What is Inhibitory Control?

Introduction

Inhibitory control, also known as response inhibition, is a cognitive process – and more specifically an executive function – that permits an individual to inhibit their impulses and natural, habitual, or dominant behavioural responses to stimuli (e.g. prepotent responses) in order to select a more appropriate behaviour that is consistent with completing their goals.

Self-control is an important aspect of inhibitory control. For example, successfully suppressing the natural behavioural response to eat cake when one is craving it while dieting requires the use of inhibitory control.

The prefrontal cortex, caudate nucleus, and subthalamic nucleus are known to regulate inhibitory control cognition. Inhibitory control is impaired in both addiction and attention deficit hyperactivity disorder. In healthy adults and ADHD individuals, inhibitory control improves over the short term with low (therapeutic) doses of methylphenidate or amphetamine. Inhibitory control may also be improved over the long-term via consistent aerobic exercise.

Tests

An inhibitory control test is a neuropsychological test that measures an individual’s ability to override their natural, habitual, or dominant behavioural response to a stimulus in order to implement more adaptive goal-oriented behaviours. Some of the neuropsychological tests that measure inhibitory control include the Stroop task, go/no-go task, Simon task, Flanker task, anti-saccade tasks, delay of gratification tasks, and stop-signal tasks.

Gender Differences

Females tend to have a greater basal capacity to exert inhibitory control over undesired or habitual behaviours and respond differently to modulatory environmental contextual factors relative to males. For example, listening to music tends to significantly improve the rate of response inhibition in females, but reduces the rate of response inhibition in males.

What is Gray’s Biopsychological Theory of Personality?

Introduction

The biopsychological theory of personality is a model of the general biological processes relevant for human psychology, behaviour, and personality. The model, proposed by research psychologist Jeffrey Alan Gray in 1970, is well-supported by subsequent research and has general acceptance among professionals.

Gray hypothesized the existence of two brain-based systems for controlling a person’s interactions with their environment: the behavioural inhibition system (BIS) and the behavioural activation system (BAS). BIS is related to sensitivity to punishment and avoidance motivation. BAS is associated with sensitivity to reward and approach motivation. Psychological scales have been designed to measure these hypothesized systems and study individual differences in personality. Neuroticism, a widely studied personality dimension related to emotional functioning, is positively correlated with BIS scales and negatively correlated with BAS scales.

Brief History

The biopsychological theory of personality is similar to another one of Gray’s theories, reinforcement sensitivity theory. The Biopsychological Theory of Personality was created after Gray disagreed with Hans Eysenck’s arousal theory that dealt with biological personality traits. Eysenck looked at the ascending reticular activating system (ARAS) for answering questions about personality. The ARAS is part of the brain structure and has been proposed to deal with cortical arousal, hence the term arousal theory. Eysenck compared levels of arousal to a scale of introversion versus extraversion. The comparison of these two scales was then used to describe individual personalities and their corresponding behavioural patterns. Gray disagreed with Eysenck’s theory because Gray believed that things such as personality traits could not be explained by just classical conditioning. Instead, Gray developed his theory which is based more heavily on physiological responses than Eysenck’s theory.

Gray had a lot of support for his theories and experimented with animals to test his hypotheses. Using animal subjects allows researchers to test whether different areas of the brain are responsible for different learning mechanisms. Specifically, Gray’s theory concentrated on understanding how reward or punishment related to anxiety and impulsivity measures. His research and further studies have found that reward and punishment are under the control of separate systems and as a result people can have different sensitivities to such rewarding or punishing stimuli.

Behavioural Inhibition System

The behavioural inhibition system (BIS), as proposed by Gray, is a neuropsychological system that predicts an individual’s response to anxiety-relevant cues in a given environment. This system is activated in times of punishment, boring things, or negative events. By responding to cues such as negative stimuli or events that involve punishment or frustration, this system ultimately results in avoidance of such negative and unpleasant events. According to Gray’s Theory, the BIS is related to sensitivity to punishment as well as avoidance motivation. It has also been proposed that the BIS is the causal basis of anxiety. High activity of the BIS means a heightened sensitivity to non-reward, punishment, and novel experience. This higher level of sensitivity to these cues results in a natural avoidance of such environments in order to prevent negative experiences such as fear, anxiety, frustration, and sadness. People who are highly sensitive to punishment perceive punishments as more aversive and are more likely to be distracted by punishments.

The physiological mechanism behind the BIS is believed to be the septohippocampal system and its monoaminergic afferents from the brainstem. Using a voxel-based morphometry analysis, the volume of the regions mentioned was assessed to view individual differences. Findings may suggest a correlation between the volume and anxiety-related personality traits. Results were found in the orbitofrontal cortex, the precuneus, the amygdala, and the prefrontal cortex.

Behavioural Activation System

The behavioural activation system (BAS), in contrast to the BIS, is based on a model of appetitive motivation – in this case, an individual’s disposition to pursue and achieve goals. The BAS is aroused when it receives cues corresponding to rewards and controls actions that are not related to punishment, rather actions regulating approachment type behaviours. This system has an association with hope. According to Gray’s theory, the BAS is sensitive to conditioned appealing stimuli, and is associated with impulsivity. It is also thought to be related to sensitivity to reward as well as approach motivation. The BAS is sensitive to non-punishment and reward. Individuals with a highly active BAS show higher levels of positive emotions such as elation, happiness, and hope in response to environmental cues consistent with non-punishment and reward, along with goal-achievement. In terms of personality, these individuals are also more likely to engage in goal-directed efforts and experience these positive emotions when exposed to impending reward. The physiological mechanism for BAS is not known as well as BIS, but is believed to be related to catecholaminergic and dopaminergic pathways in the brain. Dopamine is a neurotransmitter commonly linked with positive emotions, which could explain the susceptibility to elation and happiness upon achieving goals which has been observed. People with a highly active BAS have been shown to learn better by reward than by punishment, inverse to BIS as mentioned above. BAS is considered to include trait impulsivity that is also related to psychopathological disorders such as ADHD, substance use disorder, and alcohol use disorder. The higher the BAS score, or the higher the impulsive, the more it is likely to be related to psycho-pathological or dis-inhibitory disorders. Certain aspects of the dopaminergic reward system activate when reward cues and reinforcers are presented, including biological rewards such as food and sex. These brain areas, which were highlighted during multiple fMRI studies, are the same areas associated with BAS.

Compare and Contrast

Together, the two systems work in an inverse relationship. In other words, when a specific situation occurs, an organism can approach the situation with one of the two systems. The systems will not be stimulated at the same time and which system is dominant depends on the situation in terms of punishment versus reward. This phenomenon of the differentiation between the two systems is thought to occur because of the distinct areas in the brain that becomes activated in response to different stimuli. This difference was noted years ago through electrical stimulation of the brain.

The behavioural activation system and behavioural inhibition system differ in their physiological pathways in the brain. The inhibition system has been shown to be linked to the septo-hippocampal system which appears to have a close correlation to a serotonergic pathway, with similarities in their innervations and stress responses. On the other hand, the activation, or reward system, is thought to be associated more with a mesolimbic dopaminergic system as opposed to the serotonergic system.

The two systems proposed by Gray differ in their motivations and physiological responses. Gray also proposed that individuals can vary widely in their responsiveness of the behavioural inhibition system and the behavioural activation system. It has been found that someone who is sensitive to their BIS will be more receptive to the negative cues as compared to someone who is sensitive to their BAS and therefore responds more to cues in the environment that relate to that system, specifically positive or rewarding cues. Researchers besides Gray have shown interest in this theory and have created questionnaires that measure BIS and BAS sensitivity. Carver and White have been the primary researchers responsible for the questionnaire. Carver and White created a scale that has been shown to validly measure levels of individual scores of BIS and BAS. This measure focuses on the differences in incentive motivations and aversive motivations. As previously mentioned these motivations correlate to impulsivity and anxiety respectively.

Applications

Since the development of the BAS and BIS, tests have been created to see how individuals rate in each area. The questionnaire is called the Behavioural Inhibition System and Behavioural Activation System Questionnaire.

People can be tested based on their activation of either systems by using an EEG. These tests will conclude whether a person has a more active BIS or BAS. The two systems are independent of each other.

These tests can determine different things about a person’s personality. They can determine if a person has more positive or negative moods. Using psychological test scales designed to correlate with the attributes of these hypothesized systems, neuroticism has been found to be positively correlated with the BIS scale, and negatively correlated with the BAS scale.

According to Richard Depue’s BAS dysregulation theory of bipolar disorders, now doctors and other professionals can determine if a person with bipolar disorder is on the brink of a manic or depressive episode based on how they rate on a scale of BAS and BIS sensitivity. Essentially, this dysregulation theory proposes that people with BAS dysregulation have an extraordinarily sensitive behavioural activation system and their BAS is hyper-responsive to behavioural approach system cues. If a person with bipolar disorder self-reports high sensitivity to BAS, it means that a manic episode could occur faster. Also, if a person with bipolar disorder reports high sensitivity to BIS it could indicate a depressive phase. A better understanding of BAS dysregulation theory can inform psychosocial intervention (e.g. cognitive behavioural therapy, psychoeducation, interpersonal and social rhythm therapy, etc.).

The BAS/BIS Questionnaire can also be used in the cases of criminal profiling. Previous research as reported by researchers MacAndrew and Steele in 1991 compared two groups on opposite spectrum levels of fear and the response of a variety of questions. The two groups in the study varied on levels of BIS, either high or low, and were selected by the researchers. One group was composed of women who had experienced anxiety attacks and together made up the high BIS group. The low BIS group was composed of convicted prostitutes who had been found to take part in illegal behaviour. Main findings showed that the responses to the questionnaires were distinctly different between the high BIS group and the low BIS group, with the convicted women scoring lower. Results from this study demonstrate that questionnaires can be used as a valid measurement to show differences in the behavioural inhibition systems of different types of people. Gray also introduced his SPSRQ questionnaire to measure sensitivity to reward (SR) and sensitivity to punishment (SP) in anxiety (2012). It is a specifically designed questionnaire linking to Gray’s theory referencing the SR to the BAS and the SP to the BIS.

Future Research or Implications

As mentioned previously, psychological disorders have been analysed in terms of the behavioural inhibition and activation systems. Understanding the differences between the systems may relate to an understanding of different types of disorders that involve anxiety and impulsivity. To date, there are many types of anxiety disorders that deal with avoidance theories and future research could show that the behavioural activation system plays a large role in such disorders and may have future implications for treatment of patients.

What is Conduct Disorder?

Introduction

Conduct disorder (CD) is a mental disorder diagnosed in childhood or adolescence that presents itself through a repetitive and persistent pattern of behaviour that includes theft, lies, physical violence that may lead to destruction and wanton breaking of rules, in which the basic rights of others or major age-appropriate norms are violated.

These behaviours are often referred to as “antisocial behaviours.” It is often seen as the precursor to antisocial personality disorder, which is per definition not diagnosed until the individual is 18 years old. Conduct disorder may result from parental rejection and neglect and can be treated with family therapy, as well as behavioural modifications and pharmacotherapy. Conduct disorder is estimated to affect 51.1 million people globally as of 2013.

Signs and Symptoms

One of the symptoms of conduct disorder is a lower level of fear. Research performed on the impact of toddlers exposed to fear and distress shows that negative emotionality (fear) predicts toddlers’ empathy-related response to distress. The findings support that if a caregiver is able to respond to infant cues, the toddler has a better ability to respond to fear and distress. If a child does not learn how to handle fear or distress the child will be more likely to lash out at other children. If the caregiver is able to provide therapeutic intervention teaching children at risk better empathy skills, the child will have a lower incident level of conduct disorder.

Increased instances of violent and antisocial behaviour are also associated with the condition; examples may range from pushing, hitting and biting when the child is young, progressing towards beating and inflicted cruelty as the child becomes older.

Conduct disorder can present with limited prosocial emotions, lack of remorse or guilt, lack of empathy, lack of concern for performance, and shallow or deficient affect. Symptoms vary by individual, but the four main groups of symptoms are described below.

Aggression to People and Animals

  • Often bullies, threatens or intimidates others.
  • Often initiates physical fights.
  • Has used a weapon that can cause serious physical harm to others (e.g., a bat, brick, broken bottle, knife, gun).
  • Has been physically cruel to people.
  • Has been physically cruel to animals.
  • Has stolen while confronting a victim (e.g. mugging, purse snatching, extortion, armed robbery).
  • Has forced someone into sexual activity (rape or molestation).
  • Feels no remorse or empathy towards the harm, fear, or pain they may have inflicted on others.

Destruction of Property

  • Has deliberately engaged in fire setting with the intention of causing serious damage.
  • Has deliberately destroyed others’ property (other than by fire setting).

Deceitfulness or Theft

  • Has broken into someone else’s house, building, or car.
  • Often lies to obtain goods or favours or to avoid obligations (i.e. “cons” others).
  • Has stolen items of nontrivial value without confronting a victim (e.g. shoplifting, but without breaking and entering; forgery).

Serious Violations of Rules

  • Often stays out at night despite parental prohibitions, beginning before age 13 years.
  • Has run away from home overnight at least twice while living in parental or parental surrogate home (or once without returning for a lengthy period).
  • Is often truant from school, beginning before age 13 years.

The lack of empathy these individuals have and the aggression that accompanies this carelessness for the consequences is dangerous – not only for the individual but for those around them.

Developmental Course

Currently, two possible developmental courses are thought to lead to conduct disorder. The first is known as the “childhood-onset type” and occurs when conduct disorder symptoms are present before the age of 10 years. This course is often linked to a more persistent life course and more pervasive behaviours. Specifically, children in this group have greater levels of ADHD symptoms, neuropsychological deficits, more academic problems, increased family dysfunction and higher likelihood of aggression and violence.

There is debate among professionals regarding the validity and appropriateness of diagnosing young children with conduct disorder. The characteristics of the diagnosis are commonly seen in young children who are referred to mental health professionals. A premature diagnosis made in young children, and thus labelling and stigmatising an individual, may be inappropriate. It is also argued that some children may not in fact have conduct disorder, but are engaging in developmentally appropriate disruptive behaviour.

The second developmental course is known as the “adolescent-onset type” and occurs when conduct disorder symptoms are present after the age of 10 years. Individuals with adolescent-onset conduct disorder exhibit less impairment than those with the childhood-onset type and are not characterised by similar psychopathology. At times, these individuals will remit in their deviant patterns before adulthood. Research has shown that there is a greater number of children with adolescent-onset conduct disorder than those with childhood-onset, suggesting that adolescent-onset conduct disorder is an exaggeration of developmental behaviours that are typically seen in adolescence, such as rebellion against authority figures and rejection of conventional values. However, this argument is not established and empirical research suggests that these subgroups are not as valid as once thought.

In addition to these two courses that are recognised by the DSM, there appears to be a relationship among oppositional defiant disorder, conduct disorder, and antisocial personality disorder. Specifically, research has demonstrated continuity in the disorders such that conduct disorder is often diagnosed in children who have been previously diagnosed with oppositional defiant disorder, and most adults with antisocial personality disorder were previously diagnosed with conduct disorder. For example, some research has shown that 90% of children diagnosed with conduct disorder had a previous diagnosis of oppositional defiant disorder. Moreover, both disorders share relevant risk factors and disruptive behaviours, suggesting that oppositional defiant disorder (ODD) is a developmental precursor and milder variant of conduct disorder. However, this is not to say that this trajectory occurs in all individuals. In fact, only about 25% of children with oppositional defiant disorder will receive a later diagnosis of conduct disorder. Correspondingly, there is an established link between conduct disorder and the diagnosis of antisocial personality disorder as an adult. In fact, the current diagnostic criteria for antisocial personality disorder require a conduct disorder diagnosis before the age of 15. However, again, only 25-40% of youths with conduct disorder will develop an antisocial personality disorder. Nonetheless, many of the individuals who do not meet full criteria for antisocial personality disorder still exhibit a pattern of social and personal impairments or antisocial behaviours. These developmental trajectories suggest the existence of antisocial pathways in certain individuals, which have important implications for both research and treatment.

Associated Conditions

Children with conduct disorder have a high risk of developing other adjustment problems. Specifically, risk factors associated with conduct disorder and the effects of conduct disorder symptomatology on a child’s psychosocial context have been linked to overlapping with other psychological disorders. In this way, there seems to be reciprocal effects of comorbidity with certain disorders, leading to increased overall risk for these youth.

Attention Deficit Hyperactivity Disorder

ADHD is the condition most commonly associated with conduct disorders, with approximately 25-30% of boys and 50-55% of girls with conduct disorder having a comorbid ADHD diagnosis. While it is unlikely that ADHD alone is a risk factor for developing conduct disorder, children who exhibit hyperactivity and impulsivity along with aggression is associated with the early onset of conduct problems. Moreover, children with comorbid conduct disorder and ADHD show more severe aggression.

Substance Use Disorders

Conduct disorder is also highly associated with both substance use and abuse. Children with conduct disorder have an earlier onset of substance use, as compared to their peers, and also tend to use multiple substances. However, substance use disorders themselves can directly or indirectly cause conduct disorder like traits in about half of adolescents who have a substance use disorder. As mentioned above, it seems that there is a transactional relationship between substance use and conduct problems, such that aggressive behaviours increase substance use, which leads to increased aggressive behaviour.

Substance use in conduct disorder can lead to antisocial behaviour in adulthood.

Schizophrenia

Conduct disorder is a precursor to schizophrenia in a minority of cases, with about 40% of men and 31% of women with schizophrenia meeting criteria for childhood conduct disorder.

Cause

While the cause of conduct disorder is complicated by an intricate interplay of biological and environmental factors, identifying underlying mechanisms is crucial for obtaining accurate assessment and implementing effective treatment. These mechanisms serve as the fundamental building blocks on which evidence-based treatments are developed. Despite the complexities, several domains have been implicated in the development of conduct disorder including cognitive variables, neurological factors, intraindividual factors, familial and peer influences, and wider contextual factors. These factors may also vary based on the age of onset, with different variables related to early (e.g. neurodevelopmental basis) and adolescent (e.g. social/peer relationships) onset.

Risks

The development of conduct disorder is not immutable or predetermined. A number of interactive risk and protective factors exist that can influence and change outcomes, and in most cases conduct disorder develops due to an interaction and gradual accumulation of risk factors. In addition to the risk factors identified under cause, several other variables place youth at increased risk for developing the disorder, including child physical abuse, in-utero alcohol exposure, and maternal smoking during pregnancy. Protective factors have also been identified, and most notably include high IQ, being female, positive social orientations, good coping skills, and supportive family and community relationships.

However, a correlation between a particular risk factor and a later developmental outcome (such as conduct disorder) cannot be taken as definitive evidence for a causal link. Co-variation between two variables can arise, for instance, if they represent age-specific expressions of similar underlying genetic factors. For example, the tendency to smoke during pregnancy (SDP) is subject to substantial genetic influence, as is conduct disorder. Thus, the genes that dispose the mother to SDP may also dispose the child to CD following mitotic transmission. Indeed, Rice et al. (2009) found that in mother-fetus pairs that were not genetically related (by virtue of in-vitro fertilisation), no link between SDP and later conduct problems arose. Thus, the distinction between causality and correlation is an important consideration.

Learning Disabilities

While language impairments are most common, approximately 20-25% of youth with conduct disorder have some type of learning disability. Although the relationship between the disorders is complex, it seems as if learning disabilities result from a combination of ADHD, a history of academic difficulty and failure, and long-standing socialisation difficulties with family and peers. However, confounding variables, such as language deficits, SES disadvantage, or neurodevelopmental delay also need to be considered in this relationship, as they could help explain some of the association between conduct disorder and learning problems.

Cognitive Factors

In terms of cognitive function, intelligence and cognitive deficits are common amongst youths with conduct disorder, particularly those with early-onset and have intelligence quotients (IQ) one standard deviation below the mean and severe deficits in verbal reasoning and executive function. Executive function difficulties may manifest in terms of one’s ability to shift between tasks, plan as well as organise, and also inhibit a prepotent response. These findings hold true even after taking into account other variables such as socioeconomic status (SES), and education. However, IQ and executive function deficits are only one piece of the puzzle, and the magnitude of their influence is increased during transactional processes with environmental factors.

Brain Differences

Beyond difficulties in executive function, neurological research on youth with conduct disorder also demonstrate differences in brain anatomy and function that reflect the behaviours and mental anomalies associated in conduct disorder. Compared to normal controls, youths with early and adolescent onset of conduct disorder displayed reduced responses in brain regions associated with social behaviour (i.e. amygdala, ventromedial prefrontal cortex, insula, and orbitofrontal cortex). In addition, youths with conduct disorder also demonstrated less responsiveness in the orbitofrontal regions of the brain during a stimulus-reinforcement and reward task. This provides a neural explanation for why youths with conduct disorder may be more likely to repeat poor decision making patterns. Lastly, youths with conduct disorder display a reduction in grey matter volume in the amygdala, which may account for the fear conditioning deficits. This reduction has been linked to difficulty processing social emotional stimuli, regardless of the age of onset. Aside from the differences in neuroanatomy and activation patterns between youth with conduct disorder and controls, neurochemical profiles also vary between groups. Individuals with conduct disorder are characterised as having reduced serotonin and cortisol levels (e.g. reduced hypothalamic-pituitary-adrenal (HPA) axis), as well as reduced autonomic nervous system (ANS) functioning. These reductions are associated with the inability to regulate mood and impulsive behaviours, weakened signals of anxiety and fear, and decreased self-esteem. Taken together, these findings may account for some of the variance in the psychological and behavioural patterns of youth with conduct disorder.

Intra-Individual Factors

Aside from findings related to neurological and neurochemical profiles of youth with conduct disorder, intraindividual factors such as genetics may also be relevant. Having a sibling or parent with conduct disorder increases the likelihood of having the disorder, with a heritability rate of .53. There also tends to be a stronger genetic link for individuals with childhood-onset compared to adolescent onset. In addition, youth with conduct disorder also exhibit polymorphism in the monoamine oxidase A gene, low resting heart rates, and increased testosterone.

Family and Peer Influences

Elements of the family and social environment may also play a role in the development and maintenance of conduct disorder. For instance, antisocial behaviour suggestive of conduct disorder is associated with single parent status, parental divorce, large family size, and the young age of mothers. However, these factors are difficult to tease apart from other demographic variables that are known to be linked with conduct disorder, including poverty and low socioeconomic status. Family functioning and parent-child interactions also play a substantial role in childhood aggression and conduct disorder, with low levels of parental involvement, inadequate supervision, and unpredictable discipline practices reinforcing youth’s defiant behaviours. Peer influences have also been related to the development of antisocial behaviour in youth, particularly peer rejection in childhood and association with deviant peers. Peer rejection is not only a marker of a number of externalizing disorders, but also a contributing factor for the continuity of the disorders over time. Hinshaw and Lee (2003) also explain that association with deviant peers has been thought to influence the development of conduct disorder in two ways: 1) a “selection” process whereby youth with aggressive characteristics choose deviant friends, and 2) a “facilitation” process whereby deviant peer networks bolster patterns of antisocial behaviour. In a separate study by Bonin and colleagues, parenting programmes were shown to positively affect child behaviour and reduce costs to the public sector.

Wider Contextual Factors

In addition to the individual and social factors associated with conduct disorder, research has highlighted the importance of environment and context in youth with antisocial behaviour. However, it is important to note that these are not static factors, but rather transactional in nature (e.g. individuals are influenced by and also influence their environment). For instance, neighbourhood safety and exposure to violence have been studied in conjunction with conduct disorder, but it is not simply the case that youth with aggressive tendencies reside in violent neighbourhoods. Transactional models propose that youth may resort to violence more often as a result of exposure to community violence, but their predisposition towards violence also contributes to neighbourhood climate.

Diagnosis

Conduct disorder is classified in the fourth edition of Diagnostic and Statistical Manual of Mental Disorders (DSM). It is diagnosed based on a prolonged pattern of antisocial behaviour such as serious violation of laws and social norms and rules in people younger than the age of 18. Similar criteria are used in those over the age of 18 for the diagnosis of antisocial personality disorder. No proposed revisions for the main criteria of conduct disorder exist in the DSM-5; there is a recommendation by the work group to add an additional specifier for callous and unemotional traits. According to DSM-5 criteria for conduct disorder, there are four categories that could be present in the child’s behaviour: aggression to people and animals, destruction of property, deceitfulness or theft, and serious violation of rules.

Almost all adolescents who have a substance use disorder have conduct disorder-like traits, but after successful treatment of the substance use disorder, about half of these adolescents no longer display conduct disorder-like symptoms. Therefore, it is important to exclude a substance-induced cause and instead address the substance use disorder prior to making a psychiatric diagnosis of conduct disorder.

Treatment

First-line treatment is psychotherapy based on behaviour modification and problem-solving skills. This treatment seeks to integrate individual, school, and family settings. Parent-management training can also be helpful. No medications have been FDA approved for Conduct Disorder, but Risperidone (a second-generation antipsychotic) has the most evidence to support its use for aggression in children who have not responded to behavioural and psychosocial interventions. Selective Serotonin Reuptake Inhibitors (SSRIs) are also sometimes used to treat irritability in these patients.

Prognosis

About 25-40% of youths diagnosed with conduct disorder qualify for a diagnosis of antisocial personality disorder when they reach adulthood. For those that do not develop ASPD, most still exhibit social dysfunction in adult life.

Epidemiology

Conduct disorder is estimated to affect 51.1 million people globally as of 2013. The percentage of children affected by conduct disorder is estimated to range from 1-10%. However, among incarcerated youth or youth in juvenile detention facilities, rates of conduct disorder are between 23% and 87%.

Sex Differences

The majority of research on conduct disorder suggests that there are a significantly greater number of males than females with the diagnosis, with some reports demonstrating a threefold to fourfold difference in prevalence. However, this difference may be somewhat biased by the diagnostic criteria which focus on more overt behaviours, such as aggression and fighting, which are more often exhibited by males. Females are more likely to be characterised by covert behaviours, such as stealing or running away. Moreover, conduct disorder in females is linked to several negative outcomes, such as antisocial personality disorder and early pregnancy, suggesting that sex differences in disruptive behaviours need to be more fully understood.

Females are more responsive to peer pressure including feelings of guilt than males.

Racial Differences

Research on racial or cultural differences on the prevalence or presentation of conduct disorder is limited. However, according to studies on American youth, it appears that African-American youth are more often diagnosed with conduct disorder, while Asian-American youth are about one-third as likely to develop conduct disorder when compared to White American youth. It has been widely theorised for decades that this disparity is due to unconscious bias in those who give the diagnosis.

What is Neuropsychology?

Introduction

Neuropsychology is a branch of psychology that is concerned with how a person’s cognition and behaviour are related to the brain and the rest of the nervous system. Professionals in this branch of psychology often focus on how injuries or illnesses of the brain affect cognitive and behavioural functions.

It is both an experimental and clinical field of psychology, thus aiming to understand how behaviour and cognition are influenced by brain function and concerned with the diagnosis and treatment of behavioural and cognitive effects of neurological disorders. Whereas classical neurology focuses on the pathology of the nervous system and classical psychology is largely divorced from it, neuropsychology seeks to discover how the brain correlates with the mind through the study of neurological patients. It thus shares concepts and concerns with neuropsychiatry and with behavioural neurology in general. The term neuropsychology has been applied to lesion studies in humans and animals. It has also been applied in efforts to record electrical activity from individual cells (or groups of cells) in higher primates (including some studies of human patients).

In practice, neuropsychologists tend to work in research settings (universities, laboratories or research institutions), clinical settings (medical hospitals or rehabilitation settings, often involved in assessing or treating patients with neuropsychological problems), or forensic settings or industry (often as clinical-trial consultants where CNS function is a concern).

Brief History

Neuropsychology is a relatively new discipline within the field of psychology. The first textbook defining the field, Fundamentals of Human Neuropsychology, was initially published by Kolb and Whishaw in 1980. However, the history of its development can be traced back to the Third Dynasty in ancient Egypt, perhaps even earlier. There is much debate as to when societies started considering the functions of different organs. For many centuries, the brain was thought useless and was often discarded during burial processes and autopsies. As the field of medicine developed its understanding of human anatomy and physiology, different theories were developed as to why the body functioned the way it did. Many times, bodily functions were approached from a religious point of view and abnormalities were blamed on bad spirits and the gods. The brain has not always been considered the centre of the functioning body. It has taken hundreds of years to develop our understanding of the brain and how it affects our behaviours.

Ancient Egypt

In ancient Egypt, writings on medicine date from the time of the priest Imhotep. They took a more scientific approach to medicine and disease, describing the brain, trauma, abnormalities, and remedies for reference for future physicians. Despite this, Egyptians saw the heart, not the brain, as the seat of the soul.

Aristotle

Aristotle reinforced this focus on the heart which originated in Egypt. He believed the heart to be in control of mental processes, and looked on the brain, due to its inert nature, as a mechanism for cooling the heat generated by the heart. He drew his conclusions based on the empirical study of animals. He found that while their brains were cold to the touch and that such contact did not trigger any movements, the heart was warm and active, accelerating and slowing dependent on mood. Such beliefs were upheld by many for years to come, persisting through the Middle Ages and the Renaissance period until they began to falter in the 17th century due to further research. The influence of Aristotle in the development of neuropsychology is evident within language used in modern day, since we “follow our hearts” and “learn by the heart.”

Hippocrates

Hippocrates viewed the brain as the seat of the soul. He drew a connection between the brain and behaviours of the body, writing: “The brain exercises the greatest power in the man.” Apart from moving the focus from the heart as the “seat of the soul” to the brain, Hippocrates did not go into much detail about its actual functioning. However, by switching the attention of the medical community to the brain, his theory led to more scientific discovery of the organ responsible for our behaviours. For years to come, scientists were inspired to explore the functions of the body and to find concrete explanations for both normal and abnormal behaviours. Scientific discovery led them to believe that there were natural and organically occurring reasons to explain various functions of the body, and it could all be traced back to the brain. Hippocrates introduced the concept of the mind – which was widely seen as a separate function apart from the actual brain organ.

René Descartes

Philosopher René Descartes expanded upon this idea and is most widely known for his work on the mind-body problem. Often Descartes’s ideas were looked upon as overly philosophical and lacking in sufficient scientific foundation. Descartes focused much of his anatomical experimentation on the brain, paying special attention to the pineal gland – which he argued was the actual “seat of the soul.” Still deeply rooted in a spiritual outlook towards the scientific world, the body was said to be mortal, and the soul immortal. The pineal gland was then thought to be the very place at which the mind would interact with the mortal and machine-like body. At the time, Descartes was convinced the mind had control over the behaviours of the body (controlling the person) – but also that the body could have influence over the mind, which is referred to as dualism. This idea that the mind essentially had control over the body, but the body could resist or even influence other behaviours, was a major turning point in the way many physiologists would look at the brain. The capabilities of the mind were observed to do much more than simply react, but also to be rational and function in organised, thoughtful ways – much more complex than he thought the animal world to be. These ideas, although disregarded by many and cast aside for years led the medical community to expand their own ideas of the brain and begin to understand in new ways just how intricate the workings of the brain really were, and the complete effects it had on daily life, as well as which treatments would be the most beneficial to helping those people living with a dysfunctional mind. The mind-body problem, spurred by René Descartes, continues to this day with many philosophical arguments both for and against his ideas. However controversial they were and remain today, the fresh and well-thought-out perspective Descartes presented has had long-lasting effects on the various disciplines of medicine, psychology and much more, especially in putting an emphasis on separating the mind from the body in order to explain observable behaviours.

Thomas Willis

It was in the mid-17th century that another major contributor to the field of neuropsychology emerged. Thomas Willis studied at Oxford University and took a physiological approach to the brain and behaviour. It was Willis who coined the words ‘hemisphere’ and ‘lobe’ when referring to the brain. He was one of the earliest to use the words ‘neurology’ and ‘psychology’. Rejecting the idea that humans were the only beings capable of rational thought, Willis looked at specialised structures of the brain. He theorised that higher structures accounted for complex functions, whereas lower structures were responsible for functions similar to those seen in other animals, consisting mostly of reactions and automatic responses. He was particularly interested in people who suffered from manic disorders and hysteria. His research constituted some of the first times that psychiatry and neurology came together to study individuals. Through his in-depth study of the brain and behaviour, Willis concluded that automated responses such as breathing, heartbeats and other various motor activities were carried out within the lower region of the brain. Although much of his work has been made obsolete, his ideas presented the brain as more complex than previously imagined, and led the way for future pioneers to understand and build upon his theories, especially when it came to looking at disorders and dysfunctions in the brain.

Franz Joseph Gall

Neuroanatomist and physiologist Franz Joseph Gall made major progress in understanding the brain. He theorized that personality was directly related to features and structures within the brain. However, Gall’s major contribution within the field of neuroscience is his invention of phrenology. This new discipline looked at the brain as an organ of the mind, where the shape of the skull could ultimately determine one’s intelligence and personality. This theory was like many circulating at the time, as many scientists were taking into account physical features of the face and body, head size, anatomical structure, and levels of intelligence; only Gall looked primarily at the brain. There was much debate over the validity of Gall’s claims however, because he was often found to be wrong in his predictions. He was once sent a cast of René Descartes’ skull, and through his method of phrenology claimed the subject must have had a limited capacity for reasoning and higher cognition. As controversial and false as many of Gall’s claims were, his contributions to understanding cortical regions of the brain and localised activity continued to advance understanding of the brain, personality, and behaviour. His work is considered crucial to having laid a firm foundation in the field of neuropsychology, which would flourish over the next few decades.

Jean-Baptiste Bouillaud

Towards the late 19th century, the belief that the size of ones skull could determine their level of intelligence was discarded as science and medicine moved forward. A physician by the name of Jean-Baptiste Bouillaud expanded upon the ideas of Gall and took a closer look at the idea of distinct cortical regions of the brain each having their own independent function. Bouillaud was specifically interested in speech and wrote many publications on the anterior region of the brain being responsible for carrying out the act of ones speech, a discovery that had stemmed from the research of Gall. He was also one of the first to use larger samples for research although it took many years for that method to be accepted. By looking at over a hundred different case studies, Bouillaud came to discover that it was through different areas of the brain that speech is completed and understood. By observing people with brain damage, his theory was made more concrete. Bouillaud, along with many other pioneers of the time made great advances within the field of neurology, especially when it came to localisation of function. There are many arguable debates as to who deserves the most credit for such discoveries, and often, people remain unmentioned, but Paul Broca is perhaps one of the most famous and well known contributors to neuropsychology – often referred to as “the father” of the discipline.

Paul Broca

Inspired by the advances being made in the area of localised function within the brain, Paul Broca committed much of his study to the phenomena of how speech is understood and produced. Through his study, it was discovered and expanded upon that we articulate via the left hemisphere. Broca’s observations and methods are widely considered to be where neuropsychology really takes form as a recognisable and respected discipline. Armed with the understanding that specific, independent areas of the brain are responsible for articulation and understanding of speech, the brains abilities were finally being acknowledged as the complex and highly intricate organ that it is. Broca was essentially the first to fully break away from the ideas of phrenology and delve deeper into a more scientific and psychological view of the brain.

Karl Spencer Lashley

Lashley’s works and theories that follow are summarised in his book Brain Mechanisms and Intelligence. Lashley’s theory of the Engram was the driving force for much of his research. An engram was believed to be a part of the brain where a specific memory was stored. He continued to use the training/ablation method that Franz had taught him. He would train a rat to learn a maze and then use systematic lesions and removed sections of cortical tissue to see if the rat forgot what it had learned.

Through his research with the rats, he learned that forgetting was dependent on the amount of tissue removed and not where it was removed from. He called this mass action and he believed that it was a general rule that governed how brain tissue would respond, independent of the type of learning. But we know now that mass action was a misinterpretation of his empirical results, because in order to run a maze the rats required multiple cortical areas. Cutting into small individual parts alone will not impair the rats’ brains much, but taking large sections removes multiple cortical areas at one time, affecting various functions such as sight, motor coordination and memory, making the animal unable to run a maze properly.

Lashley also proposed that a portion of a functional area could carry out the role of the entire area, even when the rest of the area has been removed. He called this phenomenon equipotentiality. We know now that he was seeing evidence of plasticity in the brain: within certain constraints the brain has the ability for certain areas to take over the functions of other areas if those areas should fail or be removed – although not to the extent initially argued by Lashley.

Approaches

Experimental neuropsychology is an approach that uses methods from experimental psychology to uncover the relationship between the nervous system and cognitive function. The majority of work involves studying healthy humans in a laboratory setting, although a minority of researchers may conduct animal experiments. Human work in this area often takes advantage of specific features of our nervous system (for example that visual information presented to a specific visual field is preferentially processed by the cortical hemisphere on the opposite side) to make links between neuroanatomy and psychological function.

Clinical neuropsychology is the application of neuropsychological knowledge to the assessment (see neuropsychological test and neuropsychological assessment), management, and rehabilitation of people who have suffered illness or injury (particularly to the brain) which has caused neurocognitive problems. In particular they bring a psychological viewpoint to treatment, to understand how such illness and injury may affect and be affected by psychological factors. They also can offer an opinion as to whether a person is demonstrating difficulties due to brain pathology or as a consequence of an emotional or another (potentially) reversible cause or both. For example, a test might show that both patients X and Y are unable to name items that they have been previously exposed to within the past 20 minutes (indicating possible dementia). If patient Y can name some of them with further prompting (e.g. given a categorical clue such as being told that the item they could not name is a fruit), this allows a more specific diagnosis than simply dementia (Y appears to have the vascular type which is due to brain pathology but is usually at least somewhat reversible). Clinical neuropsychologists often work in hospital settings in an interdisciplinary medical team; others work in private practice and may provide expert input into medico-legal proceedings.

Cognitive neuropsychology is a relatively new development and has emerged as a distillation of the complementary approaches of both experimental and clinical neuropsychology. It seeks to understand the mind and brain by studying people who have suffered brain injury or neurological illness. One model of neuropsychological functioning is known as functional localisation. This is based on the principle that if a specific cognitive problem can be found after an injury to a specific area of the brain, it is possible that this part of the brain is in some way involved. However, there may be reason to believe that the link between mental functions and neural regions is not so simple. An alternative model of the link between mind and brain, such as parallel processing, may have more explanatory power for the workings and dysfunction of the human brain. Yet another approach investigates how the pattern of errors produced by brain-damaged individuals can constrain our understanding of mental representations and processes without reference to the underlying neural structure. A more recent but related approach is cognitive neuropsychiatry which seeks to understand the normal function of mind and brain by studying psychiatric or mental illness.

Connectionism is the use of artificial neural networks to model specific cognitive processes using what are considered to be simplified but plausible models of how neurons operate. Once trained to perform a specific cognitive task these networks are often damaged or ‘lesioned’ to simulate brain injury or impairment in an attempt to understand and compare the results to the effects of brain injury in humans.

Functional neuroimaging uses specific neuroimaging technologies to take readings from the brain, usually when a person is doing a particular task, in an attempt to understand how the activation of particular brain areas is related to the task. In particular, the growth of methodologies to employ cognitive testing within established functional magnetic resonance imaging (fMRI) techniques to study brain-behaviour relations is having a notable influence on neuropsychological research.

In practice these approaches are not mutually exclusive and most neuropsychologists select the best approach or approaches for the task to be completed.

Methods and Tools

Standardised Neuropsychological Tests

These tasks have been designed so the performance on the task can be linked to specific neurocognitive processes. These tests are typically standardised, meaning that they have been administered to a specific group (or groups) of individuals before being used in individual clinical cases. The data resulting from standardisation are known as normative data. After these data have been collected and analysed, they are used as the comparative standard against which individual performances can be compared. Examples of neuropsychological tests include: the Wechsler Memory Scale (WMS), the Wechsler Adult Intelligence Scale (WAIS), Boston Naming Test, the Wisconsin Card Sorting Test, the Benton Visual Retention Test, and the Controlled Oral Word Association.

Brain Scans

The use of brain scans to investigate the structure or function of the brain is common, either as simply a way of better assessing brain injury with high resolution pictures, or by examining the relative activations of different brain areas. Such technologies may include fMRI (functional magnetic resonance imaging) and positron emission tomography (PET), which yields data related to functioning, as well as MRI (magnetic resonance imaging) and computed axial tomography (CAT or CT), which yields structural data.

Global Brain Project

Brain models based on mouse and monkey have been developed based on theoretical neuroscience involving working memory and attention, while mapping brain activity based on time constants validated by measurements of neuronal activity in various layers of the brain. These methods also map to decision states of behaviour in simple tasks that involve binary outcomes.

Electrophysiology

The use of electrophysiological measures designed to measure the activation of the brain by measuring the electrical or magnetic field produced by the nervous system. This may include electroencephalography (EEG) or magneto-encephalography (MEG).

Experimental Tasks

The use of designed experimental tasks, often controlled by computer and typically measuring reaction time and accuracy on a particular tasks thought to be related to a specific neurocognitive process. An example of this is the Cambridge Neuropsychological Test Automated Battery (CANTAB) or CNS Vital Signs (CNSVS).

What is Antisocial Personality Disorder?

Introduction

Antisocial personality disorder (ASPD or infrequently APD) is a personality disorder characterised by a long-term pattern of disregard for, or violation of, the rights of others. A weak or non-existent conscience is often apparent, as well as a history of legal problems or impulsive and aggressive behaviour.

Antisocial personality disorder is defined in the Diagnostic and Statistical Manual of Mental Disorders (DSM), while the equivalent concept of dissocial personality disorder (DPD) is defined in the International Statistical Classification of Diseases and Related Health Problems (ICD); the primary theoretical distinction between the two is that antisocial personality disorder focuses on observable behaviours, while dissocial personality disorder focuses on affective deficits. Otherwise, both manuals provide similar criteria for diagnosing the disorder. Both have also stated that their diagnoses have been referred to, or include what is referred to, as psychopathy or sociopathy. However, some researchers have drawn distinctions between the concepts of antisocial personality disorder and psychopathy, with many researchers arguing that psychopathy is a disorder that overlaps with but is distinguishable from ASPD.

Brief History

The first version of the DSM in 1952 listed sociopathic personality disturbance. This category was for individuals who were considered “…ill primarily in terms of society and of conformity with the prevailing milieu, and not only in terms of personal discomfort and relations with other individuals”. There were four subtypes, referred to as “reactions”: antisocial, dyssocial, sexual, and addiction. The antisocial reaction was said to include people who were “always in trouble” and not learning from it, maintaining “no loyalties”, frequently callous and lacking responsibility, with an ability to “rationalise” their behaviour. The category was described as more specific and limited than the existing concepts of “constitutional psychopathic state” or “psychopathic personality” which had had a very broad meaning; the narrower definition was in line with criteria advanced by Hervey M. Cleckley from 1941, while the term sociopathic had been advanced by George Partridge in 1928 when studying the early environmental influence on psychopaths. Partridge discovered the correlation between antisocial psychopathic disorder and parental rejection experienced in early childhood.

The DSM-II in 1968 rearranged the categories and “antisocial personality” was now listed as one of ten personality disorders but still described similarly, to be applied to individuals who are: “basically unsocialised”, in repeated conflicts with society, incapable of significant loyalty, selfish, irresponsible, unable to feel guilt or learn from prior experiences, and who tend to blame others and rationalise. The manual preface contains “special instructions” including “Antisocial personality should always be specified as mild, moderate, or severe.” The DSM-II warned that a history of legal or social offenses was not by itself enough to justify the diagnosis, and that a “group delinquent reaction” of childhood or adolescence or “social maladjustment without manifest psychiatric disorder” should be ruled out first. The dyssocial personality type was relegated in the DSM-II to “dyssocial behaviour” for individuals who are predatory and follow more or less criminal pursuits, such as racketeers, dishonest gamblers, prostitutes, and dope peddlers. (DSM-I classified this condition as sociopathic personality disorder, dyssocial type). It would later resurface as the name of a diagnosis in the ICD manual produced by the WHO, later spelled dissocial personality disorder and considered approximately equivalent to the ASPD diagnosis.

The DSM-III in 1980 included the full term antisocial personality disorder and, as with other disorders, there was now a full checklist of symptoms focused on observable behaviours to enhance consistency in diagnosis between different psychiatrists (‘inter-rater reliability’). The ASPD symptom list was based on the Research Diagnostic Criteria developed from the so-called Feighner Criteria from 1972, and in turn largely credited to influential research by sociologist Lee Robins published in 1966 as “Deviant Children Grown Up”. However, Robins has previously clarified that while the new criteria of prior childhood conduct problems came from her work, she and co-researcher psychiatrist Patricia O’Neal got the diagnostic criteria they used from Lee’s husband the psychiatrist Eli Robins, one of the authors of the Feighner criteria who had been using them as part of diagnostic interviews.

The DSM-IV maintained the trend for behavioural antisocial symptoms while noting “This pattern has also been referred to as psychopathy, sociopathy, or dyssocial personality disorder” and re-including in the ‘Associated Features’ text summary some of the underlying personality traits from the older diagnoses. The DSM-5 has the same diagnosis of antisocial personality disorder. The Pocket Guide to the DSM-5 Diagnostic Exam suggests that a person with ASPD may present “with psychopathic features” if he or she exhibits “a lack of anxiety or fear and a bold, efficacious interpersonal style”.

Epidemiology

As seen in two North American studies and two European studies, ASPD is more commonly seen in men than in women, with men three to five times more likely to be diagnosed with ASPD than women. The prevalence of ASPD is even higher in selected populations, like prisons, where there is a preponderance of violent offenders. It has been found that the prevalence of ASPD among prisoners is just under 50%. Similarly, the prevalence of ASPD is higher among patients in alcohol or other drug (AOD) use treatment programmes than in the general population, suggesting a link between ASPD and AOD use and dependence. As part of the Epidemiological Catchment Area (ECA) study, men with ASPD were found to be three to five times more likely to excessively use alcohol and illicit substances than those men without ASPD. While ASPD occurs more often in men than women, there was found to be increased severity of this substance use in women with ASPD. In a study conducted with both men and women with ASPD, women were more likely to misuse substances compared to their male counterparts.

Individuals with ASPD are at an elevated risk for suicide. Some studies suggest this increase in suicidality is in part due to the association between suicide and symptoms or trends within ASPD, such as criminality and substance use. Offspring of ASPD victims are also at risk. Some research suggests that negative or traumatic experiences in childhood, perhaps as a result of the choices a parent with ASPD might make, can be a predictor of delinquency later on in the child’s life. Additionally, with variability between situations, children of a parent with ASPD may suffer consequences of delinquency if they’re raised in an environment in which crime and violence is common. Suicide is a leading cause of death among youth who display antisocial behaviour, especially when mixed with delinquency. Incarceration, which could come as a consequence of actions from a victim of ASPD, is a predictor for suicide ideation in youth.

Signs and Symptoms

Antisocial personality disorder is defined by a pervasive and persistent disregard for morals, social norms, and the rights and feelings of others. Individuals with this personality disorder will typically have no compunction in exploiting others in harmful ways for their own gain or pleasure and frequently manipulate and deceive other people. While some do so through a façade of superficial charm, others do so through intimidation and violence. They may display arrogance, think lowly and negatively of others, and lack remorse for their harmful actions and have a callous attitude to those they have harmed. Irresponsibility is a core characteristic of this disorder; most have significant difficulties in maintaining stable employment as well as fulfilling their social and financial obligations, and people with this disorder often lead exploitative, unlawful, or parasitic lifestyles.

Those with antisocial personality disorder are often impulsive and reckless, failing to consider or disregarding the consequences of their actions. They may repeatedly disregard and jeopardise their own safety and the safety of others, which can place both themselves and other people in danger. They are often aggressive and hostile, with poorly regulated tempers, and can lash out violently with provocation or frustration. Individuals are prone to substance use disorders and addiction, and the non-medical use of various psychoactive substances is common in this population. These behaviours lead such individuals into frequent conflict with the law, and many people with ASPD have extensive histories of antisocial behaviour and criminal infractions stemming back to adolescence or childhood.

Serious problems with interpersonal relationships are often seen in those with the disorder. People with antisocial personality disorder usually form poor attachments and emotional bonds, and interpersonal relationships often revolve around the exploitation and abuse of others. They may have difficulties in sustaining and maintaining relationships, and some have difficulty entering them.

Conduct Disorder

While antisocial personality disorder is a mental disorder diagnosed in adulthood, it has its precedent in childhood. The DSM-5’s criteria for ASPD require that the individual have conduct problems evident by the age of 15. Persistent antisocial behaviour, as well as a lack of regard for others in childhood and adolescence, is known as conduct disorder and is the precursor of ASPD. About 25-40% of youths with conduct disorder will be diagnosed with ASPD in adulthood.

Conduct disorder (CD) is a disorder diagnosed in childhood that parallels the characteristics found in ASPD and is characterised by a repetitive and persistent pattern of behaviour in which the basic rights of others or major age-appropriate norms are violated. Children with the disorder often display impulsive and aggressive behaviour, may be callous and deceitful, and may repeatedly engage in petty crime such as stealing or vandalism or get into fights with other children and adults. This behaviour is typically persistent and may be difficult to deter with threat or punishment. Attention deficit hyperactivity disorder (ADHD) is common in this population, and children with the disorder may also engage in substance use. CD is differentiated from oppositional defiant disorder (ODD) in that children with ODD do not commit aggressive or antisocial acts against other people, animals, and property, though many children diagnosed with ODD are subsequently re-diagnosed with CD.

Two developmental courses for CD have been identified based on the age at which the symptoms become present. The first is known as the “childhood-onset type” and occurs when conduct disorder symptoms are present before the age of 10 years. This course is often linked to a more persistent life course and more pervasive behaviours, and children in this group express greater levels of ADHD symptoms, neuropsychological deficits, more academic problems, increased family dysfunction, and higher likelihood of aggression and violence. The second is known as the “adolescent-onset type” and occurs when conduct disorder develops after the age of 10 years. Compared to the childhood-onset type, less impairment in various cognitive and emotional functions are present, and the adolescent-onset variety may remit by adulthood. In addition to this differentiation, the DSM-5 provides a specifier for a callous and unemotional interpersonal style, which reflects characteristics seen in psychopathy and are believed to be a childhood precursor to this disorder. Compared to the adolescent-onset subtype, the childhood-onset subtype, especially if callous and unemotional traits are present, tends to have a worse treatment outcome.

Comorbidity

ASPD commonly coexists with the following conditions:

  • Anxiety disorders.
  • Depressive disorder.
  • Impulse control disorders.
  • Substance-related disorders.
  • Somatization disorder.
  • Attention deficit hyperactivity disorder.
  • Bipolar disorder.
  • Borderline personality disorder.
  • Histrionic personality disorder.
  • Narcissistic personality disorder.
  • Sadistic personality disorder.

When combined with alcoholism, people may show frontal function deficits on neuropsychological tests greater than those associated with each condition. Alcohol Use Disorder is likely caused by lack of impulse and behavioural control exhibited by Antisocial Personality Disorder patients. The rates of ASPD tends to be around 40-50% in male alcohol and opiate addicts. However, it is important to remember this is not a causal relationship, but rather a plausible consequence of cognitive deficits as a result of ASPD.

Causes

Personality disorders are seen to be caused by a combination and interaction of genetic and environmental influences. Genetically, it is the intrinsic temperamental tendencies as determined by their genetically influenced physiology, and environmentally, it is the social and cultural experiences of a person in childhood and adolescence encompassing their family dynamics, peer influences, and social values. People with an antisocial or alcoholic parent are considered to be at higher risk. Fire-setting and cruelty to animals during childhood are also linked to the development of antisocial personality. The condition is more common in males than in females, and among people who are in prison.

Genetic

Research into genetic associations in antisocial personality disorder suggests that ASPD has some or even a strong genetic basis. Prevalence of ASPD is higher in people related to someone afflicted by the disorder. Twin studies, which are designed to discern between genetic and environmental effects, have reported significant genetic influences on antisocial behaviour and conduct disorder.

In the specific genes that may be involved, one gene that has seen particular interest in its correlation with antisocial behaviour is the gene that encodes for Monoamine oxidase A (MAO-A), an enzyme that breaks down monoamine neurotransmitters such as serotonin and norephinephrine. Various studies examining the genes’ relationship to behaviour have suggested that variants of the gene that results in less MAO-A being produced, such as the 2R and 3R alleles of the promoter region, have associations with aggressive behaviour in men. The association is also influenced by negative experience in early life, with children possessing a low-activity variant (MAOA-L) who experience such maltreatment being more likely to develop antisocial behaviour than those with the high-activity variant (MAOA-H). Even when environmental interactions (e.g. emotional abuse) are controlled for, a small association between MAOA-L and aggressive and antisocial behaviour remains.

The gene that encodes for the serotonin transporter (SCL6A4), a gene that is heavily researched for its associations with other mental disorders, is another gene of interest in antisocial behaviour and personality traits. Genetic associations studies have suggested that the short “S” allele is associated with impulsive antisocial behaviour and ASPD in the inmate population. However, research into psychopathy find that the long “L” allele is associated with the Factor 1 traits of psychopathy, which describes its core affective (e.g. lack of empathy, fearlessness) and interpersonal (e.g. grandiosity, manipulativeness) personality disturbances. This is suggestive of two different forms, one associated more with impulsive behaviour and emotional dysregulation, and the other with predatory aggression and affective disturbance, of the disorder.

Various other gene candidates for ASPD have been identified by a genome-wide association study published in 2016. Several of these gene candidates are shared with attention-deficit hyperactivity disorder, with which ASPD is comorbid. Furthermore, the study found that those who carry 4 mutations on chromosome 6 are 1.5 times more likely to develop antisocial personality disorder than those who do not.

Physiological

Hormones and Neurotransmitters

Traumatic events can lead to a disruption of the standard development of the central nervous system, which can generate a release of hormones that can change normal patterns of development. Aggressiveness and impulsivity are among the possible symptoms of ASPD. Testosterone is a hormone that plays an important role in aggressiveness in the brain. For instance, criminals who have committed violent crimes tend to have higher levels of testosterone than the average person. The effect of testosterone is counteracted by cortisol which facilitates the cognitive control of impulsive tendencies.

One of the neurotransmitters that has been discussed in individuals with ASPD is serotonin, also known as 5HT.[41] A meta-analysis of 20 studies found significantly lower 5-HIAA levels (indicating lower serotonin levels), especially in those who are younger than 30 years of age.

While it has been shown that lower levels of serotonin may be associated with ASPD, there has also been evidence that decreased serotonin function is highly correlated with impulsiveness and aggression across a number of different experimental paradigms. Impulsivity is not only linked with irregularities in 5HT metabolism, but may be the most essential psychopathological aspect linked with such dysfunction. Correspondingly, the DSM classifies “impulsivity or failure to plan ahead” and “irritability and aggressiveness” as two of seven sub-criteria in category A of the diagnostic criteria of ASPD.

Some studies have found a relationship between monoamine oxidase A and antisocial behaviour, including conduct disorder and symptoms of adult ASPD, in maltreated children.

Neurological

Antisocial behaviour may be related to head trauma. Antisocial behaviour is associated with decreased grey matter in the right lentiform nucleus, left insula, and frontopolar cortex. Increased volumes have been observed in the right fusiform gyrus, inferior parietal cortex, right cingulate gyrus, and post central cortex.

Intellectual and cognitive ability is consistently found to be impaired or reduced in the ASPD population. Contrary to stereotypes in popular culture of the “psychopathic genius”, antisocial personality disorder is associated with both reduced overall intelligence and specific reductions in individual aspects of cognitive ability. These deficits also occur in general-population samples of people with antisocial traits and in children with the precursors to antisocial personality disorder.

People that exhibit antisocial behaviour demonstrate decreased activity in the prefrontal cortex. The association is more apparent in functional neuroimaging as opposed to structural neuroimaging. The prefrontal cortex is involved in many executive functions, including behaviour inhibitions, planning ahead, determining consequences of action, and differentiating between right and wrong. However, some investigators have questioned whether the reduced volume in prefrontal regions is associated with antisocial personality disorder, or whether they result from co-morbid disorders, such as substance use disorder or childhood maltreatment. Moreover, it remains an open question whether the relationship is causal, i.e. whether the anatomical abnormality causes the psychological and behavioural abnormality, or vice versa.

Cavum septi pellucidi (CSP) is a marker for limbic neural maldevelopment, and its presence has been loosely associated with certain mental disorders, such as schizophrenia and post-traumatic stress disorder. One study found that those with CSP had significantly higher levels of antisocial personality, psychopathy, arrests and convictions compared with controls.

Environmental

Family Environment

Some studies suggest that the social and home environment has contributed to the development of antisocial behaviour. The parents of these children have been shown to display antisocial behaviour, which could be adopted by their children. A lack of parental stimulation and affection during early development leads to sensitization of the child’s stress response systems, which is thought to lead to underdevelopment of the child’s brain that deals with emotion, empathy and ability to connect to other humans on an emotional level. According to Dr. Bruce Perry in his book The Boy Who Was Raised as a Dog, “the [infant’s developing] brain needs patterned, repetitive stimuli to develop properly. Spastic, unpredictable relief from fear, loneliness, discomfort, and hunger keeps a baby’s stress system on high alert. An environment of intermittent care punctuated by total abandonment may be the worst of all worlds for a child.”

Cultural Influences

The sociocultural perspective of clinical psychology views disorders as influenced by cultural aspects; since cultural norms differ significantly, mental disorders such as ASPD are viewed differently. Robert D. Hare has suggested that the rise in ASPD that has been reported in the United States may be linked to changes in cultural mores, the latter serving to validate the behavioural tendencies of many individuals with ASPD. While the rise reported may be in part merely a byproduct of the widening use (and abuse) of diagnostic techniques, given Eric Berne’s division between individuals with active and latent ASPD – the latter keeping themselves in check by attachment to an external source of control like the law, traditional standards, or religion – it has been suggested that the erosion of collective standards may indeed serve to release the individual with latent ASPD from their previously prosocial behaviour.

There is also a continuous debate as to the extent to which the legal system should be involved in the identification and admittance of patients with preliminary symptoms of ASPD. Controversial clinical psychiatrist Pierre-Édouard Carbonneau suggested that the problem with legal forced admittance is the rate of failure when diagnosing ASPD. He states that the possibility of diagnosing and coercing a patient into prescribing medication to someone without ASPD, but is diagnosed with it could be potentially disastrous, but the possibility of not diagnosing it and seeing a patient go untreated because of a lack of sufficient evidence of cultural or environmental influences is something a psychiatrist must ignore, and in his words, “play it safe”.

ICD-10

The World Health Organisation’s (WHO’s) International Statistical Classification of Diseases and Related Health Problems, tenth edition (ICD-10), has a diagnosis called dissocial personality disorder (F60.2):

It is characterised by at least 3 of the following:

  • Callous unconcern for the feelings of others;
  • Gross and persistent attitude of irresponsibility and disregard for social norms, rules, and obligations;
  • Incapacity to maintain enduring relationships, though having no difficulty in establishing them;
  • Very low tolerance to frustration and a low threshold for discharge of aggression, including violence;
  • Incapacity to experience guilt or to profit from experience, particularly punishment; and/or
  • Marked readiness to blame others or to offer plausible rationalisations for the behaviour that has brought the person into conflict with society.

The ICD states that this diagnosis includes “amoral, antisocial, asocial, psychopathic, and sociopathic personality”. Although the disorder is not synonymous with conduct disorder, presence of conduct disorder during childhood or adolescence may further support the diagnosis of dissocial personality disorder. There may also be persistent irritability as an associated feature.

It is a requirement of the ICD-10 that a diagnosis of any specific personality disorder also satisfies a set of general personality disorder criteria.

Psychopathy

Psychopathy is commonly defined as a personality disorder characterised partly by antisocial behaviour, a diminished capacity for empathy and remorse, and poor behavioural controls. Psychopathic traits are assessed using various measurement tools, including Canadian researcher Robert D. Hare’s Psychopathy Checklist, Revised (PCL-R). “Psychopathy” is not the official title of any diagnosis in the DSM or ICD; nor is it an official title used by other major psychiatric organisations. The DSM and ICD, however, state that their antisocial diagnoses are at times referred to (or include what is referred to) as psychopathy or sociopathy.

American psychiatrist Hervey Cleckley’s work on psychopathy formed the basis of the diagnostic criteria for ASPD, and the DSM states ASPD is often referred to as psychopathy. However, critics argue ASPD is not synonymous with psychopathy as the diagnostic criteria are not the same, since criteria relating to personality traits are emphasized relatively less in the former. These differences exist in part because it was believed such traits were difficult to measure reliably and it was “easier to agree on the behaviours that typify a disorder than on the reasons why they occur”.

Although the diagnosis of ASPD covers two to three times as many prisoners than the diagnosis of psychopathy, Robert Hare believes the PCL-R is better able to predict future criminality, violence, and recidivism than a diagnosis of ASPD. He suggests there are differences between PCL-R-diagnosed psychopaths and non-psychopaths on “processing and use of linguistic and emotional information”, while such differences are potentially smaller between those diagnosed with ASPD and without. Additionally, Hare argued confusion regarding how to diagnose ASPD, confusion regarding the difference between ASPD and psychopathy, as well as the differing future prognoses regarding recidivism and treatability, may have serious consequences in settings such as court cases where psychopathy is often seen as aggravating the crime.

Nonetheless, psychopathy has been proposed as a specifier under an alternative model for ASPD. In the DSM-5, under “Alternative DSM-5 Model for Personality Disorders”, ASPD with psychopathic features is described as characterised by “a lack of anxiety or fear and by a bold interpersonal style that may mask maladaptive behaviours (e.g. fraudulence).” Low levels of withdrawal and high levels of attention-seeking combined with low anxiety are associated with “social potency” and “stress immunity” in psychopathy. Under the specifier, affective and interpersonal characteristics are comparatively emphasized over behavioural components.

Treatment

ASPD is considered to be among the most difficult personality disorders to treat. Rendering an effective treatment for ASPD is further complicated due to the inability to look at comparative studies between psychopathy and ASPD due to differing diagnostic criteria, differences in defining and measuring outcomes and a focus on treating incarcerated patients rather than those in the community. Because of their very low or absent capacity for remorse, individuals with ASPD often lack sufficient motivation and fail to see the costs associated with antisocial acts. They may only simulate remorse rather than truly commit to change: they can be seductively charming and dishonest, and may manipulate staff and fellow patients during treatment. Studies have shown that outpatient therapy is not likely to be successful, but the extent to which persons with ASPD are entirely unresponsive to treatment may have been exaggerated.

Most treatment done is for those in the criminal justice system to whom the treatment regimes are given as part of their imprisonment. Those with ASPD may stay in treatment only as required by an external source, such as parole conditions. Residential programmes that provide a carefully controlled environment of structure and supervision along with peer confrontation have been recommended. There has been some research on the treatment of ASPD that indicated positive results for therapeutic interventions. Psychotherapy also known as talk therapy is found to help treat patients with ASPD. Schema therapy is also being investigated as a treatment for ASPD. A review by Charles M. Borduin features the strong influence of Multisystemic therapy (MST) that could potentially improve this imperative issue. However, this treatment requires complete cooperation and participation of all family members. Some studies have found that the presence of ASPD does not significantly interfere with treatment for other disorders, such as substance use, although others have reported contradictory findings.

Therapists working with individuals with ASPD may have considerable negative feelings toward patients with extensive histories of aggressive, exploitative, and abusive behaviours. Rather than attempt to develop a sense of conscience in these individuals, which is extremely difficult considering the nature of the disorder, therapeutic techniques are focused on rational and utilitarian arguments against repeating past mistakes. These approaches would focus on the tangible, material value of prosocial behaviour and abstaining from antisocial behaviour. However, the impulsive and aggressive nature of those with this disorder may limit the effectiveness of even this form of therapy.

The use of medications in treating antisocial personality disorder is still poorly explored, and no medications have been approved by the FDA to specifically treat ASPD. A 2020 Cochrane review of studies that explored the use of pharmaceuticals in ASPD patients, of which 8 studies met the selection criteria for review, concluded that the current body of evidence was inconclusive for recommendations concerning the use of pharmaceuticals in treating the various issues of ASPD. Nonetheless, psychiatric medications such as antipsychotics, antidepressants, and mood stabilizers can be used to control symptoms such as aggression and impulsivity, as well as treat disorders that may co-occur with ASPD for which medications are indicated.

Prognosis

According to Professor Emily Simonoff of the Institute of Psychiatry, Psychology and Neuroscience there are many variables that are consistently connected to ASPD, such as: childhood hyperactivity and conduct disorder, criminality in adulthood, lower IQ scores and reading problems. The strongest relationship between these variables and ASPD are childhood hyperactivity and conduct disorder. Additionally, children who grow up with a predisposition of ASPD and interact with other delinquent children are likely to later be diagnosed with ASPD. Like many disorders, genetics play a role in this disorder but the environment holds an undeniable role in its development.

Boys are twice as likely to meet all of the diagnostic criteria for ASPD than girls (40% versus 25%) and they will often start showing symptoms of the disorder much earlier in life. Children that do not show symptoms of the disease through age 15 will not develop ASPD later in life. If adults exhibit milder symptoms of ASPD, it is likely that they never met the criteria for the disorder in their childhood and were consequently never diagnosed. Overall, symptoms of ASPD tend to peak in late-teens and early twenties, but can often reduce or improve through age 40.

ASPD is ultimately a lifelong disorder that has chronic consequences, though some of these can be moderated over time. There may be a high variability of the long-term outlook of antisocial personality disorder. The treatment of this disorder can be successful, but it entails unique difficulties. It is unlikely to see rapid change especially when the condition is severe. In fact, past studies revealed that remission rates were small, with up to only 31% rates of improvement instead of remittance. As a result of the characteristics of ASPD (e.g. displaying charm in effort of personal gain, manipulation), patients seeking treatment (mandated or otherwise) may appear to be “cured” in order to get out of treatment. According to definitions found in the DSM-5, people with ASPD can be deceitful and intimidating in their relationships. When they are caught doing something wrong, they often appear to be unaffected and unemotional about the consequences. Over time, continual behaviour that lacks empathy and concern may lead to someone with ASPD taking advantage of the kindness of others, including his or her therapist.

Without proper treatment, individuals suffering with ASPD could lead a life that brings about harm to themselves or others. This can be detrimental to their families and careers. ASPD victims suffer from lack of interpersonal skills (e.g. lack of remorse, lack of empathy, lack of emotional-processing skills). As a result of the inability to create and maintain healthy relationships due to the lack of interpersonal skills, individuals with ASPD may find themselves in predicaments such as divorce, unemployment, homelessness and even premature death by suicide. They also see higher rates of committed crime, reaching peaks in their late teens and often committing higher-severity crimes in their younger ages of diagnoses. Comorbidity of other mental illnesses such as Depression or substance use disorder is prevalent among ASPD victims. People with ASPD are also more likely to commit homicides and other crimes. Those who are imprisoned longer often see higher rates of improvement with symptoms of ASPD than others who have been imprisoned for a shorter amount of time.

According to one study, aggressive tendencies show in about 72% of all male patients diagnosed with ASPD. About 29% of the men studied with ASPD also showed a prevalence of pre-meditated aggression. Based on the evidence in the study, the researchers concluded that aggression in patients with ASPD is mostly impulsive, though there are some long-term evidences of pre-meditated aggressions. It often occurs that those with higher psychopathic traits will exhibit the pre-meditated aggressions to those around them. Over the course of a patient’s life with ASPD, he or she can exhibit this aggressive behaviour and harm those close to him or her.

Additionally, many people (especially adults) who have been diagnosed with ASPD become burdens to their close relatives, peers, and caretakers. Harvard Medical School recommends that time and resources be spent treating victims who have been affected by someone with ASPD, because the patient with ASPD may not respond to the administered therapies. In fact, a patient with ASPD may only accept treatment when ordered by a court, which will make their course of treatment difficult and severe. Because of the challenges in treatment, the patient’s family and close friends must take an active role in decisions about therapies that are offered to the patient. Ultimately, there must be a group effort to aid the long-term effects of the disorder.

What is Histrionic Personality Disorder?

Introduction

Histrionic personality disorder (HPD) is defined by the American Psychiatric Association as a personality disorder characterised by a pattern of excessive attention-seeking behaviours, usually beginning in early childhood, including inappropriate seduction and an excessive desire for approval.

Individuals diagnosed with the disorder are said to be lively, dramatic, vivacious, enthusiastic, and flirtatious. Women are diagnosed with HPD roughly 4 times as often as men. It affects 2-3% of the general population and 10-15% in inpatient and outpatient mental health institutions.

HPD lies in the dramatic cluster of personality disorders. People with HPD have a high desire for attention, make loud and inappropriate appearances, exaggerate their behaviours and emotions, and crave stimulation. They may exhibit sexually provocative behaviour, express strong emotions with an impressionistic style, and can be easily influenced by others. Associated features include egocentrism, self-indulgence, continuous longing for appreciation, and persistent manipulative behaviour to achieve their own needs.

Signs and Symptoms

People with HPD are usually high-functioning, both socially and professionally. They usually have good social skills, despite tending to use them to manipulate others into making them the centre of attention. HPD may also affect a person’s social and romantic relationships, as well as their ability to cope with losses or failures. They may seek treatment for clinical depression when romantic (or other close personal) relationships end.

Individuals with HPD often fail to see their own personal situation realistically, instead dramatising and exaggerating their difficulties. They may go through frequent job changes, as they become easily bored and may prefer withdrawing from frustration (instead of facing it). Because they tend to crave novelty and excitement, they may place themselves in risky situations. All of these factors may lead to greater risk of developing clinical depression.

Additional characteristics may include:

  • Exhibitionist behaviour.
  • Constant seeking of reassurance or approval.
  • Excessive sensitivity to criticism or disapproval.
  • Pride of own personality and unwillingness to change, viewing any change as a threat.
  • Inappropriately seductive appearance or behaviour of a sexual nature.
  • Using factitious somatic symptoms (of physical illness) or psychological disorders to garner attention.
  • Craving attention.
  • Low tolerance for frustration or delayed gratification.
  • Rapidly shifting emotional states that may appear superficial or exaggerated to others.
  • Tendency to believe that relationships are more intimate than they actually are.
  • Making rash decisions.
  • Blaming personal failures or disappointments on others.
  • Being easily influenced by others, especially those who treat them approvingly.
  • Being overly dramatic and emotional.
  • Influenced by the suggestions of others.

Some people with histrionic traits or personality disorder change their seduction technique into a more maternal or paternal style as they age.

Mnemonic

A mnemonic that can be used to remember the characteristics of histrionic personality disorder is shortened as “PRAISE ME”:

  • Provocative (or seductive) behaviour.
  • Relationships are considered more intimate than they actually are.
  • Attention-seeking.
  • Influenced easily by others or circumstances.
  • Speech (style) wants to impress; lacks detail.
  • Emotional lability; shallowness.
  • Make-up; physical appearance is used to draw attention to self.
  • Exaggerated emotions; theatrical.

Causes

Little research has been done to find evidence of what causes histrionic personality disorder. Although direct causes are inconclusive, various theories and studies suggest multiple possible causes, of a neurochemical, genetic, psychoanalytic, or environmental nature. Traits such as extravagance, vanity, and seductiveness of hysteria have similar qualities to women diagnosed with HPD. HPD symptoms typically do not fully develop until the age of 15, while the onset of treatment only occurs, on average, at approximately 40 years of age.

Neurochemical/Physiological

Studies have shown that there is a strong correlation between the function of neurotransmitters and the Cluster B personality disorders such as HPD. Individuals diagnosed with HPD have highly responsive noradrenergic systems which is responsible for the synthesis, storage, and release of the neurotransmitter, norepinephrine. High levels of norepinephrine leads to anxiety-proneness, dependency, and high sociability.

Genetic

Twin studies have aided in breaking down the genetic vs. environment debate. A twin study conducted by the Department of Psychology at Oslo University attempted to establish a correlation between genetic and Cluster B personality disorders. With a test sample of 221 twins, 92 monozygotic and 129 dizygotic, researchers interviewed the subjects using the Structured Clinical Interview for DSM-III-R Personality Disorders (SCID-II) and concluded that there was a correlation of 0.67 that histrionic personality disorder is hereditary.

Psychoanalytic Theory

Though criticised as being unsupported by scientific evidence, psychoanalytic theories incriminate authoritarian or distant attitudes by one (mainly the mother) or both parents, along with conditional love based on expectations the child can never fully meet. Using psychoanalysis, Freud believed that lustfulness was a projection of the patient’s lack of ability to love unconditionally and develop cognitively to maturity, and that such patients were overall emotionally shallow. He believed the reason for being unable to love could have resulted from a traumatic experience, such as the death of a close relative during childhood or divorce of one’s parents, which gave the wrong impression of committed relationships. Exposure to one or multiple traumatic occurrences of a close friend or family member’s leaving (via abandonment or mortality) would make the person unable to form true and affectionate attachments towards other people.

HPD and Antisocial Personality Disorder

Another theory suggests a possible relationship between histrionic personality disorder and antisocial personality disorder. Research has found 2/3 of patients diagnosed with histrionic personality disorder also meet criteria similar to those of the antisocial personality disorder, which suggests both disorders based towards sex-type expressions may have the same underlying cause. Women are hypersexualised in the media consistently, ingraining thoughts that the only way women are to get attention is by exploiting themselves, and when seductiveness is not enough, theatrics are the next step in achieving attention. Men can just as well be flirtatious towards multiple women yet feel no empathy or sense of compassion towards them. They may also become the centre of attention by exhibiting the “Don Juan” macho figure as a role-play.

Some family history studies have found that histrionic personality disorder, as well as borderline and antisocial personality disorders, tend to run in families, but it is unclear if this is due to genetic or environmental factors. Both examples suggest that predisposition could be a factor as to why certain people are diagnosed with histrionic personality disorder, however little is known about whether or not the disorder is influenced by any biological compound or is genetically inheritable. Little research has been conducted to determine the biological sources, if any, of this disorder.

Diagnosis

The person’s appearance, behaviour and history, along with a psychological evaluation, are usually sufficient to establish a diagnosis. There is no test to confirm this diagnosis. Because the criteria are subjective, some people may be wrongly diagnosed.

DSM 5

The current edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM 5) defines histrionic personality disorder (in Cluster B) as:

A pervasive pattern of excessive emotionality and attention-seeking, beginning by early adulthood and present in a variety of contexts, as indicated by five (or more) of the following:

  • Is uncomfortable in situations in which he or she is not the centre of attention.
  • Interaction with others is often characterised by inappropriate sexually seductive or provocative behaviour.
  • Displays rapidly shifting and shallow expression of emotions.
  • Consistently uses physical appearance to draw attention to self.
  • Has a style of speech that is excessively impressionistic and lacking in detail.
  • Shows self-dramatisation, theatricality, and exaggerated expression of emotion.
  • Is suggestible, i.e. easily influenced by others or circumstances.
  • Considers relationships to be more intimate than they actually are.

The DSM 5 requires that a diagnosis for any specific personality disorder also satisfies a set of general personality disorder criteria.

ICD-10

The World Health Organization’s ICD-10 lists histrionic personality disorder as:

A personality disorder characterised by:

  • Shallow and labile affectivity.
  • Self-dramatisation.
  • Theatricality.
  • Exaggerated expression of emotions.
  • Suggestibility.
  • Egocentricity.
  • Self-indulgence.
  • Lack of consideration for others.
  • Easily hurt feelings.
  • Continuous seeking for appreciation, excitement and attention.

It is a requirement of ICD-10 that a diagnosis of any specific personality disorder also satisfies a set of general personality disorder criteria.

Comorbidity

Most histrionics also have other mental disorders. Comorbid conditions include: antisocial, dependent, borderline, and narcissistic personality disorders, as well as depression, anxiety disorders, panic disorder, somatoform disorders, anorexia nervosa, substance use disorder and attachment disorders, including reactive attachment disorder.

Millon’s Subtypes

Theodore Millon identified six subtypes of histrionic personality disorder. Any individual histrionic may exhibit none or one of the following (as outlined in the table below).

SubtypeDescriptionPersonality Traits
Appeasing histrionicIncluding dependent and compulsive features.Seeks to placate, mend, patch up, smooth over troubles; knack for settling differences, moderating tempers by yielding, compromising, conceding; sacrifices self for commendation; fruitlessly placates the unplacatable.
Vivacious histrionicThe seductiveness of the histrionic mixed with the energy typical of hypomania.
Some narcissistic features can also be present.
Vigorous, charming, bubbly, brisk, spirited, flippant, impulsive; seeks momentary cheerfulness and playful adventures; animated, energetic, ebullient.
Tempestuous histrionicIncluding negativistic features.Impulsive, out of control; moody complaints, sulking; precipitous emotion, stormy, impassioned, easily wrought-up, periodically inflamed, turbulent.
Disingenuous histrionicIncluding antisocial features.Underhanded, double-dealing, scheming, contriving, plotting, crafty, false-hearted; egocentric, insincere, deceitful, calculating, guileful.
Theatrical histrionicVariant of “pure” pattern.Affected, mannered, put-on; postures are striking, eyecatching, graphic; markets self-appearance; is synthesized, stagy; simulates desirable/dramatic poses.
Infantile histrionicIncluding borderline features.Labile, high-strung, volatile emotions; childlike hysteria and nascent pouting; demanding, overwrought; fastens and clutches to another; is excessively attached, hangs on, stays fused to and clinging.

Treatment

Treatment is often prompted by depression associated with dissolved romantic relationships. Medication does little to affect the personality disorder, but may be helpful with symptoms such as depression. The only successful method studied and proven to succeed is to fully break contact with their lovers in order to gain a sense of stability and independence once again. Treatment for HPD itself involves psychotherapy, including cognitive therapy.

Interviews and Self-Report Methods

In general clinical practice with assessment of personality disorders, one form of interview is the most popular; an unstructured interview. The actual preferred method is a semi-structured interview but there is reluctance to use this type of interview because they can seem impractical or superficial. The reason that a semi-structured interview is preferred over an unstructured interview is that semi-structured interviews tend to be more objective, systematic, replicable, and comprehensive. Unstructured interviews, despite their popularity, tend to have problems with unreliability and are susceptible to errors leading to false assumptions of the client.

One of the single most successful methods for assessing personality disorders by researchers of normal personality functioning is the self-report inventory following up with a semi-structured interview. There are some disadvantages with the self-report inventory method that with histrionic personality disorder there is a distortion in character, self-presentation, and self-image. This cannot be assessed simply by asking most clients if they match the criteria for the disorder. Most projective testing depend less on the ability or willingness of the person to provide an accurate description of the self, but there is currently limited empirical evidence on projective testing to assess histrionic personality disorder.

Functional Analytic Psychotherapy

Another way to treat histrionic personality disorder after identification is through functional analytic psychotherapy. The job of a Functional Analytic Psychotherapist is to identify the interpersonal problems with the patient as they happen in session or out of session. Initial goals of functional analytic psychotherapy are set by the therapist and include behaviours that fit the client’s needs for improvement. Functional analytic psychotherapy differs from the traditional psychotherapy due to the fact that the therapist directly addresses the patterns of behaviour as they occur in-session.

The in-session behaviours of the patient or client are considered to be examples of their patterns of poor interpersonal communication and to adjust their neurotic defences. To do this, the therapist must act on the client’s behaviour as it happens in real time and give feedback on how the client’s behaviour is affecting their relationship during therapy. The therapist also helps the client with histrionic personality disorder by denoting behaviours that happen outside of treatment; these behaviours are termed “Outside Problems” and “Outside Improvements”. This allows the therapist to assist in problems and improvements outside of session and to verbally support the client and condition optimal patterns of behaviour. This then can reflect on how they are advancing in-session and outside of session by generalising their behaviours over time for changes or improvement.

Coding Client and Therapist Behaviours

This is called coding client and therapist behaviour. In these sessions there is a certain set of dialogue or script that can be forced by the therapist for the client to give insight on their behaviours and reasoning. Here is an example a hypothetical conversation. T = therapist C = Client. This coded dialogue can be transcribed as:

  • ECRB – Evoking clinically relevant behaviour:
    • T: Tell me how you feel coming in here today (CRB2).
    • C: Well, to be honest, I was nervous. Sometimes I feel worried about how things will go, but I am really glad I am here.
  • CRB1 – In-session problems:
    • C: Whatever, you always say that. (becomes quiet). I don’t know what I am doing talking so much.
  • CRB2 – In-session improvements.
  • TCRB1 – Clinically relevant response to client problems.
    • T: Now you seem to be withdrawing from me. That makes it hard for me to give you what you might need from me right now. What do you think you want from me as we are talking right now?”.
  • TCRB2 – Responses to client improvement:
    • T: That’s great. I am glad you’re here, too. I look forward to talking to you.

Functional Ideographic Assessment Template

Another example of treatment besides coding is functional ideographic assessment template. The functional ideographic assessment template, also known as FIAT, was used as a way to generalize the clinical processes of functional analytic psychotherapy. The template was made by a combined effort of therapists and can be used to represent the behaviours that are a focus for this treatment. Using the FIAT therapists can create a common language to get stable and accurate communication results through functional analytic psychotherapy at the ease of the client; as well as the therapist.

Epidemiology

The survey data from the National epidemiological survey from 2001-2002 suggests a prevalence of HPD of 1.84%. Major character traits may be inherited, while other traits may be due to a combination of genetics and environment, including childhood experiences. This personality is seen more often in women than in men. Approximately 65% of HPD diagnoses are women while 35% are men. In Marcie Kaplan’s A Women’s View of DSM-III, she argues that women are overdiagnosed due to potential biases and expresses that even healthy women are often automatically diagnosed with HPD.

Many symptoms representing HPD in the DSM are exaggerations of traditional feminine behaviours. In a peer and self-review study, it showed that femininity was correlated with histrionic, dependent and narcissistic personality disorders. Although two thirds of HPD diagnoses are female, there have been a few exceptions. Whether or not the rate will be significantly higher than the rate of women within a particular clinical setting depends upon many factors that are mostly independent of the differential sex prevalence for HPD. Those with HPD are more likely to look for multiple people for attention, which leads to marital problems due to jealousy and lack of trust from the other party. This makes them more likely to become divorced or separated once married. With few studies done to find direct causations between HPD and culture, cultural and social aspects play a role in inhibiting and exhibiting HPD behaviours.

Brief History

Histrionic personality disorder stems from Etruscan histrio which means “an actor”. Hysteria can be described as an exaggerated or uncontrollable emotion that people, especially in groups, experience. Beliefs about hysteria have varied throughout time. It wasn’t until Sigmund Freud who studied histrionic personality disorder in a psychological manner. “The roots of histrionic personality can be traced to cases of hysterical neurosis described by Freud.” He developed the psychoanalytic theory in the late 19th century and the results from his development led to split concepts of hysteria. One concept labelled as hysterical neurosis (also known as conversion disorder) and the other concept labelled as hysterical character (currently known as histrionic personality disorder). These two concepts must not be confused with each other, as they are two separate and different ideas.

Histrionic personality disorder is also known as hysterical personality. Hysterical personality has evolved in the past 400 years and it first appeared in the DSM II (Diagnostic and Statistical Manual of Mental Disorders, 2nd edition) under the name hysterical personality disorder. The name we know today as histrionic personality disorder is due to the name change in DSM III, third edition. Renaming hysterical personality to histrionic personality disorder is believed to be because of possible negative connotations to the roots of hysteria, such as intense sexual expressions, demon possessions, etc.

Histrionic personality disorder has gone through many changes. From hysteria, to hysterical character, to hysterical personality disorder, to what it is listed as in the most current DSM, DSM-5.[clarification needed] “Hysteria is one of the oldest documented medical disorders.” Hysteria dates back to both ancient Greek and Egyptian writings. Most of the writings related hysteria and women together, similar to today where the epidemiology of histrionic personality disorder is generally more prevalent in women and also frequently diagnosed in women.

Ancient Times

  • Ancient Egypt:
    • First description of the mental disorder, hysteria, dates back to 1900 BC in Ancient Egypt. Biological issues, such as the uterus movement in the female body, were seen as the cause of hysteria.
    • Traditional symptoms and descriptions of hysteria can be found in the Ebers Papyrus, the oldest medical document.
  • Ancient Greece:
    • Similar to ancient Egyptians, the ancient Greeks saw hysteria being related to the uterus.
    • Hippocrates (5th century BC) is the first to use the term hysteria.
    • Hippocrates believed hysteria was a disease that lies in the movement of uterus (from the Greek ὑστέρα hystera “uterus”).
    • Hippocrates’s theory was that since a woman’s body is cold and wet compared to a man’s body which is warm and dry, the uterus is prone to illness, especially if deprived from sex.
    • He saw sex as the cleansing of the body so that being overemotional was due to sex deprivation.
  • According to History Channel’s Ancients Behaving Badly, Cleopatra and Nero had histrionic personality disorder.

Middle Ages

  • The Trotula:
    • A group of three texts from the 12th century, discusses women’s diseases and disorders as understood during this time period, including hysteria.
    • Trota of Salerno, a female medical practitioner from 12th-century Italy, is an authoritative figure behind one of the texts of the Trotula.
    • Authoritative in that it is her treatments and theories that are presented in the text.
    • Some people believe Trota’s teachings resonated with those of Hippocrates.

Renaissance

  • The uterus was still the explanation of hysteria, the concept of women being inferior to men was still present, and hysteria was still the symbol for femininity.

Modern Age

  • Thomas Willis (17th century) introduces a new concept of hysteria.
    • Thomas Willis believed that the causes of hysteria was not linked to the uterus of the female, but to the brain and nervous system.
  • Hysteria was consequence of social conflicts during the Salem witch trials.
  • Witchcraft and sorcery was later considered absurd during the Age of Enlightenment in the late 17th century and 18th century.
    • Hysteria starts to form in a more scientific way, especially neurologically.
    • New ideas formed during this time and one of them was that if hysteria is connected to the brain, men could possess it too, not just women.
  • Franz Mesmer (18th century) treated patients suffering from hysteria with his method called mesmerism, or animal magnetism.
  • Jean-Martin Charcot (19th century) studied effects of hypnosis in hysteria.
    • Charcot states that hysteria is a neurological disorder and that it is actually very common in men.

Contemporary Age

  • Sigmund Freud’s work with Josef Breuer, Studies on Hysteria, contributes to a psychoanalytic theory of hysteria.
  • Freud believed that hysteria was caused by a lack of libidinal evolution.

Social Implications

The prevalence of histrionic personality disorder in women is apparent and urges a re-evaluation of cultural notions of normal emotional behaviour. The diagnostic approach classifies histrionic personality disorder behaviour as “excessive”, considering it in reference to a social understanding of normal emotionality.

What is Labelling Theory?

Introduction

Labelling theory posits that self-identity and the behaviour of individuals may be determined or influenced by the terms used to describe or classify them.

It is associated with the concepts of self-fulfilling prophecy and stereotyping. Labelling theory holds that deviance is not inherent in an act, but instead focuses on the tendency of majorities to negatively label minorities or those seen as deviant from standard cultural norms. The theory was prominent during the 1960s and 1970s, and some modified versions of the theory have developed and are still currently popular. Stigma is defined as a powerfully negative label that changes a person’s self-concept and social identity.

Labelling theory is closely related to social-construction and symbolic-interaction analysis. Labelling theory was developed by sociologists during the 1960s. Howard Saul Becker’s book Outsiders was extremely influential in the development of this theory and its rise to popularity.

Labelling theory is also connected to other fields besides crime. For instance there is the labelling theory that corresponds to homosexuality. Alfred Kinsey and his colleagues were the main advocates in separating the difference between the role of a “homosexual” and the acts one does. An example is the idea that males performing feminine acts would imply that they are homosexual. Thomas J. Scheff states that labelling also plays a part with the “mentally ill”. The label does not refer to criminal but rather acts that are not socially accepted due to mental disorders.

Theoretical Foundations

Labelling theory attributes its origins to French sociologist Émile Durkheim and his 1897 book, Suicide. Durkheim found that crime is not so much a violation of a penal code as it is an act that outrages society. He was the first to suggest that deviant labelling satisfies that function and satisfies society’s need to control the behaviour.

As a contributor to American Pragmatism and later a member of the Chicago School, George Herbert Mead posited that the self is socially constructed and reconstructed through the interactions which each person has with the community. The labelling theory suggests that people obtain labels from how others view their tendencies or behaviours. Each individual is aware of how they are judged by others because he or she has attempted many different roles and functions in social interactions and has been able to gauge the reactions of those present.

This theoretically builds a subjective conception of the self, but as others intrude into the reality of that individual’s life, this represents “objective” (intersubjective) data which may require a re-evaluation of that conception depending on the authoritativeness of the others’ judgment. Family and friends may judge differently from random strangers. More socially representative individuals such as police officers or judges may be able to make more globally respected judgments. If deviance is a failure to conform to the rules observed by most of the group, the reaction of the group is to label the person as having offended against their social or moral norms of behaviour. This is the power of the group: to designate breaches of their rules as deviant and to treat the person differently depending on the seriousness of the breach. The more differential the treatment, the more the individual’s self-image is affected.

Labelling theory concerns itself mostly not with the normal roles that define our lives, but with those very special roles that society provides for deviant behaviour, called deviant roles, stigmatic roles, or social stigma. A social role is a set of expectations we have about a behaviour. Social roles are necessary for the organization and functioning of any society or group. We expect the postman, for example, to adhere to certain fixed rules about how he does his job. “Deviance” for a sociologist does not mean morally wrong, but rather behaviour that is condemned by society. Deviant behaviour can include both criminal and non-criminal activities.

Investigators found that deviant roles powerfully affect how we perceive those who are assigned those roles. They also affect how the deviant actor perceives himself and his relationship to society. The deviant roles and the labels attached to them function as a form of social stigma. Always inherent in the deviant role is the attribution of some form of “pollution” or difference that marks the labelled person as different from others. Society uses these stigmatic roles to them to control and limit deviant behaviour: “If you proceed in this behavior, you will become a member of that group of people.”

Whether a breach of a given rule will be stigmatised will depend on the significance of the moral or other tenet it represents. For example, adultery may be considered a breach of an informal rule or it may be criminalised depending on the status of marriage, morality, and religion within the community. In most Western countries, adultery is not a crime. Attaching the label “adulterer” may have some unfortunate consequences but they are not generally severe. But in some Islamic countries, zina is a crime and proof of extramarital activity may lead to severe consequences for all concerned.

Stigma is usually the result of laws enacted against the behaviour. Laws protecting slavery or outlawing homosexuality, for instance, will over time form deviant roles connected with those behaviours. Those who are assigned those roles will be seen as less human and reliable. Deviant roles are the sources of negative stereotypes, which tend to support society’s disapproval of the behaviour.

George Herbert Mead

One of the founders of social interactionism, George Herbert Mead, focused on the internal processes of how the mind constructs one’s self-image. In Mind, Self, and Society (1934), he showed how infants come to know persons first and only later come to know things. According to Mead, thought is both a social and pragmatic process, based on the model of two persons discussing how to solve a problem. Mead’s central concept is the self, the part of an individual’s personality composed of self-awareness and self-image. Our self-image is, in fact, constructed of ideas about what we think others are thinking about us. While we make fun of those who visibly talk to themselves, they have only failed to do what the rest of us do in keeping the internal conversation to ourselves. Human behaviour, Mead stated, is the result of meanings created by the social interaction of conversation, both real and imaginary.

Thomas Scheff

Thomas J. Scheff (1966), professor emeritus of Sociology at UCSB, published the book Being Mentally III: A Sociological Theory. According to Scheff, society has perceptions about people with mental illness. He stated that everyone in the society learns the stereotyped imagery of mental disorder through ordinary social interaction. From childhood, people learn to use terms like “crazy,” “loony,” “nuts,” and associated them with disturbed behaviours. The media also contributes to this bias against mentally ill patients by associating them with violent crimes. Scheff believes that mental illness is a label given to a person who has a behaviour which is away from the social norms of the society and is treated as a social deviance in the society. Once a person is given a label of “mentally ill person”, they receive a set of uniform responses from the society, which are generally negative in nature. These responses from the society compel to the person to take the role of a “mentally ill person” as they start internalising the same. When the individual takes on the role of being mentally ill as their central identity, they become a stable mental ill person. Chronic mental illness is thus a social role and the societal reaction is the most determinant of one’s entry into this role of chronically ill. According to Scheff hospitalisation of a mentally ill person further reinforces this social role and forces them to take this role as their self-perception. Once the person is institutionalised for mental disorder, they have been publicly labelled as “crazy” and forced to become a member of a deviant social group. It then becomes difficult for a deviant person to return to their former level of functioning as the status of ‘patient’ causes unfavourable evaluations by self and by others.

Frank Tannenbaum

Frank Tannenbaum is considered the grandfather of labelling theory. His Crime and Community (1938), describing the social interaction involved in crime, is considered a pivotal foundation of modern criminology. While the criminal differs little or not at all from others in the original impulse to first commit a crime, social interaction accounts for continued acts that develop a pattern of interest to sociologists.

Tannenbaum first introduced the idea of “tagging.” While conducting his studies with delinquent youth, he found that a negative tag or label often contributed to further involvement in delinquent activities. This initial tagging may cause the individual to adopt it as part of their identity. The crux of Tannenbaum’s argument is that the greater the attention placed on this label, the more likely the person is to identify themselves as the label.

Kerry Townsend (2001) writes about the revolution in criminology caused by Tannenbaum’s work:

“The roots of Frank Tannenbaum’s theoretical model, known as the ‘dramatization of evil’ or labeling theory, surfaces in the mid- to late-thirties. At this time, the ‘New Deal’ legislation had not defeated the woes of the Great Depression, and, although dwindling, immigration into the United States continued.[7] The social climate was one of disillusionment with the government. The class structure was one of cultural isolationism; cultural relativity had not yet taken hold. ‘The persistence of the class structure, despite the welfare reforms and controls over big business, was unmistakable.'[7]:117 The Positivist School of Criminological thought was still dominant, and in many states, the sterilization movement was underway. The emphasis on biological determinism and internal explanations of crime were the preeminent force in the theories of the early thirties. This dominance by the Positivist School changed in the late thirties with the introduction of conflict and social explanations of crime and criminality.” “One of the central tenets of the theory is to encourage the end of labeling process. In the words of Frank Tannenbaum, ‘the way out is through a refusal to dramatize the evil”, the justice system attempts to do this through diversion programs. The growth of the theory and its current application, both practical and theoretical, provide a solid foundation for continued popularity.”

Edwin Lemert

Sociologist Edwin Lemert (1951) introduced the concept of “secondary deviance.” The primary deviance is the experience connected to the overt behaviour, say drug addiction and its practical demands and consequences. Secondary deviation is the role created to deal with society’s condemnation of the behaviour of a person.

With other sociologists of his time, Lemert saw how all deviant acts are social acts, a result of the cooperation of society. In studying drug addiction, Lemert observed a very powerful and subtle force at work. Besides the physical addiction to the drug and all the economic and social disruptions it caused, there was an intensely intellectual process at work concerning one’s own identity and the justification for the behaviour: “I do these things because I am this way.”

There might be certain subjective and personal motives that might first lead a person to drink or shoplift. But the activity itself tells us little about the person’s self-image or its relationship to the activity. Lemert writes: “His acts are repeated and organised subjectively and transformed into active roles and become the social criteria for assigning status.…When a person begins to employ his deviant behaviour or a role based on it as a means of defence, attack, or adjustment to the overt and covert problems created by the consequent societal reaction to him, his deviation is secondary.”

Howard Becker

While it was Lemert who introduced the key concepts of labelling theory, it was Howard Becker who became their successor. He first began describing the process of how a person adopts a deviant role in a study of dance musicians, with whom he once worked. He later studied the identity formation of marijuana smokers. This study was the basis of his Outsiders published in 1963. This work became the manifesto of the labelling theory movement among sociologists. In his opening, Becker writes:

“…social groups create deviance by making rules whose infraction creates deviance, and by applying those rules to particular people and labeling them as outsiders. From this point of view, deviance is not a quality of the act the person commits, but rather a consequence of the application by other of rules and sanctions to an ‘offender.’ The deviant is one to whom that label has been successfully applied; deviant behavior is behavior that people so label.”

While society uses the stigmatic label to justify its condemnation, the deviant actor uses it to justify his actions. He wrote: “To put a complex argument in a few words: instead of the deviant motives leading to the deviant behavior, it is the other way around, the deviant behavior in time produces the deviant motivation.”

Becker’s immensely popular views were also subjected to a barrage of criticism, most of it blaming him for neglecting the influence of other biological, genetic effects and personal responsibility. In a later 1973 edition of his work, he answered his critics. He wrote that sociologists, while dedicated to studying society, are often careful not to look too closely. Instead, he wrote: “I prefer to think of what we study as collective action. People act, as Mead and Blumer have made clearest, together. They do what they do with an eye on what others have done, are doing now, and may do in the future. One tries to fit his own line of action into the actions of others, just as each of them likewise adjusts his own developing actions to what he sees and expects others to do.”

Francis Cullen reported in 1984 that Becker was probably too generous with his critics. After 20 years, Becker’s views, far from being supplanted, have been corrected and absorbed into an expanded “structuring perspective.”

Albert Memmi

In The Colonizer and the Colonized (1965), Albert Memmi described the deep psychological effects of the social stigma created by the domination of one group by another. He wrote:

The longer the oppression lasts, the more profoundly it affects him (the oppressed). It ends by becoming so familiar to him that he believes it is part of his own constitution, that he accepts it and could not imagine his recovery from it. This acceptance is the crowning point of oppression.

In Dominated Man (1968), Memmi turned his attention to the motivation of stigmatic labelling: it justifies the exploitation or criminalisation of the victim. He wrote:

Why does the accuser feel obliged to accuse in order to justify himself? Because he feels guilty toward his victim. Because he feels that his attitude and his behavior are essentially unjust and fraudulent.… Proof? In almost every case, the punishment has already been inflicted. The victim of racism is already living under the weight of disgrace and oppression.… In order to justify such punishment and misfortune, a process of rationalization is set in motion, by which to explain the ghetto and colonial exploitation.

Central to stigmatic labelling is the attribution of an inherent fault: It is as if one says, “There must be something wrong with these people. Otherwise, why would we treat them so badly?”

Erving Goffman

Perhaps the most important contributor to labelling theory was Erving Goffman, President of the American Sociological Association (ASA), and one of America’s most cited sociologists. His most popular books include The Presentation of Self in Everyday Life, Interaction Ritual, and Frame Analysis.

His most important contribution to labelling theory, however, was Stigma: Notes on the Management of Spoiled Identity published in 1963. Unlike other authors who examined the process of adopting a deviant identity, Goffman explored the ways people managed that identity and controlled information about it.

Goffman’s Key Insights

The modern nation state’s heightened demand for normalcy. Today’s stigmas are the result not so much of ancient or religious prohibitions, but of a new demand for normalcy:

“The notion of the ‘normal human being’ may have its source in the medical approach to humanity, or in the tendency of large-scale bureaucratic organizations such as the nation state, to treat all members in some respects as equal. Whatever its origins, it seems to provide the basic imagery through which laymen currently conceive themselves.”

Living in a divided world, deviants split their worlds into:

  1. Forbidden places where discovery means exposure and danger;
  2. Places where people of that kind are painfully tolerated; and
  3. Places where one’s kind is exposed without need to dissimulate or conceal.

Dealing with others is fraught with great complexity and ambiguity:

“When normals and stigmatized do in fact enter one another’s immediate presence, especially when they attempt to maintain a joint conversational encounter, there occurs one of the primal scenes of sociology; for, in many cases, these moments will be the ones when the causes and effects of stigma will be directly confronted by both sides.” “What are unthinking routines for normals can become management problems for the discreditable.… The person with a secret failing, then, must be alive to the social situation as a scanner of possibilities, and is therefore likely to be alienated from the simpler world in which those around them apparently dwell.”

Society’s demands are filled with contradictions:

On the one hand, a stigmatized person may be told that he is no different from others. On the other hand, he must declare his status as “a resident alien who stands for his group.” It requires that the stigmatized individual cheerfully and unselfconsciously accept himself as essentially the same as normals, while at the same time he voluntarily withholds himself from those situations in which normals would find it difficult to give lip service to their similar acceptance of him. “One has to convey the impression that the burden of the stigma is not too heavy yet keep himself at the required distance. “A phantom acceptance is allowed to provide the base for a phantom normalcy.”

Familiarity need not reduce contempt. In spite of the common belief that openness and exposure will decrease stereotypes and repression, the opposite is true:

“Thus, whether we interact with strangers or intimates, we will still find that the fingertips of society have reached bluntly into the contact, even here putting us in our place.”

David Matza

In On Becoming Deviant (1969), sociologist David Matza gives the most vivid and graphic account of the process of adopting a deviant role. The acts of authorities in outlawing a proscribed behaviour can have two effects, keeping most out of the behaviour, but also offering new opportunities for creating deviant identities. He says the concept of “affinity” does little to explain the dedication to the behaviour. “Instead, it may be regarded as a natural biographical tendency born of personal and social circumstances that suggests but hardly compels a direction or movement.”

What gives force to that movement is the development of a new identity:

“To be cast as a thief, as a prostitute, or more generally, a deviant, is to further compound and hasten the process of becoming that very thing.”

“In shocked discovery, the subject now concretely understands that there are serious people who really go around building their lives around his activities—stopping him, correcting him, devoted to him. They keep records on the course of his life, even develop theories on how he got that way…. Pressed by such a display, the subject may begin to add meaning and gravity to his deviant activities. But he may do so in a way not especially intended by agents of the state.”

“The meaningful issue of identity is whether this activity, or any of my activities can stand for me, or be regarded as proper indications of my being. I have done a theft, been signified a thief. am I a thief? To answer affirmatively, we must be able to conceive a special relationship between being and doing—a unity capable of being indicated. That building of meaning has a notable quality.”

The “Criminal”

As an application of phenomenology, the theory hypothesizes that the labels applied to individuals influence their behaviour, particularly the application of negative or stigmatising labels (such as “criminal” or “felon”) promote deviant behaviour, becoming a self-fulfilling prophecy, i.e. an individual who is labelled has little choice but to conform to the essential meaning of that judgment. Consequently, labelling theory postulates that it is possible to prevent social deviance via a limited social shaming reaction in “labellers” and replacing moral indignation with tolerance. Emphasis is placed on the rehabilitation of offenders through an alteration of their labels. Related prevention policies include client empowerment schemes, mediation and conciliation, victim-offender forgiveness ceremonies (restorative justice), restitution, reparation, and alternatives to prison programmes involving diversion. Labelling theory has been accused of promoting impractical policy implications, and criticised for failing to explain society’s most serious offenses.

Some offenses, including the use of violence, are universally recognised as wrong. Hence, labelling either habitual criminals or those who have caused serious harm as “criminals” is not constructive. Society may use more specific labels such as “murderer” or “rapist” or “child abuser” to demonstrate more clearly after the event the extent of its disapproval, but there is a slightly mechanical determinism in asserting that the application of a label will invariably modify the behaviour of the one labelled. Further, if one of the functions of the penal system is to reduce recidivism, applying a long-term label may cause prejudice against the offender, resulting in the inability to maintain employment and social relationships.

The “Mentally Ill”

The social construction of deviant behaviour plays an important role in the labelling process that occurs in society. This process involves not only the labelling of criminally deviant behaviour, which is behaviour that does not fit socially constructed norms, but also labelling that which reflects stereotyped or stigmatised behaviour of the “mentally ill”. In 1961 Thomas Szasz, in The Myth of Mental Illness, asked, “Who defines whom as troublesome or mentally sick?… [the one] who first seizes the word imposes reality on the other; [the one] who defines thus dominates and lives; and [the one] who is defined is subjugated and may be killed.” Thomas J. Scheff in Being Mentally Ill challenged common perceptions of mental illness by claiming that mental illness is manifested solely as a result of societal influence. He argued that society views certain actions as deviant and, in order to come to terms with and understand these actions, often places the label of mental illness on those who exhibit them. Certain expectations are then placed on these individuals and, over time, they unconsciously change their behaviour to fulfil them. Criteria for different mental illnesses are not consistently fulfilled by those who are diagnosed with them because all of these people suffer from the same disorder, they are simply fulfilled because the “mentally ill” believe they are supposed to act a certain way so, over time, come to do so. Scheff’s theory had many critics, most notably Walter Gove who consistently argued against Scheff with an almost opposite theory; he believed that society has no influence at all on “mental illness”. Instead, any societal perceptions of the “mentally ill” come about as a direct result of these people’s behaviours. Most sociologists’ views of labelling and mental illness have fallen somewhere between the extremes of Gove and Scheff. On the other hand, it is almost impossible to deny, given both common sense and research findings, that society’s negative perceptions of “crazy” people has had some effect on them. It seems that, realistically, labelling can accentuate and prolong the issues termed “mental illness”, but it is rarely the full cause.

Many other studies have been conducted in this general vein. To provide a few examples, several studies have indicated that most people associate being labelled mentally ill as being just as, or even more, stigmatising than being seen as a drug addict, ex-convict, or prostitute (for example: Brand & Claiborn 1976). Additionally, Page’s 1977 study found that self declared “ex-mental patients” are much less likely to be offered apartment leases or hired for jobs. Clearly, these studies and the dozens of others like them serve to demonstrate that labelling can have a very real and very large effect on the mentally ill. However, labelling has not been proven to be the sole cause of any symptoms of mental illness.

Peggy Thoits (1999) discusses the process of labelling someone with a mental illness in her article, “Sociological Approaches to Mental Illness”. Working off Thomas Scheff’s (1966) theory, Thoits claims that people who are labelled as mentally ill are stereotypically portrayed as unpredictable, dangerous, and unable to care for themselves. She also claims that “people who are labeled as deviant and treated as deviant become deviant.” This statement can be broken down into two processes, one that involves the effects of self-labelling and the other differential treatment from society based on the individual’s label. Therefore, if society sees mentally ill individuals as unpredictable, dangerous and reliant on others, then a person who may not actually be mentally ill but has been labelled as such, could become mentally ill.

The label of “mentally ill” may help a person seek help, for example psychotherapy or medication. Labels, while they can be stigmatising, can also lead those who bear them down the road to proper treatment and (hopefully) recovery. If one believes that “being mentally ill” is more than just believing one should fulfill a set of diagnostic criteria (as Scheff would argue; see above), then one would probably also agree that there are some who are labelled “mentally ill” who need help. It has been claimed that this could not happen if “we” did not have a way to categorise (and therefore label) them, although there are actually plenty of approaches to these phenomena that do not use categorical classifications and diagnostic terms, for example spectrum or continuum models. Here, people vary along different dimensions, and everyone falls at different points on each dimension.

Proponents of hard labelling, as opposed to soft labelling, believe that mental illness does not exist, but is merely deviance from norms of society, causing people to believe in mental illness. They view them as socially constructed illnesses and psychotic disorders.

The “Homosexual”

The application of labelling theory to homosexuality has been extremely controversial. It was Alfred Kinsey and his colleagues who pointed out the big discrepancy between the behaviour and the role attached to it. They had observed the often negative consequences of labelling and repeatedly condemned labelling people as homosexual:

It is amazing to observe how many psychologists and psychiatrists have accepted this sort of propaganda, and have come to believe that homosexual males and females are discretely different from persons who respond to natural stimuli. Instead of using these terms as substantives which stand for persons, or even as adjectives to describe persons, they may better be used to describe the nature of the overt sexual relations, or of the stimuli to which an individual erotically responds.… It would clarify our thinking if the terms could be dropped completely out of our vocabulary.

Males do not represent two discrete populations, heterosexual and homosexual.… Only the human mind invents categories and tries to force facts into pigeonholes. The living world is a continuum in each and every one of its aspects.

The classification of sexual behavior as masturbatory, heterosexual, or homosexual, is, therefore, unfortunate if it suggests that only different types of persons seek out or accept each kind of sexual activity. There is nothing known in the anatomy or physiology of sexual response and orgasm which distinguishes masturbatory, heterosexual, or homosexual reactions.

In regard to sexual behavior, it has been possible to maintain this dichotomy only by placing all persons who are exclusively heterosexual in a heterosexual category and all persons who have any amount of experience with their own sex, even including those with the slightest experience, in a homosexual category.… The attempt to maintain a simple dichotomy on these matters exposes the traditional biases which are likely to enter whenever the heterosexual or homosexual classification of an individual is involved.

Erving Goffman’s Stigma: Notes on the Management of Spoiled Identity distinguished between the behaviour and the role assigned to it:

The term “homosexual” is generally used to refer to anyone who engages in overt sexual practices with a member of his own sex, the practice being called “homosexuality.” This usage appears to be based on a medical and legal frame of reference and provides much too broad and heterogenous a categorization for use here. I refer only to individuals who participate in a special community of understanding wherein members of one’s own sex are defined as the most desirable sexual objects, and sociability is energetically organized around the pursuit and entertainment of these objects.

Labeling theory was also applied to homosexuality by Evelyn Hookerand by Leznoff and Westley (1956), who published the first sociological study of the gay community. Erving Goffman and Howard Becker used the lives of gay-identified persons in their theories of labelling and interactionism. Simon and Gagnon likewise wrote: “It is necessary to move away from the obsessive concern with the sexuality of the individual, and attempt to see the homosexual in terms of the broader attachments that he must make to live in the world around him.” British sociologist Mary McIntosh reflected the enthusiasm of Europeans for labelling theory in her 1968 study, “The Homosexual Role:”

“The vantage-point of comparative sociology enables us to see that the conception of homosexuality as a condition is, itself, a possible object of study. This conception and the behavior it supports operate as a form of social control in a society in which homosexuality is condemned.… It is interesting to notice that homosexuals themselves welcome and support the notion that homosexuality as a condition. For just as the rigid categorization deters people from drifting into deviancy, so it appears to foreclose on the possibility of drifting back into normalcy and thus removes the element of anxious choice. It appears to justify the deviant behavior of the homosexual as being appropriate for him as a member of the homosexual category. The deviancy can thus be seen as legitimate for him and he can continue in it without rejecting the norm of society.”

Sara Fein and Elaine M. Nuehring (1981) were among the many who supported the application of labelling theory to homosexuality. They saw the gay role functioning as a “master status” around which other roles become organized. This brings a whole new set of problems and restrictions:

Placement in a social category constituting a master status prohibits individuals from choosing the extent of their involvement in various categories. Members of the stigmatized group lose the opportunity to establish their own personal system of evaluation and group membership as well as the ability to arrive at their own ranking of each personal characteristic.… For example, newly self-acknowledged homosexual individuals cannot take for granted that they share the world with others who hold congruent interpretations and assumptions; their behavior and motives, both past and present, will be interpreted in light of their stigma.

Perhaps the strongest proponent of labelling theory was Edward Sagarin. In his book, Deviants and Deviance, he wrote, “There are no homosexuals, transvestites, chemical addicts, suicidogenics, delinquents, criminals, or other such entities, in the sense of people having such identities.” Sagarin’s position was roundly condemned by academics in the gay community. Sagarin had written some gay novels under the pseudonym of Donald Webster Cory. According to reports, he later abandoned his gay identity and began promoting an interactionist view of homosexuality.

A number of authors adopted a modified, non-deviant, labelling theory. They rejected the stigmatic function of the gay role, but found it useful in describing the process of coming out and reconciling one’s homosexual experiences with the social role. Their works includes:

  • Homosexuals and the Military (1971);
  • Coming Out in the Gay World (1971);
  • Homosexual Identity: Commitment, Adjustment, and Significant Others (1973);
  • Male Homosexuals: Their Problems and Adaptations (1974);
  • Identity and Community in the Gay World (1974);
  • Components of Sexual Identity (1977);
  • Homosexualities: A Study of Diversity Among Men and Women (1978);
  • On ‘Doing’ and ‘Being’ Gay: Sexual Behavior and Homosexual Male Self-Identity (1978);
  • Homosexual Identity Formation: A Theoretical Model (1979, Cass identity model);
  • Becoming Homosexual: A model of Gay Identity Acquisition (1979);
  • Sexual Preference: Its Development in Men and Women (1981); and
  • Developmental Stages of the Coming Out Process (1982).

Barry Adam (1976) took those authors to task for ignoring the force of the oppression in creating identities and their inferiorising effects. Drawing upon the works of Albert Memmi, Adam showed how gay-identified persons, like Jews and blacks, internalise the hatred to justify their limitations of life choices. He saw the gravitation towards ghettos was evidence of the self-limitations:

A certain romantic liberalism runs through the literature, evident from attempts to paper over or discount the very real problems of inferiorization. Some researchers seem bent on ‘rescuing’ their subjects from ‘defamation’ by ignoring the problems of defeatism and complicit self-destruction. Avoidance of dispiriting reflection upon the day-to-day practice of dominated people appears to spring from a desire to ‘enhance’ the reputation of the dominated and magically relieve their plight. Careful observation has been sacrificed to the ‘power of positive thinking.’

Strong defence of labelling theory also arose within the gay community. Dan Slater of the Los Angeles Homosexual Information Centre said, “There is no such thing as a homosexual lifestyle. There is no such thing as gay pride or anything like that. Homosexuality is simply based on the sex act. Gay consciousness and all the rest are separatist and defeatist attitudes going back to centuries-old and out-moded conceptions that homosexuals are, indeed, different from other people.” In a later article, Slater (1971) stated the gay movement was going in the wrong direction:

Is it the purpose of the movement to try to assert sexual rights for everyone or create a political and social cult out of homosexuality? …Persons who perform homosexual acts or other non-conforming acts are sexually free. They want others enlightened. They want hostile laws changed, but they resent the attempt to organize their lives around homosexuality just as much as they resent the centuries-old attempt to organize their lives around heterosexuality.

William DuBay (1967) describes gay identity as one strategy for dealing with society’s oppression. It solves some problems but creates many more, replacing a closet of secrecy with one of gay identity. A better strategy, he suggests, is to reject the label and live as if the oppression did not exist. Quoting Goffman, he writes, “But of course what is a good adjustment for the individual can be an even better one for society.”

DuBay contends that the attempt to define homosexuality as a class of persons to be protected against discrimination as defined in the statutes has not reduced the oppression. The goal of the movement instead should be to gain acceptance of homosexual relationships as useful and productive for both society and the family. The movement has lost the high moral ground by sponsoring the “flight from choice” and not taking up the moral issues. “Persons whom we confine to back rooms and bars other societies have honored as tenders of children, astrologers, dancers, chanters, minstrels, jesters, artists, shamans, sacred warriors and judges, seers, healers, weavers of tales and magic.”

DuBay refers to the “gay trajectory,” in which a person first wraps himself in the gay role, organising his personality and his life around sexual behaviour. He might flee from his family and home town to a large gay centre. There, the bedevilling force of the stigma will introduce him to more excessive modes of deviance such as promiscuity, prostitution, alcoholism, and drugs. Many resist such temptations and try to normalise their life, but the fast lanes of gay society are littered with the casualties of gay identity. Some come to reject the label entirely. “Accomplishing the forbidden, they are neither gay nor straight. Again learning to choose, they develop the ability to make the ban ambiguous, taking responsibility and refusing explanations of their behaviors.”

John Henry Mackay (1985) writes about a gay hustler in Berlin adopting such a solution: “What was self-evident, natural, and not the least sick did not require an excuse through an explanation.… It was love just like any other love. Whoever could not or would not accept it as love was mistaken.”

There are those who reject the “gay label” for reasons other than shame or negative connotations. They do not reject their homosexuality. It is “gay” as an adjective they reject. Writer Alan Bennett and fashion icon André Leon Talley reject being labelled as a gay writer, a gay fashion designer. These men are openly gay, but believe when gay is used as an adjective, the label confines them.

Modified Labelling Theory

Bruce Link and colleagues (1989) had conducted several studies which point to the influence that labelling can have on mental patients. Through these studies, taking place in 1987, 1989, and 1997, Link advanced a “modified labelling theory” indicating that expectations of labelling can have a large negative effect, that these expectations often cause patients to withdraw from society, and that those labelled as having a mental disorder are constantly being rejected from society in seemingly minor ways but that, when taken as a whole, all of these small slights can drastically alter their self concepts. They come to both anticipate and perceive negative societal reactions to them, and this potentially damages their quality of life.

Modified labelling theory has been described as a “sophisticated social-psychological model of ‘why labels matter.'” In 2000, results from a prospective two-year study of patients discharged from a mental hospital (in the context of deinstitutionalisation) showed that stigma was a powerful and persistent force in their lives, and that experiences of social rejection were a persistent source of social stress. Efforts to cope with labels, such as not telling anyone, educating people about mental distress/disorder, withdrawing from stigmatising situations, could result in further social isolation and reinforce negative self-concepts. Sometimes an identity as a low self-esteem minority in society would be accepted. The stigma was associated with diminished motivation and ability to “make it in mainstream society” and with “a state of social and psychological vulnerability to prolonged and recurrent problems”. There was an up and down pattern in self-esteem, however, and it was suggested that, rather than simply gradual erosion of self-worth and increasing self-deprecating tendencies, people were sometimes managing, but struggling, to maintain consistent feelings of self-worth. Ultimately, “a cadre of patients had developed an entrenched, negative view of themselves, and their experiences of rejection appear to be a key element in the construction of these self-related feelings” and “hostile neighbourhoods may not only affect their self-concept but may also ultimately impact the patient’s mental health status and how successful they are.”

What is the Mood & Feelings Questionnaire?

Introduction

The Mood and Feelings Questionnaire (MFQ) is a survey that measures depressive symptoms in children and young adults.

Background

It was developed by Adrian Angold and Elizabeth J. Costello in 1987, and validity data were gathered as part of the Great Smokey Mountain epidemiological study in Western North Carolina.

The questionnaire consists of a variety of statements describing feelings or behaviours that may manifest as depressive symptoms in children between the ages of 6 and 17. The subject is asked to indicate how much each statement applies to their recent experiences. The Mood and Feelings Questionnaire has six versions, short (13 item) and long (33 item) forms of each of the following:

  • A youth self-report;
  • A version that a parent would complete; and
  • A self-report version for adults.

Several peer-reviewed studies have found the Mood and Feelings Questionnaire to be a reliable and valid measure of depression in children. Compared to many other depression scales for youth, it has more extensive coverage of symptoms and more age-appropriate wording and content.

Scoring and Interpretation

The MFQ has several tests, one short and one long, with the short questionnaire including 13 questions and the long questionnaire consisting of 33 questions. Scoring of the MFQ works by summing the point values allocated to each question. The responses and their allocated point values are as follows:

  • “not true” = 0 points.
  • “somewhat true” = 1 point.
  • “true” = 2 points.

Scores on the short MFQ range from 0 to 26, whereas scores on the long version range from 0 to 66. Higher score are indicative of increased depressive symptom severity. Scores larger than 12 on the short version or larger than 27 on the long version are suggestive of likely depression and warrant further clinical assessment.

Validity

The Mood and Feelings Questionnaire, along with the Short Mood and Feelings Questionnaire, shows reasonable psychometric properties for identifying children in early adolescence with a depressive disorder. Secondly, the MFQ does not significantly differentiate between children with depression versus children with anxiety disorders. Finally, the MFQ has been translated into Arabic, Spanish and Norwegian, but testing of these versions is more limited.

Limitations

Questionnaires like the Mood and Feelings Questionnaire should not act as a substitute for thorough clinical evaluations for both the child and parent.

What is Catatonia?

Introduction

Catatonia is a neuropsychiatric behavioural syndrome that is characterised by abnormal movements, immobility, abnormal behaviours, and withdrawal. The onset of catatonia can be acute or subtle and symptoms can wax, wane, or change during episodes. There are several subtypes of catatonia: akinetic catatonia, excited catatonia, malignant catatonia, and other forms.

Although catatonia has historically been related to schizophrenia (catatonic schizophrenia), catatonia is most often seen in mood disorders. It is now known that catatonic symptoms are nonspecific and may be observed in other mental, neurologic, and medical conditions. Catatonia is not a stand-alone diagnosis (although some experts disagree), and the term is used to describe a feature of the underlying disorder.

Recognising and treating catatonia is very important as failure to do this can lead to poor outcomes and can be potentially fatal. Treatment with benzodiazepines or ECT can lead to remission of catatonia. There is growing evidence of the effectiveness of the NMDA receptor antagonists amantadine and memantine for benzodiazepine-resistant catatonia. Antipsychotics are sometimes employed, but they can worsen symptoms and have serious adverse effects.

Brief History

It was first described in 1874 by Karl Ludwig Kahlbaum as Die Katatonie oder das Spannungsirresein (Catatonia or Tension Insanity).

Aetiology/Causes

Catatonia is almost always secondary to another underlying illness, often a psychiatric disorder. Mood disorders such as a bipolar disorder and depression are the most common aetiologies to progress to catatonia. Other psychiatric associations include schizophrenia and other primary psychotic disorders. It also is related to autism spectrum disorders.

Catatonia is also seen in many medical disorders, including infections (such as encephalitis), autoimmune disorders, meningitis, focal neurological lesions (including strokes), alcohol withdrawal, abrupt or overly rapid benzodiazepine withdrawal, cerebrovascular disease, neoplasms, head injury, and some metabolic conditions (homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcaemia).

Epidemiology

Catatonia has been mostly studied in acutely ill psychiatric patients. Catatonia frequently goes unrecognised, leading to the belief that the syndrome is rare, however, this is not true and prevalence has been reported to be as high as 10% in patients with acute psychiatric illnesses. 21-46% of all catatonia cases can be attributed to a general medical condition.

Pathogenesis/Mechanism

The pathophysiology that leads to catatonia is still poorly understood and a definite mechanism remains unknown. Neurologic studies have implicated several pathways, however, it remains unclear whether these findings are the cause or the consequence of the disorder.

Abnormalities in GABA, glutamate signalling, serotonin, and dopamine transmission are believed to be implicated in catatonia.

Furthermore, it has also been hypothesized that pathways that connect the basal ganglia with the cortex and thalamus is involved in the development of catatonia.

Signs and Symptoms

The presentation of a patient with catatonia varies greatly depending on the subtype, underlying cause and it can be acute or subtle.

Because most patients with catatonia have an underlying psychiatric illness, the majority will present with worsening depression, mania, or psychosis followed by catatonia symptoms. Catatonia presents as a motor disturbance in which patients will display marked reduction in movement, marked agitation, or a mixture of both despite having the physical capacity to move normally. These patients may be unable to start an action or stop one. Movements and mannerisms may be repetitive, or purposeless.

The most common signs of catatonia are immobility, mutism, withdrawal and refusal to eat, staring, negativism, posturing (rigidity), rigidity, waxy flexibility/catalepsy, stereotypy (purposeless, repetitive movements), echolalia or echopraxia, verbigeration (repeat meaningless phrases). It should not be assumed that patients presenting with catatonia are unaware of their surroundings as some patients can recall in detail their catatonic state and their actions.

There are several subtypes of catatonia and they are characterised by the specific movement disturbance and associated features. Although catatonia can be divided into various subtypes, the natural history of catatonia is often fluctuant and different states can exist within the same individual.

Subtypes

  • Retarded/Withdrawn Catatonia:
    • This form of catatonia is characterised by decreased response to external stimuli, immobility or inhibited movement, mutism, staring, posturing, and negativism.
    • Patients may sit or stand in the same position for hours, may hold odd positions, and may resist movement of their extremities.
  • Excited Catatonia:
    • Excited catatonia is characterised by odd mannerisms/gestures, performing purposeless or inappropriate actions, excessive motor activity restlessness, stereotypy, impulsivity, agitation, combativeness.
    • Speech and actions may be repetitive or mimic another person’s.
    • People in this state are extremely hyperactive and may have delusions and hallucinations.
    • Catatonic excitement is commonly cited as one of the most dangerous mental states in psychiatry.
  • Malignant Catatonia:
    • Malignant catatonia is a life-threatening condition that may progress rapidly within a few days. It is characterised by fever, abnormalities in blood pressure, heart rate, respiratory rate, diaphoresis (sweating), and delirium.
    • Certain lab findings are common with this presentation, however, they are nonspecific which means that they are also present in other conditions and do not diagnose catatonia.
    • These lab findings include: leukocytosis, elevated creatine kinase, low serum iron.
    • The signs and symptoms of malignant catatonia overlap significantly with neuroleptic malignant syndrome (NMS) and so a careful history, review of medications, and physical exam are critical to properly differentiate these conditions.
    • For example, if the patient has waxy flexibility and holds a position against gravity when passively moved into that position, then it is likely catatonia.
    • If the patient has a “lead-pipe rigidity” then NMS should be the prime suspect.

Diagnosis

There is not yet a definitive consensus regarding diagnostic criteria of catatonia. In the American Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the World Health Organisation’s eleventh edition of the International Classification of Disease (ICD-11) the classification is more homogeneous than in earlier editions. Prominent researchers in the field have other suggestions for diagnostic criteria.

DSM-5 Classification

The DSM-5 does not classify catatonia as an independent disorder, but rather it classifies it as catatonia associated with another mental disorder, due to another medical condition, or as unspecified catatonia. Catatonia is diagnosed by the presence of three or more of the following 12 psychomotor symptoms in association with the above mentioned mental disorder, medical condition, or unspecified.

  • Stupor: no psycho-motor activity; not actively relating to environment.
  • Catalepsy: passive induction of a posture held against gravity.
  • Waxy flexibility: allowing positioning by examiner and maintaining that position.
  • Mutism: no, or very little, verbal response (exclude if known aphasia).
  • Negativism: opposition or no response to instructions or external stimuli.
  • Posturing: spontaneous and active maintenance of a posture against gravity.
  • Mannerisms that are odd, circumstantial caricatures of normal actions.
  • Stereotypy: repetitive, abnormally frequent, non-goal-directed movements.
  • Agitation, not influenced by external stimuli.
  • Grimacing: keeping a fixed facial expression.
  • Echolalia: mimicking another’s speech.
  • Echopraxia: mimicking another’s movements.

Other disorders (additional code 293.89 [F06.1] to indicate the presence of the co-morbid catatonia):

  • Catatonia associated with autism spectrum disorder.
  • Catatonia associated with schizophrenia spectrum and other psychotic disorders.
  • Catatonia associated with brief psychotic disorder.
  • Catatonia associated with schizophreniform disorder.
  • Catatonia associated with schizoaffective disorder.
  • Catatonia associated with substance-induced psychotic disorder.
  • Catatonia associated with bipolar and related disorders.
  • Catatonia associated with major depressive disorder.
  • Catatonic disorder due to another medical condition.
  • If catatonic symptoms are present but do not form the catatonic syndrome, a medication- or substance-induced aetiology should first be considered.

ICD-11 Classification

In ICD-11 catatonia is defined as a syndrome of primarily psychomotor disturbances that is characterised by the simultaneous occurrence of several symptoms such as stupor; catalepsy; waxy flexibility; mutism; negativism; posturing; mannerisms; stereotypies; psychomotor agitation; grimacing; echolalia and echopraxia. Catatonia may occur in the context of specific mental disorders, including mood disorders, schizophrenia or other primary psychotic disorders, and Neurodevelopmental disorders, and may be induced by psychoactive substances, including medications. Catatonia may also be caused by a medical condition not classified under mental, behavioural, or neurodevelopmental disorders.

Assessment/Physical

Catatonia is often overlooked and under-diagnosed. Patients with catatonia most commonly have an underlying psychiatric disorder, for this reason, physicians may overlook signs of catatonia due to the severity of the psychosis the patient is presenting with. Furthermore, the patient may not be presenting with the common signs of catatonia such as mutism and posturing. Additionally, the motor abnormalities seen in catatonia are also present in psychiatric disorders. For example, a patient with mania will show increased motor activity that may progress to excited catatonia. One way in which physicians can differentiate between the two is to observe the motor abnormality. Patients with mania present with increased goal-directed activity. On the other hand, the increased activity in catatonia is not goal-directed and often repetitive.

Catatonia is a clinical diagnosis and there is no specific laboratory test to diagnose it. However, certain testing can help determine what is causing the catatonia. An EEG will likely show diffuse slowing. If a seizure activity is driving the syndrome, then an EEG would also be helpful in detecting this. CT or MRI will not show catatonia; however, they might reveal abnormalities that might be leading to the syndrome. Metabolic screens, inflammatory markers, or autoantibodies may reveal reversible medical causes of catatonia.

Vital signs should be frequently monitored as catatonia can progress to malignant catatonia which is life-threatening. Malignant catatonia is characterised by fever, hypertension, tachycardia, and tachypnoea.

Rating Scale

Various rating scales for catatonia have been developed, however, their utility for clinical care has not been well established. The most commonly used scale is the Bush-Francis Catatonia Rating Scale (BFCRS) (downloadable PDF). The scale is composed of 23 items with the first 14 items being used as the screening tool. If 2 of the 14 are positive, this prompts for further evaluation and completion of the remaining 9 items.

A diagnosis can be supported by the lorazepam challenge or the zolpidem challenge. While proven useful in the past, barbiturates are no longer commonly used in psychiatry; thus the option of either benzodiazepines or ECT.

Differential Diagnosis

The differential diagnosis of catatonia is extensive as signs and symptoms of catatonia may overlap significantly with those of other conditions. Therefore, a careful and detailed history, medication review, and physical exam are key to diagnosing catatonia and differentiating it from other conditions. Furthermore, some of these conditions can themselves lead to catatonia. The differential diagnosis is as follows:

  • Neuroleptic malignant syndrome (NMS):
    • Malignant catatonia and NMS are both life-threatening conditions that share many of the same characteristics including fever, autonomic instability, rigidity, and delirium.
    • Lab values of low serum iron, elevated creatine kinase, and white blood cell count are also shared by the two disorders further complicating the diagnosis.
    • Some experts consider NMS a drug-induced form of catatonia, however, it has not been established as a subtype.
    • There are features of malignant catatonia (posturing, impulsivity, etc) that are absent from NSM and the lab results are not as consistent in malignant catatonia as they are in NMS.
    • NMS is a drug-induced condition associated with antipsychotics, particularly, first generation antipsychotics.
    • Therefore, discontinuing antipsychotics and starting benzodiazepines is a treatment for this condition, and similarly it is helpful in catatonia as well.
  • Anti-NMDA receptor encephalitis:
    • Anti-NMDA receptor encephalitis is an autoimmune disorder characterised by neuropsychiatric features and the presence of IgG antibodies.
    • The presentation of anti-NMDAR encephalitis has been categorized into 5 phases: prodromal phase, psychotic phase, unresponsive phase, hyperkinetic phase, and recovery phase.
    • The psychotic phase progresses into the unresponsive phase characterized by mutism, decreased motor activity, and catatonia.
  • Serotonin syndrome:
    • Both serotonin syndrome and malignant catatonia may present with signs and symptoms of delirium, autonomic instability, hyperthermia, and rigidity.
    • Again, similar to the presentation in NSM. However, patients with Serotonin syndrome have a history of ingestion of serotonergic drugs (Ex: SSRI).
    • These patients will also present with hyperreflexia, myoclonus, nausea, vomiting, and diarrhoea.
  • Malignant hyperthermia:
    • Malignant hyperthermia and malignant catatonia share features of autonomic instability, hyperthermia, and rigidity.
    • However, malignant hyperthermia is a hereditary disorder of skeletal muscle that makes these patients susceptible to exposure to halogenated anaesthetics and/or depolarising muscle relaxants like succinylcholine.
    • Malignant hyperthermia most commonly occurs in the intraoperative or postoperative periods. Other signs and symptoms of malignant hyperthermia include metabolic and respiratory acidosis, hyperkalaemia, and cardiac arrhythmias.
  • Akinetic mutism:
    • Akinetic mutism is a neurological disorder characterised by a decrease in goal-directed behaviour and motivation, however, the patient has an intact level of consciousness.
    • Patients may present with apathy, and may seem indifferent to pain, hunger, or thirst.
    • Akinetic mutism has been associated with structural damage in a variety of brain areas.
    • Akinetic mutism and catatonia may both manifest with immobility, mutism, and waxy flexibility.
    • Differentiating both disorders is the fact that akinetic mutism does not present with echolalia, echopraxia, or posturing.
    • Furthermore, it is not responsive to benzodiazepines as is the case for catatonia.
  • Elective mutism:
    • Elective mutism has an anxious aetiology but has also been associated with personality disorders.
    • Patients with this disorder fail to speak with some individuals but will speak with others.
    • Likewise, they may refuse to speak in certain situations, for example, a child who refuses to speak at school but is conversational at home.
    • This disorder is distinguished from catatonia by the absence of any other signs/symptoms.
  • Non-convulsive status epilepticus:
    • Non-convulsive status epilepticus is seizure activity with no accompanying tonic-clonic movements.
    • It can present with stupor, similar to catatonia, and they both respond to benzodiazepines.
    • Non-convulsive status epilepticus is diagnosed by the presence of seizure activity seen on electroencephalogram (EEG).
    • Catatonia on the other hand, is associated with normal EEG or diffuse slowing.
  • Delirium:
    • Delirium is characterised by fluctuating disturbed perception and consciousness in the ill individual.
    • It has hypoactive and hyperactive or mixed forms. People with hyperactive delirium present similarly to those with excited catatonia and have symptoms of restlessness, agitation and aggression.
    • Those with hypoactive delirium present with similarly to retarded catatonia, withdrawn and quiet.
    • However, catatonia also includes other distinguishing features including posturing and rigidity as well as a positive response to benzodiazepines.
  • Locked-in syndrome:
    • Patients with locked-in syndrome present with immobility and mutism, however, unlike patients with catatonia who are unmotivated to communicate, patients with locked-in syndrome try to communicate with eye movements and blinking.
    • Furthermore, locked-in syndrome is caused by damage to the brainstem.
  • Stiff-person syndrome:
    • Catatonia and stiff-person syndrome are similar in that they may both present with rigidity, autonomic instability and a positive response to benzodiazepines.
    • However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies and other catatonic signs such as mutism and posturing are not part of the syndrome.
  • Parkinson’s disease:
    • Untreated late-stage Parkinson’s disease may present similarly to retarded catatonia with symptoms of immobility, rigidity, and difficulty speaking.
    • Further complicating the diagnosis is the fact that many patients with Parkinson’s disease will have major depressive disorder which may be the underlying cause of catatonia.
    • Parkinson’s disease can be distinguished from catatonia by a positive response to levodopa.
    • Catatonia on the other hand will show a positive response to benzodiazepines.

Treatment

The initial treatment of catatonia is to stop medication that could be potentially leading to the syndrome. These may include steroids, stimulants, anticonvulsants, neuroleptics, dopamine blockers, etc. The next step is to provide a “lorazepam challenge,” in which patients are given 2 mg of IV lorazepam (or another benzodiazepine). Most patients with catatonia will respond significantly to this within the first 15-30 minutes. If no change is observed during the first dose, then a second dose is given and the patient is re-examined. If the patient responds to the lorazepam challenge, then lorazepam can be scheduled at interval doses until the catatonia resolves. The lorazepam must be tapered slowly, otherwise, the catatonia symptoms may return. The underlying cause of the catatonia should also be treated during this time. If within a week the catatonia is not resolved, then ECT can be used to reverse the symptoms. ECT in combination with benzodiazepines is used to treat malignant catatonia. In France, zolpidem has also been used in diagnosis, and response may occur within the same time period. Ultimately the underlying cause needs to be treated.

Electroconvulsive therapy (ECT) is an effective treatment for catatonia that is well acknowledged. ECT has also shown favourable outcomes in patients with chronic catatonia. However, it has been pointed out that further high quality randomised controlled trials are needed to evaluate the efficacy, tolerance, and protocols of ECT in catatonia.

Antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic.

Excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, NMDA antagonists such as amantadine or memantine may be used. Amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. Memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. Topiramate is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of AMPA receptors.

Complications, Outcomes, and Recurrence

Patients may suffer several complications from being in a catatonic state. The nature of these complications will depend on the type of catatonia being experienced by the patient. For example, patients presenting with retarded catatonia may have refusal to eat which will in turn lead to malnutrition and dehydration. Furthermore, if immobility is a symptom the patient is presenting with, then they may develop pressure ulcers, muscle contractions, and are at risk of developing deep vein thrombosis (DVT) and pulmonary embolus (PE). Patients with excited catatonia may be aggressive and violent, and physical trauma may result from this. Catatonia may progress to the malignant type which will present with autonomic instability and may be life threatening. Other complications also include the development of pneumonia and neuroleptic malignant syndrome.[2]

Patients who experience an episode of catatonia are more likely to suffer recurrence. Treatment response for patients with catatonia is 50-70% and these patients have a good prognosis. However, failure to respond to medication is a very poor prognosis. Many of these patients will require long-term and continuous mental health care. For patients with catatonia with underlying schizophrenia, the prognosis is much poorer.

What is Behaviour Therapy?

Introduction

Behaviour therapy or behavioural psychotherapy is a broad term referring to clinical psychotherapy that uses techniques derived from behaviourism and/or cognitive psychology.

It looks at specific, learned behaviours and how the environment, or other people’s mental states, influences those behaviours, and consists of techniques based on learning theory, such as respondent or operant conditioning. Behaviourists who practice these techniques are either behaviour analysts or cognitive-behavioural therapists. They tend to look for treatment outcomes that are objectively measurable. Behaviour therapy does not involve one specific method but it has a wide range of techniques that can be used to treat a person’s psychological problems.

Behavioural psychotherapy is sometimes juxtaposed with cognitive psychotherapy, while cognitive behavioural therapy integrates aspects of both approaches, such as cognitive restructuring, positive reinforcement, habituation (or desensitisation), counterconditioning, and modelling.

Applied behaviour analysis (ABA) is the application of behaviour analysis that focuses on functionally assessing how behaviour is influenced by the observable learning environment and how to change such behaviour through contingency management or exposure therapies, which are used throughout clinical behaviour analysis therapies or other interventions based on the same learning principles.

Cognitive-behavioural therapy views cognition and emotions as preceding overt behaviour and implements treatment plans in psychotherapy to lessen the issue by managing competing thoughts and emotions, often in conjunction with behavioural learning principles.

A 2013 Cochrane review comparing behaviour therapies to psychological therapies found them to be equally effective, although at the time the evidence base that evaluates the benefits and harms of behaviour therapies was felt to be weak.

Brief History

Precursors of certain fundamental aspects of behaviour therapy have been identified in various ancient philosophical traditions, particularly Stoicism. For example, Wolpe and Lazarus wrote,

While the modern behavior therapist deliberately applies principles of learning to this therapeutic operations, empirical behavior therapy is probably as old as civilization – if we consider civilization as having started when man first did things to further the well-being of other men. From the time that this became a feature of human life there must have been occasions when a man complained of his ills to another who advised or persuaded him of a course of action. In a broad sense, this could be called behavior therapy whenever the behavior itself was conceived as the therapeutic agent. Ancient writings contain innumerable behavioral prescriptions that accord with this broad conception of behavior therapy.

The first use of the term behaviour modification appears to have been by Edward Thorndike in 1911. His article Provisional Laws of Acquired Behaviour or Learning makes frequent use of the term “modifying behaviour”. Through early research in the 1940s and the 1950s the term was used by Joseph Wolpe’s research group. The experimental tradition in clinical psychology used it to refer to psycho-therapeutic techniques derived from empirical research. It has since come to refer mainly to techniques for increasing adaptive behaviour through reinforcement and decreasing maladaptive behaviour through extinction or punishment (with emphasis on the former). Two related terms are behaviour therapy and applied behaviour analysis. Since techniques derived from behavioural psychology tend to be the most effective in altering behaviour, most practitioners consider behaviour modification along with behaviour therapy and applied behaviour analysis to be founded in behaviourism. While behaviour modification and applied behaviour analysis typically uses interventions based on the same behavioural principles, many behaviour modifiers who are not applied behaviour analysts tend to use packages of interventions and do not conduct functional assessments before intervening.

Possibly the first occurrence of the term “behaviour therapy” was in a 1953 research project by B.F. Skinner, Ogden Lindsley, Nathan Azrin and Harry C. Solomon. The paper talked about operant conditioning and how it could be used to help improve the functioning of people who were diagnosed with chronic schizophrenia. Early pioneers in behaviour therapy include Joseph Wolpe and Hans Eysenck.

In general, behaviour therapy is seen as having three distinct points of origin: South Africa (Wolpe’s group), The United States (Skinner), and the United Kingdom (Rachman and Eysenck). Each had its own distinct approach to viewing behaviour problems. Eysenck in particular viewed behaviour problems as an interplay between personality characteristics, environment, and behaviour. Skinner’s group in the United States took more of an operant conditioning focus. The operant focus created a functional approach to assessment and interventions focused on contingency management such as the token economy and behavioural activation. Skinner’s student Ogden Lindsley is credited with forming a movement called precision teaching, which developed a particular type of graphing programme called the standard celeration chart to monitor the progress of clients. Skinner became interested in the individualising of programs for improved learning in those with or without disabilities and worked with Fred S. Keller to develop programmed instruction. Programmed instruction had some clinical success in aphasia rehabilitation. Gerald Patterson used programme instruction to develop his parenting text for children with conduct problems. With age, respondent conditioning appears to slow but operant conditioning remains relatively stable. While the concept had its share of advocates and critics in the west, its introduction in the Asian setting, particularly in India in the early 1970s and its grand success were testament to the famous Indian psychologist H. Narayan Murthy’s enduring commitment to the principles of behavioural therapy and biofeedback.

While many behaviour therapists remain staunchly committed to the basic operant and respondent paradigm, in the second half of the 20th century, many therapists coupled behaviour therapy with the cognitive therapy, of Aaron Beck, Albert Ellis, and Donald Meichenbaum to form cognitive behaviour therapy (CBT). In some areas the cognitive component had an additive effect (for example, evidence suggests that cognitive interventions improve the result of social phobia treatment) but in other areas it did not enhance the treatment, which led to the pursuit of third generation behaviour therapies. Third generation behaviour therapy uses basic principles of operant and respondent psychology but couples them with functional analysis and a clinical formulation/case conceptualisation of verbal behaviour more inline with view of the behaviour analysts. Some research supports these therapies as being more effective in some cases than cognitive therapy, but overall the question is still in need of answers.

Theoretical Basis

The behavioural approach to therapy assumes that behaviour that is associated with psychological problems develops through the same processes of learning that affects the development of other behaviours. Therefore, behaviourists see personality problems in the way that personality was developed. They do not look at behaviour disorders as something a person has, but consider that it reflects how learning has influenced certain people to behave in a certain way in certain situations.

Behaviour therapy is based upon the principles of classical conditioning developed by Ivan Pavlov and operant conditioning developed by B.F. Skinner. Classical conditioning happens when a neutral stimulus comes right before another stimulus that triggers a reflexive response. The idea is that if the neutral stimulus and whatever other stimulus that triggers a response is paired together often enough that the neutral stimulus will produce the reflexive response. Operant conditioning has to do with rewards and punishments and how they can either strengthen or weaken certain behaviours.

Contingency management programmes are a direct product of research from operant conditioning.

Current Forms

Behavioural therapy based on operant and respondent principles has considerable evidence base to support its usage. This approach remains a vital area of clinical psychology and is often termed clinical behaviour analysis. Behavioural psychotherapy has become increasingly contextual in recent years. Behavioural psychotherapy has developed greater interest in recent years in personality disorders as well as a greater focus on acceptance and complex case conceptualisations.

Functional Analytic Psychotherapy

One current form of behavioural psychotherapy is functional analytic psychotherapy. Functional analytic psychotherapy is a longer duration behaviour therapy. Functional analytic therapy focuses on in-session use of reinforcement and is primarily a relationally-based therapy. As with most of the behavioural psychotherapies, functional analytic psychotherapy is contextual in its origins and nature. and draws heavily on radical behaviourism and functional contextualism.

Functional analytic psychotherapy holds to a process model of research, which makes it unique compared to traditional behaviour therapy and cognitive behavioural therapy.

Functional analytic psychotherapy has a strong research support. Recent functional analytic psychotherapy research efforts are focusing on management of aggressive inpatients.

Assessment

Behaviour therapists complete a functional analysis or a functional assessment that looks at four important areas: stimulus, organism, response and consequences. The stimulus is the condition or environmental trigger that causes behaviour. An organism involves the internal responses of a person, like physiological responses, emotions and cognition. A response is the behaviour that a person exhibits and the consequences are the result of the behaviour. These four things are incorporated into an assessment done by the behaviour therapist.

Most behaviour therapists use objective assessment methods like structured interviews, objective psychological tests or different behavioural rating forms. These types of assessments are used so that the behaviour therapist can determine exactly what a client’s problem may be and establish a baseline for any maladaptive responses that the client may have. By having this baseline, as therapy continues this same measure can be used to check a client’s progress, which can help determine if the therapy is working. Behaviour therapists do not typically ask the why questions but tend to be more focused on the how, when, where and what questions. Tests such as the Rorschach inkblot test or personality tests like the MMPI (Minnesota Multiphasic Personality Inventory) are not commonly used for behavioural assessment because they are based on personality trait theory assuming that a person’s answer to these methods can predict behaviour. Behaviour assessment is more focused on the observations of a persons behaviour in their natural environment.

Behavioural assessment specifically attempts to find out what the environmental and self-imposed variables are. These variables are the things that are allowing a person to maintain their maladaptive feelings, thoughts and behaviours. In a behavioural assessment “person variables” are also considered. These “person variables” come from a person’s social learning history and they affect the way in which the environment affects that person’s behaviour. An example of a person variable would be behavioural competence. Behavioural competence looks at whether a person has the appropriate skills and behaviours that are necessary when performing a specific response to a certain situation or stimuli.

When making a behavioural assessment the behaviour therapist wants to answer two questions:

  1. What are the different factors (environmental or psychological) that are maintaining the maladaptive behaviour; and
  2. What type of behaviour therapy or technique that can help the individual improve most effectively.

The first question involves looking at all aspects of a person, which can be summed up by the acronym BASIC ID. This acronym stands for behaviour, affective responses, sensory reactions, imagery, cognitive processes, interpersonal relationships and drug use.

Clinical Applications

Behaviour therapy based its core interventions on functional analysis. Just a few of the many problems that behaviour therapy have functionally analysed include intimacy in couples relationships, forgiveness in couples, chronic pain, stress-related behaviour problems of being an adult child of a person with an alcohol use disorder, anorexia, chronic distress, substance abuse, depression, anxiety, insomnia and obesity.

Functional analysis has even been applied to problems that therapists commonly encounter like client resistance, partially engaged clients and involuntary clients. Applications to these problems have left clinicians with considerable tools for enhancing therapeutic effectiveness. One way to enhance therapeutic effectiveness is to use positive reinforcement or operant conditioning. Although behaviour therapy is based on the general learning model, it can be applied in a lot of different treatment packages that can be specifically developed to deal with problematic behaviours. Some of the more well known types of treatments are: Relaxation training, systematic desensitisation, virtual reality exposure, exposure and response prevention techniques, social skills training, modelling, behavioural rehearsal and homework, and aversion therapy and punishment.

Relaxation training involves clients learning to lower arousal to reduce their stress by tensing and releasing certain muscle groups throughout their body. Systematic desensitisation is a treatment in which the client slowly substitutes a new learned response for a maladaptive response by moving up a hierarchy of situations involving fear. Systematic desensitisation is based in part on counter conditioning. Counter conditioning is learning new ways to change one response for another and in the case of desensitisation it is substituting that maladaptive behaviour for a more relaxing behaviour. Exposure and response prevention techniques (also known as flooding and response prevention) is the general technique in which a therapist exposes an individual to anxiety-provoking stimuli while keeping them from having any avoidance responses.

Virtual reality therapy provides realistic, computer-based simulations of troublesome situations. The modelling process involves a person being subjected to watching other individuals who demonstrate behaviour that is considered adaptive and that should be adopted by the client. This exposure involves not only the cues of the “model person” as well as the situations of a certain behaviour that way the relationship can be seen between the appropriateness of a certain behaviour and situation in which that behaviour occurs is demonstrated. With the behavioural rehearsal and homework treatment a client gets a desired behaviour during a therapy session and then they practice and record that behaviour between their sessions. Aversion therapy and punishment is a technique in which an aversive (painful or unpleasant) stimulus is used to decrease unwanted behaviours from occurring. It is concerned with two procedures:

  1. The procedures are used to decrease the likelihood of the frequency of a certain behaviour; and
  2. Procedures that will reduce the attractiveness of certain behaviours and the stimuli that elicit them.

The punishment side of aversion therapy is when an aversive stimulus is presented at the same time that a negative stimulus and then they are stopped at the same time when a positive stimulus or response is presented. Examples of the type of negative stimulus or punishment that can be used is shock therapy treatments, aversive drug treatments as well as response cost contingent punishment which involves taking away a reward.

Applied behaviour analysis is using behavioural methods to modify certain behaviours that are seen as being important socially or personally. There are four main characteristics of applied behaviour analysis:

  • First behaviour analysis is focused mainly on overt behaviours in an applied setting.
    • Treatments are developed as a way to alter the relationship between those overt behaviours and their consequences.
  • Another characteristic of applied behaviour analysis is how it (behaviour analysis) goes about evaluating treatment effects.
    • The individual subject is where the focus of study is on, the investigation is centred on the one individual being treated.
  • A third characteristic is that it focuses on what the environment does to cause significant behaviour changes.
  • Finally the last characteristic of applied behaviour analysis is the use of those techniques that stem from operant and classical conditioning such as providing reinforcement, punishment, stimulus control and any other learning principles that may apply.

Social skills training teaches clients skills to access reinforcers and lessen life punishment. Operant conditioning procedures in meta-analysis had the largest effect size for training social skills, followed by modelling, coaching, and social cognitive techniques in that order. Social skills training has some empirical support particularly for schizophrenia. However, with schizophrenia, behavioural programmes have generally lost favour.

Some other techniques that have been used in behaviour therapy are contingency contracting, response costs, token economies, biofeedback, and using shaping and grading task assignments.

Shaping and graded task assignments are used when behaviour that needs to be learned is complex. The complex behaviours that need to be learned are broken down into simpler steps where the person can achieve small things gradually building up to the more complex behaviour. Each step approximates the eventual goal and helps the person to expand their activities in a gradual way. This behaviour is used when a person feels that something in their lives can not be changed and life’s tasks appear to be overwhelming.

Another technique of behaviour therapy involves holding a client or patient accountable of their behaviours in an effort to change them. This is called a contingency contract, which is a formal written contract between two or more people that defines the specific expected behaviours that you wish to change and the rewards and punishments that go along with that behaviour. In order for a contingency contract to be official it needs to have five elements. First it must state what each person will get if they successfully complete the desired behaviour. Secondly those people involved have to monitor the behaviours. Third, if the desired behaviour is not being performed in the way that was agreed upon in the contract the punishments that were defined in the contract must be done. Fourth if the persons involved are complying with the contract they must receive bonuses. The last element involves documenting the compliance and noncompliance while using this treatment in order to give the persons involved consistent feedback about the target behaviour and the provision of reinforcers.

Token economies is a behaviour therapy technique where clients are reinforced with tokens that are considered a type of currency that can be used to purchase desired rewards, like being able to watch television or getting a snack that they want when they perform designated behaviours. Token economies are mainly used in institutional and therapeutic settings. In order for a token economy to be effective there must be consistency in administering the program by the entire staff. Procedures must be clearly defined so that there is no confusion among the clients. Instead of looking for ways to punish the patients or to deny them of rewards, the staff has to reinforce the positive behaviours so that the clients will increase the occurrence of the desired behaviour. Over time the tokens need to be replaced with less tangible rewards such as compliments so that the client will be prepared when they leave the institution and won’t expect to get something every time they perform a desired behaviour.

Closely related to token economies is a technique called response costs. This technique can either be used with or without token economies. Response costs is the punishment side of token economies where there is a loss of a reward or privilege after someone performs an undesirable behaviour. Like token economies this technique is used mainly in institutional and therapeutic settings.

Considerable policy implications have been inspired by behavioural views of various forms of psychopathology. One form of behaviour therapy, habit reversal training, has been found to be highly effective for treating tics.

In Rehabilitation

Currently, there is a greater call for behavioural psychologists to be involved in rehabilitation efforts.

Treatment of Mental Disorders

Two large studies done by the Faculty of Health Sciences at Simon Fraser University indicates that both behaviour therapy and cognitive-behavioural therapy (CBT) are equally effective for OCD. CBT has been shown to perform slightly better at treating co-occurring depression.

Considerable policy implications have been inspired by behavioural views of various forms of psychopathology. One form of behaviour therapy (habit reversal training) has been found to be highly effective for treating tics.

There has been a development towards combining techniques to treat psychiatric disorders. Cognitive interventions are used to enhance the effects of more established behavioural interventions based on operant and classical conditioning. An increased effort has also been placed to address the interpersonal context of behaviour.

Behaviour therapy can be applied to a number of mental disorders and in many cases is more effective for specific disorders as compared to others. Behaviour therapy techniques can be used to deal with any phobias that a person may have. Desensitisation has also been applied to other issues such as dealing with anger, if a person has trouble sleeping and certain speech disorders. Desensitisation does not occur over night, there is a process of treatment. Desensitisation is done on a hierarchy and happens over a number of sessions. The hierarchy goes from situations that make a person less anxious or nervous up to things that are considered to be extreme for the patient.

Modelling has been used in dealing with fears and phobias. Modelling has been used in the treatment of fear of snakes as well as a fear of water.

Aversive therapy techniques have been used to treat sexual deviations as well as alcohol use disorder.

Exposure and prevention procedure techniques can be used to treat people who have anxiety problems as well as any fears or phobias. These procedures have also been used to help people dealing with any anger issues as well as pathological grievers (people who have distressing thoughts about a deceased person).

Virtual reality therapy deals with fear of heights, fear of flying, and a variety of other anxiety disorders. VRT has also been applied to help people with substance abuse problems reduce their responsiveness to certain cues that trigger their need to use drugs.

Shaping and graded task assignments has been used in dealing with suicide and depressed or inhibited individuals. This is used when a patient feel hopeless and they have no way of changing their lives. This hopelessness involves how the person reacts and responds to someone else and certain situations and their perceived powerlessness to change that situation that adds to the hopelessness. For a person with suicidal ideation, it is important to start with small steps. Because that person may perceive everything as being a big step, the smaller you start the easier it will be for the person to master each step. This technique has also been applied to people dealing with agoraphobia, or fear of being in public places or doing something embarrassing.

Contingency contracting has been used to deal with behaviour problems in delinquents and when dealing with on task behaviours in students.

Token economies are used in controlled environments and are found mostly in psychiatric hospitals. They can be used to help patients with different mental illnesses but it doesn’t focus on the treatment of the mental illness but instead on the behavioural aspects of a patient. The response cost technique has been used to address a variety of behaviours such as smoking, overeating, stuttering, and psychotic talk.

Treatment Outcomes

Systematic desensitisation has been shown to successfully treat phobias about heights, driving, insects as well as any anxiety that a person may have. Anxiety can include social anxiety, anxiety about public speaking as well as test anxiety. It has been shown that the use of systematic desensitisation is an effective technique that can be applied to a number of problems that a person may have.

When using modelling procedures this technique is often compared to another behavioural therapy technique. When compared to desensitisation, the modelling technique does appear to be less effective. However it is clear that the greater the interaction between the patient and the subject he is modelling the greater the effectiveness of the treatment.

While undergoing exposure therapy, a person typically needs five sessions to assess the treatment’s effectiveness. After five sessions, exposure treatment has been shown to provide benefit to the patient. However, it is still recommended treatment continue beyond the initial five sessions.

Virtual reality therapy (VRT) has shown to be effective for a fear of heights. It has also been shown to help with the treatment of a variety of anxiety disorders. Due to the costs associated with VRT, therapists are still awaiting results of controlled trials investigating VRT, to assess which applications demonstrate the best results.

For those with suicidal ideation, treatment depends on how severe the person’s depression and sense of hopelessness is. If these things are severe, the person’s response to completing small steps will not be of importance to them, because they don’t consider the success an accomplishment. Generally, in those not suffering from severe depression or fear, this technique has been successful, as completion of simpler activities builds their confidences and allows them to progress to more complex situations.

Contingency contracts have been seen to be effective in changing any undesired behaviours of individuals. It has been seen to be effective in treating behaviour problems in delinquents regardless of the specific characteristics of the contract.

Token economies have been shown to be effective when treating patients in psychiatric wards who had chronic schizophrenia. The results showed that the contingent tokens were controlling the behaviour of the patients.

Response costs has been shown to work in suppressing a variety of behaviours such as smoking, overeating or stuttering with a diverse group of clinical populations ranging from sociopaths to school children. These behaviours that have been suppressed using this technique often do not recover when the punishment contingency is withdrawn. Also undesirable side effects that are usually seen with punishment are not typically found when using the response cost technique.

Third Generation

The third-generation behaviour therapy movement has been called clinical behaviour analysis because it represents a movement away from cognitivism and back toward radical behaviourism and other forms of behaviourism, in particular functional analysis and behavioural models of verbal behaviour. This area includes acceptance and commitment therapy (ACT), cognitive behavioural analysis system of psychotherapy (CBASP), behavioural activation (BA), dialectical behavioural therapy, functional analytic psychotherapy (FAP), integrative behavioural couples therapy, metacognitive therapy and metacognitive training. These approaches are squarely within the applied behaviour analysis tradition of behaviour therapy.

ACT may be the most well-researched of all the third-generation behaviour therapy models. It is based on relational frame theory. Other authors object to the term “third generation” or “third wave” and incorporate many of the “third wave” therapeutic techniques under the general umbrella term of modern cognitive behavioural therapies.

Functional analytic psychotherapy is based on a functional analysis of the therapeutic relationship. It places a greater emphasis on the therapeutic context and returns to the use of in-session reinforcement. In general, 40 years of research supports the idea that in-session reinforcement of behaviour can lead to behavioural change.

Behavioural activation emerged from a component analysis of cognitive behaviour therapy. This research found no additive effect for the cognitive component. Behavioural activation is based on a matching model of reinforcement. A recent review of the research, supports the notion that the use of behavioural activation is clinically important for the treatment of depression.

Integrative behavioural couples therapy developed from dissatisfaction with traditional behavioural couples therapy. Integrative behavioural couples therapy looks to Skinner (1969) for the difference between contingency-shaped and rule-governed behaviour. It couples this analysis with a thorough functional assessment of the couple’s relationship. Recent efforts have used radical behavioural concepts to interpret a number of clinical phenomena including forgiveness.

Organisations

Many organisations exist for behaviour therapists around the world. In the United States, the American Psychological Association’s Division 25 is the division for behaviour analysis. The Association for Contextual Behaviour Therapy is another professional organisation. ACBS is home to many clinicians with specific interest in third generation behaviour therapy. Doctoral-level behaviour analysts who are psychologists belong to American Psychological Association’s division 25 – Behaviour analysis. APA offers a diploma in behavioural psychology.

The Association for Behavioural and Cognitive Therapies (formerly the Association for the Advancement of Behaviour Therapy) is for those with a more cognitive orientation. The ABCT also has an interest group in behaviour analysis, which focuses on clinical behaviour analysis. In addition, the Association for Behavioural an Cognitive Therapies has a special interest group on addictions.

Characteristics

By nature, behavioural therapies are empirical (data-driven), contextual (focused on the environment and context), functional (interested in the effect or consequence a behaviour ultimately has), probabilistic (viewing behaviour as statistically predictable), monistic (rejecting mind–body dualism and treating the person as a unit), and relational (analysing bidirectional interactions).

Behavioural therapy develops, adds and provides behavioural intervention strategies and programs for clients, and training to people who care to facilitate successful lives in the communities.

Training

Recent efforts in behavioural psychotherapy have focused on the supervision process. A key point of behavioural models of supervision is that the supervisory process parallels the behavioural psychotherapy.

Methods

  • Behaviour management.
  • Behaviour modification.
  • Clinical behaviour analysis.
  • Contingency management.
  • Covert conditioning.
  • Decoupling.
  • Exposure and response prevention.
  • Flooding.
  • Habit reversal training.
  • Matching law.
  • Modelling.
  • Observational learning.
  • Operant conditioning.
  • Professional practice of behaviour analysis.
  • Respondent conditioning.
  • Stimulus control.
  • Systematic desensitisation.

Reference

Skinner, B.F. (1969). Contingencies of Reinforcement: A Theoretical Analysis. New York: Meredith Corporation.