Evaluation of the 'Jumping to conclusions' bias in different subgroups of the at-risk mental state: from cognitive basic symptoms to UHR criteria.

BACKGROUND: Patients with psychosis display the so-called 'Jumping to Conclusions' bias (JTC) - a tendency for hasty decision-making in probabilistic reasoning tasks. So far, only a few studies have evaluated the JTC bias in 'at-risk mental state' (ARMS) patients, specifically in ARMS samples fulfilling 'ultra-high risk' (UHR) criteria, thus not allowing for comparisons between different ARMS subgroups. METHOD: In the framework of the PREVENT (secondary prevention of schizophrenia) study, a JTC task was applied to 188 patients either fulfilling UHR criteria or presenting with cognitive basic symptoms (BS). Similar data were available for 30 healthy control participants matched for age, gender, education and premorbid verbal intelligence. ARMS patients were identified by the Structured Interview for Prodromal Symptoms (SIPS) and the Schizophrenia Proneness Instrument - Adult Version (SPI-A). RESULTS: The mean number of draws to decision (DTD) significantly differed between ARM -subgroups: UHR patients made significantly less draws to make a decision than ARMS patients with only cognitive BS. Furthermore, UHR patients tended to fulfil behavioural criteria for JTC more often than BS patients. In a secondary analysis, ARMS patients were much hastier in their decision-making than controls. In patients, DTD was moderately associated with positive and negative symptoms as well as disorganization and excitement. CONCLUSIONS: Our data indicate an enhanced JTC bias in the UHR group compared to ARMS patients with only cognitive BS. This underscores the importance of reasoning deficits within cognitive theories of the developing psychosis. Interactions with the liability to psychotic transitions and therapeutic interventions should be unravelled in longitudinal studies.

Obsessive-compulsive symptoms in at-risk mental states for psychosis: associations with clinical impairment and cognitive function.

OBJECTIVE: Obsessive-compulsive symptoms (OCS) constitute a major comorbidity in schizophrenia. Prevalence estimations of OCS for patients with at-risk mental states (ARMS) for psychosis vary largely. It is unclear how ARMS patients with or without comorbid OCS differ regarding general psychosocial functioning, psychotic and affective symptoms and neurocognitive abilities. METHOD: At-risk mental states patients (n = 233) from the interventional trial PREVENT (Secondary Prevention of Schizophrenia) were stratified according to the presence or absence of comorbid OCS and compared on several clinical variables. RESULTS: Patients, who fulfilled the criteria for obsessive-compulsive disorder (OCD) or presented with subclinical OCS (ARMSposOCS sample), did not significantly differ from patients without OCS (ARMSnegOCS) with regard to gender, age, premorbid verbal intelligence and levels of education. Furthermore, similar severity of depressive syndromes, basic cognitive, attenuated psychotic and brief limited intermittent psychotic symptoms were found. However, ARMSposOCS patients showed more impairment of psychosocial functioning and higher general psychopathology. In contrast, they scored higher in cognitive tasks measuring working memory and immediate verbal memory. CONCLUSION: Findings extend upon previous results due to the multidimensional assessment. Subsequent longitudinal studies might elucidate how comorbid OCS influence differential treatment response, especially to cognitive behavioural interventions and the transition rates to psychosis.

[Sleep disorders in schizophrenia]. / Schlafstörungen bei schizophrenen Erkrankungen.

Difficulties initiating and maintaining sleep as well as circadian rhythm disorders are very common in schizophrenia. Sleeping disorders occur as early signs of the first manifestation of illness as well as early signs of relapse. They bear a relation to positive symptoms and disorganisation of thought. Polysomnographic investigations with schizophrenic patients typically demonstrate a prolonged sleep-onset latency and a decrease in sleep efficiency and slow wave sleep. In particular, distortions of deep sleep can affect neocortical plasticity and cognition negatively. The considerable sleeping disorders are often not sufficiently taken into account in clinical routine. Particularly older antipsychotic medication like Haloperidol can affect the circadian and sleep-wake rhythms negatively. Therefore, pathophysiological changes of sleep within the scope of schizophrenic disorders and their potential implications are discussed in this outline. Regarding therapy, psychoeducative approaches are discussed as well as the administration of antipsychotic medication in accordance with the recommendations of sleep medicine professionals.

[Impact of cannabis consumption on brain development and the risk of developing psychotic disorders]. / Einflüsse von Cannabiskonsum auf die Gehirnentwicklung und das Erkrankungsrisiko für schizophrene Psychosen.

Cannabis consumption has varying effects over the whole life span, especially on achievements in the areas of schooling, professional life and performance in a social environment. Data from studies on remission from neurocognitive deficits following chronic cannabis consumption are ambiguous. The outcome range included everything from complete remission over considerable lasting deficits up to even chronic psychotic disorders. The data seem to be consistent however, when a differentiation between early begin of consumption (before the age of 16) and late begin of consumption is taken into account. Mainly those cannabis users with an early begin of consumption are prone to developing lasting neurocognitive deficits and even a decrease in grey substance volume, as well as an increase in the risk of psychosis. The correlation of this outcome with cannabis consumption during a phase of brain development that includes the consolidation of higher cognitive functions, awareness of social cues, planning of concepts and motivation as well as tools of functional control, is highly convincing. The endocannabinoid system reaches the point of highest receptor density during this age of 16/17 years, and many of the above-mentioned developmental processes are modulated by this system. A chronic damage to this system (e.g., down-regulation or desensitisation of CB1 receptors by exogenous cannabinoids) therefore holds the potential for permanent neurophysiological as well as neurocognitive deficits, and also for the development of psychotic disorders.