Introduction

Antisocial Personality Disorder (ASPD) is a personality disorder that is characterized by a reckless disregard for one’s own and others safety; individuals with this disorder are known for violating legal and social norms with little to no consideration of outcomes (Glenn Johnson and Raine 2013). Within the general population, the prevalence of ASPD is about 3% (Glenn Johnson and Raine 2013). More concerningly, general prison population studies have demonstrated that 47% of incarcerated individuals have ASPD (Fazel and Danesh 2002). Unfortunately, there is still no official cause or treatment option for the disorder. The vast pathophysiology that ASPD individuals exhibit has deemed this personality disorder one of the more difficult ones to treat (Glenn Johnson and Raine 2013). Researchers have attempted to further elucidate the development of the disorder using neurological methods as well as by attempting to connect genetic and environmental aspects that could relate to its onset. Brain regions that have been most implicated in the disorder include the prefrontal cortex, superior temporal gyrus, amygdala-hippocampal complex, and the anterior cingulate cortex (Yang, Glenn and Raine 2008). In healthy individuals, the prefrontal cortex specifically is involved in executive functioning and also has implications in the emotional aspects of empathy (Yuan and Raz 2014; Balconi and Vanutelli 2017). A specific region of the prefrontal cortex, the ventromedial prefrontal cortex/orbitofrontal cortex (vmPFC/OFC), can be further studied in humans in order to attempt to understand the cause of certain symptomology present in ASPD, namely emotional dysregulation and impulsivity. By focusing on these specific symptoms and by studying the vmPFC/OFC from an impulsivity and empathic standpoint respectively, one can investigate whether the vmPFC/OFC is crucial to understanding the emotional dysregulation and impulsivity experienced in individuals with ASPD. 

Characterization of Antisocial Personality Disorder 

The main characteristics that underlie antisocial personality disorder are failure to comply with social norms, guiltless behavior and a general disregard for others (Black 2015). According to the American Psychiatric Association Diagnostic and Statistical Manual V (2013), ASPD is considered a Cluster B Disorder, along with Borderline, Histrionic and Narcissistic personality disorder. These disorders are characterized by certain cluster traits, such as emotional dysregulation, impulsivity or even antisocial attitudes. The APA DSM V (2013) has specific criteria for diagnosing antisocial personality disorder. An individual must primarily have an impairment in personality functioning in which self-functioning and interpersonal functioning are impaired. In order to be considered impaired in self functioning, one must have identity issues in which personal gain and power drive one’s self esteem; in this regard, the individual is only focused on themselves and is deemed ego-centric. Impairment in self-functioning can also be seen in terms of an individual’s self-direction, wherein an individual disregards social norms and ethical behaviors. In order to be considered impaired in interpersonal functioning, one must also have deficits in either empathy or intimacy. A person who has dysfunctions in empathy shows no concern for others and does not feel bad after hurting another person. Deceit and coercion in relationships are characteristics of impairments in intimacy that a person with ASPD may have. Significant impairment in personality functioning is not the only criteria needed to be diagnosed with ASPD. The DSM V (2013) also denotes the fact that the individual must have pathological personality traits that demonstrate antagonism and disinhibition. Impulsivity and risk taking are key features of the pathological personality trait of disinhibition. 

Researchers are able to use self-reports and DSM diagnostic criteria to consider the disorder from a variety of perspectives. When considering ASPD from a research perspective, the literature typically uses participants who have been diagnosed with ASPD using the DSM V or DSM IV criteria; it is important to note the criteria for diagnosis has not changed with the new edition of the DSM. An interesting feature about diagnosing ASPD is the fact that an individual must be at least 18 years of age to be diagnosed. If the person is younger than this and demonstrates the symptomatology of ASPD their diagnosis would be considered conduct disorder. ASPD-like characteristics can be studied in healthy individuals using Personality Diagnostic Questionnaire-4 (Fossati et al. 2004). This method allows for studies to not be solely based on those with the most extreme characterizations of the disorder. Using both self-report measures and DSM diagnostic criteria allows researchers to investigative the vast symptomatology at hand, namely emotional dysregulation and impulsivity. In addition to using diagnostic measures and self-reports, it is important to consider the underlying neuronal mechanisms that manifest in the disease. 

Neurological Aspects of Antisocial Personality Disorder

ASPD can be considered through a neurological perspective in order to gain insight into the symptoms that patients exhibit. One of the key brain areas that many researchers focus on when investigating ASPD is the prefrontal cortex (PFC). It has been shown that individuals with ASPD have reduced cortical thickness in regions like the superior frontal gyrus, orbitofrontal cortex, and middle frontal gyrus, along with the insular cortex, precuneus, and triangularis (Jiang 2016). Although neurological deficits and or decreases in cortical thickness may be present throughout the brain, it seems as though deficits in regions of the frontal gyrus are most prevalent. Raine et al. (2000) investigated prefrontal gray and white matter in ASPD individuals using magnetic resonance imaging (MRI) and compared them to healthy controls. Autonomic activity was also assessed by measuring skin conductance response and heart rate in both groups during a social stressor. When it came to the ASPD group, an 11% reduction in gray matter volume was found compared to controls. Interestingly, compared to controls undergoing a stressor, ASPD individuals even showed reduced autonomic activity when it came to heart rate and skin conductance response. These results demonstrated that ASPD could be characterized by impairments in autonomic functioning that stem from decreased gray matter. Jiang et al. (2017) further investigated neural deficits in ASPD patients by using a more specific route - diffusion tensor imaging (DTI) - to investigate white matter integrity. Fractional anisotropy, which is a measure within DTI, was shown to be decreased in major white matter fiber bundles in ASPD patients. These fibers are particularly important in frontoparietal and frontotemporal networks. The uncinate fasciculus values of fractional anisotropy were also reduced, and this fiber specifically connects limbic region systems to the orbitofrontal cortex. The results indicate that the PFC itself may not be the only part of the brain that is impaired in ASPD - there could also be deficits in underlying networks connecting to it. 

In order to assess neurological aspects of ASPD, researchers have also looked at activation levels in certain brain areas, as opposed to just volumes of brain regions. Along these lines, Goesthals et al. (2005) were interested in brain perfusion and impulsivity-related personality disorders like borderline personality disorder (BPD) and antisocial personality disorder. For the purposes of the study, researchers used brain perfusion single photon emission computed tomography (SPECT), which uses regional cerebral blood flow as an indicator of activation. Brains of ASPD, BPD, and healthy controls were compared, and decreased regional cerebral blood flow in the right prefrontal cortex and temporal cortex were found using SPECT imaging in both the BPD and ASPD patients. Based on what the literature has demonstrated, a common denominator has been implicated in many of the studies regarding neural deficits in ASPD: the prefrontal cortex. More specifically, a region that seems to be most implicated is the ventromedial cortex/orbitofrontal cortex, which is a region within the PFC. To further elucidate whether the vmPFC/OFC is relevant in this disorder, one must consider this brain region’s role in the emotional dysregulation present in ASPD along with another major characteristic of the disorder: impulsivity.  

Emotional Dysregulation in Antisocial Personality Disorder

One of the key features of Cluster B personality disorders is the cluster trait of emotional dysregulation (APA 2013). Emotional dysregulation itself can be defined by excessive or reduced emotional intensity, or even by an inability to perceive not only one’s own emotions, but also those of others (Dadomo el al. 2017). Zlotnick (1999) investigated affective dysregulation and childhood abuse among incarcerated women to see its relation to ASPD, BPD, and posttraumatic stress disorder (PTSD). When controlling for BPD and PTSD, it was evident that there was a significant relationship between affective dysregulation and ASPD with no significant association with history of childhood abuse. This study demonstrates that affective dysregulation is a key factor in ASPD. Antisocial personality disorder’s main feature, when it comes to emotional dysregulation, is insufficient emotion (Shiota and Kalat, 2018, p. 434-435). Studies have demonstrated that individuals with ASPD experience minimal prefrontal cortex and amygdala activity when witnessing others that are suffering (as cited in Thompson, Ramos & Willett 2014 in Shiota and Kalat, 2018, p. 434-435). Interestingly, Timmermann et al. (2017) investigated impairment of facial emotion recognition in individuals with ASPD compared to healthy controls and further questioned whether oxytocin levels had any effect on this impairment. The researchers were able to demonstrate that individuals with ASPD do in fact have a deficit in recognizing faces of fearful and happy individuals. Furthermore, increasing levels of oxytocin was able to improve recognition in ASPD individuals when it came to both happy and fearful faces. The researchers explain oxytocin’s effects by indicating that it may reduce aggression in ASPD individuals and may even increase social reward, ultimately allowing them to have a correct perception of another individual. 

The characteristic of insufficient emotional processing is evident in the fact that ASPD individuals are able to hurt others without feeling any remorse about it (Shiota and Kalat, 2018, p. 434-435). Accordingly, these individuals have no regard for their own safety or the safety of others around them (Shiota and Kalat, 2018, p. 434-435). A study conducted by Kumari et al. (2009) investigated neural and behavioral responses to threats in men with either schizophrenia (SZ) or ASPD who have had a history of serious violence. The participants of the study were presented with “safe” and “threat of electric shock” conditions and they were evaluated for shock anticipation and fear using a self-report. When it came to the ASPD group, these participants showed the lowest levels of shock anticipation and fear, compared to the SZ group, who had high levels and similar violence history. This study provides insight into the defective emotional regulation individuals with ASPD demonstrate, especially when it comes to the lack of emotion felt to anticipation of a negative event like a shock. 

As seen in the DSM V (2013) diagnostic criteria for ASPD, these individuals also have impairments in empathy. According to Shiota and Kalat (2018), there are two main components of empathy: empathic accuracy and emotional empathy. Having empathic accuracy means that one is able to understand the thought process of another person and even elucidate how they are feeling. Along similar lines, emotional empathy is the idea of being able to put oneself in someone else’s shoes and understand how they are feeling. Individuals with ASPD characteristics have been shown to lack emotional empathy;  they have no regard for how others are feeling (p. 269-270). Based on the literature, it is clear that there are several facets of emotional dysregulation within ASPD, but it is not the only symptom of the disorder. To further understand ASPD, one can consider the disorder through the standpoint of impulsivity. 

Impulsivity as a Key feature of ASPD

A key feature of ASPD is the fact that individuals with the disorder are shown to be impulsive (Glenn Johnson and Raine 2013). As explained in the DSM V (2013), ASPD individuals have pathological personality traits relating to the “domain” of disinhibition. Disinhibition is characterized by irresponsibility, impulsivity, and/or risk-taking behavior. The DSM V (2013) characterization of impulsivity entails the characteristics of responding to immediate stimuli and acting in the moment along with acting without a plan or consideration of outcomes. Before considering impulsivity in individuals with ASPD, or in healthy individuals, it is important to understand that impulsivity is not unidimensional. There are several ways impulsivity can be categorized. Two of the main types of impulsivity are choice impulsivity and response/motor impulsivity. According to Dalley, Everitt and Robbins (2011), choice impulsivity is characterized by the inability to refrain from choosing an immediate and small reward rather than a delayed and much larger reward. In other words, individuals with deficits in choice impulsivity lack the ability to inhibit actions toward immediate options. This type of impulsivity is usually studied through delayed discounting paradigms where individuals are offered a small amount of money today or some large amount of money one month later. Motor/response impulsivity, on the other hand, is mainly characterized by acting without thinking and the inability to have voluntary control over a response (Dalley, Everitt and Robbins 2011). A Go/No-go task can be used to assess this type of impulsivity as it allows researchers to examine a participant’s ability to withhold an initial response by having them respond to “go” stimuli and make no response to “no-go” stimuli (Mitchell and Potenza 2014). Another method used to assess response impulsivity is the Stop-Signal Task (SST), which assesses the stopping of an ongoing action in participants (Mitchell and Potenza 2014). A very common self-report used to assess facets of impulsivity is the Barratt Impulsiveness Scale (BIS-11), which contains factors of attentional impulsivity, motor impulsivity as well as non-planning impulsivity (Patton, Stanford and Barratt 1995). Other personality questionnaires, like the Eysenck personality inventory, also contain measures of impulsivity and are commonly used to study the trait (Mitchell and Potenza 2014). 

Fossati el al. (2003) used a variety of these self-report measures to examine the relationship of impulsivity and aggressiveness with ASPD traits using 747 undergraduate university students. For the purposes of the study, the research group used the Personality Diagnostic Questionnaire-4 to asses ASPD like traits and correlated this measure with Barratts Impulsivity Scale-11 and Buss-Durkees Hostility Inventory. Interestingly, the researchers found that ASPD symptoms correlated with physical and indirect aggression as well as motor impulsiveness. In this regard, it could be speculated that motor or response impulsivity is one type of impulsivity relevant in the symptomology within ASPD diagnosis. Further evidence by Chamberlain el al. (2016) implicated impaired inhibitory control and decision making as a factor of the pathophysiology of ASPD. These researchers used the Eysenck questionnaire and stop-signal paradigm to assess impulsivity in young adults with ASPD. As expected, ASPD was found to be correlated with higher impulsivity as well as impairments in response inhibition as assessed by the stop-signal task. It is evident that response/motor impulsivity is a relevant feature in ASPD. Impulsivity and impulse control can also be considered from a neurological perspective as well. Jiang et al. (2016) demonstrated that in ASPD individuals, the cortical thickness of regions in the PFC such as the superior frontal gyrus (SFG), middle frontal gyrus (MFG), and orbitofrontal cortex (OFC) are shown to be decreased compared to healthy adults. Even more interestingly, the research group correlated this cortical thickness with a measure of impulse control and demonstrated that the cortical thickness in the SFG, MFG, and OFC, along with several non-PFC regions, was positively correlated with impulse control. This is an indication that these regions may be necessary for inhibiting impulsive behaviors and it further implicates the OFC as a key brain region for understanding ASPD symptomatology. 

The vmPFC/OFC: Insights into Emotional Dysregulation and Impulsivity in ASPD

The ventromedial prefrontal cortex/orbitofrontal cortex is a brain region that can be used to understand the symptomatology of emotional dysregulation and impulsivity in ASPD. As mentioned, it is evident that the OFC is implicated in impulsivity in that decreases in the cortical thickness of this region have been shown to be correlated with an increase in total score on the Barret Impulsivity Scale in healthy individuals (Matsuo el al. 2008). Schilling et al. (2012) found similar results using high-resolution magnetic resonance scans in healthy adults. The researchers studied cortical thickness within the entire cortex in relation to impulsiveness. These adults were assessed for impulsivity using the Barratt Impulsiveness Scale-11. The middle frontal gyrus cortical thickness had a significantly negative relationship with attention and non-planning impulsivity along with total BIS scores. Accordingly, BIS total and motor impulsivity scores were significantly negatively correlated with the cortical thickness of the orbitofrontal cortex and the superior frontal gyrus. These findings regarding the OFC and impulsivity in healthy adults are important because, as mentioned earlier, individuals with ASPD have reduced cortical thickness in regions like the superior frontal gyrus, orbitofrontal cortex, and middle frontal gyrus, along with other regions (Jiang 2016). In this regard, it can be speculated that the decreased in cortical thickness within the vmPFC/OFC is related to the motor impulsivity demonstrated in ASPD individuals. Not only can the vmPFC/OFC be implicated in the impulsivity symptomatology of ASPD, it could also be speculated that defects in this region could explain the emotional dysregulation symptomology present in individuals with the disorder.

 When it comes to emotional dysregulation it is evident that ASPD individuals lack emotional empathy in that they have a hard time figuring out how others are feeling. Along the same lines, ASPD individuals have impairments recognizing faces of fearful and happy individuals (Timmerman et al. 2017). The literature on the vmPFC/OFC can be used to elucidate this symptomatology. Shamay-Tsorry el al. (2003) studied individuals with prefrontal cortex brain damage and attempted to characterize whether they have empathy deficits because previous research had shown that individuals with brain injury tend to have impaired empathic responses. In the study, the researchers examined empathic responses in patients with localized lesions in their PFC and compared them to control healthy patients. They demonstrated that the nine individuals who had the most deficit in empathy were those with right ventromedial prefrontal cortex lesions. Another group of researchers, Tranel, Bechara, and Denburg (2002), investigated the differences in the functional roles in the left and right ventromedial prefrontal cortices. Despite having a relatively low number of participants, the researchers were able to find major deficits in emotional processing, and even a lack of an anticipatory skin conductance response, during a gambling task in the four individuals who had unilateral lesion to their right ventromedial prefrontal cortex (vmPFC). On the other hand, normal emotional and personality processing along with normal anticipatory skin conductance responses, were present in those with left vmPFC responses. This study demonstrated that the right vmPFC may be necessary for eliciting an emotional response as well as an autonomic one. Along the same lines, a study conducted by Beadle, Paradiso and Tranel (2018) investigated 8 patients with damage to the vmPFC in their relation to empathic and neutral experimental conditions, using a within subject design. Empathy was assessed using empathy induction in which the patient in the experimental condition listened to other individuals talk about the struggles in their life. Individuals who offered more money in the rounds were deemed more empathetic; empathy was also measured using self-report. In line with previous literature, individuals with vmPFC damage were found to be less likely to help someone who was suffering. This study demonstrated the role of vmPFC in emotion, especially when it comes to empathy. Ultimately, multiple sources of independent literature have shown that there are underlying commonalities between emotional dysregulation and impulsivity when it comes to impairments in the vmPFC/OFC. 

Conclusion

Of the various features that are necessary for the diagnosis of ASPD, two symptoms that seem to have a common underlying cause are emotional dysregulation and impulsivity. Relating the current literature on emotional dysregulation and impulsivity has allowed for a better understanding of how this symptomology arises in ASPD. When independently considering impulsivity and emotional dysregulation as well as the common neurological findings present in ASPD patients, the brain region that seems to be always implicated is the ventromedial prefrontal cortex/orbitofrontal cortex. These implications can help elucidate whether some of the ASPD symptomology, namely emotional dysregulation and impulsivity, are a result of impairments in the vmPFC/OFC. Understanding the potential neurological cause of the symptomology in ASPD is one step toward developing treatments for the disorder. Although ASPD has a vast symptomology, gaining understanding that the vmPFC/OFC has some implication in the disorder’s symptoms can bring the medical field closer to understanding the reckless behavior of individuals who are diagnosed with the disorder. Ultimately, it will allow researchers and the government to understand the reason that 47% of incarcerated individuals suffer with ASPD (Fazel and Danesh 2002).

Limitations 

When considering a disorder as complex as ASPD, it is relevant to address potential limitations to the findings demonstrated in the literature. It is important to be cautious of the samples used in the experiments conducted as many of the research papers regarding ASPD are conducted on individuals who are in prison. This could skew the data toward only the most severe cases of the disorder. This is important to consider when researchers make generalizations about the symptomology at hand. The other caveat to studying ASPD is the lack of research articles on the topic. Not only are there not many papers assessing the disorder, those that do assess it typically have low generalizability as there are not many participants involved. Additionally, it is important to consider the fact that many personality disorders are co-morbid with one another. People with ASPD could have other disorders like depression or bipolar disorder that could influence their symptomology. When it comes to studying brain regions themselves, it is important to consider the fact that many of the brain regions work together. In this regard, it may be evident that the vmPFC/OFC is implicated in the symptomology of the disorder, but it could be that there are more underlying connections and signals implicated as well.

Future Studies

ASPD is characterized by impulsivity and emotional dysregulation, but more research needs to be conducted in order to attempt to find a more specific link between these symptoms and the vmPFC/OFC, along with other brain regions. Although there was a plethora of information regarding impulsivity and ASPD, it was difficult to find recent studies on emotional dysregulation or empathy in general. For this reason, more studies need to be done to address the types of emotional dysregulation present in these individuals. It would also be interesting to consider the other brain regions that could be involved in the disorder. For example, using diffusion tensor imaging, Jiang et al. (2017) had demonstrated  that a major white matter fiber known as the uncinate fasciculus was reduced in individuals with ASPD. This fiber specifically connects limbic region systems to the orbitofrontal cortex, so it may be worth investigating what limbic regions are sending signals to the vmPFC/OFC as these may be playing a role in the symptomology as well. Overall, it is clear that there is a neurological cause to the disorder, so further brain studies involving diffusion tensor imaging and functional MRI would be worth conducting in order to get a better understanding of the brain deficits as a whole. 

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