Motivation and emotion/Book/2010/Antisocial personality disorder
Conscience is the window of our spirit, evil is the curtain.
Imagine - if you can - not having a conscience, none at all. No feelings of remorse, guilt and no limiting concern for strangers, friends or family. You are not held back by any of your desires by any moral compass. You have no internal restraints, and you are unhampered by any pangs of expectation. Do you crave money, power, control? What job would you do? The CEO of a company where you are able to work on your employees vulnerabilities through manipulation? Maybe you are a parent, a teacher (Stout, 2005)? Maybe you are involved in crime, or a law enforcement officer yourself? Such experience is often called Antisocial Personality Disorder or ASPD by mental health professionals, psychologists and professionals in the medical field.
Most psychological disorders reflect disturbances in a number of areas, including emotional processing and emotional responding (Kring & Banchowski, 1999). The nature of emotional impairment varies between disorders. In ASPD, there is a deficit in the experience of the perception and expression of emotion. These disturbances reflect a disruption in one or more components of emotional processing, and are also linked to aetiological factors at both neurobiological and psychological levels like (Kring & Banchowski, 1999). These emotional disturbances are salient to the disorder itself, with emotions influencing, interacting and contributing to the experience of the disorder itself.
This chapter discusses motivational aspects of ASPD. In particular, there are significant motivationally adaptive systems that are impaired or dysfunctional in ASPD, particularly core emotional processes which are deficient and that there is 'dulled' physiological functioning underlying the manifestation of the disorder. The clinical description and Diagnostic and Statistical Manual (DSM) classification of ASPD will be discussed including neurobiological theories, and the functioning of the main brain areas. We will also look into the main motivational theories of ASPD and discuss the emotional deficits in some detail. Physiological functioning and anxiety will be touched on as well as the difference between psychopathy and ASPD.
So, as you read the following chapter ask yourself these questions;
- How does motivation relate to psychological disorders, specifically ASPD?
- What psychological processes underlie the manifestation of the disorder?
- What motivates an individual with ASPD to behave in a maladaptive way?
The Latin root of motivation means ‘to move’, so in a sense the basic definition of motivation is action. There are two pivotal questions as to what motivation is. The first is what causes behaviour, and the second is why does behaviour vary in its intensity (Reeve, 2009)? It is an essential question to daily life, as many ask themselves or others why we do what we do. Essentially, the study of motivation concerns those processes that give behaviour its energy and direction (Elliot, 2006).
As individuals, we are guided by our internal motives which encompass our needs, cognitions and emotions. We motivate ourselves to eat when we feel hungry (need), when we are sad (emotion/psychological need) we may talk to a friend, and we may discuss and make decisions about what is making us sad (cognitions) (Elliot, 2006). Within these categories, we also experience physiological levels of arousal, feelings, behave or function in creative ways, and express or communicate this to others in our environment. For more information, see What is motivation?
Motivation and ASPD
So why do people with ASPD behave the way they do?
Motivation includes both approach and avoidance tendencies. We as individuals either can be approach-oriented or avoidance-oriented (Elliot, 2006). When we are approach-oriented (e.g., interest, joy, desire, reward) we welcome an opportunity to behave in a certain way which motivates us to achieve this. When we are avoidance oriented (e.g., fear, frustration, violence) we attempt to avoid aversive, anxiety provoking stimuli (we want to escape from and disengage); and we adjust our behaviour (Elliot). As such, we as individuals seek sensation seeking stimulation through these behaviours that motivate us towards goals and too adapt socially, psychologically, physically and emotionally. Individuals with ASPD though, have been shown to display behaviours that are not congruent with typical approach or avoidance tendencies in certain social, environmental, and interpersonal situations. These individuals may not express anger when anger is appropriate, and not feel the same level of fear or experience the ‘flight or fight’ response as much as others in times of danger.
Anti social personality disorder is a psychological disorder characterised by maladaptive personality traits. Personality traits are enduring patterns of perceiving, relating to and thinking about the environment and oneself that are exhibited in a wide range of social and personal contexts (APA, 2000). A personality disorder is said to exist when these traits become inflexible and maladaptive and cause either significant functional impairment or subjective distress. The DSM-IV-TR classifies personality disorders in three clusters. Cluster B is where antisocial personality disorder sits (Durand & Barlow, 2006).
DSM Classification of ASPD
- Diagnostic Criteria for Antisocial Personality Disorder
A. There is a pervasive pattern of disregard for and violation of the rights of others occurring since the age of 15 years, as indicated by three (or more) of the following:
- Failure to conform to social norms with respect to lawful behaviours as indicated by repeatedly performing acts that are grounds for arrest
- Deceitfulness, as indicated by repeated lying, use of aliases, or conning others for personal profit or pleasure
- Impulsivity or failure to plan ahead
- Irritability and aggressiveness, as indicated by repeated physical fights or assaults
- Reckless disregard for the safety of self or others
- Consistent irresponsibility, as indicated by repeated failure to sustain consistent work behaviour or honour financial obligations
- Lack of remorse, as indicated by being indifferent to or rationalising having hurt, mistreated or stolen from another
B. The individual is at least 18 years of age
C. There is evidence of conduct disorder with onset before age of 15 years
D. The occurrence of antisocial behaviour is not exclusively during the course of a Schizophrenia or Manic Episode.
American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental disorders: (4th Edition). Washington DC, pp. 706.
Steve is a 32 year old man who has ASPD. He has always had difficulties maintaining his accommodation, and as such, is often transient with no stability. Steve has had many relationships, yet often these relationships end after three months due to his repeated physical abuse towards his partner and penchant for buying prostitutes. Steve has had numerous employment prospects as he is quite intelligent, yet he often looses his job after a short period of time due to lack or appropriate interpersonal skills. Steve has a criminal history of petty crimes involving minor fraud, and driving under the influence. Steve has never committed a violent offence, yet he does state that it is possible in the future "if he needs to".
Steve is a chronic alcoholic and an avid gambler. He will often spend the majority of his money on this. Steve does not believe this is a problem, as he states that he always feels 'numb' anyway, so what’s the point? Steve has a violent family history, suffering physical abuse at the hands of his stepfather and having an alcoholic mother. Steve when questioned on this does not believe this is the reason he is abusive himself, or that this is why he drinks chronically.
Steve admits he sometimes thinks that there is something a bit 'odd' about himself, yet he believes this is not a problem, and he 'kinds of enjoys not 'caring'. Steve's mental health worker believes Steve lacks the insight to change his behaviours and has difficulty maintaining or adhering to behaviour modification strategies. Steve has moved in and out of the mental health system for years, many workers state that he is a pleasure to work with due to his charm, yet is also frustrating as he lacks the ability to see the 'error of his ways'.
Clinical Description and Symptomology in ASPD
Individuals with ASPD tend to have long histories of violating the rights of others, and as such they are often described as aggressive. They frequently show no remorse for their actions, and it is very common for them to be substance abusers (83%). ASPD appears to be associated with low socioeconomic status and urban settings (APA, 2000). The overall prevalence of ASPD is approximately 3% of males and 1% of females. The Course of ASPD appears to be chronic, with a ‘tapering off’ of symptoms after the age of approximately 40 (Kring & Banchowoksi, 1999). ASPD is more common amongst first degree biological relatives (Durand & Barlow, 2006). The risk to biological females is higher than with first degree relatives of biological males.
Those with ASPD lack empathy and tend to be callous, cynical and contemptuous of the feelings, rights, and sufferings of others. They may have inflated and arrogant self appraisal and may be excessively opinionated, self assured or cocky (APA, 2000). They may display a glib, superficial charm. They can be irresponsible and exploitative in their sexual relationships. They may have a history of many sexual partners, and may not have ever sustained a monogamous relationship (Durand & Barlow, 2006). They may be irresponsible as parents, as evidenced through malnutrition of their children; illness in their child due to lack of hygiene; a failure to arrange for caretakers of the child when away from home; and the child may be dependent on others for food or shelter, there may also be repeated squandering of household money required for necessities. These individuals may become impoverished or even homeless, or may spend years in correctional institutions (APA, 2000). Individuals with the disorder may complain of; an inability to tolerate boredom, tension and a depressed mood (Durand & Barlow, 2006).
Neurobiological Processing and Theories of ASPD
So what processes underlie the manifestation of the disorder?
In the following section we will discuss neurobiological research and theory to discover the answer.
Deficiency in Emotion Regulation and the Amygdala
The neurobiological processing of ASPD is centred on two main brain areas, the amygdala and the prefrontal cortex. The amygdala will be discussed here as it plays a main role in the neurobiological processes in ASPD. The amygdala is an almond shaped structure located in the medial temporal lobes. Along with other brain systems, the amygdala is part of the limbic system that regulates the expression of emotion and emotional memory (Blair & Mitchell, 2009). The amygdala is also responsible for multiple physiological cues, such as fear. It has also been shown to have a role in emotional states of aggression, maternal, sexual and eating behaviours (Delisi, Umphress & Vaughn, 2009).
Due to this the amygdala mediates defensive behaviour in stages of fear and anxiety, is involved in instrumental learning and aversive conditioning; and is activated in response to fearful and sad facial expressions (Delisi et al., 2009). In individuals with ASPD, the amygdala has been shown to be somewhat dysfunctional in its ability to interpret emotions and the processing of punishment and reward behaviours (Blair & Mitchell, 2009).
Those with antisocial personalities show reduced neural responses to threatening stimuli, aversive conditioning, emotional response in anticipation of imagined life events and reduced startle reflex to aversive stimuli which will be discussed later (Delisi et al., 2009). The amygdala is responsible for two capacities that are essential for successful socialisation. The ability to elicit an aversive emotional response to distress or fear in other people, and the capacity to internalise the ‘right and wrong’ of this. Individuals with ASPD are lacking in both these capacities, showing significantly reduced autonomic response to distress cues of others, including decreased fear recognition. Due to this, they are unable to empathise with others because of the lack of stimulus-response and stimulus-reinforcement associations, leading to maladaptive motivations for behaviours (Blair & Mitchell, 2009).
Decety, Michalaska, Akitsuki and Lahey (2009) studied young people diagnosed with conduct disorder, a known developmental disorder that can lead to ASPD. They investigated the brains response of the young people while they viewed pain and empathy eliciting stimuli. These young people showed less amygdala and prefrontal cortex ‘coupling’ and activity when they were watching pain inflicted on another (Decety et al... 2009).
As you can see, the neurobiological processing of individuals with ASPD is significantly impaired compared to those without the disorder. Next we will examine the main neurobiological theories about ASPD.
Neurobiological Theories about ASPD
There are three main theories on the underlying neurobiological functioning of ASPD. Each theory ties into the other, giving a better overall better understanding of the processes that are involved in the presentation of the disorder.
According to this hypothesis, ASPD sufferers have low levels of cortical arousal. The Yerkes-Dodson law states that individuals who have a very high or very low levels of arousal tend to experience negative affect and perform poorly in many situations. Individuals with a medium level of arousal tend to be relatively content and perform better in most situations (Durand & Barlow, 2006). Due to this, low levels of arousal are hypothesised to be characteristic of ASPD sufferers; and are the primary cause of antisocial and risk taking behaviours (Durand & Barlow). Basically, they seek constant stimulation to reach a higher level of arousal.
A related theory, the cortical immaturity hypothesis states that the cerebral cortex in ASPD sufferers is relatively primitive in its stages of development. Often this is reported to explain why ASPD sufferers have impulsive and childlike behaviours (Durand & Barlow, 2006). This could also explain the constant drive for stimulation of those with ASPD, and the common feelings of boredom and 'listlessness'.
The Fearlessness Hypothesis
According to this theory, ASPD sufferers possess a higher threshold for experiencing and reacting to fear than most other individuals. This fearlessness is said to give rise to all the major features of the disorder (Durand & Barlow, 2006).
The fearlessness is secured by the inability to respond to and learn from the punishing consequences of antisocial and violent behaviour. The startle reflex when viewing aversive stimuli is often used to measure fearlessness in sufferers of ASPD. This has led researchers to conclude that these individuals have problems with passive avoidance or punishment induced behavioural inhibition. Due to this, societal control over individual’s violence will have little effect as social correction has no effect on their behaviour (Honk & Shutter, 2006).
Lykken (1957) begun to explore the low fear model in ASPD many years ago, using the concept passive avoidance. In his aversive conditioning paradigms it was repeatedly shown that individuals with ASPD traits have a lesser tendency to avoid behaviour that had previously been associated with a punishment in the form of a shock (as cited in Honk & Shutter, 2006). This was later shown by Fowles (2000), in use of physiological responses to aversive stimuli and startle reflex simulations. Subsequent research has found that individuals with ASPD do poorly on anxiety mediated avoidance learning (Honk & Shutter, 2006). As a result, individuals with ASPD are seen as ‘having no fear’ and ‘blunted response in times of high stress and fear’ (Honk & Shutter). Later in the chapter anxiety and physiological response will be discussed in relation to these fearlessness and blunted affect response.
Gray’s (1987) Biological Personality Theory
Gray theorises that there are two main brain systems that regulate withdrawal and approach behaviour in response to environmental stimuli. The behavioural inhibition system (BIS) and the behavioural activation system (BAS). The BIS serves to alert the person to the possibility of danger and punishment. It is sensitive to signals of non-reward and novelty, resulting in behavioural inhibition in anticipation of possible threats; as well as increments of arousal and attention (Bjornebekk, 2007). Activity in the BIS gives rise to feelings of anxiety and induces passive avoidance, enabling the individual to scan the environment for further cues. The BAS is sensitive to reward and is connected to approach behaviour. An individual with high BAS reactivity will have greater motivational reaction to conditioned stimulus for reward, and is more aware of cues of reward, as well as cues for non-punishment or escape from punishment (Bjornebekk, 2007). Activity in the BAS produces impulsive behaviour, inducing the individual to pursue vigorously an action that might result in reward, with little regard for negative consequences (Bjornebekk, 2007)
Reactivity in the BIS and the BAS is thought to explain some of the main aspects of the motivation for antisocial behaviour. This will be further discussed in detail in motivation-avoidance behaviours under Motivation in ASPD.
Motivation in ASPD
Motivational Theory and Research on ASPD
Individuals with ASPD have profound adjustment problems is spite of above average intelligence and social skills. In light of this intact reasoning and executive functioning ability and the mismatch between their maladaptive behaviours in the environment such as school, employment and interpersonal relationships, researchers examine motivational theories of ASPD (Newman, Schmitt & Voss, 1997). Some have theorised that the ability to perform, yet experiences of chronic maladjustment in individuals with ASPD, is due to a lack of motivation to conform. Research has looked into apparent inabilities to learn from punishment and reward, and deficient emotional responses to these cues. It has largely be concluded that individuals with ASPD differ in their behavioural reactions to a variety of motivational signals which is further complicated by diminished affect, anxiety and physiological responding (Newman, Schmitt & Voss, 1997).
Response Modulation Hypothesis
Individuals with ASPD have difficulty in learning to inhibit punished responses (Newman, Schmitt & Voss, 1997). Yet they appear to have no difficulty in avoiding punishment if avoidance learning is their only goal, the avoidance contingency is made salient at the start of a task, and if positive and negative feedback are provided during the extended intertrial interval. This pattern of results is suggested to be due to their inability to process contextual information that is unexpected or peripheral to a dominant response (Newman, Schmitt & Voss, 1997). This finding was hypothesised by Patterson and Newman (1997) as response modulation. Response modulation involves an automatic shift of attention from the effortful implementation of goal directed behaviour to its evaluation. The idea was been extended by Newman and Wallace (1997) to propose that a defect in the automatic processing that underlies the ability to screen, detect and redirect attention in response to significant stimuli provides a strong mechanisms for motivational, affective and cognitive idiosyncrasies in ASPD (Newman, Schmitt & Voss, 1997).
The response modulation hypothesis hypothesis has been extended to predict that deficient avoidant learning will be specific to conditions requiring individuals to suspend dominant responses to negative feedback (Arnett, Smith & Newman, 1997). This means that individuals with ASPD are equally responsive to rewards and punishment in most situations, but have difficulty inhibiting a dominant response set when cues for punishment are present as they are less adept at interrupting BAS activation (Arnett, Smith & Newman). More generally, the response modulation hypothesis states a situation specific deficiency in the processing of contextual cues regardless of whether these involve threat of punishment, whereas the hypotheses that involve low fear or insensitivity to punishment cues of the individual with ASPD yield predictions that are specific to the punishment stimuli (Newman, Schmitt & Voss, 1997).
Newman, Schmitt and Voss (1997) conducted a study to formulate the generalisablity of the response modulation hypothesis. They studied 112 male, minimum security inmates at a prison in the USA. The study aimed to examine the effect of neutral motivational cues unrelated to punishment on those with ASPD. Using a picture task, participants were asked to locate two pictures or words that were related, with each corresponding picture confused with the wrong label attached. Each participant was informed they would receive 5 cents for responses that were quicker; aiming to formulate motivation and a dominant response set. What they found was that those who scored the highest in ASPD traits and lowest in anxiety had the hardest time with the task; showing the slowest response time. Newman, Schmitt and Voss' (1997) hypothesis that individuals with ASPD show deficiencies in interpreting motivationally neutral cues was supported.
So the response modulation hypothesis means that those with ASPD have difficulty suspending reward orienting behaviour in order to accommodate feedback from the environment (Kring & Bachowoski, 1999). Rather then saying there is impairment in either the BAS or BIS systems, this model predicts that a primary disturbance is in the deficit of the reciprocal inhibition of the activation and inhibition systems. This model can also account for cognitive characteristics like attention, but can also account for notable emotional features of ASPD like low fear and low anxiety (Kring & Bachowoski, 1999). Much of the above theory can explain why those with ASPD have problems with impulse control (i.e. substance abuse, risky behaviours) and long-term management of their daily lives (i.e. long term employment and relationships).
Approach and Avoidance Motivation in ASPD
Arnett, Smith and Newman (1997) sought to study sensitivity to reward in ASPD, using only the behavioural activation system (BAS) in context. Fowles (1980) asserted that individuals with ASPD show normal BAS activity or ‘normal approach and active avoidance’ in regards to rewards and cues. Yet Arnett et al. (1997) found that ASPD sufferers show exaggerated BAS activity, especially in regards to rewards. They also found that they experience a poor response modulation or variation due to failures to suspend goal directed behaviour when punishment was encountered (Arnett, Smith & Newman, 1997). This has been called the approach / avoidance theory of motivation in ASPD. This was also hypothesised by Arnett to be mediated by a hypersensitivity to reward not just punishment for individuals with ASPD; as it has been previously hypothesised that individuals with ASPD appear to be sensitive to punishment (Arnett, Smith & Newman, 1997).
Through two consecutive studies on 63 male inmates at a Wisconsin prison in America, Arnett, Smith and Newman (1997) studied goal directed reward and punishment behaviour on those with ASPD. They asked the participants to respond to five response buttons on a computer screen. Each participant was asked to press a button for when the lights flashed green. A tone would sound if the participant got it right, and there was no tone if they got the flash wrong. Participants were told they would receive 5 cents each ‘round’ if they received 80 right (out of 120 rounds). The participants with ASPD showed a mediated goal directed behaviour only when reward was evident, not for when no reward was present (Arnett, Smith & Newman, 1997).
The Motivational Imbalance Model
As discussed, Gray (1987) theorised that there were two main systems that regulate withdrawal and approach behaviour in response to external stimuli, the BAS and the BIS. Extending on this theory, Fowles (1980) and Arnett (1997) have conceptualised the motivational imbalance model of behaviour. Arnett argues that the inhibitory properties of the key motivational systems create the maladaptive tendencies in ASPD. This has been found when individuals show insensitivity for punishment particularly when reward is pending (as cited in Honk & Shutter, 2006).
Fowles (1980) believes that a weak or deficient BIS occurs in ASPD. Normally cues for punishment act as inputs to the BIS and various emotional and behavioural consequences ensue. In contrast, a weak BIS means that the punishment cues are less likely to activate the BIS. In the absence of this engagement, there is no inhibition for ongoing behaviour, reflection and the experience of anxiety (Kring & Bachowoski, 1999). Due to this, the behavioural problems that occur in ASPD arise because the psychological processes that normally function to motivate adaptive, socially acceptable behaviour do not occur in the presence of punishment.
The BAS and BIS are two motivationally adaptive systems typically referred to as goal directed approach and withdrawal systems. Although it is not clearly discussed by motivation theorists, discrete emotions can be aligned with activity in either the approach or avoidance behaviours of ASPD (Kring & Bachorowski, 1999). Some emotions for example, can be directly meaningful to motivations systems. “Anger” can lead to overt aggression or active avoidance. Yet we must remember, especially in ASPD, that positive emotions are not always associated with approach behaviours, the same for negative emotions in avoidance activity, which can be seen in the literature on ASPD (Kring & Bachowoski, 1999). Which leads us to the imbalance that is found in the motivational phenomenology of ASPD.
What is most notable is the ability to apply this theory to the potential rates of recidivism found in conduct disorder and ASPD. By not being able to suspend and coordinate adaptive behaviours after a crime, for example, the individual with ASPD may find it difficult to suspend committing more offences after being charged with a crime (i.e. the punishment).
Emotional Processing Deficits in ASPD
It is clear, through much research on ASPD, that the experience of the disorder is emphasised by deficient emotional processes, lack of emotional reactions, lack of anxiety and a disjunction between the actual and experiential components of emotion (McKendrick, Sullivan, Bank & Sacks, 2006). These individuals are cognitively intact, but are unable to appreciate the emotional significance of their behaviours. Due to this, the lack of affect experienced has a direct impact on their motivations and subsequent behaviours. As such, the maladaptive behaviours that are present in ASPD directly motivate the individual in responding to external and internal cues differently than those without the disorder (Kosson, Suchy, Mayer & Libby, 2002).
Based on the research performed on emotion in ASPD there has been a consensus that these individuals have difficulty responding to expressions of certain emotions more so than others (Reidy, Zeichner & Hunnicut-Ferguson, 2008). As seen in the fearlessness hypothesis, and also found in expressions of sadness, those with ASPD react and experience these expressions at a higher threshold than those without the disorder. Using lexical decision tasks (LDTs), researchers study this response. LDTs involve classifying letter strings of words or non words on a computer, which are emotional (love, hate, pain, happy) or neutral (table, chair, book, later) categories, and participants respond as quickly as they can (Lorenz & Newman, 2002). The LDT measures the network activation of the stimulus words, with faster reaction times to the words suggesting less activation. For example, individuals prone to anger should respond faster to anger words, and those with deficits in the experience of fear or sadness will respond slower to corresponding words (Reidy, Zeichner & Hunnicut-Ferguson, 2008). LDT research has also been supported by its ability to measure implicit and uncontrollable thought process, furthering its reliability.
Individuals with ASPD show more emotional facilitation to negative words than positive ones, and show a longer response time specifically when viewing angry or sad emotional categories. Lorenz and Newman (2002) performed a LDT on 237 male and 172 female inmates residing in a American correctional institution. Each participant was assessed on the DSM ratings of ASPD and Hare’s psychopathology ratings. They found the participants with ASPD showed higher facilitation to the negative words than control subjects. They also found that this sensitivity was also present for positive words showing higher levels of emotion facilitation (Lorenz & Newman, 2002).
Habel, Kuhn, Salluom, Devos and Shneider (2002) studied the emotional discrimination and emotional reactivity to mood induction of those with ASPD. Thirty-three participants were shown a facial discrimination test consisting of happy and sad facial expressions. They found that individuals with ASPD had an impaired ability to discriminate the different emotions in the faces, concluding that those with ASPD had significant deficits in their internal emotional reactions (Habel et al.). Kosson, Suchy, Mayer and Libby (2002) furthered this finding by adding the facial expression of disgust and finding that individuals with ASPD had deficient abilities in determining this emotion, more so than for sadness and anger.
Physiology and Anxiety in ASPD
Individuals with ASPD have been found to have reduced anxiety and less intense physiological responses to emotional experiences than those without the disorder (Patrick, Bradley & Lang, 1993).
In one of the earliest studies, Lykken (1957) hypothesised that individuals with ASPD experienced little to no anxiety, and had lowered physiological responses than those not diagnosed with the disorder. Using questionnaires and electrodermal response activity (facial response, heart rate and skin conductance) he studied participants with ASPD and a control group with no diagnosis (as cited in Patrick, Bradley & Lang, 1993). He found reduced anxiety levels in the individuals who had ASPD, also finding they had low electrodermal responses to shocking stimuli. He theorised after these findings that individuals with ASPD symptomology have less intense emotional reactions to many everyday experiences which is believed to underlie the manifestation of lack of affect and emotional depth (Patrick, Cuthbert & Lang, 1994).
Further empirical evidence has suggested that individuals with ASPD have ‘dulled’ physical responses to stressors, shocking stimuli and aversive experimental events (Schneider, Habel, Kessler, Posse, Grodd & Muller-Gartner, 2000), often found when using electrophysiological methods such as those used by Lykken. This blunted experience has been hypothesised to contribute to the reduced anxiety experienced, yet some researchers have begun to conclude that some individuals who score highly in ASPD and Psychopathy traits show a hypersensitivity to shocking stimuli, with heightened physiological responses and anxiety (Patrick, Bradley & Lang, 1993).
To further research physiological responses in those with ASPD, researchers use a technique called startle reflex modulation. Startle reflex is measured through eye blink responses to aversive and pleasant stimuli (Patrick, Bradley & Lang, 1993). This reflex is hypothesised to be able to measure the physiological response when participants of a study are viewing images, words, or some form of stimulus that the researcher is attempting to elicit arousal levels from. Startle reflex modulation has been seen to have the ability to show involuntary movements of the eyes as the probe is un-warned (Patrick, Bradley & Lang 1993). Researchers have found that they are able to see the valence (directionality of the elicited action disposition; either approach or avoidance), anxiety and varied physiological responses when individuals with ASPD are studied; especially when this startle reflex is paired with EMG (electromyographic) activity, facial response, heart rate monitors and skin conductance (Patrick, Bradley & Lang, 1993).
What is empathy, and can you imagine what it would be like not to have any?
Empathy is the natural ability to understand the emotions and feelings of others, whether one actually witnessed his or her situation, perceived it from a photograph, read about it in a fiction book or merely imagined it (Decety & Jackson, 2004). It is a phenomenological experience that is not a learned skill as when we are born the building blocks for it are already in the brain; it is just waiting for development and interaction with others to be shaped. Empathy denotes a familiarity of similarity with someone else’s plight, or a self/other awareness that is commonly referred to as being able to ‘put yourself in someone else’s shoes’ (Decety & Jackson). Certain disorders though are characterised by a lack of empathy, including ASPD.
Empathy can be found organically in most individuals, and it is thought that the right prefrontal cortex contains the capacity to reason about the feelings of others (Decety & Jackson, 2004). The tendency to have a low concern of the needs of others and the consequences of ones own actions seem to be common for many personality disorders, most specifically though with ASPD. This ‘empathy deficit’ in ASPD is theorised to come from the reduced ability to read and feel another’s emotional state, particularly sadness and fear (Decety & Jackson). The lack of empathy is ascribed to disrupted affective processing, as many such individuals have their executive and cognitive functions ‘intact’. Therefore, individuals with ASPD may be very good at perceiving others' intentions, while disregarding the emotional content, and taking advantage. In essence, they can simulate the emotions they cannot experience, but must rely on cognitive inputs to process such experiences in their ‘theory of mind mechanism’ (Decety & Jackson).
For an individual who is able to experience empathy, the thought of not feeling for others is an alarming dichotomy, yet it goes a long way in explaining the antisocial acts that often come from maladaptive disorders such as ASPD, especially considering the indiscriminate self appraisal, selfishness and apparent 'lack or morals'.
Criminality, Psychopathology and ASPD
ASPD is one of the most common mental disorders seen in those who commit crimes and end up incarcerated. The assumption that all criminals are antisocial is not true though (McKendrick, Sullivan, Banks and Sacks, 2006). ASPD and Psychopathy are conceptually quite similar, and the words are often used interchangeably (Kosson, Lorenz & Newman, 2006). At the measurement level, ASPD focuses more on affective and interpersonal features and their links to broad antisocial tendencies, while Psychopathy emphasises explicit anti-sociality, such as violent crime and underlying personality traits (Hare & Neumann, 2009). Most people who meet the criteria with Psychopathy also meet the criteria for ASPD, yet they qualify for a similar, yet different diagnosis (Hare & Neumann, 2009). As such, not all people with ASPD have a criminal history and many lead relatively successful lives in the community (Durand & Barlow, 2006).
Individuals with ASPD experience a range of maladaptive psychological experiences. Neurological research reveals that the amygdala and related brain regions process interpret and respond to certain emotions in a deficient way. Through neurobiological theory we have seen that those with ASPD have a higher threshold for experiencing fear, that their withdrawal and approach behaviour motivates their antisocial tendencies, and they experience underarousal. Through motivational theory it can be seen that individuals have difficulty inhibiting behaviours after punishment and reward and that these tie into the inability to respond appropriately to approach and avoidance behaviours. This chapter also discussed the imbalance found in the behavioural inhibition and activation systems in response to external stimuli.
The emotional processing deficits found in ASPD show that these individuals lack in emotional reactions and interpretation and have difficulty interpreting and the emotions of others. Furthermore, these individuals show less anxiety when viewing shocking and aversive stimuli, and have been shown to have 'blunted' physiological responses. Finally, those with ASPD are often labeled psychopathic, yet those with psychopathic traits require a similar, yet different diagnosis (Hare & Newmann, 2009).
When you feel the pain of another's heartbreak, or the joy of someone else's success imagine that taken away and you will have a small idea of what it is like to live with ASPD.
He who feels nothing is an empty man.
Glossary of terms
- Amygdala: An almond shaped structure located in the medial temporal lobes in the brain. Part of the limbic system it regulates the expression of emotion and emotional memory
- Antisocial Personality Disorder: A personality disorder that is characterised by a pervasive pattern of disregard for, and violation of, the rights of others that begins in childhood or early adolescence and continues into adulthood.
- Anxiety: A psychological and physiological state characterized by cognitive, somatic, emotional, and behavioral components. These components combine to create an unpleasant feeling that is typically associated with uneasiness, apprehension, fear, or worry.
- Avoidance motivation: That individuals experience approach behaviour when rewards are evident, and avoidance behaviour when punishment is encountered.
- Behavioural Inhibition system (BIS): System which alerts individuals to the possibility of danger and punishment, preparing for anticipation of potential threats, arousal and attention.
- Behavioural Activation system (BAS): System which is connected to approach behaviour, and is sensitive to reward, which increases motivational reactions.
- Electro dermal response: Used in physiological testing to measure facial response, skin conductance and heart rate.
- Emotion: Emotion is the complex psychophysiological experience of an individual's state of mind as interacting with biochemical (internal) and environmental (external) influences.
- Empathy: Empathy is the capacity to share the sadness or happiness of another individual being through consciousness rather than physically. Empathy develops the ability to have compassion towards other beings.
- Fearlessness Hypothesis: That individuals with ASPD have a higher threshold for experiencing and reacting to fear.
- Lexical Decision Task: A common task used to measure emotion; involves classifying letter strings of words or non words as quickly as possible on a computer, which are emotional (love, hate, happy) or neutral (table, chair, book, later).
- Motivation: Concerns the processes that give behaviour its energy and direction.
- Motivational Imbalance Model: Consists of the behavioural activation system (BAS) and the behavioural inhibition system (BIS), when one or both systems are maladaptive and inhibiting appropriate approach and avoidance behaviour.
- Prefrontal cortex: The prefrontal cortex (PFC) is the anterior part of the frontal lobes of the brain, lying in front of the motor and premotor areas. This brain region has been implicated in planning complex cognitive behaviours, personality expression, decision making and moderating correct social behavior
- Response modulation: Involves the automatic shift of attention from the effortful implementation of goal directed behaviour to its evaluation.
- Startle reflex modulation: Physiological testing method of measuring the amount of eye blinks per minute on individuals while viewing images, words or some form of stimulus the researcher is attempting to elicit arousal levels from.
- Under arousal hypothesis: Hypothesizes that individuals with ASPD have low levels of cortical arousal; as those with low or very high levels experience negative affect- while those who experience a medium level tend to be relatively content.
- Valance: Directionality of the elicited action disposition; either approach or avoidance.
The following related textbook chapters:
- What is motivation?
- What is emotion?
- Antisocial Personality Disorder and emotion
- Emotion and psychopathy
- Motivation and anxiety
- Neurobiology of aggression
American Psychiatric Association (2000). Diagnostic and Statistical Manual of mental disorders- Text Revision: (4th Edition). Washington DC.
Arnett, P. A., Smith. S. S., & Newman, J. P. (1997). Approach and avoidance motivation in psychopathic criminal offenders during passive avoidance. Journal of Personality and Social Psychology, 72 (6), 1413-1428.
Blair, R. J. R., & Mitchell, D.G.V. (2009). Psychopathy, attention and emotion. Psychological Medicine, 39 (4), 543-555.
Bjornebekk, G. (2007). Dispositions related to sensitivity in the neurobiological basis for activation of approach-avoidance motivation, antisocial attributes and individual differences in aggressive behaviour. Social Behaviour and Personality, 35 (9), 1251-1264.
Decety, J., & Jackson, P.L. (2004). The Functional architecture of empathy. Behavioural and Cognitive Neuroscience Review, 3 (2), 71-100.
DeLisi, M., Umphress, Z.R., & Vaughn, M. G. (2009). The Criminology of the amygdala. Criminal Justice and Behaviour, 36 (11), 1241-1252.
Durand, V. M. & Barlow, D. H. (2006). Essentials of Abnormal Psychology (4th Edition). Belmont, CA: Wadsworth.
Elliot, A. J. (2006). The hierarchical model of approach-avoidance motivation. Motivation and Emotion, 30, 111-116.
Glass, S. J., & Newman, J. P. (2009). Emotion processing in the criminal psychopath: The role of attention in emotion facilitated memory. Journal of Abnormal Psychology, 118 (1), 229-234.
Habel, U., Kuhn, E., Salloum, J.B., Devos, H., & Schnieder, F. (2002). Emotional processing in psychopathic personality. Aggressive Behaviour, 28, 394-400.
Hare, R.D., & Neumann, C.S. (2009). Psychopathy: Assessment and Forensic Implications. Canadian Journal of Psychiatry, 54 (12), 791-802.
Kosson, D. S., Lorenz, A. R., & Newman, J. P. (2006). Effects of co-morbid Psychopathy on criminal offending and emotion Processing in male offenders with antisocial personality disorder. Journal of Abnormal Psychology, 115 (4), 798-806.
Kosson, D. S., Suchy, Y., Mayer, A. R., & Libby, J. (2002). Facial affect recognition in criminal psychopaths. Emotion, 2 (4), 398-411.
Kring, A. M., & Bachorowski, J. (1999). Emotions and psychopathology. Cognition and Emotion, 13 (5), 575-599.
Lorenz, A., R., & Newman, J., P. (2002). Utilisation of emotion cues in male and female offenders with antisocial personality disorder: Results from a lexical decision task. Journal of Abnormal Psychology, 111 (3), 513-516.
McKendrick, K., Sullivan, C., Bank, S., & Sacks, S. (2006). Modified therapeutic community treatment for offenders with MICA disorders: Antisocial personality disorder and treatment outcomes. Journal of Offender rehabilitation, 44 (2/3), 133-159.
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.
Patrick, C., J., Bradley, M., M. & Lang, P. J. (1993). Emotion in the Criminal Psychopath: Startle Reflex Modulation. Journal of Abnormal Psychology, 102 (1), 82-92.
Patrick, C. J., Cuthbert, B. N., & Lang, P. J. (1994). Emotion in the criminal psychopath: Fear Image processing. Journal of Abnormal Psychology, 103 (3), 523-534.
Reidy, D., Zeichner, A., & Hunnicut-Ferguson, K. (2008). Psychopathy traits and the processing of emotional words: Results of a Lexical decision task. Cognition and Emotion, 22 (6), 1174-1186.
Reeve,J. (2009). Understanding Motivation and Emotion, Fifth Edition. Iowa; John Wiley & Sons.
Schneider, F., Habel, U., Kessler, C., Posse, S., Grodd, W., & Muller-Gartner, H. (2000). Functional Imaging of conditioned Aversive emotional responses in antisocial personality disorder. Neuropsychobiology, 42, 192-201.
Stout, M. (2005). The Sociopath next door. New York: Broadway Books.
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.