PAST WORK & FINDINGS
Risk for aggression and violence
A series of our studies show that key individual differences (gender, personality, genes) modulate the extent to which stress leads to aggressive behavior, and this work has identified emotional processes that may differ across these groups. For example:
Increases in emotional activation (defensive startle response) in response to stress are related to engagement in aggressive behavior among men high on negative emotional traits or hostility (Verona, Patrick, & Lang, 2002), among men carrying the short allele of the serotonin transporter gene (Verona, Joiner, Johnson, & Bender, 2006), and among normal men but not women (Verona & Curtin, 2006; Verona & Kilmer, 2007).
These set of results suggests that those at higher risk for aggression seem to show stronger associative links between negative affective systems and behavioral activation, which may explain their problems with controlling aggression under emotional situations .
In fact, Verona, Sadeh, & Curtin (2009) tested the hypothesis that the activation of behavior approach mechanisms may underlie stress-induced increases in aggression. We demonstrated that exposure to stress led to greater left prefrontal EEG activity (commonly interpreted as evidence of enhanced approach motivation) and subsequent increases in laboratory aggression. Importantly, left frontal asymmetry in response to stress exposure predicted increases in subsequent aggressive behavior, a finding that did not emerge in the no-stress condition. These results suggest that stress reactivity involving approach activation represents risk for behavioral dysregulation and possibly externalizing disorders.
Externalizing, Psychopathy, and Comorbid Syndromes
Some of our work has focused on identifying broader dimensions of psychopathology by examining the co-occurrence of externalizing disorders, psychopathic traits, and related syndromes (borderline, narcissism, suicidality).
For example, in a series of studies we have shown that suicide risk is related to the impulsive-antisocial traits of psychopathy (Verona et al., 2001, 2005; Javdani, Sadeh, & Verona, 2011), and to the externalizing dimension of psychopathology (Verona et al., 2005). The interpersonal-affective traits, however, are not related to suicide-related behaviors, or the unique variance in these traits is negatively related to suicide risk and self-harm.
Psychopathic traits are also differentially related to other personality disorders. In Schoenleber, Sadeh, and Verona (2011), we described how the grandiose and vulnerable dimensions of narcissism respectively parallel primary and secondary forms of psychopathy in terms of inter-relationships with psychopathy factors (Factor 1 and 2) and other correlates. In terms of Borderliine Personality Disorder (BPD), although the impulsive-antisocial traits are linked to BPD in both men and women, in women the interpersonal-affective traits can exacerbate risk for BPD among women high on the impulsive-antisocial traits (Sprague et al., 2012; Kruepke & Verona, under review).
These studies illustrate dimensions of psychopathology that link the impulsive-antisocial traits of psychopathy, vulnerable narcissism and borderline, and suicidality--suggesting a dysregulated dimension of psychopathology. This dimension is in contrast to one that includes the affective-interpersonal traits of psychopathy, low risk for internalizing psychopathology and grandiose narcissism--suggesting potentially a more adaptive dimension linked to primary psychopathy. Our newer studies examining intimate partner violence, sexual violence, and sex work relationships to psychopathic traits may also help in identifying distinct vulnerability factors explaining the co-occurrence of various risky and/or destructive behaviors that may represent distinct dimensions of psychopathology.
Etiological Heterogeneity in Psychopathic Personality
One main goal of our research is to elucidate the different pathways to criminal and violent behavior, and examination of the different facets of psychopathy (impulsive-antisocial traits vs. affective-interpersonal deficits) suggests at least two etiological pathways, and the possible mechanisms involved in these pathways. Main findings include the following:
We have shown different genetic contributions to the impulsivity and interpersonal-affective deficits of psychopathy using candidate gene studies (Sadeh et al., 2010, 2013). We showed that youth and adults homozygous for the short allele of the serotonin transporter genotype (5HTTLPR) evidenced more impulsivity and impulsive-antisocial traits of psychopathy, respectively, than those homozygous for the long allele. The long allele, however, was associated with higher callous-unemotional and primary psychoapthic traits. Further, the impulsive and irresponsible lifestyle features of psychopathy were higher among low-activity than high-activity MAO-A carriers. Results suggest that psychopathy may be etiologically multi-determined.
Several of our studies have uncovered differential patterns of cognitive and affective processing and cognition-emotion interactions in primary psychopathy (or Factor 1) and impulsive-antisocial traits (or Factor 2).
Within a forensic-clinical sample, Sadeh & Verona (2012, Cognitive, Affective & Behavioral Neuroscience) showed that the affective-interpersonal features of psychopathy related to aberrant processing of emotion at initial perception (visual N1) and deficits in later defensive fear reactivity (FPS), but only when picture stimuli were visually-complex. In contrast, the impulsive-antisocial features of psychopathy were associated with decreased sensitivity to picture complexity (visual N1) and unrelated to emotional processing as assessed by ERP and startle.
In another electrophysiological study (Verona, Sprague, & Sadeh, 2012, Journal of Abnormal Psychology), we reported that inhibitory control demands (No-Go vs. Go) failed to modulate frontal-P3 amplitude to negative emotional words in persons scoring high on psychopathy and persons with antisocial personality disorder (APD), but in different ways. The psychopathic group showed blunted processing of negative emotional words regardless of inhibitory control demands, consistent with research on emotional deficits in psychopathy. In contrast, the APD group demonstrated enhanced processing of negative emotion words in both Go and No-Go trials, suggesting a failure to modulate negative emotional processing when inhibitory control is required.
A recent study from our lab (Bresin et al., 2015, Journal of Abnormal Psychology) showed that interpersonal-affective traits of psychopathy were related to increased behavioral adjustment following errors and to enhanced monitoring of errors (thus, better cognitive control). Impulsive-antisocial traits were not consistently related to error adjustment across the studies, although these traits were related to a deficient monitoring of errors.
Together, this line of work has established that the development of criminal deviance may involve multiple etiological processe: (1) with affective-interpersonal traits reflecting core deficits in defensive emotional activation and/or selective attention but normal or enhanced executive functioning, and (2) the impulsive-antisocial traits reflecting tendencies toward emotional dysregulation and deficits in executive functioning. Current work continues to examine distinct cognitive-affective deficits and brain mechanisms involved in emotional and behavioral problems in individuals with criminal or violent histories.