Brain Patterns in Antisocial Personality Disorder

Brain Patterns in Antisocial Personality Disorders
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Including a review of an article written by Schiffer et al.
for the Psychiatry Research: Neuroimaging journal in January of 2014.

Antisocial Personality Disorder (ASPD) is a personality disorder classified by the American Psychiatric Association, characterized by a lack of empathy for others in various forms, ranging from psychotic behavior to social isolation. Underlying all of these behaviors are functions of the brain that are abnormal or otherwise compromised; the Amygdala and Ventromedial Prefrontal Cortex are key areas of the brain that deal with social behaviors, emotional responses and psychosis, and thus their structures and functions are of great importance to the classification and possible treatment of ASPD. It has been noted that lesions or damage to these areas of the brain can result in ASPD-like symptoms in individuals. Using fMRI scans to create blood oxygen level dependent images, activity in specific parts of the brain has been recorded and differences between the typical and atypical brain are being studied. These images combined with testing results show clear differences in brain function between individuals that function normally in society and individuals with a history of impaired social interactions. Using the information from these types of studies, extrapolation of possible means of treating patients with ASP can be made, and is being studied extensively, though there is no clear cut cure for the mental disorder at the moment.

The Brain

The Amygdala

The amygdala is the area of the brain largely responsible for memory, decision-making and emotional reaction, and are located deep within the temporal lobe of the brain in humans. It can be subdivided into its compositional nuclei; the cortical nucleus, medial nucleus, central nucleus, intercalated cell clusters and the basolateral complex. The basolateral complex in particular has been noted to associate stimuli with aversive effects in fear conditioning responses; in the case of individuals with antisocial personality disorders, often one contributing factor is negative response to the actions of others that create a lasting fear or anxiety, the effects of which are observed as activity in this area [1].

The Ventromedial Prefrontal Cortex

The ventromedial prefrontal cortex (vmPFC) is located at the most inferior part of the frontal lobe in the cerebral hemispheres, and has roles in the processing of risk, fear, decision-making and the inhibition of emotional response. The areas of the brain matter that are associated with the vmPFC are not universally agreed upon, the consensus that it is connected to the amygdala, ventral tegmental area, temporal lobe, olfactory system and dorsomedial thalamus is accepted [2]. Through inputs from these areas of the brain, signals can be relayed to many others, including the amygdala, lateral hypothalamus and hippocampus [3].

Being connected to the ventral tegmental area implies that dopamine may be active in this area of the brain, further supported by the direct bi-directional connection with the amygdala. As such, social function, including empathy for others, motivation and anxiety, are all being actively researched with respect to this area of the brain. Studies done by Boes et al in 2011[4] showed that early-onset vmPFC activity can cause impaired moral judgment and severe tendencies towards antisocial personalities. Similarly, patients with bilateral lesions to this area develop inabilities to make decisions in general when placed in realistic scenarios, however when left with only hypotheticals, their intellectual ability appears to be normal, pointing towards a social activator for the ventromedial prefrontal cortex that links its function directly to social settings and removes it in other scenarios [5].

Neural Mechanisms of Cognitive Control

When studying antisocial personality disorder, the individuals in question must meet very specific standards in order to ensure they can be classified into this category before being studied. Work done by Schiffer et al. in January of 2014[6] explored the neural mechanism of cognitive control by comparing violent offenders with clear presentation of an antisocial personality disorder. Schiffer et al explored the differences between high-end and low-end psychopathy in individuals who expressed antisocial personalities, with the high-end psychopathy being exhibited in violent offenders and the opposite exhibited in non-offenders. One theory they explored was conflict theory, the concept that the more conflict in a situation, the more anxiety the individual will feel, and thus a reaction may be triggered in individuals with higher propensities toward psychopathy, as the ventromedial prefrontal cortex in this group would be unable to inhibit the emotional response. Schiffer et al decided to test this theory using the simple Stroop color test; a test of impulsive behavior in response to incongruity.

Schiffer et al selected 21 male violent offenders along with 23 non-offenders, and established the base difference between the two groups by recording their dependence on drugs, their antisocial characteristics and their impulsivity. Then, through 240 trials of the Stroop test, four analyses were made, being error interference, reaction time interference, post-conflict adjustments and post error adjustments. Throughout the tests, the individuals were subjected to an MR Scanner producing blood oxygen level dependent images so as to record the areas of activity in the brain during the test. As expected, interference played no major role and was similar between the two groups, however post-conflict adjustment appeared much more significant in the non-offender group, though further investigation into this data showed that the overall change in post-conflict adjustments over the course of the tests may have been similar. This piece of information is key; post-conflict adjustments shows emotional learning and reaction to the incongruity in front of them, and while the offender category showed less prevalence of this overall, they still did develop a haphazard adjustment system at the same rate as the non-offender group. This points towards the possibility of therapeutic work to at least partially relieve antisocial personality disorders, as it shows that progress is not impossible, despite where the individual may be starting.

Figure 1
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Figure 1 above shows the areas affected by (a) contrast incongruent - congruent and (b) error - congruent across all subjects.

The results of the fMRI scans were also as predicted. In figure one to the right, the regions of activity were highlighted as done by Schiffer et al. Activity during conflict, being activity during incongruent trials subtract activity during congruent trials, was recorded in the left superior temporal cortex and anterior cingulate cortex moreso in the non-offender group. Both of these regions of the brain are influenced by the ventromedial prefrontal cortex. Conversely, the left amygdala showed greater activity in the offender group than the non-offender group during conflict-related activity, and was the only region of the brain to show this pattern. These patterns are instrumental to understanding the conflict-related behavior of individuals with personality disorders.

The amygdala activity during these tests being localized to the left amygdala in the offender group is significant; Schiffer et al included in their report that all offender group members were male offenders with violent tendencies. The amygdala, being one of the most studied regions of the brain, has shown differences between the male and female brain; the male amygdala tends to be more active on the right side during stress, whereas the female brain is the opposite, being more active on the left side [7]. Furthermore, it is the right amygdala that appears to link the negative emotion with the response to the stimuli; in individuals such as Schiffer's incarcerated male offenders, right amygdala overactivity would be expected rather than left amygdala. Proposals brought up by Schiffer explain the discrepancy by growing support for more generalized roles of the anterior cingulate cortex mediating the differences in the amygdala during stress response with respect to antisocial personality disorders, and explain that the offenders with ASPD may show left amygdala responses due to more distracting stimuli reducing activity in the normal areas of the brain. Activity in the left anterior cingulate cortex was negatively associated with psychopathy, which then points towards cognitive control mediated by this area being the result of the antisocial behaviors rather than psychopathy, the former taking precedence in decision-making over the latter in at least this situation [8].

Possible Treatments

Medicative responses to personality disorders have widely been tried and tested throughout the last number of years, with varying degrees of success. Work done with attention deficits have established the social standard for medicative responses to personality disorders, including drugs like Ritalin and Adderall, but more recent studies show that the evidence in support of these medications is dwindling and that they may not be as effective as once thought [9]. In light of this, proposals by Schiffer et al in their study may be more effective with enough refinement. As it stands, the difference between the offender and non-offender brain activity during the Stroop test were very distinct, and any potential treatment would have a lot to correct in order to be successful. The most interesting point to look at is the finding that the offender brain and non-offender brain both showed similar post-conflict adjustment scores; as stated before, this means that the two groups both showed signs of adjusting to the stressful situation and showed potential to improve. For a treatment to be defined, further work into the extent of the antisocial personality adjustments needs to be done; any plateaus where the individual will not improve any further need to be found if they exist, and need to be researched for another possible treatment, and additionally, work needs to be done to determine if these adjustment effects will prove to be long term. As it stands, the paper done by Schifffer et al is a strong start towards discovering potential therapeutic or other treatments for personality disorders and lays a proper groundwork for future experimentation.

1. Amunts K, Kedo O, Kindler M, Pieperhoff P, Mohlberg H, Shah N, Habel U, Schneider F, Zilles K. Cytoarchitectonic mapping of the human amygdala, hippocampal region and entorhinal cortex: intersubject variability and probability maps. (2005).
2. Finger, E. C.; Marsh, A. A.; Mitchell, D. G.; Reid, M. E.; Sims, C.; Budhani, S.; Kosson, D. S.; Chen, G.; Towbin, K. E.; Leibenluft, E.; Pine, D. S.; Blair, J. R. Abnormal Ventromedial Prefrontal Cortex Function in Children with Psychopathic Traits During Reversal Learning. (2008).
3. Carlson, Neil R. Physiology of Behavior. 11th ed. Boston: Pearson, 2013. Print.
4. Aaron D Boes et al. Behavioral effects of congenital ventromedial prefrontal cortex malformation. (2011).
5. Bechara A, Tranel D, Damasio H. Characterization of the decision-making deficit of patients with ventromedial prefrontal cortex lesions. (2000).
6. Schiffer B, Pawliczek C, Muller B, Forsting M, Gizewski E, Leygraf N, Hodgins S. Neural mechanisms underlying cognitive control of men with lifelong antisocial behavior. (2014).
7. Lanteaume, L. et al. Emotion induction after direct intracerebral stimulations of human amygdala. (2007).
8. C.S. Carter, V. van Veen. Anterior cingulate cortex and conflict detection: an update of theory and data. (2007).
9. Sharpe K. Medication: the smart pill oversell. (2014).

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