Factors contributing to social cognition impairment in borderline personality disorder and schizophrenia.

Social cognition (SC) deficits have been described both in patients with schizophrenia and borderline personality disorder (BPD). However, while the former tend towards simplistic mental state attributions (undermentalizing), the latter are more likely to make overly complex mental state inferences (overmentalizing). Performance on complex SC tasks has been shown to correlate with neurocognitive ability, emotion perception, a history of trauma, and overconfidence in errors. However, it is unclear how these factors relate to different aspects of SC deficits. Aim of the present study was to examine the pathways of SC impairment by investigating performance profiles and their predictors comparatively in BPD and schizophrenia. Participants were 44 patients with BPD, 36 patients with schizophrenia, and 38 healthy controls. Undermentalizing and overmentalizing were assessed with an ecologically valid SC task. Patients with BPD exhibited increased overmentalizing, whereas patients with schizophrenia showed a more extensive deficit pattern, their main error type being undermentalizing. Overconfidence in errors was the most important predictor for overmentalizing, while undermentalizing depended mainly on verbal memory and emotion perception. Thus, BPD und schizophrenia exhibited different SC impairment patterns, and different types of SC errors were predicted by different factors. These findings have implications for the optimization of treatment approaches.

Dopamine effects on evidence gathering and integration.

BACKGROUND: Disturbances in evidence gathering and disconfirmatory evidence integration have been associated with the presence of or propensity for delusions. Previous evidence suggests that these 2 types of reasoning bias might be differentially affected by antipsychotic medication. We aimed to investigate the effects of a dopaminergic agonist (L-dopa) and a dopaminergic antagonist (haloperidol) on evidence gathering and disconfirmatory evidence integration after single-dose administration in healthy individuals. METHODS: The study used a randomized, double-blind, placebo-controlled, 3-way crossover design. Participants were healthy individuals aged 18-40 years. We administered a new data-gathering task designed to increase sensitivity to change compared with traditional tasks. The Bias Against Disconfirmatory Evidence (BADE) task was used as a measure of disconfirmatory evidence integration. RESULTS: We included 30 individuals in our study. In the data-gathering task, dopaminergic modulation had no significant effect on the amount of evidence gathered before reaching a decision. In contrast, the ability of participants to integrate disconfirmatory evidence showed a significant linear dopaminergic modulation pattern (highest with haloperidol, intermediate with placebo, lowest with L-dopa), with the difference between haloperidol and L-dopa marginally reaching significance. LIMITATIONS: Although the doses used for haloperidol and L-dopa were similar to those used in previous studies, drug plasma level measurements would have added to the validity of findings. CONCLUSION: Evidence gathering and disconfirmatory evidence integration might be differentially influenced by dopaminergic agents. Our findings are in support of a dual-disturbance account of delusions and provide a plausible neurobiological basis for the use of interventions targeted at improving reasoning biases as an adjunctive treatment in patients with psychotic disorders.