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).

The pandemic caused by coronavirus disease 2019 (COVID-19) has forced governments to implement strict social mitigation strategies to reduce the morbidity and mortality from acute infections. These strategies, however, carry a significant risk for mental health, which can lead to increased short-term and long-term mortality and is currently not included in modeling the impact of the pandemic.

We used years of life lost (YLL) as the main outcome measure, applied to Switzerland as an example. We focused on suicide, depression, alcohol use disorder, childhood trauma due to domestic violence, changes in marital status, and social isolation, as these are known to increase YLL in the context of imposed restriction in social contact and freedom of movement. We stipulated a minimum duration of mitigation of 3 months based on current public health plans.

The study projects that the average person would suffer 0.205 YLL due to psychosocial consequence of COVID-19 mitigation measures. However, this loss would be entirely borne by 2.1% of the population, who will suffer an average of 9.79 YLL.

The results presented here are likely to underestimate the true impact of the mitigation strategies on YLL. However, they highlight the need for public health models to expand their scope in order to provide better estimates of the risks and benefits of mitigation.

Serotonergic neurotransmission plays a key role in seasonal changes of mood and behaviour. Higher serotonin transporter availability in healthy human subjects in times of lesser light has been reported in recent studies. Furthermore, seasonal alterations of postsynaptic serotonin-1A receptors have been suggested by a recent animal study. Following that, this study aimed at identifying seasonal alterations of serotonin-1A receptor binding in the living human brain.

Thirty-six healthy, drug-naïve subjects were investigated using PET and the specific tracer [carbonyl-11C]WAY-100635. Regional serotonin-1A receptor binding (5-HT1A BPND) was related to the individual exposure to global radiation. Furthermore, the subjects were divided into two groups depending on individual exposure to global radiation, and the group differences in regional 5-HT1A BPND were determined.

Correlation analysis controlled for age and gender revealed highly significant positive correlations between regional postsynaptic 5-HT1A BPND and global radiation accumulated for 5 days (r=.32 to .48, p=.030 to .002). Highly significant differences in 5-HT1A BPND binding between subjects with low compared to high exposure to global radiation were revealed (T=-2.63 to -3.77, p .013 to .001). 20% to 30% lower 5-HT1A BPND was found in the subject group exposed to lower amount of global radiation.

Seasonal factors such as exposure to global radiation influence postsynaptic serotonin-1A receptor binding in various brain regions in healthy human subjects. In combination with seasonal alterations in serotonin turnover and 5-HTT availability revealed in recent studies, our results provide an essential contribution of molecular mechanisms in seasonal changes of human serotonergic neurotransmission.

Regional alterations of serotonergic neurotransmission and functional activation in the amygdalar region of patients with major depression are underpinning its important role in affective disorders. In this study we used fMRI and PET to describe functional and molecular alterations associtated with an astrocytoma in the left amygdalar region in a patient with organic depressive disorder compared to control subjects.

The serotonin-1A (5-HT1A) receptor binding (BPND) was quantified with PET (30 frames, 90 min, 4.4 mm FWHM) in 36 subjects using the radioligand [carbonyl-11C]WAY-100635, and a reference tissue model (MRTM2). In fMRI (3T, EPI inplane resolution 1.6*2.7 mm, 10 AC-PC orientated slices, ST = 3 mm, TE/TR = 31/1000 ms), 32 participants performed emotion discrimination and sensorimotor control tasks. Statistical analysis with SPM5 and unpaired t-tests were performed on molecular and functional data separately.

The astrocytoma was delineated in the serotonin-1A receptor distribution showing (p < 0.01, uncorrected) regional BPND decrease. The ipsilateral thalamus and bilateral habenula regions displayed (p < 0.001; uncorrected) BPND increase. The fMRI data showed significantly (p < 0.05; uncorrected) reduced activation in the affected amygdalar region, ipsilateral fusiform gyrus, bilateral orbitofrontal cortex and temporal regions and increased activation in the contralateral temporal pole.

Lower serotonin-1A receptor binding in the left amydala region reflects the glial provenance of the tumor. The increased receptor binding in the habenulae might be associated with altered monoaminergic neurotransmission and depressive symptoms according to the influence of the habenulae on monoaminergic nuclei. The functional data demonstrate neuroplastic changes beyond affected areas and might indicate compensatory mechanisms.

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.

Maximal serotonin transporter (5-HTT) densities have been found in the cingulate cortex, a cortical region that has been critically implicated in emotion processing and the pathophysiology of Major Depressive Disorder. Furthermore, serotonin (5-HT) re-uptake inhibition is the first line strategy in the treatment of depression.

Since 5-HTTs are not restricted to neuronal cells, 5-HT uptake velocity (Vmax) can be easily measured on blood platelets subserving as peripheral model of neuronal 5-HTT function and related measures of neural activation.

To determine whether peripheral 5-HTT uptake velocity is related to neural activation in the cingulate cortex during emotion processing.

48 healthy subjects underwent an fMRI paradigm comprising emotional (angry/fearful faces and scenes) and neutral stimuli (simple shapes). 5-HT Vmax was determined in platelets. Subjects were genotyped for a common triallelic polymorphism in the promoter region of the 5-HTT gene (5-HTTLPR).

Significant negative correlations between Vmax and BOLD-signal in the anterior and posterior portion of the cingulate cortex have been found. Cluster maxima within both regions were detected in the subgenual anterior cortex (−1.5, 28.5, −3.5, t = −3.77) and the ventral posterior cingulate cortex (−4.5, −49.5,14.5, t = −3.06). Genotype did not impact on this relationship.

Our results indicate a clear dependency between a peripheral marker, platelet 5-HT uptake velocity, and neural activity in portions of the cingulate cortex for the first time.

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.

Citalopram is a widely applied SSRI in patients suffering from affective disorder. It is a racemic mixture of the S- and R-enantiomer of citalopram, consisting of equal parts of S-citalopram and R-citalopram, respectively. It has been shown that the inhibitory potency in serotonin reuptake of S-citalopram is much higher compared to R-citalopram, and it is assumed that S-citalopram is the main carrier of the antidepressant effect.

Here we investigated the effects of the two SSRIs Citalopram (50% S-, 50% R-citalopram) and Escitalopram (100% S-citalopram) on brain networks during emotion processing using pharmacological functional magnetic resonance imaging (fMRI) and dynamic causal modelling (DCM), an advanced tool to investigate functional integration between different brain regions.

Our results are based on a placebo-controlled, randomized, double-blind, cross-over pharmacological study in 16 healthy subjects during three fMRI scanning sessions performing a facial emotional discrimination paradigm (Windischberger, Neuroimage, 2010). 32 models of pharmacological modulation within the amygdalar-parahippocampal-orbitofrontal network were analysed using Bayesian Model Averaging (BMA) as implemented in SPM8.

S-citalopram showed statistically significant modulatory effects on forward amygdala-orbitofrontal and bidirectional amygdala-parahippocampal connections. No significant modulatory effects of R-citalopram were found.

This is the first fMRI study that showed stimulus-specific differential effects of the two enantiomeres R- and S-citalopram at the neural connectivity level. Our results corroborate studies in rats where escitalopram-induced increases in extracellular serotonin levels were found attenuated when R-citalopram was coinjected. Taken together this might explain the response differences between study drugs as demonstrated in previous clinical trials.

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.

Violence at work is a major concern in healthcare services. Prevention programs have been implemented, albeit being scarce in Italy.

The Bolzano psychiatric department adopted a de-escalation model developed by the Institut-für-Professionelles-Deeskalations-Management (ProDeMa®). It includes evaluation, prevention, and practical training aimed at preventing/reducing patients’ aggressive behavior toward healthcare workers.

In 2015, health professionals were interviewed by using a ProDeMa® 11-item questionnaire that assessed the type and frequency of endured patients’ aggressive behavior, as well as the conditions capable of producing or preventing it. One-way ANOVA with Tukey post-hoc test was used for comparisons.

A total of 165/211 (78%) surveyed workers (mean age ± DE = 44.9 ± 7.7; females = 64.6%) completed the questionnaire, of whom 21% employed at the inpatients unit (INP), 37% at the outpatients unit (OUTP), 42% at the rehabilitation facility (REHAB). The one-year number of verbal aggressions (VA) was 9766, with INP (mean ± SD = 15.2 ± 29.6) vs. OUTP (mean ± SD = 6.2 ± 30.6) vs. REHAB (mean ± SD = 8.4 ± 26.1). The one-year number of physical aggressions (PA) was 1502, with INP (mean ± SD = 3.3 ± 12.2) vs. OUTP (mean ± SD = 0.1 ± 0.5) vs. REHAB (mean ± SD = 0.1 ± 0.7). The one-year number of injuries (IN) was 200, with INP (mean ± SD = 0.5 ± 1.9) vs. OUTP (mean ± SD = 0.1 ± 0.5) vs. REHAB (mean ± SD = 0.1 ± 0.2). ANOVA showed significant differences in terms of mean verbal/physical aggression and injuries among the three workplaces (P-values = 0.000), with post-hoc Tukey test showing a significant difference of INP vs. REHAB and OUTP. The most frequent risk factors identified by the staff for precipitating aggression included rigid rules (15.1%) and inadequate communication (9.1%).

The three types of violence are common in all facilities of our Department.

The authors have not supplied their declaration of competing interest.

Obsessive–compulsive disorder (OCD) patients typically overmonitor their own behavior, as shown by symptoms of excessive doubt and checking. Although this is well established for the patients’ relationship with external stimuli in the environment, no study has explored their monitoring of internal body signals, a process known to be affected in anxiety-related syndromes. Here, we explored this issue through a cardiac interoception task that measures sensing of heartbeats. Our aim was to explore key behavioral and electrophysiological aspects of internal-cue monitoring in OCD, while examining their potential distinctiveness in this condition.

We administered a heartbeat detection (HBD) task (with related interoceptive confidence and awareness measures) to three matched groups (OCD patients, panic disorder patients, healthy controls) and recorded ongoing modulations of two task-relevant electrophysiological markers: the heart evoked potential (HEP) and the motor potential (MP).

Behaviorally, OCD patients outperformed controls and panic patients in the HBD task. Moreover, they exhibited greater amplitude modulation of both the HEP and the MP during cardiac interoception. However, they evinced poorer confidence and awareness of their interoceptive skills.

Convergent behavioral and electrophysiological data showed that overactive monitoring in OCD extends to the sensing of internal bodily signals. Moreover, this pattern discriminated OCD from panic patients, suggesting a condition-distinctive alteration. Our results highlight the potential of exploring interoceptive processes in the OCD spectrum to better characterize the population's cognitive profile. Finally, these findings may lay new bridges between somatic theories of emotion and cognitive models of OCD.