The Social Support Questionnaire (SSQ) is a quantitative, psychometrically sound survey questionnaire intended to measure social support and satisfaction with said social support from the perspective of the interviewee.
Degree of social support has been shown to influence the onset and course of certain psychiatric disorders such as clinical depression or schizophrenia. The SSQ was approved for public release in 1981 by Irwin Sarason, Henry Levine, Robert Basham and Barbara Sarason under the University of Washington Department of Psychology and consists of 27 questions. Overall, the SSQ has good test-retest reliability and convergent internal construct validity.
The questionnaire is designed so that each question has a two-part answer. The first part asks the interviewee to list up to nine people available to provide support that meet the criteria stated in the question. These support individuals are specified using their initials in addition to the relationship to the interviewee. Example questions from the first part includes questions such as “Whom could you count on to help if you had just been fired from your job or expelled from school?” and “Whom do you feel would help if a family member very close to you died?”.
The second part asks the interviewee to specify how satisfied they are with each of the people stated in the first part. The SSQ respondents use a 6 -point Likert scale to indicate their degree of satisfaction with the support from the above people ranging from “1 – very dissatisfied” to “6 – very satisfied”.
The Social Support Questionnaire has multiple short forms such as the SSQ3 and the SSQ6.
The SSQ is based on 4 original studies. The first study set out to determine whether the SSQ had the desired psychometric properties. The second study tried to relate SSQ and a diversity of personality measures such as anxiety, depression and hostility in connection with the Multiple Affect Adjective Checklist. The third study considered the relationship between social support, the prior year’s negative and positive life events, internal-external locus of control and self- esteem in conjunction with the Life Experiences Survey. The fourth study tested the idea that social support could serve as a buffer when faced with difficult life situations via trying to solve a maze and subsequently completing the Cognitive Interference Questionnaire.
The overall support score (SSQN) is calculated by taking an average of the individual scores across the 27 items. A high score on the SSQ indicates more optimism about life than a low score. Respondents with low SSQ scores have a higher prevalence of negative life events and illness. Scoring is as follows:
Add the total number of people for all 27 items (questions). (Max. is 243). Divide by 27 for average item score. This gives you SSQ Number Score, or SSQN.
Add the total satisfaction scores for all 27 items (questions). (Max is 162). Divide by 27 for average item score. This gives you SSQ Satisfaction score or SSQS.
Finally, you can average the above for the total number of people that are family members – this results in the SSQ family score.
According to Sarason, the SSQ takes between fifteen and eighteen minutes to properly administer and has “good” test-retest reliability.
The SSQ was compared with the depression scale and validity tests show significant negative correlation ranging from -0.22 to -0.43. The SSQ and the optimism scale have a correlation of 0.57. The SSQ and the satisfaction score have a correlation of 0.34. The SSQ has high internal consistency among items.
The SSQ has been used to show that higher levels of social support correlated with less suicide ideation in Military Medical University Soldiers in Iran in 2015. A low level of social support is an important risk factor in women for dysmenorrhea or menstrual cramps. Low Social Support is the strongest predictor of dysmenorrhea when compared to affect, personality and alexithymia.
The SSQ3 is a short form of the SSQ and has only three questions. The SSQ3 has acceptable test-test reliability and correlation with personality variables as compared to the long form of the Social Support Questionnaire. The internal reliability was borderline but this low level of internal reliability is as expected since there are only three questions.
The SSQ6 is a short form of the SSQ. The SSQ6 has been shown to have high correlation with: the SSQ, SSQ personality variables and internal reliability. In the development of the SSQ6, the research suggests that professed social support in adults may be a connected to “early attachment experience.” The SSQ6 consists of the below 6 questions:
Whom can you really count on to be dependable when you need help?
Whom can you really count on to help you feel more relaxed when you are under pressure or tense?
Who accepts you totally, including both your worst and your best points?
Whom can you really count on to care about you, regardless of what is happening to you?
Whom can you really count on to help you feel better when you are feeling generally down-in-the-dumps?
Whom can you count on to console you when you are very upset?
Interpersonal Support Evaluation List (ISEL)
The Interpersonal Support Evaluation List includes 40 items (questions) with four sub-scales in the areas of Tangible Support, Belonging Support, Self-Esteem Support and Appraisal Support. The interviewee rates each item based on how true or false they feel the item is for themselves. The four total response options are “Definitely True”, “Probably True”, “Probably False”, and “Definitely False”.
1990 – Joseph Zubin, Lithuanian-American psychologist and academic (b. 1900).
Joseph Zubin (09 October 1900 to 18 December 1990) was a Lithuanian-born American educational psychologist and an authority on schizophrenia who is commemorated by the Joseph Zubin Awards.
Zubin was born 09 October 1900 in Raseiniai, Lithuania, but moved to the US in 1908 and grew up in Baltimore. His first degree was in chemistry at Johns Hopkins University in 1921, and he earned a PhD in educational psychology at Columbia University in 1932. In 1934 he married Winifred Anderson (who survived him) and they had three children (2 sons, David and Jonathan, and a daughter, Winfred). At his death on 18 December 1990, he had seven grandchildren.
Clozapine is a psychiatric medication and is the first atypical antipsychotic (also called second-generation antipsychotic). It is primarily used to treat people with schizophrenia and schizoaffective disorders who have had an inadequate response to other antipsychotics or who have been unable to tolerate other drugs due to extrapyramidal side effects. It is also used for the treatment of psychosis in Parkinson’s disease. Clozapine is regarded as the gold-standard treatment when other medication has been insufficiently effective and its use is recommended by multiple international treatment guidelines, after resistance to earlier neuroleptic treatment is established.
The role of clozapine in treatment-resistant schizophrenia was established by a 1988 landmark study in which clozapine showed marked benefits compared to chlorpromazine in a group of patients with protracted psychosis who had already shown an inadequate response to other antipsychotics. While there are significant side effects, clozapine remains the most effective treatment when one or more other antipsychotics have had an inadequate response. The use of clozapine is associated with multiple improved outcomes, including a reduced rate of all-cause mortality, suicide and hospitalisation. In a 2013 network comparative meta-analysis of 15 antipsychotic drugs, clozapine was found to be significantly more effective than all other drugs. In a 2021 UK study, the majority of patients (over 85% of respondents) who took clozapine preferred it to their previous therapies, felt better on it and wanted to keep taking it. In a 2000 Canadian survey of 130 patients, the majority reported better satisfaction, quality of life, compliance with treatment, thinking, mood, and alertness.
Compared to other antipsychotics, clozapine has an increased risk of blood dyscrasias, in particular agranulocytosis, in the first 18 weeks of treatment. After one year, this risk reduces to that associated with most antipsychotics. Clozapine’s use is therefore reserved for people who have not responded to two other antipsychotics and is only done with stringent blood monitoring. Overall, despite the concerns relating to blood and other side effects, clozapine use is associated with a reduced mortality, especially from suicide which is a major cause of premature death in people with schizophrenia. The risk of clozapine related agranulocytosis and neutropenia warranted the mandatory use of stringent risk monitoring and management systems, which have reduced the risk of death from these adverse events to around 1 in 7,700. The association between clozapine use and specific bloods dyscrasias was first noted in the 1970s when eight deaths from agranulocytosis were noted in Finland. At the time it was not clear if this exceeded the established rate of this side effect which is also found in other antipsychotics and although the drug was not completely withdrawn, its use became limited. Clozapine became widely available in the early 1990s and remains the only treatment likely to be effective in treating resistant schizophrenia.
Common adverse effects include drowsiness, constipation, hypersalivation (increased saliva production), tachycardia, low blood pressure, blurred vision, weight gain, and dizziness. Clozapine is not normally associated with tardive dyskinesia (TD) and is recommended as the drug of choice when this is present, although some case reports describe clozapine-induced TD. Other serious risks include seizures, inflammation of the heart, high blood sugar levels, constipation. The use of this drug can rarely result in clozapine-induced gastric hypomotility syndrome which may lead to bowel obstruction and death, and in older people with psychosis, as a result of dementia it may lead to an increased risk of death. The mechanism of action is not entirely clear in the current medical literature. Clozapine is on the World Health Organization’s List of Essential Medicines. It is available as a generic medication.
Clozapine was synthesized in 1958 by Wander AG, a Swiss pharmaceutical company, based on the chemical structure of the tricyclic antidepressant imipramine. The first test in humans in 1962 was considered a failure. Trials in Germany in 1965 and 1966 as well as a trial in Vienna in 1966 were successful. In 1967 Wander AG was acquired by Sandoz. Further trials took place in 1972 when clozapine was released in Switzerland and Austria as Leponex. Two years later it was released in West Germany and in Finland in 1975. Early testing was performed in the United States around the same time. In 1975, 16 cases of agranulocytosis leading to 8 deaths in clozapine-treated patients, reported from 6 hospitals mostly in southwestern Finland, led to concern. Analysis of the Finnish cases revealed that all the agranulocytosis cases had occurred within the first 18 weeks of treatment and the authors proposed blood monitoring during this period. The rate of agranulocytosis in Finland appeared to be 20 times higher than in the rest of the world and there was speculation that this may have been due a unique genetic diversity in the region. Whilst the drug continued to be manufactured by Sandoz, and remained available in Europe, development in the US halted.
Interest in clozapine continued in an investigational capacity in the United States because, even in the 1980s, the duration of hospitalisation, especially in State Hospitals for those with treatment resistant schizophrenia might often be measured in years rather than days. The role of clozapine in treatment resistant schizophrenia was established by the landmark Clozaril Collaborative Study Group Study #30 in which clozapine showed marked benefits compared to chlorpromazine in a group of patients with protracted psychosis and who had already shown an inadequate response to other antipsychotics. This involved both stringent blood monitoring and a double-blind design with the power to demonstrate superiority over standard antipsychotic treatment. The inclusion criteria were patients who had failed to respond to at least three previous antipsychotics and had then not responded to a single blind treatment with haloperidol (mean dose 61 mg +/- 14 mg/d). Two hundred and sixty-eight were randomised were to double blind trials of clozapine (up to 900 mg/d) or chlorpromazine (up to 1800 mg/d). 30% of the clozapine patients responded compared to 4% of the controls, with significantly greater improvement on the Brief Psychiatric Rating Scale, Clinical Global Impression Scale, and Nurses’ Observation Scale for Inpatient Evaluation; this improvement included “negative” as well as positive symptom areas. Following this study, the US Food and Drug Administration (FDA) approved its use in 1990. Cautious of this risk, however, the FDA required a black box warning for specific side effects including agranulocytosis, and took the unique step of requiring patients to be registered in a formal system of tracking so that blood count levels could be evaluated on a systematic basis.
In December 2002, clozapine was approved in the US for reducing the risk of suicide in people with schizophrenia or schizoaffective judged to be at chronic risk for suicidal behaviour. In 2005, the FDA approved criteria to allow reduced blood monitoring frequency. In 2015, the individual manufacturer Patient Registries were consolidated by request of the FDA into a single shared Patient Registry Called The Clozapine REMS Registry. Despite the demonstrated safety of the new FDA monitoring requirements, which have lower neutrophil levels and do not include total white cell counts, international monitoring has not been standardised.
Clozapine is a dibenzodiazepine that is structurally very similar to loxapine (originally deemed a typical antipsychotic). It is slightly soluble in water, soluble in acetone, and highly soluble in chloroform. Its solubility in water is 0.1889 mg/L (25 °C). Its manufacturer, Novartis, claims a solubility of <0.01% in water (<100 mg/L).
Clozapine is usually used for people diagnosed with schizophrenia who have had an inadequate response to other antipsychotics or who have been unable to tolerate other drugs due to extrapyramidal side effects. It is also used for the treatment of psychosis in Parkinson’s Disease. It is regarded as the gold-standard treatment when other medication has been insufficiently effective and its use is recommended by multiple international treatment guidelines, supported by systematic reviews and meta-analysis. Whilst all current guidelines reserve clozapine to individuals when two other antipsychotics evidence indicates that clozapine might be used as a second line drug. Clozapine treatment has been demonstrated to produced improved outcomes in multiple domains including; a reduced risk of hospitalisation, a reduced risk of drug discontinuation, a reduction in overall symptoms and has improved efficacy in the treatment of positive psychotic symptoms of schizophrenia. Despite a range of side effects patients report good levels of satisfaction and long term adherence is favourable compared to other antipsychotics. Very long term follow-up studies reveal multiple benefits in terms of reduced mortality, with a particularly strong effect for reduced death by suicide, clozapine is the only antipsychotic known to have an effect reducing the risk of suicide or attempted suicide. Clozapine has a significant anti-aggressive effect. Clozapine is widely used in secure and forensic mental health settings where improvements in aggression, shortened admission and reductions in restrictive practice such as seclusion have been found. In secure hospitals and other settings clozapine has also been used in the treatment of borderline and antisocial personality disorder when this has been associated with violence or self-harm. Although oral treatment is almost universal clozapine has on occasion been enforced using either nasogastric or a short acting injection although in almost 50% of the approximately 100 reported cases patients agreed to take oral medication prior to the use of a coercive intervention. Clozapine has also been used off-label to treat catatonia with success in over 80% of cases.
On the basis of systematic reviews clozapine is recommended in some treatment guidelines as a third or fourth line treatment for bipolar disorder. Bipolar disorder is an unlicensed indication for clozapine.
Severe Personality Disorders
Clozapine is also used in emotionally unstable personality disorder and a randomised controlled trial is currently underway. The use of clozapine to treat personality disorder is uncommon and unlicensed.
Whilst clozapine is usually initiated in hospital setting community initiation is also available. Before clozapine can be initiated multiple assessments and baseline investigations are performed. In the UK and Ireland there must be an assessment that the patient satisfies the criteria for prescription; treatment resistant schizophrenia, intolerance due to extrapyramidal symptoms of other antipsychotics or psychosis in Parkinson’s disease. Establishing a history of treatment resistance may include careful review of the medication history including the durations, doses and compliance of previous antipsychotic therapy and that these did not have an adequate clinical effect. A diagnostic review may also be performed. That could include review of antipsychotic plasma concentrations if available. The prescriber, patient, pharmacy and the laboratory performing blood counts are all registered with a specified clozapine provider who must be advised that there is no history of neutropenia from any cause. The clozapine providers collaborate by sharing information regarding patients who have had clozapine related neutropenia or agranulocytosis so that clozapine cannot be used again on license. Clozapine may only be dispensed after a satisfactory blood result has been received by the risk monitoring agency at which point an individual prescription may be released to an individual patient only.
Baseline tests usually also include; a physical examination including baseline weight, waist circumference and BMI, assessments of renal function and liver function, an ECG and other baseline bloods may also be taken to facilitate monitoring of possible myocarditis, these might include C reactive protein (CRP) and troponin. In Australia and New Zealand pre-clozapine echocardiograms are also commonly performed. A number of service protocols are available and there are variations in the extent of preclozapine work ups. Some might also include fasting lipids, HbA1c and prolactin. At the Maudsley Hospital in the UK the Treat service also routinely performs a wide variety of other investigations including multiple investigations for other causes of psychosis and comorbidities including; MRI brain imaging, thyroid function tests, B12, folate and serum calcium levels, infection screening for blood borne viruses including Hepatitis B and C, HIV and syphilis as well as screening for autoimmune psychosis by anti-NMDA, anti-VGKC and Anti-nuclear Antibody screening. Investigations used to monitor the possibility of clozapine related side effects such as myocarditis are also performed including baseline troponin, CRP and BNP and for neuroleptic malignant syndrome CK.
The dose of clozapine is initially low and gradually increased over a number of weeks. Initial doses may range from 6.5 to 12.5 mg/d increasing stepwise typically to doses in the range of 250-350 mg per day at which point an assessment of response will be performed. In the UK the average clozapine dose is 450 mg/d. But response is highly variable and some patients respond at much lower doses and vice versa.
During the initial dose titration phase the following are typically monitored; usually daily at first; pulse, blood pressure and since orthostatic hypotension can be problematic this should be monitored both sitting and standing. If there is a significant drop then the rate of the dose increase may be slowed, temperature.
Weekly tests include; Mandatory full blood counts are performed weekly for the first 18 weeks. In some services there will also be monitoring of markers that might indicate myocarditis; troponin, CRP and BNP although the exact tests and frequency vary between services. Weight is usually measured weekly.
Thereon other investigations and monitoring will always include full blood counts (fortnightly for 1 year then monthly). Weight, waist circumference, lipids and glucose or HbA1c may also be monitored.
Clozapine Response and Treatment Optimisation
As with other antipsychotics, and in contrast to received wisdom, responses to clozapine are typically seen soon after initiation and often within the first week. That said responses, especially those which are partial, can be delayed. Quite what an adequate trial of clozapine is, is uncertain but a recommendation is that this should be for at least 8 weeks on a plasma trough level above 350-400 micro g/L. There is considerable inter-individual variation. A significant number of patients respond at lower and also much higher plasma concentrations and some patients, especially young male smokers may never achieve these plasma levels even at doses of 900 mg/day. Options then include either increasing the dose above the licensed maximum or the addition of a drug that inhibits clozapine metabolism. Avoiding unnecessary polypharmacy is a general principle in drug treatment.
Optimising Blood Sampling
The neutrophil cut off for clozapine have shown an exceptional ability to mitigate the risk of neutropenia and agranulocytosis. There is a significant margin of safety. Some patients may have marginal neutrophil counts before and after initiation and they are at risk of premature clozapine discontinuation. A knowledge of neutrophil biology allows blood sampling optimisation. Neutrophils show a diurnal variation in response to the natural cycle of G-CSF production, they are increased in the afternoons, they are also mobilised into the circulation after exercise and smoking. Simply shifting blood sampling has been shown to avoid unnecessary discontinuations, especially in black populations. However this is a disruption to usual hospital practice. Other practical steps are to ensure that blood results become available in hours and when senior staff are available.
Underuse of Clozapine
Clozapine is widely recognised as being underused with wide variation in prescribing, especially in patients with African heritage.
Psychiatrists prescribing practices have been found to be the most significant variable regarding variance in its use. Surveys of psychiatrists attitudes to clozapine have found that many had little experience in its use, over estimated the incidence and were fearful of side effects, and did not appreciate that many patients prefer to take clozapine than other antipsychotics, are reluctant to prescribe clozapine, had little experience in its use and believed that patients treated with clozapine were less satisfied than those treated with other antipsychotics. In contrast to many psychiatrists expectations most patients believe that the blood testing and other difficulties are worth the multiple benefits that they perceive. Whilst psychiatrists fear the severe adverse effects such as agranulocytosis, patients are more concerned about hypersalivation. Clozapine is no longer actively marketed and this may also be one of the explanations for its underuse.
Despite the strong evidence and universal endorsement by national and international treatment guidelines and the experiences of patients themselves, most people eligible for clozapine are not treated with it. A large study in England found that approximately 30% of those eligible for clozapine were being treated with it. Those patients that do start clozapine usually face prolonged delay, multiple episodes of psychosis and treatments such as high dose antipsychotics or polypharmacy. Instead of two previous antipsychotics many will have been exposed to ten or more drugs which were not effective. In a study of 120 patients conducted in four hospitals in South-East London, found a mean of 9.2 episodes of antipsychotic prescription before clozapine was initiated and the mean delay in using clozapine was 5 years. Treatments that have no evidence base or are regarded as actively harmful are used instead multiple and or high-dose treatment.
Racial Disparity in the Use of Clozapine
A general finding in healthcare provision is that minority groups receive inferior treatment; this is a particular finding in the US. In the US a general finding is that compared to their white peers African American people are less likely to be prescribed the second generation antipsychotics, which are more expensive than alternatives and this was even apparent and especially so for clozapine when comparison was made in the Veterans Affairs medical system and when differences regarding socioeconomic factors were taken into account. As well as being less likely to start clozapine black patients are more likely to stop clozapine, possibly on account of benign ethnic neutropenia.
Benign Ethnic Neutropenia
Benign reductions in neutrophils are observed in individuals of all ethnic backgrounds ethnic neutropenia (BEN), neutropenia without immune dysfunction or increased liability to infection is not due to abnormal neutrophil production; although, the exact aetiology of the reduction in circulating cells remains unknown. BEN is associated with several ethnic groups, but in particular those with Black African and West African ancestry. A difficulty with the use of clozapine is that neutrophil counts have been standardised on white populations. For significant numbers of black patients the standard neutrophil count thresholds did not permit clozapine use as the thresholds did not take BEN into account. Since 2002, clozapine monitoring services in the UK have used reference ranges 0.5 × 109/l lower for patients with haematologically confirmed BEN and similar adjustments are available in the current US criteria, although with lower permissible minima. But even then significant numbers of black patients will not be eligible even though the low neutrophil counts do not in their case reflect disease. The Duffy-Null polymorphism, which protects against some types of malaria, is predictive of BEN.
Clozapine may cause serious and potentially fatal adverse effects. Clozapine carries five black box warnings, including:
Severe neutropenia (low levels of neutrophils);
Orthostatic hypotension (low blood pressure upon changing positions), including slow heart rate and fainting;
Myocarditis (inflammation of the heart); and
Risk of death when used in elderly people with dementia-related psychosis.
Lowering of the seizure threshold may be dose related. Increasing the dose slowly may decrease the risk for seizures and orthostatic hypotension.
Common effects include constipation, bed-wetting, night-time drooling, muscle stiffness, sedation, tremors, orthostatic hypotension, high blood sugar, and weight gain. The risk of developing extrapyramidal symptoms, such as tardive dyskinesia, is below that of typical antipsychotics; this may be due to clozapine’s anticholinergic effects. Extrapyramidal symptoms may subside somewhat after a person switches from another antipsychotic to clozapine. Sexual problems, like retrograde ejaculation, have been reported while taking clozapine. Despite the risk for numerous side effects, many side effects can be managed while continuing to take clozapine.
Neutropenia and Agranulocytosis
Clozapine Induced Neutropenia (CIN) occurs in approximately 3.8% of cases and Clozapine Induced Agranulocytosis (CIA) in 0.4%. These are potentially serious side effects and agranulocytosis can result in death. To mitigate this risk clozapine is only used with mandatory absolute neutrophil count (ANC) monitoring (neutrophils are the most abundant of the granulocytes); for example, in the United States, the Risk Evaluation and Mitigation Strategy (REMS). The exact schedules and blood count thresholds vary internationally and the thresholds at which clozapine can be used in the US has been lower than those currently used in the UK and Australasia for some time. The effectiveness of the risk management strategies used is such that deaths from these side effects are very rare occurring at approximately 1 in 7,700 patients treated. Almost all the adverse blood reactions occur within the first year of treatment and the majority within the first 18 weeks. After one year of treatment these risks reduce markedly to that seen in other antipsychotic drugs 0.01% or about 1 in 10,000 and the risk of death is markedly lower still. When reductions in neutrophil levels are noted on regular blood monitoring then, depending on the value, monitoring may be increased or, if the neutrophil count is sufficiently low, then clozapine is stopped immediately and can then no longer be used within the medicinal licence. Stopping clozapine almost always results in resolution of the neutrophil reduction. However severe agranulocytosis can result in spontaneous infection and death, is a severe decrease in the amount of a specific kind of white blood cell called granulocytes. Clozapine carries a black box warning for drug-induced agranulocytosis. Rapid point-of-care tests may simplify the monitoring for agranulocytosis.
A clozapine “rechallenge” is when someone that experienced agranulocytosis while taking clozapine starts taking the medication again. In countries in which the neutrophil thresholds are higher than those used in the US a simple approach is, if the lowest ANC had been above the US cut off, to reintroduce clozapine but with the US monitoring regime. This has been demonstrated in a large cohort of patients in a hospital in London in which it was found that of 115 patients who had had clozapine stopped according to the US criteria only 7 would have had clozapine stopped if the US cut offs had been used. Of these 62 were rechallenged, 59 continued to use clozapine without difficulty and only 1 had a fall in neutrophils below the US cut off. Other approaches have included the use of other drugs to support neutrophil counts including lithium or granulocyte colony-stimulating factor (G-CSF). However, if agranulocytosis still occurs during a rechallenge, the alternative options are limited.
Clozapine can rarely cause myocarditis and cardiomyopathy. A large meta-analysis of clozapine exposure to over 250,000 people revealed that these occurred in approximately 7 in 1,000 patients treated and resulted in death in 3 and 4 in 10,000 patients exposed respectively and although myocarditis occurred almost exclusively within the first 8 weeks of treatment, cardiomyopathy can occur much later on. First manifestations of illness are fever which may be accompanied by symptoms associated with upper respiratory tract, gastrointestinal or urinary tract infection. Typically C-reactive protein (CRP) increases with the onset of fever and rises in the cardiac enzyme, troponin, occur up to 5 days later. Monitoring guidelines advise checking CRP and troponin at baseline and weekly for the first 4 weeks after clozapine initiation and observing the patient for signs and symptoms of illness. Signs of heart failure are less common and may develop with the rise in troponin. A recent case-control study found that the risk of clozapine-induced myocarditis is increased with increasing rate of clozapine dose titration, increasing age and concomitant sodium valproate. A large electronic health register study has revealed that nearly 90% of cases of suspected clozapine related myocarditis are false positives. Rechallenge after clozapine induced myocarditis has been performed and a protocol for this specialist approach has been published. A systematic review of rechallenge after myocarditis has show success in over 60% of reported cases.
Another under-recognised and potentially life-threatening effect spectrum is gastrointestinal hypomotility, which may manifest as severe constipation, faecal impaction, paralytic ileus, bowel obstruction, acute megacolon, ischemia or necrosis. Colonic hypomotility has been shown to occur in up to 80% of people prescribed clozapine when gastrointestinal function is measured objectively using radiopaque markers. Clozapine-induced gastrointestinal hypomotility currently has a higher mortality rate than the better known side effect of agranulocytosis. A Cochrane review found little evidence to help guide decisions about the best treatment for gastrointestinal hypomotility caused by clozapine and other antipsychotic medication. Monitoring bowel function and the pre-emptive use of laxatives for all clozapine-treated people has been shown to improve colonic transit times and reduce serious sequelae.
Hypersalivation, or the excessive production of saliva, is one of the most common adverse effects of clozapine (30-80%). The saliva production is especially bothersome at night and first thing in the morning, as the immobility of sleep precludes the normal clearance of saliva by swallowing that occurs throughout the day. While clozapine is a muscarinic antagonist at the M1, M2, M3, and M5 receptors, clozapine is a full agonist at the M4 subset. Because M4 is highly expressed in the salivary gland, its M4 agonist activity is thought to be responsible for hypersalivation. Clozapine-induced hypersalivation is likely a dose-related phenomenon, and tends to be worse when first starting the medication. Besides decreasing the dose or slowing the initial dose titration, other interventions that have shown some benefit include systemically absorbed anticholinergic medications such as hyoscine, diphenhydramine and topical anticholinergic medications like ipratropium bromide. Mild hypersalivation may be managed by sleeping with a towel over the pillow at night.
Central Nervous System
CNS side effects include drowsiness, vertigo, headache, tremor, syncope, sleep disturbances, nightmares, restlessness, akinesia, agitation, seizures, rigidity, akathisia, confusion, fatigue, insomnia, hyperkinesia, weakness, lethargy, ataxia, slurred speech, depression, myoclonic jerks, and anxiety. Rarely seen are delusions, hallucinations, delirium, amnesia, libido increase or decrease, paranoia and irritability, abnormal EEG, worsening of psychosis, paraesthesia, status epilepticus, and obsessive compulsive symptoms. Similar to other antipsychotics clozapine rarely has been known to cause neuroleptic malignant syndrome.
Clozapine is linked to urinary incontinence, though its appearance may be under-recognised.
Abrupt withdrawal may lead to cholinergic rebound effects, such as indigestion, diarrhoea, nausea/vomiting, overabundance of saliva, profuse sweating, insomnia, and agitation. Abrupt withdrawal can also cause severe movement disorders, catatonia, and psychosis. Doctors have recommended that patients, families, and caregivers be made aware of the symptoms and risks of abrupt withdrawal of clozapine. When discontinuing clozapine, gradual dose reduction is recommended to reduce the intensity of withdrawal effects.
Weight Gain and Diabetes
In addition to hyperglycaemia, significant weight gain is frequently experienced by patients treated with clozapine. Impaired glucose metabolism and obesity have been shown to be constituents of the metabolic syndrome and may increase the risk of cardiovascular disease. The data suggest that clozapine may be more likely to cause adverse metabolic effects than some of the other atypical antipsychotics.
International adverse drug effect databases indicate that clozapine use is associated with a significantly increased incidence of and death from pneumonia and this may be one of the most significant adverse events. The mechanisms for this are unknown although it has been speculated that it may be related to hypersalivation, immune effects of clozapine’s effects on the resolution of inflammation.
Symptoms of overdose can be variable, but often include; sedation, confusion, tachycardia, seizures and ataxia. Fatalities have been reported due to clozapine overdose, though overdoses of greater than 5000 mg have been survived.
Fluvoxamine inhibits the metabolism of clozapine leading to significantly increased blood levels of clozapine.
When carbamazepine is concurrently used with clozapine, it has been shown to decrease plasma levels of clozapine significantly thereby decreasing the beneficial effects of clozapine. Patients should be monitored for “decreased therapeutic effects of clozapine if carbamazepine” is started or increased. If carbamazepine is discontinued or the dose of carbamazepine is decreased, therapeutic effects of clozapine should be monitored. The study recommends carbamazepine to not be used concurrently with clozapine due to increased risk of agranulocytosis.
Ciprofloxacin is an inhibitor of CYP1A2 and clozapine is a major CYP1A2 substrate. Randomized study reported elevation in clozapine concentration in subjects concurrently taking ciprofloxacin. Thus, the prescribing information for clozapine recommends “reducing the dose of clozapine by one-third of original dose” when ciprofloxacin and other CYP1A2 inhibitors are added to therapy, but once ciprofloxacin is removed from therapy, it is recommended to return clozapine to original dose.
Clozapine is classified as an atypical antipsychotic drug because it binds to serotonin as well as dopamine receptors.
Clozapine is an antagonist at the 5-HT2A subunit of the serotonin receptor, putatively improving depression, anxiety, and the negative cognitive symptoms associated with schizophrenia.
A direct interaction of clozapine with the GABAB receptor has also been shown. GABAB receptor-deficient mice exhibit increased extracellular dopamine levels and altered locomotor behaviour equivalent to that in schizophrenia animal models. GABAB receptor agonists and positive allosteric modulators reduce the locomotor changes in these models.
Clozapine induces the release of glutamate and D-serine, an agonist at the glycine site of the NMDA receptor, from astrocytes, and reduces the expression of astrocytic glutamate transporters. These are direct effects that are also present in astrocyte cell cultures not containing neurons. Clozapine prevents impaired NMDA receptor expression caused by NMDA receptor antagonists.
The absorption of clozapine is almost complete following oral administration, but the oral bioavailability is only 60 to 70% due to first-pass metabolism. The time to peak concentration after oral dosing is about 2.5 hours, and food does not appear to affect the bioavailability of clozapine. However, it was shown that co-administration of food decreases the rate of absorption. The elimination half-life of clozapine is about 14 hours at steady state conditions (varying with daily dose).
Clozapine is extensively metabolized in the liver, via the cytochrome P450 system, to polar metabolites suitable for elimination in the urine and faeces. The major metabolite, norclozapine (desmethyl-clozapine), is pharmacologically active. The cytochrome P450 isoenzyme 1A2 is primarily responsible for clozapine metabolism, but 2C, 2D6, 2E1 and 3A3/4 appear to play roles as well. Agents that induce (e.g. cigarette smoke) or inhibit (e.g. theophylline, ciprofloxacin, fluvoxamine) CYP1A2 may increase or decrease, respectively, the metabolism of clozapine. For example, the induction of metabolism caused by smoking means that smokers require up to double the dose of clozapine compared with non-smokers to achieve an equivalent plasma concentration.
Clozapine and norclozapine (desmethyl-clozapine) plasma levels may also be monitored, though they show a significant degree of variation and are higher in women and increase with age. Monitoring of plasma levels of clozapine and norclozapine has been shown to be useful in assessment of compliance, metabolic status, prevention of toxicity, and in dose optimisation.
Society and Culture
Despite the expense of the risk monitoring and management systems required, clozapine use is highly cost effective; with a number of studies suggesting savings of tens of thousands of dollars per patient per year compared to other antipsychotics as well as advantages regarding improvements in quality of life. Clozapine is available as a generic medication.
Clozapine in the Arts
Carrie Mathison, a fictional CIA operative in the television series Homeland, secretly takes clozapine supplied by her sister for the treatment of bipolar disorder.
In the film Out of Darkness, Diana Ross played the protagonist Paulie Cooper, “a paranoid schizophrenic” who is depicted as having a dramatic improvement on clozapine.
In the television series Last Man On Earth (2015) the character Melissa has a psychotic episode and returns home and starts acting how she did pre-pandemic. Her boyfriend Todd sees her take a medication in the morning and asks her what it is. All she will say is “Santas Penis”. Todd searches medication books and finds clozapine = Clause a peen.
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Aripiprazole, sold under the brand names Abilify and Aristada among others, is an atypical antipsychotic. It is primarily used in the treatment of schizophrenia and bipolar disorder. Other uses include as an add-on treatment in major depressive disorder (MDD), tic disorders and irritability associated with autism. It is taken by mouth or injection into a muscle. A Cochrane review found low-quality evidence of effectiveness in treating schizophrenia.
In adults, side effects with greater than 10% incidence include weight gain, headache, akathisia, insomnia, and gastro-intestinal effects like nausea and constipation, and lightheadedness. Side effects in children are similar, and include sleepiness, increased appetite, and stuffy nose. A strong desire to gamble, binge eat, shop, and engage in sexual activity may also occur.
Common side effects include vomiting, constipation, sleepiness, dizziness, weight gain and movement disorders. Serious side effects may include neuroleptic malignant syndrome, tardive dyskinesia and anaphylaxis. It is not recommended for older people with dementia-related psychosis due to an increased risk of death. In pregnancy, there is evidence of possible harm to the baby. It is not recommended in women who are breastfeeding. It has not been very well studied in people less than 18 years old. The exact mode of action is not entirely clear but may involve effects on dopamine and serotonin.
Aripiprazole was approved for medical use in the United States in 2002. It is available as a generic medication. In 2019, it was the 101st most commonly prescribed medication in the United States, with more than 6 million prescriptions. Aripiprazole was discovered in 1988 by scientists at the Japanese firm Otsuka Pharmaceutical.
Aripiprazole was discovered by scientists at Otsuka Pharmaceutical and was called OPC-14597. It was first published in 1995. Otsuka initially developed the drug, and partnered with Bristol-Myers Squibb (BMS) in 1999 to complete development, obtain approvals, and market aripiprazole.
It was approved by the US Food and Drug Administration (FDA) for schizophrenia in November 2002, and the European Medicines Agency in June 2004; for acute manic and mixed episodes associated with bipolar disorder on 01 October 2004; as an adjunct for major depressive disorder on 20 November 2007; and to treat irritability in children with autism on 20 November 2009. Likewise it was approved for use as a treatment for schizophrenia by the TGA of Australia in May 2003.
Aripiprazole has been approved by the FDA for the treatment of both acute manic and mixed episodes, in people older than ten years.
In 2006, the FDA required manufacturers to add a black box warning to the label, warning that older people who were given the drug for dementia-related psychosis were at greater risk of death.
In 2007, aripiprazole was approved by the FDA for the treatment of unipolar depression when used adjunctively with an antidepressant medication. That same year, BMS settled a case with the US government in which it paid $515 million; the case covered several drugs but the focus was on BMS’s off-label marketing of aripiprazole for children and older people with dementia.
In 2011 Otsuka and Lundbeck signed a collaboration to develop a depot formulation of apripiprazole.
As of 2013, Abilify had annual sales of US$7 billion. In 2013 BMS returned marketing rights to Otsuka, but kept manufacturing the drug. Also in 2013, Otsuka and Lundbeck received US and European marketing approval for an injectable depot formulation of aripiprazole.
Otsuka’s US patent on aripiprazole expired on 20 October 2014, but due to a paediatric extension, a generic did not become available until 20 April 2015. Barr Laboratories (now Teva Pharmaceuticals) initiated a patent challenge under the Hatch-Waxman Act in March 2007. On 15 November 2010, this challenge was rejected by the US District Court in New Jersey.
Otsuka’s European patent EP0367141 which would have expired on 26 October 2009, was extended by a Supplementary Protection Certificate (SPC) to 26 October 2014. The UK Intellectual Property Office decided on 04 March 2015 that the SPC could not be further extended by six months under Regulation (EC) No 1901/2006. Even if the decision is successfully appealed, protection in Europe will not extend beyond 26 April 2015.
From April 2013 to March 2014, sales of Abilify amounted to almost $6.9 billion.
In April 2015, the FDA announced the first generic versions. In October 2015, aripiprazole lauroxil, a prodrug of aripiprazole that is administered via intramuscular injection once every four to six weeks for the treatment of schizophrenia, was approved by the FDA.
In 2016, BMS settled cases with 42 US states that had charged BMS with off-label marketing to older people with dementia; BMS agreed to pay $19.5 million.
In November 2017, the FDA approved Abilify MyCite, a digital pill containing a sensor intended to record when its consumer takes their medication.
Aripiprazole is primarily used for the treatment of schizophrenia or bipolar disorder.
The 2016 NICE guidance for treating psychosis and schizophrenia in children and young people recommended aripiprazole as a second line treatment after risperidone for people between 15 and 17 who are having an acute exacerbation or recurrence of psychosis or schizophrenia. A 2014 NICE review of the depot formulation of the drug found that it might have a role in treatment as an alternative to other depot formulations of second generation antipsychotics for people who have trouble taking medication as directed or who prefer it.
A 2014 Cochrane review comparing aripiprazole and other atypical antipsychotics found that it is difficult to determine differences as data quality is poor. A 2011 Cochrane review comparing aripiprazole with placebo concluded that high dropout rates in clinical trials, and a lack of outcome data regarding general functioning, behaviour, mortality, economic outcomes, or cognitive functioning make it difficult to definitively conclude that aripiprazole is useful for the prevention of relapse. A Cochrane review found only low quality evidence of effectiveness in treating schizophrenia. Accordingly, part of its methodology on quality of evidence is based on quantity of qualified studies.
A 2013 review found that it is in the middle range of 15 antipsychotics for effectiveness, approximately as effective as haloperidol and quetiapine and slightly more effective than ziprasidone, chlorpromazine, and asenapine, with better tolerability compared to the other antipsychotic drugs (4th best for weight gain, 5th best for extrapyramidal symptoms, best for prolactin elevation, 2nd best for QTc prolongation, and 5th best for sedation). The authors concluded that for acute psychotic episodes aripiprazole results in benefits in some aspects of the condition.
In 2013 the World Federation of Societies for Biological Psychiatry recommended aripiprazole for the treatment of acute exacerbations of schizophrenia as a Grade 1 recommendation and evidence level A.
The British Association for Psychopharmacology similarly recommends that all persons presenting with psychosis receive treatment with an antipsychotic, and that such treatment should continue for at least 1-2 years, as “There is no doubt that antipsychotic discontinuation is strongly associated with relapse during this period”. The guideline further notes that “Established schizophrenia requires continued maintenance with doses of antipsychotic medication within the recommended range (Evidence level A)”.
The British Association for Psychopharmacology and the World Federation of Societies for Biological Psychiatry suggest that there is little difference in effectiveness between antipsychotics in prevention of relapse, and recommend that the specific choice of antipsychotic be chosen based on each person’s preference and side effect profile. The latter group recommends switching to aripiprazole when excessive weight gain is encountered during treatment with other antipsychotics
Aripiprazole is effective for the treatment of acute manic episodes of bipolar disorder in adults, children, and adolescents. Used as maintenance therapy, it is useful for the prevention of manic episodes, but is not useful for bipolar depression. Thus, it is often used in combination with an additional mood stabiliser; however, co-administration with a mood stabiliser increases the risk of extrapyramidal side effects.
Aripiprazole is an effective add-on treatment for major depressive disorder; however, there is a greater rate of side effects such as weight gain and movement disorders. The overall benefit is small to moderate and its use appears to neither improve quality of life nor functioning. Aripiprazole may interact with some antidepressants, especially selective serotonin reuptake inhibitors (SSRIs). There are interactions with fluoxetine and paroxetine and lesser interactions with sertraline, escitalopram, citalopram, and fluvoxamine, which inhibit CYP2D6, for which aripiprazole is a substrate. CYP2D6 inhibitors increase aripiprazole concentrations to 2-3 times their normal level.
Short-term data (8 weeks) shows reduced irritability, hyperactivity, inappropriate speech, and stereotypy, but no change in lethargic behaviours. Adverse effects include weight gain, sleepiness, drooling and tremors. It is suggested that children and adolescents need to be monitored regularly while taking this medication, to evaluate if this treatment option is still effective after long-term use and note if side effects are worsening. Further studies are needed to understand if this drug is helpful for children after long term use.
Aripiprazole is approved for the treatment of Tourette’s syndrome. It is effective, safe, and well-tolerated for this use per systematic reviews and meta-analyses
A 2014 systematic review and meta-analysis concluded that add-on therapy with low dose aripiprazole is an effective treatment for obsessive-compulsive disorder (OCD) that does not improve with selective serotonin reuptake inhibitors (SSRIs) alone. The conclusion was based on the results of two relatively small, short-term trials, each of which demonstrated improvements in symptoms. Risperidone, another second-generation antipsychotic, appears to be superior to aripiprazole for this indication, and is recommended by the 2007 American Psychiatric Association guidelines. However, aripiprazole is cautiously recommended by a 2017 review on antipsychotics for OCD. Aripiprazole is not currently approved for the treatment of OCD and is instead used off-label for this indication.
In adults, side effects with greater than 10% incidence include weight gain, headache, akathisia, insomnia, and gastro-intestinal effects like nausea and constipation, and lightheadedness. Side effects in children are similar, and include sleepiness, increased appetite, and stuffy nose. A strong desire to gamble, binge eat, shop, and engage in sexual activity may also occur.
Uncontrolled movement such as restlessness, tremors, and muscle stiffness may occur.
The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotics to avoid acute withdrawal syndrome or rapid relapse. Symptoms of withdrawal commonly include nausea, vomiting, and loss of appetite. Other symptoms may include restlessness, increased sweating, and trouble sleeping. Less commonly there may be a feeling of the world spinning, numbness, or muscle pains. Symptoms generally resolve after a short period of time.
There is tentative evidence that discontinuation of antipsychotics can result in psychosis. It may also result in reoccurrence of the condition that is being treated. Rarely tardive dyskinesia can occur when the medication is stopped.
Children or adults who ingested acute overdoses have usually manifested central nervous system depression ranging from mild sedation to coma; serum concentrations of aripiprazole and dehydroaripiprazole in these people were elevated by up to 3-4 fold over normal therapeutic levels; as of 2008 no deaths had been recorded.
Aripiprazole is a substrate of CYP2D6 and CYP3A4. Coadministration with medications that inhibit (e.g. paroxetine, fluoxetine) or induce (e.g. carbamazepine) these metabolic enzymes are known to increase and decrease, respectively, plasma levels of aripiprazole.
Precautions should be taken in people with an established diagnosis of diabetes mellitus who are started on atypical antipsychotics along with other medications that affect blood sugar levels and should be monitored regularly for worsening of glucose control. The liquid form (oral solution) of this medication may contain up to 15 grams of sugar per dose.
Antipsychotics like aripiprazole and stimulant medications, such as amphetamine, are traditionally thought to have opposing effects to their effects on dopamine receptors: stimulants are thought to increase dopamine in the synaptic cleft, whereas antipsychotics are thought to decrease dopamine. However, it is an oversimplification to state the interaction as such, due to the differing actions of antipsychotics and stimulants in different parts of the brain, as well as the effects of antipsychotics on non-dopaminergic receptors. This interaction frequently occurs in the setting of comorbid attention-deficit hyperactivity disorder (ADHD) (for which stimulants are commonly prescribed) and off-label treatment of aggression with antipsychotics. Aripiprazole has been reported to provide some benefit in improving cognitive functioning in people with ADHD without other psychiatric comorbidities, though the results have been disputed. The combination of antipsychotics like aripiprazole with stimulants should not be considered an absolute contraindication.
Aripiprazole’s mechanism of action is different from those of the other FDA-approved atypical antipsychotics (e.g., clozapine, olanzapine, quetiapine, ziprasidone, and risperidone). It shows differential engagement at the dopamine receptor (D2). It appears to show predominantly antagonist activity on postsynaptic D2 receptors and partial agonist activity on presynaptic D2 receptors, D3, and partially D4 and is a partial activator of serotonin (5-HT1A, 5-HT2A, 5-HT2B, 5-HT6, and 5-HT7). It also shows lower and likely insignificant effect on histamine (H1), epinephrine/norepinephrine (α), and otherwise dopamine (D4), as well as the serotonin transporter. Aripiprazole acts by modulating neurotransmission overactivity of dopamine, which is thought to mitigate schizophrenia symptoms.
As a pharmacologically unique antipsychotic with pronounced functional selectivity, characterization of this dopamine D2 partial agonist (with an intrinsic activity of ~25%) as being similar to a full agonist but at a reduced level of activity presents a misleading oversimplification of its actions; for example, among other effects, aripiprazole has been shown, in vitro, to bind to and/or induce receptor conformations (i.e. facilitate receptor shapes) in such a way as to not only prevent receptor internalisation (and, thus, lower receptor density) but even to lower the rate of receptor internalisation below that of neurons not in the presence of agonists (including dopamine) or antagonists. It is often the nature of partial agonists, including aripiprazole, to display a stabilising effect (such as on mood in this case) with agonistic activity when there are low levels of endogenous neurotransmitters (such as dopamine) and antagonistic activity in the presence of high levels of agonists associated with events such as mania, psychosis, and drug use. In addition to aripiprazole’s partial agonism and functional selectivity characteristics, its effectiveness may be mediated by its very high dopamine D2 receptor occupancy (approximately 32%, 53%, 72%, 80%, and 97% at daily dosages of 0.5 mg, 1 mg, 2 mg, 10 mg, and 40 mg respectively) as well as balanced selectivity for pre- and postsynaptic receptors (as suggested by its equal affinity for both D2S and D2L receptor forms). Aripiprazole has been characterised as possessing predominantly antagonistic activity on postsynaptic D2 receptors and partial agonist activity on presynaptic D2 receptors; however, while this explanation intuitively explains the drug’s efficacy as an antipsychotic, as degree of agonism is a function of more than a drug’s inherent properties as well as in vitro demonstration of aripiprazole’s partial agonism in cells expressing postsynaptic (D2L) receptors, it was noted that “It is unlikely that the differential actions of aripiprazole as an agonist, antagonist, or partial agonist were entirely due to differences in relative D2 receptor expression since aripiprazole was an antagonist in cells with the highest level of expression (4.6 pmol/mg) and a partial agonist in cells with an intermediate level of expression (0.5-1 pmol/mg). Instead, the current data are most parsimoniously explained by the ‘functional selectivity’ hypothesis of Lawler et al (1999)”. Aripiprazole is also a partial agonist of the D3 receptor. In healthy human volunteers, D2 and D3 receptor occupancy levels are high, with average levels ranging between approximately 71% at 2 mg/day to approximately 96% at 40 mg/day. Most atypical antipsychotics bind preferentially to extrastriatal receptors, but aripiprazole appears to be less preferential in this regard, as binding rates are high throughout the brain.
Aripiprazole is also a partial agonist of the serotonin 5-HT1A receptor (intrinsic activity = 68%). Casting doubt on the significance of aripiprazole’s agonism of 5-HT1A receptors, a PET scan study of 12 patients receiving doses ranging from 10 to 30 mg found 5-HT1A receptor occupancy to be only 16% compared to ~90% for D2. It is a very weak partial agonist of the 5-HT2A receptor (intrinsic activity = 12.7%), and like other atypical antipsychotics, displays a functional antagonist profile at this receptor. The drug differs from other atypical antipsychotics in having higher affinity for the D2 receptor than for the 5-HT2A receptor. At the 5-HT2B receptor, aripiprazole has both great binding affinity and acts as a potent inverse agonist, “Aripiprazole decreased PI hydrolysis from a basal level of 61% down to a low of 30% at 1000 nM, with an EC50 of 11 nM”. Unlike other antipsychotics, aripiprazole is a high-efficacy partial agonist of the 5-HT2C receptor (intrinsic activity = 82%) and with relatively weak affinity; this property may underlie the minimal weight gain seen in the course of therapy. At the 5-HT7 receptor, aripiprazole is a very weak partial agonist with barely measurable intrinsic activity, and hence is a functional antagonist of this receptor. Aripiprazole also shows lower but likely clinically insignificant affinity for a number of other sites, such as the histamine H1, α-adrenergic, and dopamine D4 receptors as well as the serotonin transporter, while it has negligible affinity for the muscarinic acetylcholine receptors.
Since the actions of aripiprazole differ markedly across receptor systems aripiprazole was sometimes an antagonist (e.g. at 5-HT6 and D2L), sometimes an inverse agonist (e.g. 5-HT2B), sometimes a partial agonist (e.g. D2L), and sometimes a full agonist (D3, D4). Aripiprazole was frequently found to be a partial agonist, with an intrinsic activity that could be low (D2L, 5-HT2A, 5-HT7), intermediate (5-HT1A), or high (D4, 5-HT2C). This mixture of agonist actions at D2-dopamine receptors is consistent with the hypothesis that aripiprazole has ‘functionally selective’ actions. The ‘functional-selectivity’ hypothesis proposes that a mixture of agonist/partial agonist/antagonist actions are likely. According to this hypothesis, agonists may induce structural changes in receptor conformations that are differentially ‘sensed’ by the local complement of G proteins to induce a variety of functional actions depending upon the precise cellular milieu. The diverse actions of aripiprazole at D2-dopamine receptors are clearly cell-type specific (e.g. agonism, antagonism, partial agonism), and are most parsimoniously explained by the ‘functional selectivity’ hypothesis.
Since 5-HT2C receptors have been implicated in the control of depression, OCD, and appetite, agonism at the 5-HT2C receptor might be associated with therapeutic potential in obsessive compulsive disorder, obesity, and depression. 5-HT2C agonism has been demonstrated to induce anorexia via enhancement of serotonergic neurotransmission via activation of 5-HT2C receptors; it is conceivable that the 5-HT2C agonist actions of aripiprazole may, thus, be partly responsible for the minimal weight gain associated with this compound in clinical trials. In terms of potential action as an anti-obsessional agent, it is worthwhile noting that a variety of 5-HT2A/5-HT2C agonists have shown promise as anti-obsessional agents, yet many of these compounds are hallucinogenic, presumably due to 5-HT2A activation. Aripiprazole has a favourable pharmacological profile in being a 5-HT2A antagonist and a 5-HT2C partial agonist. Based on this profile, one can predict that aripiprazole may have anti-obsessional and anorectic actions in humans.
Wood and Reavill’s (2007) review of published and unpublished data proposed that, at therapeutically relevant doses, aripiprazole may act essentially as a selective partial agonist of the D2 receptor without significantly affecting the majority of serotonin receptors. A positron emission tomography imaging study found that 10 to 30 mg/day aripiprazole resulted in 85 to 95% occupancy of the D2 receptor in various brain areas (putamen, caudate, ventral striatum) versus 54 to 60% occupancy of the 5-HT2A receptor and only 16% occupancy of the 5-HT1A receptor. It has been suggested that the low occupancy of the 5-HT1A receptor by aripiprazole may have been an erroneous measurement however.
Aripiprazole acts by modulating neurotransmission overactivity on the dopaminergic mesolimbic pathway, which is thought to be a cause of positive schizophrenia symptoms. Due to its agonist activity on D2 receptors, aripiprazole may also increase dopaminergic activity to optimal levels in the mesocortical pathways where it is reduce.
Aripiprazole displays linear kinetics and has an elimination half-life of approximately 75 hours. Steady-state plasma concentrations are achieved in about 14 days. Cmax (maximum plasma concentration) is achieved 3-5 hours after oral dosing. Bioavailability of the oral tablets is about 90% and the drug undergoes extensive hepatic metabolization (dehydrogenation, hydroxylation, and N-dealkylation), principally by the enzymes CYP2D6 and CYP3A4. Its only known active metabolite is dehydro-aripiprazole, which typically accumulates to approximately 40% of the aripiprazole concentration. The parenteral drug is excreted only in traces, and its metabolites, active or not, are excreted via faeces and urine.
Aripiprazole is a phenylpiperazine and is chemically related to nefazodone, etoperidone, and trazodone. It is unusual in having twelve known crystalline polymorphs.
Society and Culture
Aripiprazole has been described as the prototypical third-generation antipsychotic, as opposed to first-generation (typical) antipsychotics like haloperidol and second-generation (atypical) antipsychotics like clozapine. It has received this classification due to its partial agonism of dopamine receptors, and is the first of its kind in this regard among antipsychotics, which before aripiprazole acted only as dopamine receptor antagonists. The introduction of aripiprazole has led to a paradigm shift from a dopamine antagonist-based approach to a dopamine agonist-based approach for antipsychotic drug development.
Attention Deficit Hyperactivity Disorder
Aripiprazole was under development for the treatment of attention-deficit hyperactivity disorder (ADHD), but development for this indication was discontinued. A 2017 meta review found only preliminary evidence (studies with small sample sizes and methodological problems) for aripiprazole in the treatment of ADHD. A 2013 systematic review of aripiprazole for ADHD similarly reported that there is insufficient evidence of effectiveness to support aripiprazole as a treatment for the condition. Although all 6 non-controlled open-label studies in the review reported effectiveness, two small randomised controlled trials found that aripiprazole did not significantly decrease ADHD symptoms. A high rate of adverse effects with aripiprazole such as weight gain, sedation, and headache was noted. Most research on aripiprazole for ADHD is in children and adolescents. Evidence on aripiprazole specifically for adult ADHD appears to be limited to a single case report.
Aripiprazole has been studied for the treatment of amphetamine dependence and other substance use disorders, but more research is needed to support aripiprazole for these potential uses. Available evidence of aripiprazole for amphetamine dependence is mixed. Some studies have reported attenuation of the effects of amphetamines by aripiprazole, whereas other studies have reported both enhancement of the effects of amphetamines and increased use of amphetamines by aripiprazole. As such, aripiprazole may not only be ineffective but potentially harmful for treatment of amphetamine dependence, and caution is warranted with regard to its use for such purposes.
Aripiprazole is under development for the treatment of agitation and pervasive child development disorders. As of May 2021, it is in phase 3 clinical trials for these indications.
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Frances Elena Farmer (19 September 1913 to 01 August 1970) was an American actress and television hostess. She appeared in over a dozen feature films over the course of her career, though she garnered notoriety for the various sensationalised accounts of her life, especially her involuntary commitment to psychiatric hospitals and subsequent mental health struggles.
A native of Seattle, Washington, Farmer began acting in stage productions while a student at the University of Washington. After graduating, she began performing in stock theatre before signing a film contract with Paramount Pictures on her 22nd birthday in September 1935. She made her film debut in the B film Too Many Parents (1936), followed by another B picture, Border Flight, before being given the lead role opposite Bing Crosby in the musical Western Rhythm on the Range (1936). Unhappy with the opportunities the studio gave her, Farmer returned to stock theatre in 1937 before being cast in the original Broadway production of Clifford Odets’s Golden Boy, staged by New York City’s Group Theatre. She followed this with two Broadway productions directed by Elia Kazan in 1939, but a battle with depression and binge drinking caused her to drop out of a subsequent Ernest Hemingway stage adaptation.
Farmer returned to Los Angeles, earning supporting roles in the comedy World Premiere (1941) and the film noir Among the Living (1941). In 1942, publicity of her reportedly erratic behaviour began to surface and, after several arrests and committals to psychiatric institutions, Farmer was diagnosed with paranoid schizophrenia. At the request of her family, particularly her mother, she was committed to an institution in her home state of Washington, where she remained a patient until 1950. Farmer attempted an acting comeback, mainly appearing as a television host in Indianapolis on her own series, Frances Farmer Presents. Her final film role was in the 1958 drama The Party Crashers, after which she spent the majority of the 1960s occasionally performing in local theatre productions staged by Purdue University. In the spring of 1970, she was diagnosed with oesophageal cancer, from which she died on 01 August 1970, aged 56.
Farmer has been the subject of various works, including two feature films and several books, many of which focus on her time spent institutionalised, during which she claimed to have been subject to various systemic abuses. Her posthumously released, ghostwritten, and widely discredited autobiography, Will There Really Be a Morning? (1972), details these claims, but has been exposed as a largely fictional work by a friend of Farmer’s to clear debts. Another discredited 1978 biography of her life, Shadowland, alleged that Farmer underwent a transorbital lobotomy during her institutionalisation, but the author has since stated in court that he fabricated this incident and several other aspects of the book. A 1982 biographical film based on this book depicted these events as true, resulting in renewed interest in her life and career.
Adam Phillips (born 19 September 1954) is a British psychoanalytic psychotherapist and essayist.
Since 2003 he has been the general editor of the new Penguin Modern Classics translations of Sigmund Freud. He is also a regular contributor to the London Review of Books.
Joan Acocella, writing in The New Yorker, described Phillips as “Britain’s foremost psychoanalytic writer”, an opinion echoed by historian Élisabeth Roudinesco in Le Monde.
Paraphrenia is a mental disorder characterised by an organised system of paranoid delusions with or without hallucinations (the positive symptoms of schizophrenia) and without deterioration of intellect or personality (its negative symptom).
This disorder is also distinguished from schizophrenia by a lower hereditary occurrence, less premorbid maladjustment, and a slower rate of progression. Onset of symptoms generally occurs later in life, near the age of 60. The prevalence of the disorder among the elderly is between 0.1% and 4%.
In the Russian psychiatric manuals, paraphrenia (or paraphrenic syndrome) is the last stage of development of paranoid schizophrenia. “Systematised paraphrenia” (with systematised delusions i. e. delusions with complex logical structure) and “expansive-paranoid paraphrenia” (with expansive/grandiose delusions and persecutory delusions) are the variants of paranoid schizophrenia (F20.0). Sometimes systematised paraphrenia can be seen with delusional disorder (F22.0). The word is from Ancient Greek: παρά – beside, near + φρήν – intellect, mind.
The term paraphrenia was originally popularised by Karl Ludwig Kahlbaum in 1863 to describe the tendency of certain psychiatric disorders to occur during certain transitional periods in life (describing paraphrenia hebetica as the insanity of the adolescence and paraphrenia senilis as the insanity of the elders.
The term was also used by Sigmund Freud for a short time starting in 1911 as an alternative to the terms schizophrenia and dementia praecox, which in his estimation did not correctly identify the underlying condition, and by Emil Kraepelin in 1912/1913, who changed its meaning to describe paraphrenia as it is understood today, as a small group of individuals that have many of the symptoms of schizophrenia with a lack of deterioration and thought disorder. Kraepelin’s study was discredited by Wilhelm Mayer in 1921 when he conducted a follow-up study using Kraepelin’s data. His study suggested that there was little to no discrimination between schizophrenia and paraphrenia; given enough time, patients presenting with paraphrenia will merge into the schizophrenic pool. However, Meyer’s data are open to various interpretations. In 1952, Roth and Morrissey conducted a large study in which they surveyed the mental hospital admissions of older patients. They characterised patients as having:
“paraphrenic delusions which… occurred in each case in the setting of a well-preserved intellect and personality, were often ‘primary’ in character, and were usually associated with the passivity failings or other volitional disturbances and hallucinations in clear consciousness pathognomonic of schizophrenia”.
In recent medicine, the term paraphrenia has been replaced by the diagnosis of “very late-onset schizophrenia-like psychosis” and has also been called “atypical psychoses, delusional disorder, psychoses not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults” by psychotherapists. Current studies, however, recognize the condition as “a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients.”
Signs and Symptoms
The main symptoms of paraphrenia are paranoid delusions and hallucinations. The delusions often involve the individual being the subject of persecution, although they can also be erotic, hypochondriacal, or grandiose in nature. The majority of hallucinations associated with paraphrenia are auditory, with 75% of patients reporting such an experience; however, visual, tactile, and olfactory hallucinations have also been reported. The paranoia and hallucinations can combine in the form of “threatening or accusatory voices coming from neighbouring houses [and] are frequently reported by the patients as disturbing and undeserved”. Patients also present with a lack of symptoms commonly found in other mental disorders similar to paraphrenia. There is no significant deterioration of intellect, personality, or habits and patients often remain clean and mostly self-sufficient. Patients also remain oriented well in time and space.
Paraphrenia is different from schizophrenia because, while both disorders result in delusions and hallucinations, individuals with schizophrenia exhibit changes and deterioration of personality whereas individuals with paraphrenia maintain a well-preserved personality and affective response.
Paraphrenia is often associated with a physical change in the brain, such as a tumour, stroke, ventricular enlargement, or neurodegenerative process. Research that reviewed the relationship between organic brain lesions and the development of delusions suggested that “brain lesions which lead to subcortical dysfunction could produce delusions when elaborated by an intact cortex”.
Many patients who present with paraphrenia have significant auditory or visual loss, are socially isolated with a lack of social contact, do not have a permanent home, are unmarried and without children, and have maladaptive personality traits. While these factors do not cause paraphrenia, they do make individuals more likely to develop the disorder later in life.
While the diagnosis of paraphrenia is absent from recent revisions of the DSM and the ICD, many studies have recognised the condition as “a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients.” As such, paraphrenia is seen as being distinct from both schizophrenia and progressive dementia in old age. Ravindran (1999) developed a list of criteria for the diagnosis of paraphrenia, which agrees with much of the research done up to the time it was published.
A delusional disorder of at least six months duration characterized by the following:
Preoccupation with one or more semi-systematised delusions, often accompanied by auditory hallucinations.
Affect notably well-preserved and appropriate. Ability to maintain rapport with others.
Flat or grossly inappropriate affect.
Grossly disorganised behaviour at times other than during the acute episode.
Disturbance of behaviour understandable in relation to the content of the delusions and hallucinations.
Only partly meets criterion A for schizophrenia. No significant organic brain disorder.
Research suggests that paraphrenics respond well to antipsychotic drug therapy if doctors can successfully achieve sufficient compliance. Herbert found that Stelazine combined with Disipal was an effective treatment. It promoted the discharging of patients and kept discharged patients from being readmitted later. While behaviour therapy may help patients reduce their preoccupation with delusions, psychotherapy is not currently of primary value.
Individuals who develop paraphrenia have a life expectancy similar to the normal population. Recovery from the psychotic symptoms seems to be rare, and in most cases paraphrenia results in in-patient status for the remainder of the life of the patient. Patients experience a slow deterioration of cognitive functions and the disorder can lead to dementia in some cases, but this development is no greater than the normal population.
Studies suggest that the prevalence of paraphrenia in the elderly population is around 2-4%.
While paraphrenia can occur in both men and women, it is more common in women, even after the difference has been adjusted for life expectancies. The ratio of women with paraphrenia to men with paraphrenia is anywhere from 3:1 to 45:2.
It is seen mainly in patients over the age of 60, but has been known to occur in patients in their 40s and 50s.
Personality Type and Living Situation
It is suggested that individuals who develop paraphrenia later in life have premorbid personalities, and can be described as “quarrelsome, religious, suspicious or sensitive, unsociable and cold-hearted.” Many patients were also described as being solitary, eccentric, isolated and difficult individuals; these characteristics were also long-standing rather than introduced by the disorder. Most of the traits recognised prior to the onset of paraphrenia in individuals can be grouped as either paranoid or schizoid. Patients presenting with paraphrenia were most often found to be living by themselves (either single, widowed, or divorced). There have also been reports of low marriage rate among paraphrenics and these individuals also have few or no children (possibly because of this premorbid personality).
The development of paranoia and hallucinations in old age have been related to both auditory and visual impairment, and individuals with paraphrenia often present with one or both of these impairments. Hearing loss in paraphrenics is associated with early age of onset, long duration, and profound auditory loss.
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Metacognition is an awareness of one’s thought processes and an understanding of the patterns behind them. The term comes from the root word meta, meaning “beyond”, or “on top of”. Metacognition can take many forms, such as reflecting on one’s ways of thinking and knowing when and how to use particular strategies for problem-solving. There are generally two components of metacognition:
Knowledge about cognition; and
Regulation of cognition.
Metamemory, defined as knowing about memory and mnemonic strategies, is an especially important form of metacognition. Academic research on metacognitive processing across cultures is in the early stages, but there are indications that further work may provide better outcomes in cross-cultural learning between teachers and students.
Writings on metacognition date back at least as far as two works by the Greek philosopher Aristotle (384-322 BC): On the Soul and the Parva Naturalia.
This higher-level cognition was given the label metacognition by American developmental psychologist John H. Flavell (1976).
The term metacognition literally means ‘above cognition’, and is used to indicate cognition about cognition, or more informally, thinking about thinking. Flavell defined metacognition as knowledge about cognition and control of cognition. For example, a person is engaging in metacognition if they notice that they are having more trouble learning A than B, or if it strikes them that they should double-check C before accepting it as fact. J.H. Flavell (1976, p. 232). Andreas Demetriou’s theory (one of the neo-Piagetian theories of cognitive development) used the term hyper-cognition to refer to self-monitoring, self-representation, and self-regulation processes, which are regarded as integral components of the human mind. Moreover, with his colleagues, he showed that these processes participate in general intelligence, together with processing efficiency and reasoning, which have traditionally been considered to compose fluid intelligence.
Metacognition also involves thinking about one’s own thinking process such as study skills, memory capabilities, and the ability to monitor learning. This concept needs to be explicitly taught along with content instruction.
Metacognitive knowledge is about one’s own cognitive processes and the understanding of how to regulate those processes to maximize learning.
Some types of metacognitive knowledge would include:
Content Knowledge (Declarative Knowledge)
Content knowledge (declarative knowledge) which is understanding one’s own capabilities, such as a student evaluating their own knowledge of a subject in a class. It is notable that not all metacognition is accurate. Studies have shown that students often mistake lack of effort with understanding in evaluating themselves and their overall knowledge of a concept. Also, greater confidence in having performed well is associated with less accurate metacognitive judgment of the performance.
Task Knowledge (Procedural Knowledge)
Task knowledge (procedural knowledge), which is how one perceives the difficulty of a task which is the content, length, and the type of assignment. The study mentioned in Content knowledge also deals with a person’s ability to evaluate the difficulty of a task related to their overall performance on the task. Again, the accuracy of this knowledge was skewed as students who thought their way was better/easier also seemed to perform worse on evaluations, while students who were rigorously and continually evaluated reported to not be as confident but still did better on initial evaluations.
Strategic Knowledge (Conditional Knowledge)
Strategic knowledge (conditional knowledge) which is one’s own capability for using strategies to learn information. Young children are not particularly good at this; it is not until students are in upper elementary school that they begin to develop an understanding of effective strategies.
Metacognition is a general term encompassing the study of memory-monitoring and self-regulation, meta-reasoning, consciousness/awareness and autonoetic consciousness/self-awareness. In practice these capacities are used to regulate one’s own cognition, to maximise one’s potential to think, learn and to the evaluation of proper ethical/moral rules. It can also lead to a reduction in response time for a given situation as a result of heightened awareness, and potentially reduce the time to complete problems or tasks.
In the domain of experimental psychology, an influential distinction in metacognition (proposed by T.O. Nelson & L. Narens) is between Monitoring – making judgements about the strength of one’s memories – and Control – using those judgments to guide behaviour (in particular, to guide study choices). Dunlosky, Serra, and Baker (2007) covered this distinction in a review of metamemory research that focused on how findings from this domain can be applied to other areas of applied research.
In the domain of cognitive neuroscience, metacognitive monitoring and control has been viewed as a function of the prefrontal cortex, which receives (monitors) sensory signals from other cortical regions and implements control using feedback loops (see chapters by Schwartz & Bacon and Shimamura, in Dunlosky & Bjork, 2008).
Metacognition is studied in the domain of artificial intelligence and modelling. Therefore, it is the domain of interest of emergent systemics.
Metacognition is classified into three components:
Metacognitive knowledge (also called metacognitive awareness) is what individuals know about themselves and others as cognitive processors.
Metacognitive regulation is the regulation of cognition and learning experiences through a set of activities that help people control their learning.
Metacognitive experiences are those experiences that have something to do with the current, on-going cognitive endeavour.
Metacognition refers to a level of thinking that involves active control over the process of thinking that is used in learning situations. Planning the way to approach a learning task, monitoring comprehension, and evaluating the progress towards the completion of a task: these are skills that are metacognitive in their nature.
Metacognition includes at least three different types of metacognitive awareness when considering metacognitive knowledge:
Declarative knowledge: refers to knowledge about oneself as a learner and about what factors can influence one’s performance. Declarative knowledge can also be referred to as “world knowledge”.
Procedural knowledge: refers to knowledge about doing things. This type of knowledge is displayed as heuristics and strategies. A high degree of procedural knowledge can allow individuals to perform tasks more automatically. This is achieved through a large variety of strategies that can be accessed more efficiently.
Conditional knowledge: refers to knowing when and why to use declarative and procedural knowledge. It allows students to allocate their resources when using strategies. This in turn allows the strategies to become more effective.
Similar to metacognitive knowledge, metacognitive regulation or “regulation of cognition” contains three skills that are essential.
Planning: refers to the appropriate selection of strategies and the correct allocation of resources that affect task performance.
Monitoring: refers to one’s awareness of comprehension and task performance
Evaluating: refers to appraising the final product of a task and the efficiency at which the task was performed. This can include re-evaluating strategies that were used.
Similarly, maintaining motivation to see a task to completion is also a metacognitive skill. The ability to become aware of distracting stimuli – both internal and external – and sustain effort over time also involves metacognitive or executive functions. The theory that metacognition has a critical role to play in successful learning means it is important that it be demonstrated by both students and teachers.
Students who underwent metacognitive training including pretesting, self evaluation, and creating study plans performed better on exams. They are self-regulated learners who utilise the “right tool for the job” and modify learning strategies and skills based on their awareness of effectiveness. Individuals with a high level of metacognitive knowledge and skill identify blocks to learning as early as possible and change “tools” or strategies to ensure goal attainment. Swanson (1990) found that metacognitive knowledge can compensate for IQ and lack of prior knowledge when comparing fifth and sixth grade students’ problem solving. Students with a high-metacognition were reported to have used fewer strategies, but solved problems more effectively than low-metacognition students, regardless of IQ or prior knowledge. In one study examining students who send text messages during college lectures, it was suggested that students with higher metacognitive abilities were less likely than other students to have their learning affected by using a mobile phone in class.
The fundamental cause of the trouble is that in the modern world the stupid are cocksure while the intelligent are full of doubt. Bertrand Russell.
Metacognologists are aware of their own strengths and weaknesses, the nature of the task at hand, and available “tools” or skills. A broader repertoire of “tools” also assists in goal attainment. When “tools” are general, generic, and context independent, they are more likely to be useful in different types of learning situations.
Another distinction in metacognition is executive management and strategic knowledge. Executive management processes involve planning, monitoring, evaluating and revising one’s own thinking processes and products. Strategic knowledge involves knowing what (factual or declarative knowledge), knowing when and why (conditional or contextual knowledge) and knowing how (procedural or methodological knowledge). Both executive management and strategic knowledge metacognition are needed to self-regulate one’s own thinking and learning.
Finally, there is no distinction between domain-general and domain-specific metacognitive skills. This means that metacognitive skills are domain-general in nature and there are no specific skills for certain subject areas. The metacognitive skills that are used to review an essay are the same as those that are used to verify an answer to a math question.
Although metacognition has thus far been discussed in relation to the self, recent research in the field has suggested that this view is overly restrictive. Instead, it is argued that metacognition research should also include beliefs about others’ mental processes, the influence of culture on those beliefs, and on beliefs about ourselves. This “expansionist view” proposes that it is impossible to fully understand metacognition without considering the situational norms and cultural expectations that influence those same conceptions. This combination of social psychology and metacognition is referred to as social metacognition.
Social metacognition can include ideas and perceptions that relate to social cognition. Additionally, social metacognition can include judging the cognition of others, such as judging the perceptions and emotional states of others. This is in part because the process of judging others is similar to judging the self. However, individuals have less information about the people they are judging; therefore, judging others tends to be more inaccurate. Having similar cognitions can buffer against this inaccuracy and can be helpful for teams or organisations, as well as interpersonal relationships.
Social Metacognition and the Self Concept
An example of the interaction between social metacognition and self-concept can be found in examining implicit theories about the self. Implicit theories can cover a wide range of constructs about how the self operates, but two are especially relevant here; entity theory and incrementalist theory. Entity theory proposes that an individual’s self-attributes and abilities are fixed and stable, while incrementalist theory proposes that these same constructs can be changed through effort and experience. Entity theorists are susceptible to learned helplessness because they may feel that circumstances are outside their control (i.e. there is nothing that could have been done to make things better), thus they may give up easily. Incremental theorists react differently when faced with failure: they desire to master challenges, and therefore adopt a mastery-oriented pattern. They immediately began to consider various ways that they could approach the task differently, and they increase their efforts. Cultural beliefs can act on this as well. For example, a person who has accepted a cultural belief that memory loss is an unavoidable consequence of old age may avoid cognitively demanding tasks as they age, thus accelerating cognitive decline. Similarly, a woman who is aware of the stereotype that purports that women are not good at mathematics may perform worse on tests of mathematical ability or avoid mathematics altogether. These examples demonstrate that the metacognitive beliefs people hold about the self – which may be socially or culturally transmitted – can have important effects on persistence, performance, and motivation.
Attitudes as a Function of Social Metacognition
The way that individuals think about attitude greatly affects the way that they behave. Metacognitions about attitudes influence how individuals act, and especially how they interact with others.
Some metacognitive characteristics of attitudes include importance, certainty, and perceived knowledge, and they influence behaviour in different ways. Attitude importance is the strongest predictor of behaviour and can predict information seeking behaviours in individuals. Attitude importance is also more likely to influence behaviour than certainty of the attitude. When considering a social behaviour like voting a person may hold high importance but low certainty. This means that they will likely vote, even if they are unsure whom to vote for. Meanwhile, a person who is very certain of who they want to vote for, may not actually vote if it is of low importance to them. This also applies to interpersonal relationships. A person might hold a lot of favourable knowledge about their family, but they may not maintain close relations with their family if it is of low importance.
Metacognitive characteristics of attitudes may be key to understanding how attitudes change. Research shows that the frequency of positive or negative thoughts is the biggest factor in attitude change. A person may believe that climate change is occurring but have negative thoughts toward it such as “If I accept the responsibilities of climate change, I must change my lifestyle”. These individuals would not likely change their behaviour compared to someone that thinks positively about the same issue such as “By using less electricity, I will be helping the planet”.
Another way to increase the likelihood of behaviour change is by influencing the source of the attitude. An individual’s personal thoughts and ideas have a much greater impact on the attitude compared to ideas of others. Therefore, when people view lifestyle changes as coming from themselves, the effects are more powerful than if the changes were coming from a friend or family member. These thoughts can be re-framed in a way that emphasizes personal importance, such as “I want to stop smoking because it is important to me” rather than “quitting smoking is important to my family”. More research needs to be conducted on culture differences and importance of group ideology, which may alter these results.
Social Metacognition and Stereotypes
People have secondary cognitions about the appropriateness, justifiability, and social judgability of their own stereotypic beliefs. People know that it is typically unacceptable to make stereotypical judgments and make conscious efforts not to do so. Subtle social cues can influence these conscious efforts. For example, when given a false sense of confidence about their ability to judge others, people will return to relying on social stereotypes. Cultural backgrounds influence social metacognitive assumptions, including stereotypes. For example, cultures without the stereotype that memory declines with old age display no age differences in memory performance.
When it comes to making judgements about other people, implicit theories about the stability versus malleability of human characteristics predict differences in social stereotyping as well. Holding an entity theory of traits increases the tendency for people to see similarity among group members and utilise stereotyped judgments. For example, compared to those holding incremental beliefs, people who hold entity beliefs of traits use more stereotypical trait judgements of ethnic and occupational groups as well as form more extreme trait judgments of new groups. When an individual’s assumptions about a group combine with their implicit theories, more stereotypical judgements may be formed. Stereotypes that one believes others hold about them are called metastereotypes.
In Nonhuman Primates
Beran, Smith, and Perdue (2013) found that chimpanzees showed metacognitive monitoring in the information-seeking task. In their studies, three language-trained chimpanzees were asked to use the keyboard to name the food item in order to get the food. The food in the container was either visible to them or they had to move toward the container to see its contents. Studies shown that chimpanzees were more often to check what was in the container first if the food in the container was hidden. But when the food was visible to them, the chimpanzees were more likely to directly approach the keyboard and reported the identity of the food without looking again in the container. Their results suggested that chimpanzees know what they have seen and show effective information-seeking behaviour when information is incomplete.
Rhesus Macaques (Macaca Mulatta)
Morgan et al. (2014) investigated whether rhesus macaques can make both retrospective and prospective metacognitive judgements on the same memory task. Risk choices were introduced to assess the monkey’s confidence about their memories. Two male rhesus monkeys (Macaca mulatta) were trained in a computerised token economy task first in which they can accumulate tokens to exchange food rewards. Monkeys were presented with multiple images of common objects simultaneously and then a moving border appearing on the screen indicating the target. Immediately following the presentation, the target images and some distractors were shown in the test. During the training phase, monkeys received immediate feedback after they made responses. They can earn two tokens if they make correct choices but lost two tokens if they were wrong.
In Experiment 1, the confidence rating was introduced after they completed their responses in order to test the retrospective metamemory judgements. After each response, a high-risk and a low-risk choice were provided to the monkeys. They could earn one token regardless of their accuracy if they choose the low-risk option. When they chose high-risk, they were rewarded with three tokens if their memory response was correct on that trial but lost three tokens if they made incorrect responses. Morgan and colleagues (2014) found a significant positive correlation between memory accuracy and risk choice in two rhesus monkeys. That is, they were more likely to select the high-risk option if they answered correctly in the working memory task but select the low-risk option if they were failed in the memory task.
Then Morgan et al. (2014) examine monkeys’ prospective metacognitive monitoring skills in Experiment 2. This study employed the same design except that two monkeys were asked to make low-risk or high-risk confidence judgement before they make actual responses to measure their judgements about future events. Similarly, the monkeys were more often to choose high-risk confidence judgment before answering correctly in working memory task and tended to choose the low-risk option before providing an incorrect response. These two studies indicated that rhesus monkeys can accurately monitor their performance and provided evidence of metacognitive abilities in monkeys.
In addition to nonhuman primates, other animals are also shown metacognition. Foote and Crystal (2007) provided the first evidence that rats have the knowledge of what they know in a perceptual discrimination task. Rats were required to classify brief noises as short or long. Some noises with intermediate durations were difficult to discriminate as short or long. Rats were provided with an option to decline to take the test on some trials but were forced to make responses on other trials. If they chose to take the test and respond correctly, they would receive a high reward but no reward if their classification of noises was incorrect. But if the rats decline to take the test, they would be guaranteed a smaller reward. The results showed that rats were more likely to decline to take the test when the difficulty of noise discrimination increased, suggesting rats knew they do not have the correct answers and declined to take the test to receive the reward. Another finding is that the performance was better when they had chosen to take the test compared with if the rats were forced to make responses, proving that some uncertain trials were declined to improve the accuracy.
These responses pattern might be attributed to actively monitor their own mental states. Alternatively, external cues such as environmental cue associations could be used to explain their behaviours in the discrimination task. Rats might have learned the association between intermediate stimuli and the decline option over time. Longer response latencies or some features inherent to stimuli can serve as discriminative cues to decline tests. Therefore, Templer, Lee, and Preston (2017) utilised an olfactory-based delayed match to sample (DMTS) memory task to assess whether rats were capable of metacognitive responding adaptively. Rats were exposed to sample odour first and chose to either decline or take the four-choice memory test after a delay. The correct choices of odour were associated with high reward and incorrect choices have no reward. The decline options were accompanied by a small reward.
In experiment 2, some “no-sample” trials were added in the memory test in which no odour was provided before the test. They hypothesized that rats would decline more often when there was no sample odour presented compared with odour presented if rats could internally assess the memory strength. Alternatively, if the decline option was motivated by external environmental cues, the rats would be less likely to decline the test because no available external cues were presented. The results showed that rats were more likely to decline the test in no-sample trials relative to normal sample trials, supporting the notion that rats can track their internal memory strength.
To rule out other potential possibilities, they also manipulated memory strength by providing the sampled odour twice and varying the retention interval between the learning and the test. Templer and colleagues (2017) found rats were less likely to decline the test if they had been exposed to the sample twice, suggesting that their memory strength for these samples was increased. Longer delayed sample test was more often declined than short delayed test because their memory was better after the short delay. Overall, their series of studies demonstrated that rats could distinguish between remembering and forgetting and rule out the possibilities that decline use was modulated by the external cues such as environmental cue associations.
Research on metacognition of pigeons has shown limited success. Inman and Shettleworth (1999) employed the delayed match to sample (DMTS) procedure to test pigeons’ metacognition. Pigeons were presented with one of three sample shapes (a triangle, a square, or a star) and then they were required to peck the matched sample when three stimuli simultaneously appeared on the screen at the end of the retention interval. A safe key was also presented in some trials next to three sample stimuli which allow them to decline that trial. Pigeons received a high reward for pecking correct stimuli, a middle-level reward for pecking the safe key, and nothing if they pecked the wrong stimuli. Inman and Shettleworth’s (1999) first experiment found that pigeons’ accuracies were lower and they were more likely to choose the safe key as the retention interval between presentation of stimuli and test increased. However, in Experiment 2, when pigeons were presented with the option to escape or take the test before the test phase, there was no relationship between choosing the safe key and longer retention interval. Adams and Santi (2011) also employed the DMTS procedure in a perceptual discrimination task during which pigeons were trained to discriminate between durations of illumination. Pigeons did not choose the escape option more often as the retention interval increased during initial testing. After extended training, they learned to escape the difficult trials. However, these patterns might be attributed to the possibility that pigeons learned the association between escape responses and longer retention delay.
In addition to DMTS paradigm, Castro and Wasserman (2013) proved that pigeons can exhibit adaptive and efficient information-seeking behaviour in the same-different discrimination task. Two arrays of items were presented simultaneously in which the two sets of items were either identical or different from one another. Pigeons were required to distinguish between the two arrays of items in which the level of difficulty was varied. Pigeons were provided with an “Information” button and a “Go” button on some trials that they could increase the number of items in the arrays to make the discrimination easier or they can prompt to make responses by pecking the Go button. Castro and Wasserman found that the more difficult the task, the more often pigeons chose the information button to solve the discrimination task. This behavioural pattern indicated that pigeons could evaluate the difficulty of the task internally and actively search for information when is necessary.
Dogs have shown a certain level of metacognition that they are sensitive to information they have acquired or not. Belger & Bräuer (2018) examined whether dogs could seek additional information when facing uncertain situations. The experimenter put the reward behind one of the two fences in which dogs can see or cannot see where the reward was hidden. After that, dogs were encouraged to find the reward by walking around one fence. The dogs checked more frequently before selecting the fence when they did not see the baiting process compared with when they saw where the reward was hidden. However, contrary to apes, dogs did not show more checking behaviours when the delay between baiting the reward and selecting the fence was longer. Their findings suggested that dogs have some aspect of information-searching behaviours but less flexibly compared to apes.
Smith et al. (1995) evaluated whether dolphins have the ability of metacognitive monitoring in an auditory threshold paradigm. A bottlenosed dolphin was trained to discriminate between high-frequency tones and low-frequency tones. An escape option was available on some trials associated with a small reward. Their studies showed that dolphins could appropriately use the uncertain response when the trials were difficult to discriminate.
There is consensus that nonhuman primates, especially great apes and rhesus monkeys, exhibit metacognitive control and monitoring behaviours. But less convergent evidence was found in other animals such as rats and pigeons. Some researchers criticised these methods and posited that these performances might be accounted for by low-level conditioning mechanisms. Animals learned the association between reward and external stimuli through simple reinforcement models. However, many studies have demonstrated that the reinforcement model alone cannot explain animals’ behavioural patterns. Animals have shown adaptive metacognitive behaviour even with the absence of concrete reward.
Metacognitive-like processes are especially ubiquitous when it comes to the discussion of self-regulated learning. Self-regulation requires metacognition by looking at one’s awareness of their learning and planning further learning methodology. Attentive metacognition is a salient feature of good self-regulated learners, but does not guarantee automatic application. Reinforcing collective discussion of metacognition is a salient feature of self-critical and self-regulating social groups. The activities of strategy selection and application include those concerned with an ongoing attempt to plan, check, monitor, select, revise, evaluate, etc.
Metacognition is ‘stable’ in that learners’ initial decisions derive from the pertinent facts about their cognition through years of learning experience. Simultaneously, it is also ‘situated’ in the sense that it depends on learners’ familiarity with the task, motivation, emotion, and so forth. Individuals need to regulate their thoughts about the strategy they are using and adjust it based on the situation to which the strategy is being applied. At a professional level, this has led to emphasis on the development of reflective practice, particularly in the education and health-care professions.
Recently, the notion has been applied to the study of second language learners in the field of TESOL and applied linguistics in general (e.g. Wenden, 1987; Zhang, 2001, 2010). This new development has been much related to Flavell (1979), where the notion of metacognition is elaborated within a tripartite theoretical framework. Learner metacognition is defined and investigated by examining their person knowledge, task knowledge and strategy knowledge.
Wenden (1991) has proposed and used this framework and Zhang (2001) has adopted this approach and investigated second language learners’ metacognition or metacognitive knowledge. In addition to exploring the relationships between learner metacognition and performance, researchers are also interested in the effects of metacognitively-oriented strategic instruction on reading comprehension (e.g. Garner, 1994, in first language contexts, and Chamot, 2005; Zhang, 2010). The efforts are aimed at developing learner autonomy, interdependence and self-regulation.
Metacognition helps people to perform many cognitive tasks more effectively. Strategies for promoting metacognition include self-questioning (e.g. “What do I already know about this topic? How have I solved problems like this before?”), thinking aloud while performing a task, and making graphic representations (e.g. concept maps, flow charts, semantic webs) of one’s thoughts and knowledge. Carr, 2002, argues that the physical act of writing plays a large part in the development of metacognitive skills.
Strategy Evaluation matrices (SEM) can help to improve the knowledge of cognition component of metacognition. The SEM works by identifying the declarative (Column 1), procedural (Column 2) and conditional (Column 3 and 4) knowledge about specific strategies. The SEM can help individuals identify the strength and weaknesses about certain strategies as well as introduce them to new strategies that they can add to their repertoire.
A regulation checklist (RC) is a useful strategy for improving the regulation of cognition aspect of one’s metacognition. RCs help individuals to implement a sequence of thoughts that allow them to go over their own metacognition. King (1991) found that fifth-grade students who used a regulation checklist outperformed control students when looking at a variety of questions including written problem solving, asking strategic questions, and elaborating information.
Examples of strategies that can be taught to students are word analysis skills, active reading strategies, listening skills, organisational skills and creating mnemonic devices.
Walker and Walker have developed a model of metacognition in school learning termed Steering Cognition, which describes the capacity of the mind to exert conscious control over its reasoning and processing strategies in relation to the external learning task. Studies have shown that pupils with an ability to exert metacognitive regulation over their attentional and reasoning strategies used when engaged in maths, and then shift those strategies when engaged in science or then English literature learning, associate with higher academic outcomes at secondary school.
“Metastrategic knowledge” (MSK) is a sub-component of metacognition that is defined as general knowledge about higher order thinking strategies. MSK had been defined as “general knowledge about the cognitive procedures that are being manipulated”. The knowledge involved in MSK consists of “making generalizations and drawing rules regarding a thinking strategy” and of “naming” the thinking strategy.
The important conscious act of a metastrategic strategy is the “conscious” awareness that one is performing a form of higher order thinking. MSK is an awareness of the type of thinking strategies being used in specific instances and it consists of the following abilities:
Making generalisations and drawing rules regarding a thinking strategy;
Naming the thinking strategy,
Explaining when, why and how such a thinking strategy should be used;
When it should not be used;
What are the disadvantages of not using appropriate strategies; and
What task characteristics call for the use of the strategy.
MSK deals with the broader picture of the conceptual problem. It creates rules to describe and understand the physical world around the people who utilise these processes called higher-order thinking. This is the capability of the individual to take apart complex problems in order to understand the components in problem. These are the building blocks to understanding the “big picture” (of the main problem) through reflection and problem solving.
Both social and cognitive dimensions of sporting expertise can be adequately explained from a metacognitive perspective according to recent research. The potential of metacognitive inferences and domain-general skills including psychological skills training are integral to the genesis of expert performance. Moreover, the contribution of both mental imagery (e.g. mental practice) and attentional strategies (e.g. routines) to our understanding of expertise and metacognition is noteworthy. The potential of metacognition to illuminate our understanding of action was first highlighted by Aidan Moran who discussed the role of meta-attention in 1996. A recent research initiative, a research seminar series called META funded by the BPS, is exploring the role of the related constructs of meta-motivation, meta-emotion, and thinking and action (metacognition).
Sparks of Interest
In the context of mental health, metacognition can be loosely defined as the process that “reinforces one’s subjective sense of being a self and allows for becoming aware that some of one’s thoughts and feelings are symptoms of an illness”. The interest in metacognition emerged from a concern for an individual’s ability to understand their own mental status compared to others as well as the ability to cope with the source of their distress. These insights into an individual’s mental health status can have a profound effect on overall prognosis and recovery. Metacognition brings many unique insights into the normal daily functioning of a human being. It also demonstrates that a lack of these insights compromises ‘normal’ functioning. This leads to less healthy functioning. In the autism spectrum, it is speculated that there is a profound deficit in Theory of Mind. In people who identify as alcoholics, there is a belief that the need to control cognition is an independent predictor of alcohol use over anxiety. Alcohol may be used as a coping strategy for controlling unwanted thoughts and emotions formed by negative perceptions. This is sometimes referred to as self medication.
Adrian Wells’ and Gerald Matthews’ theory proposes that when faced with an undesired choice, an individual can operate in two distinct modes: “object” and “metacognitive”. Object mode interprets perceived stimuli as truth, where metacognitive mode understands thoughts as cues that have to be weighted and evaluated. They are not as easily trusted. There are targeted interventions unique of each patient, that gives rise to the belief that assistance in increasing metacognition in people diagnosed with schizophrenia is possible through tailored psychotherapy. With a customised therapy in place clients then have the potential to develop greater ability to engage in complex self-reflection. This can ultimately be pivotal in the patient’s recovery process. In the obsessive-compulsive spectrum, cognitive formulations have greater attention to intrusive thoughts related to the disorder. “Cognitive self-consciousness” are the tendencies to focus attention on thought. Patients with OCD exemplify varying degrees of these “intrusive thoughts”. Patients also with generalised anxiety disorder (GAD) also show negative thought process in their cognition.
Cognitive-attentional syndrome (CAS) characterises a metacognitive model of emotion disorder (CAS is consistent with the attention strategy of excessively focusing on the source of a threat). This ultimately develops through the client’s own beliefs. Metacognitive therapy attempts to correct this change in the CAS. One of the techniques in this model is called attention training (ATT). It was designed to diminish the worry and anxiety by a sense of control and cognitive awareness. ATT also trains clients to detect threats and test how controllable reality appears to be.
Following the work of Asher Koriat, who regards confidence as central aspect of metacognition, metacognitive training for psychosis aims at decreasing overconfidence in patients with schizophrenia and raising awareness of cognitive biases. According to a meta-analysis, this type of intervention improves delusions and hallucinations.
Works of Art as Metacognitive Artefacts
The concept of metacognition has also been applied to reader-response criticism. Narrative works of art, including novels, movies and musical compositions, can be characterised as metacognitive artefacts which are designed by the artist to anticipate and regulate the beliefs and cognitive processes of the recipient, for instance, how and in which order events and their causes and identities are revealed to the reader of a detective story. As Menakhem Perry has pointed out, mere order has profound effects on the aesthetical meaning of a text. Narrative works of art contain a representation of their own ideal reception process. They are something of a tool with which the creators of the work wish to attain certain aesthetical and even moral effects.
There is an intimate, dynamic interplay between mind wandering and metacognition. Metacognition serves to correct the wandering mind, suppressing spontaneous thoughts and bringing attention back to more “worthwhile” tasks.
The concept of metacognition has also been applied to collective teams and organisations in general, termed organisational metacognition.
Educational psychology: Branch of psychology concerned with the scientific study of human learning.
Educational technology: Use of technology in education to improve learning and teaching.
Epistemology: Branch of philosophy concerning knowledge.
Introspection: Examining one’s own thoughts and feelings.
Learning styles: Largely debunked theories that aim to account for differences in individuals’ learning.
Metaphilosophy: Philosophy of philosophy.
Münchhausen trilemma: A thought experiment used to demonstrate the impossibility of proving any truth.
Metatheory: Theory whose subject matter is itself a theory.
Mindstream: Buddhist concept of continuity of mind.
Mirror test: Animal self-awareness test to determine self-recognition in a mirror.
Phenomenology (philosophy): Philosophical method and schools of philosophy.
Phenomenology (psychology): Psychological study of subjective experience.
Psychological effects of Internet use.
Second-order cybernetics: Recursive application of cybernetics to itself and the reflexive practice of cybernetics according to this critique.
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Olmstead v. L.C., 527 U.S. 581 (1999), is a United States Supreme Court case regarding discrimination against people with mental disabilities.
The Supreme Court held that under the Americans with Disabilities Act, individuals with mental disabilities have the right to live in the community rather than in institutions if, in the words of the opinion of the Court, “the State’s treatment professionals have determined that community placement is appropriate, the transfer from institutional care to a less restrictive setting is not opposed by the affected individual, and the placement can be reasonably accommodated, taking into account the resources available to the State and the needs of others with mental disabilities.”
The case was brought by the Atlanta Legal Aid Society, Inc.
Tommy Olmstead, Commissioner, Georgia Department of Human Resources, et al. v. L. C., by Zimring, guardian ad litem and next friend, et al. (Olmstead v. L.C.) was a case filed in 1995 and decided in 1999 before the United States Supreme Court. The plaintiffs, L.C. (Lois Curtis) and E.W. (Elaine Wilson, deceased 04 December 2005), two women were diagnosed with schizophrenia, intellectual disability and personality disorder. They had both been treated in institutional settings and in community based treatments in the state of Georgia.
Guardian ad litem: A legal guardian is a person who has been appointed by a court or otherwise has the legal authority to care for the personal and property interests of another person, called a ward.
Next Friend: In common law, a next friend is a person who represents another person who is underage, or, because of disability or otherwise, is unable to maintain a suit on his or her own behalf and who does not have a legal guardian. Also known as litigation friends.
Following clinical assessments by state employees, both plaintiffs were determined to be better suited for treatment in a community-based setting rather than in the institution. The plaintiffs remained confined in the institution, each for several years after the initial treatment was concluded. Both sued the state of Georgia to prevent them from being inappropriately treated and housed in the institutional setting.
Opinion of the Court
The case rose to the level of the United States Supreme Court, which decided the case in 1999, and plays a major role in determining that mental illness is a form of disability and therefore covered under the Americans with Disabilities Act (ADA). Title II of the ADA applies to ‘public entities’ and include ‘state and local governments’ and ‘any department, agency or special purpose district’ and protects any ‘qualified person with a disability’ from exclusion from participation in or denied the benefits of services, programs, or activities of a public entity.
The Supreme Court decided mental illness is a form of disability and that “unjustified isolation” of a person with a disability is a form of discrimination under Title II of the ADA. The Supreme Court held that community placement is only required and appropriate (i.e. institutionalisation is unjustified), when:
The State’s treatment professionals have determined that community placement is appropriate;
The transfer from institutional care to a less restrictive setting is not opposed by the affected individual; and
The placement can be reasonably accommodated, taking into account the resources available to the State and the needs of others with mental disabilities.
Unjustified isolation is discrimination based on disability. Olmstead v. L.C., 527 U.S. 581, 587 (1999).
The Supreme Court explained that this holding “reflects two evident judgments.”
First, “institutional placement of persons who can handle and benefit from community settings perpetuates unwarranted assumptions that persons so isolated are incapable or unworthy of participating in community life.”
Second, historically “confinement in an institution severely diminishes the everyday life activities of individuals, including family relations, social contacts, work options, economic independence, educational advancement, and cultural enrichment.” Id. at 600-601.
However, a majority of Justices in Olmstead also recognized an ongoing role for publicly and privately operated institutions:
“We emphasize that nothing in the ADA or its implementing regulations condones termination of institutional settings for persons unable to handle or benefit from community settings…Nor is there any federal requirement that community-based treatment be imposed on patients who do not desire it.” Id. at 601-602.
A plurality of Justices noted: “[N]o placement outside the institution may ever be appropriate . . . ‘Some individuals, whether mentally retarded or mentally ill, are not prepared at particular times – perhaps in the short run, perhaps in the long run – for the risks and exposure of the less protective environment of community settings ’ for these persons, ‘institutional settings are needed and must remain available’” (quoting Amicus Curiae Brief for the American Psychiatric Association, et al). “As already observed [by the majority], the ADA is not reasonably read to impel States to phase out institutions, placing patients in need of close care at risk… ‘Each disabled person is entitled to treatment in the most integrated setting possible for that person—recognizing on a case-by-case basis, that setting may be an institution’[quoting VOR’s Amici Curiae brief].” Id. at 605.
Justice Kennedy noted in his concurring opinion, “It would be unreasonable, it would be a tragic event, then, were the Americans with Disabilities Act of 1990 (ADA) to be interpreted so that states had some incentive, for fear of litigation to drive those in need of medical care and treatment out of appropriate care and into settings with too little assistance and supervision.” Id. at 610.
The Supreme Court did not reach the question of whether there is a constitutional right to community services in the most integrated setting.
About ten years after the Olmstead decision, the State of Georgia and the United States Department of Justice entered a settlement agreement to cease all admissions of individuals with developmental disabilities to state-operated, federally licensed institutions (“State Hospitals”) and, by 01 July 2015, “transition all individuals with developmental disabilities in the State Hospitals from the Hospitals to community settings,” according to a Department of Justice Fact Sheet about the settlement. The settlement also calls for serving 9,000 individuals with mental illness in community settings. Recently, the federal court’s Independent Reviewer for the settlement found significant health and safety risks, including many deaths, plaguing former State Hospital residents due to their transition from a licensed facility home to community-settings per the settlement. The Court has approved a moratorium on such transfers until the safety of those impacted can be assured.
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In psychology and psychiatry, clanging refers to a mode of speech characterised by association of words based upon sound rather than concepts.
For example, this may include compulsive rhyming or alliteration without apparent logical connection between words.
This is associated with the irregular thinking apparent in psychotic mental illnesses (e.g. mania and schizophrenia). Gustav Aschaffenburg found that manic individuals generated these “clang-associations” roughly 10-50 times more than non-manic individuals. Aschaffenburg also found that the frequency of these associations increased for all individuals as they became more fatigued.
Clanging refers specifically to behaviour that is situationally inappropriate. While a poet rhyming is not evidence of mental illness, disorganised speech that impedes the patient’s ability to communicate is a disorder in itself, often seen in schizophrenia.
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