Deficit of social cognition in subjects with surgically treated frontal lobe lesions and in subjects affected by schizophrenia.
Ontology highlight
ABSTRACT: The ability of humans to predict and explain other people's behaviour by attributing independent mental states such as desires and beliefs to them, is considered to be due to our ability to construct a "Theory of Mind". Recently, several neuroimaging studies have implicated the medial frontal lobes as playing a critical role in a dedicated "mentalizing" or "Theory of Mind" network in the human brain. In this study we compare the performance of patients with right and left medial prefrontal lobe lesions in theory of mind and in social cognition tasks, with the performance of people with schizophrenia. We report a similar social cognitive profile between patients with prefrontal lobe lesions and schizophrenic subjects in terms of understanding of false beliefs, in understanding social situations and in using tactical strategies. These findings are relevant for the functional anatomy of "Theory of Mind".
Project description:Social behaviour of healthy humans and its neural correlates have been extensively studied in social neuroscience and neuroeconomics. Whereas it is well established that several types of epilepsies, such as frontal lobe epilepsy, lead to social cognitive impairments, experimental evidence on how these translate into behavioural symptoms is scarce. Furthermore, it is unclear whether social cognitive or behavioural disturbances have an impact on therapy adherence, which is critical for effective disease management, but generally low in these patients. In order to investigate the relationship between social cognition, social behaviour, and therapy adherence in patients with frontal lobe epilepsies (FLE), we designed a study combining conventional neuropsychological with behavioural economic and functional magnetic resonance imaging (fMRI) methodology. Fifteen patients and 15 healthy controls played a prisoners' dilemma game (an established game to operationalize social behaviour) while undergoing fMRI. Additionally, social cognitive, basic neuropsychological variables, and therapy adherence were assessed. Our results implicate that social behaviour is indeed affected and can be quantified using neuroeconomic methods in patients with FLE. Impaired social behaviour in these patients might be a consequence of altered brain activation in the medial prefrontal cortex and play a role in low therapy adherence. Finally, this study serves as an example of how to integrate neuroeconomic methods in neurology.
Project description:Many tests of specific 'executive functions' show deficits after frontal lobe lesions. These deficits appear on a background of reduced fluid intelligence, best measured with tests of novel problem solving. For a range of specific executive tests, we ask how far frontal deficits can be explained by a general fluid intelligence loss. For some widely used tests, e.g. Wisconsin Card Sorting, we find that fluid intelligence entirely explains frontal deficits. When patients and controls are matched on fluid intelligence, no further frontal deficit remains. For these tasks too, deficits are unrelated to lesion location within the frontal lobe. A second group of tasks, including tests of both cognitive (e.g. Hotel, Proverbs) and social (Faux Pas) function, shows a different pattern. Deficits are not fully explained by fluid intelligence and the data suggest association with lesions in the right anterior frontal cortex. Understanding of frontal lobe deficits may be clarified by separating reduced fluid intelligence, important in most or all tasks, from other more specific impairments and their associated regions of damage.
Project description:Intracranial lesions in children often have good prognoses, allowing long-term survival. Cognitive functions, crucial for life quality, need more attention. Previous research has focused on adults, with pediatric studies limited by varied lesions and complex treatments. This study aims to evaluate cognitive and brain network changes in children with frontal lobe lesions, which significantly impact cognitive function, using a before-and-after comparison. The study enrolled 20 children with frontal lesions who underwent fMRI and cognitive tests before and after surgery, with only surgical treatment initially. Brain network changes were evaluated using functional metrics, and cognitive shifts were measured through test scores. Correlations were analyzed to explore brain mechanisms behind cognitive changes. Additionally, 20 healthy children underwent the same assessments for baseline data. Preliminary evidence of cognitive recovery, notably in social cognition, was observed about three months post-surgery, potentially linked to increased functional connectivity between the right lingual gyrus and right middle temporal gyrus. Children with frontal lobe lesions have demonstrated short-term postoperative cognitive improvement and associated reorganization and repair of brain networks, though this capacity for repair may diminish over time. This underscores the importance of timely rehabilitation interventions. This study offers unique insights into cognitive neuroscience and potential rehabilitation targets.
Project description:Self- disgust is an adverse self-conscious emotion that plays an important role in psychopathology and well-being. However, self-disgust has received little attention in the emotion literature, therefore our understanding of the processes underlying the experience of self-disgust is relatively scarce, although neuropsychological and neuroimaging studies support the idea that this emotion may heavily rely on frontal lobe-related cognition. To test this hypothesis, in two studies we investigated the relationship between state and trait levels of self-disgust, cognition and emotion regulation in healthy adults. Specifically, in Study 1 we tested the hypothesis that emotion regulation strategies (avoidance, suppression, and cognitive reappraisal) mediate the relationship between inhibition ability and state and trait levels of self-disgust. In Study 2, we followed a more comprehensive approach to test the hypothesis that frontal lobe-related cognitive processes (updating, Theory of Mind-ToM-, and self-attention) are closely related to the experience of self-disgust in healthy adults. Overall, across these studies, we found evidence to support the idea that inhibition ability and ToM may play a role in the experience of state and trait self-disgust, respectively. However, we did not find consistent evidence across the two studies to support the notion held in the literature that the experience of self- conscious emotions, in this case self-disgust, is heavily dependent on frontal lobe-related cognition.
Project description:Cortical abnormalities are considered a neurobiological characteristic of schizophrenia. However, the pattern of such deficits as they progress over the illness remains poorly understood. The goal of this project was to assess the progression of cortical thinning in frontal and temporal cortical regions in schizophrenia, and determine whether relationships exist between them and neuropsychological and clinical symptom profiles. As part of a larger longitudinal 2-year follow-up study, schizophrenia (n=20) and healthy participants (n=20) group-matched for age, gender, and recent-alcohol use, were selected. Using MRI, estimates of gray matter thickness were derived from primary anatomical gyri of the frontal and temporal lobes using surface-based algorithms. These values were entered into repeated-measures analysis of variance models to determine group status and time effects. Change values in cortical regions were correlated with changes in neuropsychological functioning and clinical symptomatology. Results revealed exaggerated cortical thinning of the middle frontal, superior temporal, and middle temporal gyri in schizophrenia participants. These thickness changes strongly influenced volumetric reductions, but were not related to shrinking surface area. Neuropsychological and clinical symptom profiles were stable in the schizophrenia participants despite these neuroanatomic changes. Overall it appears that ongoing abnormalities in the cerebral cortex continue after initial onset of schizophrenia, particularly the lateral aspects of frontal and temporal regions, and do not relate to neuropsychological or clinical measures over time. Maintenance of neuropsychological performance and clinical stability in the face of changing neuroanatomical structure suggests the involvement of alternative compensatory mechanisms.
Project description:Schizophrenia is a neurodevelopmental psychiatric disorder characterized by a variety of structural brain abnormalities that appear to progress across the course of illness. Schizophrenia also is highly heritable, and one gene that has emerged as a possible susceptibility factor is G72. G72 influences brain development and activity by an as-yet unclear mechanism, and multiple studies have reported associations between G72 and schizophrenia. We were interested in linking these domains of investigation by determining whether G72 also influences the rate of longitudinal structural brain changes in individuals with schizophrenia. As part of the Iowa Longitudinal Study of Recent Onset Psychoses, we genotyped four G72 polymorphisms previously associated with schizophrenia in 110 subjects with schizophrenia or schizoaffective disorder from whom we had obtained two brain MRI scans an average of 3 years apart. The four polymorphisms captured three haplotypes, one of which was strongly associated with an increased rate of frontal lobe volume decrement. This same haplotype was also associated with more severe psychotic symptoms at the time of the second scan. These data thus suggest that variation in G72 modulates the progressive brain changes that characterize schizophrenia.
Project description:The purpose of this pilot study was to assess the efficacy of a new social cognition (SC) remediation intervention, the Social Cognition Individualized Activities Lab (SoCIAL), for subjects with schizophrenia. The training includes a module for emotion recognition and one for theory of mind. A comparison with a validated cognitive remediation intervention, the Social Skills And Neurocognitive Individualized Training (SSANIT), was conducted to verify the efficacy of the SoCIAL in improving SC. Ten stabilized patients with schizophrenia accepted to participate. Five patients were randomized to SoCIAL and five to SSANIT. The SoCIAL intervention includes individual sessions of neurocognitive individualized training (NIT) and group sessions of SC training. SSANIT includes individual sessions of NIT and group sessions of social skills individualized training. The interventions were matched for the overall treatment duration (20 weeks) and for the frequency of the sessions (two times a week, one for SoCIAL or social skills individualized training and one for NIT, with a duration of 80 minutes for each session). Results showed a significant treatment effect (effect size: Cohen's d 0.32) on the primary outcome; in fact, only the SoCIAL intervention improved theory of mind. Patients receiving the SoCIAL intervention also showed an improvement of avolition. These preliminary findings support further development of the SoCIAL and suggest that cognitive remediation should include an SC module.
Project description:OBJECTIVES:This study had 2 objectives: First, to explore the gender-related differences in emotional processing (EP) and theory of mind-both cognitive (CToM) and affective (AToM)-in patients with schizophrenia and in a control group of healthy subjects; and, second, to examine, from a gender perspective, the possible association between EP and CToM in the AToM performance. METHODS:Forty patients with schizophrenia/schizoaffective disorder were recruited and matched by gender, age and years of education with 40 healthy subjects. EP was measured by the pictures of facial affect (POFA) test. CToM was measured using first- and second-order false-belief (FB) stories. AToM was measured by the reading the mind in the eyes test (RMET). Group and gender differences in CToM were analysed using the X2 test, whereas EP and AToM were analysed using the non-parametric Mann-Whitney U Test and a general linear model. Results were adjusted by intelligence quotient and negative symptomatology. RESULTS:Patients with schizophrenia underperformed against healthy subjects in the POFA test, second-order FB, and RMET, but not in first-order FB. No significant gender differences were found. However, there was a trend showing that females outperformed males in the POFA ( P = 0.056). Group ( P < 0.001), POFA ( P < 0.001) and second-order FB ( P = 0.022) were the best factors predicting RMET performance (adjusted R2 = 0.584). CONCLUSIONS:Our results suggest that the illness is the main factor related to the deficit in social cognition, except for the basic aspects of the CToM that were unimpaired in most patients. Nevertheless, the influence of female gender in EP should not be neglected in any group. Finally, the hierarchal interaction between these domains is discussed.
Project description:BackgroundStudies on cognition in multiple system atrophy (MSA) patients are limited.MethodsA total of 110 MSA patients were evaluated using Addenbrooke's Cognitive Examination-Revised (ACE-R), Frontal Assessment Battery (FAB), Frontal Behavioral Inventory (FBI), and Unified MSA Rating Scale (UMSARS) tests. Fifty-five age-, sex-, education- and domicile-matched healthy controls were recruited to perform the FAB and ACE-R scales.ResultsApproximately 32.7% of the patients had global cognitive deficits with the most impaired domain being verbal fluency and visuospatial ability (26.4%), followed by memory (24.5%), language (20%) and orientation/attention (20%) based on a cut-off score of ACE-R ≤ 70. A total of 41.6% of the patients had frontal lobe dysfunction, with inhibitory control (60.9%) as the most impaired domain based on a cut-off score of FAB ≤14. Most patients (57.2%) showed moderate frontal behavior changes (FBI score 4-15), with incontinence (64.5%) as the most impaired domain. The binary logistic regression model revealed that an education level < 9 years (OR:13.312, 95% CI:2.931-60.469, P = 0.001) and UMSARS ≥ 40 (OR: 2.444, 95%CI: 1.002-5.962, P< 0.049) were potential determinants of abnormal ACE-R, while MSA-C (OR: 4.326, 95%CI: 1.631-11.477, P = 0.003), an education level < 9 years (OR:2.809 95% CI:1.060-7.444, P = 0.038) and UMSARS ≥ 40 (OR:5.396, 95%CI: 2.103-13.846, P < 0.0001) were potential determinants of abnormal FAB.ConclusionsCognitive impairment is common in Chinese MSA patients. MSA-C patients with low education levels and severe motor symptoms are likely to experience frontal lobe dysfunction, while MSA patients with low education levels and severe motor symptoms are likely to experience global cognitive deficits. These findings strongly suggest that cognitive impairment should not be an exclusion criterion for the diagnosis of MSA.
Project description:Abnormalities of prefrontal cortical function are prominent features of schizophrenia and have been associated with genetic risk, suggesting that susceptibility genes for schizophrenia may impact on the molecular mechanisms of prefrontal function. A potential susceptibility mechanism involves regulation of prefrontal dopamine, which modulates the response of prefrontal neurons during working memory. We examined the relationship of a common functional polymorphism (Val(108/158) Met) in the catechol-O-methyltransferase (COMT) gene, which accounts for a 4-fold variation in enzyme activity and dopamine catabolism, with both prefrontally mediated cognition and prefrontal cortical physiology. In 175 patients with schizophrenia, 219 unaffected siblings, and 55 controls, COMT genotype was related in allele dosage fashion to performance on the Wisconsin Card Sorting Test of executive cognition and explained 4% of variance (P = 0.001) in frequency of perseverative errors. Consistent with other evidence that dopamine enhances prefrontal neuronal function, the load of the low-activity Met allele predicted enhanced cognitive performance. We then examined the effect of COMT genotype on prefrontal physiology during a working memory task in three separate subgroups (n = 11-16) assayed with functional MRI. Met allele load consistently predicted a more efficient physiological response in prefrontal cortex. Finally, in a family-based association analysis of 104 trios, we found a significant increase in transmission of the Val allele to the schizophrenic offspring. These data suggest that the COMT Val allele, because it increases prefrontal dopamine catabolism, impairs prefrontal cognition and physiology, and by this mechanism slightly increases risk for schizophrenia.