in four practitioners endorsed psychopharmacological intervention as a treatment option for the DSM-5-APS case. The lack of evidence of psychopharmacological interventions in CHR-P situations emphasizes that the least harmful interventions should be recommended. Thus, our findings indicated a need for raising awareness regarding the CHR-P paradigm and its treatment as well as the development of solid guidelines that can be implemented in clinical practice.

A meta-analysis of theory of mind and 'mentalization' in borderline personality disorder: a true neuro-social-cognitive or meta-social-cognitive impairment?

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Resting state functional connectivity in adolescent synthetic cannabinoid users with and without attention-deficit/hyperactivity disorder.

OBJECTIVE: Synthetic cannabinoids (SCs) have become increasingly popular in recent years, especially among adolescents. The first aim of the current study was to examine resting-state functional connectivity (rsFC) in SC users compared to controls. Our second aim was to examine the influence of comorbid attention-deficit/hyperactivity disorder (ADHD) symptomatology on rsFC changes in SC users compared to controls. METHODS: Resting-state functional magnetic resonance imaging (fMRI) analysis included 25 SC users (14 without ADHD and 11 with ADHD combined type) and 12 control subjects. RESULTS: We found (i) higher rsFC between the default mode network (DMN) and salience network, dorsal attention network and cingulo-opercular network, and (ii) lower rsFC within the DMN and between the DMN and visual network in SC users compared to controls. There were no significant differences between SC users with ADHD and controls, nor were there any significant differences between SC users with and without ADHD. CONCLUSIONS: We found the first evidence of abnormalities within and between resting state networks in adolescent SC users without ADHD. In contrast, SC users with ADHD showed no differences compared to controls. These results suggest that comorbidity of ADHD and substance dependence may show different rsFC alterations than substance use alone.

Meta-analysis of neurocognitive deficits in unaffected relatives of obsessive-compulsive disorder (OCD): comparison with healthy controls and patients with OCD.

BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

Peripheral inflammatory and neurotrophic biomarkers of cognitive impairment in schizophrenia: a meta-analysis.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Neurococognitive and neuroimaging correlates of obesity and components of metabolic syndrome in bipolar disorder: a systematic review.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Rich club and reward network connectivity as endophenotypes for alcohol dependence: a diffusion tensor imaging study.

We aimed to examine the whole-brain white matter connectivity and local topology of reward system nodes in patients with alcohol use disorder (AUD) and unaffected siblings, relative to healthy comparison individuals. Diffusion-weighted magnetic resonance imaging scans were acquired from 18 patients with AUD, 15 unaffected siblings of AUD patients and 15 healthy controls. Structural networks were examined using network-based statistic and connectomic analysis. Connectomic analysis showed a significant ordered difference in normalized rich club organization (AUD < Siblings < Controls). We also found rank ordered differences (Control > Sibling > AUD) for both nodal clustering coefficient and nodal local efficiency in reward system nodes, particularly left caudate, right putamen and left hippocampus. Network-based statistic analyses showed that AUD group had significantly weaker connectivity than controls in the right hemisphere, mostly in the edges connecting putamen and hippocampus with other brain regions. Our results suggest that reward system network abnormalities, especially in subcortical structures, and impairments in rich-club organization might be related to the familial predisposition for AUD.

Relationship between social-cognitive and social-perceptual aspects of theory of mind and neurocognitive deficits, insight level and schizotypal traits in obsessive-compulsive disorder.

OBJECTIVE: The primary aim of the current study was to investigate different aspects of theory of mind (ToM), including social-cognitive (ToM-reasoning) and social-perceptual (ToM-decoding) in obsessive-compulsive disorder (OCD). We also aimed to investigate the relationship between ToM, neurocognition and a number of clinical variables including overvalued ideas, schizotypal personality traits, level of insight, and disease severity. METHOD: Thirty-four patients who have been diagnosed with OCD according to DSM-IV and 30 healthy controls were included in the study. All participants were given a neuropsychological battery including tasks measuring ToM-reasoning, ToM-decoding and other neurocognitive functions. Schizotypal Personality Questionnaire (SPQ), Yale Brown Obsession and Compulsion Scale (YBOC-S) and Overvalued Ideas Scale (OVIS) were also administered to the participants. RESULTS: Patients with OCD showed significant deficits in both aspects of ToM. ToM performances of patients showed a significant positive correlation with neurocognitive functions. When controlled for general cognition factor, patient-control difference for ToM-reasoning (F = 3,917; p = 0,05), but not ToM-decoding, remained statistically significant. ToM-reasoning impairment of patients was significantly related to the severity of OCD symptoms and poor insight (p = 0,026 and p = 0,045, respectively). On the other hand, general cognitive factor (ß = 0,778; t = 3,146; p = 0,04) was found to be the only significant predictor of ToM-reasoning in OCD patients in the multiple linear regression model. CONCLUSION: OCD is associated with ToM impairment, which is related to schizotypal traits, disease severity and poor insight, yet neurocognitive deficits also significantly contribute to this finding. However, ToM-reasoning impairment could be considered as a relatively distinct feature of OCD, which is partly separate from general cognitive deficits.

Revising Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, criteria for the bipolar disorders: Phase I of the AREDOC project.

OBJECTIVE: To derive new criteria sets for defining manic and hypomanic episodes (and thus for defining the bipolar I and II disorders), an international Task Force was assembled and termed AREDOC reflecting its role of Assessment, Revision and Evaluation of DSM and other Operational Criteria. This paper reports on the first phase of its deliberations and interim criteria recommendations. METHOD: The first stage of the process consisted of reviewing Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, and recent International Classification of Diseases criteria, identifying their limitations and generating modified criteria sets for further in-depth consideration. Task Force members responded to recommendations for modifying criteria and from these the most problematic issues were identified. RESULTS: Principal issues focussed on by Task Force members were how best to differentiate mania and hypomania, how to judge 'impairment' (both in and of itself and allowing that functioning may sometimes improve during hypomanic episodes) and concern that rejecting some criteria (e.g. an imposed duration period) might risk false-positive diagnoses of the bipolar disorders. CONCLUSION: This first-stage report summarises the clinical opinions of international experts in the diagnosis and management of the bipolar disorders, allowing readers to contemplate diagnostic parameters that may influence their clinical decisions. The findings meaningfully inform subsequent Task Force stages (involving a further commentary stage followed by an empirical study) that are expected to generate improved symptom criteria for diagnosing the bipolar I and II disorders with greater precision and to clarify whether they differ dimensionally or categorically.

Meta-Analysis of Social Cognition in Mild Cognitive Impairment.

Social cognitive abilities are impaired in Alzheimer disease and other dementias. Recent studies suggested that social cognitive abilities might be also impaired in mild cognitive impairment (MCI). Current meta-analysis aimed to summarize available evidence for deficits in theory of mind (ToM) and emotion recognition in MCI. In this meta-analysis of 17 studies, facial emotion recognition and ToM performances of 513 individuals with MCI and 693 healthy controls were compared. Mild cognitive impairment was associated with significant impairments falling in the medium effect sizes range in ToM ( d = 0.63) and facial emotion recognition ( d = 0.58). Among individual emotions, recognition of fear and sadness were particularly impaired. There were no significant between-group differences in recognition of disgust, happiness, and surprise. Social cognitive deficits were more severe in multidomain MCI. There is a need for longitudinal studies investigating the potential role of social cognitive impairment in predicting conversion to dementia.

Social Cognition in Multiple Sclerosis: a Meta-Analysis.

Multiple sclerosis (MS) is associated with cognitive decline and impairment in social functioning. Accumulating evidence suggests that patients with MS are impaired in social cognition, including theory of mind (ToM) and emotion recognition. In this meta-analysis of 24 studies, facial emotion recognition and ToM performances of 989 patients with MS and 836 healthy controls were compared. MS was associated with significant impairments with medium effect sizes in ToM (d = 0.57) and facial emotion recognition (d = 0.61). Among individual emotions recognition of fear and anger were particularly impaired. The severity of social cognitive deficits was significantly associated with non-social cognitive impairment. These deficits in social cognition may underpin difficulties in social functioning in MS. However, there is a need for further studies investigating the longitudinal evolution of social cognitive deficits and their neural correlates in MS.

Meta-Analysis of Facial Emotion Recognition in Behavioral Variant Frontotemporal Dementia: Comparison With Alzheimer Disease and Healthy Controls.

Behavioral disturbances and lack of empathy are distinctive clinical features of behavioral variant frontotemporal dementia (bvFTD) in comparison to Alzheimer disease (AD). The aim of this meta-analytic review was to compare facial emotion recognition performances of bvFTD with healthy controls and AD. The current meta-analysis included a total of 19 studies and involved comparisons of 288 individuals with bvFTD and 329 healthy controls and 162 bvFTD and 147 patients with AD. Facial emotion recognition was significantly impaired in bvFTD in comparison to the healthy controls (d = 1.81) and AD (d = 1.23). In bvFTD, recognition of negative emotions, especially anger (d = 1.48) and disgust (d = 1.41), were severely impaired. Emotion recognition was significantly impaired in bvFTD in comparison to AD in all emotions other than happiness. Impairment of emotion recognition is a relatively specific feature of bvFTD. Routine assessment of social-cognitive abilities including emotion recognition can be helpful in better differentiating between cortical dementias such as bvFTD and AD.

Social cognition in temporal lobe epilepsy: A systematic review and meta-analysis.

Objective: There is increasing evidence suggesting that social cognitive abilities are impaired in temporal lobe epilepsy (TLE), the most common form of focal epilepsies. Methods: In this meta-analysis, 31 studies investigating theory of mind (ToM) and facial emotion recognition performances of 1356 patients with TLE (351 postsurgery) and 859 healthy controls were included. Results: Patients with TLE had significant deficits in ToM (d = 0.73­0.89) and recognition of facial emotions. There were no significant differences in severity of social cognitive deficits between patients with TLE with or without medial temporal lobectomy. Earlier onset of seizures was associated with ToM impairment. Right-sided TLE was associated with more severe deficits in recognition of fear, sadness, and disgust. Conclusions: Social cognitive information processing is impaired in TLE, and the potential role of these deficits in functional impairment needs to be further investigated.