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There is accumulating evidence that youths with antisocial behavior or psychopathic traits show deficits in facial emotion recognition, but little is known about the neural mechanisms underlying these impairments. A number of neuroimaging studies have investigated brain activity during facial emotion processing in youths with Conduct Disorder (CD) and adults with psychopathy, but few of these studies tested for group differences in effective connectivity-i.e. changes in connectivity during emotion processing. Using functional magnetic resonance imaging and psycho-physiological interaction methods, we investigated the impact of CD and psychopathic traits on amygdala activity and effective connectivity in 46 male youths with CD and 25 typically-developing controls when processing emotional faces. All participants were aged 16-21 years. Relative to controls, youths with CD showed reduced amygdala activity when processing angry or sad faces relative to neutral faces, but the groups did not significantly differ in amygdala-related effective connectivity. In contrast, psychopathic traits were negatively correlated with amygdala-ventral anterior cingulate cortex connectivity for angry vs neutral faces, but were unrelated to amygdala responses to angry or sad faces. These findings suggest that CD and psychopathic traits have differential effects on amygdala activation and functional interactions between limbic regions during facial emotion processing.

Objective: Conduct disorder (CD) in females is associated with negative adult outcomes including mental health problems and personality disorders. Although recent neuroimaging studies have reported changes in neural activity during facial emotion processing in males with CD or callous-unemotional (CU) traits, there have been no neuroimaging studies specifically assessing females with CD. We addressed this gap by investigating whether female adolescents with CD show atypical neural activation when processing emotional or neutral faces., Method: We acquired functional magnetic resonance imaging (fMRI) data from 20 female adolescents with CD and 20 female control participants while they viewed angry, sad, and neutral faces., Results: An omnibus group (CD, control) by facial emotion (angry, sad, neutral) analysis of variance (ANOVA) revealed main effects of facial emotion in superior temporal cortex, fusiform gyrus, ventrolateral prefrontal cortex and insula, and main effects of group in medial orbitofrontal cortex (OFC) and right anterior insula. Female participants with CD showed reduced medial OFC and increased anterior insula responses relative to healthy controls. There were no significant group × facial emotion interactions. Lifetime CD symptoms were negatively correlated with amygdala, superior temporal cortex, fusiform gyrus, and dorsolateral prefrontal cortex activity for the contrast "all-faces versus fixation." CU traits were negatively correlated with fusiform gyrus activity for the contrast sad versus neutral faces., Conclusion: Females with CD showed atypical neural activation during the processing of all facial expressions, irrespective of valence. Our results demonstrate that severity of CD symptoms and CU traits is important in explaining abnormal patterns of neural activity., (Copyright © 2014 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.)

The visual cortex is sensitive to emotional stimuli. This sensitivity is typically assumed to arise when amygdala modulates visual cortex via backwards connections. Using human fMRI, we compared dynamic causal connectivity models of sensitivity with fearful faces. This model comparison tested whether amygdala modulates distinct cortical areas, depending on dynamic or static face presentation. The ventral temporal fusiform face area showed sensitivity to fearful expressions in static faces. However, for dynamic faces, we found fear sensitivity in dorsal motion-sensitive areas within hMT+/V5 and superior temporal sulcus. The model with the greatest evidence included connections modulated by dynamic and static fear from amygdala to dorsal and ventral temporal areas, respectively. According to this functional architecture, amygdala could enhance encoding of fearful expression movements from video and the form of fearful expressions from static images. The amygdala may therefore optimize visual encoding of socially charged and salient information.

Background: Reduced levels of serotonin (5-HT) within prefrontal cortex (PFC)-amygdala circuits have long been implicated in impulsive aggression. However, whether lowering 5-HT alters the dynamic interplay between the PFC and the amygdala has not been directly tested in humans. It is known that manipulating 5-HT via acute tryptophan depletion (ATD) causes variable effects on brain responses to a variety of emotional stimuli, but it remains unclear whether ATD affects functional connectivity in neural networks involved in processing social signals of aggression (e.g., angry faces)., Methods: Thirty healthy individuals were enrolled in a randomized, double-blind, placebo-controlled ATD study. On each treatment, brain responses to angry, sad, and neutral faces were measured with functional magnetic resonance imaging. Two methods (psycho-physiological-interaction in a general linear model and dynamic causal modeling) were used to assess the impact of ATD on the functional connectivity between PFC and amygdala., Results: Data from 19 subjects were available for the final analyses. A whole-brain psycho-physiological-interaction in a general linear model showed that ATD significantly modulated the connectivity between the amygdala and two PFC regions (ventral anterior cingulate cortex and ventrolateral PFC) when processing angry vs. neutral and angry vs. sad but not sad vs. neutral faces. Dynamic causal modeling corroborated and extended these findings by showing that 5-HT depletion reduced the influence of processing angry vs. neutral faces on circuits within PFC and on PFC-amygdala pathways., Conclusions: We provide strong support for neurobiological accounts positing that 5-HT significantly influences PFC-amygdala circuits implicated in aggression and other affective behaviors., (Copyright © 2012 Society of Biological Psychiatry. All rights reserved.)

Objective: Previous research suggested that structural and functional abnormalities within the amygdala and orbitofrontal cortex contribute to the pathophysiology of Conduct Disorder (CD). Here, we investigated whether the integrity of the white-matter pathways connecting these regions is abnormal and thus may represent a putative neurobiological marker for CD., Methods: Diffusion Tensor Imaging (DTI) was used to investigate white-matter microstructural integrity in male adolescents with childhood-onset CD, compared with healthy controls matched in age, sex, intelligence, and socioeconomic status. Two approaches were employed to analyze DTI data: voxel-based morphometry of fractional anisotropy (FA), an index of white-matter integrity, and virtual dissection of white-matter pathways using tractography., Results: Adolescents with CD displayed higher FA within the right external capsule relative to controls (T = 6.08, P<0.05, Family-Wise Error, whole-brain correction). Tractography analyses showed that FA values within the uncinate fascicle (connecting the amygdala and orbitofrontal cortex) were abnormally increased in individuals with CD relative to controls. This was in contrast with the inferior frontal-occipital fascicle, which showed no significant group differences in FA. The finding of increased FA in the uncinate fascicle remained significant when factoring out the contribution of attention-deficit/hyperactivity disorder symptoms. There were no group differences in the number of streamlines in either of these anatomical tracts., Conclusions: These results provide evidence that CD is associated with white-matter microstructural abnormalities in the anatomical tract that connects the amygdala and orbitofrontal cortex, the uncinate fascicle. These results implicate abnormal maturation of white-matter pathways which are fundamental in the regulation of emotional behavior in CD.

Cognitive research has long been aware of the relationship between individual differences in personality and performance on behavioural tasks. However, within the field of cognitive neuroscience, the way in which such differences manifest at a neural level has received relatively little attention. We review recent research addressing the relationship between personality traits and the neural response to viewing facial signals of emotion. In one section, we discuss work demonstrating the relationship between anxiety and the amygdala response to facial signals of threat. A second section considers research showing that individual differences in reward drive (behavioural activation system), a trait linked to aggression, influence the neural responsivity and connectivity between brain regions implicated in aggression when viewing facial signals of anger. Finally, we address recent criticisms of the correlational approach to fMRI analyses and conclude that when used appropriately, analyses examining the relationship between personality and brain activity provide a useful tool for understanding the neural basis of facial expression processing and emotion processing in general.

Previous research has found that a common polymorphism in the serotonin transporter gene (5-HTTLPR) is an important mediator of individual differences in brain responses associated with emotional behaviour. In particular, relative to individuals homozygous for the l-allele, carriers of the s-allele display heightened amygdala activation to emotional compared to non-emotional stimuli. However, there is some debate as to whether this difference is driven by increased activation to emotional stimuli, resting baseline differences between the groups, or decreased activation to neutral stimuli. We performed functional imaging during an implicit facial expression processing task in which participants viewed angry, sad and neutral faces. In addition to neutral faces, we included two further baseline conditions, houses and fixation. We found increased amygdala activation in s-allele carriers relative to l-homozygotes in response to angry faces compared to neutral faces, houses and fixation. When comparing neutral faces to houses or fixation, we found no significant difference in amygdala response between the two groups. In addition, there was no significant difference between the groups in response to fixation when compared with a houses baseline. Overall, these results suggest that the increased amygdala response observed in s-allele carriers to emotional faces is primarily driven by an increased response to emotional faces rather than a decreased response to neutral faces or an increased resting baseline. The results are discussed in relation to the tonic and phasic hypotheses of 5-HTTLPR-mediated modulation of amygdala activity., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Effective photojournalism provokes an emotional reaction and leaves a lasting impression upon the viewer. Striking and memorable images are often said to possess 'impact'. Within cognitive neuroscience memorable emotional images evoke a greater amygdala response. Research to date has focused on arousal as a causative factor, while the contribution of appraisal dimensions relating to salience of an item, goal relevance, or impact are yet to be addressed. We explored how differences in ratings of impact influenced amygdala activity to negative emotional images matched for valence, arousal and other factors. Increased amygdala activation was found to high impact when compared to neutral images, or high impact when compared to low impact images (matched for arousal). Our findings demonstrate that the amygdala response to emotional stimuli is not a function of arousal (or valence) alone and accord more with the proposal that the amygdala responds to the significance or relevance of an event.

For some people facial expressions of aggression are intimidating, for others they are perceived as provocative, evoking an aggressive response. Identifying the key neurobiological factors that underlie this variation is fundamental to our understanding of aggressive behaviour. The amygdala and the ventral anterior cingulate cortex (ACC) have been implicated in aggression. Using functional magnetic resonance imaging (fMRI), we studied how the interaction between these regions is influenced by the drive to obtain reward (reward-drive or appetitive motivation), a personality trait consistently associated with aggression. Two distinct techniques showed that the connectivity between the ventral ACC and the amygdala was strongly correlated with personality, with high reward-drive participants displaying reduced negative connectivity. Furthermore, the direction of this effect was restricted from ventral ACC to the amygdala but not vice versa. The personality-mediated variation in the pathway from the ventral anterior cingulate cortex to the amygdala provides an account of why signals of aggression are interpreted as provocative by some individuals more than others.

A neuroimaging study in monkeys has shown that separate regions of the amygdala are responsive to facial expression and gaze/head orientation.

Studies in humans suggest that the amygdala plays a role in processing social information. A key component of social information processing is what developmental psychologists call "theory of mind": the ability to infer others' mental states. Recent studies have raised the possibility that the amygdala is involved in theory of mind, showing amygdala activation during a theory of mind task, or showing impairment on theory of mind tasks in a patient with amygdala damage acquired in childhood. Here, we present the first evidence of theory of mind deficits following amygdala damage acquired in adulthood. Two participants, D.R. and S.E., with acquired bilateral amygdala damage showed difficulties with two theory of mind tasks, "Recognition of Faux Pas" (for D.R., z=-5.17; for S.E., z=-1.83) and "Reading the Mind in the Eyes" (for S.E., z=-1.91; for D.R., z=-1.4). The items on which D.R. and S.E. made errors on these tasks were uncorrelated with the items that control participants found most difficult, indicating that these deficits cannot be attributed solely to the cognitive difficulty of the tasks. These results indicate that the amygdala's critical role in theory of mind may not be just in development, but also in "on-line" theory of mind processing in the adult brain.

Advantageous inequality (AI) aversion, or paying at a personal cost to achieve equal reward distribution, represents a unique feature of human behavior. Here, we show that individuals have strong preferences for fairness in both disadvantageous (DI) and advantageous inequality (AI) situations, such that they alter others' payoff at a personal financial cost. At the neural level, we found that both types of inequality activated the putamen, orbitofrontal cortex, and insula, regions implicated in motivation. Individual difference analyses found that those who spent more money to increase others' payoff had stronger activity in putamen when they encountered AI and less functional connectivity between putamen and both orbitofrontal cortex and anterior insula. Conversely, those who spent more money to reduce others' payoff had stronger activity in amygdala in response to DI and less functional connectivity between amygdala and ventral anterior cingulate cortex. These dissociations suggest that both types of inequality are processed by similar brain areas, yet modulated by different neural pathways. Hum Brain Mapp 35:3290-3301, 2014. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Background: Conduct disorder (CD) in female adolescents is associated with a range of negative outcomes, including teenage pregnancy and antisocial personality disorder. Although recent studies have documented changes in brain structure and function in male adolescents with CD, there have been no neuroimaging studies of female adolescents with CD. Our primary objective was to investigate whether female adolescents with CD show changes in grey matter volume. Our secondary aim was to assess for sex differences in the relationship between CD and brain structure. Methods: Female adolescents with CD ( n = 22) and healthy control participants matched in age, performance IQ and handedness ( n = 20) underwent structural magnetic resonance imaging. Group comparisons of grey matter volume were performed using voxel-based morphometry. We also tested for sex differences using archive data obtained from male CD and control participants. Results: Female adolescents with CD showed reduced bilateral anterior insula and right striatal grey matter volumes compared with healthy controls. Aggressive CD symptoms were negatively correlated with right dorsolateral prefrontal cortex volume, whereas callous-unemotional traits were positively correlated with bilateral orbitofrontal cortex volume. The sex differences analyses revealed a main effect of diagnosis on right amygdala volume (reflecting reduced amygdala volume in the combined CD group relative to controls) and sex-by-diagnosis interactions in bilateral anterior insula. Conclusions: We observed structural abnormalities in brain regions involved in emotion processing, reward and empathy in female adolescents with CD, which broadly overlap with those reported in previous studies of CD in male adolescents. [ABSTRACT FROM AUTHOR]

Eating is not only triggered by hunger but also by the sight of foods. Viewing appetizing foods alone can induce food craving and eating, although there is considerable variation in this "external food sensitivity" (EFS). Because increased EFS is associated with overeating, identifying its neural correlates is important for understanding the current epidemic of obesity. Animal research has identified the ventral striatum, amygdala, hypothalamus, medial prefrontal and premotor cortices as key interacting structures for feeding. However, it is unclear whether a similar network exists in humans and how it is affected by EFS. Using functional magnetic resonance imaging, we showed that viewing appetizing compared with bland foods produced changes in connectivity among the human ventral striatum, amygdala, anterior cingulate and premotor cortex that were strongly correlated with EFS. Differences in the dynamic interactions within the human appetitive network in response to pictures of appetizing foods may determine an individual's risk of obesity. [ABSTRACT FROM AUTHOR]

The "behavioral approach system" (BAS) (Gray, 1990) has been primarily associated with reward processing and positive affect. However, additional research has demonstrated that the BAS plays a role in aggressive behavior, heightened experience of anger, and increased attention to facial signals of aggression. Using functional magnetic resonance imaging, we show that variation in the BAS trait in healthy participants predicts activation in neural regions implicated in aggression when participants view facial signals of aggression in others. Increased BAS drive (appetitive motivation) was associated with increased amygdala activation and decreased ventral anterior cingulate and ventral striatal activation to facial signals of aggression, relative to sad and neutral expressions. In contrast, increased behavioral inhibition was associated with increased activation in the dorsal anterior cingulate, a region involved in the perception of fear and threat. Our results provide the first demonstration that appetitive motivation constitutes a significant factor governing the function of neural regions implicated in aggression, and have implications for understanding clinical disorders of aggression. [ABSTRACT FROM AUTHOR]

A network of interconnected brain regions, including orbitofrontal, ventral striatal, amygdala, and midbrain areas, has been widely implicated in a number of aspects of food reward. However, in humans, sensitivity to reward can vary significantly from one person to the next. Individuals high in this trait experience more frequent and intense food cravings and are more likely to be overweight or develop eating disorders associated with excessive food intake. Using functional magnetic resonance imaging, we report that individual variation in trait reward sensitivity (as measured by the Behavioral Activation Scale) is highly correlated with activation to images of appetizing foods (e.g., chocolate cake, pizza) in a fronto-striatal-amygdala-midbrain network. Our findings demonstrate that there is considerable personality-linked variability in the neural response to food cues in healthy participants and provide important insight into the neurobiological factors underlying vulnerability to certain eating problems (e.g., hyperphagic obesity). [ABSTRACT FROM AUTHOR]

We report three experiments investigating the recognition of emotion from facial expressions across the adult life span. Increasing age produced a progressive reduction in the recognition of fear and, to a lesser extent, anger. In contrast, older participants showed no reduction in recognition of disgust, rather there was some evidence of an improvement. The results are discussed in terms of studies from the neuropsychological and functional imaging literature that indicate that separate brain regions may underlie the emotions fear and disgust. We suggest that the dissociable effects found for fear and disgust are consistent with the differential effects of ageing on brain regions involved in these emotions. [Copyright &y& Elsevier]

Recent theories distinguish anxiety from fear in the brain. Anxiety is associated with activation in ventromedial prefrontal cortex and hippocampus, while fear is associated with activation in periaqueductal gray, with amygdala involved in processing aspects of both emotional responses. These theories propose that the amount of information available about threat determines which of the two defensive responses is elicited, with fear and anxiety associated with well-defined and uncertain threats respectively. However, a direct test of this hypothesis is lacking. Here we provide such a test using fMRI to record participants’ brain activity while they performed a computer-based task which required to press a button to move an artificial agent to a target position while an artificial predator chased the agent. In one condition (associated with fear) the predator was visible, while in another condition (associated with anxiety) the predator was invisible. Ventromedial prefrontal cortex, hippocampus, and amygdala showed increased activity when the predator was invisible compared to visible, while the opposite effect was observed in periaqueductal gray. We also observed that participants with high but not low trait-anxiety showed an hippocampal activation with invisible threat at an earlier time stage during the trial. These findings help clarify the neural mechanisms that underlie different defensive emotions and shed light on how these mechanisms may contribute to exaggerated anxiety. [ABSTRACT FROM AUTHOR]

Abstract: It is not known how 5-HTTLPR genotype×childhood adversity (CA) interactions that are associated with an increased risk for affective disorders in population studies operate at the neural systems level. We hypothesized that healthy adolescents at increased genetic and environmental risk for developing mood disorders (depression and anxiety) would demonstrate increased amygdala reactivity to emotional stimuli compared to those with only one such risk factor or those with none. Participants (n=67) were classified into one of 4 groups dependent on being homozygous for the long or short alleles within the serotonin-transporter-linked polymorphic region (5-HTTLPR) of the SLC6A4 gene and exposure to CA in the first 11years of life (present or absent). A functional magnetic resonance imaging investigation was undertaken which involved viewing emotionally-salient face stimuli. In addition, we assessed the role of other variables hypothesized to influence amygdala reactivity, namely recent negative life-events (RNLE) assessed at ages 14 and 17, current anxiety symptoms and psychiatric history. We replicated prior findings demonstrating moderation by gene variants in 5-HTTLPR, but found no support for an effect of CA on amygdala reactivity. We also found a significant effect of RNLE aged 17 with amygdala reactivity demonstrating additive, but not interactive effects with 5-HTTLPR. A whole-brain analysis found a 5-HTTLPR×CA interaction in the lingual gyrus whereby CA appears to differentially modify neural reactivity depending on genotype. These results demonstrate that two different forms of environmental adversities interplay with 5-HTTLPR and thereby differentially impact amygdala and cortical reactivity. [Copyright &y& Elsevier]