ANOVA to test whether BPD patients exhibited weaker posttask increase in the amygdala intrinsic FC with the prefrontal cortex (PFC), compared to non-patients. Subsequently, we explored whether the results are common for personality disorders characterized by emotional problems, using additional data of 21 cluster-C personality disorder patients. In contrast to non-patients, BPD patients failed to show increased posttask amygdala resting-state FC with the medial, dorsolateral, ventrolateral PFC, and superior temporal gyrus, but surprisingly exhibited decreased FC with the posterior cingulate cortex and increased FC with the superior parietal lobule. In BPD patients, the emotion regulation task failed to increase resting-state amygdala FC with brain regions essential for effortful emotion regulation, which suggests: (a) altered cognitive control typically used to indirectly alleviate distress by reinterpreting the meaning of emotional stimuli; (b) impaired direct regulation of emotional responses, which might be Abstract Emotion instability in borderline personality disorder (BPD) has been associated with an impaired frontolimbic inhibitory network. However, functional connectivity (FC) underlying altered emotion regulation in BPD has yet to be established. Here, we used resting-state fMRI to investigate enduring effects of effortful emotion regulation on the amygdala intrinsic FC in BPD. In this multicenter study, resting-state fMRI was acquired before and after an emotion regulation task in 48 BPD patients and 39 non-patient comparison individuals. The bilateral amygdalae were used as a seed in the whole-brain FC analysis and two-way mixed Blazej M. Baczkowski and Linda van Zutphen have contributed equally to this work. common for personality disorders; (c) avoidance of selfrelated appraisals induced by social emotional stimuli. Electronic supplementary material

A number of recent studies have challenged the hypothesis that patients with obsessive-compulsive disorder (OCD) display global memory deficits. An alleviated form of the memory deficit hypothesis posits that OCD patients share deficits to vividly recall memory episodes. According to the latter view, checking rituals can be understood as counter-productive coping strategies to "enrich" memory episodes in order to make them more distinctive. A source memory task was administered to 27 OCD (17 checkers) and 51 healthy participants. Along with confidence judgments, a remember-know procedure was employed to assess whether OCD patients display problems with conscious/vivid recollection. Patients with or without checking compulsions did not exhibit differences to controls on source memory accuracy and meta-memory. Patients forgot more self-generated items, which, however, was related to comorbid depressive but not OCD symptoms. Findings challenge the ubiquity of memory deficits in OCD. To account for the inconclusive pattern of results in the literature, it is suggested that patients mistrust their memories and adopt checking rituals only when perceived responsibility is inflated.

The majority of patients with schizophrenia display neurocognitive deficits (e.g., memory impairment) as well as inflated cognitive biases (e.g., jumping to conclusions). Both cognitive domains are implicated in the pathogenesis of the disorder and are known to compromise functional outcome. At present, there is a dearth of effective treatment options. A total of 90 patients with schizophrenia were recruited online (a diagnosis of schizophrenia had been confirmed in a large subgroup during a previous hospital admission). Subsequent to a baseline assessment encompassing psychopathology, self-reported cognition as well as objective memory and reasoning tests, patients were randomized to one of three conditions: standard cognitive remediation (mybraintraining), metacognition-augmented cognition remediation (CR) condition (variant of mybraintraining which encouraged patients to reduce speed of decision-making and attenuate response confidence when participants made high-confidence judgements and hasty incorrect decisions) and a waitlist control group. Patients were retested after 6 weeks and again 3 months after the second assessment. Groups did not differ on psychopathology and neurocognitive parameters at any timepoint. However, at follow-up the metacognitive-augmented CR group displayed a significant reduction on jumping to conclusions and overconfidence. Treatment adherence correlated with a reduction of depression; gains in the training exercises from the standard mybraintraining condition were correlated with improved objective memory performance. The study suggests that metacognition-augmented CR may ameliorate cognitive biases but not neurocognition. The study ties in well with prior research showing that neurocognitive dysfunctions are rather resistant to change; the failure to detect significant improvement of CR or metacognition-augmented CR on psychopathology and neurocognition over time may partly be attributed to a number of methodological limitations of our study (low psychopathology and chronicity of participants, low “dosage,” narrow range of tests, self-report psychopathology scales).