This document summarizes research on the neurological basis and treatment of antisocial personality disorder (ASPD). Studies have found deficits in brain areas like the prefrontal cortex, limbic system, and hippocampus in individuals with ASPD. Lower levels of serotonin have also been linked to ASPD. Treatments for ASPD are limited due to the manipulative nature of those with the disorder and low treatment seeking. More research is needed to better understand the causes of ASPD and develop effective treatments.

1. Running head: ANTISOCIAL PERSONALITY DISORER 1
Antisocial Personality Disorder: Neurological Research and Treatment
My Nguyen
Liberty University

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Abstract
Antisocial personality disorder (ASPD) belonged to Axis II – personality disorder and
intellectual disability – of The Diagnostic and Statistical Manual of Mental Disorders (DMS-IV-
R). Individuals diagnosed with ASPD consistently display a disregard and violation of others
while lacking empathy and remorse. They behave aggressively and impulsively, regularly act
based on their desires and take risky or dangerous decisions. The present study discussed several
experiments and researches exploring the cause of ASPD biologically and neurologically.
Findings indicated deficits in brain areas of individuals with ASPD, as well as impaired
cognitive and behavioral functioning. Due to the nature of the disorder, few treatments exist and
most are inadequate in addressing the problem. More researches regarding ASPD can be
conducted in the future to further understand the disorder, and determine possible treatments.
Key words: antisocial personality disorder, physiological, treatments, literature review

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Antisocial Personality Disorder: Neurological Research and Treatment
Antisocial Personality Disorder (ASPD) is a diagnosis for individuals who exhibit
patterns of antisocial traits and behaviors. According to The Diagnostic and Statistical Manual of
Mental Disorders (5th ed.; DSM-5; American Psychiatric Association, 2013), these individuals
are impaired not only in self-personality, but also in interpersonal relationship. In the popular
culture, people are more familiar with terms such as psychopathy or sociopathy. Nonetheless,
ASPD is the closest disorder classified by the DSM-5 to these mental illnesses. A person must be
at least 18 years old to be diagnosed with ASPD; however, people typically display behavioral
problems when they are young. Prominently, in one research, nearly one fifth of the teenagers
who had conduct disorder (CD) developed ASPD (Washburn et al., 2007). In the United States’
population, the prevalence rate of ASPD was 4.3%; moreover, the number varied between race,
ethnicity and gender, in which the highest rates were among male and white people (Goldstein et
al., 2016). Additionally, ASPD had a high comorbidity with other disorders, including substance
abuse, bipolar, borderline, and schizotypal personality disorder. Some features of ASPD are
disregard or violation of rights of others, violence, lack of empathy and remorse, recklessness,
and impulsivity (American Psychiatric Association, 2013).
While it is fascinating for researchers to look at ASPD, the cause of the disorder is not
clearly determined. Several experiments examined the abnormality in the brain, including the
prefrontal cortex, the limbic system, and the hippocampus (Raine, Lencz, Bihrle, LaCasse, &
Colletti, 2000; Laakso et al., 2001; Raine, Lee, Yang, & Colletti, 2010). Even within Type II
personality disorder, ASPD is extremely difficult to treat, and most treatments are deemed
ineffective. Rarely do individuals with ASPD seek the help of a psychologist unless they are
forced into treatment. Furthermore, those with ASPD diagnosis are uncooperative and it is

4. ANTISOCIAL PERRSONALITY DISORDER 4
challenging to create a therapeutic alliance with their manipulative natures (Glenn, 2013).
Consequently, the paper presented several researches to investigate the possible causes of ASPD
neurologically, and inspected the existing treatments and their effectiveness.
The Psychological of Antisocial Personality Disorder
ASPD manifests in each individual in a different way; however, there are many common
traits. These people display impairment in personality, such as being egoistic, or setting goals
based solely on personal gain, pleasure, or power (American Psychiatric Association, 2013).
They are unable to conform to normal behaviors, and frequently break the rules or laws. More
importantly, some of the most distinct characteristics of ASPD individuals are their lacks of
empathy and intimacy. They neither feel concerned for nor understand the sufferings of others;
they also do not experience remorse after committing an immoral, unethical or illegal behavior.
Due to the deceitful nature, ASPD people cannot form intimate relationships. They are
mainly interested in exploiting others, through intimidation, force, or trickery, which is
consistent with their ego-centrism characters. A psychologist described a criminal with ASPD as
being extremely manipulative, and he himself was manipulated various times over by this patient
(Hare, 1993). Indeed, psychopaths are sometimes described charming, and they utilize this
feature effectively; they would use several means to influence others to achieve their desires
(American Psychiatric Association, 2013). Besides being manipulative, ASPD individuals
usually lie; they are dishonest, and can be tremendously hostile towards those who hinder them.
Other prevalent traits of patients diagnosed with ASPD are recklessness, impulsivity, and
irresponsibility (American Psychiatric Association, 2013). Resulting from their disregards of
others, they simply do not care about commitments or obligations, and fail to keep promises and
agreements. They are prone to boredom; hence, they would take huge risks and engage in

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dangerous situations or activities. For these combined reasons, the population that researchers
tend to look for psychopathic individuals are prisoners; approximately 30% of the investigated
sample of criminals meet the criteria for ASPD diagnostics (O’Conner, 2008).
While most people exhibit certain aspects of the above mentioned traits at least once in
their lifetime, psychopaths and sociopaths express these behaviors fairly consistently across
situations and time. To be diagnosed with ASPD, a person would not display the characteristics
only under the influence of substances, or medical conditions, and ASPD must not be deemed as
a normal stage of development (American Psychiatric Association, 2013). One of the exceptional
indicators of ASPD is animal abusing which in turn evolves into violence towards human and a
variety of antisocial behaviors (Arluke, Levin, Luke, & Ascione, 1999). While not all people
with ASPD are criminals or would commit criminal acts, their behaviors and cognitive process
are undeniably pathological.
Physiological Attribution
Psychological Mechanism
Theorists had attempted to explain the cause of ASPD through several models, including
psychodynamic, behavioral, and cognitive. The present paper, however, focused on addressing
the biological factors. Psychologists had looked at the dysfunction of several brain areas. One of
the earlier studies analyzed the prefrontal cortex. Raine, Lencz, Bihrle, LaCasse, and Colletti
(2000) conducted an experiment with 82 men, 21 of which were diagnosed with ASPD. The
researcher performed psychopathic personality, psychophysiological assessment, and magnetic
resonance imaging (MRI). The results indicated a reduction in prefrontal gray matter volume in
the individuals with ASPD, but their white matter is similar to other participants. While the
research was rudimentary, it yielded exciting results and was the guide post for future

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experimenters. With a similar idea in assessing the cortical region of the brain, another study
examined a sample of 58 right-handed males containing 14 people with ASPD diagnoses
(Narayan et al., 2007). After completing the image analysis, the experimenters revealed a
statistically significant correlation between participants with ASPD and thinning of several
regions of the brain, including the medial inferior frontal cortices, and the right hemisphere
sensory motor areas. On the other hand, Laakso et al. (2001) inspected the relationship between
psychopathy and the posterior hippocampus. Through examining 18 male violence offenders
diagnosed with ASPD, the experiment implied a link between low volume of the posterior
hippocampus and psychopathic behavior. In details, there existed a negative correlation between
the hippocampal volumes and the scores of the participants on the Psychopathy Checklist-
Revised. In the same light, other experiments also focused on the region that contains the
hippocampus – the limbic system. Raine, Lee, Yang, and Colletti (2010) looked at the presence
of the cavum septum pellucidum (CSP) – the premature form of the limbic system. The
preservation of CSP indicates a maldevelopment of an infant. The findings illustrated a
significantly high level of ASPD diagnoses in individuals with CSP. Finally, Dolan and Park’s
(2002) research suggested that ASPD was also associated with deficit in the ventromedial
prefrontal (VMPFC) and dorsolateral prefrontal (DLPFC) when examining 29 males diagnosed
with the disorder.
While some psychologists were looking for an explanation in brain areas, others
inspected the levels of neurotransmitters and other chemicals within the brain. A long held belief
of many researchers is that the serotonin level of an individual may be a contributor to ASPD.
Studies have shown that most participants diagnosed with ASPD have a significantly lower
serotonin turn-over rate – indicated by low cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid

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(5-HIAA), and an abnormal serotonergic level (Linnoila, Virkkunen, Scheinin, Nuutila, Rimon,
& Goodwin, 1983; Virkkunen, Goldman, Nielsen, & Linnoila, 1995; Moss, Yao, & Panzak,
1990; Moore, Scarpa, & Raine, 2002). The findings were fairly consistent and compatible
throughout literature. Thus, it is safe to infer that serotonin is one of the main components
attributing to ASPD.
Psychological vs. Physiological
ASPD manifests in a person through malfunctioned cognitive processes and behaviors.
Researches showed that ASPD was linked with a decrease in the volume of prefrontal cortex, or
the deficiency of the orbitofrontal cortex (Raine et al., 2000; Meyers et al., 1992). This region of
the brain has been linked to the executive function which means a deficit in one could result in
the others. It was mentioned that ASPD patients are impulsive, aggressive, and reckless. These
behaviors are controlled by the frontal cortex, which regulates cognitive control, planning, and
working memory. Therefore, when patients diagnosed with ASPD are unable to control
themselves and think rationally and carefully, it is likely that they would commit dangerous
and/or risky actions. Furthermore, people with ASPD would frequently disregard and/or violate
others’ rights; they are manipulative and only commit an action to benefit them. This
phenomenon could be the result of their inability to understand and regulate emotion, which in
turn leads to lack of empathy. The processing of emotion is linked to the DLPFC, and researches
have confirmed the correlation between these behaviors and a deficit in there (Dolan, & Parks,
2002; Blair, & Frith, 2000). Correspondingly, the impaired hippocampus and limbic system,
including the amygdala, contributed to a deficit in the capability to learn fear response,
regulation of aggression and negative emotion, social attach, and bonding (Laasko et al., 2001;
Raine et al., 2010; Schneider et al., 2000). Along with a cognitive deficit that results in a lack of

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social anxiety, ASPD individuals take part in risky actions, commit violent and criminal actions,
and lack remorse afterwards.
Imaging Studies
Structural Imaging. In assessing ASPD, MRI – a method to create pictures of detail
structures of the brain using magnetic field and radio wave energy – was a widely used method.
Raine et al. (2000) conducted a midsagittal and four parasagittal scans in order to construct the
image of the gray and white matter of the prefrontal cortex. The results indicated a reduction of
gray matter volume. On the other hand, Raine et al. (2010) performed the scan to identify the
existence of CSP in ASPD individuals compared to a control group with normal septum
pellucidum. In another experiment, the MRI was combined with a statistical map of the brain,
showing that ASPD was linked to the thinning of several areas throughout the prefrontal context,
including the medial inferior frontal area, the lateral sensory motor cortex, and the posterior
region of the intraparietal sulcus (Narayan et al., 2007). Remarkably, a case study employed the
MRI scan on a patient called J.Z., who had an acquired ASPD (Meyers, Berman, Scheibel, &
Hayman, 1992). After a brain surgery, the patient’s character differed vastly and leaned towards
antisocial behaviors. The scan revealed cerebral damage in the left orbitofrontal lobe, indicating
a relation between ASPD and this region of the brain.
Functional Imaging. Other types of scans centering in the physiological activities of the
brain were employed to investigate ASPD. A functional magnetic resonance imaging (fMRI)
study revealed a decrease in functional connectivity between the attention network and default
mode network (Tang, Jiang, Liao, Wang, & Luo, 2013). Moreover, a patient group with ASPD
had a different pattern of activation in the brain while doing a Go/NoGo task; in particular, the
stimulation was more extended and bilateral compared to the control group (Völlm et al., 2004).

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In addition, another study discovered a difference between ASPD individuals and control group
in the activation of the amygdala during the habituation stage of conditioning (Schneider et al.,
2000). Similarly, electroencephalogram (EEG) test reported an abnormality in slow wave of the
ASPD (Calzada-Reyes, Alvarez-Amador, Galán-García, & Valdés-Sosa, 2012). A negative
correlation between the activation of the left-hemisphere and diagnoses of ASPD was also
presented (Deckel, Hesselbrock, & Bauer, 1996). Finally, a single photon emission computerized
tomography (SPECT) scan detected a deviation in the pattern of relative blood flows of ASPD
individuals in the process of handling emotional words (Intrator et al., 1997). As had been noted,
patients/individuals diagnosed with ASPD exhibited both structural and functional abnormality
in the brain.
Animal Models
ASPD is composed of many personality traits; for this reason, it is nearly inaccessible in
animals. However, studies have tried to determine several noticeable symptoms in behavior and
regulation of the disorder in animal model, such as aggression, violence, and antisocial behavior.
Sluyter et al. (2003) compared the model of genes in mice with data of male humans. The two
models of mice inspected were short and long attack latency (SAL and LAL). Respectively, the
models were compared with Persisters – persistently displayed antisocial behavior – and
Abstainer – never manifest behavior – man. The mice were put into a cage to measure whether
the male mouse would attack a standard opponent. The findings indicated that the animal model
was accountable as antisocial behavior characteristics are consistent between SAL and Persisters,
as well as LAL and Abstainer. Even though aggression was the component with the most
concentration in the study, it can be assumed that genetic elements played a role in the
expression of ASPD. Correspondingly, when looking at primates, researchers discovered the link

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between serotonin and aggression. The results of a longitudinal study detected the decrease of
CSF 5-HIAA concentration in rhesus macaque females as they displayed spontaneous
aggression, similar to human (Higley et al., 1996). Indeed, in spite of the fact that ASPD cannot
be diagnosed directly in animal, researches focused on the aggressive aspect of behavior yielded
promising results for application on human.
Neurological Systems
As a consequence of the deficit and impairment in the brain of ASPD individuals, they
experience neurological dysfunction. Prominently, the affected systems are executive function,
emotional processing, and autonomic activities. The executive function is involved in the ability
to plan, inhibitory control, and working memories, etc. Studies suggested that people diagnosed
with ASPD had severe impairment in this system, exhibiting the inability to plan ahead, deficit in
working memory, and trouble in shifting attention (Dolan, & Park, 2002). They suffered from
tasks requiring these skills, such as the “Towel of London”, “Go/NoGo”, matching samples and
attention shifting tasks. Moreover, the reduced capacity of inhibitory control model indicated a
lower cognitive control and self-regulation (Tang et al., 2013; Blair, 2001; Dinn, & Harris,
2000). Additionally, ASPD is characterized with the failure to process emotion. Patients with the
disorder experience difficulty in emotion regulation and emotion processing; hence, they are
impaired in processing empathy and fearful stimuli (Tang et al., 2013; Blair, & Frith, 2000). At
the same time, low autonomic activities of these individuals during a social influence of stressor
result in the deficiency in learning fear behavior, as well as incapability to process feedback
information to determine the appropriate consequences following an action (Raine et al., 2000;
Dinn, & Harris, 2000).

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Treatments
Personality disorders, in general, are refractory, since they are compositions of
personality traits instead of symptoms. Even within these disorders, ASPD is undeniably one of
the hardest, with either therapy or medication. The problems are more psychological than
physiological, thus most medical treatments yield fruitless results and are deemed ineffective
(Glenn, Johnson, & Raine, 2013). Psychologists have attempted to investigate possible
treatments by studying the possible dysfunctional problem, focusing on behavior problems,
emotional regulation and processing, such as aggression, and impulsivity. However, most studies
looked at individuals with comorbid disorders, namely substance abuse, depression, and anxiety
(Dolan, & Coid, 1993). Several experiments aimed to elevate the symptoms of ASPD using
antidepressant drugs, such as SSRIs, or MAOIs, and especially sertraline (Dunlop et al., 2011).
These drugs mainly inhibit the reuptake of several neurotransmitters, including serotonin, which
is linked to ASPD. By increasing the level of serotonin in the brain, psychologists hoped to
reduce aggression and violence from the patients. Correspondingly, researches have expanded to
the use of atypical antipsychotic, notably quetiapine, to decrease irritability, impulsivity, and
aggressiveness (Walker, Thomas, & Allen, 2003). While the precise mechanism of quetiapine is
unclear, similar to most antipsychotic, this drug might contribute to the relief of symptoms by
blocking the receptors on the dopamine pathway. An effect on the activity of the limbic systems
is probably induced, as this region of the brain is linked to ASPD. Other medicines or drugs
receive little support as well as limited researches.
One of the latest hypotheses on treatments for ASPD focused on ACE inhibitors
(Hobgood, 2013). The author theorized that by blocking the sympathetic nervous system and
raising dopamine levels, ACE inhibitors would be able to treat ASPD effectively. Specifically,

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the hypothesis stated that blocking Renin angiotensin would be beneficial since Renin seems to
increase aggression traits. More researches need to be conducted in order to further analyzed
Hobgood’s hypothesis; however, the reasoning behind the mechanism suggested promising
findings.
Conclusions
Antisocial personality disorder is characterized by impulsivity, risk taking, violence, and
aggressiveness. Individuals diagnosed with this disorder experience impairment in self-
regulation and interpersonal relationship. They do not conform to the norm; rather, they ignore
others and only commit actions that would benefit themselves. Due to proneness to boredom,
ASPD people are likely to engage in risky and dangerous behaviors, and sometimes violently
attack others if they are obstructed. Psychopaths are also said to be charming and manipulative;
they are fraudulent and frequently lies.
Researchers have examined possible contributors to ASPD neurologically. Findings
suggested that ASPD is associated with deficits in several regions of the brain, such as the
prefrontal cortex, including the dorsolateral prefrontal cortex and the orbitofrontal cortex, the
limbic systems, and the hippocampus. Other experiments indicated an abnormal level of
serotonin turn-over in the brain. Ultimately, the deficits lead to malfunctioning neurological
systems, mainly the executive functioning, emotion processing and autonomic responses.
Biological and neurological treatments regarding ASPD are scarce and considered
ineffective. Some psychologists employ antidepressant or atypical antipsychotic medicine to
elevate symptoms of ASPD. Even though they can be effective to some extent, researches need
to be conducted in order to determine the treatment that would bring most benefits in the future.

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