Neuroticism and psychopathy predict brain activation during moral and nonmoral emotion regulation

Functional neuroimaging has identified brain regions associated with voluntary regulation of emotion, including the prefrontal cortex and amygdala. The neural mechanisms underlying individual differences in emotion regulation have not been extensively studied. We investigated the neural correlates of neuroticism and psychopathic personality traits in the context of an emotion regulation task. Results showed that amygdala activity elicited by unpleasant pictures was positively correlated with neuroticism and negatively correlated with a specific psychopathic trait related to emotional underreactivity. During active attempts to decrease emotional responses to unpleasant pictures, superior and ventrolateral prefrontal activity was positively correlated with psychopathy, but not with neuroticism. In contrast, dorsolateral prefrontal activity was positively correlated with neuroticism, but not with psychopathy. Psychopathy was also negatively correlated with medial prefrontal activity in response to pictures depicting moral violations, suggesting reduced emotional responses to moral stimuli in individuals with high levels of psychopathic traits. These results demonstrate dissociable influences of different personality traits on neural activity associated with responses to emotional stimuli and on the recruitment of regulation-related brain activity during the active down-regulation of responses to negative emotional stimuli. These results have implications for the etiology of trait-based psychopathology involving emotional dysregulation.     

Psychopathy,frustration, and reactive aggression: The role of ventromedial prefrontal cortex

Psychopathy is a developmental disorder marked by emotional hyporesponsiveness and an increased risk for instrumental and reactive aggression. The increased risk for reactive aggression is the focus of the current paper. It will be argued that the increased risk for reactive aggression does not relate to an increased sensitivity to threatening stimuli since psychopathy is associated with a reduced sensitivity to threat. Instead, it is argued that the increased risk for reactive aggression relates to an increased risk for frustration; i.e., the emotional state following the performance of an action in the expectation of a particular reward and not receiving this reward. Two impairments seen in psychopathy would increase the risk for frustration and consequent potential reactive aggression; impairments in stimulus‐reinforcement learning and reversal learning. It is argued that both are known consequences of impairment in ventromedial prefrontal cortex, one of the regions principally implicated in psychopathy.     

Aberrant neural processing of moral violations in criminal psychopaths

A defining characteristic of psychopathy is the willingness to intentionally commit moral transgressions against others without guilt or remorse. Despite this "moral insensitivity," the behavioral and neural correlates of moral decision-making in psychopathy have not been well studied. To address this issue, the authors used functional magnetic resonance imaging (fMRI) to record hemodynamic activity in 72 incarcerated male adults, stratified into psychopathic (n = 16) and nonpsychopathic (n = 16) groups based on scores from the Hare Psychopathy Checklist-Revised (R. D. Hare, 2003), while they made decisions regarding the severity of moral violations of pictures that did or did not depict moral situations. Consistent with hypotheses, an analysis of brain activity during the evaluation of pictures depicting moral violations in psychopaths versus nonpsychopaths showed atypical activity in several regions involved in moral decision-making. This included reduced moral/nonmoral picture distinctions in the ventromedial prefrontal cortex and anterior temporal cortex in psychopaths relative to nonpsychopaths. In a separate analysis, the association between severity of moral violation ratings and brain activity across participants was compared in psychopaths versus nonpsychopaths. Results revealed a positive association between amygdala activity and severity ratings that was greater in nonpsychopaths than psychopaths, and a negative association between posterior temporal activity and severity ratings that was greater in psychopaths than nonpsychopaths. These results reveal potential neural underpinnings of moral insensitivity in psychopathy and are discussed with reference to neurobiological models of morality and psychopathy.     

催产素影响恐惧习得和消退的认知神经机制

恐惧是一种基本的情绪, 在人类的生存和适应中发挥着重要作用。先前的研究表明, 杏仁核、背侧前扣带回、脑岛等脑区是条件化恐惧习得的认知神经基础, 杏仁核、海马和腹内侧前额叶等脑区在恐惧消退过程中发挥重要作用。研究发现, 催产素与恐惧习得和恐惧消退过程密切相关。恐惧习得过程中, 催产素影响杏仁核、背侧前扣带回的活动, 影响杏仁核与背侧前扣带回和脑干间的功能连接, 促进或抑制恐惧习得过程; 恐惧消退过程中, 催产素影响了杏仁核和腹内侧前额叶的活动, 并且影响杏仁核与内侧前额叶和海马间的功能连接, 促进或抑制恐惧消退过程。未来研究应从性别差异、神经网络模型、身心发育和病理研究等角度展开, 力图深入理解催产素影响恐惧情绪加工的认知神经机制。     

睡眠剥夺影响恐惧情绪加工的认知神经机制

睡眠剥夺与恐惧情绪加工的各个过程息息相关。睡眠剥夺损害了恐惧的习得过程, 而且影响着杏仁核、内侧前额叶的活动及它们之间的功能连接; 睡眠剥夺削弱了恐惧记忆的巩固和再巩固过程, 不仅破坏了恐惧记忆再巩固过程相关蛋白质和酶的合成, 同时也影响着海马、杏仁核、内侧前额叶的活动以及它们之间的功能连接; 睡眠剥夺损害了恐惧的消退, 同时也改变了海马、杏仁核等相关脑区的活动模式。未来的研究应从睡眠剥夺影响恐惧情绪加工的认知神经机制、睡眠剥夺与恐惧情绪相关障碍的关系等角度展开, 力图深入理解睡眠剥夺影响恐惧情绪加工的认知神经机制。     

Spiking Phineas Gage: a neurocomputational theory of cognitive-affective integration in decision making

The authors present a neurological theory of how cognitive information and emotional information are integrated in the nucleus accumbens during effective decision making. They describe how the nucleus accumbens acts as a gateway to integrate cognitive information from the ventromedial prefrontal cortex and the hippocampus with emotional information from the amygdala. The authors have modeled this integration by a network of spiking artificial neurons organized into separate areas and used this computational model to simulate 2 kinds of cognitive-affective integration. The model simulates successful performance by people with normal cognitive-affective integration. The model also simulates the historical case of Phineas Gage as well as subsequent patients whose ability to make decisions became impeded by damage to the ventromedial prefrontal cortex.     

Inhibition of action, thought, and emotion: A selective neurobiological review

The neural bases of inhibitory function are reviewed, covering data from paradigms assessing inhibition of motor responses (antisaccade, go/nogo, stop-signal), cognitive sets (e.g., Wisconsin Card Sort Test), and emotion (fear extinction). The frontal cortex supports performance on these paradigms, but the specific neural circuitry varies: response inhibition depends upon fronto-basal ganglia networks, inhibition of cognitive sets is supported by orbitofrontal cortex, and retention of fear extinction reflects ventromedial prefrontal cortex–amygdala interactions. Inhibition is thus neurobiologically heterogeneous, although right ventrolateral prefrontal cortex may support a general inhibitory process. Dysfunctions in these circuits may contribute to psychopathological conditions marked by inhibitory deficits.     

Amygdala functional connectivity is reduced after the cold pressor task

The amygdala forms a crucial link between central pain and stress systems. Previous research indicates that psychological stress affects amygdala activity, but it is less clear how painful stressors influence subsequent amygdala functional connectivity. In the present study, we used pulsed arterial spin labeling (PASL) to investigate differences in healthy male adults’ resting-state amygdala functional connectivity following a cold pressor versus a control task, with the stressor and control conditions being conducted on different days. During the period of peak cortisol response to acute stress (approximately 15–30 min after stressor onset), participants were asked to rest for 6 min with their eyes closed during a PASL scanning sequence. The cold pressor task led to reduced resting-state functional connectivity between the amygdalae and orbitofrontal cortex (OFC) and ventromedial prefrontal cortex, and this occurred irrespective of cortisol release. The stressor also induced greater inverse connectivity between the left amygdala and dorsal anterior cingulate cortex (ACC), a brain region implicated in the down-regulation of amygdala responsivity. Furthermore, the degree of poststressor left amygdala decoupling with the lateral OFC varied according to self-reported pain intensity during the cold pressor task. These findings indicate that the cold pressor task alters amygdala interactions with prefrontal and ACC regions 15–30 min after the stressor, and that these altered functional connectivity patterns are related to pain perception rather than cortisol feedback.     

Ecstasy and agony: activation of the human amygdala in positive and negative emotion

Considerable evidence indicates that the amygdala plays a critical role in negative, aversive human emotions. Although researchers have speculated that the amygdala plays a role in positive emotion, little relevant evidence exists. We examined the neural correlates of positive and negative emotion using positron emission tomography (PET), focusing on the amygdala. Participants viewed positive and negative photographs, as well as interesting and uninteresting neutral photographs, during PET scanning. The left amygdala and ventromedial prefrontal cortex were activated during positive emotion, and bilateral amygdala activation occurred during negative emotion. High-interest, unusual photographs also elicited left-amygdala activation, a finding consistent with suggestions that the amygdala is involved in vigilance reactions to associatively ambiguous stimuli. The current results constitute the first neuroimaging evidence for a role of the amygdala in positive emotional reactions elicited by visual stimuli. Although the amygdala appears to play a more extensive role in negative emotion, it is involved in positive emotion as well.     

The neurodevelopmental basis of math anxiety

Math anxiety is a negative emotional reaction to situations involving mathematical problem solving. Math anxiety has a detrimental impact on an individual's long-term professional success, but its neurodevelopmental origins are unknown. In a functional MRI study on 7- to 9-year-old children, we showed that math anxiety was associated with hyperactivity in right amygdala regions that are important for processing negative emotions. In addition, we found that math anxiety was associated with reduced activity in posterior parietal and dorsolateral prefrontal cortex regions involved in mathematical reasoning. Multivariate classification analysis revealed distinct multivoxel activity patterns, which were independent of overall activation levels in the right amygdala. Furthermore, effective connectivity between the amygdala and ventromedial prefrontal cortex regions that regulate negative emotions was elevated in children with math anxiety. These effects were specific to math anxiety and unrelated to general anxiety, intelligence, working memory, or reading ability. Our study identified the neural correlates of math anxiety for the first time, and our findings have significant implications for its early identification and treatment.     

Pure correlates of exploration and exploitation in the human brain

Balancing exploration and exploitation is a fundamental problem in reinforcement learning. Previous neuroimaging studies of the exploration–exploitation dilemma could not completely disentangle these two processes, making it difficult to unambiguously identify their neural signatures. We overcome this problem using a task in which subjects can either observe (pure exploration) or bet (pure exploitation). Insula and dorsal anterior cingulate cortex showed significantly greater activity on observe trials compared to bet trials, suggesting that these regions play a role in driving exploration. A model-based analysis of task performance suggested that subjects chose to observe until a critical evidence threshold was reached. We observed a neural signature of this evidence accumulation process in the ventromedial prefrontal cortex. These findings support theories positing an important role for anterior cingulate cortex in exploration, while also providing a new perspective on the roles of insula and ventromedial prefrontal cortex.     

The interplay of attention and emotion: top-down attention modulates amygdala activation in psychopathy

Psychopathic behavior has long been attributed to a fundamental deficit in fear that arises from impaired amygdala function. Growing evidence has demonstrated that fear-potentiated startle (FPS) and other psychopathy-related deficits are moderated by focus of attention, but to date, no work on adult psychopathy has examined attentional modulation of the amygdala or concomitant recruitment of relevant attention-related circuitry. Consistent with previous FPS findings, here we report that psychopathy-related differences in amygdala activation appear and disappear as a function of goal-directed attention. Specifically, decreased amygdala activity was observed in psychopathic offenders only when attention was engaged in an alternative goal-relevant task prior to presenting threat-relevant information. Under this condition, psychopaths also exhibited greater activation in selective-attention regions of the lateral prefrontal cortex (LPFC) than did nonpsychopaths, and this increased LPFC activation mediated psychopathy’s association with decreased amygdala activation. In contrast, when explicitly attending to threat, amygdala activation did not differ in psychopaths and nonpsychopaths. This pattern of amygdala activation highlights the potential role of LPFC in mediating the failure of psychopathic individuals to process fear and other important information when it is peripheral to the primary focus of goal-directed attention.     

Psychopathy, risk taking, and attention: a differentiated test of the somatic marker hypothesis

A. R. Damasio's (1994) somatic marker hypothesis relates psychopathy to deficits in the ventromedial prefrontal cortex. Using the gambling task (A. Bechara, A. R. Damasio, H. Damasio, & S. Anderson, 1994), the authors tested this premise and the role of attention as a moderator. Forty-nine male prison inmates were assessed with the Psychopathy Checklist--Revised (R. D. Hare, 1991), the gambling task, and standardized tests on attention-concentration, and intelligence. Results revealed no general relation between psychopathy and gambling task performance. However, psychopathic inmates with low attention scores gambled worse than did the attentive ones. They also had more previous convictions. In nonpsychopathic individuals, attention had no impact. Different processing strategies for psychopathic and nonpsychopathic individuals are proposed to explain these findings.     

Individual differences in harm-related moral values are associated with functional integration of large-scale brain networks of emotional regulation

Emotions affects moral judgements, and controlled cognitive processes regulate those emotional responses during moral decision making. However, the neurobiological basis of this interaction is unclear. We used a graph theory measurement called participation coefficient (‘PC’) to quantify the resting-state functional connectivity within and between four meta-analytic groupings (MAGs) associated with emotion generation and regulation, to test whether that measurement predicts individual differences in moral foundations-based values. We found that the PC of one of the MAGs (MAG2) was positively correlated with one of the five recognized moral foundations–the one based on harm avoidance. We also found that increased inter-module connectivity between the ventromedial prefrontal cortex, dorsolateral prefrontal cortex and middle temporal gyrus with other nodes in the four MAGs was likewise associated with higher endorsement of the Harm foundation. These results suggest that individuals' sensitivity to harm is associated with functional integration of large-scale brain networks of emotional regulation. These findings add to our knowledge of how individual variations in our moral values could be reflected by intrinsic brain network organization and deepen our understanding of the relationship between emotion and cognition during evaluations of moral values.     

情绪大脑机制研究的进展

文章综述情绪大脑机制研究的最新进展。情绪的脑机制——大脑回路,包括前额皮层、杏仁核、海马、前部扣带回、腹侧纹状体等。前额皮层中的不对称性与趋近和退缩系统有关,左前额皮层与趋近系统和积极感情有关,右前额皮层与消极感情和退缩有关。杏仁核易被消极的感情刺激所激活,尤其是恐惧。海马在情绪的背景调节中起着重要作用。前额皮层和杏仁核激活不对称性的个体差异是情绪个体差异的生理基础。情绪的中枢回路有可塑性。     

Neurodevelopmental changes in the circuits underlying empathy and sympathy from childhood to adulthood

Empathy and sympathy play crucial roles in much of human social interaction and are necessary components for healthy coexistence. Sympathy is thought to be a proxy for motivating prosocial behavior and providing the affective and motivational base for moral development. The purpose of the present study was to use functional MRI to characterize developmental changes in brain activation in the neural circuits underpinning empathy and sympathy. Fifty-seven individuals, whose age ranged from 7 to 40 years old, were presented with short animated visual stimuli depicting painful and non-painful situations. These situations involved either a person whose pain was accidentally caused or a person whose pain was intentionally inflicted by another individual to elicit empathic (feeling as the other) or sympathetic (feeling concern for the other) emotions, respectively. Results demonstrate monotonic age-related changes in the amygdala, supplementary motor area, and posterior insula when participants were exposed to painful situations that were accidentally caused. When participants observed painful situations intentionally inflicted by another individual, age-related changes were detected in the dorsolateral prefrontal and ventromedial prefrontal cortex, with a gradual shift in that latter region from its medial to its lateral portion. This pattern of activation reflects a change from a visceral emotional response critical for the analysis of the affective significance of stimuli to a more evaluative function. Further, these data provide evidence for partially distinct neural mechanisms subserving empathy and sympathy, and demonstrate the usefulness of a developmental neurobiological approach to the new emerging area of moral neuroscience.     

成瘾人群跨期选择的神经机制及干预方法

成瘾可分为物质成瘾和行为成瘾, 两类成瘾人群在跨期选择上都表现出高时间折扣率的缺陷, 但也有各自的特异性特征。成瘾人群跨期选择缺陷的神经基础主要集中在评估网络(腹内侧前额叶、纹状体、后扣带皮层等)、认知控制网络(前额叶皮层、前扣带皮层等)和预期想象网络(海马、杏仁核等); 可利用心理训练来改善成瘾人群跨期选择缺陷, 其干预方法包括工作记忆训练、预期想象训练、金钱管理指导等。未来研究应该从成瘾者跨期选择缺陷的认知机制、3个神经网络系统的交互作用机理、行为遗传学以及开发有效的干预方法等方面展开大量研究。     

A model of amygdala–hippocampal–prefrontal interaction in fear conditioning and extinction in animals

Empirical research has shown that the amygdala, hippocampus, and ventromedial prefrontal cortex (vmPFC) are involved in fear conditioning. However, the functional contribution of each brain area and the nature of their interactions are not clearly understood. Here, we extend existing neural network models of the functional roles of the hippocampus in classical conditioning to include interactions with the amygdala and prefrontal cortex. We apply the model to fear conditioning, in which animals learn physiological (e.g. heart rate) and behavioral (e.g. freezing) responses to stimuli that have been paired with a highly aversive event (e.g. electrical shock). The key feature of our model is that learning of these conditioned responses in the central nucleus of the amygdala is modulated by two separate processes, one from basolateral amygdala and signaling a positive prediction error, and one from the vmPFC, via the intercalated cells of the amygdala, and signaling a negative prediction error. In addition, we propose that hippocampal input to both vmPFC and basolateral amygdala is essential for contextual modulation of fear acquisition and extinction. The model is sufficient to account for a body of data from various animal fear conditioning paradigms, including acquisition, extinction, reacquisition, and context specificity effects. Consistent with studies on lesioned animals, our model shows that damage to the vmPFC impairs extinction, while damage to the hippocampus impairs extinction in a different context (e.g., a different conditioning chamber from that used in initial training in animal experiments). We also discuss model limitations and predictions, including the effects of number of training trials on fear conditioning.     

Recalling safety: cooperative functions of the ventromedial prefrontal cortex and the hippocampus in extinction

Anxiety disorders are commonly treated with exposure-based therapies that rely on extinction of conditioned fear. Persistent fear and anxiety following exposure therapy could reflect a deficit in the recall of extinction learning. Animal models of fear learning have elucidated a neural circuit for extinction learning and recall that includes the amygdala, ventromedial prefrontal cortex (vmPFC), and hippocampus. Whereas the amygdala is important for extinction learning, the vmPFC is a site of neural plasticity that allows for the inhibition of fear during extinction recall. We suggest that the vmPFC receives convergent information from other brain regions, such as contextual information from the hippocampus, to determine the circumstances under which extinction or fear will be recalled. Imaging studies of human fear conditioning and extinction lend credence to this extinction network. Understanding the neural circuitry underlying extinction recall will lead to more effective therapies for disorders of fear and anxiety.     

The functional neuroanatomy of emotion and affective style

Recently, there has been a convergence in lesion and neuroimaging data in the identification of circuits underlying positive and negative emotion in the human brain. Emphasis is placed on the prefrontal cortex (PFC) and the amygdala as two key components of this circuitry. Emotion guides action and organizes behavior towards salient goals. To accomplish this, it is essential that the organism have a means of representing affect in the absence of immediate elicitors. It is proposed that the PFC plays a crucial role in affective working memory. The ventromedial sector of the PFC is most directly involved in the representation of elementary positive and negative emotional states while the dorsolateral PFC may be involved in the representation of the goal states towards which these elementary positive and negative states are directed. The amygdala has been consistently identified as playing a crucial role in both the perception of emotional cues and the production of emotional responses, with some evidence suggesting that it is particularly involved with fear-related negative affect. Individual differences in amygdala activation are implicated in dispositional affective styles and increased reactivity to negative incentives. The ventral striatum, anterior cingulate and insular cortex also provide unique contributions to emotional processing.