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Sarah J. Brislin and Christopher J. Patrick
Antisocial personality disorder (ASPD) and psychopathy are related but distinguishable conditions with long histories in the mental health field. Mirroring developments in the broader literatures on personality disorders and general psychopathology, a shift has occurred toward viewing these conditions as continuous-dimensional and multifaceted in nature rather than discrete and unitary. In this chapter, we begin with a description of the history of these diagnoses, focusing on theoretical accounts and methods of assessment. Second we discuss current conceptions of ASPD and psychopathy and how these two diagnostic conditions differ in terms of their symptomatic features and etiologic bases. Next, we describe dimensional approaches to assessing psychopathy and three phenotypic-dispositional constructs that have recently been used as a framework for conceptualizing ASPD and psychopathy. These dispositions, termed boldness, meanness, and disinhibition, are viewed as contributing to distinct symptom configurations recognizable as ASPD and psychopathy, and help to account for how these conditions relate to other forms of psychopathology. In line with recent trends toward conceptualizing and studying clinical problems in biobehavioral terms, we next consider how these three dispositional facets relate to biobehavioral systems/processes. Drawing on what has been learned about these dispositional constructs and their biobehavioral bases, we conclude with suggestions as to steps that can be taken to advance our understanding of ASPD and psychopathy, with a particular focus on multi-method assessments and targeted treatments.
Historic Descriptions of ASPD and Psychopathy
Individuals who exhibit impulsive, aggressive, disinhibited behavior without signs of thought disturbance have long been of interest to mental health scholars and practitioners. Whether described as manie sans delire (“insanity without delirium”) as suggested by Phillippe Pinel (1801), “moral insanity” as proposed by James Prichard (1837), or “moral weakness” as preferred by Benjamin Rush (1823) – early psychopathology experts grappled with the etiology of this pattern of norm-violating behaviors. While some early experts postulated that this symptom pattern arises from deficits in moral development, J. L. Koch (1841–1908) was the first to use the term psychopathic, connoting “in-born” and “biologically-based,” which he applied to a broad array of psychiatric conditions. Kraepelin (1915), by contrast, used the label “psychopathic personalities” for a narrower set of characterological (personality-based) conditions that resemble modern conceptions of ASPD and psychopathy.
Conceptions of antisocial behavior and psychopathy remained vague and diffuse into the twentieth century. In 1941, Hervey Cleckley’s book The Mask of Sanity introduced a much more focused definition for the term “psychopathic,” based on his clinical observation and scholarly analysis of many psychiatric inpatient cases. Cleckley characterized psychopathy as a distinct and severe form of psychopathology masked by an appearance of good psychological health. Sixteen symptom criteria broadly covering impulsive and deviant behavior, shallow emotions, and a lack of close relationships – evident in a context of ostensible psychological stability (normal or higher intelligence, social poise, lack of “neurotic” [internalizing] features or thought disorder symptoms) – were proposed as a concrete basis for diagnosing psychopathy. By contrast, other forensic researchers at the time (e.g., McCord & McCord, 1964) emphasized the importance of a predatory affective-interpersonal style and lack of remorse while excluding indications of psychological well-being from their conceptualization. These contrasting views are still evident in alternative conceptualizations of psychopathy in use today.
Differing conceptualizations of psychopathy are also evident in proposed subtyping schemes for this condition. One of the first of these, by Karpman (1941), described a subset of antisocial individuals who exhibited high levels of anxiousness and depressivity along with disinhibitory features of psychopathy such as impulsiveness, rebelliousness, and aggression. He labeled these individuals “secondary psychopaths” and posited that their psychopathic symptomatology arose from adverse early environments. On the other hand, mirroring Cleckley’s “masked pathology” conception, Karpman characterized “primary psychopathy” as involving low anxiousness and a lack of emotional sensitivity alongside salient antisocial behavior. Evidence for this distinction was provided by research demonstrating differing responses in laboratory tasks for these two subtypes, with the primary type exhibiting a failure to inhibit punished responses and reduced physiological arousal during anticipation of pain relative to the secondary type (Lykken, 1957). Based on empirical evidence of this and other types reported over the years, Lykken (1995) proposed that primary psychopathy reflects low dispositional fear whereas secondary psychopathy arises from temperamentally-based oversensitivity to reward cues.
The first two editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM-I and II; American Psychiatric Association [APA], 1952, 1968) defined ASPD (termed “Antisocial Reaction” in DSM-I and “Antisocial Personality” in DSM-II) in prototypic-descriptive terms that aligned with Cleckley’s characterization of psychopathy. In addition to a history of rule- and law-breaking behavior, these early DSM editions included callousness towards others, lack of guilt, and lack of ability to learn from punishment as characteristic features. In an effort to address well-documented deficiencies in the reliability of psychiatric diagnoses made using DSM-I and II, prototype descriptions were replaced with criterion-based diagnoses in DSM-III (APA, 1980), and the criteria for ASPD (labeled as such within this edition) consisted of behavioral symptoms including irresponsible, aggressive, and unlawful conduct, and the presence of behavioral deviancy before age 15.
In the revised third edition (DSM-III-R; APA, 1987), a criterion pertaining to lack of remorse was added, and this criterion was retained in DSM-IV (APA, 1994). The diagnostic criteria for personality disorders in this edition of the DSM were carried over to the main Diagnostic Criteria and Codes portion (Section II) of the current fifth edition (DSM-5; APA, 2013), and thus the criteria for ASPD remain the same as those in DSM-IV.
As with prior editions of the DSM, the definition of ASPD in DSM-5 does not fully capture psychopathy – in particular, providing only partial, inadequate coverage of affective-interpersonal features considered most central to this condition (Hare, 1996; Lynam & Vachon, 2012; Patrick & Drislane, 2015). Consequently, even though the diagnosis of “antisocial personality” was originally included in the DSM system to represent the syndrome of psychopathy, drift occurred across successive editions of this system. As a result, differences between the phenotypic presentations of the two disorders are often muddied by misconceptions about diagnostic differentiation. In the next section, we discuss in more specific detail points of overlap and distinctiveness between the two diagnoses as currently defined.
Current Definitions of ASPD and Psychopathy
ASPD: DSM-5 Definitions
Section II of DSM-5 (APA, 2013) defines ASPD as a pattern of behavioral deviancy with onset in childhood (before age 15) that persists into adulthood. The child symptom criteria match those for conduct disorder, and the adult criteria include impulsiveness, irresponsibility, irritability or aggression, unlawful behavior, disregard for the safety of self or others, and a lack of remorse. In addition to overlapping with psychopathy, ASPD exhibits systematic comorbidity with other DSM disorders (Black, Gunter, Loveless, Allen, & Sieleni, 2010) – most notably substance use disorders and other impulse control disorders (e.g., attention deficit hyperactivity disorder, nonsubstance addictions, borderline personality). We consider this pattern of comorbidity again at a later point in this chapter, where we discuss evidence indicating that the co-occurrence among these different disorders can be accounted for by a common externalizing factor (Krueger et al., 2002).
The DSM-5 (APA, 2013) contains an alternative dimensional-trait system for personality disorders, in Section III, titled “Emerging Measures and Models.” This alternative system represents conditions of these types in terms of pathological personality traits from five domains: Disinhibition, Antagonism, Negative Affect, Detachment, and Psychoticism. ASPD is characterized by high levels of Disinhibition, Antagonism, and Negative Affect, while psychopathy is specified as including additional lower order traits – low anxiousness, low social withdrawal, and high attention seeking. A self-report instrument, the Personality Inventory for DSM-5 (PID-5; Krueger, Derringer, Markon, Watson, & Skodol, 2012), was developed as a means to index the personality traits specified within the Section III trait system.
Psychopathy: Interview- and Questionnaire-Based Measures
Currently, the clinician administered Psychopathy Checklist – Revised (PCL-R; Hare, 2003) is the most commonly used method for assessing psychopathy in correctional and forensic hospital settings. The PCL-R is rated using information obtained from a structured clinical interview and a review of institutional file records, and includes 20 items; each item is rated on a 0–2 scale, resulting in a maximum score of 40. The PCL-R was developed to differentiate offenders judged to be high versus low in resemblance to Cleckley’s clinical description of psychopathy, utilizing a global rating system. As such, the PCL-R includes items that index the affective-interpersonal deficits included in Cleckley’s description along with items pertaining to criminal behaviors and attitudes. For many years, research studies using the PCL-R focused on subgroups of offender participants classified as psychopathic versus nonpsychopathic based on low and high cutoffs for overall symptom scores (e.g., >30 and <20, respectively).
However, recent research has moved toward use of continuous scores, for symptom subdimensions (factors) as well as for the PCL-R as a whole. The focus on subdimensions derives from structural analyses of the inventory (e.g., Harpur, Hare, & Hakstian, 1989) demonstrating two broad factors underlying its items: Factor 1, encompassing interpersonal-affective features of psychopathy, and Factor 2, reflecting impulsive-antisocial symptoms. Following the delineation of these factors, further analytic work revealed that Factor 1 could be subdivided into distinct Interpersonal and Affective facets (Cooke & Michie, 2001) and that Factor 2 could be subdivided into an impulsive-irresponsible (“Lifestyle”) facet and an Antisocial facet (Hare, 2003; Hare & Neumann, 2008).
While intercorrelated, the factors and facets of the PCL-R exhibit diverging relations with assorted criterion variables. Factor 1, for example, is selectively associated with narcissism, instrumental aggression, and low levels of anxiety and depression (Hare, 2003; Hicks & Patrick, 2006). Factor 2, on the other hand, is associated with reactive aggression, substance use problems, and suicidal behavior (Hare, 1991, 2003; Verona, Patrick, & Joiner, 2001). Factor 2 also accounts for most of the overlap between PCL-R psychopathy and ASPD. The PCL-R factors also show divergent relations with physiological criterion measures (e.g., Drislane, Vaidyanathan, & Patrick, 2013; Vaidyanathan, Hall, Patrick, & Bernat, 2011; Venables & Patrick, 2012), as discussed later in this chapter.
In addition to containing factors/facets that show contrasting associations with criterion variables, studies using the classification technique of model-based cluster analysis have identified distinct variants (“subtypes”) of high-PCL-R scoring offenders. The first study of this sort, by Hicks, Markon, Patrick, Krueger, and Newman (2004), identified two subtypes of psychopathic criminals on the basis of personality trait profiles: an “emotionally stable” subtype and an “aggressive” subtype. A subsequent study by Skeem, Johansson, Andershed, Kerr, and Louden (2007) that clustered high PCL-R offenders based on psychopathy facet scores and anxiety-scale scores also identified two subgroups, differentiated in particular by low versus high anxiousness, which they termed “primary” and “secondary.” A further study by Hicks, Vaidyanathan, and Patrick (2010), focusing on female offenders clustered on the basis of personality trait profiles, reported a similar pair of subtypes, with the secondary (high-anxious) psychopathic group showing greater violent behavior and substance abuse, along with more mental health problems of other types, than the primary (low-anxious) group.
Self-report instruments are also widely used to assess psychopathy. Some of these, such as Paulhus, Neumann, & Hare’s (2014) Self-Report Psychopathy Scale (SRP) and Levenson and colleagues’ (Levenson, Kiehl, & Fitzpatrick, 1995) Self-Report Psychopathy (LSRP) measure, were developed to parallel the PCL-R. These instruments, like the PCL-R, contain correlated but distinct subdimensions (“factors” or “facets”). Other self-report inventories exist that were developed separately from the PCL-R. These include the Psychopathic Personality Inventory (PPI; Lilienfeld & Andrews, 1996; Lilienfeld & Widows, 2005), the Elemental Psychopathy Assessment (EPA; Lynam et al., 2011), and the Triarchic Psychopathic Measure (TriPM; Patrick, 2010). Rather than emulating the item content of the PCL-R, these inventories rely more broadly on historic conceptualizations and theoretic perspectives, and approach psychopathy from a trait-based (rather than syndrome-based) perspective. These measures are discussed in detail later in this chapter, as they provide points of intersection for psychopathy with broad models of personality.
As a final point, it should be noted that cluster analytic studies of individuals assessed using self-report measures of psychopathy have also revealed distinct subgroups of high scorers resembling those identified in PCL-R/offender studies (e.g., Drislane et al., 2015; Falkenbach, Stern & Creevy, 2014). Specifically, such studies have generally revealed a “primary” subtype exhibiting low anxiousness and high social assertiveness along with prominent antisocial deviance, and a “secondary” subtype exhibiting high anxiousness, high negative affectivity, and internalizing disorder symptoms along with alienation, hostility, aggressiveness, and substance problems. Individuals in the secondary group more often report histories of childhood abuse.
Dimensional Approaches to Diagnosis
In this next section, we discuss advances in the field of general psychopathology – in particular, growing empirical evidence supporting a continuous-dimensional characterization of personality and clinical disorders. Following this, we describe how these advances relate to developments in the study of psychopathy and ASPD.
For some time now, there has been a general consensus that personality pathology is dimensional rather than categorical in nature. For example, researchers in the 1980s examined the distribution of personality disorder symptoms specified in DSM-III-R (APA, 1987) and were unable to find evidence for a clear distinction between individuals diagnosed with and without personality disorders (e.g., Kass, Skodol, Charles, Spitzer, & Williams, 1985; Widiger, Hurt, Frances, Clarkin, & Gilmore, 1984; Zimmerman & Coryell, 1990). In response to these findings, it was suggested that personality pathology should be conceptualized in terms of general trait frameworks such as the Five-Factor Model (FFM; Costa & McCrae, 1992).
Research has produced evidence to suggest that episodic clinical disorders are also better conceptualized as dimensional in nature, rather than discrete. In particular, empirical evidence points to gradations in severity of symptomatology and systematic overlap among different disorders as support for a dimensional conceptualization. For example, based on patterns of comorbidity among adult DSM-III-R disorders, Krueger (1999) proposed that two underlying core psychopathological processes – internalizing (encompassing anxious-misery and fear subfactors) and externalizing – give rise to common mental disorders. These higher order dimensions of psychopathology have also been found consistently in studies of child psychopathology (Achenbach & Edelbrock, 1978, 1984).
In subsequent work, Krueger and colleagues (Krueger, McGue, & Iacono, 2001) sought to interface internalizing and externalizing factors of psychopathology with normal range personality, as indexed by the Multidimensional Personality Questionnaire (MPQ; Tellegen, 2011). These investigators found internalizing to be associated with high negative emotionality (NEM) and low positive emotionality (PEM), and externalizing to be associated with low constraint (CON) and high NEM. These findings support a view of comorbidity as arising from variations in basic temperament dispositions that contribute to a range of adverse outcomes (Clark, Watson, & Mineka, 1994).
In a move toward implementing the dimensional approach to diagnosis in the formal psychiatric nosology, Section III of DSM-5 – titled “Emerging Measures and Models” – includes a system for characterizing personality pathology in terms of continuous traits, organized within broader dispositional domains. Recently, a more comprehensive dimensional model of psychopathology, encompassing episodic clinical syndromes as well as personality disorders, has been advanced. This model, termed the Hierarchical Taxonomy of Psychopathology (HiTOP; Kotov et al., 2017), characterizes psychopathological syndromes and their affiliated symptoms in a multilevel system that reflects empirically-observed patterns of covariation among them. The levels of the HiTOP model range from specific symptom dimensions at the lowest level to a general psychopathology factor at the highest level – with symptom clusters (“components”), disorders (“syndromes”), and disorder dimensions (“spectra”) in between. The model considers higher levels of the psychopathology hierarchy (syndromes, spectra) to be related to broad dimensions of normative personality.
Reflecting these advances in conceptualizing personality disorders, and psychopathological conditions more broadly, a shift has occurred in the study of psychopathy and ASPD toward viewing these disorders as multifaceted and encompassing different configurations of trait-based proclivities. This shift is reflected, for example, in a move toward use of dimensional terminology in published work (e.g., “individuals high in psychopathic traits,” in place of “psychopaths”), changes in research design (i.e., away from extreme-group studies toward continuous-score studies), and a broadening of target populations for study (i.e., to include younger and older individuals from the general community, along with institutionalized and clinic-referred samples). Recent studies have shown that both psychopathy and ASPD are represented effectively within the DSM-5 Section III trait system as operationalized by the PID-5 (e.g., Strickland, Drislane, Lucy, Krueger, & Patrick, 2013).
In the next section we describe the triarchic model, a biobehavioral trait framework that can be used to integrate alternative historic conceptions of psychopathy and antisocial behavior as well as facilitate neurobiological investigations. The triarchic model is also compatible with broader dimensional models of psychopathology such as the DSM-5 Section III and HiTOP models.
Triarchic Model
The triarchic model of psychopathy (Patrick, Fowles, & Krueger, 2009) posits that three distinct dispositional constructs account for the observable symptoms and correlates of psychopathy: boldness, which encompasses social dominance, venturesomeness, and emotional resilience, and connects with the biobehavioral process of defensive reactivity; meanness, which entails low empathy, callousness, and aggressive manipulation of others, and relates to biobehavioral systems for social caring and connectedness; and disinhibition, which involves deficient planfulness/control, irresponsibility, and emotional dysregulation, and is associated with the biobehavioral process of inhibitory control.
These triarchic model dispositions are represented to varying degrees in pre-existing psychopathy assessment instruments, including those mentioned above (Drislane, Patrick, & Arsal, 2014; Sellbom & Phillips, 2013). In addition, the triarchic model connects to established models of general personality including the FFM (Poy, Segarra, Esteller, López, & Moltó, 2014) and Tellegen’s (2011) Multidimensional Personality framework (Brislin, Drislane, Smith, Edens, & Patrick, 2015). The representation of triarchic model constructs within these well-established measures and models provides a link between their nomological networks, allowing for different facets and factors of psychopathy to be interfaced with broader psychopathology domains.
The Triarchic Psychopathy Measure (TriPM; Drislane et al., 2014; Patrick, 2010) was developed as a specific operationalization of the triarchic model constructs. The TriPM is a 58-item self-report inventory that yields scores on boldness, meanness, and disinhibition. While the TriPM was developed specifically to index the triarchic dispositional constructs, it is viewed as just one means for operationalizing these constructs. Consistent with the idea of the triarchic constructs as linked to normative personality traits and represented in different conceptualizations of psychopathy, research has shown that these constructs can be effectively indexed using items from existing psychopathy inventories (Hall et al., 2014; Drislane et al., 2015) as well as omnibus measures of personality (Brislin et al., 2015; Drislane, Brislin, Jones, & Patrick, 2018).
In the subsections that follow, we describe referents in the literature for each of the triarchic model constructs – disinhibition, meanness, and boldness – and we discuss what we have learned about these dispositional constructs through systematic research focusing on each. In particular, each construct is discussed as it relates to current models of personality, common measurement tools, and correlates across modalities (methods) of measurement. We also consider how different configurations of these dispositional tendencies might give rise to alternative clinical presentations of ASPD and psychopathy. In the final major section following this, we consider how the three triarchic model constructs can help to clarify the nature and bases of psychopathic symptomatology in neurobiological terms.
Disinhibition
A pervasive lack of behavioral restraint is central to all definitions of ASPD and psychopathy. Represented in the disinhibitory-behavioral features of the PCL-R (Factor 2), the Self-Centered Impulsivity factor of the PPI-R, and the DSM criteria for ASPD, impulsive and disinhibited behaviors are a core, common feature of these two disorders. Thomas Achenbach first delineated externalizing as a dimension of psychopathology, along with a second major dimension labeled internalizing, in factor analytic work focusing on child mental disorders. He conceptualized externalizing problems as products of conflict directed toward the external world, and internalizing problems as arising from psychological turmoil maintained within (Achenbach, 1966, 1974). These empirically derived constructs mapped onto broad categories of child psychiatric conditions as defined at the time, with externalizing encompassing “undercontrolled” conditions marked by aggression and rule-breaking, and internalizing encompassing “overcontrolled” conditions involving anxiousness, social withdrawal, and depressivity (Achenbach & Edelbrock, 1978). This work was the first to present evidence that psychopathologic conditions that had been defined up to that point as discrete and categorical might share common liabilities, resulting in systematic patterns of comorbidity.
Subsequent to this, Gorenstein and Newman (1980) advanced the idea of a disinhibitory spectrum encompassing ASPD, alcohol use problems, hyperactivity, impulsivity, and psychopathy. Citing findings demonstrating systematic comorbidity among these conditions (i.e., individuals meeting diagnostic criteria for one of these conditions would frequently meet criteria for others), these investigators proposed that these different conditions arise from a shared liability. Viewed in this way, it became important to clarify the nature and etiologic bases of this liability, as a basis for improving the parsimony of clinical diagnoses and providing a broad-range target for treatment (Krueger, 1999; Krueger, Caspi, Moffitt, & Silva, 1998).
Gorenstein and Newman’s (1980) conceptualization set the stage for further research directed at clarifying patterns of comorbidity among mental disorders using advanced statistical modeling methods. Research focusing on patterns of overlap among common adult forms of psychopathology yielded factors compatible with those reported for childhood disorders – namely, an externalizing factor, reflecting covariance between substance use problems and antisocial personality, and an internalizing factor, reflecting the covariation between anxious-fearful and depressive disorders (Kendler, Prescott, Myers, & Neale, 2003; Krueger, 1999; Krueger et al., 1998). Following from this work, Krueger and colleagues (2002) used twin-modeling analyses to demonstrate a strong heritable basis (i.e., ~80 percent of variance attributable to additive genetic influences) to the broad externalizing factor reflecting the variance in common among child and adult symptoms of ASPD, substance use problems, and disinhibitory personality traits. Based on this evidence, these investigators proposed that a common dispositional liability contributes to differing conditions of this sort, with the precise symptomatic expression determined by disorder-specific etiological influences. Research conducted subsequent to this study supports the conclusion that externalizing proneness is highly heritable, and indicates that it operates in a similar way across genders (Hicks et al., 2007; Kendler et al., 2003; Krueger et al., 2002).
The externalizing spectrum was delineated in further detail by Krueger and colleagues (Krueger, Markon, Patrick, Benning, & Kramer, 2007). These investigators mapped out a multifaceted model of this problem domain in the form of a self-report instrument for use in research on disinhibitory psychopathology: the Externalizing Spectrum Inventory (ESI). The ESI quantifies externalizing problems and traits through 23 content scales that load together onto a general externalizing proneness factor, with residual variances of certain scales also loading onto separate callous aggression and substance abuse factors. The general externalizing factor reflects proclivities toward nonplanfulness, impulsiveness, irresponsibility, mistrust, and rule-breaking – consistent with the idea of a broad dispositional liability involving deficient behavioral and emotional control. This externalizing factor demonstrates strong associations with the impulsive-antisocial (Factor 2) dimension of psychopathy, whether assessed by self-report (PPI-R) or clinician rating (PCL-R; Venables & Patrick, 2012; Venables, Hall, & Patrick, 2014), and accounts for much of the overlap between ASPD and psychopathy (Venables et al., 2014; Wall, Wygant, & Sellbom, 2015).
The TriPM Disinhibition scale was developed to index the general factor of the ESI model, and it shows robust associations with Factor 2 of the PCL-R, the Self-Centered Impulsivity factor of the PPI, and FFM Neuroticism and low Conscientiousness (Patrick & Drislane, 2015; Sellbom & Phillips, 2013; Poy et al., 2014). In addition, recent research has demonstrated that disinhibition as indexed by the TriPM is well represented in the trait-based definition for ASPD in Section III of DSM-5. Specifically, Strickland et al. (2013) reported that TriPM Disinhibition demonstrated appreciable correlations with traits from the Section III domains of Disinhibition, Antagonism, and Detachment, as indexed by the PID-5; as noted earlier, Section III defines ASPD in terms of traits from these domains.
Disinhibition also demonstrates robust and reliable associations with impulse-related conditions apart from ASPD and psychopathy. For example, disinhibition as indexed by the ESI general factor is positively associated with substance use disorders (alcohol, cannabis, other drugs; Nelson, Strickland, Krueger, Arbisi, & Patrick, 2016; Venables & Patrick, 2012). Disinhibition also demonstrates associations with the hyperactive-impulsive symptoms of attention deficit/hyperactivity disorder (Young, Stallings, Corley, Krauter, & Hewitt, 2000; Young et al., 2009), which are theorized to reflect a weakened behavioral inhibition system (Barkley, 1997). In addition, externalizing proneness has been found to be predictive of suicidal behaviors both on its own and in conjunction with high levels of dispositional fear (Venables, Sellbom, et al., 2015). This interactive aspect of personality traits may account for convergence and divergence among correlates of ASPD and psychopathy, as individuals high in psychopathy are characterized by relatively low levels of internalizing problems and suicidal behaviors.
Meanness
Meanness (or callous unemotionality; Frick, Ray, Thornton, & Kahn, 2014) is a core feature of psychopathic personality and is represented, in part, in the DSM-5 definition of ASPD. The affective facet of the PCL-R contains criteria relating to callousness, lack of remorse, and shallow affect, intended to capture the emotional insensitivity and predatory-exploitative tendencies described in historical conceptualizations of psychopathy. ASPD as defined in DSM-5 Section II includes a “lack of remorse” symptom. While this single symptom provides only partial coverage of core affective features of psychopathy (Hare, 2003), it does represent guiltlessness and to some extent callous disregard. Given its limited role in the criterion-based diagnosis of ASPD and the heterogeneous nature of this DSM diagnosis, meanness has largely been studied within the child and adult psychopathy literatures.
Meanness, though not recognized as such, has been represented in adult measures of psychopathy for some time. The PCL-R assesses for this facet of psychopathy through four items that index lack of remorse, shallow affect, deficient empathy, and failure to accept responsibility for one’s actions (Hare, 2003). These items covary to form a “deficient affective experience” subdimension (Cooke & Michie, 2001). The self-report based PPI-R (Lilienfeld & Widows, 2005) includes specific representation of meanness in its Coldheartedness subscale, which indexes manipulative disregard for others and lack of emotional sensitivity, as distinct from impulsive and fearless tendencies (Drislane et al., 2014).
Meanness has also been studied from a developmental perspective, by child psychopathy researchers interested in how this dispositional tendency (termed “callous-unemotional traits” in their writings) manifests at a young age and develops over time. Initially, adult measures of psychopathy, most notably the PCL-R, served as referents for developing measures suitable for use with children and adolescents. The interview-based PCL:Youth Version (PCL:YV) assesses meanness based on the same four symptoms included in the adult version, with slight modifications to the scoring criteria to enhance relevancy for adolescent-aged subjects. The informant-rated Antisocial Process Screening Device (APSD; Frick & Hare, 2001), also patterned after the PCL-R, is designed for use with younger individuals (aged 6–13). Self-report measures have also been developed to index callous-unemotional traits in youth. One of these, the Inventory of Callous-Unemotional Traits (ICU; Frick, 2004), was developed to measure the affective (meanness) facet of psychopathy with greater specificity – using the callous-unemotional items of the APSD as a referent. Along with four items taken directly from the APSD, the ICU includes 20 other items intended to provide greater content coverage of the affective features of psychopathy. Another youth-oriented inventory patterned after the PCL-R, the Youth Psychopathic Traits Inventory (YPI; Andershed, Gustafson, Kerr, & Stattin, 2002), assesses psychopathy in terms of three dimensions: callous-unemotional, grandiose-manipulative, and impulsive-irresponsible. These different interview, informant, and self-report based measures are widely used in child and adolescent research; however, they are largely based on adult conceptualizations of psychopathy and since critics have expressed concerns about their structural coherency and validity (Salekin, Andershed, & Clark, 2018), it is likely that new or revised instruments will be proposed in the coming years.
Meanness is also represented in the ESI externalizing model (Krueger et al., 2007). As noted above, residual variances in certain subscales of the ESI – in particular, those indexing empathy (reversed), relational aggression, and destructive aggression – define a distinct Callous-Aggression factor. As a counterpart to the TriPM Disinhibition scale, which measures general externalizing proneness, the Meanness scale of the TriPM was developed to index the ESI Callous-Aggression factor through items from scales that load most strongly onto this factor in the ESI structural model. This scale shows selective associations with other indices of meanness including PPI Coldheartedness and the PCL-R’s Affective facet (Patrick & Drislane, 2015) – as well as with key neurobiological measures (as described in the next major section).
With regard to DSM-5 ASPD, research demonstrates that TriPM Meanness is related most strongly to traits from the DSM-5 Section III domain of Antagonism, and to lesser degree with traits from the Disinhibition and Detachment domains (Strickland et al., 2013). The balanced representation of traits associated with Antagonism and Disinhibition in the Section III definition of ASPD results in a more callousness-infused characterization of this condition than in Section II of the manual.
Apart from ASPD, meanness exhibits associations mainly with other erratic-dramatic (Cluster B) personality disorders in the DSM – in particular, narcissistic personality disorder (Paulhus & Williams, 2002). Meanness shows some relationship as well with substance use problems, but this appears attributable to its overlap with disinhibition (Venables & Patrick, 2012). Meanness is well represented in normal-range personality models, demonstrating a significant negative association with FFM Agreeableness (Poy et al., 2014) and significant positive and negative associations, respectively, with MPQ Aggression and Social Closeness (Brislin et al., 2015).
Boldness
Cleckley (1976) described boldness when he highlighted the “mask” features of psychopathic individuals. Indeed, features that marked these psychiatric patients as unusual and interesting were their charm and social poise, lack of anxiety or internalizing problems, and low suicide risk. Lykken (1957, 1995), Hare (1965), and Fowles (1980) all reported evidence in support of the idea of psychopathy involving low fear and nonanxiousness. Although clearly represented in Cleckley’s description of psychopathy (see Crego & Widiger, 2016) and in contemporary measures of this condition (Drislane et al., 2014), boldness does not enter into the DSM diagnosis of ASPD (Venables et al., 2014), and as described below, is largely unrelated to disorders associated with ASPD.
One of the first measures to represent boldness as a distinct facet of psychopathic personality was the PPI (Lilienfeld & Andrews, 1996). Factor analytic work on the structure of the PPI (Benning, Patrick, Hicks, Blonigen, & Krueger, 2003) demonstrated the presence of a Fearless Dominance (PPI-FD) factor – reflecting social assertiveness, immunity to stressful experience, and fearless risk-taking – separate from the PPI’s impulsive-antisocial (Self-Centered Impulsivity; Lilienfeld & Widows, 2005) factor. Boldness, operationalized as PPI-FD, appears not to be represented in the Section II conception of DSM-5 ASPD: a meta-analytic study by Miller and Lynam (2012) reported that FD was only weakly correlated with symptoms of ASPD and unassociated or only weakly associated with other externalizing conditions (e.g., aggression, substance abuse). By contrast, this meta-analytic study reported that FD was associated to a robust negative degree with internalizing psychopathology, consistent with Cleckley’s clinical description of psychopathic individuals.
Despite its prominent role in historic conceptualizations and early research on psychopathic personality, the role of boldness has been recently questioned as a component of psychopathy. A particular point of concern has been that that PPI-FD scores are only modestly correlated with scores on Factor 1 of the PCL-R and unassociated with Factor 2 scores (Miller & Lynam, 2012), suggesting weak relevance to this well-established clinical measure of psychopathy. However, when examined on a facet level, PPI-FD has been found to be robustly and consistently associated with the Interpersonal facet of the PCL-R, encompassing glibness/charm, grandiosity, and manipulativeness (Hall et al., 2014; Venables et al., 2014; Wall et al., 2015) – features considered “core” to psychopathy (Harpur, Hare, & Hakstian, 1989). Of note, PPI-FD is assessed in a different modality (self-report) than the PCL-R (clinical interview), a factor known to attenuate convergent relations (Blonigen et al., 2010). Indeed, PPI-FD correlates to a higher degree with various self-report based measures including the SRP, YPI, EPA, and with Miller and colleagues’ (Miller, Lynam, Widiger, & Leukefeld, 2001) FFM-based psychopathy prototype (Drislane et al., 2014; Lilienfeld et al., 2016; Poy et al., 2014), though it is not represented in certain others (e.g., LSRP; Drislane et al., 2014). PPI-FD has also been found to differentiate primary and secondary variants of psychopathy in cluster analytic work focusing on high PCL-R scoring offenders (Hicks et al., 2004).
Boldness is one of three major facets of psychopathy identified by the triarchic model (Patrick et al., 2009). The TriPM Boldness scale is one commonly used operationalization of the construct, developed to assess fearless proclivities in the domains of interpersonal behavior, affective experience, and venturesomeness. Within the triarchic model, boldness is characterized as overlapping to a modest degree with meanness and as uncorrelated with disinhibition.
Section III of the DSM-5 includes a psychopathy specifier for the trait-based definition of ASPD. This specifier consists of traits related to low anxiousness and social assertiveness (i.e., lack of social withdrawal and attention seeking). As expected given the traits composing it, this specifier (when operationalized using the PID-5) correlates appreciably with established indicators of boldness including PPI-FD and TriPM Boldness (Anderson, Sellbom, Wygant, Salekin, & Krueger, 2014). Reciprocally, Strickland et al. (2013) reported that TriPM Boldness, when controlling for modest overlap with TriPM Meanness, showed a positive association with the PID-5 trait domain of Antagonism, as well as negative associations with trait domains of Negative Affect and Detachment – demonstrating that boldness as assessed by the TriPM encompasses both maladaptive (i.e., disagreeable) as well as adaptive (i.e., stable/assertive) features.
In line with the idea that boldness operates as a mask of psychological well-being, higher levels of PPI-FD are negatively associated with social phobia and other fear conditions, while correlating positively with grandiose-narcissistic tendencies (Benning, Patrick, & Iacono, 2005). Moderate negative associations between PPI-FD and internalizing disorders symptoms more broadly (i.e., symptoms of mood as well as anxiety disorders) have been consistently found (see Miller & Lynam, 2012, for meta-analytic evidence). Though related weakly if at all to ASPD, PPI-FD shows robust positive and negative associations with two other Cluster B personality disorders‐narcissistic and borderline, respectively (Miller & Lynam, 2012).
Boldness also has clear ties to established models of normal range personality, including the FFM (Costa & McCrae, 1992) and Tellegen’s three-factor MPQ model (Tellegen & Waller, 2008). Boldness, as defined by PPI-FD, shows moderate-level associations with FFM traits of Extraversion (+) and Neuroticism (‒), and a modest positive association with Openness to Experience (Miller & Lynam, 2012). With respect to the MPQ model, PPI-FD is associated with high Social Potency (domain of Positive Emotionality), low stress reactivity (domain of Negative Emotionality), and low harm avoidance (domain of Constraint; Benning et al., 2003). These findings provide support for the perspective that boldness is associated both with psychologically adaptive characteristics and with fearless, risk taking behavior.
Connections to Biobehavioral Systems and Processes
Trait based models of personality such as the triarchic model provide a framework for linking ASPD and psychopathy to scientific initiatives to incorporate data from neural and behavioral modalities into the assessment and conceptualization of clinical disorders. Initiatives such as the NIMH’s Research Domain Criteria (RDoC) system have called for integrating variables from biological and neurophysiological modalities with more standard assessment measures to move the field towards a neurobiologically-informed science of psychopathology. Similarly, the National Institute on Alcohol Abuse and Alcoholism (see Kwako, Momenan, Litten, Koob, & Goldman, 2016) and the National Research Council (2015) are also promoting the use of measures other than self- and other-report. In this final major section, we discuss psychopathy and ASPD in relation to three biobehavioral processes: inhibitory control, empathic sensitivity, and defensive reactivity. These processes connect clearly to the triarchic model phenotypes and provide a basis for linking what we know about psychological aspects of psychopathy and ASPD with neurophysiological and behavioral variables.
Inhibitory Control
Inhibitory control is a biobehavioral process presumed to reflect frontal-brain based differences in the capability to restrain behavior and regulate emotional reactivity (Patrick, Durbin, & Moser, 2012). This biobehavioral process interfaces with the triarchic model construct of disinhibition (i.e., externalizing proneness). Across many studies, individuals high in externalizing demonstrate patterns of dysregulated responding in the context of inhibitory control tasks administered in laboratory settings. For example, Fein, Klein, and Finn (2004) reported that individuals with substance use problems and high levels of externalizing behaviors exhibited a propensity to make risky choices during a simulated gambling task. In another study involving twins, Young and colleagues (2009) administered a set of lab-based tasks (Stroop, stop-signal, antisaccade) that called for participants to override prepotent responses, and used the covariance among performance measures from these tasks to define an “executive function” (EF) factor. Scores on this EF factor were negatively correlated with externalizing proneness, and twin modeling analyses demonstrated that this phenotypic association was attributable largely to shared genetic influences (Young et al., 2009).
Other work has shown that the ability to regulate autonomic nervous system responses (i.e., cardiovascular, electrodermal) is related both to cognitive functioning and externalizing psychopathology. Evidence for a relationship with cognitive functioning comes from work demonstrating facilitative effects of autonomic regulation on memory performance (Clark, Naritoku, Smith, Browning, & Jensen, 1999) and the ability to manage attentional demands (Borenstein & Seuss, 2000). Evidence for a relationship with externalizing proneness comes from studies demonstrating that individuals exhibiting antisocial behavior show reduced baseline levels of autonomic activity but increased autonomic reactivity in response to stress (Lorber, 2004; Ortiz & Raine, 2004). Other studies have reported elevated HR variability in antisocial individuals and interpreted this as evidence for weak vagal-parasympathetic regulation (Ortiz & Raine, 2004). Consistent with results from behavioral performance studies (e.g., Fein et al., 2004; Young et al., 2009), these psychophysiological findings support a link between externalizing proneness and inhibitory control deficits.
Multiple lines of neurophysiological evidence also indicate that externalizing proneness reflects, in part, impairment in anterior brain systems that regulate affect and behavior. In studies using electroencephalographic (EEG) methods to measure electrocortical activity, individuals high in externalizing proneness show reductions in event-related potential (ERP) response during cognitive processing tasks (Patrick et al., 2012). Reduced amplitude of the P3 component of the ERP response to target stimuli in an oddball task paradigm is the best-established brain response indicator of externalizing proneness (Iacono, Carlson, Malone, & McGue, 2002; Patrick et al., 2006). This association between externalizing and P300 has been shown to be attributable mainly to shared genetic influences (Hicks et al., 2007; Yancey, Venables, Hicks, & Patrick, 2013). In addition to blunted P3 response to oddball-target stimuli, blunted P3 in relation to stimuli in other cognitive tasks is also associated with high levels of externalizing (Nelson, Patrick, & Bernat, 2011). In addition to reduced P3 response in different tasks, individuals high in externalizing proneness show reduced amplitude of the error-related negativity (ERN), a negative-going cortical response that follows incorrect responses in a performance task (Dikman & Allen, 2000; Hall, Bernat, & Patrick, 2007), suggesting difficulties in endogenous error-monitoring. Taken together, findings for these ERP measures provide further evidence that externalizing proneness (disinhibition) is related to impairments in cognitive processing and control.
Neuroimaging studies have also produced evidence for differential brain reactivity on the part of externalizing-prone individuals in visual processing paradigms. For example, Foell and colleagues (2015) found that individuals high in trait disinhibition showed increased amygdala reactivity to affective pictures in the context of a pre-cueing task that enabled participants to anticipate picture presentations before their occurrence. The authors’ interpretation was that high-disinhibited individuals failed to anticipate the occurrence of pictures, and thereby down-regulate their emotional reactions, in a normal way. Other neuroimaging research has demonstrated abnormal patterns of functional connectivity among particular brain regions in high-externalizing individuals (Abram et al., 2015).
Taken together, findings from these various lines of research suggest that highly disinhibited individuals show impaired processing of or attention to events occurring within an ongoing task, and that this results in reduced recognition of implicit and explicit task contingencies. In turn, this is consistent with Patrick and Bernat’s (2009) conceptualization of trait disinhibition as involving a failure to link and integrate ongoing stimulus events and response outcomes with situation-relevant memories related to goals and consequences. These neurocognitive impairments disrupt automatic processes needed to anticipate, reflect upon, and self-regulate emotions and behaviors.
Empathic Sensitivity
Psychopathy is characterized by distinct affective and interpersonal features. A lack of concern for the well-being of others coupled with restricted emotional sensitivity are conceptualized to give rise to aggressive and manipulative behaviors. Consistent with this behavioral presentation, children and adults high in trait callousness demonstrate difficulties in processing emotions, empathizing with others, and altering their behavior when punished. Multiple studies have found that children and adults high in trait callousness are less likely to recognize, react to, or pay attention to affective faces – particularly fearful faces (Brislin et al., 2018; Brislin & Patrick, 2019; Dawel, O’Kearney, McKone, & Palermo, 2012; Marsh et al., 2008). Research studies have also found that callousness is associated with slower modification of behavior following punishment (Blair, 2001).
These differences in reactivity to affective faces and punishment cues are also accompanied by differences in neural responses, in high-callous youth as well as adults. Different studies have reported decreased amygdala reactivity to fearful faces in children high in callous-unemotional traits (Jones, Laurens, Herba, Barker, & Viding, 2009; Marsh et al., 2008; Viding et al., 2012). Consistent with the idea that blunted response to negative emotional cues allows high-callous individuals to act aggressively without an affective appreciation of the harm they cause to others, Lozier and colleagues (Lozier, Cardinale, VanMeter, & Marsh, 2014) found that reduced amygdala reactivity mediated the well-established association between trait callousness and proactive aggression. Recent work in adults using ERP measurement has also determined that reduced responsiveness to fearful face stimuli occurs early in the processing of such stimuli (Brislin et al., 2018; Brislin & Patrick, 2019).
Neurophysiological studies have also found that trait callousness is associated with decreased responsiveness to painful stimulation. Studies using both fMRI and ERP measurement (Cheng, Hung, & Decety, 2012; Lockwood et al., 2013; Marsh et al., 2013; Michalska, Zeffiro, & Decety, 2016; Yoder, Lahey, & Decety, 2016) have revealed evidence for reduced activity and altered connectivity in areas of the brain associated with empathy for pain (i.e., anterior insula, posterior insula, anterior cingulate cortex, amygdala) in individuals with high levels of callousness. Additionally, trait callousness has been found to be associated with heightened pain tolerance (Miller, Rausher, Hyatt, Maples, & Zeichner, 2014; Brislin, Buchman-Schmitt, Joiner, & Patrick, 2016). Further research is needed on how the physical experience of pain and neural empathic response to the pain of others are associated, and in turn, how they relate to trait callousness.
Lastly, studies with younger samples have consistently revealed evidence for differential neural reactivity to punishment in high-callous participants. Typically developing youth and those diagnosed with ADHD show a reduction in ventromedial prefrontal cortex (vmPFC) activity following an unexpected punishment (Finger et al., 2008). By contrast, youth high in both conduct problems and callousness do not demonstrate this reduction in vmPFC activation (Finger et al., 2008). In another study where children were taught that certain stimuli were “good” and others “bad” (because they were either rewarded or unrewarded), children high in callousness demonstrated less reactivity in orbitofrontal cortex (OFC) and caudate regions early in the task, and less OFC responsiveness to reward (Finger et al., 2011). In other work, Cohn et al. (2013) demonstrated that callousness in delinquent boys was negatively associated with anterior cingulate cortex (ACC) activity during fear conditioning. However, more work is needed on punishment responsiveness, as recent studies have suggested that these deficits may not be unique to callousness, but instead may occur in children with conduct problems more broadly (White et al., 2013, 2014). Indeed, the finding of deficits in error monitoring in high-externalizing adults appears consistent with this latter possibility. Further research using dimensional assessments of both callousness and disinhibition and measurement of neural reactivity in different tasks within the same participants will be needed to resolve this issue.
Defensive Reactivity
Psychopathy is also characterized by a weak defensive reactivity system, as evidenced for example by deficient startle potentiation in the presence of threat cues. Research with adult offenders has indicated that variations in defensive reactivity as indexed by startle modulation are most associated with the affective-interpersonal (Factor 1) features of psychopathy (e.g., Patrick, 1994; Vaidyanathan et al., 2011). Other work with non-offender samples has shown that scales that index boldness – the triarchic model construct most uniquely associated with psychopathy Factor 1 (Venables et al., 2014) – are associated with variations in aversive startle potentiation (Benning et al., 2005; Dvorak-Bertsch, Curtin, Rubinstein, & Newman, 2009; Esteller, Poy, & Moltó, 2016; Vaidyanathan, Patrick, & Bernat, 2009). Boldness is also associated with decreased electrodermal activation during anticipation of noxious stimulus events (Dindo & Fowles, 2011).
Defensive reactivity has also been studied through examination of electrocortical response to sudden unexpected noise probes. In this context, P3 amplitude can be viewed as indexing the coordination of cognitive resources to determine if sustained defensive mobilization is needed (Herbert, Kissler, Junghöfer, Peyk, & Rockstroh, 2006). Researchers have found that the affective-interpersonal component (Factor 1) of the PCL-R is associated with a reduced P3 brain response to abrupt noise probes occurring during viewing of picture stimuli (Drislane et al., 2013; Patrick et al., 2012). Similarly, PCL-R Factor 1 has been found to be associated with decreased elaborative response to aversive images, reflected in blunted late positive potential (LPP) response (Venables, Hall, Yancey, & Patrick, 2015). The LPP is a longer-latency, more persistent ERP component that is thought to reflect sustained processing of motivationally salient stimuli. The finding of blunted LPP response to aversive stimuli in individuals high in PCL-R Factor 1 is therefore consistent with the hypothesis that weak defensive reactivity is a distinct substrate for the fearless (bold) clinical presentation of individuals high in psychopathic traits.
In sum, these findings suggest that the defensive reactivity system contributes, through the boldness phenotype, to psychopathic traits. However, the defensive reactivity continuum is not psychopathy specific. While clinical presentations of psychopathy marked by boldness appear to occupy the low pole of this continuum, fear disorders appear to lie at the other end, where increased startle reactivity during negative emotional cueing is characteristic.
Future Directions
Psychoneurometric Measurement Models
Recent initiatives have called for a shift toward characterizing psychological disorders in terms of behavioral and neurobiological indicators in concert with traditional report-based measures. As discussed in earlier portions of this chapter, externalizing proneness, trait callousness, and threat sensitivity have correlates in behavior and neurobiology. The psychoneurometric measurement approach (Patrick et al., 2012; Patrick, Iacono, & Venables, 2019; Yancey et al., 2016) was proposed as a framework for conceptualizing and quantifying clinically-relevant attributes across differing modalities (methods) of measurement. This approach relies on the idea that psychological attributes, when conceptualized in neurobehavioral terms, can be quantified using variables from different measurement domains.
Using a psychoneurometric approach, researchers have formulated multi-method measurement models for the constructs of threat sensitivity (Yancey, Venables, & Patrick, 2016), akin to boldness in reverse (Kramer, Patrick, Krueger, & Gasperi, 2012), and inhibitory control (Venables et al., 2018), akin to disinhibition in reverse (Patrick et al., 2012, 2013). In these studies, a latent variable representation of the target attribute was defined using indicators from modalities of self-report and physiology, along with behavioral response in the case of inhibitory control. And in each case, the latent multi-method factor showed substantially more balanced associations with criterion measures from different modalities (methods) of measurement than individual modality indicators or modality factors.
These multi-method measurement models for threat sensitivity (/boldness) and inhibitory control (/disinhibition) can serve as valuable platforms for investigating the role of biobehavioral systems and processes in psychopathy, and clarifying how it relates to and differs from ASPD and other forms of psychopathology. Further work is still needed to investigate interrelations among known indicators of meanness, and biological correlates of empathic sensitivity as described earlier may provide a suitable starting point for this. Along with reshaping clinical assessments to incorporate non-report measures, work of this kind can provide insight into the functional role that neural and behavioral variables identified as indicators play in a given phenotype. Along with advancing our understanding of basic processes underlying differing expressions of psychopathy and ASPD, multi-method assessments of these biobehavioral attributes can serve as important referents for neuropsychologically oriented treatments.
Clinical Implications
ASPD and psychopathy have long been characterized as either highly resistant to treatment or even untreatable. These conditions certainly are challenging for clinicians as their core characteristics are at odds with motivation for change, treatment compliance, and therapeutic rapport (Skeem, Polaschek, Patrick, & Lilienfeld, 2011). Nonetheless, treatments that focus on targeting phenotypic facets of psychopathy as opposed to the disorder as a discrete taxon have shown some promise. For example, Caldwell and colleagues (Caldwell, Skeem, Salekin, & Van Rybrock, 2006) implemented a treatment program with children high in psychopathic traits that focused on reward instead of punishment, targeted self-interest, and taught empathy skills, and found decreased recidivism over a two-year follow-up period. Interventions that are tailored to the specific cognitive and emotional deficits that underlie externalizing proneness, trait callousness, and threat sensitivity may treatments with improved effectiveness.
Treatments targeting behavioral and physiological deficits associated with disinhibition could focus on the use of feedback-based response modification. In line with the idea that disinhibition is a core disposition that contributes to an aggressive, dysregulated clinical presentation, studies by Kahn and colleagues (e.g., Kahn, Ducharme, Travers, & Gonzalez-Heydrich, 2009) have shown that children who participated in a video game intervention, the Regulate and Gain Emotional (RAGE) Control procedure, learned how to focus, respond effectively, and keep their heart rates down other demanding tasks. While this project in its early stages, the utility of this treatment appears promising, as it may be more engaging than a CBT-based therapy for children and adults who are high in disinhibition. Another study by Konicar et al. (2015) provided instruction to high-psychopathic participants in how to regulate their cortical activity through biofeedback training, in a manner designed to enhance cognitive control capacity. These investigators found that improved cognitive control resulting from the biofeedback training was associated with decreased self-reported aggressive and impulsive behaviors, and improvements in both behavioral-inhibition performance and ERN reactivity in a laboratory-based task (Konicar et al., 2015).
To target callousness (meanness), treatments can integrate biofeedback with another targeted component – attentional retraining. Attentional retraining focuses on modifying attentional biases through reward cues. This method has been used primarily in treatment of anxiety disorders, but could theoretically be applied to teach individuals high in callousness to attend to distress cues. As individuals high in this attribute demonstrate poor attention to emotional face cues, attentional retraining could be used to teach these individuals to attend to faces and correctly identify them. A biofeedback component in which high-callous individuals are rewarded for increasing their emotional arousal to negatively valenced images could promote improvements in attending and responding appropriately to emotional cues in others. This approach to treatment is hypothetical at this point, but warrants future examination.
Given evidence for boldness as a dispositional characteristic with relevance to psychopathy, targeted treatments for this phenotypic facet also warrant consideration. When boldness co-occurs with high levels of meanness or disinhibition, it may be useful to focus treatment on enhancing threat sensitivity to more normative levels. For example, attentional retraining could be used in a manner opposite to how it is used to treat anxiety patients – in order to enhance attentiveness toward threatening or aversive stimuli. As with targeted treatments for meanness, research is needed to determine whether attention-oriented therapy can produce change in this psychopathy facet.
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