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The Development of Severe and Chronic Violence Among Youth: The Role of Psychopathic Traits and Reward Processing

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Abstract

Psychopathic traits are a manifestation of a personality pathology that comprises a core affective-interpersonal dysfunction (callous-unemotional traits) and an impulsive-antisocial behavioral component. Of particular importance, psychopathic traits are associated with the perpetration of some of the most severe acts of violence, and they appear to indicate a subset of youth at risk for earlier onset, greater frequency, and persistence of violent offending. Although these youth represent a minority of the population, they commit a significant proportion of the violence in the general community. In our review, we highlight evidence of a unique neurobiological predisposition that underlies the core affective deficits and describe contemporary accounts for the developmental processes leading to the antisocial behavior associated with psychopathy. Current evidence suggests that, for this subset of youth, the structure and function of neural circuitry supporting emotion processing, reward learning, decision making, and the development of emotion related to empathy may be crucial to understanding why they are at risk for violence. In particular, a reward dominant pattern of neurobehavioral conditioning may explain how these youth progress to some of the most severe and persistent forms of violence. However, this pattern of conditioning may also be essential to the primary prevention of such deleterious behavior. We suspect that effective strategies to prevent such violence may ultimately be informed by understanding these affective and motivational mechanisms.

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Notes

  1. There has been significant debate about the role of criminality in the construct of psychopathy. It is beyond the scope of this paper to review these issues here and interested readers are referred elsewhere [21–23] for a more detailed overview. Despite this debate it is generally recognized that violence is certainly a correlate if not a consequence of psychopathy [20].

  2. There exist several disparate methods of assessing psychopathic traits in youth including clinician rated instruments, teacher report, parent report, and self-report instruments. Importantly, there are a number of critical issues related to the convergence (or lack of convergence) among these alternative assessment methods [48]. Although a number of measures have been validated for research purposes, expert rater devices employing clinician interview and file review are most widely used for clinical and forensic decision making purposes.

  3. The population attributable risk indicates the number (or proportion) of cases (i.e., violent incidents) that would not occur in a population if the factor (i.e., psychopathy) were eliminated. In other words, it indicates the percentage of violence that would be prevented.

  4. Cope et al. [60] reported Pearson effect sizes (r = .40). We converted to Cohen’s d using the formula: d = \(\surd \frac{{4{r^2}}}{{1 - {r^2}}}\).

  5. In another study with a longer follow-up period, Vincent et al. [65] reported that predictive power was primarily due to the behavioral features of psychopathic traits leading the authors to speculate that the predictive utility of the CU features may be greatest at younger ages and diminish post adolescence. In a related vein, Stockdale et al. [66] found that all of the psychopathy facets significantly predicted violent youth recidivism but when looking at adult recidivism the interpersonal and affective traits were not significantly associated. However, it may not be unexpected that the behavioral features would become a stronger predictor of violence as youth age and accumulate violent perpetrations [67]. This would create a scenario of criterion contamination where violence assessed as part of the behavioral features of psychopathy would have more covariance with violent behavior assessed as the criterion than would the CU features. Thus, this covariance does not negate the potential etiological role CU traits may play in the development of violence [67].

  6. It bears mentioning that as of yet, no genetic studies have been conducted with adult populations assessed and diagnosed as psychopathic via the PCL measures (i.e., scoring above 30).

  7. Koenigs [87] offers some cautions for comparing imaging data from child/adolescent populations to adult populations—even among healthy populations.

  8. Recent studies suggest that it is under specific conditions involving competing contingencies or task demands that individuals with psychopathic traits demonstrate deficient amygdala response to noxious stimuli or punishment cues [109]. Because functioning in the real world almost always presents competing contingencies, there are likely many conditions in which psychopathic traits predict a reduced neural response to punishment cues.

  9. In contrast to impaired emotional empathy, youth with CU traits show no impairments in cognitive empathy which is the ability to understand the intentions or beliefs of others in order to predict their behavior [31]. However, Brook and Kosson [111] reported impairments on a laboratory measures of cognitive empathy among adult psychopaths.

  10. Evidence suggestive of a selective emotion processing deficit in combination with diminished amygdala activity has strengthened theories that psychopathy is associated with a “fear deficit”. However, the underlying emotion deficit in psychopathy and accompanying neurocognitive dysfunction has been the subject of a widely studied and controversial debate in the field of psychopathy research. Although it is generally agreed that psychopathy and CU traits are associated with a lack of empathy, there is ongoing discussion as to whether the emotion processing deficits linked to reduced amygdala response in psychopathy are absolute or moderated by attention [109, 113, 114]. Consistent with the former interpretation, there is evidence that children with CU traits exhibit reduced activation in amygdala in response to fearful facial expressions [102, 103] and affective Theory of Mind scenarios (e.g., imagining the emotional states of others) [101]. Consistent with the latter interpretation, instructing psychopathic youth and adults to attend to important features of emotional cues (such as the eyes in fear expressions) ameliorate fear recognition deficits and diminished amygdala response [115–118]. In support of both of these theories, a recent neuroimaging study reported that youth with psychopathic traits show reduced recruitment of brain regions in the dorsal endogenous attention network in response to fearful facial expressions [115]. These findings corroborate integrated neurobiological theories of psychopathy that implicate both amygdala dysfunction and downstream attention processing [119]. Even among controversies regarding whether psychopathy is marked by a distinct impairment in processing fear or whether attention modulates the manner in which individuals respond to emotion cues, there is clear evidence that psychopathy is associated with marked dysfunction in emotion-relevant brain circuitry and the ability to demonstrate emotional empathy towards others.

  11. Reward has often been thought to reflect a hedonic state or conscious state of pleasure. However, competing theories suggest that the exact nature of reward at the neurochemical level is not clear and may represent motivation, wanting, liking, or strictly reflect positive reinforcement defined as increased probability of behavior occurring in the future [130–132]. We use the term reward to reflect reinforcement (i.e., increases the likelihood of the behavior occurring in future) without suggestion of the means by which it does so (i.e., motivation, wanting, liking, anhedonia, etc.).

  12. A complete review of the empirical literature on cognitive dysfunction in psychopathy is beyond the scope of this review; however, there is also substantial evidence of deterioration in cognitive efficiency under approach motivation conditions [29, 145] and for specific impairments in processing peripheral stimuli under approach motivation conditions [99, 109] which are likely to further reduce the ability to modify approach behavior based upon punishment cues.

  13. We should reiterate at this point the heterogeneity among measures of psychopathic traits in youth [48]. Although a number of studies have measured CU traits in children under the age of 6 [38, 41–45], the nascent state of this literature indicates the need for further refinement before such assessment methods could be put into practice.

  14. In terms of youth violence prevention, universal programs are those administered to everyone within a defined population regardless of risk; selected programs are directed to a population who is at-risk for youth violence but has yet to engage in violent behavior; and indicated programs are those that target individuals who show early signs of engaging in violence [162].

  15. These numbers are updated to 2016 dollars from 2010 dollars using the Consumer Price Index.

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Authors and Affiliations

  1. Division of Violence Prevention, Centers for Disease Control & Prevention, Atlanta, GA, USA

    Dennis E. Reidy & Megan C. Kearns

  2. Department of Psychology and Neuroscience, Millsaps College, Jackson, MS, USA

    Elizabeth Krusemark

  3. Department of Psychiatry, University of Wisconsin-Madison, Madison, WI, USA

    Elizabeth Krusemark

  4. Department of Psychology, Rosalind Franklin University of Medicine & Science, North Chicago, IL, USA

    David S. Kosson

  5. School of Social Work, Wayne State University, Detroit, MI, USA

    Joanne Smith-Darden

  6. Departments of Psychology & Neuroscience, University of New Mexico, Albuquerque, NM, USA

    Kent A. Kiehl

  7. The Nonprofit Mind Research Network, Albuquerque, NM, USA

    Kent A. Kiehl

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  1. Dennis E. Reidy
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  2. Elizabeth Krusemark
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Reidy, D.E., Krusemark, E., Kosson, D.S. et al. The Development of Severe and Chronic Violence Among Youth: The Role of Psychopathic Traits and Reward Processing. Child Psychiatry Hum Dev 48, 967–982 (2017). https://doi.org/10.1007/s10578-017-0720-5

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