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Antisocial personality disorder (ASPD) and violence result from a loss of mentalizing. Mentalization-based treatment for antisocial personality disorder (MBT-ASPD) is delivered primarily as a group intervention. Individuals with ASPD are more likely to learn from those whom they consider to be similar to themselves, so the task of the MBT clinician is to generate constructive group interactions during which learning can take place. Common mentalizing profiles of people with ASPD are outlined and examples of the formulation that can be used are given. The chapter discusses how to engage patients in treatment using the formulation, and it provides examples of how to prevent dropout by creating an atmosphere of equality within the group. A range of clinical problems that are commonly encountered when running groups for people with ASPD are outlined, and suggestions on how to intervene in these scenarios are given.
Social mentalizing informs the theory and practice of mentalization-based treatment for adolescents (MBT-A). Adolescence is, among other things, a time for establishing a self-identity and learning about how to interact effectively with a peer group. A focus on balancing mentalizing in peer and family interactions is crucial, with special attention to hypermentalizing and the alien self. Involvement of families and schools in treatment is necessary. MBT-A includes individual, family, and group therapy, and its overall aim is to develop the patient’s independence. Crucial aspects of achieving this goal include building up relational stability and supporting the patient’s sense of agency and autonomy within their relational networks.
This study was carried out to map psychosis spectrum disorder risk factors.
Objectives
Our goal was to find what kind of instrumental methods may help to detect latent liabilities for schizophrenia and bipolar affective disorder
Methods
Using online questionnaires n=710 students were screened. Groups were formed based on the inclusion criteria: N = 25 people prone to mood swings, N = 30 people prone to odd experiences and delusive thinking, and a normal control group with N = 30 people. Personality, temperament, self-experiences, affectivity scales, and cognitive screening were conducted in addition to actigraphy coupled with a mobile application for detecting subjective experiences (EMA). Furthermore, instrumental examination of self-agency, testing time interval discrimination and (re)production, eye-tracking, EEG-microstates, and laboratory testing of inflammatory, immunologic and cardio-metabolic measures of allostatic load were applied.
Results
Self-experience disorders: both risk groups showed significantly higher scores than the control group (CG). Self-agency: based on incorrectly attributed responses, the positive schizotypy risk factor (PSF) group differed from the CG (p = 0.003). Antisaccade study: the PSF group showed a difference from the CG (p = 0.002). Actigraphy: based on the distributions of diurnal cumulative activities, it distinguished those with a cyclothymic risk factor (CTF) from the CG (67% probability in the k-means clustering procedure).
Conclusions
Healthy students with a latent liability for schizotypy or bipolarity could be distinguished by some targeted laboratory methods. Susceptibility for bipolarity was indicated by actigraphic analyzes, and the risk for schizotypal development was indicated by deficiencies in the self-agency experience and by anti-saccadic eye movement disorders.
The sense of self-agency, i.e., experiencing oneself as the cause of one's own actions, is impaired in patients with schizophrenia. Normally, inferences of self-agency are enhanced when actual outcomes match with pre-activated outcome information, where this pre-activation can result from explicitly set goals (i.e., goal-based route) or implicitly primed outcome information (i.e., prime-based route). Previous research suggests that patients show specific impairments in the prime-based route, implicating that they do not rely on matches between implicitly available outcome information and actual action-outcomes when inferring self-agency. The question remains: Why? Here, we examine whether neurocognitive functioning and self-serving bias (SSB) may explain abnormalities in patients’ agency inferences.
Methods
Thirty-six patients and 36 healthy controls performed a commonly used agency inference task to measure goal- and prime-based self-agency inferences. Neurocognitive functioning was assessed with the Brief Assessment of Cognition in Schizophrenia (BACS) and the SSB was assessed with the Internal Personal and Situational Attributions Questionnaire.
Results
Results showed a substantial smaller effect of primed outcome information on agency experiences in patients compared with healthy controls. Whereas patients and controls differed on BACS and marginally on SSB scores, these differences were not related to patients’ impairments in prime-based agency inferences.
Conclusions
Patients showed impairments in prime-based agency inferences, thereby replicating previous studies. This finding could not be explained by cognitive dysfunction or SSB. Results are discussed in the context of the recent surge to understand and examine deficits in agency experiences in schizophrenia.
An area of recent interest in schizophrenia research is to investigate specific neural and cognitive abnormalities associated with symptoms of this disorder.
Objective:
To establish clinical, cognitive and neural correlates of self-monitoring deficits in schizophrenia, which according to various theoretical models can account for the first-rank symptoms of this disorder.
Methods:
Relevant data were identified from PubMed and PsycInfo searches up to July 2006 using combinations of keywords including ‘self-monitoring’, ‘symptoms’, ‘self-agency’, ‘neuropsychological’, ‘cognitive’, ‘brain activity’, ‘PET’ and ‘fMRI’.
Conclusions:
Self-monitoring deficit is most consistently observed in patients with schizophrenia with auditory hallucinations and passivity experiences. This deficit may not be schizophrenia specific. At present, there are insufficient direct data to reach meaningful conclusions about the cognitive correlates of this deficit. Functional neuroimaging studies in patients with schizophrenia with auditory hallucinations point to defective engagement of the neural regions known to be involved in self-monitoring in healthy people. Further multimodal studies using validated cognitive and clinical measures, self-monitoring paradigms and appropriate imaging tools to analyze patients with schizophrenia with and without self-monitoring deficits are required to increase our understanding of this topic.
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