Neuropsychological conditions, severed linkage, and disrupted neural network are highly involved in the development of antisocial personality disorder. Research in neuroscience is starting to uncover the biological substrates justifying the cause of ASPD. There are several and complex models used to unravel the mystery behind the brain’s role in the development of antisocial personality condition. Each of them offered significant clues in linking the condition with the neurological impairment in the prefrontal cortex of the brain. In this study, the previous researches will be explored to justify claims that the biological substrate of ASPD condition is the impairment of ventromedial sector of the prefrontal cortex of the brain. Journals and clinical studies will be used to establish connection between neurological impairment and ASPD.
Antisocial personality disorder (ASPD) is commonly referred to as one of the most destructive psychiatric condition characterized by the patient’s lack of pervasive disregard to the rights of others or the law. ASPD is often associated to criminal attitudes wherein the patient shows history of violence and tend to develop chronic behaviors manipulates, exploits, and disrupts the norms of social conformity. The concept of ASPD continued to be the subject of neuropsychological study to determine the biological substrates that relates to the lack of impulse control. Narayan et al. (2007) asserted that the biological substrates of ASPD are relatively similar to neurophysiologic patterns determined among people with violent and aggressive behavior. In order to further understand the biological nature of ASPD the study will explore the pathological evidences from previous diagnosis of the condition. Recent neuropsychological studies of ASPD at the onset of Schizophrenia suggest cortical thinning in the pre-frontal cortex of the brain (Narayan et al. 1422). Therefore, it can be assumed that the biological substrate of ASPD lies on the neurobiological impairments in the pre-frontal cortex of the brain. However, proving this assumption will employ investigating the differences in the structure of the pre-frontal cortex of individuals diagnosed with ASPD.
Neural Basis of ASPD
The most prominent and replicated findings in the biological substrates of ASPD relates to the perceived abnormalities in the prefrontal cortex of the brain. However, the determination of the neurological structure that indicates the occurrence of ASPD poses significant challenge due to the weakness of imaging methodologies in visualizing the neurological pattern that ASPD creates. In the frontal lobe, functional abnormalities and structure can be observed by comparing the results of a functional fMRI study. Antisocial individuals tend to demonstrate aggressive and violent behavior triggered by uncontrolled impulses in the brain. New et al. (2002) suggests that the lack of impulse control resulting to violent and aggressive behavior was due to the reduced frontal functioning. This neurological change was found to be consistent among the most violent criminals and psychiatric patients. Studying patients with similar damage in the prefrontal cortex helps in conforming its implication in the development of antisocial behavior.
Strikingly, observed lesions in the orbitofrontal/ventromedial and prefrontal cortex among patients showed similar indications of impulsivity, lying, financial irresponsibility, failure to hold career, failure to achieve future goals and rule breaking. These attitudes are highly attributed to antisocial tendencies and the damage in the said region of the brain is crucial in keeping impulse control (Damasio). Based on this assumption, it can be suggested that the ventromedial prefrontal cortex is detrimental in generating aversive acts and emotional responsiveness. It was speculated earlier that neurobiological impairments in the pre-frontal cortex of the brain is the biological substrate in the development of ASPD. Based on the results of the previous studies by New et al. (2002) and Damasio (1998), it suggests that the damage in ventromedial region of the prefrontal cortex triggers the development of ASPD among individuals. Therefore, comparing the extent of damage in the aforementioned region of the brain determines the probabilities of ASPD development among individuals.
Other Biological Basis
The level of aggressiveness and antisocial behavior among ASPD patients has been correlated to the parasympathetic nervous system as the main biological trigger for aggression. In addition to deficiency, low resting heart rate also proposes a neutral substrate that is common among psychopathic and conduct-disordered individuals. The commonality of the condition among the aforementioned disorders suggests a correlative pattern that points to the cause of antisocial behavior from biological perspective. Ultimately, the central nervous system in general poses liability in the development of antisocial behavior apart from the conceived correlation of prefrontal cortex damages to ASPD. Other biological substrate found to be the causal factor in antisocial behavior tackles the neuroendocrine and genetic vulnerabilities according to Blair (2001). From genetics perspective, ASPD is a result of inherited impulsivity, which is a prerequisite to developing antisocial behavior. On the other hand, dopaminergic neurotransmission and serotonergic vulnerabilities are highly associated to the conduct abnormalities.
These predisposing vulnerabilities are attributed to functional abnormalities that occur in the orbitofrontal region of the brain. This region of the brain generates emotion and decision-making similar to the function performed by ventromedial sector, which is involved in behavioral operation (Bechara, Damasio and Damasio). The majority of previous neurological-based studies suggest the same brain area responsible in the development of ASPD. These studies provide significant contribution to the establishment of the assumption that damages in the prefrontal cortex is the biological substrate of ASPD. Damages occurred in the ventromedial sector profoundly disrupts social behavior. Although cognitive abilities are still preserved despite of the damages in ventromedial sector, the well-adopted individual is still likely to lose ability to observe proper social conventions and make moral decisions.
The role of the prefrontal cortex is to regulate the emotional and socially significant behavioral attributes including decision-making. Impairment in either sector of the prefrontal cortex profoundly affects the social cognitive capacity of individuals particularly with the presence of lesions in the said region of the brain as clinical research suggests. Therefore, the biological substrate of psychological behavior rests upon the level of normative condition in the prefrontal cortex. Since the prefrontal region is where the ventromedial sector is found, predisposing vulnerabilities are likely to occur including antisocial behavior (Bechara, Damasio and Damasio) in the event of damage by lesion. In addition to the correlation found between damages in the ventromedial sector and antisocial behavior development; the said sector of the brain also serves as the dispositional linkage between bio regulatory state and factual knowledge.
It is apparent that disruption in its structure provides the substrate justification to impairment of recognizing and responding appropriately to myriad of complex social situation (Anderson et al.). In the context of normal social interaction, a certain configuration is required in order for actions and actors to make immediate response to complex situations. The ventromedial sector responsible for appropriating the necessary components for valid response in a complex social situation plays a significant role in ensuring that the responses are within the norms of social convention. However, acquired damages due to biological, hereditary, and consequential reasons disrupt the normal neurological pattern for recognizing and responding to complex situations and moral reasoning. When a person is faced with factual aspects of a certain situation, pertinent dispositions are automatically activated in the higher associated cortices (Anderson et al.). This will lead to recollection of facts from previous experiences and at the same time activates the linkage in the ventromedial prefrontal sector where emotional disposition is located. However, if the ventromedial sector is damaged, the neurological patterns and linkages are compromised leading to inappropriate reasoning and response. In addition, results of the actions are considered as the product of previously learned factual emotional set (Blair) distorted because of damage in the ventromedial sector encompass by antisocial behavior.
Environmental stimulus, childhood experiences, and external influences are normally attributed in the development of antisocial behavior as psychology discourse normally based its observation. However, biological substrates provide a stronger and factual argument on the causes of antisocial behavior. The prefrontal cortex of the brain contains the neurological components are critical to emotional regulation in which apparent damages such as lesion in the particular region of the brain causes the condition. Aggressiveness and violent behavior demonstrated by most notorious of criminals and psychopaths are similar to those demonstrated by people suffering antisocial personality disorder. There is a greater connection between behavioral change and conditional changes in the prefrontal cortex of the brain particularly in the ventromedial sector.
It was assumed earlier that neurobiological impairments in the pre-frontal cortex of the brain are detrimental in the development of ASPD. Based on the study and evidence from previous research, it was clear that the early assumption was correct because impairments caused by damage in the ventromedial sector of the prefrontal cortex affects the emotional, moral reasoning and decision-making capacity of individuals asserting more violent and aggressive behavior particularly in complex social situations. These behaviors are highly attributed to ASPD, which justifies the conclusion that damages in the prefrontal cortex is a biological substrate to antisocial personality disorder.
Anderson, Steven W., Antoine Bechara, Hanna Damasio, Daniel Tranel, and Antonio R. Damasio. "Impairment of social and moral behavior related to early damage in human prefrontal cortex." Nature Neuroscience 2.11 (1999): 1032-1037. Print.
Behcara, Antoine, Hanna Damasio, and Antonio R. Damasio. "Emotion, Decision Making and the Orbitofrontal Cortex." Cereb. Cortex 10.3 (2000): 295-307. Web. <10.1093/cercor/10.3.295>.
Blair, R J. "ADVANCES IN NEUROPSYCHIATRY: Neurocognitive models of aggression, the antisocial personality disorders, and psychopathy." Journal of Neurology Neurosurgery and Psychiatry 71 (2001): 727–731. Print.
Damasio, Antonio R. "Emotion in the Perspective of an Integrated Nervous System." Brain Research Reviews 26 (1998): n. pag. Print.
Narayan, Veena M., Katherine L. Narr, Veena Kumari, Roger P. Woods, Paul M. Thompson, Arthur W. Toga, and Tonmoy Sharma. "Regional Cortical Thinning in Subjects With Violent Antisocial Personality Disorder or Schizophrenia." Am J Psychiatry 164 (2007): 1418–1427. Web. 11 Nov. 2013. <http://psychiatryonline.org/data/Journals/AJP/3830/07aj1418.PDF>.
New, A. S., Erin A. Hazlett, Monte S. Buchsbaum, Marianne Goodman, Diedre Reynolds, Vivian Mitropoulou, Larry Sprung, Robert B. Shaw, Harold Koenigsberg, Jimcy Platholi, Jeremy Silverman, and Larry J. Siever. "Blunted Prefrontal Cortical 18Fluorodeoxyglucose Positron Emission Tomography Response to Meta-Chlorophenylpiperazine in Impulsive Aggression." Archives of General Psychiatry 59 (2002): 621-629. Print.