The bed nucleus of the stria terminalis (BNST), a portion of the ‘extended amygdala’, is implicated in the pathophysiology of anxiety and addiction disorders. Its small size and connection to other small regions prevents standard imaging techniques from easily capturing it and its connectivity with confidence. Seed-based resting state functional connectivity is an established method for mapping functional connections across the brain from a region of interest. We therefore mapped the BNST resting state network with high spatial resolution using 7 Tesla fMRI, demonstrating the in vivo reproduction of many human BNST connections previously described only in animal research. We identify strong BNST functional connectivity in amygdala, hippocampus and thalamic subregions, caudate, periaqueductal gray, hypothalamus and cortical areas such as the medial PFC and precuneus. This work, which demonstrates the power of ultra-high field for mapping functional connections in the human, is an important step towards elucidating cortical and subcortical regions and subregions of the BNST network.

Background Anxiety patients exhibit deficits in cognitive tasks that require prefrontal control of attention, including those that tap working memory (WM). However, it is unclear whether these deficits reflect threat-related processes or symptoms of the disorder. Here we distinguish between these hypotheses by determining the effect of shock threat vs. safety on the neural substrates of WM performance in anxiety patients and healthy controls. Methods Patients, diagnosed with generalized and/or social anxiety disorder, and controls performed blocks of an N-back WM task during periods of safety and threat of shock. We recorded BOLD activity during the task, and investigated the effect of clinical anxiety (patients vs. controls) and threat on WM load-related BOLD activation. Results Behaviorally, patients showed an overall impairment in both accuracy and reaction time compared to controls, independent of threat. At the neural level, patients showed less WM load-related activation in the dorsolateral prefrontal cortex, a region critical for cognitive control. In addition, patients showed less WM load-related deactivation in the ventromedial prefrontal cortex and posterior cingulate cortex, which are regions of the default mode network. Most importantly, these effects were not modulated by threat. Conclusions This work suggests that the cognitive deficits seen in anxiety patients may represent a key component of clinical anxiety, rather than a consequence of threat.

Antisocial behaviors cause harm, directly or indirectly, to others’ welfare. The novel coronavirus pandemic has increased the urgency of understanding a specific form of antisociality: behaviors that increase risk of disease transmission. Because disease transmission-linked behaviors tend to be interpreted and responded to differently than other antisocial behaviors, it is unclear whether general indices of antisociality predict contamination-relevant behaviors. In a pre-registered study using an online U.S. sample, we found that individuals reporting high levels of antisociality engage in fewer social distancing measures: they report leaving their homes more frequently (p = .024) and standing closer to others while outside (p < .001). These relationships were observed after controlling for sociodemographic variables, illness risk, and use of protective equipment. Independently, higher education and leaving home for work were also associated with reduced distancing behavior. Antisociality was not significantly associated with level of worry about the coronavirus. These findings suggest that more antisocial individuals may pose health risks to themselves and their community during the COVID-19 pandemic.

Anxiety can have both detrimental and facilitatory cognitive effects. This study investigates the neural substrates of a replicated facilitatory effect of anxiety on sustained attention and response inhibition. This effect consisted of improved performance on the Sustained Attention to Response Task (a Go-NoGo task consisting of 91% Go and 9% NoGo trials) in threat (unpredictable electrical shock) vs safe (no shock) conditions. This study uses the same experimental design with fMRI and relies on an event-related analysis of BOLD signal changes. Findings reveal that threat-related cognitive facilitation (improved NoGo accuracy) is associated with greater activation of a right-lateralized frontoparietal group of regions previously implicated in sustained attention and response inhibition. Moreover, these same regions show decreased activation in the Go trials preceding NoGo errors. During NoGo trials, striatal activity is also greater in the threat vs safe condition, consistent with the notion of enhanced inhibitory processing under threat. These findings identify potential mechanisms by which threat of unpredictable shock can facilitate distinct cognitive functions. A greater understanding of the complex interaction of the anxious state and cognitive processes may have critical clinical implications.