Background-Research on the neural circuitry underlying fear extinction has led to the examination of d-cycloserine (DCS), a partial agonist at the NMDA receptor in the amygdala, as a method of enhancing exposure therapy outcome. Preliminary results have supported the use of DCS to augment exposure therapy in adult anxiety disorders; however, no data have been reported in any childhood anxiety disorder. Thus, we sought to preliminarily examine if weight-adjusted DCS doses (25 or 50mg) enhanced the overall efficacy of cognitive-behavioral therapy (CBT) for pediatric obsessive-compulsive disorder (OCD).

Over the past 25 years, our understanding of the risks conferred by "behavioral inhibition to the unfamiliar" (BI) has grown tremendously, yet many questions remain. BI represents the persistent tendency to show extreme reticence, fearfulness, or avoidance in novel situations or with unfamiliar people. Prospective studies of high-risk offspring, selected community children, and unselected epidemiologic samples converge to suggest that BI confers specific risk for social anxiety disorder in early and middle childhood and adolescence. Later outcomes are less clear, with some studies suggesting associations with depression or panic disorder. Studies that find broad associations between BI and anxiety proneness in general may be limited by the absence of information about parental psychopathology (an important potential confound associated with both BI and anxiety disorders in offspring). A critical area for further inquiry is the degree to which BI confers risk for social anxiety disorder in the absence of family history of anxiety disorders. Additionally, although progress has been made in identifying risk factors, protective factors, and treatments that may influence the course of BI and associated anxiety, more work is needed. Also, several exciting inroads have been made into the genetic and neurobiologic underpinnings of BI, and future studies promise greater elucidation of these areas. For now, the clinical take-home message is that preschool-age children presenting with extreme and persistent BI are at elevated risk for social anxiety disorder and possibly for other future disorders; preliminary evidence suggests that these children may be helped by early cognitive-behavioral intervention.

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Findings suggest that EFDs do not serve as trait markers for developing anxiety or depression but appear to be symptomatic of current disorder.

This study investigated the neural basis of individual variation in emotion regulation, specifically the ability to reappraise negative stimuli so as to down-regulate negative affect. Brain functions in young adults were measured with functional Magnetic Resonance Imaging during three conditions: (i) attending to neutral pictures; (ii) attending to negative pictures and (iii) reappraising negative pictures. Resting-state functional connectivity was measured with amygdala and dorsolateral prefrontal cortical (DLPFC) seed regions frequently associated with emotion regulation. Participants reported more negative affect after attending to negative than neutral pictures, and less negative affect following reappraisal. Both attending to negative vs neutral pictures and reappraising vs attending to negative pictures yielded widespread activations that were significantly right-lateralized for attending to negative pictures and left-lateralized for reappraising negative pictures. Across participants, more successful reappraisal correlated with less trait anxiety and more positive daily emotion, greater activation in medial and lateral prefrontal regions, and lesser resting-state functional connectivity between (a) right amygdala and both medial prefrontal and posterior cingulate cortices, and (b) bilateral DLPFC and posterior visual cortices. The ability to regulate emotion, a source of resilience or of risk for distress, appears to vary in relation to differences in intrinsic functional brain architecture.

This study evaluated the efficacy of a four-session Cognitive Bias Modification-Interpretation program for 45 depressed adolescents and young adults (14–21 years old; 12 males, 33 females; Beck Depressive Inventory, Second Edition ≥ 14) randomized to an active intervention condition (repeated exposure to positive outcomes of depression-relevant ambiguous scenarios; n=23) or a control condition (n=22). Both conditions experienced reductions on a Test of Interpretation Bias at post-treatment, with no significant between-group differences. When limited to those with negative bias at baseline, the intervention group showed greater improvement in interpretation bias at mid- and post-treatment. In addition, the intervention group overall had greater improvements in self-reported negative cognitions than the control group at post-intervention and two-week follow-up. However, there were no differences between groups in depression or anxiety symptom change. Potential factors contributing to mixed findings are discussed.

These findings suggest that a new Child Behavior Checklist-ASD profile consisting of the Child Behavior Checklist-Withdrawn, Social, and Thought Problems scales could serve as a rapid and cost-effective screening instrument to help identify cases likely to meet clinical criteria for ASDs in the clinical setting.

The past two decades have witnessed significant growth in our understanding of the developmental antecedents of anxiety disorders. In this article, we review studies of offspring at risk for anxiety disorders, longitudinal studies of the course of anxiety disorders in clinical, epidemiologic, and at-risk samples, studies of hypothesized temperamental risk factors for anxiety, and give a brief overview of the literature on environmental risk factors. Clear developmental antecedents to anxiety disorders identified include (1) childhood anxiety disorders [in particular, separation anxiety and overanxious disorder/general anxiety disorder (GAD)], (2) behavioral inhibition which predicts later social phobia, (3) anxiety sensitivity which predicts later panic disorder, and (4) negative affectivity, which predicts a spectrum of psychopathology including anxiety disorders. Further prospective studies are needed to examine the roles of environmental factors such as parenting practices, peer influences, stressful life events, and perinatal stressors. Future studies could benefit from (1) beginning earlier in development and following individuals into adulthood, (2) assessing the overlap between multiple temperamental constructs, (3) greater use of observational measures of temperament and of parent-child and peer interactions, (4) greater attention to parental psychopathology which may confound associations noted, (5) exploration of other features of anxiety disorders (neurofunctional correlates, cognitive features, other aspects of emotional regulation) as potential precursors, and (6) intervention studies exploring whether modifying developmental antecedents can alter the course of anxiety disorders.