What is the Positive and Negative Syndrome Scale?

Introduction

The Positive and Negative Syndrome Scale (PANSS) is a medical scale used for measuring symptom severity of patients with schizophrenia.

It was published in 1987 by Stanley Kay, Lewis Opler, and Abraham Fiszbein. It is widely used in the study of antipsychotic therapy. The scale is known as the “gold standard” that all assessments of psychotic behavioural disorders should follow.

The name refers to the two types of symptoms in schizophrenia, as defined by the American Psychiatric Association:

  • Positive symptoms, which refer to an excess or distortion of normal functions (e.g. hallucinations and delusions); and
  • Negative symptoms, which represent a diminution or loss of normal functions.

Some of these functions which may be lost include normal thoughts, actions, ability to tell fantasies from reality, and the ability to properly express emotions.

The PANSS is a relatively brief interview, requiring 45 to 50 minutes to administer. The interviewer must be trained to a standardised level of reliability.

Interview Items

To assess a patient using PANSS, an approximately 45-minute clinical interview is conducted. The patient is rated from 1 to 7 on 30 different symptoms based on the interview as well as reports of family members or primary care hospital workers.

  • Positive scale:
    • 7 Items, (minimum score = 7, maximum score = 49):
      • Delusions.
      • Conceptual disorganisation.
      • Hallucinations.
      • Excitement.
      • Grandiosity.
      • Suspiciousness/persecution.
      • Hostility.
  • Negative scale:
    • 7 Items, (minimum score = 7, maximum score = 49):
      • Blunted affect.
      • Emotional withdrawal.
      • Poor rapport.
      • Passive/apathetic social withdrawal.
      • Difficulty in abstract thinking.
      • Lack of spontaneity and flow of conversation.
      • Stereotyped thinking.
  • General Psychopathology scale:
    • 16 Items, (minimum score = 16, maximum score = 112):
      • Somatic concern.
      • Anxiety.
      • Guilt feelings.
      • Tension.
      • Mannerisms and posturing.
      • Depression.
      • Motor retardation.
      • Uncooperativeness.
      • Unusual thought content.
      • Disorientation.
      • Poor attention.
      • Lack of judgement and insight.
      • Disturbance of volition.
      • Poor impulse control.
      • Preoccupation.
      • Active social avoidance.

PANSS Total score minimum = 30, maximum = 210

Scoring

As 1 rather than 0 is given as the lowest score for each item, a patient can not score lower than 30 for the total PANSS score. Scores are often given separately for the positive items, negative items, and general psychopathology. In their original publication on the PANSS scale, Stanley Kay and colleagues tested the scale on 101 adult patients (20-68 years-old) with schizophrenia and the mean scores were,

  • Positive scale = 18.20.
  • Negative scale = 21.01.
  • General psychopathology = 37.74.

Based on meta-analytic results, an alternative five-factor solution of the PANSS was proposed with positive symptoms, negative symptoms, disorganisation, excitement, and emotional distress.

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What is Mania?

Introduction

Mania, also known as manic syndrome, is a mental and behavioural disorder defined as a state of abnormally elevated arousal, affect, and energy level, or “a state of heightened overall activation with enhanced affective expression together with lability of affect.”

During a manic episode, an individual will experience rapidly changing emotions and moods, highly influenced by surrounding stimuli. Although mania is often conceived as a “mirror image” to depression, the heightened mood can be either euphoric or dysphoric. As the mania intensifies, irritability can be more pronounced and result in anxiety or anger.

The symptoms of mania include elevated mood (either euphoric or irritable), flight of ideas and pressure of speech, increased energy, decreased need and desire for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states. However, in full-blown mania, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behaviour.

Refer to Bipolar I Disorder, Bipolar II Disorder, and Mixed Affective State.

Etymology

The nosology of the various stages of a manic episode has changed over the decades. The word derives from the Ancient Greek μανία (manía), “madness, frenzy” and the verb μαίνομαι (maínomai), “to be mad, to rage, to be furious”.

Causes and Diagnosis

Mania is a syndrome with multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (such as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, such as multiple sclerosis; certain medications may perpetuate a manic state, for example prednisone; or substances prone to abuse, especially stimulants, such as caffeine and cocaine. In the current DSM-5, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterised as either mild, moderate, or severe, with certain diagnostic criteria (e.g. catatonia, psychosis). Mania is divided into three stages:

  • Hypomania, or stage I;
  • Acute mania, or stage II; and
  • Delirious mania (delirium), or stage III.

This “staging” of a manic episode is useful from a descriptive and differential diagnostic point of view.

Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardised tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic/hypomanic bipolar patient needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have “gone manic” severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.

Classification

Mixed States

Refer to Mixed Affective State.

In a mixed affective state, the individual, though meeting the general criteria for a hypomanic (discussed below) or manic episode, experiences three or more concurrent depressive symptoms. This has caused some speculation, among clinicians, that mania and depression, rather than constituting “true” polar opposites, are, rather, two independent axes in a unipolar – bipolar spectrum.

A mixed affective state, especially with prominent manic symptoms, places the patient at a greater risk for suicide. Depression on its own is a risk factor but, when coupled with an increase in energy and goal-directed activity, the patient is far more likely to act with violence on suicidal impulses.

Hypomania

Refer to Hypomania.

Hypomania, which means “less than mania”, is a lowered state of mania that does little to impair function or decrease quality of life. It may, in fact, increase productivity and creativity. In hypomania, there is less need for sleep and both goal-motivated behaviour and metabolism increase. Some studies exploring brain metabolism in subjects with hypomania, however, did not find any conclusive link; while there are studies that reported abnormalities, some failed to detect differences. Though the elevated mood and energy level typical of hypomania could be seen as a benefit, true mania itself generally has many undesirable consequences including suicidal tendencies, and hypomania can, if the prominent mood is irritable as opposed to euphoric, be a rather unpleasant experience. In addition, the exaggerated case of hypomania can lead to problems. For instance, trait-based positivity for a person could make them more engaging and outgoing, and cause them to have a positive outlook in life. When exaggerated in hypomania, however, such a person can display excessive optimism, grandiosity, and poor decision making, often with little regard to the consequences.

Associated Disorders

A single manic episode, in the absence of secondary causes, (i.e. substance use disorders, pharmacologics, or general medical conditions) is often sufficient to diagnose bipolar I disorder. Hypomania may be indicative of bipolar II disorder. Manic episodes are often complicated by delusions and/or hallucinations; and if the psychotic features persist for a duration significantly longer than the episode of typical mania (two weeks or more), a diagnosis of schizoaffective disorder is more appropriate. Certain obsessive-compulsive spectrum disorders as well as impulse control disorders share the suffix “-mania,” namely, kleptomania, pyromania, and trichotillomania. Despite the unfortunate association implied by the name, however, no connection exists between mania or bipolar disorder and these disorders. Furthermore, evidence indicates a B12 deficiency can also cause symptoms characteristic of mania and psychosis.

Hyperthyroidism can produce similar symptoms to those of mania, such as agitation, elevated mood, increased energy, hyperactivity, sleep disturbances and sometimes, especially in severe cases, psychosis.

Signs and Symptoms

A manic episode is defined in the American Psychiatric Association’s diagnostic manual as a “distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration, if hospitalisation is necessary),” where the mood is not caused by drugs/medication or a non-mental medical illness (e.g. hyperthyroidism), and: (a) is causing obvious difficulties at work or in social relationships and activities, or (b) requires admission to hospital to protect the person or others, or (c) the person is suffering psychosis.

To be classified as a manic episode, while the disturbed mood and an increase in goal-directed activity or energy is present, at least three (or four, if only irritability is present) of the following must have been consistently present:

  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep (e.g. feels rested after 3 hours of sleep).
  • More talkative than usual, or acts pressured to keep talking.
  • Flights of ideas or subjective experience that thoughts are racing.
  • Increase in goal-directed activity, or psychomotor acceleration.
  • Distractibility (too easily drawn to unimportant or irrelevant external stimuli).
  • Excessive involvement in activities with a high likelihood of painful consequences.(e.g. extravagant shopping, improbable commercial schemes, hypersexuality).

Though the activities one participates in while in a manic state are not always negative, those with the potential to have negative outcomes are far more likely.

If the person is concurrently depressed, they are said to be having a mixed episode.

The World Health Organisation’s classification system defines a manic episode as one where mood is higher than the person’s situation warrants and may vary from relaxed high spirits to barely controllable exuberance, is accompanied by hyperactivity, a compulsion to speak, a reduced sleep requirement, difficulty sustaining attention, and/or often increased distractibility. Frequently, confidence and self-esteem are excessively enlarged, and grand, extravagant ideas are expressed. Behaviour that is out-of-character and risky, foolish or inappropriate may result from a loss of normal social restraint.

Some people also have physical symptoms, such as sweating, pacing, and weight loss. In full-blown mania, often the manic person will feel as though their goal(s) are of paramount importance, that there are no consequences, or that negative consequences would be minimal, and that they need not exercise restraint in the pursuit of what they are after. Hypomania is different, as it may cause little or no impairment in function. The hypomanic person’s connection with the external world, and its standards of interaction, remain intact, although intensity of moods is heightened. But those who suffer from prolonged unresolved hypomania do run the risk of developing full mania, and may cross that “line” without even realising they have done so.

One of the signature symptoms of mania (and to a lesser extent, hypomania) is what many have described as racing thoughts. These are usually instances in which the manic person is excessively distracted by objectively unimportant stimuli. This experience creates an absent-mindedness where the manic individual’s thoughts totally preoccupy them, making them unable to keep track of time, or be aware of anything besides the flow of thoughts. Racing thoughts also interfere with the ability to fall asleep.

Manic states are always relative to the normal state of intensity of the afflicted individual; thus, already irritable patients may find themselves losing their tempers even more quickly, and an academically gifted person may, during the hypomanic stage, adopt seemingly “genius” characteristics and an ability to perform and articulate at a level far beyond that which they would be capable of during euthymia. A very simple indicator of a manic state would be if a heretofore clinically depressed patient suddenly becomes inordinately energetic, enthusiastic, cheerful, aggressive, or “over-happy”. Other, often less obvious, elements of mania include delusions (generally of either grandeur or persecution, according to whether the predominant mood is euphoric or irritable), hypersensitivity, hypervigilance, hypersexuality, hyper-religiosity, hyperactivity and impulsivity, a compulsion to over explain (typically accompanied by pressure of speech), grandiose schemes and ideas, and a decreased need for sleep (for example, feeling rested after only 3 or 4 hours of sleep). In the case of the latter, the eyes of such patients may both look and seem abnormally “wide open”, rarely blinking, and may contribute to some clinicians’ erroneous belief that these patients are under the influence of a stimulant drug, when the patient, in fact, is either not on any mind-altering substances or is actually on a depressant drug. Individuals may also engage in out-of-character behaviour during the episode, such as questionable business transactions, wasteful expenditures of money (e.g. spending sprees), risky sexual activity, abuse of recreational substances, excessive gambling, reckless behaviour (such as extreme speeding or other daredevil activity), abnormal social interaction (e.g. over-familiarity and conversing with strangers), or highly vocal arguments. These behaviours may increase stress in personal relationships, lead to problems at work, and increase the risk of altercations with law enforcement. There is a high risk of impulsively taking part in activities potentially harmful to the self and others.

Although “severely elevated mood” sounds somewhat desirable and enjoyable, the experience of mania is ultimately often quite unpleasant and sometimes disturbing, if not frightening, for the person involved and for those close to them, and it may lead to impulsive behaviour that may later be regretted. It can also often be complicated by the sufferer’s lack of judgment and insight regarding periods of exacerbation of characteristic states. Manic patients are frequently grandiose, obsessive, impulsive, irritable, belligerent, and frequently deny anything is wrong with them. Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprived psychosis may appear, further complicating the ability to think clearly. Racing thoughts and misperceptions lead to frustration and decreased ability to communicate with others.

Mania may also, as earlier mentioned, be divided into three “stages”. Stage I corresponds with hypomania and may feature typical hypomanic characteristics, such as gregariousness and euphoria. In stages II and III mania, however, the patient may be extraordinarily irritable, psychotic or even delirious. These latter two stages are referred to as acute and delirious (or Bell’s), respectively.

Cause

Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69%. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medication possibly include glutaminergic agents and drugs that alter the hypothalamic-pituitary-adrenal (HPA) axis. Lifestyle triggers include irregular sleep-wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.

Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioural changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behaviour. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behaviour in preclinical models.

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.

Deep brain stimulation of the subthalamic nucleus in Parkinson’s disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.

Mania can also be caused by physical trauma or illness. When the causes are physical, it is called secondary mania.

Mechanism

Refer to Biology of Bipolar Disorder.

The mechanism underlying mania is unknown, but the neurocognitive profile of mania is highly consistent with dysfunction in the right prefrontal cortex, a common finding in neuroimaging studies. Various lines of evidence from post-mortem studies and the putative mechanisms of anti-manic agents point to abnormalities in GSK-3, dopamine, Protein kinase C and Inositol monophosphatase.

Meta analysis of neuroimaging studies demonstrate increased thalamic activity, and bilaterally reduced inferior frontal gyrus activation. Activity in the amygdala and other subcortical structures such as the ventral striatum tend to be increased, although results are inconsistent and likely dependent upon task characteristics such as valence. Reduced functional connectivity between the ventral prefrontal cortex and amygdala along with variable findings supports a hypothesis of general dysregulation of subcortical structures by the prefrontal cortex. A bias towards positively valenced stimuli, and increased responsiveness in reward circuitry may predispose towards mania. Mania tends to be associated with right hemisphere lesions, while depression tends to be associated with left hemisphere lesions.

Post-mortem examinations of bipolar disorder demonstrate increased expression of Protein Kinase C (PKC). While limited, some studies demonstrate manipulation of PKC in animals produces behavioural changes mirroring mania, and treatment with PKC inhibitor tamoxifen (also an anti-oestrogen drug) demonstrates antimanic effects. Traditional antimanic drugs also demonstrate PKC inhibiting properties, among other effects such as GSK3 inhibition.

Manic episodes may be triggered by dopamine receptor agonists, and this combined with tentative reports of increased VMAT2 activity, measured via PET scans of radioligand binding, suggests a role of dopamine in mania. Decreased cerebrospinal fluid levels of the serotonin metabolite 5-HIAA have been found in manic patients too, which may be explained by a failure of serotonergic regulation and dopaminergic hyperactivity.

Limited evidence suggests that mania is associated with behavioural reward hypersensitivity, as well as with neural reward hypersensitivity. Electrophysiological evidence supporting this comes from studies associating left frontal EEG activity with mania. As left frontal EEG activity is generally thought to be a reflection of behavioural activation system activity, this is thought to support a role for reward hypersensitivity in mania. Tentative evidence also comes from one study that reported an association between manic traits and feedback negativity during receipt of monetary reward or loss. Neuroimaging evidence during acute mania is sparse, but one study reported elevated orbitofrontal cortex activity to monetary reward, and another study reported elevated striatal activity to reward omission. The latter finding was interpreted in the context of either elevated baseline activity (resulting in a null finding of reward hypersensitivity), or reduced ability to discriminate between reward and punishment, still supporting reward hyperactivity in mania. Punishment hyposensitivity, as reflected in a number of neuroimaging studies as reduced lateral orbitofrontal response to punishment, has been proposed as a mechanism of reward hypersensitivity in mania.

Diagnosis

In the ICD-10 there are several disorders with the manic syndrome:

  • Organic manic disorder (F06.30).
  • Mania without psychotic symptoms (F30.1).
  • Mania with psychotic symptoms (F30.2).
  • Other manic episodes (F30.8).
  • Unspecified manic episode (F30.9).
  • Manic type of schizoaffective disorder (F25.0).
  • Bipolar affective disorder, current episode manic without psychotic symptoms (F31.1).
  • Bipolar affective disorder, current episode manic with psychotic symptoms (F31.2).

Treatment

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.

The acute treatment of a manic episode of bipolar disorder involves the utilisation of either a mood stabiliser (Carbamazepine, valproate, lithium, or lamotrigine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, or aripiprazole). The use of antipsychotic agents in the treatment of acute mania was reviewed by Tohen and Vieta in 2009.

When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilise the patient’s mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.

Lithium is the classic mood stabiliser to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine and topiramate, both anticonvulsants as well.

In some cases, long-acting benzodiazepines, particularly clonazepam, are used after other options are exhausted. In more urgent circumstances, such as in emergency rooms, lorazepam, combined with haloperidol, is used to promptly alleviate symptoms of agitation, aggression, and psychosis.

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilisers in these patients. Some atypical antidepressants, however, such as mirtazepine and trazodone have been occasionally used after other options have failed.

Society and Culture

In Electroboy: A Memoir of Mania by Andy Behrman, he describes his experience of mania as “the most perfect prescription glasses with which to see the world… life appears in front of you like an oversized movie screen”. Behrman indicates early in his memoir that he sees himself not as a person suffering from an uncontrollable disabling illness, but as a director of the movie that is his vivid and emotionally alive life. There is some evidence that people in the creative industries suffer from bipolar disorder more often than those in other occupations. Winston Churchill had periods of manic symptoms that may have been both an asset and a liability.

English actor Stephen Fry, who suffers from bipolar disorder, recounts manic behaviour during his adolescence: “When I was about 17 … going around London on two stolen credit cards, it was a sort of fantastic reinvention of myself, an attempt to. I bought ridiculous suits with stiff collars and silk ties from the 1920s, and would go to the Savoy and Ritz and drink cocktails.” While he has experienced suicidal thoughts, he says the manic side of his condition has had positive contributions on his life.

What is Hypomania?

Introduction

Hypomania (literally “under mania” or “less than mania”) is a mental and behavioural disorder, characterised essentially by an apparently non-contextual elevation of mood (euphoria) which contributes to persistently disinhibited behaviour.

The individual afflicted may suffer with irritability, not necessarily less severe than full mania; in fact, the presence of marked irritability is a documented feature of hypomanic and mixed episodes in Bipolar type II. According to DSM-5 criteria, hypomania is distinct from mania in that there is no significant functional impairment; mania, by DSM-5 definition, does include significant functional impairment and may have psychotic features.

Characteristic behaviours of persons experiencing hypomania are a notable decrease in the need for sleep, an overall increase in energy, unusual behaviours and actions, and a markedly distinctive increase in talkativeness and confidence, commonly exhibited with a flight of creative ideas. Other symptoms related to this may include feelings of grandiosity, distractibility, and hypersexuality. While hypomanic behaviour often generates productivity and excitement, it can become troublesome if the subject engages in risky or otherwise inadvisable behaviours, and/or the symptoms manifest themselves in trouble with everyday life events. When manic episodes are separated into stages of a progression according to symptomatic severity and associated features, hypomania constitutes the first stage of the syndrome, wherein the cardinal features (euphoria or heightened irritability, pressure of speech and activity, increased energy, decreased need for sleep, and flight of ideas) are most plainly evident.

Refer to Bipolar I Disorder, Bipolar II Disorder, and Mixed Affective State.

Etymology

The Ancient Greek physician Hippocrates called one personality type ‘hypomanic’ (Greek: ὑπομαινόμενοι, hypomainómenoi). In 19th century psychiatry, when mania had a broad meaning of insanity, hypomania was equated by some to concepts of ‘partial insanity’ or monomania. A more specific usage was advanced by the German neuro-psychiatrist Emanuel Ernst Mendel in 1881, who wrote, “I recommend, taking into consideration the word used by Hippocrates, to name those types of mania that show a less severe phenomenological picture, ‘hypomania'”. Narrower operational definitions of hypomania were developed in the 1960s and 1970s.

Signs and Symptoms

Individuals in a hypomanic state have a decreased need for sleep, are extremely gregarious and competitive, and have a great deal of energy. They are, otherwise, often fully functioning (unlike individuals suffering from a full manic episode).

Distinctive Markers

Specifically, hypomania is distinguished from mania by the absence of psychotic symptoms, and by its lesser degree of impact on functioning.

Hypomania is a feature of bipolar II disorder and cyclothymia, but can also occur in schizoaffective disorder. Hypomania is also a feature of bipolar I disorder; it arises in sequential procession as the mood disorder fluctuates between normal mood (euthymia) and mania. Some individuals with bipolar I disorder have hypomanic as well as manic episodes. Hypomania can also occur when moods progress downwards from a manic mood state to a normal mood. Hypomania is sometimes credited with increasing creativity and productive energy. Numerous people with bipolar disorder have credited hypomania with giving them an edge in their theatre of work.

People who experience hyperthymia, or “chronic hypomania”, encounter the same symptoms as hypomania but on a longer-term basis.

Associated Disorders

Cyclothymia, a condition of continuous mood fluctuations, is characterised by oscillating experiences of hypomania and depression that fail to meet the diagnostic criteria for either manic or major depressive episodes. These periods are often interspersed with periods of relatively normal (euthymic) functioning.

When a patient presents with a history of at least one episode of both hypomania and major depression, each of which meet the diagnostic criteria, bipolar II disorder is diagnosed. In some cases, depressive episodes routinely occur during the fall or winter and hypomanic ones in the spring or summer. In such cases, one speaks of a “seasonal pattern”.

If left untreated, and in those so predisposed, hypomania may transition into mania, which may be psychotic, in which case bipolar I disorder is the correct diagnosis.

Causes

Often in those who have experienced their first episode of hypomania – generally without psychotic features – there may be a long or recent history of depression or a mix of hypomania combined with depression (known as mixed-state) prior to the emergence of manic symptoms. This commonly surfaces in the mid to late teens. Because the teenage years are typically an emotionally charged time of life, it is not unusual for mood swings to be passed off as normal hormonal teen behaviour and for a diagnosis of bipolar disorder to be missed until there is evidence of an obvious manic or hypomanic phase.

In cases of drug-induced hypomanic episodes in unipolar depressives, the hypomania can almost invariably be eliminated by lowering medication dosage, withdrawing the drug entirely, or changing to a different medication if discontinuation of treatment is not possible.

Hypomania can be associated with narcissistic personality disorder.

Psychopathology

Mania and hypomania are usually studied together as components of bipolar disorders, and the pathophysiology is usually assumed to be the same. Given that norepinephrine and dopaminergic drugs are capable of triggering hypomania, theories relating to monoamine hyperactivity have been proposed. A theory unifying depression and mania in bipolar individuals proposes that decreased serotonergic regulation of other monoamines can result in either depressive or manic symptoms. Lesions on the right side frontal and temporal lobes have further been associated with mania.

Diagnosis

The DSM-IV-TR defines a hypomanic episode as including, over the course of at least four days, elevated mood plus three of the following symptoms OR irritable mood plus four of the following symptoms, when the behaviours are clearly different from how the person typically acts when not depressed:

  • Pressured speech.
  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep.
  • Flight of ideas or the subjective experience that thoughts are racing.
  • Easily distracted.
  • Increase in goal-directed activity (e.g. social activity, at work, or hypersexuality), or psychomotor agitation.
  • Involvement in pleasurable activities that may have a high potential for negative psycho-social or physical consequences (e.g. the person engages in unrestrained buying sprees, sexual indiscretions, reckless driving, physical and verbal conflicts, foolish business investments, quitting a job to pursue some grandiose goal, etc.).

Treatment

Medications

Antimanic drugs are used to control acute attacks and prevent recurring episodes of hypomania combined with a range of psychological therapies. The recommended length of treatment ranges from 2 years to 5 years. Anti-depressants may also be required for existing treatments but are avoided in patients who have had a recent history with hypomania. Sertraline has often been debated to have side effects that can trigger hypomania.

What is Habit Reversal Training?

Introduction

Habit reversal training (HRT) is a “multicomponent behavioural treatment package originally developed to address a wide variety of repetitive behaviour disorders”.

Behavioural disorders treated with HRT include tics, trichotillomania, nail biting, thumb sucking, skin picking, temporomandibular disorder (TMJ), lip-cheek biting and stuttering. It consists of five components: awareness training, competing response training, contingency management, relaxation training, and generalisation training.

Research on the efficacy of HRT for behavioural disorders have produced consistent, large effect sizes (approximately 0.80 across the disorders). It has met the standard of a well-established treatment for stuttering, thumb sucking, nail biting, and TMJ disorders. According to a meta-analysis from 2012, decoupling, a self-help variant of HRT, also shows efficacy.

For Tic Disorders

In the case of tics, these components are intended to increase tic awareness, develop a competing response to the tic, and build treatment motivation and compliance. HRT is based on the presence of a premonitory urge, or sensation occurring before a tic. HRT involves replacing a tic with a competing response – a more comfortable or acceptable movement or sound – when a patient feels a premonitory urge building.

Controlled trials have demonstrated that HRT is an acceptable, tolerable, effective and durable treatment for tics; HRT reduces the severity of vocal tics, and results in enduring improvement of tics when compared with supportive therapy. HRT has been shown to be more effective than supportive therapy and, in some studies, medication. HRT is not yet proven or widely accepted, but large-scale trials are ongoing and should provide better information about its efficacy in treating Tourette syndrome. Studies through 2006 are:

“characterized by a number of design limitations, including relatively small sample sizes, limited characterization of study participants, limited data on children and adolescents, lack of attention to the assessment of treatment integrity and adherence, and limited attention to the identification of potential clinical and neurocognitive mechanisms and predictors of treatment response”. (Piacentini & Chang, 2006, p.227).

Additional controlled studies of HRT are needed to address whether HRT, medication, or a combination of both is most effective, but in the interim, “HRT either alone or in combination with medication should be considered as a viable treatment” for tic disorders.

Comprehensive Behavioural Intervention for Tics

Comprehensive Behavioural Intervention for Tics (CBIT), based on HRT, is a first-line treatment for Tourette syndrome and tic disorders. With a high level of confidence, CBIT has been shown to be more likely to lead to a reduction in tics than other supportive therapies or psychoeducation. Some limitations are: children younger than ten may not understand the treatment, people with severe tics or ADHD may not be able to suppress their tics or sustain the required focus to benefit from behavioural treatments, there is a lack of therapists trained in behavioural interventions, finding practitioners outside of specialty clinics can be difficult, and costs may limit accessibility. Whether increased awareness of tics through HRT/CBIT (as opposed to moving attention away from them) leads to further increases in tics later in life is a subject of discussion among TS experts.

Reference

Piacentini, J.C. & Chang, S.W. (2006) Behavioral Treatments for Tic Suppression: Habit Reversal Training. Advances in Neurology. 99, pp.227-233.

What is Body-Focused Repetitive Behaviour?

Introduction

Body-focused repetitive behaviour (BFRB) is an umbrella name for impulse control behaviours involving compulsively damaging one’s physical appearance or causing physical injury.

Body-focused repetitive behaviour disorders (BFRBDs) in ICD-11 is in development.

BFRB disorders are currently estimated to be under the obsessive-compulsive spectrum.

Cause(s)

The cause of BFRBs is unknown.

Emotional variables may have a differential impact on the expression of BFRBs.

Research has suggested that the urge to repetitive self-injury is similar to a BFRB but others have argued that for some the condition is more akin to a substance abuse disorder.

Researchers are investigating a possible genetic component.

Onset

BFRBs most often begin in late childhood or in the early teens.

Diagnosis

Types

The main BFRB disorders are:

  • Skin:
    • Dermatillomania (excoriation disorder), skin picking.
    • Dermatophagia, skin nibbling.
  • Mouth:
    • Morsicatio buccarum, cheek biting.
    • Morsicatio labiorum, inner lip biting.
    • Morsicatio linguarum, tongue biting.
  • Hands:
    • Onychophagia, nail biting.
    • Onychotillomania, nail picking.
  • Nose:
    • Rhinotillexomania, compulsive nose picking.
  • Hair:
    • Trichophagia, hair nibbling.
    • Trichotemnomania, hair cutting.
    • Trichotillomania, hair pulling.
  • Eyes:
    • Mucus fishing syndrome – compulsion to remove or “fish” strands of mucus from the eye.

Treatment

Psychotherapy

Treatment can include behaviour modification therapy, medication, and family therapy. The evidence base criteria for BFRBs is strict and methodical. Individual behavioural therapy has been shown as a “probably effective” evidence-based therapy to help with thumb sucking, and possibly nail biting. Cognitive behavioural therapy was cited as experimental evidence based therapy to treat trichotillomania and nail biting; a systematic review found best evidence for habit reversal training and decoupling. Another form of treatment that focuses on mindfulness, stimuli and rewards has proven effective in some people. However, no treatment was deemed well-established to treat any form of BFRBs.

Pharmacotherapy

Excoriation disorder, and trichotillomania have been treated with inositol and N-acetylcysteine.

Prevalence

BFRBs are among the most poorly understood, misdiagnosed, and undertreated groups of disorders. BFRBs may affect at least 1 out of 20 people. These collections of symptoms have been known for a number of years, but only recently have appeared in widespread medical literature. Trichotillomania alone is believed to affect 10 million people in the United States.

What is the Association for Behaviour Analysis International?

Introduction

The Association for Behaviour Analysis International (ABAI) is a professional association of psychologists, educators, and practitioners whose scholarship and practice derive from the work of B.F. Skinner.

ABAI organises conferences in the US and abroad, publishes journals, and offers accreditation programs for behaviour analysis training programmes. As of March 2021, ABAI has 97 regional associate chapters both in the United States and abroad, many of which offer their own annual conferences. As of 2019, ABAI had over 9,000 members and membership in its affiliate chapters was greater than 28,000.

Refer to Clinical Behaviour Analysis, Applied Behaviour Analysis, and Licensed Behaviour Analyst.

Brief History

The Association for Behaviour Analysis International (ABAI) was founded in 1974 as the MidWestern Association for Behaviour Analysis (MABA) to serve as an interdisciplinary group of professionals, paraprofessionals, and students. Behaviour analysis was well-represented in the Midwest of the US, but many behaviour analysts were disappointed with the level of support their relatively new field received at the existing psychology conferences. Gerald Mertens and Israel Goldiamond organised the first two-day conference, which was held at the University of Chicago, and speakers included, Sidney Bijou, James Dinsmoor, Roger Ulrich and Goldiamond.

MABA’s first headquarters were located on the campus of Western Michigan University (WMU) in Kalamazoo, Michigan. By 1977, the annual conference was extended four days and included 550 events, and MABA had grown to 1,190 members from 42 states and five foreign countries.

In 1978, MABA began publishing its first journal, The Behaviour Analyst (renamed Perspectives in Behavioural Science in 2018), and in 1979, the organisation changed its name to the Association for Behaviour Analysis (ABA), subsequently adopting the name Association for Behaviour Analysis International (ABAI). In 2001, it sponsored its first international meeting in Venice, Italy.

Association for Behaviour Analysis (ABA) began offering APA credits for the first time in 1994, at their 20th Annual Convention in Atlanta, GA. While the BACB solidified itself in the field, ABA offered its first BACB credits in 2000 at their 26th Annual Convention in Washington, DC.

Activities

Conferences

ABAI organises conferences related to the theory and practice of behaviour analysis. In addition to the annual conference, which is held at a location in the US or Canada, every other year, ABAI hosts an international conference. The association also holds an annual autism conference and has hosted several single-track conferences on topics of special interest to behaviour analysts, such as theory and philosophy, climate change, behavioural economics, and education.

Many conference sessions offer approved continuing education credits (CEUs) for practitioners who wish to maintain their professional certification. Among the organisations that approve ABAI presentations for CEU credit are the American Psychological Association, the National Association of School Psychologists, and the Behaviour Analyst Certification Board.

Accreditation Programme

ABAI operates an accreditation programme for universities offering master’s and doctoral degrees in behaviour analysis. Degree programs that achieve ABAI accreditation meet the organization’s standards of training and will satisfy the Behaviour Analyst Certification Board requirements to achieve certification as a behaviour analyst.

Society for the Advancement of Behaviour Analysis

ABAI is supported by the Society for the Advancement of Behaviour Analysis (SABA), a 501(c)(3) organisation that accepts tax-exempt charitable contributions. SABA maintains a number of funds to support research in child development, international development, public awareness of behavioural science, and diversity, equity, and inclusion. SABA also provides grants to support student research, student travel to the annual ABAI conference, and graduate research focused on issues of diversity, equity, and inclusion.

Position Statements

As of 2021, ABAI had released six policy statements on: right to effective behavioural treatment (1989), student’s right to effective education (1990), facilitated communication (1995), restraint and seclusion (2010), sexual harassment (2019), and commitment to equity (2020).

Awards

SABA administers an awards programme at the annual convention of ABAI that recognises distinguished service to behaviour analysis, scientific translation, international dissemination of behaviour analysis, effective presentation of behaviour analysis in the mass media, and enduring programmatic contributions to behaviour analysis. Past recipients of the award for distinguished service to behaviour analysis include Sidney Bijou, James Dinsmoor, A. Charles Catania, Jack Michael and Murray Sidman.

Journals

The Association of Applied Behaviour Analysis International publishes six peer-reviewed journals.

  • Perspectives on Behaviour Science, is ABAI’s first journal, published from 1978-2017 as The Behaviour Analyst. It is a semiannual journal publishing articles on theoretical, experimental, and applied topics in behaviour analysis, including literature reviews, re-interpretations of published data, and articles on behaviourism as a philosophy.
  • The Analysis of Verbal Behaviour is a collection of experiments and theoretical papers regarding verbal behaviour and applied behaviour analysis.
  • Behaviour Analysis in Practice is a peer-reviewed journal that includes articles on how to efficiently practice applied behaviour analysis.
  • The Psychological Record includes articles concerning behavioural analysis, behavioural science, and behaviour theory. It was founded in 1937 by Jacob Robert Kantor. Its first experimental area editor was B.F. Skinner. After being published most recently at Southern Illinois University at Carbondale, the journal was adopted as an official publication of ABAI. The Psychological Record publishes empirical and conceptual articles related to the field of behaviour analysis, behaviour science, and behaviour theory.
  • Behaviour and Social Issues, is an interdisciplinary journal publishing articles analysing human social behaviour, particularly with regard to understanding and influencing significant social problems such as social justice, human rights, and sustainability.
  • Education and Treatment of Children.

What is Obsessive-Compulsive Disorder?

Introduction

Obsessive–compulsive disorder (OCD) is a mental and behavioural disorder in which a person has intrusive thoughts (called “obsessions”) and/or feels the need to perform certain routines repeatedly (called “compulsions”) to an extent where it induces distress or impairs one’s general functioning.

Obsessions are unwanted and persistent thoughts, mental images or urges. These obsessions generate feelings of anxiety, disgust, or unease. Some common obsessions include but are not limited to fear of contamination, obsession with symmetry, and unwanted thoughts about religion, sex, and/or harm.

Some compulsions include but are not limited to excessive hand washing or cleaning, arranging things in a particular way, having to perform actions according to specific rules, counting, constantly seeking reassurance, and compulsive checking behaviour. Most adults are aware that the behaviours do not make sense. Compulsions are done to achieve relief from the distress caused by obsessions. These compulsions occur to such a degree that the person’s daily life is negatively affected. They typically take up at least an hour of each day but can fill a person’s day in severe cases. The condition is associated with tics, anxiety disorder, and an increased risk of suicide.

The cause is unknown. There appear to be some genetic components, with both identical twins more often affected than both non-identical twins. Risk factors include a history of child abuse or other stress-inducing events. Some cases have been documented to occur following streptococcal infections. The diagnosis is based on the symptoms and requires ruling out other drug-related or medical causes. Rating scales such as the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) can be used to assess the severity. Other disorders with similar symptoms include anxiety disorder, major depressive disorder, eating disorders, tic disorders, and obsessive-compulsive personality disorder.

Treatment may involve psychotherapy, such as cognitive behavioural therapy (CBT), and antidepressants, such as selective serotonin reuptake inhibitors (SSRIs) or clomipramine. CBT for OCD involves increasing exposure to fears and obsessions while preventing the compulsive behaviour that would normally accompany the obsessions. Contrary to this, metacognitive therapy encourages the ritual behaviours in order to alter the relationship to one’s thoughts about them. While clomipramine appears to work as well as do SSRIs, it has greater side effects and thus is typically reserved as a second-line treatment. Atypical antipsychotics may be useful when used in addition to an SSRI in treatment-resistant cases but are also associated with an increased risk of side effects. Without treatment, the condition often lasts decades.

Obsessive-compulsive disorder affects about 2.3% of people at some point in their lives while rates during any given year are about 1.2%. It is unusual for symptoms to begin after the age of 35, and half of people develop problems before 20. Males and females are affected about equally and OCD occurs worldwide. The phrase obsessive-compulsive is sometimes used in an informal manner unrelated to OCD to describe someone as being excessively meticulous, perfectionistic, absorbed, or otherwise fixated.

Brief History

In the 7th century AD, John Climacus records an instance of a young monk plagued by constant and overwhelming “temptations to blasphemy” consulting an older monk,  who told him, “My son, I take upon myself all the sins which these temptations have led you, or may lead you, to commit. All I require of you is that for the future you pay no attention to them whatsoever.”  The Cloud of Unknowing, a Christian mystical text from the late 14th century, recommends dealing with recurring obsessions by first attempting to ignore them,  and, if that fails, “cower under them like a poor wretch and a coward overcome in battle, and reckon it to be a waste of your time for you to strive any longer against them”,  a technique now known as “emotional flooding”. 

From the 14th to the 16th century in Europe, it was believed that people who experienced blasphemous, sexual or other obsessive thoughts were possessed by the devil.  Based on this reasoning, treatment involved banishing the “evil” from the “possessed” person through exorcism. The vast majority of people who thought that they were possessed by the devil did not suffer from hallucinations or other “spectacular symptoms”,  but “complained of anxiety, religious fears, and evil thoughts.”  In 1584, a woman from Kent, England, named Mrs. Davie, described by a justice of the peace as “a good wife”,  was nearly burned at the stake after she confessed that she experienced constant, unwanted urges to murder her family.

The English term obsessive-compulsive arose as a translation of German Zwangsvorstellung (‘obsession’) used in the first conceptions of OCD by Carl Westphal. Westphal’s description went on to influence Pierre Janet, who further documented features of OCD. In the early 1910s, Sigmund Freud attributed obsessive-compulsive behaviour to unconscious conflicts that manifest as symptoms. Freud describes the clinical history of a typical case of “touching phobia” as starting in early childhood, when the person has a strong desire to touch an item. In response, the person develops an “external prohibition” against this type of touching. However, this “prohibition does not succeed in abolishing” the desire to touch; all it can do is repress the desire and “force it into the unconscious.” Freudian psychoanalysis remained the dominant treatment for OCD until the mid-1980s,  even though medicinal and therapeutic treatments were known and available, because it was widely thought that these treatments would be detrimental to the effectiveness of the psychotherapy.  In the mid-1980s, this approach changed  and practitioners began treating OCD primarily with medicine and practical therapy rather than through psychoanalysis.

Notable Cases

John Bunyan (1628-1688), the author of The Pilgrim’s Progress, displayed symptoms of OCD (which had not yet been named).  During the most severe period of his condition, he would mutter the same phrase over and over again to himself while rocking back and forth.  He later described his obsessions in his autobiography Grace Abounding to the Chief of Sinners,  stating, “These things may seem ridiculous to others, even as ridiculous as they were in themselves, but to me they were the most tormenting cogitations.”  He wrote two pamphlets advising those suffering from similar anxieties.  In one of them, he warns against indulging in compulsions:  “Have care of putting off your trouble of spirit in the wrong way: by promising to reform yourself and lead a new life, by your performances or duties”.

British poet, essayist and lexicographer Samuel Johnson (1709-1784) also suffered from OCD.  He had elaborate rituals for crossing the thresholds of doorways, and repeatedly walked up and down staircases counting the steps.  He would touch every post on the street as he walked past,  only step in the middles of paving stones,  and repeatedly perform tasks as though they had not been done properly the first time. 

The American aviator and filmmaker Howard Hughes is known to have had OCD. Friends of Hughes have also mentioned his obsession with minor flaws in clothing. This was conveyed in The Aviator (2004), a film biography of Hughes.

Signs and Symptoms

OCD can present with a wide variety of symptoms. Certain groups of symptoms usually occur together. These groups are sometimes viewed as dimensions or clusters that may reflect an underlying process. The standard assessment tool for OCD, the Yale-Brown Obsessive Compulsive Scale (Y-BOCS), has 13 predefined categories of symptoms. These symptoms fit into three to five groupings. A meta-analytic review of symptom structures found a four-factor structure (grouping) to be most reliable. The observed groups included a “symmetry factor”, a “forbidden thoughts factor”, a “cleaning factor”, and a “hoarding factor”. The “symmetry factor” correlated highly with obsessions related to ordering, counting, and symmetry, as well as repeating compulsions. The “forbidden thoughts factor” correlated highly with intrusive and distressing thoughts of a violent, religious, or sexual nature. The “cleaning factor” correlated highly with obsessions about contamination and compulsions related to cleaning. The “hoarding factor” only involved hoarding-related obsessions and compulsions and was identified as being distinct from other symptom groupings.

While OCD has been considered a homogeneous disorder from a neuropsychological perspective, many of the putative neuropsychological deficits may be the result of comorbid disorders. Furthermore, some subtypes have been associated with improvement in performance on certain tasks such as pattern recognition (washing subtype) and spatial working memory (obsessive thought subtype). Subgroups have also been distinguished by neuroimaging findings and treatment response. Neuroimaging studies on this have been too few, and the subtypes examined have differed too much to draw any conclusions. On the other hand, subtype-dependent treatment response has been studied, and the hoarding subtype has consistently responded least to treatment.

The phrase obsessive-compulsive is sometimes used in an informal manner unrelated to OCD to describe someone as being excessively meticulous, perfectionistic, absorbed, or otherwise fixated.

Obsessions

Obsessions are thoughts that recur and persist despite efforts to ignore or confront them. People with OCD frequently perform tasks, or compulsions, to seek relief from obsession-related anxiety. Within and among individuals, the initial obsessions or intrusive thoughts vary in their clarity and vividness. A relatively vague obsession could involve a general sense of disarray or tension accompanied by a belief that life cannot proceed as normal while the imbalance remains. A more intense obsession could be a preoccupation with the thought or image of a close family member or friend dying or intrusions related to “relationship rightness”. Other obsessions concern the possibility that someone or something other than oneself – such as God, the devil or disease – will harm either the person or the people or things about which the person cares. Other individuals with OCD may experience the sensation of invisible protrusions emanating from their bodies or feel that inanimate objects are ensouled.

Some people with OCD experience sexual obsessions that may involve intrusive thoughts or images of “kissing, touching, fondling, oral sex, anal sex, intercourse, incest and rape” with “strangers, acquaintances, parents, children, family members, friends, coworkers, animals and religious figures”, and can include “heterosexual or homosexual content” with persons of any age. As with other intrusive, unpleasant thoughts or images, some disquieting sexual thoughts at times are normal, but people with OCD may attach extraordinary significance to the thoughts. For example, obsessive fears about sexual orientation can appear to the person with OCD, and even to those around him or her, as a crisis of sexual identity. Furthermore, the doubt that accompanies OCD leads to uncertainty regarding whether one might act on the troubling thoughts, resulting in self-criticism or self-loathing.

Most people with OCD understand that their notions do not correspond with reality; however, they feel that they must act as though their notions are correct. For example, an individual who engages in compulsive hoarding might be inclined to treat inorganic matter as if it had the sentience or rights of living organisms, while accepting that such behaviour is irrational on a more intellectual level. There is a debate as to whether hoarding should be considered with other OCD symptoms.

OCD sometimes manifests without overt compulsions, which may be termed primarily obsessional OCD. OCD without overt compulsions could, by one estimate, characterise as many as 50-60% of OCD cases.

Compulsions

Some people with OCD perform compulsive rituals because they inexplicably feel that they must do so, while others act compulsively to mitigate the anxiety that stems from obsessive thoughts. The person might feel that these actions will somehow either prevent a dreaded event from occurring or will push the event from his or her thoughts. In any case, the person’s reasoning is so idiosyncratic or distorted that it results in significant distress for the person or for those around him or her. Excessive skin picking, hair pulling, nail biting and other body-focused repetitive behaviour disorders are all on the obsessive-compulsive spectrum. Some individuals with OCD are aware that their behaviours are not rational, but feel compelled to follow through with them to fend off feelings of panic or dread.

Some common compulsions include hand washing, cleaning, checking things (such as locks on doors), repeating actions (such as turning on and off switches), ordering items in a certain way and requesting reassurance. Compulsions are different from tics (such as touching, tapping, rubbing or blinking) and stereotyped movements (such as head banging, body rocking or self-biting), which are usually not as complex and are not precipitated by obsessions. It can sometimes be difficult to tell the difference between compulsions and complex tics. About 10% to 40% of individuals with OCD also have a lifetime tic disorder.

People rely on compulsions as an escape from their obsessive thoughts; however, they are aware that the relief is only temporary, and that the intrusive thoughts will soon return. Some people use compulsions to avoid situations that may trigger their obsessions. Compulsions may be actions directly related to the obsession, such as someone obsessed with contamination compulsively washing their hands, but they can be unrelated actions as well.

Although some people perform actions repeatedly, they do not necessarily perform these actions compulsively. For example, bedtime routines, learning a new skill and religious practices are not compulsions. Whether behaviours are compulsions or mere habit depends on the context in which the behaviours are performed. For example, arranging and ordering books for eight hours a day would be expected of one who works in a library, but would seem abnormal in other situations. In other words, habits tend to bring efficiency to one’s life, while compulsions tend to disrupt it.

In addition to experiencing the anxiety and fear that typically accompany OCD, sufferers may spend hours performing such compulsions every day. In such situations, it can become difficult for the person to fulfil his or her work, family or social roles. In some cases, these behaviours can also cause adverse physical symptoms. For example, people who obsessively wash their hands with antibacterial soap and hot water can make their skin red and raw with dermatitis.

People with OCD can use rationalisations to explain their behaviour; however, these rationalisations do not apply to the overall behaviour but to each instance individually. For example, a person compulsively checking the front door may argue that the time taken and stress caused by one more check is much less than the time and stress associated with being robbed, and thus checking is the better option. In practice, after that check, the person is still not sure and deems it is better to perform one more check, and this reasoning can continue for as long as necessary.

In cognitive behavioural therapy, OCD patients are asked to overcome intrusive thoughts by not indulging in any compulsions. They are taught that rituals keep OCD strong, while not performing them causes the OCD to become weaker. For body-focused repetitive behaviours (BFRB), such as trichotillomania, skin picking and onychophagia (nail biting), behavioural interventions such as habit reversal training and decoupling are recommended for the treatment of compulsive behaviours.

Insight

The DSM-V contains three specifiers for the level of insight in OCD. Good or fair insight is characterised by the acknowledgment that obsessive-compulsive beliefs are or may not be true. Poor insight is characterised by the belief that obsessive-compulsive beliefs are probably true. Absence of insight makes obsessive-compulsive beliefs delusional thoughts, and occurs in about 4% of people with OCD.

Overvalued Ideas

Some people with OCD exhibit what is known as overvalued ideas. In such cases, the person with OCD will truly be uncertain whether the fears that cause them to perform their compulsions are irrational. After some discussion, it is possible to convince the individual that their fears may be unfounded. It may be more difficult to practice ERP therapy on such people because they may be unwilling to cooperate, at least initially. There are severe cases in which the person has an unshakable belief in the context of OCD that is difficult to differentiate from psychotic disorders.

Cognitive Performance

Though OCD was once believed to be associated with above-average intelligence, this does not appear to necessarily be the case. A 2013 review reported that people with OCD may sometimes have mild but wide-ranging cognitive deficits, most significantly those affecting spatial memory and to a lesser extent with verbal memory, fluency, executive function and processing speed, while auditory attention was not significantly affected. People with OCD show impairment in formulating an organisational strategy for coding information, set-shifting and motor and cognitive inhibition.

Specific subtypes of symptom dimensions in OCD have been associated with specific cognitive deficits. For example, the results of one meta-analysis comparing washing and checking symptoms reported that washers outperformed checkers on eight out of ten cognitive tests. The symptom dimension of contamination and cleaning may be associated with higher scores on tests of inhibition and verbal memory.

Children

Approximately 1-2% of children are affected by OCD. Obsessive-compulsive disorder symptoms tend to develop more frequently in children 10-14 years of age, with males displaying symptoms at an earlier age and at a more severe level than do females. In children, symptoms can be grouped into at least four types.

Associated Conditions

People with OCD may be diagnosed with other conditions as well as, or instead of, OCD, such as obsessive-compulsive personality disorder, major depressive disorder, bipolar disorder, generalised anxiety disorder, anorexia nervosa, social anxiety disorder, bulimia nervosa, Tourette syndrome, transformation obsession, autism spectrum disorder, attention deficit hyperactivity disorder, dermatillomania (compulsive skin picking), body dysmorphic disorder and trichotillomania (hair pulling). More than 50% of people with OCD experience suicidal tendencies, and 15% have attempted suicide. Depression, anxiety and prior suicide attempts increase the risk of future suicide attempts.

Individuals with OCD have also been found to be affected by delayed sleep phase syndrome at a substantially higher rate than is the general public. Moreover, severe OCD symptoms are consistently associated with greater sleep disturbance. Reduced total sleep time and sleep efficiency have been observed in people with OCD, with delayed sleep onset and offset and an increased prevalence of delayed sleep phase disorder.

Some research has demonstrated a link between drug addiction and OCD. For example, there is a higher risk of drug addiction among those with any anxiety disorder (possibly as a way of coping with the heightened levels of anxiety), but drug addiction among people with OCD may serve as a type of compulsive behaviour and not just as a coping mechanism. Depression is also extremely prevalent among people with OCD. One explanation for the high depression rate among OCD populations was posited by Mineka, Watson and Clark (1998), who explained that people with OCD (or any other anxiety disorder) may feel depressed because of an “out of control” type of feeling.

Someone exhibiting OCD signs does not necessarily have OCD. Behaviours that present as (or seem to be) obsessive or compulsive can also be found in a number of other conditions, including obsessive-compulsive personality disorder (OCPD), autism spectrum disorder or disorders in which perseveration is a possible feature (ADHD, PTSD, bodily disorders or habit problems), or subclinically.

Some with OCD present with features typically associated with Tourette syndrome, such as compulsions that may appear to resemble motor tics; this has been termed “tic-related OCD” or “Tourettic OCD”.

OCD frequently occurs comorbidly with both bipolar disorder and major depressive disorder. Between 60 and 80% of those with OCD experience a major depressive episode in their lifetime. Comorbidity rates have been reported at between 19 and 90% because of methodological differences. Between 9-35% of those with bipolar disorder also have OCD, compared to 1-2% in the general population. About 50% of those with OCD experience cyclothymic traits or hypomanic episodes. OCD is also associated with anxiety disorders. Lifetime comorbidity for OCD has been reported at 22% for specific phobia, 18% for social anxiety disorder, 12% for panic disorder, and 30% for generalized anxiety disorder. The comorbidity rate for OCD and ADHD has been reported to be as high as 51%.

Causes

Refer to Causes of OCD.

The cause is unknown. Both environmental and genetic factors are believed to play a role. Risk factors include a history of child abuse or other stress-inducing event.

Drug-Induced OCD

Many different types of medication can create/induce OCD in patients without previous symptoms. A new chapter about OCD in the DSM-5 (2013) now specifically includes drug-induced OCD.

Atypical antipsychotics (second-generation antipsychotics) such as olanzapine (Zyprexa) have been proven to induce de novo OCD in patients.

Genetics

There appear to be some genetic components with identical twins more often affected than non-identical twins. Further, individuals with OCD are more likely to have first-degree family members exhibiting the same disorders than do matched controls. In cases in which OCD develops during childhood, there is a much stronger familial link in the disorder than with cases in which OCD develops later in adulthood. In general, genetic factors account for 45-65% of the variability in OCD symptoms in children diagnosed with the disorder. A 2007 study found evidence supporting the possibility of a heritable risk for OCD.

A mutation has been found in the human serotonin transporter gene hSERT in unrelated families with OCD.

A systematic review found that while neither allele was associated with OCD overall, in Caucasians the L allele was associated with OCD. Another meta-analysis observed an increased risk in those with the homozygous S allele, but found the LS genotype to be inversely associated with OCD.

A genome-wide association study found OCD to be linked with SNPs near BTBD3 and two SNPs in DLGAP1 in a trio-based analysis, but no SNP reached significance when analysed with case-control data.

One meta-analysis found a small but significant association between a polymorphism in SLC1A1 and OCD.

The relationship between OCD and COMT has been inconsistent, with one meta-analysis reporting a significant association, albeit only in men, and another meta analysis reporting no association.

It has been postulated by evolutionary psychologists that moderate versions of compulsive behaviour may have had evolutionary advantages. Examples would be moderate constant checking of hygiene, the hearth or the environment for enemies. Similarly, hoarding may have had evolutionary advantages. In this view, OCD may be the extreme statistical “tail” of such behaviours, possibly the result of a high number of predisposing genes.

Autoimmune

A controversial hypothesis is that some cases of rapid onset of OCD in children and adolescents may be caused by a syndrome connected to Group A streptococcal infections known as paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). OCD and tic disorders are hypothesized to arise in a subset of children as a result of a post-streptococcal autoimmune process. The PANDAS hypothesis is unconfirmed and unsupported by data, and two new categories have been proposed: PANS (paediatric acute-onset neuropsychiatric syndrome) and CANS (childhood acute neuropsychiatric syndrome). The CANS/PANS hypotheses include different possible mechanisms underlying acute-onset neuropsychiatric conditions, but do not exclude GABHS infections as a cause in a subset of individuals. PANDAS, PANS and CANS are the focus of clinical and laboratory research but remain unproven. Whether PANDAS is a distinct entity differing from other cases of tic disorders or OCD is debated.

A review of studies examining anti-basal ganglia antibodies in OCD found an increased risk of having anti-basal ganglia antibodies in those with OCD versus the general population.

Mechanisms

Neuroimaging

Functional neuroimaging during symptom provocation has observed abnormal activity in the orbitofrontal cortex, left dorsolateral prefrontal cortex, right premotor cortex, left superior temporal gyrus, globus pallidus externus, hippocampus and right uncus. Weaker foci of abnormal activity were found in the left caudate, posterior cingulate cortex and superior parietal lobule. However, an older meta-analysis of functional neuroimaging in OCD reported that the only consistent functional neuroimaging finding was increased activity in the orbital gyrus and head of the caudate nucleus, while ACC activation abnormalities were too inconsistent. A meta-analysis comparing affective and nonaffective tasks observed differences with controls in regions implicated in salience, habit, goal-directed behaviour, self-referential thinking and cognitive control. For nonaffective tasks, hyperactivity was observed in the insula, ACC, and head of the caudate/putamen, while hypoactivity was observed in the medial prefrontal cortex (mPFC) and posterior caudate. Affective tasks were observed to relate to increased activation in the precuneus and posterior cingulate cortex (PCC), while decreased activation was found in the pallidum, ventral anterior thalamus and posterior caudate. The involvement of the cortico-striato-thalamo-cortical loop in OCD as well as the high rates of comorbidity between OCD and ADHD have led some to draw a link in their mechanism. Observed similarities include dysfunction of the anterior cingulate cortex and prefrontal cortex, as well as shared deficits in executive functions. The involvement of the orbitofrontal cortex and dorsolateral prefrontal cortex in OCD is shared with bipolar disorder and may explain the high degree of comorbidity. Decreased volumes of the dorsolateral prefrontal cortex related to executive function has also been observed in OCD.

People with OCD evince increased grey matter volumes in bilateral lenticular nuclei, extending to the caudate nuclei, with decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri. These findings contrast with those in people with other anxiety disorders, who evince decreased (rather than increased) grey matter volumes in bilateral lenticular/caudate nuclei, as well as decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri. Increased white matter volume and decreased fractional anisotropy in anterior midline tracts has been observed in OCD, possibly indicating increased fibre crossings.

Cognitive models
Generally two categories of models for OCD have been postulated, the first involving deficits in executive function, and the second involving deficits in modulatory control. The first category of executive dysfunction is based on the observed structural and functional abnormalities in the dlPFC, striatum and thalamus. The second category involving dysfunctional modulatory control primarily relies on observed functional and structural differences in the ACC, mPFC and OFC.[91][92]

One proposed model suggests that dysfunction in the OFC leads to improper valuation of behaviors and decreased behavioral control, while the observed alterations in amygdala activations leads to exaggerated fears and representations of negative stimuli.[93]

Because of the heterogeneity of OCD symptoms, studies differentiating various symptoms have been performed. Symptom-specific neuroimaging abnormalities include the hyperactivity of caudate and ACC in checking rituals, while finding increased activity of cortical and cerebellar regions in contamination-related symptoms. Neuroimaging differentiating content of intrusive thoughts has found differences between aggressive as opposed to taboo thoughts, finding increased connectivity of the amygdala, ventral striatum and ventromedial prefrontal cortex in aggressive symptoms while observing increased connectivity between the ventral striatum and insula in sexual/religious intrusive thoughts.[94]

Another model proposes that affective dysregulation links excessive reliance on habit-based action selection[95] with compulsions. This is supported by the observation that those with OCD demonstrate decreased activation of the ventral striatum when anticipating monetary reward, as well as increased functional connectivity between the VS and the OFC. Furthermore, those with OCD demonstrate reduced performance in Pavlovian fear-extinction tasks, hyperresponsiveness in the amygdala to fearful stimuli, and hyporesponsiveness in the amygdala when exposed to positively valanced stimuli. Stimulation of the nucleus accumbens has also been observed to effectively alleviate both obsessions and compulsions, supporting the role of affective dysregulation in generating both.

Cognitive Models

Generally two categories of models for OCD have been postulated, the first involving deficits in executive function, and the second involving deficits in modulatory control. The first category of executive dysfunction is based on the observed structural and functional abnormalities in the dlPFC, striatum and thalamus. The second category involving dysfunctional modulatory control primarily relies on observed functional and structural differences in the ACC, mPFC and OFC.

One proposed model suggests that dysfunction in the OFC leads to improper valuation of behaviours and decreased behavioural control, while the observed alterations in amygdala activations leads to exaggerated fears and representations of negative stimuli.

Because of the heterogeneity of OCD symptoms, studies differentiating various symptoms have been performed. Symptom-specific neuroimaging abnormalities include the hyperactivity of caudate and ACC in checking rituals, while finding increased activity of cortical and cerebellar regions in contamination-related symptoms. Neuroimaging differentiating content of intrusive thoughts has found differences between aggressive as opposed to taboo thoughts, finding increased connectivity of the amygdala, ventral striatum and ventromedial prefrontal cortex in aggressive symptoms while observing increased connectivity between the ventral striatum and insula in sexual/religious intrusive thoughts.

Another model proposes that affective dysregulation links excessive reliance on habit-based action selection with compulsions. This is supported by the observation that those with OCD demonstrate decreased activation of the ventral striatum when anticipating monetary reward, as well as increased functional connectivity between the VS and the OFC. Furthermore, those with OCD demonstrate reduced performance in Pavlovian fear-extinction tasks, hyperresponsiveness in the amygdala to fearful stimuli, and hyporesponsiveness in the amygdala when exposed to positively valanced stimuli. Stimulation of the nucleus accumbens has also been observed to effectively alleviate both obsessions and compulsions, supporting the role of affective dysregulation in generating both.

Neurobiological

From the observation of the efficacy of antidepressants in OCD, a serotonin hypothesis of OCD has been formulated. Studies of peripheral markers of serotonin, as well as challenges with proserotonergic compounds have yielded inconsistent results, including evidence pointing towards basal hyperactivity of serotonergic systems. Serotonin receptor and transporter binding studies have yielded conflicting results, including higher and lower serotonin receptor 5-HT2A and serotonin transporter binding potentials that were normalised by treatment with SSRIs. Despite inconsistencies in the types of abnormalities found, evidence points towards dysfunction of serotonergic systems in OCD. Orbitofrontal cortex overactivity is attenuated in people who have successfully responded to SSRI medication, a result believed to be caused by increased stimulation of serotonin receptors 5-HT2A and 5-HT2C.

A complex relationship between dopamine and OCD has been observed. Although antipsychotics, which act by antagonising dopamine receptors may improve some cases of OCD, they frequently exacerbate others. Antipsychotics, in the low doses used to treat OCD, may actually increase the release of dopamine in the prefrontal cortex, through inhibiting autoreceptors. Further complicating things is the efficacy of amphetamines, decreased dopamine transporter activity observed in OCD, and low levels of D2 binding in the striatum.[100] Furthermore, increased dopamine release in the nucleus accumbens after deep brain stimulation correlates with improvement in symptoms, pointing to reduced dopamine release in the striatum playing a role in generating symptoms.

Abnormalities in glutamatergic neurotransmission have implicated in OCD. Findings such as increased cerebrospinal glutamate, less consistent abnormalities observed in neuroimaging studies and the efficacy of some glutamatergic drugs such as the glutamate-inhibiting riluzole have implicated glutamate in OCD. OCD has been associated with reduced N-Acetylaspartic acid in the mPFC, which is thought to reflect neuron density or functionality, although the exact interpretation has not been established.

Diagnosis

Formal diagnosis may be performed by a psychologist, psychiatrist, clinical social worker, or other licensed mental health professional. To be diagnosed with OCD, a person must have obsessions, compulsions, or both, according to the Diagnostic and Statistical Manual of Mental Disorders (DSM). The Quick Reference to the 2000 edition of the DSM states that several features characterize clinically significant obsessions and compulsions, and that such obsessions are recurrent and persistent thoughts, impulses or images that are experienced as intrusive and that cause marked anxiety or distress. These thoughts, impulses or images are of a degree or type that lies outside the normal range of worries about conventional problems. A person may attempt to ignore or suppress such obsessions, or to neutralize them with some other thought or action, and will tend to recognize the obsessions as idiosyncratic or irrational.

Compulsions become clinically significant when a person feels driven to perform them in response to an obsession, or according to rules that must be applied rigidly, and when the person consequently feels or causes significant distress. Therefore, while many people who do not suffer from OCD may perform actions often associated with OCD (such as ordering items in a pantry by height), the distinction with clinically significant OCD lies in the fact that the person who suffers from OCD must perform these actions to avoid significant psychological distress. These behaviours or mental acts are aimed at preventing or reducing distress or preventing some dreaded event or situation; however, these activities are not logically or practically connected to the issue, or they are excessive. In addition, at some point during the course of the disorder, the individual must realise that his or her obsessions or compulsions are unreasonable or excessive.

Moreover, the obsessions or compulsions must be time-consuming (taking up more than one hour per day) or cause impairment in social, occupational or scholastic functioning. It is helpful to quantify the severity of symptoms and impairment before and during treatment for OCD. In addition to the person’s estimate of the time spent each day harbouring obsessive-compulsive thoughts or behaviours, concrete tools can be used to gauge the person’s condition. This may be done with rating scales, such as the Yale-Brown Obsessive Compulsive Scale (Y-BOCS; expert rating) or the obsessive-compulsive inventory (OCI-R; self-rating). With measurements such as these, psychiatric consultation can be more appropriately determined because it has been standardised.

OCD is sometimes placed in a group of disorders called the obsessive-compulsive spectrum.

Differential Diagnosis

OCD is often confused with the separate condition obsessive-compulsive personality disorder (OCPD). OCD is egodystonic, meaning that the disorder is incompatible with the sufferer’s self-concept. Because egodystonic disorders go against a person’s self-concept, they tend to cause much distress. OCPD, on the other hand, is egosyntonic – marked by the person’s acceptance that the characteristics and behaviours displayed as a result are compatible with their self-image, or are otherwise appropriate, correct or reasonable.

As a result, people with OCD are often aware that their behaviour is not rational and are unhappy about their obsessions but nevertheless feel compelled by them. By contrast, people with OCPD are not aware of anything abnormal; they will readily explain why their actions are rational. It is usually impossible to convince them otherwise, and they tend to derive pleasure from their obsessions or compulsions.

Management

A form of psychotherapy called cognitive behavioural therapy (CBT) and psychotropic medications are first-line treatments for OCD. Other forms of psychotherapy, such as psychodynamics and psychoanalysis may help in managing some aspects of the disorder, but in 2007 the American Psychiatric Association (APA) noted a lack of controlled studies showing their effectiveness “in dealing with the core symptoms of OCD”.

Therapy

The specific technique used in CBT is called exposure and response prevention (ERP), which involves teaching the person to deliberately come into contact with the situations that trigger the obsessive thoughts and fears (“exposure”) without carrying out the usual compulsive acts associated with the obsession (“response prevention”), thus gradually learning to tolerate the discomfort and anxiety associated with not performing the ritualistic behaviour. At first, for example, someone might touch something only very mildly “contaminated” (such as a tissue that has been touched by another tissue that has been touched by the end of a toothpick that has touched a book that came from a “contaminated” location, such as a school). That is the “exposure”. The “ritual prevention” is not washing. Another example might be leaving the house and checking the lock only once (exposure) without going back and checking again (ritual prevention). The person fairly quickly habituates to the anxiety-producing situation and discovers that his or her anxiety level drops considerably; he or she can then progress to touching something more “contaminated” or not checking the lock at all – again, without performing the ritual behaviour of washing or checking.

ERP has a strong evidence base, and it is considered the most effective treatment for OCD. However, this claim was doubted by some researchers in 2000, who criticised the quality of many studies. A 2007 Cochrane review also found that psychological interventions derived from CBT models were more effective than treatment as usual consisting of no treatment, waiting list or non-CBT interventions. For body-focused repetitive behaviours (BFRB), behavioural interventions are recommended by reviews such as habit-reversal training and decoupling.

Psychotherapy in combination with psychiatric medication may be more effective than either option alone for individuals with severe OCD.

Medication

The medications most frequently used are the selective serotonin reuptake inhibitors (SSRIs). Clomipramine, a medication belonging to the class of tricyclic antidepressants, appears to work as well as SSRIs but has a higher rate of side effects.

SSRIs are a second-line treatment of adult obsessive compulsive disorder with mild functional impairment and as first-line treatment for those with moderate or severe impairment. In children, SSRIs can be considered as a second-line therapy in those with moderate to severe impairment, with close monitoring for psychiatric adverse effects. SSRIs are efficacious in the treatment of OCD; people treated with SSRIs are about twice as likely to respond to treatment as are those treated with placebo. Efficacy has been demonstrated both in short-term (6-24 weeks) treatment trials and in discontinuation trials with durations of 28-52 weeks.

In 2006, the National Institute of Clinical and Health Excellence (NICE) guidelines recommended antipsychotics for OCD that does not improve with SSRI treatment. For OCD there is tentative evidence for risperidone and insufficient evidence for olanzapine. Quetiapine is no better than placebo with regard to primary outcomes, but small effects were found in terms of YBOCS score. The efficacy of quetiapine and olanzapine are limited by an insufficient number of studies. A 2014 review article found two studies that indicated that aripiprazole was “effective in the short-term” and found that “[t]here was a small effect-size for risperidone or anti-psychotics in general in the short-term”; however, the study authors found “no evidence for the effectiveness of quetiapine or olanzapine in comparison to placebo.” While quetiapine may be useful when used in addition to an SSRI in treatment-resistant OCD, these drugs are often poorly tolerated, and have metabolic side effects that limit their use. None of the atypical antipsychotics appear to be useful when used alone. Another review reported that no evidence supports the use of first-generation antipsychotics in OCD.

A guideline by the APA suggested that dextroamphetamine may be considered by itself after more well-supported treatments have been tried.

Procedures

Electroconvulsive therapy (ECT) has been found to have effectiveness in some severe and refractory cases.

Surgery may be used as a last resort in people who do not improve with other treatments. In this procedure, a surgical lesion is made in an area of the brain (the cingulate cortex). In one study, 30% of participants benefitted significantly from this procedure. Deep-brain stimulation and vagus nerve stimulation are possible surgical options that do not require destruction of brain tissue. In the United States, the Food and Drug Administration (FDA) approved deep-brain stimulation for the treatment of OCD under a humanitarian device exemption requiring that the procedure be performed only in a hospital with special qualifications to do so.

In the United States, psychosurgery for OCD is a treatment of last resort and will not be performed until the person has failed several attempts at medication (at the full dosage) with augmentation, and many months of intensive cognitive-behavioural therapy with exposure and ritual/response prevention. Likewise, in the United Kingdom, psychosurgery cannot be performed unless a course of treatment from a suitably qualified cognitive-behavioural therapist has been carried out.

Children

Therapeutic treatment may be effective in reducing ritual behaviours of OCD for children and adolescents. Similar to the treatment of adults with OCD, CBT stands as an effective and validated first line of treatment of OCD in children. Family involvement, in the form of behavioural observations and reports, is a key component to the success of such treatments. Parental interventions also provide positive reinforcement for a child who exhibits appropriate behaviours as alternatives to compulsive responses. In a recent meta-analysis of evidenced-based treatment of OCD in children, family-focused individual CBT was labelled as “probably efficacious”, establishing it as one of the leading psychosocial treatments for youth with OCD. After one or two years of therapy, in which a child learns the nature of his or her obsession and acquires strategies for coping, that child may acquire a larger circle of friends, exhibit less shyness, and become less self-critical.

Although the causes of OCD in younger age groups range from brain abnormalities to psychological preoccupations, life stress such as bullying and traumatic familial deaths may also contribute to childhood cases of OCD, and acknowledging these stressors can play a role in treating the disorder.

Epidemiology

Obsessive-compulsive disorder affects about 2.3% of people at some point in their life, with the yearly rate about 1.2%. OCD occurs worldwide. It is unusual for symptoms to begin after the age of 35 and half of people develop problems before 20. Males and females are affected about equally.

Prognosis

Quality of life is reduced across all domains in OCD. While psychological or pharmacological treatment can lead to a reduction of OCD symptoms and an increase in reported quality of life, symptoms may persist at moderate levels even following adequate treatment courses, and completely symptom-free periods are uncommon. In paediatric OCD, around 40% still have the disorder in adulthood, and around 40% qualify for remission.

Society and Culture

Art, Entertainment and Media

Movies and television shows may portray idealised or incomplete representations of disorders such as OCD. Compassionate and accurate literary and on-screen depictions may help counteract the potential stigma associated with an OCD diagnosis, and lead to increased public awareness, understanding and sympathy for such disorders.

  • In the film As Good as It Gets (1997), actor Jack Nicholson portrays a man with OCD who performs ritualistic behaviours that disrupt his life.
  • The film Matchstick Men (2003), directed by Ridley Scott, portrays a con man named Roy (Nicolas Cage) with OCD who opens and closes doors three times while counting aloud before he can walk through them.
  • In the television series Monk (2002-2009), the titular character Adrian Monk fears both human contact and dirt.
  • In Turtles All the Way Down (2017), a young adult novel by author John Green, teenage main character Aza Holmes struggles with OCD that manifests as a fear of the human microbiome.
    • Throughout the story, Aza repeatedly opens an unhealed callus on her finger to drain out what she believes are pathogens.
    • The novel is based on Green’s own experiences with OCD.
    • He explained that Turtles All the Way Down is intended to show how “most people with chronic mental illnesses also live long, fulfilling lives”.
  • The British TV series Pure (2019) stars Charly Clive as a 24-year-old Marnie who is plagued by disturbing sexual thoughts, as a kind of primarily obsessional obsessive compulsive disorder.
    • The series is based on a book of the same name by Rose Cartwright.

Research

The naturally occurring sugar inositol has been suggested as a treatment for OCD.

μ-Opioids, such as hydrocodone and tramadol, may improve OCD symptoms. Administration of opiate treatment may be contraindicated in individuals concurrently taking CYP2D6 inhibitors such as fluoxetine and paroxetine.

Much current research is devoted to the therapeutic potential of the agents that affect the release of the neurotransmitter glutamate or the binding to its receptors. These include riluzole, memantine, gabapentin, N-acetylcysteine, topiramate and lamotrigine.

What is Cyclothymia?

Introduction

Cyclothymia, also known as cyclothymic disorder, is a mental and behavioural disorder that involves numerous periods of symptoms of depression and periods of symptoms of elevated mood.

These symptoms, however, are not sufficient to be a major depressive episode or a hypomanic episode. Symptoms must last for more than one year in children and two years in adults.

The cause of cyclothymia is unknown. Risk factors include a family history of bipolar disorder. Cyclothymia differs from bipolar in that major depression, mania, or hypomania have never occurred.

Treatment is generally with counselling and mood stabilisers such as lithium. It is estimated that 0.4-1% of people have cyclothymia at some point in their life. Onset is typically in late childhood to early adulthood. Males and females are affected equally often.

Brief History

In 1883, Karl Ludwig Kahlbaum identified a disorder characterised by recurring mood cycles. The disorder contained both melancholic and manic episodes that occurred in a milder form than in bipolar disorder. This condition was coined “cyclothymia” by Kahlbaum and his student Ewald Hecker. Kahlbaum developed his theory of cyclothymia through his work with people presenting with these symptoms at the Kahlbaum Sanitarium in Goerlitz, Silesia (Germany). He was recognised as a leading hypnotherapist and psychotherapist of his day. He was a progressive in the field of mental health, believing that mental illness should not carry a stigma and that people dealing with mental health issues should be treated humanely. Kalhbaum was the first to recognise that people with cyclothymia often do not seek help for the disorder due to its mild symptoms.

Cyclothymia has been conceptualised in a variety of ways, including as a subtype of bipolar disorder, a temperament, a personality trait, and a personality disorder. There is also an argument that cyclothymia should be considered a neurodevelopmental disorder. The two defining features of the disorder, according to DSM-5, are the presence of depressive and hypomanic symptoms, not meeting the threshold for a depressive or hypomanic episode. Cyclothymia is also classified as a subtype of bipolar disorder in DSM-5, but some researchers disagree with this classification and argue that it should be primarily defined as an exaggeration of mood and emotional instability. In the past, cyclothymia has been conceptualised to include other characteristics in addition to the flux between depression and hypomania, such as mood reactivity, impulsivity, and anxiety.

Symptoms

People with cyclothymia experience both depressive phases and hypomanic phases (which are less severe than a full hypomanic episode). The depressive and manic symptoms in cyclothymia last for variable amounts of time due to the unstable and reactive nature of the disorder. The depressive phases are similar to major depressive disorder and are characterised by dulled thoughts and sensations and the lack of motivation for intellectual or social activities. Most people with cyclothymia are generally fatigued and tend to sleep frequently and for long periods of time. However, other people experience insomnia.

Other symptoms of cyclothymic depression include indifference toward people or activities that used to be extremely important. Cyclothymic depression also leads to difficulty making decisions. In addition, people with this condition tend to be critical and complain easily. Suicidal thoughts are common, even in mild forms of cyclothymia. In the depressive state, people with cyclothymia also experience physical complaints including frequent headaches, tightness in the head and chest, an empty sensation in the head, weakness, weight loss, and hair loss.

The distinguishing factor between typical depression and cyclothymic depression is that in cyclothymic depression, there are instances of hypomania. People with cyclothymia can switch from the depressive state to the hypomanic state without warning to them or others. The duration and frequency of phases is unpredictable.

In the hypomanic state, people’s thoughts become faster and they become more sociable and talkative. They may engage in spending sprees, spontaneous actions, have heightened self-esteem, and greater vanity. In contrast to a regular manic state that would be associated with bipolar I, symptoms in the hypomanic phase generally occur in a less severe form.

Comorbidities

Cyclothymia commonly occurs in conjunction with other disorders. Between 20-50 percent of people with depression, anxiety, and related disorders also have cyclothymia. When people with cyclothymia seek mental health resources it tends to be for symptoms of their comorbid condition rather than for their symptoms of cyclothymia. In children and adolescents, the most common comorbidities with cyclothymia are anxiety disorders, impulse control issues, eating disorders, and ADHD. In adults, cyclothymia also tends to be comorbid with impulse control issues. Sensation-seeking behaviours occur in hypomanic states. These often include gambling and compulsive sexuality in men, or compulsive buying and binge eating in women.

In addition to sensation-related disorders, cyclothymia has also been associated with atypical depression. In one study, a connection was found between interpersonal sensitivity, mood reactivity (i.e. responding to actual or potential positive events with brighter mood), and cyclothymic mood swings, all of which are symptoms of atypical depression. Cyclothymia also tends to occur in conjunction with separation anxiety, where a person has anxiety as a result of separation from a caregiver, friend, or loved one. Other issues that tend to co-occur with cyclothymia include social anxiety, fear of rejection and a tendency toward hostility to those connected with past pain and rejection. People with cyclothymia tend to seek intense interpersonal relationships when in a hypomanic state and isolation when in a depressed state. This generally leads to short, tumultuous relationships.

Causes

The cause is unknown. Risk factors include a family history of bipolar disorder.

First-degree relatives of people with cyclothymia have major depressive disorder, bipolar I disorder, and bipolar II disorder more often than the general population. Substance-related disorders also may be at a higher risk within the family. First-degree relatives of a bipolar I individuals may have a higher risk of cyclothymic disorder than the general population.

Diagnosis

Cyclothymia is classified in DSM-5 as a subtype of bipolar disorder. The criteria are:

  • Periods of elevated mood and depressive symptoms for at least half the time during the last two years for adults and one year for children and teenagers.
  • Periods of stable moods last only two months at most.
  • Symptoms create significant problems in one or more areas of life.
  • Symptoms do not meet the criteria for bipolar disorder, major depression, or another mental disorder.
  • Symptoms are not caused by substance use or a medical condition.

The DSM-5 criteria for cyclothymia are restrictive according to some researchers. This affects the diagnosis of cyclothymia because fewer people get diagnosed than potentially could. This means that a person who has some symptoms of the disorder might not be able to get treatment because they do not meet all of the necessary criteria described in DSM-5. Furthermore, it also leads to more attention being placed on depression and other bipolar-spectrum disorders because if a person does not meet all the criteria for cyclothymia they are often given a depression or bipolar spectrum diagnosis. Improper diagnosis may lead some people with cyclothymia to be treated for a comorbid disorder rather than having their cyclothymic tendencies addressed.

Cyclothymia is often not recognised by the affected individual or medical professionals due to its ostensibly mild symptoms. In addition, it is difficult to identify and classify. Due to disagreement and misconceptions among health and mental health professionals, cyclothymia is often diagnosed as “bipolar not otherwise specified”. Cyclothymia is also often confused with borderline personality disorder due to their similar symptoms, especially in older adolescents and young adults.

Most people with the disorder present in a depressive state, not realising that their hypomanic states are abnormal. Mild manic episodes tend to be interpreted as part of the person’s personality or simply a heightened mood. In addition, the disorder often manifests during childhood or adolescence, making it even more difficult for the person to distinguish between symptoms of the disorder and their personality. For example, people may think that they just suffer from mood swings and not realise that these are a result of a psychiatric condition.

Management

Cognitive behavioural therapy (CBT) is considered potentially effective for people diagnosed with cyclothymia.

Medication can be used in addition to behavioural approaches. However, mood stabilisers should be used before antidepressants, and if antidepressants are used they should be used with caution. Antidepressants are a concern due to the possibility of inducing hypomanic switches or rapid cycling.

Epidemiology

Cyclothymia, known today as cyclothymic disorder, tends to be underdiagnosed due to its low intensity. The exact rates for cyclothymia have not been widely studied. Some studies estimate that between 5 and 8% are affected at some point in their life whereas other studies suggest a rate ranging from 0.4 to 2.5%.

Males appear to be affected equally often, though women are more likely to receive treatment. Cyclothymia is diagnosed in around fifty percent of people with depression who are evaluated in psychiatric outpatient settings.

Etymology

Cyclothymia is derived from the Greek word κυκλοθυμία (from κῦκλος kyklos, “circle” and θυμός thymos, “mood, emotion”). Therefore, it means “to cycle or circle between moods or emotions”.

Research

Whether subtypes of bipolar disorder, such as cyclothymia, truly represent separate disorders or are part of a unique bipolar spectrum is debated in research. Cyclothymia is typically not described in research studies or diagnosed in clinical settings, making it less recognisable and less understood by professionals. This absence of cyclothymia in research and clinical settings suggests that cyclothymia is either being diagnosed as another mood disorder or as a non-affective psychiatric disorder or not coming to scientific or clinical attention due to a lack of diagnostic clarity or because the nature of cyclothymia is still highly contested. Additionally, the current diagnostic criterion for cyclothymia emphasizes that symptoms are persistent, which suggests that they are enduring traits rather than a psychological state, thus, it has been argued that it should be diagnosed as a personality disorder. Since the symptoms tend to overlap with personality disorders, the validity and distinction between these two diagnostic categories has been debated.

Lastly, the tendency of cyclothymia to be comorbid with other mental disorders makes diagnosis difficult. These issues prevent consensus on the definition of cyclothymia and its relationship with other mental disorders among researchers and clinicians. This lack of consensus on an operational definition and symptom presentation is especially pronounced with children and adolescents because the diagnostic criteria have not been adequately adapted to take into account their developmental level.

Society and Culture

Actor Stephen Fry has spoken about his experience with cyclothymia, which was depicted in the documentary Stephen Fry: The Secret Life of the Manic Depressive.

Singer Charlene Soraia had cyclothymia and wrote a song about her experiences with the disorder.

What is Dysthymia?

Introduction

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.

In the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), dysthymia is a serious state of chronic depression, which persists for at least two years (one year for children and adolescents). Dysthymia is less acute than major depressive disorder, but not necessarily less severe.

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:

  1. 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.
  2. When depressed, the patient has two or more of:
    1. decreased or increased appetite
    2. decreased or increased sleep (insomnia or hypersomnia)
    3. Fatigue or low energy
    4. Reduced self-esteem
    5. Decreased concentration or problems making decisions
    6. Feelings of hopelessness or pessimism
  3. During this two-year period, the above symptoms are never absent longer than two consecutive months.
  4. During the duration of the two-year period, the patient may have had a perpetual major depressive episode.
  5. The patient has not had any manic, hypomanic, or mixed episodes.
  6. The patient has never fulfilled criteria for cyclothymic disorder.
  7. The depression does not exist only as part of a chronic psychosis (such as schizophrenia or delusional disorder).
  8. The symptoms are often not directly caused by a medical illness or by substances, including substance use or other medications.
  9. 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.

What is Antisocial Personality Disorder?

Introduction

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

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

Brief History

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

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

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

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

Epidemiology

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

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

Signs and Symptoms

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

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

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

Conduct Disorder

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

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

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

Comorbidity

ASPD commonly coexists with the following conditions:

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

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

Causes

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

Genetic

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

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

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

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

Physiological

Hormones and Neurotransmitters

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

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

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

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

Neurological

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

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

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

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

Environmental

Family Environment

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

Cultural Influences

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

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

ICD-10

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

It is characterised by at least 3 of the following:

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

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

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

Psychopathy

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

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

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

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

Treatment

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

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

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

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

Prognosis

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

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

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

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

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

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