Conceptualizing Psychopathy in Triarchic Terms: Implications for Treatment

Abstract

Clarifying the nature and origins of psychopathy is crucial to establishing effective methods for treating this severe form of pathology. The Triarchic Model of Psychopathy (Patrick, Fowles, & Krueger, 2009) is presented as a framework for resolving historic debates regarding the nature of psychopathy, and for guiding research on neurobiological influences contributing to its characteristic symptom picture. Evidence is reviewed for two distinct processes underlying “boldness” and “disinhibition” components of psychopathy in particular: underreactivity of the brain's defensive motivational system, and impairment in fronto-cortical regulatory circuitry. A third symptomatic facet, “meanness” (or callous-unemotionality) is theorized to reflect dysfunction in brain systems important for emotional empathy, and in endogenous neuromodulators such as oxytocin and vasopressin. We discuss how this variegated perspective on the nature and etiology of psychopathy can inform approaches to treatment. Specifically, focusing on feedback-based response modification and attentional retraining approaches as examples, we describe how specific neurobiologically-informed interventions might be developed to address distinct symptomatic components of psychopathy.

Keywords:

• psychopathy
• triarchic model
• boldness
• meanness
• disinhibition
• biofeedback
• attentional retraining

Notes

The Fearlessness subscale of the PPI loads on PPI-IA as well as PPI-FD (Benning et al., 2003; Ross et al., 2009). The reason appears to be that the items of this subscale reflect not just tendencies toward venturesomeness and tolerance of danger, but also boredom susceptibility and weak restraint; the venturesomeness component of PPI Fearlessness in particular accounts for its relationship with PPI-FD, whereas the boredom/weak restraint component accounts for its association with PPI-IA (Benning et al., 2005a).