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BackgroundFatigue has an adaptive function and serves as a temporary signal to rest and save energy often in response to immune activation. It may, however, also persist in a pathological condition incurring significant burden. While subjective symptoms and scientific consensus indicate that both physical and mental determinants of motivated behavior are affected in fatigue, the underlying processes are rarely examined using objective, task-based indicators.MethodsIn three consecutive studies, including validation (N = 48) and reliability assessments (N = 27), we use an experimental task to jointly objectify reward learning and effort execution as two determinants of behavioral motivation. In addition, we tested how fatigue and its acute perturbation in response to immune activation after SARS-CoV-2 vaccination are linked to these task-based indicators of motivation in a longitudinal cross-over design (N = 55).ResultsThe validation study showed the utility of the experimental task for simultaneously assessing learning, effort exertion, and its regulation based on subjective confidence. The reliability assessment over a one-week period indicated that symptoms of fatigue and task behavior are highly reliable and that repetition effects have little impact on motivated behavior. Finally, in the vaccination trial, we found significant links between fatigue and task behavior. Baseline levels of fatigue predicted how effort is gauged in dependence of current confidence about reward outcomes, and state perturbations of fatigue in the context of the SARS-CoV-2 vaccination reduced confidence during learning. Importantly, task success was significantly lower in subjects who reported high fatigue at baseline and who additionally experienced stronger increase in fatigue in response to vaccination.DiscussionOur results demonstrate that the experimental task allows to jointly assess determinants of motivated behavior, and to link its constituent processes to subjective fatigue. This suggests that our understanding of fatigue and its perturbation due to acute immune activation can benefit from objective, task-based indicators of the underlying motivational mechanisms. Future studies could build on these findings to further deepen the understanding of neurobehavioral mechanisms underlying fatigue in the context of immune activation.

Background Autism spectrum disorder (ASD) is characterized by difficulties in social communication and interaction, which have been related to atypical neural processing of rewards, especially in the social domain. Since intranasal oxytocin has been shown to modulate activation of the brain’s reward circuit, oxytocin might ameliorate the processing of social rewards in ASD and thus improve social difficulties. Methods In this randomized, double-blind, placebo-controlled, crossover fMRI study, we examined effects of a 24 IU dose of intranasal oxytocin on reward-related brain function in 37 men with ASD without intellectual impairment and 37 age- and IQ-matched control participants. Participants performed an incentive delay task that allows the investigation of neural activity associated with the anticipation and receipt of monetary and social rewards. Results Non-significant tests suggested that oxytocin did not influence neural processes related to the anticipation of social or monetary rewards in either group. Complementary Bayesian analyses indicated moderate evidence for a null model, relative to an alternative model. Our results are inconclusive regarding possible oxytocin effects on amygdala responsiveness to social rewards during reward consumption. There were no significant differences in reward-related brain function between the two groups under placebo. Conclusions Our results do not support the hypothesis that intranasal oxytocin generally enhances activation of reward-related neural circuits in men with and without ASD.

The feedback people receive on their behavior shapes the process of belief formation and self-efficacy in mastering a particular task. However, the neural and computational mechanisms of how the subjective value of self-efficacy beliefs, and the corresponding affect, influence the learning process remain unclear. We investigated these mechanisms during self-efficacy belief formation using fMRI, pupillometry, and computational modeling, and by analyzing individual differences in affective experience. Biases in the formation of self-efficacy beliefs were associated with affect, pupil dilation, and neural activity within the anterior insula, amygdala, ventral tegmental area/ substantia nigra, and mPFC. Specifically, neural and pupil responses mapped the valence of the prediction errors in correspondence with individuals’ experienced affective states and learning biases during self-efficacy belief formation. Together with the functional connectivity dynamics of the anterior insula within this network, our results provide evidence for neural and computational mechanisms of how we arrive at affected beliefs.

Being confronted with social-evaluative stress elicits a physiological and a psychological stress response. This calls for regulatory processes to manage negative affect and maintain self-related optimistic beliefs. The aim of the current study was to investigate the affect-regulating potential of self-related belief updating after exposure to social-evaluative stress, in comparison to non-social physical stress or no stress. We assessed self-related belief updating using trial-by-trial performance feedback and described the updating behavior in a mechanistic way using computational modeling. We found that social-evaluative stress was accompanied by an increase in cortisol and negative affect which was related to a shift in self-related belief updating towards the positive direction. This self-beneficial belief updating, which was absent after physical stress or control, was associated with a better recovery from stress-induced negative affect. This indicates that enhanced integration of positive self-related feedback can act as a coping strategy to deal with social-evaluative stress.

Highlights • Narcissistic Personality Disorder (NPD) is linked to low prosociality. • Here, we investigate social decision making in NPD with functional MRI (fMRI). • Prosociality and (neural tracking of) motivational conflict were low in NPD. • While reduced, prosocial behavior was not completely absent in NPD., Narcissistic Personality Disorder (NPD) entails severe impairments in interpersonal functioning that are likely driven by self-beneficial and exploitative behavior. Here, we investigate the underlying motivational and neural mechanisms of prosocial decision-making by experimentally manipulating motivational conflict between self-beneficial and prosocial incentives. One group of patients diagnosed with NPD and a group of healthy controls (CTL) were scanned using functional magnetic resonance imaging while performing a prosocial decision-making task. In this task, we systematically varied the level of conflict between self-beneficial and prosocial options on each trial. We analyzed choice behavior, response times, and neural activity in regions associated with conflict monitoring to test how motivational conflict drives prosocial choice behavior. Participants in the NPD group behaved less prosocially than the CTL group overall. Varying degrees of motivational conflict between self-beneficial and prosocial options induced response variability in both groups, but more so in the CTL group. The NPD group responded faster than the CTL group, unless choosing prosocially, which slowed response times to a level comparable to the CTL group. Additionally, neural activity tracking motivational conflict in dorsomedial prefrontal cortex was reduced in the NPD group. Collectively, low generosity in NPD appears to arise from reduced consideration of prosocial motives, which obviates motivational conflict with self-beneficial motives and entails reduced activity in neural conflict monitoring systems. Yet, our data also indicate that NPD is not marked by an absolute indifference to others’ needs. This points to potentials for improving interpersonal relationships, effectively supporting the well-being of patients and their peers.

Healthy sleep, positive general affect, and the ability to regulate emotional experiences are fundamental for well-being. In contrast, various mental disorders are associated with altered rapid eye movement (REM) sleep, negative affect, and diminished emotion regulation abilities. However, the neural processes mediating the relationship between these different phenomena are still not fully understood. In the present study of 42 healthy volunteers, we investigated the effects of selective REM sleep suppression (REMS) on general affect, as well as on feelings of social exclusion, cognitive reappraisal (CRA) of emotions, and their neural underpinnings. Using functional magnetic resonance imaging we show that, on the morning following sleep suppression, REMS increases general negative affect, enhances amygdala responses and alters its functional connectivity with anterior cingulate cortex during passively experienced experimental social exclusion. However, we did not find effects of REMS on subjective emotional ratings in response to social exclusion, their regulation using CRA, nor on functional amygdala connectivity while participants employed CRA. Our study supports the notion that REM sleep is important for affective processes, but emphasizes the need for future research to systematically investigate how REMS impacts different domains of affective experience and their neural correlates, in both healthy and (sub-)clinical populations.

Healthy sleep, positive general affect, and the ability to regulate emotional experiences are fundamental for well-being. In contrast, various mental disorders are associated with altered rapid eye movement (REM) sleep, negative affect, and diminished emotion regulation abilities. However, the neural processes mediating the relationship between these different phenomena are still not fully understood. In the present study of 42 healthy volunteers, we investigated the effects of selective REM sleep suppression (REMS) on general affect, as well as on feelings of social exclusion, emotion regulation, and their neural underpinnings. Using functional magnetic resonance imaging we show that REMS increases amygdala responses to experimental social exclusion, as well as negative affect on the morning following sleep deprivation. There was no evidence that emotional responses to experimentally induced social exclusion or their regulation using cognitive reappraisal were impacted by diminished REM sleep. Our findings indicate that general affect and amygdala activity depend on REM sleep, while specific emotional experiences possibly rely on additional psychological processes and neural systems that are less readily influenced by REMS.

Experiencing events as controllable is essential for human well-being. Based on classic psychological theory, we test how internal control beliefs impact the affective valuation of task outcomes, neural dynamics and ensuing behavioral preferences. In three consecutive studies we show that dynamics in positive affect increase, with a qualitative shift towards self-evaluative pride, when agents believe they caused a given outcome. We demonstrate that these outcomes engage brain networks processing self-referential information in the cortical midline. Here, activity in the ventromedial prefrontal cortex tracks outcome valence regarding both success as well as internal control, and covaries with positive affect in response to outcomes. These affective dynamics also relate to increased functional coupling between the ventral striatum and cortical midline structures. Finally, we show that pride predicts preferences for control, even at monetary costs. Our investigations extend recent models of positive affect and well-being, and emphasize that control beliefs drive intrinsic motivation., Human affect is shaped in part by whether desirable states are achieved under personal control. Here, the authors show that control beliefs affect happiness and pride, and how those effects relate to neural responses in the prefrontal cortex and behavioral preferences for exerting control.

Experiencing events as controllable and attributing positive outcomes to own contributions is essential for human well-being. Based on classic psychological theory we test how internal control beliefs impact the affective valuation of task outcomes, neural dynamics and ensuing behavioral preferences. In three consecutive studies with independent samples we show that dynamics in self-evaluative affect specifically increase when agents believe they caused a given task outcome. We demonstrate that these outcomes engage brain networks processing self-referential information in the cortical midline. Here, activity in the ventromedial prefrontal cortex tracks outcome valence regarding both success as well as internal control, and covaries with self-evaluative affect. These affective dynamics also relate to increased functional coupling between the ventral striatum and cortical midline structures. Finally, we show that self-evaluative affect promotes preferences for control, even at a monetary cost. Our investigations extend recent models of positive affect and well-being, and emphasize that control beliefs drive intrinsic motivation.

Embarrassment is a genuine human emotion that we experience while being publicly exposed in unfavorable situations. The embarrassment we feel informs us how we perform according to prevalent norms and moral values and helps to regulate the impression we make on others. One cornerstone of embarrassment is the capacity to take another’s perspective and reflect on the thoughts, feelings, and intentions of others. On the neural systems level, these processes of perspective taking are linked to neural activation in the medial prefrontal cortex and precuneus. In addition, the mishap and the expected negative evaluation induce affective arousal and activity in the anterior insula and anterior cingulate cortex. Both networks contribute to the experience of embarrassment and it is their orchestrated activity in the (para-) limbic system that accounts for this complex emotional phenomenon. From a conceptual point of view embarrassment thus presupposes the presence of others. This witnessing audience however also reacts to the mishaps of others and embarrassment may also be experienced vicariously. Here, processes of perspective taking also play an important role, while bystanders embody threats to another’s social integrity. Such interpersonal emotional phenomena gain particular relevance in the context of psychiatric disorders. Specifically, autism spectrum disorders and social anxiety disorders have core symptoms in the social domain that manifest in social interactions causing disturbances in social behavior and reduced well-being of affected individuals.

Witnessing others' plights can be funny for observers, but may also trigger one to empathically cringe with the victim of the predicament. In the present study, we examined the common and distinct neural networks involved in schadenfreude (i.e. pleasure derived from another's misfortune) and fremdscham (i.e. empathically sharing the embarrassment about another's misfortune). Using functional magnetic resonance imaging we examined a total of N = 34 participants while they observed social integrity threats of a misfortunate other and either reported on their schadenfreude or fremdscham. In this between-subject design, we found that despite a broad overlap in brain regions involved in social cognition, the left anterior insula (AI) was activated less if observers were asked to focus on their schadenfreude. Further, the nucleus accumben's activity exclusively covaried with the intensity of the schadenfreude experience and had a higher functional connectivity with the left AI in the context of schadenfreude than during fremdscham. With the present findings, we demonstrate that the valence and intensity of interpersonal emotions strongly depend on the experimental context and that empathy and reward circuits are involved in shaping the subjective experience.