Emotional dysregulation is thought to underlie risk for both anxiety and depressive disorders. However, despite high rates of comorbidity, anxiety and depression are phenotypically different. Apart from nosological differences (e.g., worry for anxiety, low mood for depression), it remains unclear how the emotional dysregulation inherent in individual differences in trait anxiety and depression severity present on a day-to-day basis. One approach that may facilitate addressing these questions is to utilize Ecological Momentary Assessment (EMA) using mobile phones to parse the temporal dynamics of affective experiences into specific parameters. An emerging literature in affective science suggests that risk for anxiety and depressive disorders may be associated with variation in the mean and instability/variability of emotion. Here we examine the extent to which distinct temporal dynamic parameters uniquely predict risk for anxiety versus depression. Over 10 days, 105 individuals rated their current positive and negative affective state several times each day. Using two distinct approaches to statistically assess mean and instability of positive and negative affect, we found that individual differences in trait anxiety was generally associated with increased instability of positive and negative affect whereas mean levels of positive and negative affect were generally associated with individual differences in depression. These data provide evidence that the emotional dysregulation underlying risk for mood versus anxiety disorders unfolds in distinct ways and highlights the utility in examining affective dynamics to understand psychopathology. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

STANDFIRST:: Hopelessness and despair threaten health and longevity. We urgently need strategies to counteract these effects and improve population health. Prosociality contributes to better mental and physical health for individuals, and for the communities in which they live. We propose that prosociality should be a public health priority. COMMENT:: The COVID-19 pandemic produced high levels of stress, loneliness, and mental health problems, magnifying global trends in health disparities. Hopelessness and despair are growing problems particularly in the U.S. The sharp increase in rates of poor mental health is problematic in its own right, but poor mental health also contributes to greater morbidity and mortality. Without action, we will see steep declines in global population health and related costs to society. An approach that is “more of the same” is insufficient to stem the cascading effects of emotional ill-being. Something new is desperately needed. To this point, recent work called on the discipline of psychiatry to contribute more meaningfully to the deaths of despair framework (i.e., conceptualizing rises in suicide, drug poisoning and alcoholic liver disease as due to misery of difficult social and economic circumstances). Recognizing that simply expanding mental health services cannot address the problem, the authors noted the importance of population-level prevention and targeting macro-level causes for intervention. This requires identifying upstream factors causally related to these deaths. However, factors explaining population health trends are poorly delineated and focus on risks and deficits (e.g., adverse childhood experiences, unemployment). A ‘deficit-based’ approach has limits as the absence of a risk factor does not inevitably indicate presence of a protective asset; we also need an ‘asset-based’ approach to understanding more comprehensively the forces that shape good health and buffer harmful effects of stress and adversity.

Metacognitive awareness-the ability to know that one is having a particular experience-is thought to guide optimal behavior, but its neural bases continue to be the subject of vigorous debate. Prior work has identified correlations between perceptual metacognitive ability and the structure and function of lateral prefrontal cortex (LPFC); however, evidence for a causal role of this region in promoting metacognition is controversial. Moreover, whether LPFC function promotes metacognitive awareness of perceptual and emotional features of complex, yet ubiquitous face stimuli is unknown. Here, using model-based analyses following a causal intervention to LPFC in humans, we demonstrate that LPFC function promotes metacognitive awareness of the orientation of faces-although not of their emotional expressions. Collectively, these data support the causal involvement of the prefrontal cortex in metacognitive awareness, and indicate that the role of LPFC in metacognition encompasses perceptual experiences of naturalistic social stimuli.

Humans show consistent differences in the extent to which their behavior reflects a bias toward appetitive approach-related behavior or avoidance of aversive stimuli [Elliot, A. J. Approach and avoidance motivation. In A. J. Elliot (Ed.), Handbook of approach and avoidance motivation (pp. 3-14). New York: Psychology Press, 2008]. We examined the hypothesis that in healthy participants this motivational bias (assessed by self-report and by a probabilistic learning task that allows direct comparison of the relative sensitivity to reward and punishment) reflects lateralization of dopamine signaling. Using [F-18]fallypride to measure D2/D3 binding, we found that self-reported motivational bias was predicted by the asymmetry of frontal D2 binding. Similarly, striatal and frontal asymmetries in D2 dopamine receptor binding, rather than absolute binding levels, predicted individual differences in learning from reward versus punishment. These results suggest that normal variation in asymmetry of dopamine signaling may, in part, underlie human personality and cognition.

Study objectives

Obstructive sleep apnea (OSA) is associated with significant alterations in neuronal integrity resulting from either hypoxemia and/or sleep loss. A large body of imaging research supports reductions in gray matter volume, alterations in white matter integrity and resting state activity, and functional abnormalities in response to cognitive challenge in various brain regions in patients with OSA. In this study, we used high-density electroencephalography (hdEEG), a functional imaging tool that could potentially be used during routine clinical care, to examine the regional distribution of neural activity in a non-clinical sample of untreated men and women with moderate/severe OSA.

Design

Sleep was recorded with 256-channel EEG in relatively healthy subjects with apnea-hypopnea index (AHI) > 10, as well as age-, sex-, and body mass index-matched controls selected from a research population initially recruited for a study on sleep and meditation.

Setting

Sleep laboratory.

Patients or participants

Nine subjects with AHI > 10 and nine matched controls.

Interventions

N/A.

Measurements and results

Topographic analysis of hdEEG data revealed a broadband reduction in EEG power in a circumscribed region overlying the parietal cortex in OSA subjects. This parietal reduction in neural activity was present, to some extent, across all frequency bands in all stages and episodes of nonrapid eye movement sleep.

Conclusion

This investigation suggests that regional deficits in electroencephalography (EEG) power generation may be a useful clinical marker for neural disruption in obstructive sleep apnea, and that high-density EEG may have the sensitivity to detect pathological cortical changes early in the disease process.

Compassion, the emotional response of caring for another who is suffering and that results in motivation to relieve suffering, is thought to be an emotional antecedent to altruistic behavior. However, it remains unclear whether compassion enhances altruistic behavior in a uniform way or is specific to sub-types of behavior such as altruistic helping of a victim or altruistic punishment of a transgressor. We investigated the relationship between compassion and subtypes of altruistic behavior using third-party paradigms where participants (1) witnessed an unfair economic exchange between a transgressor and a victim, and (2) had the opportunity to either spend personal funds to either economically (a) help the victim or (b) punish the transgressor. In Study 1, we examined whether individual differences in self-reported empathic concern (the emotional component of compassion) was associated with greater altruistic helping or punishment behavior in two independent samples. For participants who witnessed an unfair transaction, trait empathic concern was associated with greater helping of a victim and had no relationship to punishment. However, in those who decided to punish the transgressor, participants who reported greater empathic concern decided to punish less. In Study 2, we directly enhanced compassion using short-term online compassion meditation training to examine whether altruistic helping and punishment were increased after two weeks of training. Compared to an active reappraisal training control group, the compassion training group gave more to help the victim and did not differ in punishment of the transgressor. Together, these two studies suggest that compassion is related to greater altruistic helping of victims and is not associated with or may mitigate altruistic punishment of transgressors.

Failure to sustain positive affect over time is a hallmark of depression and other psychopathologies, but the mechanisms supporting the ability to sustain positive emotional responses are poorly understood. Here, we investigated the neural correlates associated with the persistence of positive affect in the real world by conducting two experiments in humans: an fMRI task of reward responses and an experience-sampling task measuring emotional responses to a reward obtained in the field. The magnitude of DLPFC engagement to rewards administered in the laboratory predicted reactivity of real-world positive emotion following a reward administered in the field. Sustained ventral striatum engagement in the laboratory positively predicted the duration of real-world positive emotional responses. These results suggest that common pathways are associated with the unfolding of neural processes over seconds and with the dynamics of emotions experienced over minutes. Examining such dynamics may facilitate a better understanding of the brain-behavior associations underlying emotion. Significance statement: How real-world emotion, experienced over seconds, minutes, and hours, is instantiated in the brain over the course of milliseconds and seconds is unknown. We combined a novel, real-world experience-sampling task with fMRI to examine how individual differences in real-world emotion, experienced over minutes and hours, is subserved by affective neurodynamics of brain activity over the course of seconds. When winning money in the real world, individuals sustaining positive emotion the longest were those with the most prolonged ventral striatal activity. These results suggest that common pathways are associated with the unfolding of neural processes over seconds and with the dynamics of emotions experienced over minutes. Examining such dynamics may facilitate a better understanding of the brain-behavior associations underlying emotion.

Sleeping brain activity reflects brain anatomy and physiology. The aim of this study was to use high density (256 channel) electroencephalography (EEG) during sleep to characterize topographic changes in sleep EEG power across normal aging, with high spatial resolution. Sleep was evaluated in 92 healthy adults aged 18-65 years old using full polysomnography and high density EEG. After artifact removal, spectral power density was calculated for standard frequency bands for all channels, averaged across the NREM periods of the first 3 sleep cycles. To quantify topographic changes with age, maps were generated of the Pearson's coefficient of the correlation between power and age at each electrode. Significant correlations were determined by statistical non-parametric mapping. Absolute slow wave power declined significantly with increasing age across the entire scalp, whereas declines in theta and sigma power were significant only in frontal regions. Power in fast spindle frequencies declined significantly with increasing age frontally, whereas absolute power of slow spindle frequencies showed no significant change with age. When EEG power was normalized across the scalp, a left centro-parietal region showed significantly less age-related decline in power than the rest of the scalp. This partial preservation was particularly significant in the slow wave and sigma bands. The effect of age on sleep EEG varies substantially by region and frequency band. This non-uniformity should inform the design of future investigations of aging and sleep. This study provides normative data on the effect of age on sleep EEG topography, and provides a basis from which to explore the mechanisms of normal aging as well as neurodegenerative disorders for which age is a risk factor.

Frontal EEG asymmetry is thought to reflect variations in affective style, such that greater relative right frontal activity at rest predicts enhanced emotional responding to threatening or negative stimuli, and risk of depression and anxiety disorders. A diathesis-stress model has been proposed to explain how this neuro-affective style might predispose to psychopathology, with greater right frontal activity being a vulnerability factor especially under stressful conditions. Less is known about the extent to which greater relative right frontal activity at rest might be associated with or be a diathesis for deleterious physical health outcomes. The present study examined the association between resting frontal EEG asymmetry and systemic, low-grade inflammation and tested the diathesis-stress model by examining whether childhood maltreatment exposure interacts with resting frontal asymmetry in explaining inflammation. Resting EEG, serum inflammatory biomarkers (interleukin-6, C-reactive protein, and fibrinogen) and self-reported psychological measures were available for 314 middle-aged adults (age M=55.3years, SD=11.2, 55.7% female). Analyses supported the diathesis-stress model and revealed that resting frontal EEG asymmetry was significantly associated with inflammation, but only in individuals who had experienced moderate to severe levels of childhood maltreatment. These findings suggest that, in the context of severe adversity, a trait-like tendency towards greater relative right prefrontal activity may predispose to low-grade inflammation, a risk factor for conditions with inflammatory underpinnings such as coronary heart disease.

Children with anxiety disorders (ADs) experience persistent fear and worries that are highly debilitating, conferring risk for lifelong psychopathology. Anticipatory anxiety is a core clinical feature of childhood ADs, often leading to avoidance of uncertain and novel situations. Extensive studies in non-human animals implicate amygdala dysfunction as a critical substrate for early life anxiety. To test specific amygdala-focused hypotheses in preadolescent children with ADs, we used fMRI to characterize amygdala activation during uncertain anticipation and in response to unexpected stimuli. Forty preadolescent (age 8-12 years) children, 20 unmedicated AD patients and 20 matched controls completed an anticipation task during an fMRI scan. In the task, symbolic cues preceded fear or neutral faces, such that 'certain' cues always predicted the presentation of fear or neutral faces, whereas 'uncertain' cues were equally likely to be followed by fear or neutral faces. Both AD children and controls showed robust amygdala response to faces. In response to the uncertain cues, AD children had increased amygdala activation relative to controls. Moreover, in the AD children, faces preceded by an 'uncertain' cue elicited increased amygdala activation, as compared with the same faces following a 'certain' cue. Children with ADs experience distress both in anticipation of and during novel and surprising events. Our findings suggest that increased amygdala activation may have an important role in the generation of uncertainty-related anxiety. These findings may guide the development of neuroscientifically informed treatments aimed at relieving the suffering and preventing the lifelong disability associated with pediatric ADs.