The dual-deficit model identifies unique correlates of the two major factors associated with psychopathy (Patrick, 2007). Factor 1 is associated with deficits in amygdala-mediated emotion, while Factor 2 is related to deficits in higher-order cognitive processes. Research suggests that attention to environmental and contextual cues is critical for emotion and cognition (Ochsner & Gross, 2005). Therefore, and by extension, attention may also be important to deficits in both Factor 1 and Factor 2. The present study utilizes a sample of male prisoners in order to examine the relationship between self-reported attentional control (Derryberry & Reed, 2002) and the major factors of psychopathy, as assessed by three different methods. Across all three measures, Factor 1 is associated with superior attentional control, whereas Factor 2 is related to inferior attentional control. Furthermore, results provide support for the external validity of three commonly used methods for assessing psychopathy. We propose that anomalous attentional control may contribute to both major symptom clusters associated with psychopathy.
Psychopathy is a disorder that is associated with unconstrained “antisocial impulses” (Lykken, 2006, p. 7), but is distinguished from other antisocial syndromes by an interpersonal style that includes glibness, superficial charm, and shallow affect (Cleckley, 1976). When studying the psychological processes that contribute to psychopathy, some investigators advocate parsing psychopathy into these two components so that the unique correlates of these dimensions or factors of psychopathy may be identified (Patrick, 2007).
Such dual-deficit models are predicated on the two-factor model of Hare’s Psychopathy Checklist-Revised (PCL-R; Hare, Harpur, & Hakstian, 1990).1 Here, Factor 1 reflects the interpersonal (charm, grandiosity, and deceitfulness/conning) and affective (lack of remorse, empathy, and emotional depth) features of psychopathy. Alternatively, Factor 2 describes the impulsive and chronic antisocial tendencies associated with psychopathy. According to the dual-deficit model, Factor 1 and Factor 2 are etiologically distinct.
It is suggested that the interpersonal and affective symptoms of psychopathy (i.e., PCL-R Factor 1) correspond to an amygdala-related deficit in emotion processing (Kiehl et al., 2001 and Patrick, 2007). For Patrick (2007), for instance, Factor 1 is associated with a weak defensive system that reduces behavioral and physiological reactions to threat cues directly. Consistent with this view, PCL-R Factor 1 is negatively correlated with startle potentiation during affectively negative as opposed to neutral pictures; and, negatively correlated with trait anxiety (Patrick, 2007; cf. Schmitt & Newman, 1999).
The impulsive and antisocial symptoms of psychopathy (i.e., PCL-R Factor 2), however, have been attributed to a deficit in executive control that undermines inhibition of behavior (Patrick, 1994). For Patrick (2007), the impulsive and antisocial behaviors associated with Factor 2 reflect a deficit in higher-order processes that interferes with one’s focus on threat cues, precludes activation of the defensive system, undermines inhibition of approach behavior, and indirectly results in weak defensive system functioning. In support of this model, Patrick and colleagues cite laboratory studies on externalizing disorders and the effects of alcohol which appear to provide evidence of weak cognitive control (Curtin & Fairchild, 2003, see also Patrick, 1994). Additionally, in contrast to Factor 1, Factor 2 is positively associated with trait anxiety (Patrick, 2007). Thus, the dual-deficit model suggests distinct etiologies and divergent external correlates for Factor 1 and Factor 2; with Factor 1 symptoms attributed to an emotion deficit and Factor 2 symptoms attributed to deficient higher-order cognitive processes, such as cognitive control.
A critical part of successful cognitive control is attention to the environment and use of contextual cues (Ochsner & Gross, 2005). This suggests that when examining cognitive control, it is essential to understand other cognitive processes, like attention, that may contribute to or interact with the functioning of this higher-order cognitive process. More specifically, attentional control, a process that is related to the ability to focus and shift attention may be understood as a crucial component of cognitive control (Weissman, Mangun, & Woldorff, 2002). Furthermore, since, Factor 2 is associated with cognitive deficits whereas Factor 1 is not, the Factors should be associated differentially with attentional control. Specifically, the information processing deficits associated with Factor 2 are likely to engender problems with attentional control. Conversely, the dual-deficit model makes no clear prediction about attentional control for Factor 1, as the core problem involves an emotion deficit.
In this study, we use the attention control scale (ACS, Derryberry & Reed, 2002) to evaluate the quality of attention processing associated with Factors 1 and 2, respectively. The ACS is a 20-item self-report questionnaire that taps an individual’s ability to focus and shift attention. Based on existing research, we predict that (1) Factor 2 of psychopathy will be associated with inferior attentional control and (2) Factor 1 will be uncorrelated with attentional control. Additionally, we will evaluate the consistency of the finding across three widely used measures of psychopathy: the Psychopathy Checklist-Revised (Hare, 2003), the Psychopathic Personality Inventory-Short (Lilienfeld & Andrews, 1996) and the Multidimensional Personality Questionnaire-Brief (Patrick, Curtin, & Tellegen, 2002). Although all three methods have been used to study Factor 1 and Factor 2 traits, it remains to be seen whether these alternative measures correspond to the same psychobiological processes (see Neumann, Malterer, & Newman, 2008). Finally, because Factor 1 and Factor 2 are differentially associated with trait anxiety and trait anxiety is correlated with attention control (Derryberry & Reed, 2002), we explore the potential confounding effects of anxiety.
