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What is Olanzapine?

Published on by Andrew Marshall26 Comments

Introduction

Olanzapine, sold under the trade name Zyprexa among others, is an atypical antipsychotic primarily used to treat schizophrenia and bipolar disorder.

For schizophrenia, it can be used for both new-onset disease and long-term maintenance. It is taken by mouth or by injection into a muscle.

Common side effects include weight gain, movement disorders, dizziness, feeling tired, constipation, and dry mouth. Other side effects include low blood pressure with standing, allergic reactions, neuroleptic malignant syndrome, high blood sugar, seizures, gynecomastia, erectile dysfunction, and tardive dyskinesia. In older people with dementia, its use increases the risk of death. Use in the later part of pregnancy may result in a movement disorder in the baby for some time after birth. Although how it works is not entirely clear, it blocks dopamine and serotonin receptors.

Brief History

Olanzapine was patented in 1971 and approved for medical use in the United States in 1996. It is available as a generic medication. In 2017, it was the 239th-most commonly prescribed medication in the United States, with more than two million prescriptions. Lilly also markets olanzapine in a fixed-dose combination with fluoxetine as olanzapine/fluoxetine (Symbyax).

Chemical Synthesis

The preparation of olanzapine was first disclosed in a series of patents from Eli Lilly & Co. in the 1990s. In the final two steps, 5-methyl-2-[(2-nitrophenyl)amino]-3-thiophenecarbonitrile was reduced with stannous chloride in ethanol to give the substituted thienobenzodiazepine ring system, and this was treated with methylpiperazine in a mixture of dimethyl sulfoxide and toluene as solvent to produce the drug.

Medical Uses

Schizophrenia

The first-line psychiatric treatment for schizophrenia is antipsychotic medication, with olanzapine being one such medication. Olanzapine appears to be effective in reducing symptoms of schizophrenia, treating acute exacerbations, and treating early-onset schizophrenia. The usefulness of maintenance therapy, however, is difficult to determine, as more than half of people in trials quit before the 6-week completion date. Treatment with olanzapine (like clozapine) may result in increased weight gain and increased glucose and cholesterol levels when compared to most other second-generation antipsychotic drugs used to treat schizophrenia.

Comparison

The UK National Institute for Health and Care Excellence (NICE), the British Association for Psychopharmacology, and the World Federation of Societies for Biological Psychiatry suggest that little difference in effectiveness is seen between antipsychotics in prevention of relapse, and recommend that the specific choice of antipsychotic be chosen based on a person’s preference and the drug’s side-effect profile. The US Agency for Healthcare Research and Quality concludes that olanzapine is not different from haloperidol in the treatment of positive symptoms and general psychopathology, or in overall assessment, but that it is superior for the treatment of negative and depressive symptoms. It has a lower risk of causing movement disorders than typical antipsychotics.

In a 2013 comparison of fifteen antipsychotic drugs in schizophrenia, olanzapine was ranked third in efficacy. It was 5% more effective than risperidone (fourth), 24-27% more effective than haloperidol, quetiapine, and aripiprazole, and 33% less effective than clozapine (first). A 2013 review of first-episode schizophrenia concluded that olanzapine is superior to haloperidol in providing a lower discontinuation rate, and in short-term symptom reduction, response rate, negative symptoms, depression, cognitive function, discontinuation due to poor efficacy, and long-term relapse, but not in positive symptoms or on the clinical global impressions (CGI) score. In contrast, pooled second-generation antipsychotics showed superiority to first-generation antipsychotics only against the discontinuation, negative symptoms (with a much larger effect seen among industry- compared to government-sponsored studies), and cognition scores. Olanzapine caused less extrapyramidal side effects and less akathisia, but caused significantly more weight gain, serum cholesterol increase, and triglyceride increase than haloperidol.

A 2012 review concluded that among ten atypical antipsychotics, only clozapine, olanzapine, and risperidone were better than first-generation antipsychotics. A 2011 review concluded that neither first- nor second-generation antipsychotics produce clinically meaningful changes in CGI scores, but found that olanzapine and amisulpride produce larger effects on the PANSS and BPRS batteries than five other second-generation antipsychotics or pooled first-generation antipsychotics. A 2010 Cochrane systematic review found that olanzapine may have a slight advantage in effectiveness when compared to aripiprazole, quetiapine, risperidone, and ziprasidone. No differences in effectiveness were detected when comparing olanzapine to amisulpride and clozapine. A 2014 meta-analysis of nine published trials having minimum duration six months and median duration 52 weeks concluded that olanzapine, quetiapine, and risperidone had better effects on cognitive function than amisulpride and haloperidol.

Bipolar Disorder

Olanzapine is recommended by NICE as a first-line therapy for the treatment of acute mania in bipolar disorder. Other recommended first-line treatments are haloperidol, quetiapine, and risperidone. It is recommended in combination with fluoxetine as a first-line therapy for acute bipolar depression, and as a second-line treatment by itself for the maintenance treatment of bipolar disorder.

The Network for Mood and Anxiety Treatments recommends olanzapine as a first-line maintenance treatment in bipolar disorder and the combination of olanzapine with fluoxetine as second-line treatment for bipolar depression.

A review on the efficacy of olanzapine as maintenance therapy in patients with bipolar disorder was published by Dando & Tohen in 2006. A 2014 meta-analysis concluded that olanzapine with fluoxetine was the most effective among nine treatments for bipolar depression included in the analysis.

Other Uses

Olanzapine may be useful in promoting weight gain in underweight adult outpatients with anorexia nervosa. However, no improvement of psychological symptoms was noted.

Olanzapine has been shown to be helpful in addressing a range of anxiety and depressive symptoms in individuals with schizophrenia and schizoaffective disorders, and has since been used in the treatment of a range of mood and anxiety disorders. Olanzapine is no less effective than lithium or valproate and more effective than placebo in treating bipolar disorder. It has also been used for Tourette syndrome and stuttering.

Olanzapine has been studied for the treatment of hyperactivity, aggressive behaviour, and repetitive behaviours in autism.

Olanzapine is frequently prescribed off-label for the treatment of insomnia, including difficulty falling asleep and staying asleep. The daytime sedation experienced with olanzapine is generally comparable to quetiapine and lurasidone, which is a frequent complaint in clinical trials. In some cases, the sedation due to olanzapine impaired the ability of people to wake up at a consistent time every day. Some evidence of efficacy for treating insomnia is seen, but long-term studies (especially for safety) are still needed.

Olanzapine has been recommended to be used in antiemetic regimens in people receiving chemotherapy that has a high risk for vomiting.

Specific Populations

Pregnancy and Lactation

Olanzapine is associated with the highest placental exposure of any atypical antipsychotic. Despite this, the available evidence suggests it is safe during pregnancy, although the evidence is insufficiently strong to say anything with a high degree of confidence. Olanzapine is associated with weight gain, which according to recent studies, may put olanzapine-treated patients’ offspring at a heightened risk for neural tube defects (e.g. spina bifida). Breastfeeding in women taking olanzapine is advised against because olanzapine is secreted in breast milk, with one study finding that the exposure to the infant is about 1.8% that of the mother.

Elderly

Citing an increased risk of stroke, in 2004, the Committee on the Safety of Medicines in the UK issued a warning that olanzapine and risperidone, both atypical antipsychotic medications, should not be given to elderly patients with dementia. In the US, olanzapine comes with a black box warning for increased risk of death in elderly patients. It is not approved for use in patients with dementia-related psychosis. A BBC investigation in June 2008 found that this advice was being widely ignored by British doctors. Evidence suggested that the elderly are more likely to experience weight gain on olanzapine compared to aripiprazole and risperidone.

Adverse Effects

Refer to Adverse Effects of Olanzapine.

The principal side effect of olanzapine is weight gain, which may be profound in some cases and/or associated with derangement in blood-lipid and blood-sugar profiles (see section metabolic effects). A 2013 meta-analysis of the efficacy and tolerance of 15 antipsychotic drugs (APDs) found that it had the highest propensity for causing weight gain out of the 15 APDs compared with an SMD of 0.74. Extrapyramidal side effects, although potentially serious, are infrequent to rare from olanzapine, but may include tremors and muscle rigidity.

It is not recommended to be used by IM injection in acute myocardial infarction, bradycardia, recent heart surgery, severe hypotension, sick sinus syndrome, and unstable angina.

Several patient groups are at a heightened risk of side effects from olanzapine and antipsychotics in general. Olanzapine may produce nontrivial high blood sugar in people with diabetes mellitus. Likewise, the elderly are at a greater risk of falls and accidental injury. Young males appear to be at heightened risk of dystonic reactions, although these are relatively rare with olanzapine. Most antipsychotics, including olanzapine, may disrupt the body’s natural thermoregulatory systems, thus permitting excursions to dangerous levels when situations (exposure to heat, strenuous exercise) occur.

Other side effects include galactorrhoea, amenorrhea, gynecomastia, and erectile dysfunction (impotence).

Paradoxical Effects

Olanzapine is used therapeutically to treat serious mental illness. Occasionally, it can have the opposite effect and provoke serious paradoxical reactions in a small subgroup of people, causing unusual changes in personality, thoughts, or behaviour; hallucinations and excessive thoughts about suicide have also been linked to olanzapine use.

Drug-Induced OCD

Many different types of medication can create or induce pure obsessive-compulsive disorder (OCD) in patients who have never had symptoms before. A new chapter about OCD in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (2013) now specifically includes drug-induced OCD.

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

Metabolic Effects

The US Food and Drug Administration (FDA) requires all atypical antipsychotics to include a warning about the risk of developing hyperglycaemia and diabetes, both of which are factors in the metabolic syndrome. These effects may be related to the drugs’ ability to induce weight gain, although some reports have been made of metabolic changes in the absence of weight gain. Studies have indicated that olanzapine carries a greater risk of causing and exacerbating diabetes than another commonly prescribed atypical antipsychotic, risperidone. Of all the atypical antipsychotics, olanzapine is one of the most likely to induce weight gain based on various measures. The effect is dose dependent in humans and animal models of olanzapine-induced metabolic side effects. There are some case reports of olanzapine-induced diabetic ketoacidosis. Olanzapine may decrease insulin sensitivity, though one 3-week study seems to refute this. It may also increase triglyceride levels.

Despite weight gain, a large multicentre, randomised National Institute of Mental Health study found that olanzapine was better at controlling symptoms because patients were more likely to remain on olanzapine than the other drugs. One small, open-label, nonrandomised study suggests that taking olanzapine by orally dissolving tablets may induce less weight gain, but this has not been substantiated in a blinded experimental setting.

Post-Injection Delirium/Sedation Syndrome

Postinjection delirium/sedation syndrome (PDSS) is a rare syndrome that is specific to the long-acting injectable formulation of olanzapine, olanzapine pamoate. The incidence of PDSS with olanzapine pamoate is estimated to be 0.07% of administrations, and is unique among other second-generation, long-acting antipsychotics (e.g. paliperidone palmitate), which do not appear to carry the same risk.[70] PDSS is characterised by symptoms of delirium (e.g. confusion, difficulty speaking, and uncoordinated movements) and sedation. Most people with PDSS exhibit both delirium and sedation (83%). Although less specific to PDSS, a majority of cases (67%) involved a feeling of general discomfort. PDSS may occur due to accidental injection and absorption of olanzapine pamoate into the bloodstream, where it can act more rapidly, as opposed to slowly distributing out from muscle tissue. Using the proper, intramuscular-injection technique for olanzapine pamoate helps to decrease the risk of PDSS, though it does not eliminate it entirely. This is why the FDA advises that people who are injected with olanzapine pamoate be watched for 3 hours after administration, in the event that PDSS occurs.

Animal Toxicology

Olanzapine has demonstrated carcinogenic effects in multiple studies when exposed chronically to female mice and rats, but not male mice and rats. The tumours found were in either the liver or mammary glands of the animals.

Discontinuation

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, vertigo, numbness, or muscle pains may occur. Symptoms generally resolve after a short time.

Tentative evidence indicates 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.

Overdose

Symptoms of an overdose include tachycardia, agitation, dysarthria, decreased consciousness, and coma. Death has been reported after an acute overdose of 450 mg, but also survival after an acute overdose of 2000 mg. Fatalities generally have occurred with olanzapine plasma concentrations greater than 1000 ng/mL post mortem, with concentrations up to 5200 ng/mL recorded (though this might represent confounding by dead tissue, which may release olanzapine into the blood upon death). No specific antidote for olanzapine overdose is known, and even physicians are recommended to call a certified poison control centre for information on the treatment of such a case. Olanzapine is considered moderately toxic in overdose, more toxic than quetiapine, aripiprazole, and the SSRIs, and less toxic than the monoamine oxidase inhibitors and tricyclic antidepressants.

Interactions

Drugs or agents that increase the activity of the enzyme CYP1A2, notably tobacco smoke, may significantly increase hepatic first-pass clearance of olanzapine; conversely, drugs that inhibit CYP1A2 activity (examples: ciprofloxacin, fluvoxamine) may reduce olanzapine clearance. Carbamazepine, a known enzyme inducer, has decreased the concentration/dose ration of olanzapine by 33% compared to olanzapine alone. Another enzyme inducer, ritonavir, has also been shown to decrease the body’s exposure to olanzapine, due to its induction of the enzymes CYP1A2 and uridine 5′-diphospho-glucuronosyltransferase (UGT). Probenecid increases the total exposure (area under the curve) and maximum plasma concentration of olanzapine. Although olanzapine’s metabolism includes the minor metabolic pathway of CYP2D6, the presence of the CYP2D6 inhibitor fluoxetine does not have a clinically significant effect on olanzapine’s clearance.

Pharmacology

Pharmacodynamics

Olanzapine has a higher affinity for 5-HT2A serotonin receptors than D2 dopamine receptors, which is a common property of most atypical antipsychotics, aside from the benzamide antipsychotics such as amisulpride along with the nonbenzamides aripiprazole, brexpiprazole, blonanserin, cariprazine, melperone, and perospirone.

Olanzapine had the highest affinity of any second-generation antipsychotic towards the P-glycoprotein in one in vitro study. P-glycoprotein transports a myriad of drugs across a number of different biological membranes (found in numerous body systems) including the blood-brain barrier (a semipermeable membrane that filters the contents of blood prior to it reaching the brain); P-GP inhibition could mean that less brain exposure to olanzapine results from this interaction with the P-glycoprotein. A relatively large quantity of commonly encountered foods and medications inhibit P-GP, and pharmaceuticals fairly commonly are either substrates of P-GP, or inhibit its action; both substrates and inhibitors of P-GP effectively increase the permeability of the blood-brain barrier to P-GP substrates and subsequently increase the central activity of the substrate, while reducing the local effects on the GI tract. The mediation of olanzapine in the central nervous system by P-GP means that any other substance or drug that interacts with P-GP increases the risk for toxic accumulations of both olanzapine and the other drug.

Olanzapine is a potent antagonist of the muscarinic M3 receptor, which may underlie its diabetogenic side effects. Additionally, it also exhibits a relatively low affinity for serotonin 5-HT1, GABAA, beta-adrenergic receptors, and benzodiazepine binding sites.

The mode of action of olanzapine’s antipsychotic activity is unknown. It may involve antagonism of dopamine and serotonin receptors. Antagonism of dopamine receptors is associated with extrapyramidal effects such as tardive dyskinesia (TD), and with therapeutic effects. Antagonism of muscarinic acetylcholine receptors is associated with anticholinergic side effects such as dry mouth and constipation; in addition, it may suppress or reduce the emergence of extrapyramidal effects for the duration of treatment, but it offers no protection against the development of TD. In common with other second-generation (atypical) antipsychotics, olanzapine poses a relatively low risk of extrapyramidal side effects including TD, due to its higher affinity for the 5HT2A receptor over the D2 receptor.

Antagonizing H1 histamine receptors causes sedation and may cause weight gain, although antagonistic actions at serotonin 5-HT2C and dopamine D2 receptors have also been associated with weight gain and appetite stimulation.

Pharmacokinetics

Metabolism

Olanzapine is metabolized by the cytochrome P450 (CYP) system; principally by isozyme 1A2 (CYP1A2) and to a lesser extent by CYP2D6. By these mechanisms, more than 40% of the oral dose, on average, is removed by the hepatic first-pass effect. Clearance of olanzapine appears to vary by sex; women have roughly 25% lower clearance than men. Clearance of olanzapine also varies by race; in self-identified African Americans or Blacks, olanzapine’s clearance was 26% higher. A difference in the clearance does not apparent between individuals identifying as Caucasian, Chinese, or Japanese. Routine, pharmacokinetic monitoring of olanzapine plasma levels is generally unwarranted, though unusual circumstances (e.g. the presence of drug-drug interactions) or a desire to determine if patients are taking their medicine may prompt its use.

Chemistry

Olanzapine is unusual in having four well-characterised crystalline polymorphs and many hydrated forms.

Society and Culture

Regulatory Status

Olanzapine is approved by the US FDA for:

  • Treatment – in combination with fluoxetine – of depressive episodes associated with bipolar disorder (December 2003).
  • Long-term treatment of bipolar I disorder (January 2004).
  • Long-term treatment – in combination with fluoxetine – of resistant depression (March 2009).
  • Oral formulation: acute and maintenance treatment of schizophrenia in adults, acute treatment of manic or mixed episodes associated with bipolar I disorder (monotherapy and in combination with lithium or sodium valproate).
  • Intramuscular formulation: acute agitation associated with schizophrenia and bipolar I mania in adults.
  • Oral formulation combined with fluoxetine: treatment of acute depressive episodes associated with bipolar I disorder in adults, or treatment of acute, resistant depression in adults.
  • Treatment of the manifestations of psychotic disorders (September 1996 to March 2000).
  • Short-term treatment of acute manic episodes associated with bipolar I disorder (March 2000).
  • Short-term treatment of schizophrenia instead of the management of the manifestations of psychotic disorders (March 2000).
  • Maintaining treatment response in schizophrenic patients who had been stable for about eight weeks and were then followed for a period of up to eight months (November 2000).

The drug became generic in 2011.

Sales of Zyprexa in 2008 were $2.2 billion in the US and $4.7 billion worldwide.

Controversy and Litigation

Eli Lilly has faced many lawsuits from people who claimed they developed diabetes or other diseases after taking Zyprexa, as well as by various governmental entities, insurance companies, and others. Lilly produced a large number of documents as part of the discovery phase of this litigation, which started in 2004; the documents were ruled to be confidential by a judge and placed under seal, and later themselves became the subject of litigation.

In 2006, Lilly paid $700 million to settle around 8,000 of these lawsuits, and in early 2007, Lilly settled around 18,000 suits for $500 million, which brought the total Lilly had paid to settle suits related to the drug to $1.2 billion.

A December 2006 New York Times article based on leaked company documents concluded that the company had engaged in a deliberate effort to downplay olanzapine’s side effects. The company denied these allegations and stated that the article had been based on cherry-picked documents. The documents were provided to the Times by Jim Gottstein, a lawyer who represented mentally ill patients, who obtained them from a doctor, David Egilman, who was serving as an expert consultant on the case. After the documents were leaked to online peer-to-peer, file-sharing networks by Will Hall and others in the psychiatric survivors movement, who obtained copies, in 2007 Lilly filed a protection order to stop the dissemination of some of the documents, which Judge Jack B. Weinstein of the Brooklyn Federal District Court granted. Judge Weinstein also criticized the New York Times reporter, Gottstein, and Egilman in the ruling. The Times of London also received the documents and reported that as early as 1998, Lilly considered the risk of drug-induced obesity to be a “top threat” to Zyprexa sales. On 09 October 2000, senior Lilly research physician Robert Baker noted that an academic advisory board to which he belonged was “quite impressed by the magnitude of weight gain on olanzapine and implications for glucose.”

Lilly had threatened Egilman with criminal contempt charges regarding the documents he took and provided to reporters; in September 2007, he agreed to pay Lilly $100,000 in return for the company’s agreement to drop the threat of charges.

In September 2008, Judge Weinstein issued an order to make public Lilly’s internal documents about the drug in a different suit brought by insurance companies, pension funds, and other payors.

In March 2008, Lilly settled a suit with the state of Alaska, and in October 2008, Lilly agreed to pay $62 million to 32 states and the District of Columbia to settle suits brought under state consumer protection laws.

In 2009, Eli Lilly pleaded guilty to a US federal criminal misdemeanour charge of illegally marketing Zyprexa for off-label use and agreed to pay $1.4 billion. The settlement announcement stated “Eli Lilly admits that between September 1999 and 31 March 2001, the company promoted Zyprexa in elderly populations as treatment for dementia, including Alzheimer’s dementia. Eli Lilly has agreed to pay a $515 million criminal fine and to forfeit an additional $100 million in assets.”

Trade Names

Olanzapine is generic and available under many trade names worldwide.

Dosage Forms

Olanzapine is marketed in a number of countries, with tablets ranging from 2.5 to 20 mg. Zyprexa (and generic olanzapine) is available as an orally disintegrating “wafer”, which rapidly dissolves in saliva. It is also available in 10-mg vials for intramuscular injection.

Research

Olanzapine has been studied as an antiemetic, particularly for the control of chemotherapy-induced nausea and vomiting (CINV).

In general, olanzapine appears to be about as effective as aprepitant for the prevention of CINV, though some concerns remain for its use in this population. For example, concomitant use of metoclopramide or haloperidol increases the risk for extrapyramidal symptoms. Otherwise, olanzapine appears to be fairly well tolerated for this indication, with somnolence being the most common side effect.

Olanzapine has been considered as part of an early psychosis approach for schizophrenia. The Prevention through Risk Identification, Management, and Education study, funded by the National Institute of Mental Health and Eli Lilly, tested the hypothesis that olanzapine might prevent the onset of psychosis in people at very high risk for schizophrenia. The study examined 60 patients with prodromal schizophrenia, who were at an estimated risk of 36-54% of developing schizophrenia within a year, and treated half with olanzapine and half with placebo. In this study, patients receiving olanzapine did not have a significantly lower risk of progressing to psychosis. Olanzapine was effective for treating the prodromal symptoms, but was associated with significant weight gain.

What is a Neuropsychological Test?

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Introduction

Neuropsychological tests are specifically designed tasks that are used to measure a psychological function known to be linked to a particular brain structure or pathway.

Refer to Neuropsychological Assessment.

Tests are used for research into brain function and in a clinical setting for the diagnosis of deficits. They usually involve the systematic administration of clearly defined procedures in a formal environment. Neuropsychological tests are typically administered to a single person working with an examiner in a quiet office environment, free from distractions. As such, it can be argued that neuropsychological tests at times offer an estimate of a person’s peak level of cognitive performance. Neuropsychological tests are a core component of the process of conducting neuropsychological assessment, along with personal, interpersonal and contextual factors.

Most neuropsychological tests in current use are based on traditional psychometric theory. In this model, a person’s raw score on a test is compared to a large general population normative sample, that should ideally be drawn from a comparable population to the person being examined. Normative studies frequently provide data stratified by age, level of education, and/or ethnicity, where such factors have been shown by research to affect performance on a particular test. This allows for a person’s performance to be compared to a suitable control group, and thus provide a fair assessment of their current cognitive function.

According to Larry J. Seidman, the analysis of the wide range of neuropsychological tests can be broken down into four categories. First is an analysis of overall performance, or how well people do from test to test along with how they perform in comparison to the average score. Second is left-right comparisons: how well a person performs on specific tasks that deal with the left and right side of the body. Third is pathognomic signs, or specific test results that directly relate to a distinct disorder. Finally, the last category is differential patterns, which are typically used to diagnose specific diseases or types of damage.

Categories

Most forms of cognition actually involve multiple cognitive functions working in unison, however tests can be organised into broad categories based on the cognitive function which they predominantly assess. Some tests appear under multiple headings as different versions and aspects of tests can be used to assess different functions.

Intelligence

Intelligence testing in a research context is relatively more straightforward than in a clinical context. In research, intelligence is tested and results are generally as obtained, however in a clinical setting intelligence may be impaired so estimates are required for comparison with obtained results. Premorbid estimates can be determined through a number of methods, the most common include: comparison of test results to expected achievement levels based on prior education and occupation and the use of hold tests which are based on cognitive faculties which are generally good indicators of intelligence and thought to be more resistant to cognitive damage, e.g. language.

  • National Adult Reading Test (NART).
  • Wechsler Adult Intelligence Scale (WAIS).
  • Wechsler Intelligence Scale for Children (WISC).
  • Wechsler Preschool and Primary Scale of Intelligence (WPPSI).
  • Wechsler Test of Adult Reading (WTAR).

Memory

Memory is a very broad function which includes several distinct abilities, all of which can be selectively impaired and require individual testing. There is disagreement as to the number of memory systems, depending on the psychological perspective taken. From a clinical perspective, a view of five distinct types of memory, is in most cases sufficient. Semantic memory and episodic memory (collectively called declarative memory or explicit memory); procedural memory and priming or perceptual learning (collectively called non-declarative memory or implicit memory) all four of which are long term memory systems; and working memory or short term memory. Semantic memory is memory for facts, episodic memory is autobiographical memory, procedural memory is memory for the performance of skills, priming is memory facilitated by prior exposure to a stimulus and working memory is a form of short term memory for information manipulation.

  • Benton Visual Retention Test.
  • California Verbal Learning Test.
  • Cambridge Prospective Memory Test (CAMPROMPT).
  • Gollin figure test.
  • Memory Assessment Scales (MAS).
  • Rey Auditory Verbal Learning Test.
  • Rivermead Behavioural Memory Test.
  • Test of Memory and Learning (TOMAL).
  • Mental Attributes Profiling System.
  • Wechsler Memory Scale (WMS).

Language

Language functions include speech, reading and writing, all of which can be selectively impaired.

  • Boston Diagnostic Aphasia Examination.
  • Boston Naming Test.
  • Comprehensive Aphasia Test (CAT).
  • Multilingual Aphasia Examination.

Executive Function

Executive functions is an umbrella term for a various cognitive processes and sub-processes. The executive functions include: problem solving, planning, organisational skills, selective attention, inhibitory control and some aspects of short term memory.

  • Behavioural Assessment of Dysexecutive Syndrome (BADS).
  • CNS Vital Signs (Brief Core Battery).
  • Continuous performance task (CPT).
  • Controlled Oral Word Association Test (COWAT).
  • d2 Test of Attention.
  • Delis-Kaplan Executive Function System (D-KEFS).
  • Digit Vigilance Test.
  • Figural Fluency Test.
  • Halstead Category Test.
  • Hayling and Brixton tests.
  • Kaplan Baycrest Neurocognitive Assessment (KBNA).
  • Kaufman Short Neuropsychological Assessment.
  • Paced Auditory Serial Addition Test (PASAT).
  • Rey-Osterrieth Complex Figure.
  • Ruff Figural Fluency Test.
  • Stroop task.
  • Test of Variables of Attention (T.O.V.A.).
  • Tower of London Test.
  • Trail-Making Test (TMT) or Trails A & B.
  • Wisconsin Card Sorting Test (WCST).
  • Symbol Digit Modalities Test.
  • Test of Everyday Attention (TEA).

Visuospatial

Neuropsychological tests of visuospatial function should cover the areas of visual perception, visual construction and visual integration. Though not their only functions, these tasks are to a large degree carried out by areas of the parietal lobe.

  • Clock Test.
  • Hooper Visual Organisation Task (VOT).
  • Rey-Osterrieth Complex Figure.

Dementia Specific

Dementia testing is often done by way of testing the cognitive functions that are most often impaired by the disease e.g. memory, orientation, language and problem solving. Tests such as these are by no means conclusive of deficits, but may give a good indication as to the presence or severity of dementia.

  • The Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog).
  • Clinical Dementia Rating.
  • Dementia Rating Scale.

Batteries Assessing Multiple Neuropsychological Functions

There are some test batteries which combine a range of tests to provide an overview of cognitive skills. These are usually good early tests to rule out problems in certain functions and provide an indication of functions which may need to be tested more specifically.

  • Barcelona Neuropsychological Test (BNT).
  • Cambridge Neuropsychological Test Automated Battery (CANTAB).
  • Cognistat (The Neurobehavioral Cognitive Status Examination).
  • Cognitive Assessment Screening Instrument (CASI).
  • Cognitive Function Scanner (CFS).
  • Dean-Woodcock Neuropsychology Assessment System (DWNAS).
  • General Practitioner Assessment Of Cognition (GPCOG).
  • Hooper Visual Organisation Test.
  • Luria-Nebraska Neuropsychological battery.
  • MicroCog.
  • Mini mental state examination (MMSE).
  • NEPSY.
  • Repeatable Battery for the Assessment of Neuropsychological Status.
  • Short Parallel Assessments of Neuropsychological Status (SPANS).
  • CDR Computerised Assessment System.

Automated Computerised Cognitive Tests

Traditional cognitive examinations are mostly paper and pen based. As such most of them are time consuming and require special training to be carried out. Today there is a rapidly growing number of automated computerised cognitive tests emerging, for example Brain on Track, Cogstate, CAMCI, CANTAB. Several of these new tests are shoving promising ability to discriminate between healthy individuals and different cognitive difficulties and/or to monitor cognitive impairment over time. Since these tests are easily administered to large groups of people this is opening up possibilities to, for example, regularly screen portions of the population at risk for cognitive decline and early on give adequate support and treatment.

Benefits of Neuropsychological Testing

The most beneficial factor of neuropsychological assessment is that it provides an accurate diagnosis of the disorder for the patient when it is unclear to the psychologist what exactly the patient has. This allows for accurate treatment later on in the process because treatment is driven by the exact symptoms of the disorder and how a specific patient may react to different treatments. The assessment allows the psychologist and patient to understand the severity of the deficit and to allow better decision-making by both parties. It is also helpful in understanding deteriorating diseases because the patient can be assessed multiple times to see how the disorder is progressing.

On This Day … 30 August

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People (Births)

Victor Skumin

Victor Andreevich Skumin (born 30 August 1948) is a Russian and Soviet scientist, psychiatrist, philosopher and writer.

After graduating from the Kharkiv National Medical University in 1973, in 1976, he became a psychotherapist in Kiev Institute of Cardiovascular Surgery. In 1978, he described a new disease, the Skumin syndrome. He introduced a method of psychotherapy and self-improvement based on optimistic autosuggestion for psychological rehabilitation of cardiosurgical patients (1979).

From 1980 to 1990, he was professor of psychotherapy at the Kharkiv Medical Academy of Post-graduate Education. The main result of his scientific activity was the discovery of the “syndrome of the neurotic phantom of somatic disease” and a “concept of the mental constituent of a chronic somatic disease”.

From 1990 to 1994, Skumin held positions as chaired professor of psychology and pedagogy, and of physical education and Health life at the Kharkiv State Academy of Culture. In 1994, he was elected to the post of the President-founder of the World Organisation of Culture of Health (Moscow). In 1995, Skumin became the first editor-in-chief of the journal To Health via Culture. He is known for inventing a popular term “Culture of Health” (1968).

Besides psychiatry and psychology, Skumin writes on healthy lifestyle, yoga, and philosophy. He co-authored series of illustrated books and articles on Agni Yoga, Roerichism, Russian cosmism, transhumanism, and New Age. He wrote books of fiction and lyrics for several songs.

On This Day … 29 August

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People (Births)

  • 1935 – László Garai, Hungarian psychologist and scholar.

Laszlo Garai

László Garai (born 29 August 1935) is a scholar of psychology: studies theoretical psychology, social psychology and economic psychology.

Early Life

Garai was born in Budapest. He graduated in philosophy and psychology from the Faculty of Arts of Budapest University (1959).

He obtained his Candidate degree from the Hungarian Academy of Sciences with a thesis on a specifically human basic need.

He obtained his Doctor of Science degree from the Hungarian Academy of Science with a thesis on social identity and paradoxes of its psychic elaboration.

Professional Work

László Garai started his career as editor at the Encyclopaedia Department of the Hungarian academic publishing house Akadémiai Kiadó. After the defence of his thesis above on specifically basic human need, he concluded this research as a fellow of the Institute for Philosophy of the Hungarian Academy of Sciences (1964-1971). According to his hypothesis, a paradoxical need for a needfree activity is specific for humans and substantial for their other needs. The structure of the hypothesized need is isomorphic with that of the work considered as a “specifically human basic activity” and defined as that of arranging in one and the same structure ends and means. The hypothesis is based on the activity theory of Alexei Leontiev.

He won a Keldysh Scholarship (post doctoral scholarship founded by Keldysh, president of the USSR Academy of Sciences, to support joint Soviet-Hungarian academic research projects) to the Department of scientific discoveries’ psychology in the Institute for History of Natural Sciences and Technology in the Soviet Academy of Sciences (Moscow, 1969-1970)). There Garai studied simultaneous scientific discoveries (such as that of Bolyai and Lobachevsky).

In 1970, Garai founded in the Institute for Psychology of the Hungarian Academy of Sciences a research unit that became the first in Hungary research team of economic psychology and a centre of Vygotskian theoretical research. head of that department (1971-1979) and research advisor (1998-2002). He worked at the Laboratoire Européen de Psychologie Sociale (Paris, 1971, 1973 and 1977) and directed psycho-economic research supported by the National Scientific Research Foundation (1990-2005).

Garai was a member of the advisory board of the Hungarian Ministry of Finance. He is on the editorial board of the Journal of Russian and East European Psychology.

On This Day … 28 August

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People (Births)

  • 1903 – Bruno Bettelheim, Austrian-American psychologist and author (d. 1990).

People (Deaths)

  • 1757 – David Hartley, English psychologist and philosopher (b. 1705).

Bruno Bettelheim

Bruno Bettelheim (28 August 1903 to 13 March 1990) was an Austrian-born psychologist, scholar, public intellectual and author who spent most of his academic and clinical career in the United States. An early writer on autism, Bettelheim’s work focused on the education of emotionally disturbed children, as well as Freudian psychology more generally. In the US, he later gained a position as professor at the University of Chicago and director of the Sonia Shankman Orthogenic School for Disturbed Children, and after 1973 taught at Stanford University.

Bettelheim’s ideas, which grew out of those of Sigmund Freud, theorised that children with behavioural and emotional disorders were not born that way, and could be treated through extended psychoanalytic therapy, treatment that rejected the use of psychotropic drugs and shock therapy. During the 1960s and 1970s he had an international reputation in such fields as autism, child psychiatry, and psychoanalysis.

Much of his work was discredited after his death due to fraudulent academic credentials, allegations of abusive treatment of patients under his care, accusations of plagiarism, and lack of oversight by institutions and the psychological community.

David Hartley

David Hartley FRS (baptised 21 June 1705 to 28 August 1757) was an English philosopher and founder of the Associationist school of psychology.

What is Quazepam?

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Introduction

Quazepam (marketed under brand names Doral, Dormalin) is a relatively long-acting benzodiazepine derivative drug developed by the Schering Corporation in the 1970s.

Quazepam is indicated for the treatment of insomnia including sleep induction and sleep maintenance. Quazepam induces impairment of motor function and has relatively (and uniquely) selective hypnotic and anticonvulsant properties with considerably less overdose potential than other benzodiazepines (due to its novel receptor-subtype selectively). Quazepam is an effective hypnotic which induces and maintains sleep without disruption of the sleep architecture.

Brief History

It was patented in 1970 and came into medical use in 1985.

Medical Uses

Quazepam is used for short-term treatment of insomnia related to sleep induction or sleep maintenance problems and has demonstrated superiority over other benzodiazepines such as temazepam. It had a fewer incidence of side effects than temazepam, including less sedation, amnesia, and less motor-impairment. Usual dosage is 7.5 to 15 mg orally at bedtime.

Quazepam is effective as a premedication prior to surgery.

Side Effects

Quazepam has fewer side effects than other benzodiazepines and less potential to induce tolerance and rebound effects. There is significantly less potential for quazepam to induce respiratory depression or to adversely affect motor coordination than other benzodiazepines. The different side effect profile of quazepam may be due to its more selective binding profile to type 1 benzodiazepine receptors.

  • Ataxia.
  • Daytime somnolence.
  • Hypokinesia.
  • Cognitive and performance impairments.

In September 2020, the US Food and Drug Administration (FDA) required the boxed warning be updated for all benzodiazepine medicines to describe the risks of abuse, misuse, addiction, physical dependence, and withdrawal reactions consistently across all the medicines in the class.

Tolerance and Dependence

Tolerance may occur to quazepam but more slowly than seen with other benzodiazepines such as triazolam. Quazepam causes significantly less drug tolerance and less withdrawal symptoms including less rebound insomnia upon discontinuation compared to other benzodiazepines. Quazepam may cause less rebound effects than other type1 benzodiazepine receptor selective nonbenzodiazepine drugs due to its longer half-life. Short-acting hypnotics often cause next day rebound anxiety. Quazepam due to its pharmacological profile does not cause next day rebound withdrawal effects during treatment.

No firm conclusions can be drawn, however, whether long-term use of quazepam does not produce tolerance as few, if any, long-term clinical trials extending beyond 4 weeks of chronic use have been conducted. Quazepam should be withdrawn gradually if used beyond 4 weeks of use to avoid the risk of a severe benzodiazepine withdrawal syndrome developing. Very high dosage administration over prolonged periods of time, up to 52 weeks, of quazepam in animal studies provoked severe withdrawal symptoms upon abrupt discontinuation, including excitability, hyperactivity, convulsions and the death of two of the monkeys due to withdrawal-related convulsions. More monkeys died, however, in the diazepam-treated monkeys. In addition it has now been documented in the medical literature that one of the major metabolites of quazepam, N-desalkyl-2-oxoquazepam (N-desalkylflurazepam), which is long-acting and prone to accumulation, binds unselectively to benzodiazepine receptors, thus quazepam may not differ all that much pharmacologically from other benzodiazepines.

Special Precautions

Benzodiazepines require special precaution if used in the during pregnancy, in children, alcohol or drug-dependent individuals and individuals with comorbid psychiatric disorders.

Quazepam and its active metabolites are excreted into breast milk.

Accumulation of one of the active metabolites of quazepam, N-desalkylflurazepam, may occur in the elderly. A lower dose may be required in the elderly.

Elderly

Quazepam is more tolerable for elderly patients compared to flurazepam due to its reduced next day impairments. However, another study showed marked next day impairments after repeated administration due to accumulation of quazepam and its long-acting metabolites. Thus the medical literature shows conflicts on quazepam’s side effect profile. A further study showed significant balance impairments combined with an unstable posture after administration of quazepam in test subjects. An extensive review of the medical literature regarding the management of insomnia and the elderly found that there is considerable evidence of the effectiveness and durability of non-drug treatments for insomnia in adults of all ages and that these interventions are underutilised. Compared with the benzodiazepines including quazepam, the nonbenzodiazepine sedative/hypnotics appeared to offer few, if any, significant clinical advantages in efficacy or tolerability in elderly persons. It was found that newer agents with novel mechanisms of action and improved safety profiles, such as the melatonin agonists, hold promise for the management of chronic insomnia in elderly people. Long-term use of sedative/hypnotics for insomnia lacks an evidence base and has traditionally been discouraged for reasons that include concerns about such potential adverse drug effects as cognitive impairment (anterograde amnesia), daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls. In addition, the effectiveness and safety of long-term use of these agents remain to be determined. It was concluded that more research is needed to evaluate the long-term effects of treatment and the most appropriate management strategy for elderly persons with chronic insomnia.

Interactions

The absorption rate is likely to be significantly reduced if quazepam is taken in the fasted state reducing the hypnotic effect of quazepam. If 3 or more hours have passed since eating food then some food should be eaten before taking quazepam.

Pharmacology

Quazepam is a trifluoroalkyl type of benzodiazepine. Quazepam is unique amongst benzodiazepines in that it selectively targets the GABAA α1 subunit receptors which are responsible for inducing sleep. Its mechanism of action is very similar to zolpidem and zaleplon in its pharmacology and can successfully substitute for zolpidem and zaleplon in animal studies.

Quazepam is selective for type I benzodiazepine receptors containing the α1 subunit, similar to other drugs such as zaleplon and zolpidem. As a result, quazepam has little or no muscle relaxant properties. Most other benzodiazepines are unselective and bind to type1 GABAA receptors and type2 GABAA receptors. Type1 GABAA receptors include the α1 subunit containing GABAA receptors which are responsible for hypnotic properties of the drug. Type 2 receptors include the α2, α3 and α5 subunits which are responsible for anxiolytic action, amnesia and muscle relaxant properties. Thus quazepam may have less side effects than other benzodiazepines but, it has a very long half-life of 25 hours which reduces its benefits as a hypnotic due to likely next day sedation. It also has two active metabolites with half-lives of 28 and 79 hours. Quazepam may also cause less drug tolerance than other benzodiazepines such as temazepam and triazolam perhaps due to its subtype selectivity. The longer half-life of quazepam may have the advantage however, of causing less rebound insomnia than shorter acting subtype selective nonbenzodiazepines. However, one of the major metabolites of quazepam, the N-desmethyl-2-oxoquazepam (aka N-desalkylflurazepam), binds unselectively to both type1 and type2 GABAA receptors. The N-desmethyl-2-oxoquazepam metabolite also has a very long half-life and likely contributes to the pharmacological effects of quazepam.

Pharmacokinetics

Quazepam has an absorption half-life of 0.4 hours with a peak in plasma levels after 1.75 hours. It is eliminated both renally and through faeces. The active metabolites of quazepam are 2-oxoquazepam and N-desalkyl-2-oxoquazepam. The N-desalkyl-2-oxoquazepam metabolite has only limited pharmacological activity compared to the parent compound quazepam and the active metabolite 2-oxoquazepam. Quazepam and its major active metabolite 2-oxoquazepam both show high selectivity for the type1 GABAA receptors. The elimination half-life range of quazepam is between 27 and 41 hours.

Mechanism of Action

Quazepam modulates specific GABAA receptors via the benzodiazepine site on the GABAA receptor. This modulation enhances the actions of GABA, causing an increase in opening frequency of the chloride ion channel which results in an increased influx of chloride ions into the GABAA receptors. Quazepam, unique amongst benzodiazepine drugs selectively targets type1 benzodiazepine receptors which results reduced sleep latency in promotion of sleep. Quazepam also has some anticonvulsant properties.

EEG and Sleep

Quazepam has potent sleep inducing and sleep maintaining properties. Studies in both animals and humans have demonstrated that EEG changes induced by quazepam resemble normal sleep patterns whereas other benzodiazepines disrupt normal sleep. Quazepam promotes slow wave sleep. This positive effect of quazepam on sleep architecture may be due to its high selectivity for type1 benzodiazepine receptors as demonstrated in animal and human studies. This makes quazepam unique in the benzodiazepine family of drugs.

Drug Misuse

Refer to Benzodiazepine Use Disorder.

Quazepam is a drug with the potential for misuse. Two types of drug misuse can occur, either recreational misuse where the drug is taken to achieve a high, or when the drug is continued long term against medical advice.

What is Ramelteon?

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Introduction

Ramelteon, sold under the brand name Rozerem among others, is a sleep agent medication that selectively binds to the MT1 and MT2 receptors in the suprachiasmatic nucleus (SCN), instead of binding to GABAA receptors, such as with drugs like zolpidem.

It appears to speed the onset of sleep and alter the total amount of sleep a person gets. It is approved by the US Food and Drug Administration (FDA) for long-term use.

Ramelteon does not show any appreciable binding to GABAA receptors, which are associated with anxiolytic, myorelaxant, and amnesic effects.

Brief History

Ramelteon was approved for use in the United States in July 2005.

Medical Uses

Ramelteon is approved in the United States for the treatment of insomnia characterised by difficulty with sleep onset.

A systematic review, published in 2014, concluded “ramelteon was found to be beneficial in preventing delirium in medically ill individuals when compared to placebo.”

Mechanism of Action

Ramelteon is a melatonin receptor agonist with both high affinity for melatonin MT1 and MT2 receptors and selectivity over the MT3 receptor. Ramelteon demonstrates full agonist activity in vitro in cells expressing human MT1 or MT2 receptors, and high selectivity for human MT1 and MT2 receptors compared to the MT3 receptor.

The activity of ramelteon at the MT1 and MT2 receptors is believed to contribute to its sleep-promoting properties, as these receptors, acted upon by endogenous melatonin, are thought to be involved in the maintenance of the circadian rhythm underlying the normal sleep-wake cycle. Ramelteon has no appreciable affinity for the GABA receptor complex or for receptors that bind neuropeptides, cytokines, serotonin, dopamine, noradrenaline, acetylcholine, and opioids. Ramelteon also does not interfere with the activity of a number of selected enzymes in a standard panel.

The major metabolite of ramelteon, M-II, is active and has approximately one tenth and one fifth the binding affinity of the parent molecule for the human MT1 and MT2 receptors, respectively, and is 17-25-fold less potent than ramelteon in in vitro functional assays. Although the potency of M-II at MT1 and MT2 receptors is lower than the parent drug, M-II circulates at higher concentrations than the parent producing 20-100-fold greater mean systemic exposure when compared to ramelteon. M-II has weak affinity for the serotonin 5-HT2B receptor, but no appreciable affinity for other receptors or enzymes. Similar to ramelteon, M-II does not interfere with the activity of a number of endogenous enzymes.

Adverse Effects

Ramelteon has not been shown to produce dependence and has shown no potential for abuse, and the withdrawal and rebound insomnia that is typical with GABA modulators is not present in ramelteon.

Six percent of ramelteon-treated patients in clinical trials discontinued due to an adverse event, compared with two percent in the placebo arms. The most frequent adverse events leading to discontinuation were somnolence, dizziness, nausea, fatigue, headache, and insomnia. The US official Prescribing Information warns of rare cases of anaphylactic reactions, abnormal thinking, worsening of depression or suicidal thinking in patients with pre-existing depression, and decreased testosterone and increased prolactin levels. It also notes that ramelteon is not recommended for use in patients with severe sleep apnoea.

In mice treated with ramelteon for two years, increases in liver and testicular tumours were observed, but only at doses at least 20 times greater than the recommended human dose on a milligram/kilogram basis.

Drug Interactions

Ramelteon has been evaluated for potential drug interactions with the following medications and showed no significant effects: omeprazole, theophylline, dextromethorphan, and midazolam, digoxin and warfarin. There were no clinically meaningful effects when ramelteon was co-administered with any of these drugs.

A drug interaction study showed that there were no clinically meaningful effects or an increase in adverse events when ramelteon and the SSRI Prozac (fluoxetine) were co-administered. When co-administered with ramelteon, fluvoxamine (strong CYP1A2 inhibitor) increased AUC approximately 190-fold, and the Cmax increased approximately 70-fold, compared to ramelteon administered alone. Ramelteon and fluvoxamine should not be co-administered.

Ramelteon has significant drug-drug interaction with the following drugs: amiodarone, ciprofloxacin, fluvoxamine, ticlopidine.

Ramelteon should be administered with caution in patients taking other CYP1A2 inhibitors, strong CYP3A4 inhibitors such as ketoconazole, and strong CYP2C9 inhibitors such as fluconazole.

Efficacy may be reduced when ramelteon is used in combination with potent CYP enzyme inducers such as rifampin, since ramelteon concentrations may be decreased.

What is Schema Therapy?

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Introduction

Schema therapy was developed by Jeffrey E. Young for use in treatment of personality disorders and chronic DSM Axis I disorders, such as when patients fail to respond or relapse after having been through other therapies (for example, traditional cognitive behavioural therapy, CBT). Schema therapy is an integrative psychotherapy combining theory and techniques from previously existing therapies, including CBT, psychoanalytic object relations theory, attachment theory, and Gestalt therapy.

Concepts

Four main theoretical concepts in schema therapy are early maladaptive schemas (or simply schemas), coping styles, modes, and basic emotional needs:

  1. In cognitive psychology, a schema is an organised pattern of thought and behaviour. It can also be described as a mental structure of preconceived ideas, a framework representing some aspect of the world, or a system of organizing and perceiving new information. In schema therapy, a schema specifically refers to an early maladaptive schema, defined as a pervasive self-defeating or dysfunctional theme or pattern of memories, emotions, and physical sensations, developed during childhood or adolescence and elaborated throughout one’s lifetime. Often they have the form of a belief about the self or the world. For instance, a person with an Abandonment schema could be hypersensitive (have an “emotional button” or “trigger”) about their perceived value to others, which in turn could make them feel sad and panicky in their interpersonal relationships.
  2. Coping styles are a person’s behavioural responses to schemas. There are three potential coping styles. In “avoidance” the person tries to avoid situations that activate the schema. In “surrender” the person gives into the schema, doesn’t try to fight against it, and changes their behaviour in expectation that the feared outcome is inevitable. In “counterattack”, also called “overcompensation”, the person puts extra work into not allowing the schema’s feared outcome to happen. These maladaptive coping styles (overcompensation, avoidance, or surrender) very often wind up reinforcing the schemas. Continuing the Abandonment example: having imagined a threat of abandonment in a relationship and feeling sad and panicky, a person using an avoidance coping style might then behave in ways to limit the closeness in the relationship to try to protect themselves from being abandoned. The resulting loneliness or even actual loss of the relationship could easily reinforce the person’s Abandonment schema. Another example can be given for the Defectiveness schema: A person using an avoidance coping style might avoid situations that make them feel defective, or might try to numb the feeling with addictions or distractions. A person using a surrender coping style might tolerate unfair criticism without defending themselves. A person using the counterattack/overcompensation coping style might put extra effort into being superhuman.
  3. Modes are mind states that cluster schemas and coping styles into a temporary “way of being” that a person can shift into occasionally or more frequently. For example, a Vulnerable Child mode might be a state of mind encompassing schemas of Abandonment, Defectiveness, Mistrust/Abuse and a coping style of surrendering (to the schemas).
  4. If a patient’s basic emotional needs are not met in childhood, then schemas, coping styles, and modes can develop. Some basic needs that have been identified are: connection, mutuality, reciprocity, flow, and autonomy. For example, a child with unmet needs around connection – perhaps due to parental loss to death, divorce, or addiction – might develop an Abandonment schema.

The goal of schema therapy is to help patients meet their basic emotional needs by helping the patient learn how to:

  • Heal schemas by diminishing the intensity of emotional memories comprising the schema and the intensity of bodily sensations, and by changing the cognitive patterns connected to the schema; and
  • Replace maladaptive coping styles and responses with adaptive patterns of behaviour.

Techniques used in schema therapy including limited reparenting and Gestalt therapy psychodrama techniques such as imagery re-scripting and empty chair dialogues (Refer to techniques in schema therapy, below).

There is a growing literature of outcome studies on schema therapy, where schema therapy has shown impressive results (Refer to outcome studies on schema therapy, below).

Early Maladaptive Schemas

Refer to List of Maladaptive Schemas.

Early maladaptive schemas are self-defeating emotional and cognitive patterns established from childhood and repeated throughout life. They may be made up of emotional memories of past hurt, tragedy, fear, abuse, neglect, unmet safety needs, abandonment, or lack of normal human affection in general. Early maladaptive schemas can also include bodily sensations associated with such emotional memories. Early maladaptive schemas can have different levels of severity and pervasiveness: the more severe the schema, the more intense the negative emotion when the schema is triggered and the longer it lasts; the more pervasive the schema, the greater the number of situations that trigger it.

Schema Domains

Schema domains are five broad categories of unmet needs into which are grouped 18 early maladaptive schemas identified by Young, Klosko & Weishaar (2003):

  • Disconnection/Rejection includes 5 schemas:
    • Abandonment/Instability.
    • Mistrust/Abuse.
    • Emotional Deprivation.
    • Defectiveness/Shame.
    • Social Isolation/Alienation.
  • Impaired Autonomy and/or Performance includes 4 schemas:
    • Dependence/Incompetence.
    • Vulnerability to Harm or Illness.
    • Enmeshment/Undeveloped Self.
    • Failure.
  • Impaired Limits includes 2 schemas:
    • Entitlement/Grandiosity.
    • Insufficient Self-Control and/or Self-Discipline.
  • Other-Directedness includes 3 schemas:
    • Subjugation.
    • Self-Sacrifice.
    • Approval-Seeking/Recognition-Seeking.
  • Over-vigilance/Inhibition includes 4 schemas:
    • Negativity/Pessimism.
    • Emotional Inhibition.
    • Unrelenting Standards/Hypercriticalness.
    • Punitiveness.

Schema Modes

Schema modes are momentary mind states which every human being experiences at one time or another. A schema mode consists of a cluster of schemas and coping styles. Life situations that a person finds disturbing or offensive, or arouse bad memories, are referred to as “triggers” that tend to activate schema modes. In psychologically healthy persons, schema modes are mild, flexible mind states that are easily pacified by the rest of their personality. In patients with personality disorders, schema modes are more severe, rigid mind states that may seem split off from the rest of their personality.

Identified Schema Modes

Young, Klosko & Weishaar (2003) identified 10 schema modes grouped into four categories. The four categories are: Child modes, Dysfunctional Coping modes, Dysfunctional Parent modes, and the Healthy Adult mode. The four Child modes are: Vulnerable Child, Angry Child, Impulsive/Undisciplined Child, and Happy Child. The three Dysfunctional Coping modes are: Compliant Surrenderer, Detached Protector, and Overcompensator. The two Dysfunctional Parent modes are: Punitive Parent and Demanding Parent.

Angry ChildThis is fuelled mainly by feelings of victimisation or bitterness, leading towards negativity, pessimism, jealousy, and rage. While experiencing this schema mode, a patient may have urges to yell, scream, throw/break things, or possibly even injure themselves or harm others. The Angry Child schema mode is enraged, anxious, frustrated, self-doubting, feels unsupported in ideas and vulnerable.
Impulsive ChildThis is the mode where anything goes. Behaviours of the Impulsive Child schema mode may include reckless driving, substance abuse, cutting oneself, suicidal thoughts, gambling, or fits of rage, such as punching a wall when “triggered” or laying blame of circumstantial difficulties upon innocent people. Unsafe sex, rash decisions to run away from a situation without resolution, tantrums perceived by peers as infantile, and so forth are a mere few of the behaviours which a patient in this schema mode might display. Impulsive Child is the rebellious and careless schema mode.
Detached ProtectorThis is based in escape. Patients in Detached Protector schema mode withdraw, dissociate, alienate, or hide in some way. This may be triggered by numerous stress factors or feelings of being overwhelmed. When a patient with insufficient skills is in a situation involving excessive demands, it can trigger a Detached Protector response mode. Stated simply, patients become numb in order to protect themselves from the harm or stress of what they fear is to come, or to protect themselves from fear of the unknown in general.
Abandoned ChildThis is the mode in which a patient may feel defective in some way, thrown aside, unloved, obviously alone, or may be in a “me against the world” mindset. The patient may feel as though peers, friends, family, and even the entire world have abandoned them. Behaviours of patients in Abandoned Child mode may include (but are not limited to) falling into major depression, pessimism, feeling unwanted, feeling unworthy of love, and perceiving personality traits as irredeemable flaws. Rarely, a patient’s self-perceived flaws may be intentionally withheld on the inside; when this occurs, instead of showing one’s true self, the patient may appear to others as “egotistical”, “attention-seeking”, selfish, distant, and may exhibit behaviours unlike their true nature. The patient might create a narcissistic alter-ego/persona in order to escape or hide the insecurity from others. Due to fear of rejection, of feeling disconnected from their true self and poor self-image, these patients, who truly desire companionship/affection, may instead end up pushing others away.
Punitive ParentThis is identified by beliefs of a patient that they should be harshly punished, perhaps due to feeling “defective”, or making a simple mistake. The patient may feel that they should be punished for even existing. Sadness, anger, impatience, and judgement are directed to the patient and from the patient. The Punitive Parent has great difficulty in forgiving themselves even under average circumstances in which anyone could fall short of their standards. The Punitive Parent does not wish to allow for human error or imperfection, thus punishment is what this mode seeks.
Healthy AdultThis is the mode that schema therapy aims to help a patient achieve as the long-lasting state of well-being. The Healthy Adult is comfortable making decisions, is a problem-solver, thinks before acting, is appropriately ambitious, sets limits and boundaries, nurtures self and others, forms healthy relationships, takes on all responsibility, sees things through, and enjoys/partakes in enjoyable adult activities and interests with boundaries enforced, takes care of their physical health, and values themselves. In this schema mode the patient focuses on the present day with hope and strives toward the best tomorrow possible. The Healthy Adult forgives the past, no longer sees themselves as a victim (but as a survivor), and expresses all emotions in ways which are healthy and cause no harm.

Techniques in Schema Therapy

Treatment plans in schema therapy generally encompass three basic classes of techniques: cognitive, experiential, and behavioural (in addition to the basic healing components of the therapeutic relationship). Cognitive strategies expand on standard CBT techniques such as listing pros and cons of a schema, testing the validity of a schema, or conducting a dialogue between the “schema side” and the “healthy side”. Experiential and emotion focused strategies expand on standard Gestalt therapy psychodrama and imagery techniques. Behavioural pattern-breaking strategies expand on standard behaviour therapy techniques, such as role playing an interaction and then assigning the interaction as homework. One of the most central techniques in schema therapy is the use of the therapeutic relationship, specifically through a process called “limited reparenting”.

Specific techniques often used in schema therapy include flash cards with important therapeutic messages, created in session and used by the patient between sessions, and the schema diary – a template or workbook that is filled out by the patient between sessions and that records the patient’s progress in relation to all the theoretical concepts in schema therapy.

Schema Therapy and Psychoanalysis

From an integrative psychotherapy perspective, limited reparenting and the experiential techniques, particularly around changing modes, could be seen as actively changing what psychoanalysis has described as object relations. Historically, mainstream psychoanalysis tended to reject active techniques – such as Fritz Perls’ Gestalt therapy work or Franz Alexander’s “corrective emotional experience” – but contemporary relational psychoanalysis (led by analysts such as Lewis Aron, and building on the ideas of earlier unorthodox analysts such as Sándor Ferenczi) is more open to active techniques. It is notable that in a head to head comparison of a psychoanalytic object relations treatment (Otto F. Kernberg’s transference focused psychotherapy) and schema therapy, the latter has been demonstrated to be more effective in treating Borderline Personality Disorder.

Outcome Studies on Schema Therapy

Schema Therapy vs Transference Focused Psychotherapy Outcomes

Dutch investigators, including Josephine Giesen-Bloo and Arnoud Arntz (the project leader), compared schema therapy (also known as schema focused therapy or SFT) with transference focused psychotherapy (TFP) in the treatment of borderline personality disorder. 86 patients were recruited from four mental health institutes in the Netherlands. Patients in the study received two sessions per week of SFT or TFP for three years. After three years, full recovery was achieved in 45% of the patients in the SFT condition, and in 24% of those receiving TFP. One year later, the percentage fully recovered increased to 52% in the SFT condition and 29% in the TFP condition, with 70% of the patients in the SFT group achieving “clinically significant and relevant improvement”. Moreover, the dropout rate was only 27% for SFT, compared with 50% for TFP.

Patients began to feel and function significantly better after the first year, with improvement occurring more rapidly in the SFT group. There was continuing improvement in subsequent years. Thus investigators concluded that both treatments had positive effects, with schema therapy clearly more successful.

Less Intensive Outpatient, Individual Schema Therapy

Dutch investigators, including Marjon Nadort and Arnoud Arntz, assessed the effectiveness of schema therapy in the treatment of borderline personality disorder when utilised in regular mental health care settings. A total of 62 patients were treated in eight mental health centres located in the Netherlands. The treatment was less intensive along a number of dimensions including a shift from twice weekly to once weekly sessions during the second year. Despite this, there was no lessening of effectiveness with recovery rates that were at least as high and similarly low dropout rates.

Pilot Study of Group Schema Therapy for Borderline Personality Disorder

Investigators Joan Farrell, Ida Shaw and Michael Webber at the Indiana University School of Medicine Centre for BPD Treatment & Research tested the effectiveness of adding an eight-month, 30-session schema therapy group to treatment-as-usual (TAU) for borderline personality disorder (BPD) with 32 patients. The dropout rate was 0% for those patients who received group schema therapy in addition to TAU and 25% for those who received TAU alone. At the end of treatment, 94% of the patients who received group schema therapy in addition to TAU compared to 16% of the patients receiving TAU alone no longer met BPD diagnostic criteria. The schema therapy group treatment led to significant reductions in symptoms and global improvement in functioning. The large positive treatment effects found in the group schema therapy study suggest that the group modality may augment or catalyse the active ingredients of the treatment for BPD patients. As of 2014, a collaborative randomised controlled trial is under way at 14 sites in six countries to further explore this interaction between groups and schema therapy.

What is the Assessment of Suicide Risk?

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Introduction

Suicide risk assessment is a process of estimating the likelihood for a person to attempt or die by suicide.

The goal of a thorough risk assessment is to learn about the circumstances of an individual person with regard to suicide, including warning signs, risk factors, and protective factors. Risk for suicide is re-evaluated throughout the course of care to assess the patient’s response to personal situational changes and clinical interventions. Accurate and defensible risk assessment requires a clinician to integrate a clinical judgment with the latest evidence-based practice, although accurate prediction of low base rate events, such as suicide, is inherently difficult and prone to false positives.

The assessment process is ethically complex: the concept of “imminent suicide” (implying the foreseeability of an inherently unpredictable act) is a legal construct in a clinical guise, which can be used to justify the rationing of emergency psychiatric resources or intrusion into patients’ civil liberties. Some experts recommend abandoning suicide risk assessment as it is so inaccurate. In addition suicide risk assessment is often conflated with assessment of self-harm which has little overlap with completed suicide. Instead, it is suggested that the emotional state which has caused the suicidal thoughts, feelings or behaviour should be the focus of assessment with a view to helping the patient rather than reducing the anxiety of clinician who overestimates the risk of suicide and are fearful of litigation. Given the difficulty of suicide prediction, researchers have attempted to improve the state of the art in both suicide and suicidal behaviour prediction using natural language processing and machine learning applied to electronic health records.

Refer to Suicidal Ideation, Suicide Awareness, Suicide Prevention, and Suicide Prevention Contract.

In Practice

There are risks and disadvantages to both over-estimation and under-estimation of suicide risk. Over-sensitivity to risk can have undesirable consequences, including inappropriate deprivation of patients’ rights and squandering of scarce clinical resources. On the other hand, underestimating suicidality as a result of a dismissive attitude or lack of clinical skill jeopardises patient safety and risks clinician liability. Some people may worry that asking about suicidal intentions will make suicide more likely. In reality, regarding that the enquiries are made sympathetically, it does not. Key areas to be assessed include the person’s predisposition to suicidal behaviour; identifiable precipitant or stressors such as job loss, recent death of a loved one and change of residence; the patient’s symptomatic presentation; presence of hopelessness; nature of suicidal thinking; previous suicidal behaviour; impulsivity and self-control; and protective factors.

Suicide risk assessment should distinguish between acute and chronic risk. Acute risk might be raised because of recent changes in the person’s circumstances or mental state, while chronic risk is determined by a diagnosis of a mental illness, and social and demographic factors. Bryan and Rudd (2006) suggest a model in which risk is categorized into one of four categories: Baseline, Acute, Chronic high risk, and Chronic high risk with acute exacerbation. Risk level can be described semantically (in words) e.g. as Non-existent, Mild, Moderate, Severe, or Extreme, and the clinical response can be determined accordingly. Others urge use of numbers to describe level of relative or (preferably) absolute risk of completed suicide.

Scale for Suicide Ideation

The Scale for Suicide Ideation (SSI) was developed in 1979 by Aaron T. Beck, Maria Kovacs, and Arlene Weissman to quantify intensity in suicide ideators. It was developed for use by clinicians during semi-structured interviews. The scale contained 19 items rated on a scale from 0 to 2, allowing scores between 0 and 38. The items could be grouped into three categories: “Active Suicidal Desire, Preparation, and Passive Suicidal Desire.” Initial findings showed promising reliability and validity.

Modified Scale for Suicide Ideation

The Modified Scale for Suicide Ideation (MSSI) was developed by Miller et al., using 13 items from the SSI and 5 new items. The modifications increased both reliability and validity. The scale was also changed to range from 0 to 3, yielding a total score ranging from 0 to 54. Joiner found two factors, Suicidal Desire and Ideation, and Resolved Plans and Preparation. The MSSI was also shown to have higher discrimination between groups of suicide ideators and attempters than the BDI, BHS, PSI, and SPS.

Suicide Intent Scale

The Suicide Intent Scale (SIS) was developed in order to assess the severity of suicide attempts. The scale consists of 15 questions which are scaled from 0-2, which take into account both the logistics of the suicide attempt as well as the intent. The scale has high reliability and validity. Completed suicides ranked higher in the severity of the logistics than attempted suicides (it was impossible to measure intent for the completed suicides), and those with multiple attempts had higher scores than those who only attempted suicide once.

Suicidal Affect Behaviour Cognition Scale

The Suicidal Affect Behaviour Cognition Scale (SABCS) is a six-item self-report measure based on both suicide and psychological theory, developed to assess current suicidality for clinical, screening, and research purposes. Substantial empirical evidence was found, from four independent studies, confirming the importance of assessing suicidal affect, behaviours, and cognition as a single suicidal construct. The SABCS was the first suicide risk measure to be developed through both classical test theory (CTT) and item response theory (IRT) psychometric approaches and to show significant improvements over a highly endorsed comparison measure. The SABCS was shown to have higher internal reliability, and to be a better predictor of both future suicidal behaviours and total suicidality over an existing standard.

Suicide Behaviours Questionnaire

Refer to the Suicide Behaviours Questionnaire-Revised.

The Suicide Behaviours Questionnaire (SBQ) is a self-report measure developed by Linehan in 1981. In 1988 it was transformed from a long questionnaire to a short four questions that can be completed in about 5 minutes. Answers are on a Likert scale that ranges in size for each question, based on data from the original questionnaire. It is designed for adults and results tend to correlate with other measures, such as the SSI. It is popular because it is easy to use as a screening tool, but at only four questions, fails to provide detailed information.

Life Orientation Inventory

The Life Orientation Inventory (LOI) is a self-report measure that comes in both a 30 question and 110 question form. Both forms use a 4-point Likert scale to answer items, which are divided into six sub-scales on the longer form: self-esteem vulnerability, over-investment, overdetermined misery, affective domination, alienation, and suicide tenability. This scale has strong reliability and validity, and has been shown to be able to differentiate between control, depressed, possibly suicidal, and highly suicidal individuals. It also contains 3 validity indices, similar to the MMPI. However, while useful, this inventory is now out of print.

Reasons For Living Inventory

The Reasons For Living Inventory (RFL) is theoretically based, and measures the probability of suicide based on the theory that some factors may mitigate suicidal thoughts. It was developed in 1983 by Linehan and colleagues. and contains 48 items answered on a Likert scale from 1 to 6. The measure is divided into six subscales:

  • Survival and coping beliefs;
  • Responsibility to family;
  • Child concerns;
  • Fear of suicide;
  • Fear of social disproval; and
  • Moral objections.

Scores are reported as an average for the total and each sub-scale. The scale is shown to be fairly reliable and valid, but is still mostly seen in research as compared to clinical use. Other variations of the scale include the College Students Reasons for Living Inventory, and the Brief Reasons for Living Inventory. The college students reasons for living inventory replaced the responsibility to family sub-scale with a responsibility to family and friends sub-scale and that replaced the child concerns sub-scale with a college/future concerns sub-scale. The Brief Reasons for Living Inventory uses only 12 of the items from the RFL. Prolonged stress releases hormones that damage over time the hippocampus. The hippocampus is responsible for storing memories according to context (spatial, emotional and social) as well as activating memories according to context. When the hippocampus is damaged, events will be perceived in the wrong context, or memories with the wrong context might be activated.

Nurses Global Assessment of Suicide Risk

The Nurses Global Assessment of Suicide Risk (NGASR) was developed by Cutcliffe and Barker in 2004 to help novice practitioners with assessment of suicide risk, beyond the option of the current lengthy checklists currently available. It is based on 15 items, with some such as “Evidence of a plan to commit suicide” given a weighting of 3, while others, such as “History of psychosis” are weighted with a 1, giving a maximum total score of 25. Scores of 5 or less are considered low level of risk, 6-8 are intermediate level of risk, 9-11 are high level of risk, and 12 or more are very high level of risk. Each item is supported theoretically by studies that have shown a connection between the item and suicide. However, the validity and reliability of the test as a whole have not yet been empirically tested

Demographic Factors

Within the United States, the suicide rate is 11.3 suicides per 100,000 people within the general population.

Age

In the United States, the peak age for suicide is early adulthood, with a smaller peak of incidence in the elderly. On the other hand, there is no second peak in suicide in black men or women, and a much more muted and earlier-peaking rise in suicide amongst non-Hispanic women than their male counterparts. Older white males are the leading demographic group for suicide within the United States, at 47 deaths per 100,000 individuals for non-Hispanic white men over age 85. For Americans aged 65 and older, the rate is 14.3 per 100,000. Suicide rates are also elevated among teens. For every 100,000 individuals within an age group there are 0.9 suicides in ages 10-14, 6.9 among ages 15-19, and 12.7 among ages 20-24.

Sex

China and São Tomé and Príncipe are the only countries in the world where suicide is more common among women than among men.

In the United States, suicide is around 4.5 times more common in men than in women. US men are 5 times as likely to commit suicide within the 15- to 19-year-old demographic, and 6 times as likely as women to commit suicide within the 20- to 24-year-old demographic. Gelder, Mayou and Geddes reported that women are more likely to commit suicide by taking overdose of drugs than men. Transgender individuals are at particularly high risk. Prolonged stress lasting 3 to 5 years, such clinical depression co-morbid with other conditions, can be a major factor in these cases.

Ethnicity and Culture

In the United States white persons and Native Americans have the highest suicide rates, Black persons have intermediate rates, and Hispanic persons have the lowest rates of suicide. However, Native American males in the 15-24 age group have a dramatically higher suicide rate than any other group. A similar pattern is seen in Australia, where Aboriginal people, especially young Aboriginal men, have a much higher rate of suicide than white Australians, a difference which is attributed to social marginalisation, trans-generational trauma, and high rates of alcoholism. A link may be identified between depression and stress, and suicide.

Sexual Orientation

There is evidence of elevated risk of suicide among non-heterosexual individuals (e.g. homosexual or bisexual individuals), especially among adolescents

Biographical and historical Factors

The literature on this subject consistently shows that a family history of committed suicide in first-degree relatives, adverse childhood experiences (parental loss and emotional, physical and sexual abuse), and adverse life situations (unemployment, isolation and acute psychosocial stressors) are associated with suicide risk.

Recent life events can act as precipitants. Significant interpersonal loss and family instability, such as bereavement, poor relationship with family, domestic partner violence, separation, and divorce have all been identified as risk factors. Financial stress, unemployment, and a drop in socioeconomic status can also be triggers for a suicidal crisis. This is also the case for a range of acute and chronic health problems, such as pain syndromes, or diagnoses of conditions like HIV or cancer.

Mental State

Certain clinical mental state features are predictive of suicide. An affective state of hopelessness, in other words a sense that nothing will ever get better, is a powerful predictive feature. High risk is also associated with a state of severe anger and hostility, or with agitation, anxiety, fearfulness, or apprehension. Research domain criteria symptom burdens, particularly the positive and negative valence domains, are associated with time varying risk of suicide. Specific psychotic symptoms, such as grandiose delusions, delusions of thought insertion and mind reading are thought to indicate a higher likelihood of suicidal behaviour. Command hallucinations are often considered indicative of suicide risk, but the empirical evidence for this is equivocal. Another psychiatric illness that is a high risk of suicide is schizophrenia. The risk is particularly higher in younger patients who have insight into the serious effect the illness is likely to have on their lives.

The primary and necessary mental state Federico Sanchez called idiozimia (from idios “self” and zimia “loss”), followed by suicidal thoughts, hopelessness, loss of will power, hippocampal damage due to stress hormones, and finally either the activation of a suicidal belief system, or in the case of panic or anxiety attacks the switching over to an anger attack, are the converging reasons for a suicide to occur.

Suicidal Ideation

Refer to Suicidal Ideation.

Suicidal ideation refers to the thoughts that a person has about suicide. Assessment of suicidal ideation includes assessment of the extent of preoccupation with thoughts of suicide (for example continuous or specific thoughts), specific plans, and the person’s reasons and motivation to attempt suicide.

Planning

Assessment of suicide risk includes an assessment of the degree of planning, the potential or perceived lethality of the suicide method that the person is considering, and whether the person has access to the means to carry out these plans (such as access to a firearm). A suicide plan may include the following elements:

  • Timing;
  • Availability of method;
  • Setting;
  • Actions made towards carrying out the plan (such as obtaining medicines, poisons, rope or a weapon);
  • Choosing and inspecting a setting; and
  • Rehearsing the plan.

The more detailed and specific the suicide plan, the greater the level of risk. The presence of a suicide note generally suggests more premeditation and greater suicidal intent. The assessment would always include an exploration of the timing and content of any suicide note and a discussion of its meaning with the person who wrote it.

Motivation to Die

Suicide risk assessment includes an assessment of the person’s reasons for wanting to commit suicide. Some are due to overwhelming emotions or others can have a deep philosophical belief. The causes are highly varied.

Other Motivations for Suicide

Suicide is not motivated only by a wish to die. Other motivations for suicide include being motivated to end the suffering psychologically and a person suffering from a terminal illness may intend to commit suicide as a means of managing physical pain and/or their way of dealing with possible future atrophy or death.

Reasons to Live

Balanced against reasons to die are the suicidal person’s reasons to live, and an assessment would include an enquiry into the person’s reasons for living and plans for the future.

Past suicidal Acts

There are people who commit suicide the first time they have suicidal thoughts and there are many who have suicidal thoughts and never commit suicide.

Suicide Risk and Mental Illness

All major mental disorders carry an increased risk of suicide. However, 90% of suicides can be traced to depression, linked either to manic-depression (bipolar), major depression (unipolar), schizophrenia or personality disorders, particularly borderline personality disorder. Comorbidity of mental disorders increases suicide risk, especially anxiety or panic attacks.

Anorexia nervosa has a particularly strong association with suicide: the rate of suicide is forty times greater than the general population. The lifetime risk of suicide was 18% in one study, and in another study 27% of all deaths related to anorexia nervosa were due to suicide.

The long-term suicide rate for people with schizophrenia was estimated to be between 10 and 22% based upon longitudinal studies that extrapolated 10 years of illness for lifetime, but a more recent meta-analysis has estimated that 4.9% of schizophrenics will commit suicide during their lifetimes, usually near the illness onset. Risk factors for suicide among people with schizophrenia include a history of previous suicide attempts, the degree of illness severity, comorbid depression or post-psychotic depression, social isolation, and male gender. The risk is higher for the paranoid subtype of schizophrenia, and is highest in the time immediately after discharge from hospital.

While the lifetime suicide risk for mood disorders in general is around 1%, long-term follow-up studies of people who have been hospitalised for severe depression show a suicide risk of up to 13%. People with severe depression are 20 times more likely and people with bipolar disorder are 15 times more likely to die from suicide than members of the general population. Depressed people with agitation, severe insomnia, anxiety symptoms, and co-morbid anxiety disorders are particularly at-risk. Antidepressants have been linked with suicide as Healy (2009) stated that people on antidepressant have the tendency to commit suicide after 10-14 days of commencement of antidepressant.

People with a diagnosis of a personality disorder, particularly borderline, antisocial or narcissistic personality disorders, are at a high risk of suicide. In this group, elevated suicide risk is associated with younger age, comorbid drug addiction and major mood disorders, a history of childhood sexual abuse, impulsive and antisocial personality traits, and recent reduction of psychiatric care, such as recent discharge from hospital. While some people with personality disorders may make manipulative or contingent suicide threats, the threat is likely to be non-contingent when the person is silent, passive, withdrawn, hopeless, and making few demands.

A history of excessive alcohol use is common among people who commit suicide, and alcohol intoxication at the time of the suicide attempt is a common pattern. Meta analytic research conducted in 2015 indicates that a person with co-occurring alcohol use disorder and major depression is more likely to ideate, attempt, and complete suicide than those with individual disorders.

What is the Suicide Behaviours Questionnaire-Revised?

Published on by Andrew Marshall1 Comment

Introduction

The Suicide Behaviors Questionnaire-Revised (SBQ-R) is a psychological self-report questionnaire designed to identify risk factors for suicide in children and adolescents between ages 13 and 18.

Background

The four-question test is filled out by the child and takes approximately five minutes to complete. The questionnaire has been found to be reliable and valid in recent studies. One study demonstrated that the SBQ-R had high internal consistency with a sample of university students. However, another body of research, which evaluated some of the most commonly used tools for assessing suicidal thoughts and behaviours in college-aged students, found that the SBQ-R and suicide assessment tools in general have very little overlap between them. One of the greatest strengths of the SBQ-R is that, unlike some other tools commonly used for suicidality assessment, it asks about future anticipation of suicidal thoughts or behaviours as well as past and present ones and includes a question about lifetime suicidal ideation, plans to commit suicide, and actual attempts.

Question Breakdown, Scoring, and Interpretation

Each of the four questions addresses a specific risk factor: the first concerns presence of suicidal thoughts and attempts, the second concerns frequency of suicidal thoughts, the third concerns the threat level of suicidal attempts, and the fourth concerns likelihood of future suicidal attempts. The first item has often been used on its own in order to assign individuals to a suicidal and a non-suicidal control group for studies. Each question has an individual scale, and each response corresponds to a certain point value.

Domain Breakdown

A maximum score of 18 is possible on the SBQ-R, and the following responses to the 4 questions correspond to the following point values:

Point ValueQuestion 1 ResponseQuestion 2 ResponseQuestion 3 ResponseQuestion 4 Response
0–––Never
11Never1No chance at all
22, 3a, or 3bRarely2a or 2bRather unlikely
3–Sometimes3a or 3bUnlikely
44a or 4bOften–Likely
5–Very often–Rather likely
6–––Very likely

Interpretation of Subscale Scores

A total score of 7 and higher in the general population and a total score of 8 and higher in patients with psychiatric disorders indicates significant risk of suicidal behaviour.