Amygdala hyperactivation to angry faces in intermittent explosive disorder

McCloskey, Michael S.; Phan, K. Luan; Angstadt, Mike; Fettich, Karla C.; Keedy, Sarah K.; Coccaro, Emil F.

doi:10.1016/j.jpsychires.2016.04.006

Cited by 81 publications

(76 citation statements)

References 53 publications

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“…Existing neuroimaging studies in patient groups with high levels of aggression and in healthy controls implicate a network of brain regions involved in aggression that includes the amygdala (McCloskey et al , 2016), striatum (Glenn and Yang, 2012), anterior cingulate and orbitofrontal cortex (Beyer et al , 2014). The dominant conceptual framework of how these regions regulate reactive aggression is that the prefrontal cortex inhibits or modulates subcortical activity mediating the aggressive response (Nelson and Trainor, 2007; Siever, 2008; Rosell and Siever, 2015).…”

Section: Introductionmentioning

confidence: 99%

“…Typically, brain responses to aversive facial expressions are used. For example, the involvement of the amygdala in aggression has been evaluated in patients with intermittent explosive disorder, who display a heightened amygdala response to angry faces (Coccaro et al , 2007; McCloskey et al , 2016), and in youths with conduct disorder and callous-unemotional traits, who show reduced amygdala reactivity to fearful faces (White et al , 2012). …”

Section: Introductionmentioning

confidence: 99%

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Violent offenders respond to provocations with high amygdala and striatal reactivity

Cunha-Bang

Fisher

Hjordt

et al. 2017

Social Cognitive and Affective Neuroscience

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The ability to successfully suppress impulses and angry affect is fundamental to control aggressive reactions following provocations. The aim of this study was to examine neural responses to provocations and aggression using a laboratory model of reactive aggression. We used a novel functional magnetic resonance imaging point-subtraction aggression paradigm in 44 men, of whom 18 were incarcerated violent offenders and 26 were control non-offenders. We measured brain activation following provocations (monetary subtractions), while the subjects had the possibility to behave aggressively or pursue monetary rewards. The violent offenders behaved more aggressively than controls (aggression frequency 150 vs 84, P = 0.03) and showed significantly higher brain reactivity to provocations within the amygdala and striatum, as well as reduced amygdala-prefrontal and striato-prefrontal connectivity. Amygdala reactivity to provocations was positively correlated with task-related behavior in the violent offenders. Across groups, striatal and prefrontal reactivity to provocations was positively associated with trait anger and trait aggression. These results suggest that violent individuals display abnormally high neural sensitivity to social provocations, a sensitivity related to aggressive behavior. These findings provide novel insight into the neural pathways that are sensitive to provocations, which is critical to more effectively shaped interventions that aim to reduce pathological aggressive behavior.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Violent offenders respond to provocations with high amygdala and striatal reactivity

Cunha-Bang

Fisher

Hjordt

et al. 2017

Social Cognitive and Affective Neuroscience

View full text Add to dashboard Cite

show abstract

“…In addition, the labeling of neutral faces as “angry” (proxy for hostile attribution) was correlated with history of childhood trauma in the IED participants in this study (unpublished data). Subsequent work reports that individuals with IED display a greater fMRI BOLD response to anger faces in the amygdala compared with controls (Coccaro et al, 2007; McCloskey et al, 2016) suggesting that non-verbal emotional cues related to possible threat in social situations may lead to aggressive actions through imbalances in cortico-limbic circuits (Coccaro et al, 2011), especially when those individuals have other neurobiologic abnormalities related to behavioral inhibition. This latter finding is in contrast to aggressive individuals high in callous/unemotional traits in whom fMRI BOLD responses to emotional stimuli in the amygdala is blunted compared with controls (Dolan and Fullam, 2009; Finger et al, 2011; Harenski et al, 2010; White et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Social cognition in Intermittent Explosive Disorder and aggression

Coccaro

Fanning

Keedy

et al. 2016

Journal of Psychiatric Research

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Social-emotional information processing (SEIP) was assessed in individuals with current DSM-5 Intermittent Explosive Disorder (IED: n = 100) and in healthy (n = 100) and psychiatric (n = 100) controls using a recently developed and validated self-rated questionnaire. SEIP vignettes depicted both direct aggressive and relationally aggressive scenarios of a socially ambiguous nature and were followed by questions assessing subjects' reactions and judgments about the vignettes. IED subjects differed from both healthy and psychiatric controls in all SEIP components. While hostile attribution was highly related to history of aggression, it was also directly correlated with negative emotional response. Further analysis revealed that this component, as well as response valuation and response efficiency, rather than hostile attribution, best explained history of aggressive behavior. A reformulated SEIP model, including self-reported history of childhood trauma, found that negative emotional response and response efficiency were the critical correlates for history of aggressive behavior. Psychosocial interventions of aggressive behavior in IED subjects may do well to include elements that work to reduce the emotional response to social threat and that work to restructure social cognition so that the tendency towards overt, or relationally, aggressive responding is reduced.

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“…Indeed, compared with controls, unmedicated individuals with intermittent explosive disorder showed greater amygdala response to angry (vs neutral) facial expressions [10]. Further, amygdala activation to angry faces was correlated with number of prior aggressive acts [10]. And an increased activity of the left amygdala was also observed in male borderline personality patients during anger induction and aggression phases [11].…”

Section: Neurobiological Basis Of Aggressive/violent Behavior: Insighmentioning

confidence: 95%

“…Studies with functional Magnetic Resonance Imaging (MRI) has shown that amygdala responsivity appears to be increased in aggressive individuals [9][10][11]. Indeed, compared with controls, unmedicated individuals with intermittent explosive disorder showed greater amygdala response to angry (vs neutral) facial expressions [10].…”

Section: Neurobiological Basis Of Aggressive/violent Behavior: Insighmentioning

confidence: 99%

Preventing Aggressive/Violent Behavior: A Role for Biomarkers?

Pinna

Manchia

2017

Biomark. Med.

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The burden of aggressive/violent behavior Despite a declining rate in the past 10 years, aggressive/violent behavior remains among the main causes of worldwide premature mortality [1]. Associated direct (medical and nonmedical expenditure) and indirect (longterm societal implications) socio-economic costs are also substantial [2,3]. These have been estimated in 2001 at approximately 5% of the gross national product of industrialized countries, and as much as 14% of the gross national product of low-income countries [3].In this context, policy makers have attempted to enact interventions that could prevent the development of aggression and violence in at-risk populations (i.e., abused children and troubled youth, alcohol and substance abusers, prisoners). These public health approaches that include, among the others, education, behavior change, policy, engineering and environmental support, have proven to be effective in reducing the rates of aggression/violence as well as its associated economic costs [4].Nonetheless, there is still a substantial proportion of individuals who enact aggressive/violent behavior over the lifetime course that is not targeted by these interventions. Further, such interventions are implemented only once aggressive behavior has already manifested itself.By definition, primary preventive strategies intend to avoid the manifestation of a specific disease or event before it occurs. To be effective, preventive approaches need to identify risk factors that can determine the onset of an illness or of an event in an exposed population.In the case of aggressive/violent behavior, there is a multitude of determinants (clinical, environmental and biological) that set the liability threshold for its manifestation. It is plausible that predictive models integrating different levels of information (from phenotypic to 'omics' data) might help identifying with higher accuracy individuals at risk for aggression/violence compared with those relying only, for instance, on clinical data. However, the inclusion of biological markers (henceforth biomarkers) in such models can be achieved only if they are identified in longitudinal prospective studies and are replicated in independent samples. Importantly, this process could also lead to a more precise understanding of the neurobiological underpinnings of aggression/violence.Here, we critically discuss the recent advancements in the identification of biological markers of aggression and the eventual barriers toward their implementation in predictive models. To this end, we will first briefly present the current knowledge on the neurobiological make up of aggression/violent behavior. Next, we will discuss how the phenotypic heterogeneity of aggression might have hindered the identification of reliable biomarkers. Finally, we will present data on available biological markers of aggression that might be suitable for implementation in predictive models.

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Amygdala hyperactivation to angry faces in intermittent explosive disorder

Cited by 81 publications

References 53 publications

Violent offenders respond to provocations with high amygdala and striatal reactivity

Violent offenders respond to provocations with high amygdala and striatal reactivity

Social cognition in Intermittent Explosive Disorder and aggression

Preventing Aggressive/Violent Behavior: A Role for Biomarkers?

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