No abstract available

Approximately 80% of patients presenting to emergency departments (ED) with chest pain do not have any true cardiopulmonary emergency such as acute coronary syndrome (ACS). However, psychological contributors such as anxiety are thought to be present in up to 58%, but often remain undiagnosed leading to chronic chest pain and ED recidivism.

This study examines the influence of trait anxiety on working memory (WM) in safety and threat. Interactions between experimentally induced anxiety and WM performance (on different cognitive loads) have been reported in healthy, nonanxious subjects. Differences in trait anxiety may moderate these interactions. Accordingly, these interactions may be potentiated by high trait anxiety (HTA), or show a resilient pattern that protects cognitive performance. HTA and low trait anxiety (LTA) were defined by a median split of scores on the trait component of the state-trait anxiety inventory. Sustained anxiety was evoked by a probabilistic exposure to an aversive scream, and was measured by eyeblink startle and self-report. WM was tested using an n-back task (1-, 2-, and 3-back). Results revealed that, as expected, the HTA group reported greater anxiety during the task. However, trait anxiety did not impact the modulation of WM performance by induced anxiety. Notably, HTA influenced anxiety-potentiated startle (startle during threat minus startle during safe; APS) differently as a function of memory load. Accordingly, APS decreased with increasing WM load, but HTA antagonized this reduction. The HTA group showed no impairment on the 3-back WM task despite a higher APS. The amplified APS could be associated with the increase in effort-related cognitive arousal. Furthermore, this third replication of the interaction of induced anxiety by load on WM performance testifies to the robustness of the unique interplay between anxiety and WM.

Anxiety disorders are common and can be debilitating, with effective treatments remaining hampered by an incomplete understanding of the underlying genetic etiology. Improvements have been made in understanding the genetic influences on mouse behavioral models of anxiety, yet it is unclear the extent to which genes identified in these experimental systems contribute to genetic variation in human anxiety phenotypes. Leveraging new and existing large-scale human genome-wide association studies, we tested whether sets of genes previously identified in mouse anxiety-like behavior studies contribute to a range of human anxiety disorders. When tested as individual genes, 13 mouse-identified genes were associated with human anxiety phenotypes, suggesting an overlap of individual genes contributing to both mouse models of anxiety-like behaviors and human anxiety traits. When genes were tested as sets, we did identify 14 significant associations between mouse gene sets and human anxiety, but the majority of gene sets showed no significant association with human anxiety phenotypes. These few significant associations indicate a need to identify and develop more translatable mouse models by identifying sets of genes that "match" between model systems and specific human phenotypes of interest. We suggest that continuing to develop improved behavioral paradigms and finer-scale experimental data, for instance from individual neuronal subtypes or cell-type-specific expression data, is likely to improve our understanding of the genetic etiology and underlying functional changes in anxiety disorders.

Bipolar disorder is often comorbid with anxiety, which is itself associated with poorer clinical outcomes, including suicide. A better etiologic understanding of this comorbidity could inform diagnosis and treatment. The present study aims to test whether comorbid anxiety in bipolar disorder reflects shared genetic risk factors. We also sought to assess the contribution of genetic risk for anxiety to suicide attempts in bipolar disorder. Polygenic risk scores (PRS) were calculated from published genome-wide association studies of samples of controls and cases with anxiety (n = 83,566) or bipolar disorder (n = 51,710), then scored in independent target samples (total n = 3369) of individuals with bipolar disorder who reported or denied lifetime anxiety disorders or suicidal attempts in research interviews. Participants were recruited from clinical and nonclinical settings and genotyped for common genetic variants. The results show that polygenic risk for anxiety was associated with comorbid anxiety disorders and suicide attempts in bipolar disorder, while polygenic risk for bipolar disorder was not associated with any of these variables. Our findings point out that comorbid anxiety disorders in bipolar disorder reflect a dual burden of bipolar and anxiety-related genes; the latter may also contribute to suicide attempts. Clinical care that recognizes and addresses this dual burden may help improve outcomes in people living with comorbid bipolar and anxiety disorders.

Both anxiety sensitivity (AS) and experiential avoidance (EA) have been linked to social anxiety disorder (SAD). However, previous studies did not consider their joint variance and the heterogeneity of SAD. In this mixed methods cross-sectional survey, we examined 121 online participants (age range: 16-70 years) who self-reported as socially anxious. We compared AS and EA levels in individuals with a primary fear of noticeable anxiety symptoms vs. behaving ineptly. AS and EA were highly prevalent across the sample. Surprisingly, the noticeable symptoms subtype showed slightly lower AS and EA levels than the inept behavior subtype. The noticeable symptoms subtype scored notably lower on social anxiety measures (mean = 69.8) than the inept behavior subtype (mean = 89.3). EA was uniquely associated with social anxiety in both subtypes, while AS was uniquely associated with social anxiety only in the inept behavior subtype. The joint variance explained substantially more of the noticeable symptoms subtype's social anxiety (32.5%) compared to the inept behavior subtype's (9.4%). Qualitative themes aligned with these findings, indicating a self-reinforcing dynamic between high AS, high EA, and social anxiety symptoms. Potential clinical implications are discussed. Future research should examine causality in the AS-EA-SAD dynamic, considering the heterogeneity of SAD.

The State-Trait Anxiety Inventory (STAI) and the Hamilton scale for anxiety (HARS) are two of the most important scales employed in clinical and psychological realms for the evaluation of anxiety. Although the reliability and sensibility of these scales are widely demonstrated there is an open debate on what exactly their scores reflect. Neuroimaging provides the potential to validate the quality and reliability of clinical scales through the identification of specific biomarkers. For this reason, we evaluated the neural correlates of these two scales in a large cohort of healthy individuals using structural neuroimaging methods.

A recent systematic review has reported that poor reading is reliably associated with anxiety. However, we currently lack evidence-based intervention for children who have both poor reading and anxiety (PRAX). In this study, we tested a new PRAX intervention in 8- to 12-year-old children using a double-baseline intervention case series design. Analyses of both group and individual data revealed that 12 weeks of PRAX intervention significantly improved children's reading and spelling accuracy, and significantly reduced both anxiety disorders and symptoms. These results support PRAX intervention as a treatment for comorbid reading and anxiety problems in children and pave the way to a randomised controlled trial.

Ketamine is swiftly effective in a range of neurotic disorders that are resistant to conventional antidepressant and anxiolytic drugs. The neural basis for its therapeutic action is unknown. Here we report the effects of ketamine on the EEG of patients with treatment-resistant generalized anxiety and social anxiety disorders.

Anxiety disorders are one of the most commonly reported disorders in psychiatry, causing a high medical and socio-economic burden. Recently, there has been a soaring interest in the biological basis of anxiety disorders, which is reflected in an increasing number of articles related to the topic. Due to the ambiguity of the diagnosis and a large number of underdiagnosed patients, researchers are looking for laboratory tests that could facilitate the diagnosis of anxiety disorders in clinical practice and would allow for the earliest possible implementation of appropriate treatment. Such potential biomarkers may also be useable in monitoring the efficacy of pharmacological therapy for anxiety disorders. Therefore this article reviews the literature of potential biomarkers such as components of saliva, peripheral blood, cerebrospinal fluid (CSF), and neuroimaging studies. There are promising publications in the literature that can be useful. The most valuable and promising markers of saliva are cortisol, lysozyme, and α-amylase (sAA). In the blood, in turn, we can distinguish serotonin, brain-derived serum neurotrophic factor (BDNF), cortisol, and microRNA. Structural changes in the amygdala and hippocampus are promising neuroimaging markers, while in CSF, potential markers include oxytocin and 5-Hydroxyindoleacetic acid (5-HIAA). Unfortunately, research in the field of biomarkers is hampered by insufficient knowledge about the etiopathogenesis of anxiety disorders, the significant heterogeneity of anxiety disorders, frequent comorbidities, and low specificity of biomarkers. The development of appropriate biomarker panels and their assessment using new approaches may have the prospective to overcome the above-mentioned obstacles.

Background: As an emergent public health event, COVID-19 has had a significant impact on mental health, particularly causing anxiety. Some cognitive-affective related studies have demonstrated that attentional control is related to levels of anxiety. More specifically, recent research has shown that anxiety sensitivity is uniquely associated with mental health responses to COVID-19. The aim of the current study was to investigate the role of anxiety sensitivity during COVID-19 outbreak period, especially physical and cognitive concerns, in relation to attentional control and anxiety. Methods: It is a questionnaire study. A total of 464 participants were recruited through online sampling between February and March, 2020. They were surveyed by the Attentional Control Scale (ATTC), Anxiety Sensitivity Index-3 (ASI-3) and Depression Anxiety Stress Scale-21 (DASS-21). Data were analyzed using descriptive statistics and correlation analysis. We also tested the mediating effect. Results: The results showed that attentional control is negatively correlated with physical concern, cognitive concern and anxiety. And results support that physical and cognitive concerns play a mediating role between attentional control and anxiety. Conclusions: Anxiety sensitivity plays a mediating role between attentional control and anxiety. These findings can help effective prevention and intervention of anxiety.

Socioeconomic status (SES) disparities have profound impacts on child development and health, which are linked to negative emotions and alterations in the integrity of stress-sensitive hypothalamus-pituitary-adrenal (HPA)-axis system. However, its underlying psychophysiological mechanisms remain poorly understood. Here we investigate how family SES, in concert with parental anxiety, affects children's anxiety and their integrity of HPA-axis system in two studies involving a total of 1318 children and their parents. In Study 1 with a cohort of 1088 children and their parents, we found that low-SES children relative to high-SES ones experienced a higher level of anxiety mediated by increasing parental anxiety. In Study 2 with an independent cohort of 230 children and their parents, we found that low-SES children exhibited an increase in pre-bedtime basal cortisol but a decrease in cortisol awakening response (CAR). Structural equation modeling (SEM) further revealed that the association between low SES and children's reduced CAR was mediated by increased parental and child anxiety. Our findings suggest that low-SES children are more vulnerable to anxiety and altered HPA-axis integrity, most likely mediated through increased parental anxiety.

The Anxiety-CHF (Anxiety in patients with Chronic Heart Failure) study investigated heart-focused anxiety (HFA, with the dimensions fear, attention, and avoidance of physical activity), general anxiety, depression, and quality of life (QoL) in patients with heart failure. Psychological measures were assessed before and up to 2 years after the implantation of an implantable cardioverter defibrillator (ICD) with or without cardiac resynchronization therapy defibrillator (CRT-D).

anxiety remains one of the most common disorders in typically developing children and young adults. Adolescents with Down syndrome (DS) lack diagnostic tests for evaluation.

Elite young athletes have to cope with multiple psychological demands such as training volume, mental and physical fatigue, spatial separation of family and friends or time management problems may lead to reduced mental and physical recovery. While normative data regarding symptoms of anxiety and depression for the general population is available (Hinz and Brähler, 2011), hardly any information exists for adolescents in general and young athletes in particular. Therefore, the aim of this study was to assess overall symptoms of anxiety and depression in young athletes as well as possible sex differences. The survey was carried out within the scope of the study "Resistance Training in Young Athletes" (KINGS-Study). Between August 2015 and September 2016, 326 young athletes aged (mean ± SD) 14.3 ± 1.6 years completed the Hospital Anxiety and Depression Scale (HAD Scale). Regarding the analysis of age on the anxiety and depression subscales, age groups were classified as follows: late childhood (12-14 years) and late adolescence (15-18 years). The participating young athletes were recruited from Olympic weight lifting, handball, judo, track and field athletics, boxing, soccer, gymnastics, ice speed skating, volleyball, and rowing. Anxiety and depression scores were (mean ± SD) 4.3 ± 3.0 and 2.8 ± 2.9, respectively. In the subscale anxiety, 22 cases (6.7%) showed subclinical scores and 11 cases (3.4%) showed clinical relevant score values. When analyzing the depression subscale, 31 cases (9.5%) showed subclinical score values and 12 cases (3.7%) showed clinically important values. No significant differences were found between male and female athletes (p ≥ 0.05). No statistically significant differences in the HADS scores were found between male athletes of late childhood and late adolescents (p ≥ 0.05). To the best of our knowledge, this is the first report describing questionnaire based indicators of symptoms of anxiety and depression in young athletes. Our data implies the need for sports medical as well as sports psychiatric support for young athletes. In addition, our results demonstrated that the chronological classification concerning age did not influence HAD Scale outcomes. Future research should focus on sports medical and sports psychiatric interventional approaches with the goal to prevent anxiety and depression as well as teaching coping strategies to young athletes.

The COVID-19 pandemic has had a profound negative impact on mental health symptoms and daily life functioning across the United States and worldwide. Past work has revealed that perceived stress relates to poorer outcomes, however, little work to date has examined factors that may exacerbate these outcomes, and no work to date has examined this relation in terms of COVID-19. Anxiety sensitivity is a promising individual difference factor that has shown to be related to mental health and functional impairment. Anxiety Sensitivity is also a vulnerability factor related to heightened stress perception.

Although impaired fear extinction has repeatedly been demonstrated in patients with anxiety disorders, little is known about whether these impairments persist after treatment. The current comparative exploratory study investigated fear extinction in 26 patients treated for their anxiety disorder in the years preceding the study as compared to 17 healthy control subjects. Fear-potentiated startle and subjective fear were measured in a cue and context fear conditioning paradigm within a virtual reality environment. Results indicated no differences in fear extinction between treated anxiety patients and control subjects. However, scores on the Beck Anxiety Inventory across all participants revealed impaired extinction of fear potentiated startle in subjects with high compared to low anxiety symptoms over the past week. Taken together, this exploratory study found no support for impaired fear extinction in treated anxiety patients, and implies that current anxiety symptoms rather than previous patient status determine the success of extinction.

Aversive experiences can lead to complex behavioral adaptations including increased levels of anxiety and fear generalization. The neuronal mechanisms underlying such maladaptive behavioral changes, however, are poorly understood. Here, using a combination of behavioral, physiological and optogenetic approaches in mouse, we identify a specific subpopulation of central amygdala neurons expressing protein kinase C δ (PKCδ) as key elements of the neuronal circuitry controlling anxiety. Moreover, we show that aversive experiences induce anxiety and fear generalization by regulating the activity of PKCδ(+) neurons via extrasynaptic inhibition mediated by α5 subunit-containing GABAA receptors. Our findings reveal that the neuronal circuits that mediate fear and anxiety overlap at the level of defined subpopulations of central amygdala neurons and demonstrate that persistent changes in the excitability of a single cell type can orchestrate complex behavioral changes.

Anxiety disorders are highly prevalent and disabling but seem particularly tractable to investigation with translational neuroscience methodologies. Neuroimaging has informed our understanding of the neurobiology of anxiety disorders, but research has been limited by small sample sizes and low statistical power, as well as heterogenous imaging methodology. The ENIGMA-Anxiety Working Group has brought together researchers from around the world, in a harmonized and coordinated effort to address these challenges and generate more robust and reproducible findings. This paper elaborates on the concepts and methods informing the work of the working group to date, and describes the initial approach of the four subgroups studying generalized anxiety disorder, panic disorder, social anxiety disorder, and specific phobia. At present, the ENIGMA-Anxiety database contains information about more than 100 unique samples, from 16 countries and 59 institutes. Future directions include examining additional imaging modalities, integrating imaging and genetic data, and collaborating with other ENIGMA working groups. The ENIGMA consortium creates synergy at the intersection of global mental health and clinical neuroscience, and the ENIGMA-Anxiety Working Group extends the promise of this approach to neuroimaging research on anxiety disorders.

Psychological flexibility is the main outcome of acceptance commitment therapy. Insight into the usefulness of measuring psychological flexibility is an important step to enable studies on the effectiveness of acceptance commitment therapy in middle-aged children (8-10 years). For this purpose, we examined the factor structure, the construct validity and the reliability of the Avoidance and Fusion Questionnaire for Youth. The Avoidance and Fusion Questionnaire for Youth taps psychological inflexibility (the opposite of psychological flexibility) in children and adolescents. Although the questionnaire has been extensively validated in older children, this is not the case for middle-aged children. The Avoidance and Fusion Questionnaire for Youth contains 17 items and is constituted of the subscales cognitive fusion, experiential avoidance and behavioral ineffectiveness. A shortened 8-item version also exists, the Avoidance and Fusion Questionnaire for Youth-8, which does not distinguish between these subscales. We performed a confirmatory factor analysis. Additionally, we assessed the relationship between psychological flexibility and child anxiety. Children, aged 8-10 years, were recruited via regular primary schools. Of the 459 approached children, 267 (58 %) parents signed informed consents for their children (Age: M = 9.18; SD = .79; Sex: nboys = 137, 51 %). Children completed the questionnaires during regular classes. In this sample, the 17-item version of the Avoidance and Fusion Questionnaire for Youth was less appropriate for measuring psychological inflexibility than the 8-item version. Furthermore, we found a significant positive relationship between psychological inflexibility and child anxiety. We argue that acceptance commitment therapy would be an interesting candidate for intervening early on in dysfunctional child anxiety, as acceptance commitment therapy's cognitive elements require cognitive skills that children are likely to master early on.