Dysthymia, also known as persistent depressive disorder (PDD), is a mental and behavioural disorder, specifically a disorder primarily of mood, consisting of the same cognitive and physical problems as depression, but with longer-lasting symptoms.
The concept was coined by Robert Spitzer as a replacement for the term “depressive personality” in the late 1970s.
As dysthymia is a chronic disorder, sufferers may experience symptoms for many years before it is diagnosed, if diagnosis occurs at all. As a result, they may believe that depression is a part of their character, so they may not even discuss their symptoms with doctors, family members or friends. In the DSM-5, dysthymia is replaced by persistent depressive disorder. This new condition includes both chronic major depressive disorder and the previous dysthymic disorder. The reason for this change is that there was no evidence for meaningful differences between these two conditions.
Epidemiology
Globally dysthymia occurs in about 105 million people a year (1.5% of the population). It is 38% more common in women (1.8% of women) than in men (1.3% of men). The lifetime prevalence rate of dysthymia in community settings appears to range from 3 to 6% in the United States. However, in primary care settings the rate is higher ranging from 5 to 15 percent. United States prevalence rates tend to be somewhat higher than rates in other countries.
Signs and Symptoms
Dysthymia characteristics include an extended period of depressed mood combined with at least two other symptoms which may include insomnia or hypersomnia, fatigue or low energy, eating changes (more or less), low self-esteem, or feelings of hopelessness. Poor concentration or difficulty making decisions are treated as another possible symptom. Irritability is one of the more common symptoms in children and adolescents.
Mild degrees of dysthymia may result in people withdrawing from stress and avoiding opportunities for failure. In more severe cases of dysthymia, people may withdraw from daily activities. They will usually find little pleasure in usual activities and pastimes.
Diagnosis of dysthymia can be difficult because of the subtle nature of the symptoms and patients can often hide them in social situations, making it challenging for others to detect symptoms. Additionally, dysthymia often occurs at the same time as other psychological disorders, which adds a level of complexity in determining the presence of dysthymia, particularly because there is often an overlap in the symptoms of disorders.
There is a high incidence of comorbid illness in those with dysthymia. Suicidal behaviour is also a particular problem with those with dysthymia. It is vital to look for signs of major depression, panic disorder, generalised anxiety disorder, alcohol and substance use disorders, and personality disorder.
Causes
There are no known biological causes that apply consistently to all cases of dysthymia, which suggests diverse origin of the disorder. However, there are some indications that there is a genetic predisposition to dysthymia: “The rate of depression in the families of people with dysthymia is as high as fifty percent for the early-onset form of the disorder”. Other factors linked with dysthymia include stress, social isolation, and lack of social support.
In a study using identical and fraternal twins, results indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is in part caused by heredity.
Co-Occurring Conditions
Dysthymia often co-occurs with other mental disorders. A “double depression” is the occurrence of episodes of major depression in addition to dysthymia. Switching between periods of dysthymic moods and periods of hypomanic moods is indicative of cyclothymia, which is a mild variant of bipolar disorder.
“At least three-quarters of patients with dysthymia also have a chronic physical illness or another psychiatric disorder such as one of the anxiety disorders, cyclothymia, drug addiction, or alcoholism”. Common co-occurring conditions include major depression (up to 75%), anxiety disorders (up to 50%), personality disorders (up to 40%), somatoform disorders (up to 45%) and substance use disorders (up to 50%). People with dysthymia have a higher-than-average chance of developing major depression. A 10-year follow-up study found that 95% of dysthymia patients had an episode of major depression. When an intense episode of depression occurs on top of dysthymia, the state is called “double depression.”
Double Depression
Double depression occurs when a person experiences a major depressive episode on top of the already-existing condition of dysthymia. It is difficult to treat, as sufferers accept these major depressive symptoms as a natural part of their personality or as a part of their life that is outside of their control. The fact that people with dysthymia may accept these worsening symptoms as inevitable can delay treatment. When and if such people seek out treatment, the treatment may not be very effective if only the symptoms of the major depression are addressed, but not the dysthymic symptoms. Patients with double depression tend to report significantly higher levels of hopelessness than is normal. This can be a useful symptom for mental health services providers to focus on when working with patients to treat the condition. Additionally, cognitive therapies can be effective for working with people with double depression in order to help change negative thinking patterns and give individuals a new way of seeing themselves and their environment.
It has been suggested that the best way to prevent double depression is by treating the dysthymia. A combination of antidepressants and cognitive therapies can be helpful in preventing major depressive symptoms from occurring. Additionally, exercise and good sleep hygiene (e.g. improving sleep patterns) are thought to have an additive effect on treating dysthymic symptoms and preventing them from worsening.
Pathophysiology
There is evidence that there may be neurological indicators of early onset dysthymia. There are several brain structures (corpus callosum and frontal lobe) that are different in women with dysthymia than in those without dysthymia. This may indicate that there is a developmental difference between these two groups.
Another study, which used fMRI techniques to assess the differences between individuals with dysthymia and other people, found additional support for neurological indicators of the disorder. This study found several areas of the brain that function differently. The amygdala (associated with processing emotions such as fear) was more activated in dysthymia patients. The study also observed increased activity in the insula (which is associated with sad emotions). Finally, there was increased activity in the cingulate gyrus (which serves as the bridge between attention and emotion).
A study comparing healthy individuals to people with dysthymia indicates there are other biological indicators of the disorder. An anticipated result appeared as healthy individuals expected fewer negative adjectives to apply to them, whereas people with dysthymia expected fewer positive adjectives to apply to them in the future. Biologically these groups are also differentiated in that healthy individuals showed greater neurological anticipation for all types of events (positive, neutral, or negative) than those with dysthymia. This provides neurological evidence of the dulling of emotion that individuals with dysthymia have learned to use to protect themselves from overly strong negative feelings, compared to healthy people.
There is some evidence of a genetic basis for all types of depression, including dysthymia. A study using identical and fraternal twins indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is caused in part by heredity.
A new model has recently surfaced in the literature regarding the HPA axis (structures in the brain that get activated in response to stress) and its involvement with dysthymia (e.g. phenotypic variations of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP), and down-regulation of adrenal functioning) as well as forebrain serotonergic mechanisms. Since this model is highly provisional, further research is still needed.
Diagnosis
The Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV), published by the American Psychiatric Association, characterises dysthymic disorder. The essential symptom involves the individual feeling depressed for the majority of days, and parts of the day, for at least two years. Low energy, disturbances in sleep or in appetite, and low self-esteem typically contribute to the clinical picture as well. Sufferers have often experienced dysthymia for many years before it is diagnosed. People around them often describe the sufferer in words similar to “just a moody person”. Note the following diagnostic criteria:
During a majority of days for two years or more, the adult patient reports depressed mood, or appears depressed to others for most of the day.
When depressed, the patient has two or more of:
decreased or increased appetite
decreased or increased sleep (insomnia or hypersomnia)
Fatigue or low energy
Reduced self-esteem
Decreased concentration or problems making decisions
Feelings of hopelessness or pessimism
During this two-year period, the above symptoms are never absent longer than two consecutive months.
During the duration of the two-year period, the patient may have had a perpetual major depressive episode.
The patient has not had any manic, hypomanic, or mixed episodes.
The patient has never fulfilled criteria for cyclothymic disorder.
The symptoms are often not directly caused by a medical illness or by substances, including substance use or other medications.
The symptoms may cause significant problems or distress in social, work, academic, or other major areas of life functioning.
In children and adolescents, mood can be irritable, and duration must be at least one year, in contrast to two years needed for diagnosis in adults.
Early onset (diagnosis before age 21) is associated with more frequent relapses, psychiatric hospitalisations, and more co-occurring conditions. For younger adults with dysthymia, there is a higher co-occurrence in personality abnormalities and the symptoms are likely chronic. However, in older adults suffering from dysthymia, the psychological symptoms are associated with medical conditions and/or stressful life events and losses.
Dysthymia can be contrasted with major depressive disorder by assessing the acute nature of the symptoms. Dysthymia is far more chronic (long lasting) than major depressive disorder, in which symptoms may be present for as little as 2 weeks. Also Dysthymia often presents itself at an earlier age than Major Depressive Disorder.
Prevention
Though there is no clear-cut way to prevent dysthymia from occurring, some suggestions have been made. Since dysthymia will often first occur in childhood, it is important to identify children who may be at risk. It may be beneficial to work with children in helping to control their stress, increase resilience, boost self-esteem, and provide strong networks of social support. These tactics may be helpful in warding off or delaying dysthymic symptoms.
Treatment
Persistent depressive disorder can be treated with psychotherapy and pharmacotherapy. The overall rate and degree of treatment success is somewhat lower than for non-chronic depression, and a combination of psychotherapy and pharmacotherapy shows best results.
Therapy
Psychotherapy can be effective in treating dysthymia. In a meta-analytic study from 2010, psychotherapy had a small but significant effect when compared to control groups. However, psychotherapy is significantly less effective than pharmacotherapy in direct comparisons.
There are many different types of therapy, and some are more effective than others.
The empirically most studied type of treatment is cognitive-behavioural therapy.
This type of therapy is very effective for non-chronic depression, and it appears to be also effective for chronic depression.
Cognitive behavioural analysis system of psychotherapy (CBASP) has been designed specifically to treat PDD.
Empirical results on this form of therapy are inconclusive: While one study showed remarkably high treatment success rates, a later, even larger study showed no significant benefit of adding CBASP to treatment with antidepressants.
Schema therapy and psychodynamic psychotherapy have been used for PDD, though good empirical results are lacking.
Interpersonal psychotherapy has also been said to be effective in treating the disorder, though it only shows marginal benefit when added to treatment with antidepressants.
Medications
In a 2010 meta-analysis, the benefit of pharmacotherapy was limited to selective serotonin reuptake inhibitors (SSRIs) rather than tricyclic antidepressants (TCA).
According to a 2014 meta-analysis, antidepressants are at least as effective for persistent depressive disorder as for major depressive disorder. The first line of pharmacotherapy is usually SSRIs due to their purported more tolerable nature and reduced side effects compared to the irreversible monoamine oxidase inhibitors or tricyclic antidepressants. Studies have found that the mean response to antidepressant medications for people with dysthymia is 55%, compared with a 31% response rate to a placebo. The most commonly prescribed antidepressants/SSRIs for dysthymia are escitalopram, citalopram, sertraline, fluoxetine, paroxetine, and fluvoxamine. It often takes an average of 6-8 weeks before the patient begins to feel these medications’ therapeutic effects. Additionally, STAR*D, a multi-clinic governmental study, found that people with overall depression will generally need to try different brands of medication before finding one that works specifically for them. Research shows that 1 in 4 of those who switch medications get better results regardless of whether the second medication is an SSRI or some other type of antidepressant.
In a meta-analytic study from 2005, it was found that SSRIs and TCAs are equally effective in treating dysthymia. They also found that MAOIs have a slight advantage over the use of other medication in treating this disorder. However, the author of this study cautions that MAOIs should not necessarily be the first line of defence in the treatment of dysthymia, as they are often less tolerable than their counterparts, such as SSRIs.
Tentative evidence supports the use of amisulpride to treat dysthymia but with increased side effects.
Combination Treatment
When pharmacotherapy alone is compared with combined treatment with pharmacotherapy plus psychotherapy, there is a strong trend in favour of combined treatment. Working with a psychotherapist to address the causes and effects of the disorder, in addition to taking antidepressants to help eliminate the symptoms, can be extremely beneficial. This combination is often the preferred method of treatment for those who have dysthymia. Looking at various studies involving treatment for dysthymia, 75% of people responded positively to a combination of cognitive behavioural therapy and pharmacotherapy, whereas only 48% of people responded positively to just CBT or medication alone.
A 2019 Cochrane review of 10 studies involving 840 participants could not conclude with certainty that continued pharmacotherapy with antidepressants (those used in the studies) was effective in preventing relapse or recurrence of persistent depressive disorder. The body of evidence was too small for any greater certainty although the study acknowledges that continued psychotherapy may be beneficial when compared to no treatment.
Resistance
Because of dysthymia’s chronic nature, treatment resistance is somewhat common. In such a case, augmentation is often recommended. Such treatment augmentations can include lithium pharmacology, thyroid hormone augmentation, amisulpride, buspirone, bupropion, stimulants, and mirtazapine. Additionally, if the person also suffers from seasonal affective disorder, light therapy can be useful in helping augment therapeutic effects.
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”.
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.
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.
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.
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.
“Shame on you”: The impact of shame in body-focused repetitive behaviours and binge eating.
Background
Body-focused repetitive behaviours (BFRBs), such as hair-pulling, skin-picking, and nail-biting, have been associated with difficulties in emotion regulation.
Studies have suggested that aversive emotions are important triggers for impulsive behaviours such as BFRBs and binge eating.
In particular, shame has been hypothesized to be a key emotion before and after these behaviours, but no experimental studies yet have investigated its impact on BFRBs.
The researchers aimed to evaluate the role of shame in BFRB and binge eating episodes and the presence of shame following these behaviours.
Methods
Eighteen women with BFRBs, 18 with binge eating, and 18 community controls participated in the study.
Results
Results showed that an experimental shame condition triggered more shame in the binge eating and BFRB groups than in the control group.
In addition, the shame induced condition increased the urge to engage in BFRBs, but not in binge eating.
Conclusions
Results showed that participants from the BFRB and the binge eating groups reported more shame after engaging in their pathological behaviours compared to following the neutral condition.
Future studies should replicate these findings with larger samples and different shame-inducing conditions.
Reference
Houazene, S., Leclerc, J.B., O’Connor, K. & Aardema, F. (2021) “Shame on you”: The impact of shame in body-focused repetitive behaviors and binge eating. Behaviour Research and Therapy. doi: 10.1016/j.brat.2021.103804. Online ahead of print.
Behaviourism is a systematic approach to understanding the behaviour of humans and other animals. It assumes that behaviour is either a reflex evoked by the pairing of certain antecedent stimuli in the environment, or a consequence of that individual’s history, including especially reinforcement and punishment contingencies, together with the individual’s current motivational state and controlling stimuli. Although behaviourists generally accept the important role of heredity in determining behaviour, they focus primarily on environmental events.
It combines elements of philosophy, methodology, and theory. Behaviourism emerged in the early 1900s as a reaction to depth psychology and other traditional forms of psychology, which often had difficulty making predictions that could be tested experimentally, but derived from earlier research in the late nineteenth century, such as when Edward Thorndike pioneered the law of effect, a procedure that involved the use of consequences to strengthen or weaken behaviour.
During the first half of the twentieth century, John B. Watson devised methodological behaviourism, which rejected introspective methods and sought to understand behaviour by only measuring observable behaviours and events. It was not until the 1930s that B.F. Skinner suggested that covert behaviour – including cognition and emotions – subjects to the same controlling variables as observable behaviour, which became the basis for his philosophy called radical behaviourism. While Watson and Ivan Pavlov investigated how (conditioned) neutral stimuli elicit reflexes in respondent conditioning, Skinner assessed the reinforcement histories of the discriminative (antecedent) stimuli that emits behaviour; the technique became known as operant conditioning.
The application of radical behaviourism – known as applied behaviour analysis – is used in a variety of contexts, including, for example, applied animal behaviour and organisational behaviour management to treatment of mental disorders, such as autism and substance abuse. In addition, while behaviourism and cognitive schools of psychological thought do not agree theoretically, they have complemented each other in the cognitive-behaviour therapies, which have demonstrated utility in treating certain pathologies, including simple phobias, PTSD, and mood disorders.
Branches of Behaviourism
An outline of the various branches of behaviourism can be seen the table below.
Branch
Description
Interbehaviourism
Proposed by Jacob Robert Kantor before B. F. Skinner’s writings.
Methodological Behaviourism
1. John B. Watson’s behaviourism states that only public events (motor behaviours of an individual) can be objectively observed. 2. Although it was still acknowledged that thoughts and feelings exist, they were not considered part of the science of behaviour. 3. It also laid the theoretical foundation for the early approach behaviour modification in the 1970s and early 1980s.
Psychological Behviourism
1. As proposed by Arthur W. Staats, unlike the previous behaviourisms of Skinner, Hull, and Tolman, was based upon a program of human research involving various types of human behaviour. 2. Psychological behaviourism introduces new principles of human learning. 3. Humans learn not only by the animal learning principles but also by special human learning principles. 4. Those principles involve humans’ uniquely huge learning ability. 5. Humans learn repertoires that enable them to learn other things. Human learning is thus cumulative. 6. No other animal demonstrates that ability, making the human species unique.
Radical Behaviourism
1. Skinner’s philosophy is an extension of Watson’s form of behaviourism by theorising that processes within the organism – particularly, private events, such as thoughts and feelings – are also part of the science of behaviour, and suggests that environmental variables control these internal events just as they control observable behaviours. 2. Although private events cannot be directly seen by others, they are later determined through the species’ overt behaviour. 3. Radical behaviourism forms the core philosophy behind behaviour analysis. 4. Willard Van Orman Quine used many of radical behaviourism’s ideas in his study of knowledge and language.
Teleological Behaviourism
1. Proposed by Howard Rachlin, post-Skinnerian, purposive, close to microeconomics. Focuses on objective observation as opposed to cognitive processes.
Theoretical Behaviourism
1. Proposed by J.E.R. Staddon, adds a concept of internal state to allow for the effects of context. 2. According to theoretical behaviourism, a state is a set of equivalent histories, i.e., past histories in which members of the same stimulus class produce members of the same response class (i.e., B.F. Skinner’s concept of the operant). 3. Conditioned stimuli are thus seen to control neither stimulus nor response but state. 4. Theoretical behaviourism is a logical extension of Skinner’s class-based (generic) definition of the operant.
Hullian & Post-Hullian
1. A sub-type of theoretical behaviourism. 2. Theoretical, group data, not dynamic, physiological.
Purposive
1. A sub-type of theoretical behaviourism. 2. Tolman’s behaviouristic anticipation of cognitive psychology
Modern-Day Theory: Radical Behaviourism
B.F. Skinner proposed radical behaviourism as the conceptual underpinning of the experimental analysis of behaviour. This viewpoint differs from other approaches to behavioural research in various ways, but, most notably here, it contrasts with methodological behaviourism in accepting feelings, states of mind and introspection as behaviours also subject to scientific investigation. Like methodological behaviourism, it rejects the reflex as a model of all behaviour, and it defends the science of behaviour as complementary to but independent of physiology. Radical behaviourism overlaps considerably with other western philosophical positions, such as American pragmatism.
Although John B. Watson mainly emphasized his position of methodological behaviourism throughout his career, Watson and Rosalie Rayner conducted the renowned Little Albert experiment (1920), a study in which Ivan Pavlov’s theory to respondent conditioning was first applied to eliciting a fearful reflex of crying in a human infant, and this became the launching point for understanding covert behaviour (or private events) in radical behaviourism. However, Skinner felt that aversive stimuli should only be experimented on with animals and spoke out against Watson for testing something so controversial on a human.
In 1959, Skinner observed the emotions of two pigeons by noting that they appeared angry because their feathers ruffled. The pigeons were placed together in an operant chamber, where they were aggressive as a consequence of previous reinforcement in the environment. Through stimulus control and subsequent discrimination training, whenever Skinner turned off the green light, the pigeons came to notice that the food reinforcer is discontinued following each peck and responded without aggression. Skinner concluded that humans also learn aggression and possess such emotions (as well as other private events) no differently than do nonhuman animals.
Experimental and Conceptual Innovations
This essentially philosophical position gained strength from the success of Skinner’s early experimental work with rats and pigeons, summarized in his books The Behaviour of Organisms and Schedules of Reinforcement. Of particular importance was his concept of the operant response, of which the canonical example was the rat’s lever-press. In contrast with the idea of a physiological or reflex response, an operant is a class of structurally distinct but functionally equivalent responses. For example, while a rat might press a lever with its left paw or its right paw or its tail, all of these responses operate on the world in the same way and have a common consequence. Operants are often thought of as species of responses, where the individuals differ but the class coheres in its function-shared consequences with operants and reproductive success with species. This is a clear distinction between Skinner’s theory and S-R theory.
Skinner’s empirical work expanded on earlier research on trial-and-error learning by researchers such as Thorndike and Guthrie with both conceptual reformulations – Thorndike’s notion of a stimulus-response “association” or “connection” was abandoned; and methodological ones – the use of the “free operant”, so called because the animal was now permitted to respond at its own rate rather than in a series of trials determined by the experimenter procedures. With this method, Skinner carried out substantial experimental work on the effects of different schedules and rates of reinforcement on the rates of operant responses made by rats and pigeons. He achieved remarkable success in training animals to perform unexpected responses, to emit large numbers of responses, and to demonstrate many empirical regularities at the purely behavioural level. This lent some credibility to his conceptual analysis. It is largely his conceptual analysis that made his work much more rigorous than his peers’, a point which can be seen clearly in his seminal work Are Theories of Learning Necessary? in which he criticizes what he viewed to be theoretical weaknesses then common in the study of psychology. An important descendant of the experimental analysis of behaviour is the Society for Quantitative Analysis of Behaviour.
Relation to Language
As Skinner turned from experimental work to concentrate on the philosophical underpinnings of a science of behaviour, his attention turned to human language with his 1957 book Verbal Behaviour and other language-related publications; Verbal Behaviour laid out a vocabulary and theory for functional analysis of verbal behaviour, and was strongly criticised in a review by Noam Chomsky.
Skinner did not respond in detail but claimed that Chomsky failed to understand his ideas, and the disagreements between the two and the theories involved have been further discussed. Innateness theory, which has been heavily critiqued, is opposed to behaviourist theory which claims that language is a set of habits that can be acquired by means of conditioning. According to some, the behaviourist account is a process which would be too slow to explain a phenomenon as complicated as language learning. What was important for a behaviourist’s analysis of human behaviour was not language acquisition so much as the interaction between language and overt behaviour. In an essay republished in his 1969 book Contingencies of Reinforcement, Skinner took the view that humans could construct linguistic stimuli that would then acquire control over their behaviour in the same way that external stimuli could. The possibility of such “instructional control” over behaviour meant that contingencies of reinforcement would not always produce the same effects on human behaviour as they reliably do in other animals. The focus of a radical behaviourist analysis of human behaviour therefore shifted to an attempt to understand the interaction between instructional control and contingency control, and also to understand the behavioural processes that determine what instructions are constructed and what control they acquire over behaviour. Recently, a new line of behavioural research on language was started under the name of relational frame theory.
Education
Behaviourism focuses on one particular view of learning: a change in external behaviour achieved through using reinforcement and repetition (Rote learning) to shape behaviour of learners. Skinner found that behaviours could be shaped when the use of reinforcement was implemented. Desired behaviour is rewarded, while the undesired behaviour is not rewarded. Incorporating behaviourism into the classroom allowed educators to assist their students in excelling both academically and personally. In the field of language learning, this type of teaching was called the audio-lingual method, characterised by the whole class using choral chanting of key phrases, dialogues and immediate correction.
Within the behaviourist view of learning, the “teacher” is the dominant person in the classroom and takes complete control, evaluation of learning comes from the teacher who decides what is right or wrong. The learner does not have any opportunity for evaluation or reflection within the learning process, they are simply told what is right or wrong. The conceptualisation of learning using this approach could be considered “superficial,” as the focus is on external changes in behaviour, i.e., not interested in the internal processes of learning leading to behaviour change and has no place for the emotions involved in the process.
Operant Conditioning
Operant conditioning was developed by B.F. Skinner in 1937 and deals with the management of environmental contingencies to change behaviour. In other words, behaviour is controlled by historical consequential contingencies, particularly reinforcement – a stimulus that increases the probability of performing behaviours, and punishment – a stimulus that decreases such probability. The core tools of consequences are either positive (presenting stimuli following a response), or negative (withdrawn stimuli following a response).
The following descriptions explain the concepts of four common types of consequences in operant conditioning.
Type
Description
Positive Reinforcement
1. Providing a stimulus that an individual desires to reinforce desired behaviours. 2. For example, a child loves playing video games. 3. His mother reinforced his tendency to provide a helping hands to other family members by providing more time for him to play video games.
Negative Reinforcement
1. Removing a stimulus that an individual does not desire to reinforce desired behaviours. 3. For example, a child hates being nagged to clean his room. 3. His mother reinforces his room cleaning by removing the undesired stimulus of nagging after he has cleaned.
Positive Punishment
1. Providing a stimulus that an individual does not desire to decrease undesired behaviours. 2. For example, a child hates to do chores. 3. His parents will try to reduce the undesired behaviour of failing a test by applying the undesired stimuli of having him do more chores around the house.
Negative Punishment
1. Removing a stimulus that an individual desires in order to decrease undesired behaviours. 2. For example, a child loves playing video games. 3. His parents will try to reduce the undesired behaviour of failing an exam by removing the desired stimulus of video games.
Classical experiment in operant conditioning, for example the Skinner Box, “puzzle box” or operant conditioning chamber to test the effects of operant conditioning principles on rats, cats and other species. From the study of Skinner box, he discovered that the rats learned very effectively if they were rewarded frequently with food. Skinner also found that he could shape the rats’ behaviour through the use of rewards, which could, in turn, be applied to human learning as well.
Skinner’s model was based on the premise that reinforcement is used for the desired actions or responses while punishment was used to stop the undesired actions responses that are not. This theory proved that humans or animals will repeat any action that leads to a positive outcome, and avoiding any action that leads to a negative outcome. The experiment with the pigeons showed that a positive outcome leads to learned behaviour since the pigeon learned to peck the disc in return for the reward of food.
These historical consequential contingencies subsequently leads to (antecedent) stimulus control, but in contrast to respondent conditioning where antecedent stimuli elicits reflexive behavior, operant behavior is only emitted and therefore does not force its occurrence. It includes the following controlling stimuli:
Discriminative stimulus (Sd):
An antecedent stimulus that increases the chance of the organism engaging in a behaviour.
One example of this occurred in Skinner’s laboratory.
Whenever the green light (Sd) appeared, it signalled the pigeon to perform the behaviour of pecking because it learned in the past that each time it pecked, food was presented (the positive reinforcing stimulus).
Stimulus delta (S-delta):
An antecedent stimulus that signals the organism not to perform a behaviour since it was extinguished or punished in the past.
One notable instance of this occurs when a person stops their car immediately after the traffic light turns red (S-delta).
However, the person could decide to drive through the red light, but subsequently receive a speeding ticket (the positive punishing stimulus), so this behaviour will potentially not reoccur following the presence of the S-delta.
Respondent Conditioning
Although operant conditioning plays the largest role in discussions of behavioural mechanisms, respondent conditioning (also called Pavlovian or classical conditioning) is also an important behaviour-analytic process that need not refer to mental or other internal processes. Pavlov’s experiments with dogs provide the most familiar example of the classical conditioning procedure. At the beginning, the dog was provided a meat (unconditioned stimulus, UCS, naturally elicit a response that is not controlled) to eat, resulting in increased salivation (unconditioned response, UCR, which means that a response is naturally caused by UCS). Afterwards, a bell ring was presented together with food to the dog. Although bell ring was a neutral stimulus (NS, meaning that the stimulus did not had any effect), dog would start salivate when only hearing a bell ring after a number of pairings. Eventually, the neutral stimulus (bell ring) became conditioned. Therefore, salvation was elicited as a conditioned response (the response same as the unconditioned response), pairing up with meat – the conditioned stimulus). Although Pavlov proposed some tentative physiological processes that might be involved in classical conditioning, these have not been confirmed. The idea of classical conditioning helped behaviourist John Watson discover the key mechanism behind how humans acquire the behaviours that they do, which was to find a natural reflex that produces the response being considered.
Watson’s “Behaviourist Manifesto” has three aspects that deserve special recognition: one is that psychology should be purely objective, with any interpretation of conscious experience being removed, thus leading to psychology as the “science of behaviour”; the second one is that the goals of psychology should be to predict and control behaviour (as opposed to describe and explain conscious mental states); the third one is that there is no notable distinction between human and non-human behaviour. Following Darwin’s theory of evolution, this would simply mean that human behaviour is just a more complex version in respect to behaviour displayed by other species.
In Philosophy
Behaviourism is a psychological movement that can be contrasted with philosophy of mind. The basic premise of radical behaviourism is that the study of behaviour should be a natural science, such as chemistry or physics, without any reference to hypothetical inner states of organisms as causes for their behaviour. Behaviourism takes a functional view of behaviour. According to Edmund Fantino and colleagues: “Behaviour analysis has much to offer the study of phenomena normally dominated by cognitive and social psychologists. We hope that successful application of behavioural theory and methodology will not only shed light on central problems in judgment and choice but will also generate greater appreciation of the behavioural approach.”
Behaviourist sentiments are not uncommon within philosophy of language and analytic philosophy. It is sometimes argued that Ludwig Wittgenstein defended a logical behaviourist position (e.g. the beetle in a box argument). In logical positivism (as held, e.g. by Rudolf Carnap and Carl Hempel), the meaning of psychological statements are their verification conditions, which consist of performed overt behaviour. W.V.O. Quine made use of a type of behaviourism, influenced by some of Skinner’s ideas, in his own work on language. Quine’s work in semantics differed substantially from the empiricist semantics of Carnap which he attempted to create an alternative to, couching his semantic theory in references to physical objects rather than sensations. Gilbert Ryle defended a distinct strain of philosophical behaviourism, sketched in his book The Concept of Mind. Ryle’s central claim was that instances of dualism frequently represented “category mistakes”, and hence that they were really misunderstandings of the use of ordinary language. Daniel Dennett likewise acknowledges himself to be a type of behaviourist, though he offers extensive criticism of radical behaviourism and refutes Skinner’s rejection of the value of intentional idioms and the possibility of free will.
This is Dennett’s main point in “Skinner Skinned.” Dennett argues that there is a crucial difference between explaining and explaining away… If our explanation of apparently rational behavior turns out to be extremely simple, we may want to say that the behavior was not really rational after all. But if the explanation is very complex and intricate, we may want to say not that the behavior is not rational, but that we now have a better understanding of what rationality consists in. (Compare: if we find out how a computer program solves problems in linear algebra, we don’t say it’s not really solving them, we just say we know how it does it. On the other hand, in cases like Weizenbaum’s ELIZA program, the explanation of how the computer carries on a conversation is so simple that the right thing to say seems to be that the machine isn’t really carrying on a conversation, it’s just a trick.) (Curtis Brown, Philosophy of Mind, “Behaviorism: Skinner and Dennett”).
Law of Effect and Trace Conditioning
Law of Effect:
Although Edward Thorndike’s methodology mainly dealt with reinforcing observable behaviour, it viewed cognitive antecedents as the causes of behaviour, and was theoretically much more similar to the cognitive-behaviour therapies than classical (methodological) or modern-day (radical) behaviourism.
Nevertheless, Skinner’s operant conditioning was heavily influenced by the Law of Effect’s principle of reinforcement.
Trace conditioning:
Akin to B.F. Skinner’s radical behaviourism, it is a respondent conditioning technique based on Ivan Pavlov’s concept of a “memory trace” in which the observer recalls the conditioned stimulus (CS), with the memory or recall being the unconditioned response (UR).
There is also a time delay between the CS and unconditioned stimulus (US), causing the conditioned response (CR) – particularly the reflex – to be faded over time.
Molecular versus Molar Behaviourism
Skinner’s view of behaviour is most often characterised as a “molecular” view of behaviour; that is, behaviour can be decomposed into atomistic parts or molecules. This view is inconsistent with Skinner’s complete description of behaviour as delineated in other works, including his 1981 article “Selection by Consequences”. Skinner proposed that a complete account of behaviour requires understanding of selection history at three levels: biology (the natural selection or phylogeny of the animal); behaviour (the reinforcement history or ontogeny of the behavioual repertoire of the animal); and for some species, culture (the cultural practices of the social group to which the animal belongs). This whole organism then interacts with its environment. Molecular behaviourists use notions from melioration theory, negative power function discounting or additive versions of negative power function discounting.
Molar behaviourists, such as Howard Rachlin, Richard Herrnstein, and William Baum, argue that behaviour cannot be understood by focusing on events in the moment. That is, they argue that behaviour is best understood as the ultimate product of an organism’s history and that molecular behaviourists are committing a fallacy by inventing fictitious proximal causes for behaviour. Molar behaviourists argue that standard molecular constructs, such as “associative strength”, are better replaced by molar variables such as rate of reinforcement. Thus, a molar behaviourist would describe “loving someone” as a pattern of loving behaviour over time; there is no isolated, proximal cause of loving behaviour, only a history of behaviours (of which the current behaviour might be an example) that can be summarised as “love”.
Theoretical Behaviourism
Skinner’s radical behaviourism has been highly successful experimentally, revealing new phenomena with new methods, but Skinner’s dismissal of theory limited its development. Theoretical behaviourism recognised that a historical system, an organism, has a state as well as sensitivity to stimuli and the ability to emit responses. Indeed, Skinner himself acknowledged the possibility of what he called “latent” responses in humans, even though he neglected to extend this idea to rats and pigeons. Latent responses constitute a repertoire, from which operant reinforcement can select. Theoretical behaviourism links between the brain and the behaviour that provides a real understanding of the behaviour. Rather than a mental presumption of how brain-behaviour relates.
Behaviour Analysis and Culture
Cultural analysis has always been at the philosophical core of radical behaviourism from the early days (as seen in Skinner’s Walden Two, Science & Human Behaviour, Beyond Freedom & Dignity, and About Behaviourism).
During the 1980s, behaviour analysts, most notably Sigrid Glenn, had a productive interchange with cultural anthropologist Marvin Harris (the most notable proponent of “cultural materialism”) regarding interdisciplinary work. Very recently, behaviour analysts have produced a set of basic exploratory experiments in an effort toward this end. Behaviourism is also frequently used in game development, although this application is controversial.
Behaviour Informatics and Behaviour Computing
With the fast growth of big behavioural data and applications, behaviour analysis is ubiquitous. Understanding behaviour from the informatics and computing perspective becomes increasingly critical for in-depth understanding of what, why and how behaviours are formed, interact, evolve, change and affect business and decision. Behaviour informatics and behaviour computing deeply explore behaviour intelligence and behaviour insights from the informatics and computing perspectives.
Criticisms and Limitations
In the second half of the 20th century, behaviourism was largely eclipsed as a result of the cognitive revolution. This shift was due to radical behaviourism being highly criticised for not examining mental processes, and this led to the development of the cognitive therapy movement. In the mid-20th century, three main influences arose that would inspire and shape cognitive psychology as a formal school of thought:
Noam Chomsky’s 1959 critique of behaviourism, and empiricism more generally, initiated what would come to be known as the “cognitive revolution”.
Developments in computer science would lead to parallels being drawn between human thought and the computational functionality of computers, opening entirely new areas of psychological thought. Allen Newell and Herbert Simon spent years developing the concept of artificial intelligence (AI) and later worked with cognitive psychologists regarding the implications of AI. The effective result was more of a framework conceptualisation of mental functions with their counterparts in computers (memory, storage, retrieval, etc.)
Formal recognition of the field involved the establishment of research institutions such as George Mandler’s Center for Human Information Processing in 1964. Mandler described the origins of cognitive psychology in a 2002 article in the Journal of the History of the Behavioural Sciences.
In the early years of cognitive psychology, behaviourist critics held that the empiricism it pursued was incompatible with the concept of internal mental states. Cognitive neuroscience, however, continues to gather evidence of direct correlations between physiological brain activity and putative mental states, endorsing the basis for cognitive psychology.
Behaviour Therapy
Behaviour therapy is a term referring to different types of therapies that treat mental health disorders. It identifies and helps change people’s unhealthy behaviours or destructive behaviours through learning theory and conditioning. Ivan Pavlov’s classical conditioning, as well as counterconditioning are the basis for much of clinical behaviour therapy, but also includes other techniques, including operant conditioning, or contingency management, and modelling – sometimes called observational learning. A frequently noted behaviour therapy is systematic desensitisation, which was first demonstrated by Joseph Wolpe and Arnold Lazarus.
21st-Century Behaviourism (Behaviour Analysis)
Applied behaviour analysis (ABA) – also called behavioural engineering – is a scientific discipline that applies the principles of behaviour analysis to change behaviour. ABA derived from much earlier research in the Journal of the Experimental Analysis of Behaviour, which was founded by B.F. Skinner and his colleagues at Harvard University. Nearly a decade after the study “The psychiatric nurse as a behavioural engineer” (1959) was published in that journal, which demonstrated how effective the token economy was in reinforcing more adaptive behaviour for hospitalised patients with schizophrenia and intellectual disability, it led to researchers at the University of Kansas to start the Journal of Applied Behaviour Analysis in 1968.
Although ABA and behaviour modification are similar behaviour-change technologies in that the learning environment is modified through respondent and operant conditioning, behaviour modification did not initially address the causes of the behaviour (particularly, the environmental stimuli that occurred in the past), or investigate solutions that would otherwise prevent the behaviour from reoccurring. As the evolution of ABA began to unfold in the mid-1980s, functional behaviour assessments (FBAs) were developed to clarify the function of that behaviour, so that it is accurately determined which differential reinforcement contingencies will be most effective and less likely for aversive consequences to be administered. In addition, methodological behaviourism was the theory underpinning behaviour modification since private events were not conceptualised during the 1970s and early 1980s, which contrasted from the radical behaviourism of behaviour analysis. ABA – the term that replaced behaviour modification – has emerged into a thriving field.
The independent development of behaviour analysis outside the United States also continues to develop. In the US, the American Psychological Association (APA) features a subdivision for Behaviour Analysis, titled APA Division 25: Behaviour Analysis, which has been in existence since 1964, and the interests among behaviour analysts today are wide-ranging, as indicated in a review of the 30 Special Interest Groups (SIGs) within the Association for Behaviour Analysis International (ABAI). Such interests include everything from animal behaviour and environmental conservation, to classroom instruction (such as direct instruction and precision teaching), verbal behaviour, developmental disabilities and autism, clinical psychology (i.e., forensic behaviour analysis), behavioural medicine (i.e., behavioural gerontology, AIDS prevention, and fitness training), and consumer behaviour analysis.
The field of applied animal behaviour – a sub-discipline of ABA that involves training animals – is regulated by the Animal Behaviour Society, and those who practice this technique are called applied animal behaviourists. Research on applied animal behaviour has been frequently conducted in the Applied Animal Behaviour Science journal since its founding in 1974.
ABA has also been particularly well-established in the area of developmental disabilities since the 1960s, but it was not until the late 1980s that individuals diagnosed with autism spectrum disorders were beginning to grow so rapidly and groundbreaking research was being published that parent advocacy groups started demanding for services throughout the 1990s, which encouraged the formation of the Behaviour Analyst Certification Board, a credentialing program that certifies professionally trained behaviour analysts on the national level to deliver such services. Nevertheless, the certification is applicable to all human services related to the rather broad field of behaviour analysis (other than the treatment for autism), and the ABAI currently has 14 accredited MA and PhD programmes for comprehensive study in that field.
Early behavioural interventions (EBIs) based on ABA are empirically validated for teaching children with autism and has been proven as such for over the past five decades. Since the late 1990s and throughout the twenty-first century, early ABA interventions have also been identified as the treatment of choice by the US Surgeon General, American Academy of Paediatrics, and US National Research Council.
Discrete trial training – also called early intensive behavioural intervention – is the traditional EBI technique implemented for thirty to forty hours per week that instructs a child to sit in a chair, imitate fine and gross motor behaviours, as well as learn eye contact and speech, which are taught through shaping, modelling, and prompting, with such prompting being phased out as the child begins mastering each skill. When the child becomes more verbal from discrete trials, the table-based instructions are later discontinued, and another EBI procedure known as incidental teaching is introduced in the natural environment by having the child ask for desired items kept out of their direct access, as well as allowing the child to choose the play activities that will motivate them to engage with their facilitators before teaching the child how to interact with other children their own age.
A related term for incidental teaching, called pivotal response treatment (PRT), refers to EBI procedures that exclusively entail twenty-five hours per week of naturalistic teaching (without initially using discrete trials). Current research is showing that the majority of the population learn more words at a quicker pace through PRT since only a small portion of the non-verbal autistic population have lower receptive language skills – a phrase used to describe individuals who do not pay much attention to overt stimuli or others in their environment – and the latter are the children who initially require discrete trials to acquire speech.
Organizational behaviour management, which applies contingency management procedures to model and reinforce appropriate work behaviour for employees in organisations, has developed a particularly strong following within ABA, as evidenced by the formation of the OBM Network and Journal of Organisational Behaviour Management, which was rated the third highest impact journal in applied psychology by ISI JOBM rating.
Modern-day clinical behaviour analysis has also witnessed a massive resurgence in research, with the development of relational frame theory (RFT), which is described as an extension of verbal behaviour and a “post-Skinnerian account of language and cognition.” RFT also forms the empirical basis for acceptance and commitment therapy, a therapeutic approach to counselling often used to manage such conditions as anxiety and obesity that consists of acceptance and commitment, value-based living, cognitive defusion, counterconditioning (mindfulness), and contingency management (positive reinforcement). Another evidence-based counselling technique derived from RFT is the functional analytic psychotherapy known as behavioural activation that relies on the ACL model – awareness, courage, and love – to reinforce more positive moods for those struggling with depression.
Incentive-based contingency management (CM) is the standard of care for adults with substance-use disorders; it has also been shown to be highly effective for other addictions (i.e. obesity and gambling). Although it does not directly address the underlying causes of behaviour, incentive-based CM is highly behaviour analytic as it targets the function of the client’s motivational behaviour by relying on a preference assessment, which is an assessment procedure that allows the individual to select the preferred reinforcer (in this case, the monetary value of the voucher, or the use of other incentives, such as prizes). Another evidence-based CM intervention for substance abuse is community reinforcement approach and family training that uses FBAs and counterconditioning techniques – such as behavioural skills training and relapse prevention – to model and reinforce healthier lifestyle choices which promote self-management of abstinence from drugs, alcohol, or cigarette smoking during high-risk exposure when engaging with family members, friends, and co-workers.
While schoolwide positive behaviour support consists of conducting assessments and a task analysis plan to differentially reinforce curricular supports that replace students’ disruptive behaviour in the classroom, paediatric feeding therapy incorporates a liquid chaser and chin feeder to shape proper eating behaviour for children with feeding disorders. Habit reversal training, an approach firmly grounded in counterconditioning which uses contingency management procedures to reinforce alternative behaviour, is currently the only empirically validated approach for managing tic disorders.
Some studies on exposure (desensitisation) therapies – which refer to an array of interventions based on the respondent conditioning procedure known as habituation and typically infuses counterconditioning procedures, such as meditation and breathing exercises – have recently been published in behaviour analytic journals since the 1990s, as most other research are conducted from a cognitive-behaviour therapy framework. When based on a behaviour analytic research standpoint, FBAs are implemented to precisely outline how to employ the flooding form of desensitisation (also called direct exposure therapy) for those who are unsuccessful in overcoming their specific phobia through systematic desensitisation (also known as graduated exposure therapy). These studies also reveal that systematic desensitisation is more effective for children if used in conjunction with shaping, which is further termed contact desensitisation, but this comparison has yet to be substantiated with adults.
Other widely published behaviour analytic journals include Behaviour Modification, The Behaviour Analyst, Journal of Positive Behaviour Interventions, Journal of Contextual Behavioural Science, The Analysis of Verbal Behaviour, Behaviour and Philosophy, Behaviour and Social Issues, and The Psychological Record.
Cognitive Behaviour Therapy
Cognitive behaviour therapy (CBT) is a behaviour therapy discipline that often overlaps considerably with the clinical behaviour analysis subfield of ABA, but differs in that it initially incorporates cognitive restructuring and emotional regulation to alter a person’s cognition and emotions.
A popularly noted counselling intervention known as dialectical behaviour therapy (DBT) includes the use of a chain analysis, as well as cognitive restructuring, emotional regulation, distress tolerance, counterconditioning (mindfulness), and contingency management (positive reinforcement). DBT is quite similar to acceptance and commitment therapy, but contrasts in that it derives from a CBT framework. Although DBT is most widely researched for and empirically validated to reduce the risk of suicide in psychiatric patients with borderline personality disorder, it can often be applied effectively to other mental health conditions, such as substance abuse, as well as mood and eating disorders.
Most research on exposure therapies (also called desensitisation) – ranging from eye movement desensitisation and reprocessing therapy to exposure and response prevention – are conducted through a CBT framework in non-behaviour analytic journals, and these enhanced exposure therapies are well-established in the research literature for treating phobic, post-traumatic stress, and other anxiety disorders (such as obsessive compulsive disorder, or OCD).
Cognitive-based behavioural activation (BA) – the psychotherapeutic approach used for depression – is shown to be highly effective and is widely used in clinical practice. Some large randomised control trials have indicated that cognitive-based BA is as beneficial as antidepressant medications but more efficacious than traditional cognitive therapy. Other commonly used clinical treatments derived from behavioural learning principles that are often implemented through a CBT model include community reinforcement approach and family training, and habit reversal training for substance abuse and tics, respectively.
Treating Trichotillomania – CBT for Hairpulling and Related Problems.
Author(s): Martin E. Franklin and David F. Tolin.
Year: 2010.
Edition: Reprint Edition.
Publisher: Springer.
Type(s): Hardcover, Paperback and Kindle.
Synopsis:
There is still scant clinical information on trichotillomania. This book fills the need for a full-length cognitive-behavioural treatment manual.
The authors share their considerable expertise in treating body-focused repetitive behaviour disorders (not only hair-pulling but skin-picking and nail-biting as well) in an accessible, clinically valid reference.
This is the first comprehensive, clinical, and empirically-based volume to address these disorders.
Modeling essential connections in obsessive-compulsive disorder patients using functional MRI.
Background
Obsessive-compulsive disorder (OCD) is a mental disease in which people experience uncontrollable and repetitive thoughts or behaviours.
Clinical diagnosis of OCD is achieved by using neuropsychological assessment metrics, which are often subjectively affected by psychologists and patients.
In this study, the researchers propose a classification model for OCD diagnosis using functional MR images.
Methods
Using functional connectivity (FC) matrices calculated from brain region of interest (ROI) pairs, a novel Riemann Kernel principal component analysis (PCA) model is employed for feature extraction, which preserves the topological information in the FC matrices.
Hierarchical features are then fed into an ensemble classifier based on the XGBoost algorithm.
Finally, decisive features extracted during classification are used to investigate the brain FC variations between patients with OCD and healthy controls.
Results
The proposed algorithm yielded a classification accuracy of 91.8%.
Additionally, the well-known cortico-striatal-thalamic-cortical (CSTC) circuit and cerebellum were found as highly related regions with OCD.
To further analyse the cerebellar-related function in OCD, the researchers demarcated cerebellum into three sub-regions according to their anatomical and functional property.
Using these three functional cerebellum regions as seeds for brain connectivity computation, statistical results showed that patients with OCD have decreased posterior cerebellar connections.
Conclusions
This study provides a new and efficient method to characterise patients with OCD using resting-state functional MRI.
The researchers also provide a new perspective to analyse disease-related features.
Despite of CSTC circuit, their model-driven feature analysis reported cerebellum as an OCD-related region.
This paper may provide novel insight to the understanding of genetic aetiology of OCD.
Reference
Xing, X., Jin, L., Li, Q., Yang, Q., Han, H., Xu, C., Wei, Z., Zhan, Y., Zhou, X.S., Xue, Z., Chu, X., Peng, Z. & Shi, F. (2020) Modeling essential connections in obsessive-compulsive disorder patients using functional MRI. Brain and Behavior. 10(2):e01499. doi: 10.1002/brb3.1499. Epub 2020 Jan 1.
The PTSD Behavioral Activation Workbook: Activities to Help You Rebuild Your Life from Post-Traumatic Stress Disorder (A New Harbinger Self-Help Workbook).
Author(s): Matthew Jakupcak (PhD), Amy W Wagner (PhD), Christopher R. Martell (PhD), and Matthew T Tull (PhD).
Year: 2020.
Edition: First (1st).
Publisher: New Harbinger Publications; Workbook Edition.
Type(s): Paperback and Kindle.
Synopsis:
If you suffer from post-traumatic stress disorder (PTSD), reliving the past through trauma-focused treatments may be too painful a place to start. Behavioural activation – the powerful treatment method outlined in this workbook – provides an essential foundation for recovery by shifting the focus of your trauma to the things in life that give you true fulfilment, joy, and value. This way, you can envision the kind of future you want to have, and move forward in your treatment to pursue that future.
With this breakthrough workbook, you will learn to replace unproductive coping strategies – such as avoidance – with activities that you find pleasant and meaningful. You’ll find an overview of behavioural activation: what it is, why it works, and how you can implement it into your life to begin healing the wounds of your past and paving the way for a bright future full of possibility.
If you have experienced trauma, you need real tools to help you manage your pain and jumpstart your recovery. With this compassionate and evidence-based workbook, you will find actionable solutions to help you begin healing and take that next needed step toward wellness, wholeness, and peace.
Enabling patients to cope with psychotropic medication in mental health care: Evaluation and reports of the new inventory MedSupport.
Background
This cross sectional study examined patients’ perceptions of professional support regarding use of psychotropic medication in a specialist mental health care setting.
The aims were to evaluate reliability and validity of the MedSupport inventory, and investigate possible associations between MedSupport scores and patient characteristics.
Methods
A cross-sectional study was performed.
The patients completed the MedSupport, a newly developed self-reported 6 item questionnaire on a Likert scale ranged 1 to 5 (1 = strongly disagree to 5 = strongly agree), and the Beliefs about Medicines Questionnaire.
Diagnosis and treatment information were obtained at the clinical visits and from patient records.
Among the 992 patients recruited, 567 patients (57%) used psychotropic medications, and 514 (91%) of these completed the MedSupport and were included in the study.
Results
The MedSupport showed an adequate internal consistency (Cronbach alpha.87; 95% CI.86-89) and a convergent validity toward the available variables.
The MedSupport mean score was 3.8 (standard deviation.9, median 3.8).
Increasing age and the experience of stronger needs for psychotropic medication were associated with perception of more support to cope with medication, whereas higher concern toward use of psychotropic medication was associated with perception of less support.
Patients diagnosed with behavioural and emotional disorders, onset in childhood and adolescence perceived more support than patients with Mood disorders.
Conclusions
The MedSupport inventory was suitable for assessing the patients’ perceived support from health care service regarding their medication.
Awareness of differences in patients’ perceptions might enable the service to provide special measures for patients who perceive insufficient medication support.
Reference
Drivenes, K., Vederhus, J.K., Haaland, V.Ø., Ruud, T., Hauge, Y.L., Regevik, H., Falk, R.S. & Tanum, L. (2020) Enabling patients to cope with psychotropic medication in mental health care: Evaluation and reports of the new inventory MedSupport. Medicine (Baltimore). 99(1):e18635. doi: 10.1097/MD.0000000000018635.
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