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An Introduction to Psychopathy
Psychopathy is a disorder that characterizes an individual showing pronounced emotional deficits and an increased risk for displaying antisocial behavior ( Frick, 1995;Hare, 2003). The affective component of psychopathy, often called callous-unemotional (CU) traits, is the distinguishing feature of the disorder relative to other behavioral profiles associated with an increased likelihood of antisocial behavior (Blair, 2007). CU traits refer to a lack of guilt, remorse, and empathy (Frick et al., 2005).
While it is past antisocial behavior that is particularly important in predicting future criminal activity (Walters, 2003), it is CU traits that are at the core of developmental trajectory associated with psychopathy (Frick and White, 2008). The disorder is developmental. It has been shown that CU traits in particular and the psychopathy more generally are relatively stable from childhood into adulthood (Lynam et al., 2007; Munoz and Frick, 2007). In addition, the functional impairments seen in adults with psychopathy (e.g., in responding to emotional expressions, aversive conditioning, passive avoidance learning, reversal learning, extinction) are also seen in adolescents with psychopathic tendencies (see later).
Several formal assessment tools for psychopathy exist, including the Antisocial Process Screening Device (Frick and Hare, 2001) and Psychopathy Checklist – Youth Version (Forth et al., 2007) for adolescents and the Psychopathy Checklist-Revised (Hare, 2003) for adults. Most research has identified three dimensions of behavior that compose psychopathy (Cooke et al., 2006; Frick et al., 2000; Neumann et al., 2006), though other models have been proposed (Cooke et al., 2006). These three dimensions are as follows: an affective factor that focuses on CU traits; an arrogant, deceitful, and narcissistic interpersonal style; and an impulsive, irresponsible, and antisocial behavior (Cooke et al., 2006; Frick et al., 2000; Neumann et al., 2006).
Psychopathy is not equivalent to the psychiatric conditions of conduct disorder (CD) or antisocial personality disorder (ASPD) as defined by DSM-5 or their ICD-10 counterparts. The diagnostic criteria for these disorders focus on antisocial behaviors rather than on etiological factors such as the emotion dysfunction seen in psychopathy (Blair et al., 2005). As such these psychiatric conditions describe individuals with difficulties in executive dysfunction (Moffitt, 1993), as well as individuals with symptoms stemming from CU traits. Consequently, individuals with psychopathy are a more homogenous group than those individuals meeting the criteria for CD and ASPD (Karnik et al., 2006). It should be noted, however, that DSM-5 includes the specifier for CD ‘with limited pro-social emotions,’ which stem directly from research on youth with CD and CU traits (Pardini et al., 2010; Pardini and Fite, 2010). Furthermore, the diagnosis of ASPD now includes components of psychopathy (APA, 2013). While the disorder of psychopathy will still not be equivalent to the DSM-5 diagnoses of CD and ASPD, there will be greater overlap in diagnostic conceptualization.
Psychopathy is characterized by an increased risk for antisocial behavior (Frick and Dickens, 2006; Hare, 2003). While several psychiatric disorders and neurological conditions, including CD and ASPD (APA, 2013), confer an increased risk of reactive aggression (Anderson et al., 1999; Leibenluft et al., 2003), psychopathy is unique in that it conveys increased risk for instrumental aggression (Frick et al., 2003). Furthermore, psychopathy is strongly predictive of institutional maladjustment and recidivism (Edens and Campbell, 2007; Walters, 2003), particularly violent recidivism (Edens et al., 2007;Hemphill et al., 1998).
Causes of Psychopathy
Behavioral genetics work in children and adolescents (for a review, see Viding and McCrory, 2012) suggests that CU traits and psychopathy are highly heritable. Various twin studies across different groups have found the genetic influences account for between 40 and 78% of the variance in CU traits in the population (Viding and McCrory, 2012). Critically, in a large twin sample, antisocial behavior in youth high on CU traits was highly heritable (h2 = 0.81), while antisocial behavior was much less heritable (h2 = 0.30) in youth low on CU traits (Viding et al., 2005).
Despite the evidence suggesting that genetics plays an important etiological role in psychopathy, relatively little is known about the molecular genetics of the disorder. Studies in youth suggest that the long allele of the serotonin transporter gene may be a risk factor for psychopathy (Sadeh et al., 2010 and Sadeh et al., 2013). Additionally,Hirata et al. (2013) report an association between the single-nucleotide polymorphism rs6269 of catechol-O-methyltransferase and CU traits in a modest sample of antisocial youth. Though these early findings are promising, they are preliminary and further work is needed. Furthermore, it is quite possible that different genotypes are associated with the various deficits associated with psychopathy (see Psychopathy by Stuart F. White, James R. Blair for more information).
Relatedly, antisocial behavior in psychopaths and youth with CD and CU traits appears to be less influenced by environmental factors than antisocial behavior in youth with low levels of CU traits. Poor parenting is less associated with antisocial behavior in youth with high levels of CU traits (Hipwell et al., 2007; Oxford et al., 2003; Wootton et al., 1997; Yeh et al., 2011). Moreover, youth with CD and high levels of CU traits are less likely to have a history of trauma than youth with CD and low levels of CU traits (Kahn et al., 2013;Kimonis et al., 2012). Critically, despite the increased genetic influence and reduced environmental influence on the development of psychopathy and CD with high levels of CU traits, this does not mean that psychopathy is genetically determined (Viding and McCrory, 2012). In fact, there have been data to suggest that socioeconomic status plays a role in the expression of genetic risk for psychopathy (Sadeh et al., 2010), though the mechanisms of this gene by environment interaction are not understood. Learn more about the pathophysiology of psychopathy, neural impairment impacts, development of psychopathy and the treatment of psychopathy in this article.
This excerpt was taken from the article White, S. F. and Blair, J. R. (2015). Psychopathy. International Encyclopedia of the Social & Behavioral Sciences (Second Edition), Pages 451-456,http://dx.doi.org/10.1016/B978-0-08-097086-8.56032-2
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*See the article Psychopathy by Stuart F. White and James R. Blair for references cited in this blog
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