Steffen Moritz

Jumping to conclusions in delusional and non-delusional schizophrenic patients

OBJECTIVE Several studies have provided evidence for the claim that a subgroup of (schizophrenic) patients with current delusions share a jumping to conclusions (JTC) bias. The primary aim of the present study was to investigate whether currently deluded and non-deluded schizophrenic patients perform differently on three tasks tapping probabilistic reasoning. METHOD Probabilistic reasoning was assessed in 31 schizophrenic patients, 28 psychiatric controls, and 17 healthy controls. In addition to the traditional draws to decision procedure, we employed two tasks for which participants had to judge, at each stage, the likelihood that beads come from either container (graded estimates procedure). Reaction times were recorded for the graded estimates procedure. RESULTS A JTC bias was displayed by 42% of the schizophrenic patients in the draws to decision condition, while 7% of the psychiatric patients and none of the healthy controls reached a decision after only one bead. A similar pattern of results was observed for the graded estimates procedure. This bias was more pronounced in deluded schizophrenic patients, although currently non-deluded patients also showed evidence for earlier decisions. A bias to over-adjust when confronted with potentially disconfirmatory evidence was confined to deluded schizophrenic participants. There was also evidence for an increase in JTC in the deluded group over the course of the tasks. No substantial group differences occurred with respect to reaction time parameters indicating that results are not attributable to impulsivity. DISCUSSION The findings provide further evidence for state and trait characteristics of abnormal reasoning in paranoid schizophrenia. Results are discussed in light of several competing explanations for JTC in schizophrenia.

Metacognitive training in schizophrenia: from basic research to knowledge translation and intervention

Purpose of review There has been a marked increase in the study of cognitive biases in schizophrenia, which has in part been stimulated by encouraging results with cognitive–behavioral interventions in the disorder. We summarize new evidence on cognitive biases thought to trigger or maintain positive symptoms in schizophrenia and present a new therapeutic intervention. Recent findings Recent studies indicate that patients with paranoid schizophrenia jump to conclusions, show attributional biases, share a bias against disconfirmatory evidence, are overconfident in errors, and display problems with theory of mind. Many of these biases precede the psychotic episode and may represent cognitive traits. Building upon this literature, we developed a metacognitive training program that aims to convey scientific knowledge on cognitive biases to patients and provides corrective experiences in an engaging and supportive manner. Two new studies provide preliminary evidence for the feasibility and efficacy of this approach. Summary The gap between our advanced understanding of cognitive processes in schizophrenia and its application in clinical treatment is increasingly being narrowed. Despite emerging evidence for the feasibility and efficacy of metacognitive training as a stand-alone program, its most powerful application may be in combination with individual cognitive–behavioral therapy.

Executive functioning in obsessive–compulsive disorder, unipolar depression, and schizophrenia

The present study investigated whether schizophrenic, unipolar depressive, and obsessive-compulsive psychiatric patients show a distinguishable profile in tasks considered sensitive to frontal lobe functioning. Three psychiatric samples, each comprising 25 patients with little symptomatic overlap, were compared to 70 healthy controls. Participants completed several executive tasks (Wisconsin Card Sorting Test (WCST), verbal fluency, digit span, Stroop, and Trail-Making). Except for age, which was entered as a covariate, subjects did not differ in any sociodemographic background variable. Healthy controls showed superior performance relative to depressive and schizophrenic patients who exhibited comparable deficits in all tasks. Obsessive-compulsive disorder (OCD) patients revealed dysfunctions in the Trail-Making Tests A and B and in the fluency task. Dysfunctions in the domains of working memory, verbal fluency, distractibility, and concept formation were not confined to a specific psychiatric population.

Symptom dimensions in obsessive–compulsive disorder: prediction of cognitive-behavior therapy outcome

Objective:  A significant number of patients with obsessive–compulsive disorder (OCD) fail to benefit sufficiently from treatments. This study aimed to evaluate whether certain OCD symptom dimensions were associated with cognitive‐behavioral therapy (CBT) outcome.

Cognitive Impairment in Major Depression: Association with Salivary Cortisol

BACKGROUND Cognitive deficits and elevated cortisol are hallmarks of depression. Cortisol acts via mineralocorticoid and glucocorticoid receptors, which have their highest density in the hippocampus, a brain area closely related to cognitive function. Several studies have separately examined cortisol secretion and cognitive deficits in depression. However, only few studies have assessed their association in the same patients producing inconclusive results. METHODS We examined 52 medication-free patients with major depression (37 women, 15 men; mean age 35 +/- 11 years; Hamilton Depression Scale mean score 27 +/- 5) and 50 healthy control subjects, matched for age, gender, and years of education. We applied several neuropsychological tests. Salivary cortisol levels were measured on the same day at 08:00, 12:00, 16:00, and 22:00 hours. RESULTS Compared with healthy subjects, patients had significantly higher cortisol levels and were impaired in verbal memory, visuospatial memory, working memory, and selective attention. In depressed patients, but not in healthy control subjects, we found a negative correlation between salivary cortisol levels (area under the curve) and hippocampus-related neuropsychological domains (verbal memory, visuospatial memory) and executive function. CONCLUSIONS Cognitive deficits, especially those closely related to hippocampus function, appear to be related to cortisol secretion in depressed patients. Elevated cortisol may downregulate mineralocorticoid and glucocorticoid receptors in the hippocampus, which could, in part, be responsible for cognitive deficits in depressed patients.

Source monitoring and memory confidence in schizophrenia

BACKGROUND The present study attempted to extend previous research on source monitoring deficits in schizophrenia. We hypothesized that patients would show a bias to attribute self-generated words to an external source. Furthermore, it was expected that schizophrenic patients would be overconfident regarding false memory attributions. METHOD Thirty schizophrenic and 21 healthy participants were instructed to provide a semantic association for 20 words. Subsequently, a list was read containing experimenter- and self-generated words as well as new words. The subject was required to identify each item as old/new, name the source. and state the degree of confidence for the source attribution. RESULTS Schizophrenic patients displayed a significantly increased number of source attribution errors and were significantly more confident than controls that a false source attribution response was true. The latter bias was ameliorated by higher doses of neuroleptics. CONCLUSIONS It is inferred that a core cognitive deficit underlying schizophrenia is a failure to distinguish false from true mnestic contents.

Memory and attention performance in psychiatric patients: Lack of correspondence between clinician-rated and patient-rated functioning with neuropsychological test results

In the present study, the correspondence between clinician-assessed and self-reported neurocognitive performance was contrasted with scores obtained from psychometric neuropsychological tests in 148 psychiatric in-patients. Results revealed that self-reported cognitive functioning was strongly associated with depressive symptomatology but was only poorly related to psychometric neurocognitive performance, particularly in schizophrenia. After illness denial was controlled for, the overall association between subjective and objective test performance was slightly increased but still failed to reach significance in six out of eight analyses. In approximately 20% to 40% of all cases, clinicians judged memory performance to be normal despite substantial impairment revealed by neuropsychological test results (attention parameters: 7-51%). Since (ecological) validity and reliability have been demonstrated for many neurocognitive paradigms, the present results question the validity of non-psychometric neurocognitive assessment and call for a complementation of clinical judgment with neurocognitive assessment. Reasons for decreased sensitivity of self-reported and clinician-assessed neurocognitive functioning are discussed.

The Contribution of a Cognitive Bias Against Disconfirmatory Evidence (BADE) to Delusions in Schizophrenia

A neuropsychological paradigm is introduced that provides a measure of a bias against disconfirmatory evidence (BADE), and its correspondence with delusions in people with schizophrenia and schizoaffective disorder was investigated. Fifty-two patients diagnosed with schizophrenia or schizoaffective disorder (36 were acutely delusional) and 24 healthy control participants were presented with delusion-neutral pictures in each trial, and were asked to rate the plausibility of four written interpretations of the scenario depicted by that picture. Subsequently, new pictures that provided background information about the depicted scenario were successively presented, and participants were requested to adjust their ratings, taking into account this new information. Two of the interpretations appeared tenable initially but ultimately proved to be implausible, one appeared untenable initially but eventually proved to be plausible, and one appeared untenable at all stages. A BADE was observed for delusional compared to non-delusional patients, as well as for all patients compared to controls. In addition, regardless of symptom profile, patients were more accepting of implausible interpretations than controls. The present work suggests that deficits in reasoning may contribute to the maintenance of delusions via an impairment in the processing of disconfirmatory evidence. The authors thank Jessica Bristowe, Jannine Laseleta, and Tonya Kragelj for assistance with data collection and data management, and Drs. Karin Christensen, Mahesh Menon, Elton Ngan, Eric Strachan, and Ivan Torres for comments and discussions that shaped this work. This research was supported by post-doctoral fellowships from the Mind Foundation of BC, the Canadian Psychiatric Research Foundation, and the Canadian Institutes of Health Research to TSW, scholarships from the German Academic Exchange Program (DAAD) to SM, and a grant from the Riverview Hospital Academic Steering Committee to TSW.

The Effect of State Anxiety on Paranoid Ideation and Jumping to Conclusions. An Experimental Investigation

Theoretical models of persecutory delusions have emphasized the impact of reasoning biases and negative emotion at the early stages of symptom formation. However, the causal mechanisms remain unclear. This study tests the hypothesis that state anxiety will increase paranoid ideation and that this increase will be moderated by the level of individual vulnerability and mediated by the tendency to jump to conclusions. Healthy participants (n = 90) with varying levels of vulnerability (psychosis symptoms assessed by the Community Assessment of Psychic Experiences) were randomly assigned to either an anxiety or a nonanxiety condition. Anxiety was induced by pictures from the International Affective Picture System and by in sensu exposure to individual anxiety-provoking situations. During each condition, symptoms of paranoia were assessed by a state-adapted version of the Paranoia Checklist. Jumping to conclusions (JTC) was assessed using a modified version of the beads task. Overall, participants in the anxiety condition reported significantly more paranoid thoughts and showed more JTC than participants in the neutral condition. Participants with higher baseline vulnerability were more likely to show an increase in paranoia as reaction to the anxiety manipulation. Moreover, the association of anxiety and paranoia was mediated by the increased tendency to jump to conclusions in the beads task. The results are in line with a threat anticipation conceptualization of paranoia and provide evidence for an interaction of anxiety and reasoning biases in the development of paranoid beliefs. A combination of meta-cognitive training directed at reasoning biases and promoting emotion regulation skills might prove beneficial in preventing symptoms.

Impact of comorbid depressive symptoms on neuropsychological performance in obsessive-compulsive disorder.

There is indirect evidence from previous research that several executive disturbances in obsessive-compulsive disorder (OCD) are mediated by comorbid depressive symptoms. For the present study, the authors investigated whether OCD patients with elevated Hamilton Rating Scale for Depression (HRSD) scores would exhibit deficits in tasks sensitive to the medial and dorsolateral frontal cortex as well as other executive tasks. The 36 OCD patients were split along the median according to their HRSD scores and compared with matched control subjects. Patients with high HRSD scores performed significantly worse than control subjects and patients with low HRSD scores on the Wisconsin Card Sorting Test, the Trail-Making Test (TMT, Part B), and the TMT difference score. Moreover, patients with high HRSD scores exhibited deficits on a (creative) verbal fluency task. It is suggested that comorbid depressive symptoms may have artificially inflated some executive deficit scores in previous studies.