We investigated how the brain integrates motivational and attentional signals by using a neuroimaging paradigm that provided separate estimates for transient cue- and target-related signals, in addition to sustained block-related responses. Participants performed a Posner-type task in which an endogenous cue predicted target location on 70% of trials, while motivation was manipulated by varying magnitude and valence of a cash incentive linked to task performance. Our findings revealed increased detection performance (d′) as a function of incentive value. In parallel, brain signals revealed that increases in absolute incentive magnitude led to cue- and target-specific response modulations that were independent of sustained state effects across visual cortex, fronto-parietal regions, and subcortical regions. Interestingly, state-like effects of incentive were observed in several of these brain regions, too, suggesting that both transient and sustained fMRI signals may contribute to task performance. For both cue and block periods, the effects of administering incentives were correlated with individual trait measures of reward sensitivity. Taken together, our findings support the notion that motivation improves behavioral performance in a demanding attention task by enhancing evoked responses across a distributed set of anatomical sites, many of which have been previously implicated in attentional processing. However, the effect of motivation was not simply additive as the impact of absolute incentive was greater during invalid than valid trials in several brain regions, possibly because motivation had a larger effect on reorienting than orienting attentional mechanisms at these sites.

Countercyclical risk aversion can explain major puzzles such as the high volatility of asset prices. Evidence for its existence is, however, scarce because of the host of factors that simultaneously change during financial cycles. We circumvent these problems by priming financial professionals with either a boom or a bust scenario. Subjects primed with a financial bust were substantially more fearful and risk averse than those primed with a boom, suggesting that fear may play an important role in countercyclical risk aversion. The mechanism described here is relevant for theory and may explain self-reinforcing processes that amplify market dynamics. (JEL E32, E44, G01, G11, G12)

Despite considerable interest in the neural basis of valuation, the question of how valuation affects cognitive processing has received relatively less attention. Here, we review evidence from recent behavioral and neuroimaging studies supporting the notion that motivation can enhance perceptual and executive control processes to achieve more efficient goal-directed behavior. Specifically, in the context of cognitive tasks offering monetary gains, improved behavioral performance has been repeatedly observed in conjunction with elevated neural activations in task-relevant perceptual, cognitive and reward-related regions. We address the neural basis of motivation-cognition interactions by suggesting various modes of communication between relevant neural networks: (1) global hub regions may integrate information from multiple inputs providing a communicative link between specialized networks; (2) point-to-point interactions allow for more specific cross-network communication; and (3) diffuse neuromodulatory systems can relay motivational signals to cortex and enhance signal processing. Together, these modes of communication allow information regarding motivational significance to reach relevant brain regions and shape behavior.

Although both attention and motivation affect behavior, how these 2 systems interact is currently unknown. To address this question, 2 experiments were conducted in which participants performed a spatially cued forced-choice localization task under varying levels of motivation. Participants were asked to indicate the location of a peripherally cued target while ignoring a distracter. Motivation was manipulated by varying magnitude and valence (reward and punishment) of an incentive linked to task performance. Attention was manipulated via a peripheral cue, which correctly predicted the presence of a target stimulus on 70% of the trials. Taken together, our findings revealed that the signal detection measure, reflecting perceptual sensitivity, increased as a function of incentive value during both valid and invalid trials. In addition, trend analyses revealed a linear increase in detection sensitivity as a function of incentive magnitude for both reward and punishment conditions. Our results suggest that elevated motivation leads to improved efficiency in orienting and reorienting of exogenous spatial attention and that one mechanism by which attention and motivation interact involves the sharpening of attention during motivationally salient conditions.

Our behavior is constantly accompanied by a sense of confidence and its’ precision is critical for adequate adaptation and survival. Importantly, abnormal confidence judgments that do not reflect reality may play a crucial role in pathological decision-making typically seen in psychiatric disorders. In this review, we propose abnormalities of confidence as a new model of interpreting psychiatric symptoms. We hypothesize a dysfunction of confidence at the root of psychiatric symptoms either expressed subclinically in the general population or clinically in the patient population. Our review reveals a robust association between confidence abnormalities and psychiatric symptomatology. Confidence abnormalities are present in subclinical/prodromal phases of psychiatric disorders, show a positive relationship with symptom severity, and appear to normalize after recovery. In the reviewed literature, the strongest evidence was found for a decline in confidence in (sub)clinical OCD, and for a decrease in confidence discrimination in (sub)clinical schizophrenia. We found suggestive evidence for increased/decreased confidence in addiction and depression/anxiety, respectively. Confidence abnormalities may help to understand underlying psychopathological substrates across disorders, and should thus be considered transdiagnostically. This review provides clear evidence for confidence abnormalities in different psychiatric disorders, identifies current knowledge gaps and supplies suggestions for future avenues. As such, it may guide future translational research into the underlying processes governing these abnormalities, as well as future interventions to restore them.

Deregulated EVI1 expression defines poor prognostic subsets among AML with t(11q23) and AML with t(9;11)(p22;q23). Patients with EVI1(+) MLL-rearranged AML seem to benefit from allogeneic transplantation in first CR.

Deficits in empathy enhance conflicts and human suffering. Thus, it is crucial to understand how empathy can be learned and how learning experiences shape empathy-related processes in the human brain. As a model of empathy deficits, we used the well-established suppression of empathy-related brain responses for the suffering of out-groups and tested whether and how out-group empathy is boosted by a learning intervention. During this intervention, participants received costly help equally often from an out-group member (experimental group) or an in-group member (control group). We show that receiving help from an out-group member elicits a classical learning signal (prediction error) in the anterior insular cortex. This signal in turn predicts a subsequent increase of empathy for a different out-group member (generalization). The enhancement of empathy-related insula responses by the neural prediction error signal was mediated by an establishment of positive emotions toward the out-group member. Finally, we show that surprisingly few positive learning experiences are sufficient to increase empathy. Our results specify the neural and psychological mechanisms through which learning interacts with empathy, and thus provide a neurobiological account for the plasticity of empathic reactions.empathy | in-group | learning | prediction error | fMRI

Incidental negative emotions unrelated to the current task, such as background anxiety, can strongly influence decisions. This is most evident in psychiatric disorders associated with generalized emotional disturbances. However, the neural mechanisms by which incidental emotions may affect choices remain poorly understood. Here we study the effects of incidental anxiety on human risky decision making, focusing on both behavioral preferences and their underlying neural processes. Although observable choices remained stable across affective contexts with high and low incidental anxiety, we found a clear change in neural valuation signals: during high incidental anxiety, activity in ventromedial prefrontal cortex and ventral striatum showed a marked reduction in (1) neural coding of the expected subjective value (ESV) of risky options, (2) prediction of observed choices, (3) functional coupling with other areas of the valuation system, and (4) baseline activity. At the same time, activity in the anterior insula showed an increase in coding the negative ESV of risky lotteries, and this neural activity predicted whether the risky lotteries would be rejected. This pattern of results suggests that incidental anxiety can shift the focus of neural valuation from possible positive consequences to anticipated negative consequences of choice options. Moreover, our findings show that these changes in neural value coding can occur in the absence of changes in overt behavior. This suggest a possible pathway by which background anxiety may lead to the development of chronic reward desensitization and a maladaptive focus on negative cognitions, as prevalent in affective and anxiety disorders.