Although previous behavioral studies have shown that schizophrenia patients have impaired theory of mind (ToM), the neural mechanisms associated with this impairment are poorly understood. This study aimed to identify the neural mechanisms of ToM in schizophrenia, using functional magnetic resonance imaging (fMRI) with a belief attribution task.
In the scanner, 12 schizophrenia patients and 13 healthy control subjects performed the belief attribution task with three conditions: a false belief condition, a false photograph condition, and a simple reading condition.
For the false belief versus simple reading conditions, schizophrenia patients showed reduced neural activation in areas including the temporoparietal junction (TPJ) and medial prefrontal cortex (MPFC) compared with controls. Further, during the false belief versus false photograph conditions, we observed increased activations in the TPJ and the MPFC in healthy controls, but not in schizophrenia patients. For the false photograph versus simple reading condition, both groups showed comparable neural activations.
Schizophrenia patients showed reduced task-related activation in the TPJ and the MPFC during the false belief condition compared with controls, but not for the false photograph condition. This pattern suggests that reduced activation in these regions is associated with, and specific to, impaired ToM in schizophrenia.
"mPFC and lower portion of the precuneus ; Amodio and Frith , 2006 ; Van Overwalle and Baetens , 2009 ; Mar , 2011 ; Schilbach et al . , 2012 ) during completion of false belief tasks ( which require inferring others ' representations of reality , which does not correspond with their own perception reality ; Lee et al . , 2011 ) . The observed pattern of findings suggest that Theory of Mind is not in general impaired in Schizophrenia , but that it instead reflects deficits in reasoning when complex non - factual elements are needed to understand the social environment ( Kern et al . , 2009 ; Sparks et al . , 2010 ) . Both counterfactual and false belief infer"
[Show abstract][Hide abstract] ABSTRACT: Counterfactual reasoning is a hallmark of human thought, enabling the capacity to shift from perceiving the immediate environment to an alternative, imagined perspective. Mental representations of counterfactual possibilities (e.g., imagined past events or future outcomes not yet at hand) provide the basis for learning from past experience, enable planning and prediction, support creativity and insight, and give rise to emotions and social attributions (e.g., regret and blame). Yet remarkably little is known about the psychological and neural foundations of counterfactual reasoning. In this review, we survey recent findings from psychology and neuroscience indicating that counterfactual thought depends on an integrative network of systems for affective processing, mental simulation, and cognitive control. We review evidence to elucidate how these mechanisms are systematically altered through psychiatric illness and neurological disease. We propose that counterfactual thinking depends on the coordination of multiple information processing systems that together enable adaptive behavior and goal-directed decision making and make recommendations for the study of counterfactual inference in health, aging, and disease.
Frontiers in Human Neuroscience 07/2015; 9. DOI:10.3389/fnhum.2015.00420 · 2.99 Impact Factor
"Several studies have reported aberrant activation in schizophrenia patients of MPFC and/or PCC (Blackwood et al., 2004; Holt et al., 2011a; Lee et al., 2011; Bedford et al., 2012; van der Meer et al., 2013) (CMS structures) and the LTC (Brune et al., 2008; Walter et al., 2009; Murphy et al., 2010; Pedersen et al., 2012) during SR tasks. A few studies have also linked altered CMS and LTC function during SR with subsyndromal psychotic symptoms (Brune et al., 2011; Modinos et al., 2011; Brent et al., 2014a). "
[Show abstract][Hide abstract] ABSTRACT: Background: Deficits in the capacity to reflect about the self and others (“social reflection” [SR]) have been iden- tified in schizophrenia, as well as in people with a genetic or clinical risk for the disorder. However, the neural underpinnings of these abnormalities are incompletely understood. Methods: Responses of a network of brain regions known to be involved in self and other processing (e.g., medial prefrontal cortex (MPFC), posterior cingulate cortex (PCC), and superior temporal gyrus (STG)) were measured during SR in 16 first-degree, non-psychotic relatives (RELS) of schizophrenia patients and 16 healthy con- trols (CONS). Because of prior evidence linking dysfunction in this network and delusions, associations be- tween SR-related responses of this network and subclinical delusions (measured using the Peters et al. Delusions Inventory) were also examined.
Results: Compared with CONS, RELS showed significantly less SR-related activity of the right and left PCC and STG. Moreover, response magnitudes were negatively correlated with levels of delusional thinking across both groups. Conclusions: These findings suggest that aberrant function of the neural circuitry underpinning SR is asso- ciated with the genetic liability to schizophrenia and confers vulnerability to delusional beliefs.
Schizophrenia Research 08/2014; In Press(1-3). DOI:10.1016/j.schres.2014.05.033 · 3.92 Impact Factor
"EEFFs are directly related to prefrontal areas, and the implication of the frontal lobe in ToM has been reported not only in patients with schizophrenia but also in healthy controls (Reginald et al., 2009). Decreased neural activity in frontal areas has been described when patients with schizophrenia perform affective ToM tasks (Russell et al., 2000) and cognitive ToM tasks (Lee et al., 2011). Frontal abnormalities , including reduction of gray matter in the left and right frontoinsular cortex, fronto-thalamic circuitry, and white matter reduction in the medial frontal lobe, have been described in chronic schizophrenia patients (Bora et al., 2011) as well as in first-episode patients (Berge et al., 2011; Bora et al., 2011), and these have been related with cognition and clinical symptoms. "
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to investigate the influence of neurocognition on affective and cognitive theory of mind (ToM) tasks in early phases of psychosis. In a cross-sectional study of 60 first-episode schizophrenia/schizoaffective disorder patients, the implication of neurocognition in first- and second-order ToM stories, Hinting Task, and Reading the Mind in the Eyes Test (RMET) was analyzed. Regression models were used, controlling for clinical symptoms and antipsychotic dose. Spatial span backward (odds ratio [OR], 0.34; p = 0.01) and intrusions in the Rey Auditory Verbal Learning Test (OR, 4.86; p = 0.04) were the best factors to predict second-order ToM failure. Trail Making Test B (B = 0.01; p = 0.04) and negative symptoms (B = 0.09; p = 0.01) predicted Hinting task performance while Block design (B = 0.1; p = 0.04) was related to RMET outcome. Executive functions and clinical symptoms were related to ToM performance in first-episode schizophrenia patients, although different patterns of relationship were observed in each ToM task.
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