Post-extubation dysphagia in critically ill patients is known to affect about 18 per cent of mixed medical-surgical intensive care unit patients. This study investigated the incidence of post-extubation dysphagia in adult intensive care unit patients with coronavirus disease 2019.

This study was a retrospective analysis of consecutive intensive care unit patients prospectively screened for dysphagia. Systematic screening of all extubated intensive care unit patients at our tertiary centre was performed using the Bernese intensive care unit dysphagia algorithm. The primary outcome measure was the incidence of post-extubation dysphagia.

A total of 231 critically ill adult coronavirus disease 2019 positive patients were included, and 81 patients remained in the final analysis after exclusion criteria were applied (e.g. patients transferred). Dysphagia screening positivity was 25 of 81 (30.9 per cent), with 28.2 per cent (22 of 78) having confirmed dysphagia by specialist examination within 24 hours (n = 3 lost to follow up).

In this observational study, it was observed that the incidence of dysphagia in adult critically ill coronavirus disease 2019 patients was about 31 per cent (i.e. increased when compared with a historical pre-pandemic non-coronavirus disease 2019 intensive care unit cohort).

Dysfunction in the basal ganglia has been related to impaired reward processing and anhedonia, a core symptom of Major Depressive Disorder (MDD). In particular, the ventral striatum including the nucleus accumbens is increasingly implicated in the pathophysiology of MDD, but evidence for a specific role during episodes of full remission is lacking so far.

To investigate functional connectivity patterns of resting-state activity in patients in the remitted phase of MDD (rMDD).

To determine whether rMDD is related to disruptions of functional coupling between the ventral striatum and cortical regions.

Forty-three remitted depressed patients and thirty-five healthy controls were recruited at Medical University of Vienna, Vienna, Austria, and performed a six minute resting-state fMRI scan. Seed time series were extracted from the preprocessed data using individual masks for ventral striatum and correlated with all nodes in a surface based analysis using FreeSurfer, AFNI and SUMA. The resulting correlation coefficients were then Fishertransformed, group results were determined by comparing group mean smoothed z-scores with a two-sample ttest.

Increased resting-state functional connectivity was revealed between ventral striatum (seed region) and anterior cingulate cortex as well as orbitofrontal cortex in the rMDD group compared to healthy controls.

Our preliminary data is in accordance with the idea that increased functional coupling between the ventral striatum and two major emotion processing regions, the anterior cingulate cortex and the orbitofrontal cortex, may represent a neural mechanism contributing to the maintenance of full remission of MDD.

Converging evidence suggests alterations of neural activation in the basal ganglia to represent neural correlates of Major Depressive Disorder (MDD). While a previous study reported increases of functional connectivity in resting state activity between the caudate nuclei and the posterior cingulate cortex in acutely depressed patients, it remains unclear whether this finding persists during full remission once antidepressant treatment has been discontinued.

To investigate patterns of functional coupling between the basal ganglia and cortical regions during resting-state conditions.

To determine whether increases of functional connectivity between caudate nuclei, putamen, and pallidum with cortical regions, in particular the cingulate cortex, pertain during remission of MDD.

Forty-three remitted depressed (rMDD) patients and thirty-five healthy controls were recruited at Medical University of Vienna, Vienna, Austria, and performed a six minute resting-state fMRI scan. Seed time series were extracted from the preprocessed data using individual masks for the basal ganglia and correlated with all nodes in a surface based analysis using FreeSurfer, AFNI and SUMA. The resulting correlation coefficients were then Fisher-transformed, group results were determined by comparing group mean smoothed z-scores with a two-sample t-test.

Increased resting-state functional connectivity was revealed between basal ganglia and cingulate as well as prefrontal cortex in the rMDD group compared to healthy controls.

Our preliminary results revealed increased functional coupling between the basal ganglia and wide parts of the cingulate and prefrontal cortex to possibly represent a specific neural pattern during remission of MDD.

While most neuroimaging studies have investigated acutely depressed patients, neural mechanisms underlying stable remission are rarely examined. Furthermore, the majority of previous functional MRI (fMRI) studies have focused on task-induced neural activity, while resting-state activity may be more reproducible across study centers.

To clarify patterns of functional coupling between subcortical structures and cortical resting state activity.

To determine whether alterations of functional coupling between the amygdala and cortical emotion processing regions characterize patients in the remitted phase of Major Depressive Disorder (rMDD).

Forty-three remitted depressed patients and thirty-five healthy controls were recruited at Medical University of Vienna, Vienna, Austria, and performed a six minute resting-state fMRI scan. The scans were corrected for slice timing and motion, as well as for mean white matter, mean CSF, and median gray matter signals. Seed time series were extracted using individual amygdala masks and correlated with all nodes in a surface based analysis using FreeSurfer, AFNI and SUMA. The resulting correlation coefficients were then Fisher-transformed, group results were determined by comparing group mean smoothed (to 8 mm FWHM) z-scores with a two-sample t-test.

Increased resting-state functional connectivity was revealed between amygdala (seed region) and posterior cingulate cortex as well as orbitofrontal cortex in the rMDD group compared to healthy controls.

Our preliminary results suggest altered functional coupling between amygdala and cortical emotion processing areas during resting state conditions, possibly representing a neural mechanism contributing to the maintenance of stable remission of MDD.

The natural course of Major Depressive Disorder (MDD) encompasses the occurrence of alternating intervals of major depressive episodes and remission. While several abnormalities in neural circuits related to acute MDD have been identified, the neural mechanisms underlying stable remission remain obscure.

Acute MDD is characterized by increased amygdala and subgenual anterior cingulate cortex (sACC) activation and decreased connectivity between the amygdala and the sACC. Consequently, we expect those regions to be affected during remission.

To determine whether active counter-regulatory mechanisms are implicated in the maintenance of full remission once antidepressant treatment has been discontinued.

Functional and structural magnetic resonance imaging was used to measure brain activation and volume of the amygdala and the sACC. Images were obtained from 38 healthy subjects without any psychiatric life-time diagnosis and 38 gender-matched drug-free remitted MDD patients. Furthermore, correlation analyses were performed with clinical variables.

Patients with rMDD exhibited lower activation in the amygdala and the sACC and increased functional coupling between the amygdala and sACC compared to controls. This connectivity was particularly pronounced in patients characterized by a long cumulated time of depressive episodes. Similarly, structural connectivity results showed increased association between the amygdala and sACC volume in rMDD patients compared to controls.

Remitted MDD is related to neural alterations within a neural circuit encompassing the amygdala and the sACC compared to controls. These findings suggest active counter-regulatory mechanisms likely contributing to the maintenance of remission once treatment has been discontinued.

An increasing number of treatment studies focus on impaired cognition and emotion processing in schizophrenia. In study 1 we evaluated neuronal activation with fMRI during facial emotion processing in schizophrenia patients treated with new antipsychotics. The study 2 was carried out in order to evaluate whether combinations of new antipsychotics with a cognitive training (Cogpack) or a Training of Affect Decoding (TAD) were more effective than new antipsychotics alone.

In the first study patients with schizophrenia (n=11) and matched healthy controls (n=11) viewed facial displays of emotions. FMRI was used to measure BOLD signal changes as patients alternated beween tasks requiring discrimination of emotional valence of faces and age. In the second study schizophrenic patients (n=20) were compared with a randomized group of patients in the Cogpack (N=20) and in the TAD (n=20).

The same activation patterns in the amygdala were apparent in schizophrenic patients treated with new antipsychotics and healthy controls. The cognition training group revealed significant improvements in cognitive functions and transfer effects in skills needed for daily life. In the TAD group significant improvements were found in recognition of sad facial emotions.

New antipsychotics may improve the functionality of the networks needed for emotion processing and cognition. Cogpack training and TAD, in combination with new antipsychotics, are important treatment techniques for improving social functioning relevant for rehabilitation.

Study results on decision-making (DM) abilities in suicidal individuals are conflicting. Most studies have focused on DM under ambiguity and included patients with a lifetime history of suicide attempts.

To assess DM abilities with two different instruments in recent suicide attempters.

The study sample consisted of three groups. Group 1 (SA) were currently depressed inpatients having attempted suicide within the previous six months. Group 2 (NSA) consisted of depressed inpatients without a lifetime history of suicide attempts. Group 3 (CG) was a healthy control group. Besides depression severity, impulsiveness and suicidal intent (SA group only) DM was assessed using the Iowa gambling task (IGT) for DM under ambiguity and the game of dice task (GDT) for DM under risk.

A total of 78 participants (SA group, n = 21; NSA group, n = 31; CG, n = 26) were included into the study. Significant between group differences were found regarding marital status, current partnership, smoking status, depression score, impulsiveness score and family history of psychiatric disorders (all discriminating controls from patients but not between SA and NSA groups). The three groups did not differ with regard to IGT scores. Concerning GDT, the SA group showed significantly lower scores compared to the two other groups, implying a readiness for more risky decisions in suicide attempters versus non-attempters and controls.

Suicide attempters appear to make more risky decisions compared to depressed non-attempters as well as healthy controls even if the DM under ambiguity patterns do not differ.

The authors have not supplied their declaration of competing interest.

Internet-based cognitive–behavioural treatment (ICBT) for anxiety disorders has shown some promise, but no study has yet examined unguided ICBT in primary care. This randomized controlled trial (RCT) investigated whether a transdiagnostic, unguided ICBT programme for anxiety disorders is effective in primary care settings, after a face-to-face consultation with a physician (MD). We hypothesized that care as usual (CAU) plus unguided ICBT would be superior to CAU in reducing anxiety and related symptoms among patients with social anxiety disorder (SAD), panic disorder with or without agoraphobia (PDA) and/or generalized anxiety disorder (GAD).

Adults (n = 139) with at least one of these anxiety disorders, as reported by their MD and confirmed by a structured diagnostic interview, were randomized. Unguided ICBT was provided by a novel transdiagnostic ICBT programme (‘velibra’). Primary outcomes were generic measures, such as anxiety and depression symptom severity, and diagnostic status at post-treatment (9 weeks). Secondary outcomes included anxiety disorder-specific measures, quality of life, treatment adherence, satisfaction, and general psychiatric symptomatology at follow-up (6 months after randomization).

CAU plus unguided ICBT was more effective than CAU at post-treatment, with small to medium between-group effect sizes on primary (Cohen's d = 0.41–0.47) and secondary (Cohen's d = 0.16–0.61) outcomes. Treatment gains were maintained at follow-up. In the treatment group, 28.2% of those with a SAD diagnosis, 38.3% with a PDA diagnosis, and 44.8% with a GAD diagnosis at pretreatment no longer fulfilled diagnostic criteria at post-treatment.

The unguided ICBT intervention examined is effective for anxiety disorders when delivered in primary care.