Attentional bias to threat has been implicated as a cognitive mechanism in anxiety disorders for youth. Yet, prior studies documenting this bias have largely relied on a method with questionable reliability (i.e. dot-probe task) and small samples, few of which included adolescents. The current study sought to address such limitations by examining relations between anxiety – both clinically diagnosed and dimensionally rated – and attentional bias to threat.

The study included a community sample of adolescents and employed eye-tracking methodology intended to capture possible biases across the full range of both automatic (i.e. vigilance bias) and controlled attentional processes (i.e. avoidance bias, maintenance bias). We examined both dimensional anxiety (across the full sample; n = 215) and categorical anxiety in a subset case-control analysis (n = 100) as predictors of biases.

Findings indicated that participants with an anxiety disorder oriented more slowly to angry faces than matched controls. Results did not suggest a greater likelihood of initial orienting to angry faces among our participants with anxiety disorders or those with higher dimensional ratings of anxiety. Greater anxiety severity was associated with greater dwell time to neutral faces.

This is the largest study to date examining eye-tracking metrics of attention to threat among healthy and anxious youth. Findings did not support the notion that anxiety is characterized by heightened vigilance or avoidance/maintenance of attention to threat. All effects detected were extremely small. Links between attention to threat and anxiety among adolescents may be subtle and highly dependent on experimental task dimensions.

Prevalence estimates of neurodevelopmental disorders (ND) are essential for treatment planning. However, epidemiological research has yielded highly variable rates across countries, including Spain. This study examined the prevalence and sociodemographic correlates of ND in a school sample of Spanish children and adolescents.

The Child Behaviour Checklist/Teacher's Report Form/Youth Self-Report and the Conners' Rating Scales were administered for screening purposes. Additionally, teachers provided information on reading and writing difficulties. Subjects who screened positive were interviewed for diagnostic confirmation according to the Diagnostic and Statistical Manual of Mental Disorders criteria. The final population comprised 6834 students aged 5–17. Multivariate analyses were performed to determine the influence of gender, age, educational stage, school type, socioeconomic status (SES), and ethnicity on the prevalence estimates.

A total of 1249 (18.3%) subjects met criteria for at least one ND, although only 423 had already received a diagnosis. Specifically, the following prevalence rates were found: intellectual disabilities (ID), 0.63%; communication disorders, 1.05%; autism spectrum disorder (ASD), 0.70%; attention-deficit/hyperactivity disorder (ADHD), 9.92%; specific learning disorder (SLD), 10.0%; and motor disorders, 0.76%. Students of foreign origin and from low SES evidenced higher odds of having ID. Boys were more likely to display ASD or a motor disorder. Age, SES, and ethnicity were significant predictors for SLD, while communication disorders and ADHD were also associated with gender.

The prevalence of ND among Spanish students is consistent with international studies. However, a substantial proportion had never been previously diagnosed, which emphasise the need for early detection and intervention programmes.

Little is known about the relationship between psychomotor disturbance (PMD) and treatment outcome of psychotic depression. This study examined the association between PMD and subsequent remission and relapse of treated psychotic depression.

Two hundred and sixty-nine men and women aged 18–85 years with an episode of psychotic depression were treated with open-label sertraline plus olanzapine for up to 12 weeks. Participants who remained in remission or near-remission following an 8-week stabilization phase were eligible to participate in a 36-week randomized controlled trial (RCT) that compared the efficacy and tolerability of sertraline plus olanzapine (n = 64) with sertraline plus placebo (n = 62). PMD was measured with the psychiatrist-rated sign-based CORE at acute phase baseline and at RCT baseline. Spearman's correlations and logistic regression analyses were used to analyze the association between CORE total score at acute phase baseline and remission/near-remission and CORE total score at RCT baseline and relapse.

Higher CORE total score at acute phase baseline was associated with lower frequency of remission/near-remission. Higher CORE total score at RCT baseline was associated with higher frequency of relapse, in the RCT sample as a whole, as well as in each of the two randomized groups.

PMD is associated with poorer outcome of psychotic depression treated with sertraline plus olanzapine. Future research needs to examine the neurobiology of PMD in psychotic depression in relation to treatment outcome.

The current coronavirus disease (COVID-19) has a great impact worldwide. Healthcare workers play an essential role and are one of the most exposed groups. Information about the psychosocial impact on healthcare workers is limited.

3109 healthcare workers completed a national, internet-based, cross-sectional 45-item survey between 9 and 19 April 2020. The objective is to assess the psychological impact of the COVID-19 pandemic in Spanish healthcare workers. A Psychological Stress and Adaptation at work Score (PSAS) was defined combining four modified versions of validated psychological assessment tests (A) Healthcare Stressful Test, (B) Coping Strategies Inventory, (C) Font-Roja Questionnaire and (D) Trait Meta-Mood Scale.

The highest psychosocial impact was perceived in Respiratory Medicine, the mean (S.D.) PSAS was 48.3 (13.6) and Geriatrics 47.6 (16.4). Higher distress levels were found in the geographical areas with the highest incidence of COVID-19 (>245.5 cases per 100 000 people), PSAS 46.8 (15.2); p < 0.001. The least stress respondents were asymptomatic workers PSAS, 41.3 (15.4); p < 0.001, as well as those above 60 years old, PSAS, 37.6 (16); p < 0.001. Workers who needed psychological therapy and did not receive it, were more stressed PSAS 52.5 (13.6) than those who did not need it PSAS 39.7 (13.9); p < 0.001.

The psychological impact in healthcare workers in Spain during COVID-19 emergency has been studied. The stress perceived is parallel to the number of cases per 100 000 people. Psychotherapy could have a major role to mitigate the experimented stress level.

Individuals with depression often experience widespread and persistent cognitive deficits, which might be due to brain atrophy and cerebral small vessel disease (CSVD). We therefore studied the associations between depression, markers of brain atrophy and CSVD, and cognitive functioning.

We used cross-sectional data from the population-based Maastricht study (n = 4734; mean age 59.1 ± 8.6 years, 50.2% women), which focuses on type 2 diabetes. A current episode of major depressive disorder (MDD, n = 151) was assessed by the Mini-International Neuropsychiatric Interview. Volumes of cerebral spinal fluid, white matter, gray matter and white matter hyperintensities, presence of lacunar infarcts and cerebral microbleeds, and total CSVD burden were assessed by 3 T magnetic resonance imaging. Multiple linear and logistic regression analyses tested the associations between MDD, brain markers and cognitive functioning in memory, information processing speed, and executive functioning & attention, and presence of cognitive impairment. Structural equation modeling was used to test mediation.

In fully adjusted models, MDD was associated with lower scores in information processing speed [mean difference = −0.18(−0.28;−0.08)], executive functioning & attention [mean difference = −0.13(−0.25;−0.02)], and with higher odds of cognitive impairment [odds ratio (OR) = 1.60(1.06;2.40)]. MDD was associated with CSVD in participants without type 2 diabetes [OR = 1.65(1.06;2.56)], but CSVD or other markers of brain atrophy or CSVD did not mediate the association with cognitive functioning.

MDD is associated with more impaired information processing speed and executive functioning & attention, and overall cognitive impairment. Furthermore, MDD was associated with CSVD in participants without type 2 diabetes, but this association did not explain an impaired cognitive profile.

Subanesthetic ketamine infusion therapy can produce fast-acting antidepressant effects in patients with major depression. How single and repeated ketamine treatment modulates the whole-brain functional connectome to affect clinical outcomes remains uncharacterized.

Data-driven whole brain functional connectivity (FC) analysis was used to identify the functional connections modified by ketamine treatment in patients with major depressive disorder (MDD). MDD patients (N = 61, mean age = 38, 19 women) completed baseline resting-state (RS) functional magnetic resonance imaging and depression symptom scales. Of these patients, n = 48 and n = 51, completed the same assessments 24 h after receiving one and four 0.5 mg/kg intravenous ketamine infusions. Healthy controls (HC) (n = 40, 24 women) completed baseline assessments with no intervention. Analysis of RS FC addressed effects of diagnosis, time, and remitter status.

Significant differences (p < 0.05, corrected) in RS FC were observed between HC and MDD at baseline in the somatomotor network and between association and default mode networks. These disruptions in FC in MDD patients trended toward control patterns with ketamine treatment. Furthermore, following serial ketamine infusions, significant decreases in FC were observed between the cerebellum and salience network (SN) (p < 0.05, corrected). Patient remitters showed increased FC between the cerebellum and the striatum prior to treatment that decreased following treatment, whereas non-remitters showed the opposite pattern.

Results support that ketamine treatment leads to neurofunctional plasticity between distinct neural networks that are shown as disrupted in MDD patients. Cortico-striatal-cerebellar loops that encompass the SN could be a potential biomarker for ketamine treatment.

Post-traumatic stress disorder (PTSD), anxiety, and impulsive aggression are linked to transdiagnostic neurocognitive deficits. This includes impaired inhibitory control over inappropriate responses. Prior studies showed that inhibitory control can be improved by modulating the right inferior frontal gyrus (IFG) with transcranial direct current stimulation (tDCS) in combination with inhibitory control training. However, its clinical potential remains unclear. We therefore aimed to replicate a tDCS-enhanced inhibitory control training in a clinical sample and test whether this reduces stress-related mental health symptoms.

In a preregistered double-blind randomized-controlled trial, 100 active-duty military personnel and post-active veterans with PTSD, anxiety, or impulsive aggression symptoms underwent a 5-session intervention where a stop-signal response inhibition training was combined with anodal tDCS over the right IFG for 20 min at 1.25 mA. Inhibitory control was evaluated with the emotional go/no-go task and implicit association test. Stress-related symptoms were assessed by self-report at baseline, post-intervention, and after 3-months and 1-year follow-ups.

Active relative to sham tDCS neither influenced performance during inhibitory control training nor on assessment tasks, and did also not significantly influence self-reported symptoms of PTSD, anxiety, impulsive aggression, or depression at post-assessment or follow-up.

Our results do not support the idea that anodal tDCS over the right IFG at 1.25 mA enhances response inhibition training in a clinical sample, or that this tDCS-training combination can reduce stress-related symptoms. Applying different tDCS parameters or combining tDCS with more challenging tasks might provide better conditions to modulate cognitive functioning and stress-related symptoms.

Subgenual cingulate cortex (SCC) responses to self-blaming emotion-evoking stimuli were previously found in individuals prone to self-blame with and without a history of major depressive disorder (MDD). This suggested SCC activation reflects self-blaming emotions such as guilt, which are central to models of MDD vulnerability.

Here, we re-examined these hypotheses in an independent larger sample. A total of 109 medication-free participants (70 with remitted MDD and 39 healthy controls) underwent fMRI whilst judging self- and other-blaming emotion-evoking statements. They also completed validated questionnaires of proneness to self-blaming emotions including those related to internal (autonomy) and external (sociotropy) evaluation, which were subjected to factor analysis.

An interaction between group (remitted MDD v. Control) and condition (self- v. other-blame) was observed in the right SCC (BA24). This was due to higher SCC signal for self-blame in remitted MDD and higher other-blame-selective activation in Control participants. Across the whole sample, extracted SCC activation cluster averages for self- v. other-blame were predicted by a regression model which included the reliable components derived from our factor analysis of measures of proneness to self-blaming emotions. Interestingly, this prediction was solely driven by autonomy/self-criticism, and adaptive guilt factors, with no effect of sociotropy/dependency.

Despite confirming the prediction of SCC activation in self-blame-prone individuals and those vulnerable to MDD, our results suggest that SCC activation reflects blame irrespective of where it is directed rather than selective for self. We speculate that self-critical individuals have more extended SCC representations for blame in the context of self-agency.