Dispositional negativity-the propensity to experience and express more frequent, intense, or enduring negative affect-is a fundamental dimension of childhood temperament and adult personality. Elevated levels of dispositional negativity can have profound consequences for health, wealth, and happiness, drawing the attention of clinicians, researchers, and policymakers. Here, we highlight recent advances in our understanding of the psychological and neurobiological processes linking stable individual differences in dispositional negativity to momentary emotional states. Self-report data suggest that 3 key pathways-increased stressor reactivity, tonic increases in negative affect, and increased stressor exposure-explain most of the heightened negative affect that characterizes individuals with a more negative disposition. Of these 3 pathways, tonically elevated, indiscriminate negative affect appears to be most central to daily life and most relevant to the development of psychopathology. New behavioral and biological data provide insights into the neural systems underlying these 3 pathways and motivate the hypothesis that seemingly "tonic" increases in negative affect may actually reflect increased reactivity to stressors that are remote, uncertain, or diffuse. Research focused on humans, monkeys, and rodents suggests that this indiscriminate negative affect reflects trait-like variation in the activity and connectivity of several key brain regions, including the central extended amygdala and parts of the prefrontal cortex. Collectively, these observations provide an integrative psychobiological framework for understanding the dynamic cascade of processes that bind emotional traits to emotional states and, ultimately, to emotional disorders and other kinds of adverse outcomes. (PsycINFO Database Record

The central extended amygdala (EAc)—including the bed nucleus of the stria terminalis (BST) and central nucleus of the amygdala (Ce)—plays a critical role in triggering fear and anxiety and is implicated in the development of a range of debilitating neuropsychiatric disorders. Although it is widely believed that these disorders reflect the coordinated activity of distributed neural circuits, the functional architecture of the EAc network and the degree to which the BST and the Ce show distinct patterns of functional connectivity is unclear. Here, we used a novel combination of imaging approaches to trace the connectivity of the BST and the Ce in 130 healthy, racially diverse, community‐dwelling adults. Multiband imaging, high‐precision registration techniques, and spatially unsmoothed data maximized anatomical specificity. Using newly developed seed regions, whole‐brain regression analyses revealed robust functional connectivity between the BST and Ce via the sublenticular extended amygdala, the ribbon of subcortical gray matter encompassing the ventral amygdalofugal pathway. Both regions displayed coupling with the ventromedial prefrontal cortex (vmPFC), midcingulate cortex (MCC), insula, and anterior hippocampus. The BST showed stronger connectivity with the thalamus, striatum, periaqueductal gray, and several prefrontal territories. The only regions showing stronger functional connectivity with the Ce were neighboring regions of the dorsal amygdala, amygdalohippocampal area, and anterior hippocampus. These observations provide a baseline against which to compare a range of special populations, inform our understanding of the role of the EAc in normal and pathological fear and anxiety, and showcase image registration techniques that are likely to be useful for researchers working with “deidentified” neuroimaging data.

When extreme, anxiety can become debilitating. Anxiety disorders, which often first emerge early in development, are common and challenging to treat, yet the neurocognitive mechanisms that confer increased risk have only recently started to come into focus. Here we review recent work highlighting the importance of neural circuits centered on the amygdala. We begin by describing dispositional negativity, a core dimension of childhood temperament and adult personality and an important risk factor for the development of anxiety disorders and other kinds of stress-sensitive psychopathology. Converging lines of epidemiological, neurophysiological, and mechanistic evidence indicate that the amygdala supports stable individual differences in dispositional negativity across the lifespan and contributes to the etiology of anxiety disorders in adults and youth. Hyper-vigilance and attentional biases to threat are prominent features of the anxious phenotype and there is growing evidence that they contribute to the development of psychopathology. Anatomical studies show that the amygdala is a hub, poised to govern attention to threat via projections to sensory cortex and ascending neuromodulator systems. Imaging and lesion studies demonstrate that the amygdala plays a key role in selecting and prioritizing the processing of threat-related cues. Collectively, these observations provide a neurobiologically-grounded framework for understanding the development and maintenance of anxiety disorders in adults and youth and set the stage for developing improved intervention strategies.

Objective: To identify which aspects of prosody are negatively affected subsequent to right hemisphere brain damage (RHD) and to evaluate the methodological quality of the constituent studies.Method: Twenty-one electronic databases were searched to identify articles from 1970 to February 2020 by entering keywords. Eligibility criteria for articles included a focus on adults with acquired RHD, prosody as the primary research topic, and publication in a peer-reviewed journal. A quality appraisal was conducted using a rubric adapted from Downs and Black (1998).Results: Of the 113 articles appraised as eligible and appropriate for inclusion, 71 articles were selected to undergo data extraction for both meta-analyses of population effect size estimates and qualitative synthesis. Across all domains of prosody, the effect estimate wasg= 2.51 [95% CI (1.94, 3.09),t= 8.66,p< 0.0001], based on 129 contrasts between RHD and non-brain-damaged healthy controls (NBD), indicating a significant random effects model. This effect size was driven by findings in emotional prosody,g= 2.48 [95% CI (1.76, 3.20),t= 6.88,p< 0.0001]. Overall, studies of higher quality (r_pb= 0.18,p< 0.001) and higher sample size/contrast ratio (r_pb= 0.25,p< 0.001) were more likely to report significant differences between RHD and NBD participants.Conclusions: The results confirm consistent evidence for emotional prosody deficits in the RHD population. Inconsistent evidence was observed across linguistic prosody domains and pervasive methodological issues were identified across studies, regardless of their prosody focus. These findings highlight the need for more rigorous and sufficiently high-powered designs to examine prosody subsequent to RHD, particularly within the linguistic prosody domain.

Background: Transcranial direct-current stimulation (tDCS) is a promising adjunct to therapy for chronic aphasia. Methods: This single-center, randomized, double-blind, sham-controlled efficacy trial tested the hypothesis that anodal tDCS augments language therapy in subacute aphasia. Secondarily, we compared the effect of tDCS on discourse measures and quality of life and compared the effects on naming to previous findings in chronic stroke. Right-handed English speakers with aphasia <3 months after left hemisphere ischemic stroke were included, unless they had prior neurological or psychiatric disease or injury or were taking certain medications (34 excluded; final sample, 58). Participants were randomized 1:1, controlling for age, aphasia type, and severity, to receive 20 minutes of tDCS (1 mA) or sham-tDCS in addition to fifteen 45-minute sessions of naming treatment (plus standard care). The primary outcome variable was change in naming accuracy of untrained pictures pretreatment to 1-week posttreatment. Results: Baseline characteristics were similar between the tDCS (N=30) and sham (N=28) groups: patients were 65 years old, 53% male, and 2 months from stroke onset on average. In intent-to-treat analysis, the adjusted mean change from baseline to 1-week posttreatment in picture naming was 22.3 (95% CI, 13.5–31.2) for tDCS and 18.5 (9.6–27.4) for sham and was not significantly different. Content and efficiency of picture description improved more with tDCS than sham. Groups did not differ in quality of life improvement. No patients were withdrawn due to adverse events. Conclusions: tDCS did not improve recovery of picture naming but did improve recovery of discourse. Discourse skills are critical to participation. Future research should examine tDCS in a larger sample with richer functional outcomes. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02674490.