The clinical phenomena that interest me most are psychopathy, antisocial behavior, substance abuse, and pathological fear. I have a particular interest in underlying brain systems involved in processing and reacting to emotional stimuli.
A major focus of my work over the years has been on studying emotional processing in psychopathic criminals, with results indicating that the interpersonal-affective (“Factor 1”) component of psychopathy is associated with a higher threshold for fear reactivity.
This research, together with other recent work we have done on psychopathy in non-prisoner samples using the self-reported based Psychopathic Personality Inventory (PPI; Lilienfeld & Andrews, Psy Assessment, 1996), point to "boldness" (a benign expression of temperamental fearlessness--marked by social dominance and emotional resiliency) as a key construct for understanding the phenomenon of "successful" psychopathy. My colleagues and I (Patrick, Fowles, & Krueger, Development and Psychopathology, 2009) recently advanced a triarchic conceptualization of psychopathy that emphasizes differentiable constructs of boldness, meanness, and disinhibition as important to empirical investigation of the origins and development of Psychopathy. We are now in the process of validating new interview and self-report inventories developed to assess these distinctive phenotypic components of psychopathy in a direct manner.
A related focus of my work (in collaboration with Dr. Robert Krueger) has been on developing a new integrative model of externalizing psychopathology-encompassing child and adult antisocial behavior, alcohol and drug problems, and affiliated personality traits and problem behaviors. This model, termed the externalizing spectrum model (Krueger, Markon, Patrick et al., J Abnormal Psychology, 2007), conceives of traits and problem behaviors within this domain as arising from a broad underlying vulnerability (predominantly genetic in origin) along with other specific etiologic influences that determine the distinctive expression of this vulnerability in one phenotypic form or another. The model also offers a novel research strategy for studying causal factors and processes underlying disorders of this kind. Rather than studying each disorder as a separate entity with its own unique causal underpinnings, one can study the broad dispositional factor these disorders have in common, as well as studying the unique variance associated with each individual disorder. In collaboration with my FSU colleague Dr. Ed Bernat, I have been using electrocortical (EEG/ERP) measures to elucidate brain processing differences underlying variations in general externalizing vulnerability. Our initial papers (Patrick, Bernat et al., Psychophysiology, 2006; Hall, Bernat, & Patrick, Psy Science, 2007) established reduced P300 brain response to target stimuli in an oddball task and reduced amplitude of the error-related negativity (ERN) in a speeded performance task as physiological indicators of this general vulnerability factor. We are extending this work by examining brain responses in variants of these tasks that provide for dissociation of lower-level affective processing from higher elaborative processing of task stimuli. We have found that high externalizing individuals are normally sensitive to the emotional content of exogenous stimuli, even when stimuli are presented briefly and incidentally, but that deeper elaborative processing of stimulus input is impaired in a variety of contexts. This work, currently funded by an NIMH RC1 (“Challenge”) grant, is serving as the basis for a theory of brain processing deficits underlying the general vulnerability to externalizing disorders.
A further line of research, reflecting a merging of my interests in psychopathy and anxiety/mood disorders, entails the study of a trait continuum of fear and fearlessness. This work is funded through an NIMH Center (P50) grant. I conceive of trait fear as a basic neurobiological dimension oblique to (i.e., related to, but distinct from) the broad dimension of negative affectivity that undergirds internalizing disorders. In the first phase of this research, we administered a battery of established measures of fear and fearlessness (including the Fearless Dominance scales from the PPI) to a sample of approximately 2700 adult twins and found that all scales loaded substantially on a large common factor that, like the externalizing factor, was predominantly heritable. In the second phase, which entailed follow-up lab testing of approximately 500 of these twins, we examined physiological (including brain ERP and blink startle) responses to incidental affective stimuli as possible biological (endophenotype) markers of this trait dimension. In addition, we are using electrocortical and neuro-imaging methods to evaluate whether individual differences in trait fear reflect core reactivity differences at the level of basic subcortical systems, or differences in the ability to down-regulate affect mediated by frontal brain regions. We are also examining, within this large adult twin sample, relations between dispositional fear and clinical symptoms of internalizing (anxiety and mood) disorders on one hand, and psychopathy-related personality disorders (narcissistic, histrionic, borderline, antisocial) on the other. Analyses of molecular genetic data from this study sample will also be undertaken.
Ultimately, I believe that individual differences along dimensions such as defensive reactivity and inhibitory control can be defined using physiological (including brain response) measures, and that this improved approach to phenotyping will be a key to elucidating neurobiological processes underlying psychological vulnerability and resilience).