Compromised Neurocognitive Control in Antisocial Personality Disorder

Antisocial personality disorder (ASPD) is characterized by a variety of pervasive patterns and antisocial behaviors in individuals. Most notably this includes, but is not limited to, impulsive behaviors leading to a disregard for the wellbeing of others. Furthermore, ASPD is associated with several neurocognitive deficits assumed to cause the persistence of these antisocial behaviors, as well as other aberrancies with cognition. Cognitive inflexibility, attentional deficits, and alternations in schematic processing are but a few of the cognitive anomalies exhibited in persons with ASPD. Along with the underlying neurological insults, these cognitive dysfunctions will be the primary focus of this review.

Antisocial behaviors and cognitive defects characteristic of ASPD are regulated by anomalies in several brain regions. Particular focus has been given to prefrontal brain structures, including the anterior cingulate (ACC), ventromedial (vmPFC), fusiform gyri, and hypothalamus. Problems in these areas explain the cognitive aberrancies in understanding and responding to stimuli, poor allocation of attention and maladaptive schematic processing.

Currently, a plethora of ASPD research has focused on the aforementioned prefrontal brain structures, and their relation to impulsive behaviors, emotional processing, and issues with attentional redirection. Researchers have also looked into the genetics governing ASPD, including identifying associated genes and as such, implementing appropriate therapies and treatments.
However, very few studies have looked into developing therapies based on neurocognitive defects. One such study by Lobbestael et al. implemented a schema-focused therapy approach to incarcerated individuals with ASPD [10]. The importance of cognition, and the associated neurological insults should not be downplayed, however, and will be discussed in further detail.

Cognitive Inflexibility

Ventromedial Prefrontal Cortex (vmPFC)

Cognitive flexibility refers to an individual’s ability to understand, and subsequently respond to, various circumstances by rearranging previously acquired information to fit a given situation. Inflexibility in this domain has been linked to poorer decision-making and failure to learn from negative consequences. These impairments have been documented in the literature to account for antisocial behaviors present in persons diagnosed with ASPD. The aforementioned cognitive defects, in turn, stem from various neurological abnormalities. These neurological underpinnings of executive dysfunctions have been largely attributed to the prefrontal region.

More recent studies have focused particularly on the anterior cingulate (ACC) and ventromedial (vmPFC) portions of the prefrontal cortex (PFC) [1]. ACC anomalies and their related behavioral consequences will be mentioned with regards to aberrant schematic processing in ASPD persons, but majority of research on cognitive rigidity has been done on the vmPFC. Thus, this section focuses on psychopathy as it relates to vmPFC insults.

A recent neurological imaging study conducted by Grabenhorst et al. has shown that the vmPFC functions to give a value to goal-oriented outcomes. It evaluates potential rewards and dictates subsequent actions through a neurological attractor network known as area 10. This area is also located within the vmPFC [2]. Specifically, it is in area 10 that signals are converted into a decision between alternative options. O’Doherty et al. have replicated findings from the Grabenhorst study. They too have found that vmPFC’s main function is to weigh reward values from a list of choices, and select the most appropriate option. Additionally, the study concludes that decision-making is a multistep process whereby available choices are ranked based on given values [3]. This is particularly important information for ASPD research because individuals with the disorder most evidently have problems with cognitive tasks that require multiple steps for completion [4].

Impaired Decision-making

Problems with the decision-making process and learning from previous punishments (physical, social, psychological and the like) have been noted within the ASPD population in other models as well. This includes the inability to cooperate during a stimulation of the theoretical game, the Prisoner’s Dilemma. It has been noted that while stimulating the game theory paradigm, participants diagnosed with ASPD were significantly more likely to choose behavioral options that were more selfish, profiting only themselves with each transaction [5]. This could be due to aberrancies in vmPFC processing such that uncooperative behavior is more valued than its cooperative counterpart. As well, there may be faults within signaling pathways related to area 10.

Attentional Deficits

Along with poorer decision-making skills, attentional deficits have also been associated with antisocial behaviors. This includes, most notably, abnormal facial recognition caused by a lack of attentional resources in ASPD patients. Problems with attending to fearful facial expressions in particular have been studied extensively. Current research supports the idea that the neurological anomalies underlying attentional deficits stem from hypo-responsiveness of cortical regions activated when viewing facial stimuli.

A primary research article by Pfabigan et al. outlines the differences in attentional processing systems between participants diagnosed with ASPD as compared to healthy controls. Processing facial stimuli involves multiple steps, and the study looked to investigate the discrepancies in these stages, as measured by event-related potentials (ERPs) [6]. It was found that discrepancies with neurological processing between the two groups occur early on in the stimuli recognition process, notably as early as 88 to 120 milliseconds [6].

P1 was the primary EPR used in the study, as it is known to respond to visual processing of faces. Higher P1 amplitudes are established when viewing negative information (when compared to positive or neutral information). Accordingly, the ASPD group showed significantly smaller P1 amplitudes when tested via an electroencephalogram (EEG). Figure 1 depicts the P1 amplitudes measured in Pfabigan’s article, as measured in potential per millisecond. Differences observed within P1 amplitudes cannot be explained through differences in physically processing stimuli, as all participants were able to distinguish between negative and positive emotional facial features displayed. Problems with distributing attentional resources are assumed to be the cause.

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Figure 1: P1 Amplitudes per Millisecond Measured in Participants with High/Low vs. Negative/Positive ASPD Traits [6]

Although sensory processing is in tact in ASPD individuals, it is less available to respond to emotionally salient stimuli due to problems with attentional allocation. Persons exhibiting ASPD symptoms spend significantly less time attending to facial stimuli than control groups. A large body of literature has looked into the right fusiform gyrus and left lingual gyrus as the main extrastriate areas responsible for cortical under-activation causing attentional problems seen with ASPD.

For example, other studies have demonstrated that these extrastriate cortices are less active than control groups when processing faces. Interestingly enough, when viewing fearful faces, there was an increase in the fusiform gyri of healthy control participants. In comparison, ASPD patients had decreased gyri activation [7]. Activation levels were measured using functional magnetic resonance imaging (fMRI) techniques.

Altered Schematic Processing

Schemata are mental constructs formed from preconceived notions, which are used to consolidate and categorize new information. These constructs tend to influence attentional focus, as objects and behaviors fitting into a certain schema are given more attention. However, within the ASPD population, schematic processing is altered. They tend to be unstable, cognitively cruel, quickly triggered by anger and lack a sense of empathy [8], two key emotions deregulated in antisocial persons. Specifically, this review will assess the current literature with regards to maladaptive schemas, but a large body of ASPD research focuses on these cognitive defects in terms of moral development in ASPD.

When referring to aggression, it is important to note that the term has been separated into different categories, each characterizing differing motivations behind the hostility. These categories include reactive and instrumental aggression. Reactive aggression is used as a response to provocation whereas instrumental aggression is planned and goal-directed. Unsurprisingly, individuals diagnosed with ASPD display repeated episodes of instrumental anger.

There are various neurological defects associated with instrumental aggression, including aberrant medial amygdala function, as well as dysfunctions within areas of the hypothalamus, posterior cingulate, and inferior frontal [9]. In accordance with abnormal hypothalamic function, Veit et al. utilized a competitive reaction time paradigm to investigate the different types of aggression within incarcerated criminals diagnosed with ASPD. The paradigm involved two phases: an anticipating punishment phase and a retaliation phase.

Figure 2 below features scans from Veit’s study during the retaliation period. The posterior cingulate, inferior frontal and hypothalamus are all activated during this phase, but particular attention is given to the hypothalamus in Figure 3, as it is directly correlated to Buss-Perry (BP) aggression scores. They found instrumental aggression to be most positively correlated to activation of the hypothalamus, particularly during the retaliation phase [9]. Results from the fMRI data collected show that during the punishment-anticipation phase, there was no activation of the ACC, amygdala or prefrontal regions in ASPD patients.

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Figure 2: fMRI Brain Imaging Scans during the Retaliation Phase [9]

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Figure 3: Hypothalamic Activation as it Relates to Physical Aggression [9]

Other studies have linked anger in ASPD to be heavily physiological. Although participants with ASPD did not report feeling angry in given self-assessments or schema modes, physiological measures (decreased heart rate, lower systolic blood pressure and the like) were measured to be less responsive whilst cognition was overly responsive [10]. The study concluded that with antisocial persons, baselines for maladaptive schematic processing are higher when compared to healthy controls.

The problems exhibited with schematic processing within the ASPD population lead to various behavioral irregularities, with accompanying neurological aberrancies. However, along with a cluster of other personality disorders, it is theorized that early childhood abuse is a key etiological factor in the development of maladaptive schemas. Delving into etiological factors also gives leeway to the development of new therapies for ASPD, such as schema-focused therapy. This includes reorganizing the maladaptive schema and implementing new mindsets.

Bibliography
[1] Koenigs, M. The role of prefrontal cortex in psychopathy. Reviews in the Neurosciences. 23(3), 253-262. (2012). [2] Grabenhorst F., Rolls E. Value, pleasure and choice in the ventral prefrontal cortex. Trends in Cognitive Sciences. 15(2), 56-67. (2011). [3] O’Doherty, J. Contributions of the ventromedial prefrontal cortex to goal-directed action selection. Ann N Y Acad. Sci. 1239, 118-129. (2011). [4] Burgess, J. Neurocognitive Impairment in Dramatic Personalities - Histrionic, Narcissistic, Borderline and Antisocial Disorders. Psychiatry Research. 42(3), 283-290. (1992). [5] Mokros A., Menner B., Eisenbarth H., Alpers G., Lange K. Osterheider M. Diminished cooperativeness of psychopaths in a prisoner’s dilemma game yields higher rewards. Journal of Abnormal Psychology. 117(2), 406-413. (2008). [6] Pfabigan D, Alexopoulos J., Sailer U. Exploring the Effects of Antisocial Personality Traits on Brain Potentials during Face Processing. Public Library of Science. 7(11), 1-8. (2012). [7] Deeley Q., Eileen D., Surguladze S. Facial emotion processing in criminal psychopathy - Preliminary functional magnetic resonance imaging study. British Journal of Psychiatry. 189, 533-539. (2006). [8] Mercadillo R., Diaz L., Barrios F. Neurobiology of Moral Emotions. Salud Mental 30(3), 1-11 (2007). [9] Veit R., Lotze M., Sewing S., Missenhardt H., Gaber T., Birbaumer N. Aberrant social and cerebral responding in a competitive reaction time paradigm in criminal psychopaths. NeuroImage. 49, 3365-3372. (2010). [10] Lobbestael J., Arntz C., Chakhssi F. Effects of induced anger in patients with antisocial personality disorder. Psychological Medicine. 39, 557-568. (2009).

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