Motivation and emotion/Textbook/Motivation and emotion/Textbook/Emotion/Antisocial personality disorder

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Antisocial Personality Disorder and Emotion[edit]

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Angry man

Antisocial personality disorder (ASPD) is a relatively rare disorder, which displays some very visible characteristics. It is estimated that as little as 3% of the male population is eligible for a diagnosis of ASPD, and 1% of females, but the effects of the violent and criminal behaviour displayed are felt by the wider community as this is where their crimes are often committed. But what causes people to behave in this way? Do people who behave this way have no feelings, no thought of the consequences of their actions or of the effects on other people? Hopefully those questions will be answered by the end of this chapter. Through the course of this chapter we will discuss the main characteristics of ASPD and also the causes, treatment and prevalence in the population. We will also look more closely at the role emotion, or a lack thereof, plays in ASPD. Additionally, we will look at some specific emotions related to ASPD, such as fear and anxiety.

Focus Questions

  • What are some of the characteristics of ASPD?
  • What role does emotion play in people with ASPD?
  • What are some of the main theories behind ASPD and emotion?

What is Antisocial Personality Disorder?[edit]

Antisocial personality disorder, as defined by the Diagnostic and Statistical Manual, Fourth Edition, Text Revision (APA, 2000)(DSM-IV-TR) is an ongoing disregard for the rights and feelings of others. This pattern of behaviour usually begins in childhood or adolescence and continues to develop in adulthood. For a diagnosis of antisocial personality disorder a person must be 18 years old and have displayed symptoms of conduct disorder before the age of 15.


DSM-IV-TR Criteria

A. There is a pervasive pattern of disregard for and violation of the rights of others occuring since age 15 years, as indicated by three or more of the following:

(1) failure to conform to social norms wiht respect to lawful behaviours as indicated by repeatedly performing acts that are grounds for arrest.<

(2) deceitfulness, as indicated by repeatedly lying, use of aliases, or conning others for personal profit or pleasure.

(3) impulsivity or failure to plan ahea

(4) irritability and aggressiveness, as indicated by repeated physical fights or ults

(5) reckless disregard for safety of self or others

(6) consistent irresponsibility, as indicated by repeated failure to sustain consistent work behaviour or honour financial obligations

(7) lack of remorse, as indicated by being indifferent to or rationalizing having hurt, mistreated or stolen from another

B. The individual is at least age 18 years.

C. There is evidence of Conduct Disorder with onset before age 15 years.

D. The occurrence of antisocial behaviour is not exclusively during the course of Schizophrenia or a Manic Episode. (DSM-IV-TR, 2000, p. 706)

The main characteristic of this disorder is the complete disregard for the wishes, rights or feelings of others. ASPD shares common characteristics with psychopathy, sociopathy and dyssocial personality disorder. Traits typical of ASPD are:

  • Repeated violation of the rights of others
  • Repeatedly performing criminal acts such as destroying property, harassing others, stealing or pursuing illegal occupations.
  • Deceitful or manipulative behaviour used for personal gain or pleasure
  • Lying
  • Impulsivity, and an inability to plan ahead
  • Easily irritated and aggressive, and as a consequence often get into physical fights or physically abuse others (e.g. spouses or children)
  • Recklessness and a disregard for personal safety. This can be displayed in driving behaviours, such as speeding or driving whilst intoxicated. They may also engage in unsafe sexual relationships or use substances at risky levels.
  • Irresponsible- this often leads to an inability to hold a steady job, and difficulty in handling finances.
  • Show no remorse for their behaviour. Often they will rationalise their actions by blaming the victims of their crimes (e.g. "They deserved it", "If I didn't take advantage of them someone else would have")
  • Lack of empathy and a tendency to be callous, cynical and contemptuous of the feelings, rights and suffering of others.
  • Inflated sense of self and arrogant demeanor
  • Superficial charm

For a diagnosis of antisocial personality disorder an individual must display more than three of the above symptoms over a prolonged period of time, and they must significantly impair on an individuals’ daily functioning. If you have a friend who has been in trouble with the law on one or two occasions, or know someone who impulsive, these characteristics alone do not necessarily warrant a diagnosis of ASPD.

Distinguishing between ASPD and Psychopathy
The term antisocial personality disorder and psychopathology are often used interchangeably, and although the two disorders do share common characteristics, they are not the same disorder. Psychopathology is characterised as a disorder of personality, particularly the affective deficits. ASPD focuses more so on the behavioural aspects of the disorder, such as criminality (Ogloff, 2006). Many people with psychopathy also meet the diagnostic criteria for ASPD, but not all people with ASPD meet the criteria for psychopathy (Hare & Neumann, 2009).


As with many psychological disorders, there are many factors thought to contribute to the development of ASPD. One of the strongest predictors is genetics. ASPD is more common among first degree biological relatives with the disorder than in the general population (APA, 2000). The psychodynamic model proposes that ASPD is caused by a lack of parental love, which leads to a lack of trust in others (Sperry,2003). The behavioural model suggests that antisocial behaviours are learned through imitating the behaviours or those around them (Gaynor & Baird, 2007). These theories will be discussed in more detail later in relation to emotion.


Treatment for people with ASPD tends to be very difficult and often ineffective as the patient usually does not have a desire to change, and their lack of empathy leads them to believe that they have done nothing wrong. Patients with ASPD are often difficult to treat, and due to the characteristics of the disorder such a deceit, lying and lack of regard for others they are not desirable patients. Another barrier to treatment is that it is often forced upon them by a judge, so their commitment to the treatment is often half hearted (Duggan, 2009).

Early intervention with children diagnosed with conduct disorder is thought to be one form of effective treatment. Pharmacological treatments (see pharmacology) have been tried with limited effectiveness. Cognitive therapy, which tries to get patients to think about moral issues and attempt to empathise with the needs of others has also shown limited results. Current research suggests that there is no single method of treating ASPD that gives conclusive results (Comer, 2010). The symptoms do appear to become less severe with age, and by middle age many people with ASPD are less likely to be involved in criminal activity, but they continue to have problems with interpersonal relationships, parenting and holding down a job (Paris, 2004).


The prevalence of ASPD in the general population is about 3% in males and 1% in females. These rates increase drastically in prison settings or substance abuse treatment settings (APA, 2000). Although results vary due to different methods of measurement, the prevalence of ASPD amongst prison inmates has been reported to be as little as 11% and as high as 78% (Rotter et al., 2002). However, Ogloff (2006) believes that the prevalence of ASPD, particularly in the prison population is greatly over estimated, and over diagnosed. Ogloff states that many adults in prison meet the criteria for ASPD based on the diagnostic focus on criminality, but the diagnosis may not be warranted in many cases and has led to overinflated figures from prisons.



In the introduction, emotion is defined as the complex psychophysiological experience of an individual’s state of mind as interacting with biochemical and environmental influences (Myers, 2004). Emotion involves mood, temperament, personality and motivation. Emotion plays a large part in our everyday lives, and contributes to our development. There are three main components of emotion:

  1. Behaviour- The result of an emotion, such as crying or a facial expression of fear.
  2. Physiology- The parts of the brain that are involved in producing emotion.
  3. Cognition- Processing external stimuli in relation to emotion. (Durand & Barlow, 2006).

For more information on emotion, see emotion. We will now look at the role emotion plays in people with antisocial personality disorder.

Psychodynamic Theory[edit]

Sigmund Freud

The psychodynamic theory of ASPD proposes that the disorder develops due to a lack of parental love and closeness during infancy, which leads to an individual becoming emotionally distant and mistrusting others later in life. Research supporting this theory has found that people with this disorder are more likely to have had significant childhood stress, in the form of family poverty, violence and parental conflict or divorce, indicating that there is an etiological connection between trauma and the development of ASPD (Martens, 2005). Whilst these childhood traumas do create vulnerability for the child to develop later psychological problems, the traumas alone do not cause disorders. Psychodynamic theory is not a leading theory in regard to ASPD, and as such there is little research surrounding it. However, it has been included in this section on ASPD and emotion as the theory relates specifically to emotions, or a lack thereof, experienced in childhood.

Behavioural Theory[edit]

Behavioural theorists suggest that antisocial behaviours can be learned through modelling, or imitation. Modelling is when a person imitates the actions or behaviours of those around them. As you have read previously, there is a high genetic relationship with the development of ASPD. Thus it is reasonable to conclude that as well as the genetic predisposition for the disorder, there are also environmental influences. A child who grows up with a parent with ASPD could grow up imitating the actions of that parent, including the antisocial aspects such as aggressiveness, deceitful and criminal behaviours (Paris, 2004).

Other behavioural theorists have suggested that antisocial behaviours displayed in childhood are rewarded and reinforced, often unintentionally by parents. When a child misbehaves or shows aggressive behaviours as a reaction to parents’ requests, the parents may simply give in to restore the peace. Over time the child will learn that by displaying this behaviour they get what they want and will repeatedly react in the same manner. Parent Management Training has been identified as a preventative strategy for children displaying antisocial behaviours, and improved parenting practices following the training have been linked with a reduction in undesirable behaviours in children (Kazdan & Whitley, 2006).

Genetic Influences[edit]

P genetics

Family and adoption studies suggest that genetics may be one of the main predictors in the development of ASPD. One of the first adoption studies conducted by Crowe (1974) involving ASPD investigated the rates of ASPD prevalence in adopted children who had biological mothers with a criminal history. The rate of adoptees displaying signs of ASPD was 13%, compared with just 2% for the control group of matched adoptees. The children of the criminal mothers were removed as newborn, reducing the risk of environmental influences and indicating a high genetic correlation. Although the results were significant, the sample group was quite small (N = 46). Another interesting finding from Crowe’s research was that the adoptees with criminal mothers who went on to commit acts of crime themselves spent a longer period of time in an orphanage than the control group, or the group who did not become criminals later in life, indicating that as well as a genetic predisposition, environmental influences also play a large role (Roth & Finley, 1998).

Subsequent research has supported the gene-environment interaction. An adoption study compared the likelihood of children with a parent with ASPD and the child developing conduct disorder, which is a precursor for ASPD in adulthood. The results found that if the children with the biological predisposition were exposed to chronic stress by their adopted family, in the form of marital, legal or psychiatric problems, the children were at a greater risk of developing conduct disorder. A genetic influence does not necessarily mean that a person will develop ASPD, but evidence shows that the genetic influence matched with environmental influences increases the risk (Cadoret, Yates, Troughton, Woodworth & Stewart, 1995).

Biological Theories[edit]

Underarousal Hypothesis[edit]

Yerkes-Dodson Curve

The underarousal hypothesis states that people with low levels of cortical arousal often display many of the symptoms of ASPD, such as antisocial and risk taking behaviours. According to the Yerkes-Dodson curve, people at either end of the curve, with very high or very low levels of arousal experience negative affect and have difficulty performing, whereas people within the normal range of the curve experience no negative affect and have no trouble performing tasks. Due to low levels of arousal, people with ASPD appear to become bored very easily engage in risk-seeking behaviour such as taking illicit drugs or getting into fights in an effort to increase their level of stimulation and reduce the feelings of boredom (Durand & Barlow, 2006). This hypothesis could also explain why people with ASPD have trouble with holding down a job or long term planning. Research into the effects of low cortical arousal has shown that people operate best with medium levels of cortical arousal, yet people showing low levels of arousal do not perform as well and will actively try and produce a situation where they are more stimulated. For example, if a person with low arousal levels becomes bored whilst driving they will engage in unsafe behaviours such as speeding and reckless driving to provide stimulation (Fischer, Langner, Birbaumer & Brocke, 2008). The underarousal hypothesis was developed with psychopaths and has been inferred to work with people with ASPD. As many of the characteristics displayed are the same, it can be assumed that those characteristics have the same cause.

Fearlessness Hypothesis[edit]

The fearlessness hypothesis proposes that people with ASPD have a higher threshold for fear than most individuals. This lack of fear can be seen in some of the characteristics of ASPD, such as criminality, involvement in violence and other risk taking behaviours. The fearlessness also results in an inability to respond to and learn from the negative consequences of their behaviours. As discussed earlier in regard to treatment of ASPD, many patients who present for treatment do not recognise that they have done anything wrong and show no remorse for their actions. Societal punishments, such as imprisonment or community service, for crimes committed by people with ASPD often have no effect (van Honk & Schutter, 2006). In relation to the fearlessness hypothesis, pioneering research by Lykken (1957) showed that people with ASPD traits displayed significantly lower levels of anxiety than the control group.

The Response Modulation (RM) hypothesis was derived from the fearlessness hypothesis, but investigated other aspects, as well as fear. Newman, Schmitt and Voss (1997) conducted research which supported their claim that people displaying antisocial characteristics would have difficulty processing motivationally neutral stimuli, as well as the fear related stimuli. The research findings supported the RM hypothesis, indicating that people with ASPD not only do not recognise the emotion of fear, but any peripheral stimuli which they do not feel is relevant to them.

These two hypotheses validate the claim that people with ASPD not only are unable to experience fear and display a lack of empathy, but they may in fact be unable to experience a wider range of emotions, including anxiety.

Behavioural Inhibition System[edit]

According to Gray’s model of brain functioning, the behavioural inhibition system (BIS) is responsible for an individuals’ ability to stop and recognise when they are faced with possible punishment, non-reward or situations which may lead to frustration and anxiety. The behavioural activation system (BAS) is responsible for a person’s sensitivity to reward and regulates approach behaviour. It is generally believed that people with ASPD have an imbalance between the BIS and the BAS, which leads to the fear and anxiety generally felt by most people in dangerous situations being less prominent. People with weaker BIS not only show a lack of anxiety, but also an inability to inhibit behaviours in the face of punishment. This will also result in strong reward seeking behaviour, also known as impulsivity. An additional result of a weak BIS is the inability to learn from past experiences, or past punishments (Fowles, 1980).

Antisocial Personality Disorder and Stress[edit]

Soldiers preparing for combat

Being in involved in combat is a stressful experience, and it is believed that it may lead to the development of antisocial behaviours in some people. Research from Vietnam War veterans found that there was a significant relationship between combat exposure and adult antisocial behaviours. Participants (N = 118) showed signs of antisocial behaviour indicating that there may be a relationship between combat exposure level and adult antisocial behaviours and the development or maintenance of antisocial behaviours (Resnick, Foy, Donahoe & Miller, 1989). However, the relationship between witnessing violence and the development of antisocial behaviours is still unclear.

The relationship between stress and ASPD was also discussed briefly in relation to causes, where it is thought that significant environmental/social stressors experienced during childhood could play a part in the development of the disorder, if a genetic predisposition exists.

Deficits in Emotional Processing[edit]

Research has shown that participants with ASPD demonstrated poorer performance on emotion-discrimination tasks, compared to a control group not displaying any signs of ASPD. People with ASPD have less intense emotional reactions to everyday events, and also have trouble distinguishing between positive and negative emotions. Higher levels of emotional detachment were also found, providing an insight as to why people with ASPD can so easily lie and manipulate others (Habel, Kuhn, Salloum, Devos & Schneider 2002).


ASPD is a complex disorder, and it can be difficult for people to understand how those with ASPD can act in such manipulative and deceitful ways and not feel any remorse for their actions. It is one of the few disorders that does not appear to respond to any type of treatment, either in the form of therapy or drug treatment. There are a number of theories regarding the cause of the disorder, but the most generally accepted and tested theory is that of genetic inheritance. Throughout this chapter we looked briefly at various models explaining the lack of emotion in people with ASPD. The underarousal hypothesis and the fearlessness hypothesis are two of the best know models and explain the reasons behind the thrill seeking, impulsive and aggressive behaviours displayed. Finally, the chapter looked at the role of stress in ASPD, and how the characteristic deficits in emotion may be explained. Although there has been a lot of research into ASPD, there are still a lot of gaps particularly in the areas of prevention and treatment. This chapter closes by leaving you with a few questions to consider:

  1. If a person is diagnosed with ASPD, is it possible for them to lead a "normal" life?
  2. Do you think ASPD has varying degrees of severity?
  3. What do you think is the main area that needs more research in regard to ASPD?

See also


American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders: Text Revision (4th Edition). Washington DC.

Cadoret, R. J., Yates, W. R., Troughton, E., Woodworth, G., & Stewart, M. A. (1995). Genetic-environment interaction in the genesis of aggressivity and conduct disorders. Archives of General Psychiatry, 52, 916-924.

Comer, R. J. (2010). Abnormal Psychology (7th Edition). New York: Worth Publishers.

Crowe, R. (1974). An adoption study of antisocial personality. Archives of General Psychiatry, 31, 785-791.

Duggan, C. (2009). A treatment guideline for people with antisocial personality disorder: Overcoming attitudinal barriers and evidential limitations. Criminal Behaviour and Mental Health, 19, 219-223.

Durand, V. M. & Barlow, D. H. (2006). Essentials of Abnormal Psychology (4th Edition). Belmont, CA: Thomson Wadsworth.

Fischer, T., Langner, R., Birbaumer, R., & Brocke, B. (2008). Arousal and attention: Self-chosen stimulation optimizes cortical excitability and minimises compensatory effect. Journal of Cognitive Neuroscience, 20(8), 1443-1453.

Fowles, Don C. (1980). The three arousal model: Implications of Gray’s two-factor learning theory for heart rate, electrodermal activity and psychopathy. Psychophysiology, 17(2), 87-104.

Gaynor, S.T. & Baird, S.C. (2007). Personality disorders. In D.W. Woods & J.W. Kanter (Eds.), Understanding behavior disorders: A contemporary behavioural perspective. Reno, NV: Context Press.

Habel, U., Kuhn, E., Salloum, J.B., Devos, H., & Schneider, F. (2002). Emotional processing in psychopathic personality. Aggressive Behavior, 28(5), 394-400.

Hare, Robert D. & Neumann, Craig S. (2009). Psychopathy: Assessment and forensic implications. The Canadian Psychiatric Association Journal, 54(12), 791-802.

Kazdan, Alan E. & Whitley, Moira K. (2006). Pretreatment social relations, therapeutic alliance, and improvements in parenting practices in parent management training. Journal of Consulting and Clinical Psychology, 74(2), 346-355.

Lykken, David T. (1957). A study of anxiety in the sociopathic personality. The Journal of Abnormal and Social Psychology, 55(1), 6-10.

Martens, Willem H. J. (2005). Multidimensional model of trauma and correlated antisocial personality disorder. Journal of Loss & Trauma, 10(2), 115-129.

Myers, David G. (2004). Theories of Emotion. Psychology, Seventh Edition, New York, NY: Worth Publishers, p.500.

Newman, J. P., Schmitt, W. A. & Voss, W. D. (1997). The impact of motivationally neutral cues on psychopathic individuals: Assessing the generality of the response modulation hypothesis. Journal of Abnormal Psychology, 106(4), 563-575.

Ogloff, J.R.P. (2006). Psychopathy/ antisocial personality disorder conumdrum. Australian & New Zealand Journal of Psychiatry, 40, 519-528.

Paris, J. (2004). Personality disorders over time: Implications for psychotherapy. American Journal of Psychotherapy, 58(4), 420-429.

Resnick, H. S., Foy, D. W., Donahoe, C. P., & Miller, E. N. (1989). Antisocial behaviour and post-traumatic stress disorder in Vietnam veterans. Journal of Clinical Psychology, 45(6), 860-866.

Roth, Wendy E. & Finley, Gordon E. (1998). Adoption and antisocial personality: Genetic and environmental factors associated with antisocial outcomes. Child and Adolescent Social Work Journal, 15(2), 133-151.

Rotter, M., Way, B., Steinbacher, M., Sawyer, D. & Smith, H. (2002). Personality disorders in prisons: Aren’t they all antisocial? Psychiatric Quarterly, 73(4), 337-349.

Sperry, L. (2003). Handbook of diagnosis and treatment of DSM-IV-TR personality disorders (2nd Ed.). New York: Brunner-Routledge.

Van Honk, J. & Schutter, D.J.L.G. (2006). Unmasking feigned sanity: A neurobiological model of emotion processing in primary psychopathy. Cognitive Neuropsychiatry,11(3), 285-306.

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