Moderators of Treatment Efficacy in Individualized Metacognitive Training for Psychosis (MCT+)

Individualized Metacognitive Training (MCT+) is a manualized intervention designed to improve delusional severity by reducing delusion-associated cognitive biases such as jumping-to-conclusions. Increased interest in personalized medicine stipulates the identification of patients who are more likely to benefit from specialized interventions. The present study aimed to explore baseline moderators of MCT+ efficacy on delusions and overall positive symptoms in psychosis.; We analyzed data from a randomized rater-blind controlled trial, in which 92 patients with psychotic disorders and current or past delusions were randomly assigned to either MCT+ or CogPack®, a cognitive remediation software. Baseline moderator variables consisted of jumping-to-conclusions, cognitive insight, quality of life, self-esteem, selective attention, and patients' attitudes towards their symptoms. Linear mixed-effects models were applied to investigate specific moderators of MCT+ efficacy.; In MCT+ relative to CogPack, presence of a jumping-to-conclusions bias, a lowered decision threshold, and low self-esteem were associated with larger improvements in delusional severity and/or overall positive symptoms over time. Subjective reasoning style and insight, as well as subjective attitudes towards psychosis, did not moderate the treatment efficacy of MCT+ relative to CogPack.; Participation of both treatment groups in group MCT as a part of standard care, possibly leading to additional effects on delusional severity.; Patients with low self-esteem and those who are prone to jumping-to-conclusions seem to particularly benefit from MCT+. Our results can help inform clinical practice as they provide specific criteria for selecting patients for whom MCT+ is most appropriate

Differential relationship of jumping-to-conclusions and incorrigibility with delusion severity

Reasoning biases such as jumping-to-conclusions (JTC) and incorrigibility have been suggested to contribute to the generation and maintenance of delusions. However, it is still debated whether these biases represent stable traits of patients with delusions, or are related to state fluctuations of delusion severity. The present study aimed to elucidate this question by combining a cross-sectional with a longitudinal approach. JTC, incorrigibility and delusion severity were assessed in 79 patients with a history of delusions over a 6-month period. To allow for a differentiated look into effects of time vs. symptom changes, patients were divided into patients with (D+) and without (D-) current delusions at baseline. Significant improvement of delusions was noted in D+ at follow-up. JTC did not differ between the two patient groups either at baseline or over time. In contrast, incorrigibility was significantly higher in D+ than D- at baseline; this difference remained stable throughout the 6-month follow-up period. The two biases did not significantly co-vary over time. Our results suggest a dissociation between incorrigibility and JTC as regards their relation to current presence of delusions, and tentatively support theoretical accounts attributing different roles to the two biases in the generation (JTC) and maintenance (incorrigibility) of delusions

Familial Comorbidity of Bipolar Disorder and Multiple Sclerosis: Genetic Susceptibility, Coexistence or Causal Relationship?

Our purpose in undertaking the present study was to examine the hypotheses proposed for explaining the frequent comorbidity of bipolar disorder and multiple sclerosis. One hypothesis posits that, when there is comorbidity, MS plays a causal role in psychiatric manifestations. Another suggests that both disorders have a common underlying physiological process that increases the likelihood of their co-occurrence. We examined two adult siblings with comorbidity and their relatives, including three generations of family members with psychiatric morbidity. We found an extensive multigenerational history of bipolar disorder in this family. This history would seem to support the hypothesis of a common underlying brain process (potentially genetically-based) to explain the comorbidity of BD and MS, but cannot clarify whether this comorbidity implies a relationship between the two disorders or merely reflects parallel processes of brain deterioration. We cannot, however, rule out the possibility of a subclinical MS-related process leading to the early manifestation of BD, with MS appearing much later in time, or even a third, undetermined factor, leading to familial comorbidity. Although we have insufficient information to support either hypothesis definitively, we present the familial cases as a springboard for a discussion of dilemmas related to teasing apart MS and BD comorbidity. Further observation of the clinical course of the younger family members, who have not yet shown any neurological signs, over the next few years may elucidate the current picture further