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What is a Suicide Prevention Contract?

Published on by Andrew Marshall2 Comments

Introduction

A suicide prevention contract is a contract that contains an agreement not to attempt/commit suicide.

Refer to Suicidal Ideation, Suicide Awareness, Suicide Prevention, and Assessment of Suicide Risk.

Background

It was historically used by health professionals dealing with depressive clients. Typically, the client was asked to agree to talk with the professional prior to carrying out any decision to commit suicide. Suicide prevention contracts have been shown not to be effective and have risk of harm. Suicide prevention contracts were once a “widely used but overvalued clinical and risk-management technique.” Indeed, it has been argued that such contracts “may in fact increase danger by providing psychiatrists with a false sense of security, thus decreasing their clinical vigilance.” It has also been argued that such contracts can anger or inhibit the client and introduce coercion into therapy.

On This Day … 26 August

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People (Deaths)

  • 1910 – William James, American psychologist and philosopher (b. 1842).

William James

William James (11 January 1842 to 26 August 1910) was an American philosopher, historian, and psychologist, and the first educator to offer a psychology course in the United States. James is considered to be a leading thinker of the late nineteenth century, one of the most influential philosophers of the United States, and the “Father of American psychology”.

Along with Charles Sanders Peirce, James established the philosophical school known as pragmatism, and is also cited as one of the founders of functional psychology. A Review of General Psychology analysis, published in 2002, ranked James as the 14th most eminent psychologist of the 20th century. A survey published in American Psychologist in 1991 ranked James’s reputation in second place, after Wilhelm Wundt, who is widely regarded as the founder of experimental psychology. James also developed the philosophical perspective known as radical empiricism. James’s work has influenced philosophers and academics such as Émile Durkheim, W.E.B. Du Bois, Edmund Husserl, Bertrand Russell, Ludwig Wittgenstein, Hilary Putnam, Richard Rorty, and Marilynne Robinson.

Born into a wealthy family, James was the son of the Swedenborgian theologian Henry James Sr. and the brother of both the prominent novelist Henry James and the diarist Alice James. James trained as a physician and taught anatomy at Harvard, but never practiced medicine. Instead he pursued his interests in psychology and then philosophy. James wrote widely on many topics, including epistemology, education, metaphysics, psychology, religion, and mysticism. Among his most influential books are The Principles of Psychology, a groundbreaking text in the field of psychology; Essays in Radical Empiricism, an important text in philosophy; and The Varieties of Religious Experience, an investigation of different forms of religious experience, including theories on mind-cure.

On This Day … 24 August

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People (Births)

  • 1915 – James Tiptree Jr. (Alice Bradley Sheldon), American psychologist and science fiction author (d. 1987).
  • 1923 – Arthur Jensen, American psychologist and academic (d. 2012).

People (Deaths)

  • 2004 – Elisabeth Kübler-Ross, Swiss-American psychiatrist and academic (b. 1926).

James Tiptree Jr.

Alice Bradley Sheldon (born Alice Hastings Bradley; 24 August 1915 to 19 May 1987) was an American science fiction author better known as James Tiptree Jr., a pen name she used from 1967 to her death. It was not publicly known until 1977 that James Tiptree Jr. was a woman. From 1974 to 1977 she also used the pen name Raccoona Sheldon. Sheldon was inducted into the Science Fiction Hall of Fame in 2012.

She studied for her bachelor of arts degree at American University (1957-1959), going on to achieve a doctorate at George Washington University in Experimental Psychology in 1967. She wrote her doctoral dissertation on the responses of animals to novel stimuli in differing environments. During this time, she wrote and submitted a few science fiction stories under the name James Tiptree Jr., in order to protect her academic reputation.

Arthur Jensen

Arthur Robert Jensen (24 August 1923 to 22 October 2012) was an American psychologist and writer. He was a professor of educational psychology at the University of California, Berkeley. Jensen was known for his work in psychometrics and differential psychology, the study of how and why individuals differ behaviourally from one another.

He was a major proponent of the hereditarian position in the nature and nurture debate, the position that genetics play a significant role in behavioural traits, such as intelligence and personality. He was the author of over 400 scientific papers published in refereed journals and sat on the editorial boards of the scientific journals Intelligence and Personality and Individual Differences.

Jensen was controversial, largely for his conclusions regarding the causes of race-based differences in IQ. A 2019 study found him to be the most controversial intelligence researcher among 55 persons covered.

Elisabeth Kubler-Ross

Elisabeth Kübler-Ross (08 July 1926 to 24 August 2004) was a Swiss-American psychiatrist, a pioneer in near-death studies, and author of the internationally best-selling book, On Death and Dying (1969), where she first discussed her theory of the five stages of grief, also known as the “Kübler-Ross model”.

Kübler-Ross was a 2007 inductee into the National Women’s Hall of Fame, was named by Time as one of the “100 Most Important Thinkers” of the 20th century and was the recipient of nineteen honorary degrees. By July 1982, Kübler-Ross taught 125,000 students in death and dying courses in colleges, seminaries, medical schools, hospitals, and social-work institutions. In 1970, she delivered an Ingersoll Lecture at Harvard University on the theme On Death and Dying.

What is a Neuropsychological Assessment?

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Introduction

Neuropsychological assessment was traditionally carried out to assess the extent of impairment to a particular skill and to attempt to determine the area of the brain which may have been damaged following brain injury or neurological illness.

With the advent of neuroimaging techniques, location of space-occupying lesions can now be more accurately determined through this method, so the focus has now moved on to the assessment of cognition and behaviour, including examining the effects of any brain injury or neuropathological process that a person may have experienced.

A core part of neuropsychological assessment is the administration of neuropsychological tests for the formal assessment of cognitive function, though neuropsychological testing is more than the administration and scoring of tests and screening tools. It is essential that neuropsychological assessment also include an evaluation of the person’s mental status. This is especially true in assessment of Alzheimer’s disease and other forms of dementia. Aspects of cognitive functioning that are assessed typically include orientation, new-learning/memory, intelligence, language, visuoperception, and executive function. However, clinical neuropsychological assessment is more than this and also focuses on a person’s psychological, personal, interpersonal and wider contextual circumstances.

Assessment may be carried out for a variety of reasons, such as:

  • Clinical evaluation, to understand the pattern of cognitive strengths as well as any difficulties a person may have, and to aid decision making for use in a medical or rehabilitation environment.
  • Scientific investigation, to examine a hypothesis about the structure and function of cognition to be tested, or to provide information that allows experimental testing to be seen in context of a wider cognitive profile.
  • Medico-legal assessment, to be used in a court of law as evidence in a legal claim or criminal investigation.

Miller outlined three broad goals of neuropsychological assessment. Firstly, diagnosis, to determine the nature of the underlying problem. Secondly, to understand the nature of any brain injury or resulting cognitive problem (see neurocognitive deficit) and its impact on the individual, as a means of devising a rehabilitation programme or offering advice as to an individual’s ability to carry out certain tasks (for example, fitness to drive, or returning to work). And lastly, assessments may be undertaken to measure change in functioning over time, such as to determine the consequences of a surgical procedure or the impact of a rehabilitation programme over time.

Diagnosis of a Neuropsychological Disorder

Certain types of damage to the brain will cause behavioural and cognitive difficulties. Psychologists can start screening for these problems by using either one of the following techniques or all of these combined:

History TakingThis includes gathering medical history of the patient and their family, presence or absence of developmental milestones, psychosocial history, and character, severity, and progress of any history of complaints. The psychologist can then gauge how to treat the patient and determine if there are any historical determinants for his or her behaviour.
InterviewingPsychologists use structured interviews in order to determine what kind of neurological problem the patient might be experiencing. There are a number of specific interviews, including the Short Portable Mental Status Questionnaire, Neuropsychological Impairment Scale, Patient’s Assessment of Own Functioning, and Structured Interview for the Diagnosis of Dementia.
Test-TakingScores on standardised tests of adequate predictive validity predictor well current and/or future problems. Standardised tests allow psychologists to compare a person’s results with other people’s because it has the same components and is given in the same way. It is therefore representative of the person’s behaviour and cognition. The results of a standardised test are only part of the jigsaw. Further, multidisciplinary investigations (e.g. neuroimaging, neurological) are typically needed to officially diagnose a brain-injured patient.
Intelligence TestingTesting one’s intelligence can also give a clue to whether there is a problem in the brain-behaviour connection. The Wechsler Scales are the tests most often used to determine level of intelligence. The variety of scales available, the nature of the tasks, as well as a wide gap in verbal and performance scores can give clues to whether there is a learning disability or damage to a certain area of the brain.
Testing Other AreasOther areas are also tested when a patient goes through neuropsychological assessment. These can include sensory perception, motor functions, attention, memory, auditory and visual processing, language, problem solving, planning, organisation, speed of processing, and many others. Neuropsychological assessment can test many areas of cognitive and executive functioning to determine whether a patient’s difficulty in function and behaviour has a neuropsychological basis.

Information Gathered from Assessment

Tsatsanis and Volkmar believe that assessment can provide unique information about the type of disorder a patient has which allows the psychologist to come up with a treatment plan. Neuropsychological assessment can clarify the nature of the disorder and determine the cognitive functioning associated with a disorder. Assessment can also allow the psychologist to understand the developmental progress of the disorder in order to predict future problems and come up with a successful treatment package. Different assessments can also determine if a patient will be at risk for a particular disorder. It is important to remember, however, that assessing a patient at one time is not enough to go ahead and continue treatment because of the changes in behaviour that can occur frequently. A patient must be retested multiple times in order to make sure that the current treatment is still the right treatment. For neuropsychological assessments, researchers discover the different areas of the brain that is damaged based on the cognitive and behavioural aspects of the patient.

Benefits of Assessment

The most beneficial factor of neuropsychological assessment is that is provides an accurate diagnosis of the disorder for the patient when it is unclear to the psychologist what exactly they have. 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.

One area where neuropsychological assessments can be beneficial is in forensic cases where the defendant’s competency is being questioned due to possible brain injury or damage. A neuropsychological assessment may show brain damage when neuroimaging has failed. It can also determine whether the individual is faking a disorder (malingering) in order to attain a lesser sentence.

Most neuropsychological testing can be completed in 6 to 12 hours or less. This time, however, does not include the role of the psychologist interpreting the data, scoring the test, making formulations, and writing a formal report.

Qualifications for Conducting Assessments

Neuropsychological assessments are usually conducted by doctoral-level (Ph.D., Psy.D.) psychologists trained in neuropsychology, known as clinical neuropsychologists. The definition and scope of a clinical neuropsychologist is outlined in the widely accepted Houston Conference Guidelines. They will usually have postdoctoral training in neuropsychology, neuroanatomy, and brain function. Most will be licensed and practicing psychologists in their particular field. Recent developments in the field allow for highly trained individuals such as psychometrists to administer selected instruments, though determinations regarding testing results remain the responsibility of the doctor.

On This Day … 23 August

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People (Deaths)

  • 1974 – Roberto Assagioli, Italian psychiatrist and author (b. 1888).
  • 1989 – R. D. Laing, Scottish psychiatrist and author (b. 1927).
  • 2013 – William Glasser, American psychiatrist and author (b. 1925).

Roberto Assagioli

Roberto Assagioli (27 February 1888 to 23 August 1974) was an Italian psychiatrist and pioneer in the fields of humanistic and transpersonal psychology.

Assagioli founded the psychological movement known as psychosynthesis, which is still being developed today by therapists and psychologists, who practice the psychological methods and techniques he developed. His work, expounded in two books and many monographs published as pamphlets, emphasized the possibility of progressive integration, or synthesis, of the personality.

R.D. Laing

Ronald David Laing (07 October 1927 to 23 August 1989), usually cited as R.D. Laing, was a Scottish psychiatrist who wrote extensively on mental illness – in particular, the experience of psychosis.

Laing’s views on the causes and treatment of psychopathological phenomena were influenced by his study of existential philosophy and ran counter to the chemical and electroshock methods that had become psychiatric orthodoxy. Taking the expressed feelings of the individual patient or client as valid descriptions of personal experience rather than simply as symptoms of mental illness, Laing regarded schizophrenia as a theory not a fact. Though associated in the public mind with anti-psychiatry he rejected the label. Politically, he was regarded as a thinker of the New Left. Laing was portrayed by David Tennant in the 2017 film Mad to Be Normal.

William Glasser

William Glasser (11 May 1925 to 23 August 2013) was an American psychiatrist.

Glasser was the developer of W. Edwards Deming’s workplace ideas, reality therapy and choice theory. His innovations for individual counselling, work environments and school, highlight personal choice, personal responsibility and personal transformation. Glasser positioned himself in opposition to conventional mainstream psychiatrists, who focus instead on classifying psychiatric syndromes as “illnesses” and prescribe psychotropic medications to treat mental disorders.

Based on his wide-ranging and consulting clinical experience, Glasser applied his theories to broader social issues, such as education, management, and marriage, to name a few. As a public advocate, Glasser warned the general public of potential detriments caused by older generations of psychiatry, wedded to traditional diagnosing of patients as having mental illnesses (brain disorders) and prescribing medications. In his view, patients simply act out their unhappiness and lack of meaningful personal connection with important people in their life. Glasser advocated educating the general public about mental health issues; offering, post-modern frameworks for finding and following healthy therapeutic direction.

On This Day … 21 August

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People (Births)

  • 1921 – Reuven Feuerstein, Romanian-Israeli psychologist and academic (d. 2014).

People (Deaths)

Reuven Feuerstein

Reuven Feuerstein (21 August 1921 to 29 April 2014) was an Israeli clinical, developmental, and cognitive psychologist, known for his theory of intelligence which states “it is not ‘fixed’, but rather modifiable”. Feuerstein is recognised for his work in developing the theories and applied systems of structural cognitive modifiability, mediated learning experience, cognitive map, deficient cognitive functions, learning propensity assessment device, instrumental enrichment programmes, and shaping modifying environments. These interlocked practices provide educators with the skills and tools to systematically develop students’ cognitive functions and operations to build meta-cognition.

Feuerstein was the founder and director of the International Centre for the Enhancement of Learning Potential (ICELP) in Jerusalem, Israel. For more than 50 years, Feuerstein’s theories and applied systems have been implemented in both clinical and classroom settings internationally, with more than 80 countries applying his work. Feuerstein’s theory on the malleability of intelligence has led to more than 2,000 scientific research studies and countless case studies with various learning populations.

Helen Bamber

Helen Rae Bamber OBE, née Helen Balmuth (01 May 1925 to 21 August 2014), was a British psychotherapist and human rights activist. She worked with Holocaust survivors in Germany after the concentration camps were liberated in 1945. In 1947, she returned to Britain and continued her work, helping to establish Amnesty International and later co-founding the Medical Foundation for the Care of Victims of Torture. In 2005, she created the Helen Bamber Foundation to help survivors of human rights violations.

Throughout her life, Bamber worked with those who were the most marginalised: Holocaust survivors, asylum-seekers, refugees, victims of the conflict in Northern Ireland, trafficked men, women and children, survivors of genocide, torture, rape, female genital mutilation, British former Far East prisoners of war, former hostages and other people who suffered torture abroad. She worked in many countries including Gaza, Kosovo, Uganda, Turkey and Northern Ireland.

What is Midazolam?

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Introduction

Midazolam, sold under the brand name Versed, among others, is a benzodiazepine medication used for anaesthesia, procedural sedation, trouble sleeping, and severe agitation.

It works by inducing sleepiness, decreasing anxiety, and causing a loss of ability to create new memories. It is also useful for the treatment of seizures. Midazolam can be given by mouth, intravenously, or injection into a muscle, by spraying into the nose, or through the cheek. When given intravenously, it typically begins working within five minutes; when injected into a muscle, it can take fifteen minutes to begin working. Effects last for between one and six hours.

Side effects can include a decrease in efforts to breathe, low blood pressure, and sleepiness. Tolerance to its effects and withdrawal syndrome may occur following long-term use. Paradoxical effects, such as increased activity, can occur especially in children and older people. There is evidence of risk when used during pregnancy but no evidence of harm with a single dose during breastfeeding. It belongs to the benzodiazepine class of drugs and works by increasing the activity of the GABA neurotransmitter in the brain.

Midazolam was patented in 1974 and came into medical use in 1982. It is on the World Health Organisation’s List of Essential Medicines. Midazolam is available as a generic medication. In many countries, it is a controlled substance.

Brief History

Midazolam is among about 35 benzodiazepines currently used medically, and was synthesized in 1975 by Walser and Fryer at Hoffmann-LaRoche, Inc in the United States. Owing to its water solubility, it was found to be less likely to cause thrombophlebitis than similar drugs. The anticonvulsant properties of midazolam were studied in the late 1970s, but not until the 1990s did it emerge as an effective treatment for convulsive status epilepticus. As of 2010, it is the most commonly used benzodiazepine in anaesthetic medicine. In acute medicine, midazolam has become more popular than other benzodiazepines, such as lorazepam and diazepam, because it is shorter lasting, is more potent, and causes less pain at the injection site. Midazolam is also becoming increasingly popular in veterinary medicine due to its water solubility. In 2018 it was revealed the CIA considered using Midazolam as a “truth serum” on terrorist suspects in project “Medication”.

Medical Uses

Seizures

Midazolam is sometimes used for the acute management of seizures. Long-term use for the management of epilepsy is not recommended due to the significant risk of tolerance (which renders midazolam and other benzodiazepines ineffective) and the significant side effect of sedation. A benefit of midazolam is that in children it can be given in the cheek or in the nose for acute seizures, including status epilepticus. Midazolam is effective for status epilepticus that has not improved following other treatments or when intravenous access cannot be obtained, and has advantages of being water-soluble, having a rapid onset of action and not causing metabolic acidosis from the propylene glycol vehicle (which is not required due to its solubility in water), which occurs with other benzodiazepines.

Drawbacks include a high degree of breakthrough seizures – due to the short half-life of midazolam – in over 50% of people treated, as well as treatment failure in 14-18% of people with refractory status epilepticus. Tolerance develops rapidly to the anticonvulsant effect, and the dose may need to be increased by several times to maintain anticonvulsant therapeutic effects. With prolonged use, tolerance and tachyphylaxis can occur and the elimination half-life may increase, up to days. There is evidence buccal and intranasal midazolam is easier to administer and more effective than rectally administered diazepam in the emergency control of seizures.

Procedural Sedation

Intravenous midazolam is indicated for procedural sedation (often in combination with an opioid, such as fentanyl), for preoperative sedation, for the induction of general anaesthesia, and for sedation of people who are ventilated in critical care units. Midazolam is superior to diazepam in impairing memory of endoscopy procedures, but propofol has a quicker recovery time and a better memory-impairing effect. It is the most popular benzodiazepine in the intensive care unit (ICU) because of its short elimination half-life, combined with its water solubility and its suitability for continuous infusion. However, for long-term sedation, lorazepam is preferred due to its long duration of action, and propofol has advantages over midazolam when used in the ICU for sedation, such as shorter weaning time and earlier tracheal extubation.

Midazolam is sometimes used in neonatal intensive care units. When used, additional caution is required in newborns; midazolam should not be used for longer than 72 hours due to risks of tachyphylaxis, and the possibility of development of a benzodiazepine withdrawal syndrome, as well as neurological complications. Bolus injections should be avoided due to the increased risk of cardiovascular depression, as well as neurological complications. Midazolam is also sometimes used in newborns who are receiving mechanical ventilation, although morphine is preferred, owing to its better safety profile for this indication.

Sedation using midazolam can be used to relieve anxiety and manage behaviour in children undergoing dental treatment.

Agitation

Midazolam, in combination with an antipsychotic drug, is indicated for the acute management of schizophrenia when it is associated with aggressive or out-of-control behaviour.

End of Life Care

In the final stages of end-of-life care, midazolam is routinely used at low doses via subcutaneous injection to help with agitation, myoclonus, restlessness or anxiety in the last hours or days of life. At higher doses during the last weeks of life, midazolam is considered a first line agent in palliative continuous deep sedation therapy when it is necessary to alleviate intolerable suffering not responsive to other treatments, but the need for this is rare.

Contraindications

Benzodiazepines require special precaution if used in the elderly, during pregnancy, in children, in alcohol- or other drug-dependent individuals or those with comorbid psychiatric disorders.[31] Additional caution is required in critically ill patients, as accumulation of midazolam and its active metabolites may occur.[32] Kidney or liver impairments may slow down the elimination of midazolam leading to prolonged and enhanced effects.[33][34] Contraindications include hypersensitivity, acute narrow-angle glaucoma, shock, hypotension, or head injury. Most are relative contraindications.

Side Effects

Refer to Long-term Effects of Benzodiazepine Use.

Side effects of midazolam in the elderly are listed above. People experiencing amnesia as a side effect of midazolam are generally unaware their memory is impaired, unless they had previously known it as a side effect.

Long-term use of benzodiazepines has been associated with long-lasting deficits of memory, and show only partial recovery six months after stopping benzodiazepines. It is unclear whether full recovery occurs after longer periods of abstinence. Benzodiazepines can cause or worsen depression. Paradoxical excitement occasionally occurs with benzodiazepines, including a worsening of seizures. Children and elderly individuals or those with a history of excessive alcohol use and individuals with a history of aggressive behaviour or anger are at increased risk of paradoxical effects. Paradoxical reactions are particularly associated with intravenous administration. After night-time administration of midazolam, residual ‘hangover’ effects, such as sleepiness and impaired psychomotor and cognitive functions, may persist into the next day. This may impair the ability of users to drive safely and may increase the risk of falls and hip fractures. Sedation, respiratory depression and hypotension due to a reduction in systematic vascular resistance, and an increase in heart rate can occur. If intravenous midazolam is given too quickly, hypotension may occur. A “midazolam infusion syndrome” may result from high doses, and is characterised by delayed arousal hours to days after discontinuation of midazolam, and may lead to an increase in the length of ventilatory support needed.

In susceptible individuals, midazolam has been known to cause a paradoxical reaction, a well-documented complication with benzodiazepines. When this occurs, the individual may experience anxiety, involuntary movements, aggressive or violent behaviour, uncontrollable crying or verbalisation, and other similar effects. This seems to be related to the altered state of consciousness or disinhibition produced by the drug. Paradoxical behaviour is often not recalled by the patient due to the amnesia-producing properties of the drug. In extreme situations, flumazenil can be administered to inhibit or reverse the effects of midazolam. Antipsychotic medications, such as haloperidol, have also been used for this purpose.

Midazolam is known to cause respiratory depression. In healthy humans, 0.15 mg/kg of midazolam may cause respiratory depression, which is postulated to be a central nervous system (CNS) effect. When midazolam is administered in combination with fentanyl, the incidence of hypoxemia or apnoea becomes more likely.

Although the incidence of respiratory depression/arrest is low (0.1-0.5%) when midazolam is administered alone at normal doses, the concomitant use with CNS acting drugs, mainly analgesic opiates, may increase the possibility of hypotension, respiratory depression, respiratory arrest, and death, even at therapeutic doses. Potential drug interactions involving at least one CNS depressant were observed for 84% of midazolam users who were subsequently required to receive the benzodiazepine antagonist flumazenil. Therefore, efforts directed toward monitoring drug interactions and preventing injuries from midazolam administration are expected to have a substantial impact on the safe use of this drug

Pregnancy and Breastfeeding

Midazolam, when taken during the third trimester of pregnancy, may cause risk to the neonate, including benzodiazepine withdrawal syndrome, with possible symptoms including hypotonia, apnoeic spells, cyanosis, and impaired metabolic responses to cold stress. Symptoms of hypotonia and the neonatal benzodiazepine withdrawal syndrome have been reported to persist from hours to months after birth. Other neonatal withdrawal symptoms include hyperexcitability, tremor, and gastrointestinal upset (diarrhoea or vomiting). Breastfeeding by mothers using midazolam is not recommended.

Elderly

Additional caution is required in the elderly, as they are more sensitive to the pharmacological effects of benzodiazepines, metabolise them more slowly, and are more prone to adverse effects, including drowsiness, amnesia (especially anterograde amnesia), ataxia, hangover effects, confusion, and falls.

Tolerance, Dependence, and Withdrawal

A benzodiazepine dependence occurs in about one-third of individuals who are treated with benzodiazepines for longer than 4 weeks, which typically results in tolerance and benzodiazepine withdrawal syndrome when the dose is reduced too rapidly. Midazolam infusions may induce tolerance and a withdrawal syndrome in a matter of days. The risk factors for dependence include dependent personality, use of a benzodiazepine that is short-acting, high potency and long-term use of benzodiazepines. Withdrawal symptoms from midazolam can range from insomnia and anxiety to seizures and psychosis. Withdrawal symptoms can sometimes resemble a person’s underlying condition. Gradual reduction of midazolam after regular use can minimise withdrawal and rebound effects. Tolerance and the resultant withdrawal syndrome may be due to receptor down-regulation and GABAA receptor alterations in gene expression, which causes long-term changes in the function of the GABAergic neuronal system.

Chronic users of benzodiazepine medication who are given midazolam experience reduced therapeutic effects of midazolam, due to tolerance to benzodiazepines. Prolonged infusions with midazolam results in the development of tolerance; if midazolam is given for a few days or more a withdrawal syndrome can occur. Therefore, preventing a withdrawal syndrome requires that a prolonged infusion be gradually withdrawn, and sometimes, continued tapering of dose with an oral long-acting benzodiazepine such as clorazepate dipotassium. When signs of tolerance to midazolam occur during intensive care unit sedation the addition of an opioid or propofol is recommended. Withdrawal symptoms can include irritability, abnormal reflexes, tremors, clonus, hypertonicity, delirium and seizures, nausea, vomiting, diarrhoea, tachycardia, hypertension, and tachypnoea. In those with significant dependence, sudden discontinuation may result in withdrawal symptoms such as status epilepticus that may be fatal.

Overdose

Refer to Benzodiazepine Overdose.

A midazolam overdose is considered a medical emergency and generally requires the immediate attention of medical personnel. Benzodiazepine overdose in healthy individuals is rarely life-threatening with proper medical support; however, the toxicity of benzodiazepines increases when they are combined with other CNS depressants such as alcohol, opioids, or tricyclic antidepressants. The toxicity of benzodiazepine overdose and risk of death is also increased in the elderly and those with obstructive pulmonary disease or when used intravenously. Treatment is supportive; activated charcoal can be used within an hour of the overdose. The antidote for an overdose of midazolam (or any other benzodiazepine) is flumazenil. While effective in reversing the effects of benzodiazepines it is not used in most cases as it may trigger seizures in mixed overdoses and benzodiazepine dependent individuals.

Symptoms of midazolam overdose can include:

  • Ataxia.
  • Dysarthria.
  • Nystagmus.
  • Slurred speech.
  • Somnolence (difficulty staying awake).
  • Mental confusion.
  • Hypotension.
  • Respiratory arrest.
  • Vasomotor collapse.
  • Impaired motor functions.
    • Impaired reflexes.
    • Impaired coordination.
    • Impaired balance.
  • Dizziness.
  • Coma.
  • Death.

Detection in Body Fluids

Concentrations of midazolam or its major metabolite, 1-hydroxymidazolam glucuronide, may be measured in plasma, serum, or whole blood to monitor for safety in those receiving the drug therapeutically, to confirm a diagnosis of poisoning in hospitalised patients, or to assist in a forensic investigation of a case of fatal overdosage. Patients with renal dysfunction may exhibit prolongation of elimination half-life for both the parent drug and its active metabolite, with accumulation of these two substances in the bloodstream and the appearance of adverse depressant effects.

Interactions

Protease inhibitors, nefazodone, sertraline, grapefruit, fluoxetine, erythromycin, diltiazem, clarithromycin inhibit the metabolism of midazolam, leading to a prolonged action. St John’s wort, rifapentine, rifampin, rifabutin, phenytoin enhance the metabolism of midazolam leading to a reduced action. Sedating antidepressants, antiepileptic drugs such as phenobarbital, phenytoin and carbamazepine, sedative antihistamines, opioids, antipsychotics and alcohol enhance the sedative effects of midazolam. Midazolam is metabolised almost completely by cytochrome P450-3A4. Atorvastatin administration along with midazolam results in a reduced elimination rate of midazolam. St John’s wort decreases the blood levels of midazolam. Grapefruit juice reduces intestinal 3A4 and results in less metabolism and higher plasma concentrations.

Pharmacology

Midazolam is a short-acting benzodiazepine in adults with an elimination half-life of 1.5-2.5 hours. In the elderly, as well as young children and adolescents, the elimination half-life is longer. Midazolam is metabolised into an active metabolite alpha1-hydroxymidazolam. Age-related deficits, renal and liver status affect the pharmacokinetic factors of midazolam as well as its active metabolite. However, the active metabolite of midazolam is minor and contributes to only 10% of biological activity of midazolam. Midazolam is poorly absorbed orally, with only 50% of the drug reaching the bloodstream. Midazolam is metabolised by cytochrome P450 (CYP) enzymes and by glucuronide conjugation. The therapeutic as well as adverse effects of midazolam are due to its effects on the GABAA receptors; midazolam does not activate GABAA receptors directly but, as with other benzodiazepines, it enhances the effect of the neurotransmitter GABA on the GABAA receptors (↑ frequency of Cl− channel opening) resulting in neural inhibition. Almost all of the properties can be explained by the actions of benzodiazepines on GABAA receptors. This results in the following pharmacological properties being produced: sedation, induction of sleep, reduction in anxiety, anterograde amnesia, muscle relaxation and anticonvulsant effects.

Society and Culture

Cost

Midazolam is available as a generic medication.

Availability

Midazolam is available in the United States as a syrup or as an injectable solution.

Dormicum brand midazolam is marketed by Roche as white, oval, 7.5-mg tablets in boxes of two or three blister strips of 10 tablets, and as blue, oval, 15-mg tablets in boxes of two (Dormonid 3x) blister strips of 10 tablets. The tablets are imprinted with “Roche” on one side and the dose of the tablet on the other side. Dormicum is also available as 1-, 3-, and 10-ml ampoules at a concentration of 5 mg/ml. Another manufacturer, Novell Pharmaceutical Laboratories, makes it available as Miloz in 3- and 5-ml ampoules. Midazolam is the only water-soluble benzodiazepine available. Another maker is Roxane Laboratories; the product in an oral solution, Midazolam HCl Syrup, 2 mg/ml clear, in a red to purplish-red syrup, cherry in flavour. It becomes soluble when the injectable solution is buffered to a pH of 2.9-3.7. Midazolam is also available in liquid form. It can be administered intramuscularly, intravenously, intrathecally, intranasally, buccally, or orally.

Legal Status

In the Netherlands, midazolam is a List II drug of the Opium Law. Midazolam is a Schedule IV drug under the Convention on Psychotropic Substances. In the United Kingdom, midazolam is a Schedule 3/Class C controlled drug. In the United States, midazolam (DEA number 2884) is on the Schedule IV list of the Controlled Substances Act as a non-narcotic agent with low potential for abuse.

Marketing Authorisation

In 2011, the European Medicines Agency (EMA) granted a marketing authorisation for a buccal application form of midazolam, sold under the trade name Buccolam. Buccolam was approved for the treatment of prolonged, acute, convulsive seizures in people from three months to less than 18 years of age. This was the first application of a paediatric-use marketing authorisation.

Use in Executions

The drug has been introduced for use in executions by lethal injection in certain jurisdictions in the United States in combination with other drugs. It was introduced to replace pentobarbital after the latter’s manufacturer disallowed that drug’s use for executions. Midazolam acts as a sedative to render the condemned prisoner unconscious, at which time vecuronium bromide and potassium chloride are administered, stopping the prisoner’s breathing and heart, respectively.

Midazolam has been used as part of a three-drug cocktail, with vecuronium bromide and potassium chloride in Florida and Oklahoma prisons. Midazolam has also been used along with hydromorphone in a two-drug protocol in Ohio and Arizona.

The usage of midazolam in executions became controversial after condemned inmate Clayton Lockett apparently regained consciousness and started speaking midway through his 2014 execution when the state of Oklahoma attempted to execute him with an untested three-drug lethal injection combination using 100 mg of midazolam. Prison officials reportedly discussed taking him to a hospital before he was pronounced dead of a heart attack 40 minutes after the execution began. An observing doctor stated that Lockett’s vein had ruptured. It is not clear which drug or drugs caused his death or what quantities of vecuronium bromide and potassium chloride were released before the execution was cancelled.

Notable Incidents

The state of Florida used midazolam to execute William Frederick Happ in October 2013.

The state of Ohio used midazolam in the execution of Dennis McGuire in January 2014; it took McGuire 24 minutes to die after the procedure started, and he gasped and appeared to be choking during that time, leading to questions about the dosing and timing of the drug administration, as well as the choice of drugs.

The execution of Ronald Bert Smith in the state of Alabama on 08 December 2016, “went awry soon after (midazolam) was administered” again putting the effectiveness of the drug in question.

In October 2016, the state of Ohio announced that it would resume executions in January 2017, using a formulation of midazolam, vecuronium bromide, potassium chloride, but this was blocked by a Federal judge. On 26 July 2017, Ronald Phillips was executed with a three-drug cocktail including midazolam after the Supreme Court refused to grant a stay.[86] Prior to this, the last execution in Ohio had been that of Dennis McGuire. Murderer Gary Otte’s lawyers unsuccessfully challenged his Ohio execution, arguing that midazolam might not protect him from serious pain when the other drugs are administered. He died without incident in about 14 minutes on 13 September 2017.

On 24 April 2017, the state of Arkansas carried out a double-execution of Jack Harold Jones, 52, and Marcel Williams, 46. The state of Arkansas attempted to execute eight people before its supply of midazolam expired on 30 April 2017. Two of them were granted a stay of execution, and another, Ledell T. Lee, 51, was executed on 20 April 2017.

Legal Challenges

In Glossip v. Gross, attorneys for three Oklahoma inmates argued that midazolam could not achieve the level of unconsciousness required for surgery, meaning severe pain and suffering was likely. They argued that midazolam was cruel and unusual punishment and thus contrary to the Eighth Amendment to the United States Constitution. In June 2015, the US Supreme Court ruled that they had failed to prove that midazolam was cruel and unusual when compared to known, available alternatives.

The state of Nevada is also known to use midazolam in execution procedures. In July 2018, one of the manufacturers accused state officials of obtaining the medication under false pretences. This incident was the first time a drug company successfully, though temporarily, halted an execution. A previous attempt in 2017, to halt an execution in the state of Arizona by another drug manufacturer was not successful.

What is Metapsychology?

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Introduction

Metapsychology (Greek: meta ‘beyond, transcending’, and ψυχολογία ‘psychology‘) is that aspect of any psychological theory which refers to the structure of the theory itself (hence the prefix “meta”) rather than to the entity it describes.

The psychology is about the psyche; the metapsychology is about the psychology. The term is used mostly in discourse about psychoanalysis, the psychology developed by Sigmund Freud, which was at its time regarded as a branch of science (with roots in the work of Freud’s scientific mentors and predecessors, especially Helmholtz, Brucke, Charcot, and Janet), or, more recently, as a hermeneutics of understanding (with roots in Freud’s literary sources, especially Sophocles and, to a lesser extent, Goethe and Shakespeare). Interest on the possible scientific status of psychoanalysis has been renewed in the emerging discipline of neuropsychoanalysis, whose major exemplar is Mark Solms. The hermeneutic vision of psychoanalysis is the focus of influential works by Donna Orange.

Freud and the als ob Problem

Psychoanalytic metapsychology is concerned with the fundamental structure and concepts of Freudian theory. Sigmund Freud first used the term on 13 February 1896 in a letter to Wilhelm Fliess, to refer to his addition of unconscious processes to the conscious ones of traditional psychology. On 10 March 1898, he wrote to Fiess: “It seems to me that (German: als ob) the theory of wish fulfilment has brought only the psychological solution and not the biological – or, rather, metapsychical – one. (I am going to ask you seriously, by the way, whether I may use the name metapsychology for my psychology that leads behind consciousness).”

Three years after completing his unpublished Project for a Scientific Psychology, Freud’s optimism had completely vanished. In a letter dated September 22 of that year he told Fliess: “I am not at all in disagreement with you, not at all inclined to leave psychology hanging in the air without an organic basis. But apart from this conviction, I do not know how to go on, neither theoretically nor therapeutically, and therefore must behave as if [als läge] only the psychological were under consideration. Why I cannot fit it together [the organic and the psychological] I have not even begun to fathom”. “When, in his ‘Autobiographical Study’ of 1925, Freud called his metapsychology a ‘speculative superstructure’…the elements of which could be abandoned or changed once proven inadequate, he was, in the terminology of Kant’s Critique of Judgement, proposing a psychology als ob or as if – a heuristic model of mental functioning that did not necessarily correspond with external reality.”

A salient example of Freud’s own metapsychology is his characterisation of psychoanalysis as a “simultaneously closed system, fundamentally unrelated and impervious to the external world and as an open system inherently connected and responsive to environmental influence.

In the 1910s, Freud wrote a series of twelve essays, to be collected as Preliminaries to a Metapsychology. Five of these were published independently under the titles: “Instincts and Their Vicissitudes,” “Repression,” “The Unconscious,” “A Metapsychological Supplement to the Theory of Dreams,” and “Mourning and Melancholia.” The remaining seven remained unpublished, an expression of Freud’s ambivalence about his own attempts to articulate the whole of his vision of psychoanalysis. In 1919 he wrote to Lou Andreas-Salome, “Where is my Metapsychology? In the first place it remains unwritten”. In 1920 he published Beyond the Pleasure Principle, a text with metaphysical ambitions.

Midcentury psychoanalyst David Rapaport defined the term thus: “Books on psychoanalysis usually deal with its clinical theory… there exists, however, a fragmentary—yet consistent—general theory of psychoanalysis, which comprises the premises of the special (clinical) theory, the concepts built on it, and the generalizations derived from it… named metapsychology.”

Freud’s Metapsychology

  • The topographical point of view: the psyche operates at different levels of consciousness – unconscious, preconscious, and conscious.
  • The dynamic point of view: the notion that there are psychological forces which may conflict with one another at work in the psyche.
  • The economic point of view: the psyche contains charges of energy which are transferred from one element of the psyche to another.
  • The structural point of view: the psyche consists of configurations of psychological processes which operate in different ways and reveal different rates of change – the ego, the id, and the superego.
  • The genetic point of view: the origins – or “genesis” – of psychological processes can be found in developmentally previous psychological processes.

Ego psychologist Heinz Hartmann also added ‘the adaptive” point of view’ to Freud’s metapsychology, although Lacan who interpreted metapsychology as the symbolic, the Real, and the imaginary, said “the dimension discovered by analysis is the opposite of anything which progresses through adaptation”

Criticism

Freud’s metapsychology has faced criticism, mainly from ego psychology. Object relations theorists such as Melanie Klein, shifted the focus away from intrapsychic conflicts and towards the dynamics of interpersonal relationships, leading to a unifocal theory of development that focused on the mother-child relationship. Most ego psychologists saw the structural point of view, Freud’s latest metapsychology, as the most important. Some proposed that only the structural point of view be kept in metapsychology, because the topographical point of view made an unnecessary distinction between the unconscious and the preconscious (Arlow & Brenner) and because the economic point of view was viewed as redundant (Gill).

What is a Mental Health Care Navigator?

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Introduction

A mental health care navigator is an individual who assists patients and families to find appropriate mental health caregivers, facilities and services. Individuals who are care navigators are often also trained therapists and doctors.

Overview

The need for mental health care navigators arises from the fragmentation of the mental health industry, which can often leave patients with more questions than answers. Care navigators work closely with patients and families through discussion and collaboration to provide information on best options and referrals to healthcare professionals, facilities, and organisations specialising in the patients’ needs. The difference between other mental health professionals and a care navigator is that a care navigator provides information and directs a patient to the best help rather than offering treatment. Still, care navigators may provide diagnosis and treatment planning.

Mental health care navigation is also sometimes provided by self-help books. Lloyd I. Sederer, M.D.’s The Family Guide to Mental Healthcare (W.W. Norton & Company, 2013) is a resource for patients and families searching for guidance in the mental health industry. Publishers Weekly called it a “thoughtful, compassionate, and fact-packed guide for recognizing illness and getting help.” It provides information to patients and families about recognising symptoms of mental illness, how to get diagnosis and how to choose the right therapists and treatments.

Terminology

Many mental health organisations use “navigator” and “navigation” to describe the service of providing guidance through the health care industry. Care navigators are also sometimes referred to as “system navigators.” One type of care navigator is an “educational consultant.”

Models

Models for mental health care navigation can involve many scenarios from a brief consultation to an extended process with follow-up. They offer referrals, assistance with insurance and other financial matters and general support. A highly detailed method of care navigation with long-term follow up was developed in 2011 by San Francisco-based psychiatrist and mental health expert Eli Merritt, M.D. His model involves what he calls the “3 R’s” of mental health care: “Research, Resources, and Referrals.”

It involves four steps:

Assessment & Needs IdentificationIn this preliminary, exploratory phase, care navigators meet with the individual or family seeking help. Patient history and needs are identified. Both the patient and the care navigator think through short- and long-term goals and levels of treatment sought.
Dialogue & Plan FormationThrough discussion and collaboration, both the patient and care navigator brainstorm next steps, establishing a plan that is specific to the patient’s needs.
Care CoordinationAfter information gathering and brainstorming, doctors, therapists, and other mental health options are provided to the patient. Questions of affordability arise, and patients are advised toward the best solutions for their conditions and circumstances.
ContinuityAfter guiding patients to healthcare providers, care navigators maintain communication and continuity with patients, offering assistance with any future obstacles that might arise.

On This Day … 20 August

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People (Births)

  • 1913 – Roger Wolcott Sperry, American neuropsychologist and neurobiologist, Nobel Prize laureate (d. 1994).

People (Deaths)

  • 1985 – Donald O. Hebb, Canadian psychologist and academic (b. 1904).

Roger Wolcott Sperry

Roger Wolcott Sperry (20 August 1913 to 17 April 1994) was an American neuropsychologist, neurobiologist and Nobel laureate who, together with David Hunter Hubel and Torsten Nils Wiesel, won the 1981 Nobel Prize in Physiology and Medicine for his work with split-brain research. A Review of General Psychology survey, published in 2002, ranked Sperry as the 44th most cited psychologist of the 20th century.

Education

Sperry went to Hall High School in West Hartford, Connecticut, where he was a star athlete in several sports, and did well enough academically to win a scholarship to Oberlin College. At Oberlin, he was captain of the basketball team, and he also took part in varsity baseball, football, and track. He also worked at a café on campus to help support himself. Sperry was an English major, but he took an Intro to Psychology class taught by a Professor named R.H. Stetson who had worked with William James, the father of American Psychology. This class sparked Sperry’s interest in the brain and how it can change. Stetson was disabled and had trouble getting around so Sperry would help him out by driving him to and from wherever he needed to go. This included taking Stetson to lunch with his colleagues. Sperry would just sit at the end of the table and listen to Stetson and his colleagues discuss their research and other psychological interests. This increased Sperry’s interest in Psychology even more and after he received his undergraduate degree in English from Oberlin he decided to stay and get his master’s degree in Psychology. He received his bachelor’s degree in English in 1935 and a master’s degree in psychology in 1937. He received his Ph.D. in zoology from the University of Chicago in 1941, supervised by Paul A. Weiss. Sperry then did postdoctoral research with Karl Lashley at Harvard University though most of his time was spent with Lashley at the Yerkes Primate Research Centre in Orange Park, Florida.

Career

In 1942, Sperry began work at the Yerkes Laboratories of Primate Biology, then a part of Harvard University. There he focused on experiments involving the rearranging of motor and sensory nerves. He left in 1946 to become an assistant professor, and later associate professor, at the University of Chicago. In 1949, during a routine chest x-ray, there was evidence of tuberculosis. He was sent to Saranac Lake in the Adironack Mountains in New York for treatment. It was during this time when he began writing his concepts of the mind and brain, and was first published in the American Scientist in 1952. In 1952, he became the Section Chief of Neurological Diseases and Blindness at the National Institutes of Health and finished out the year at the Marine Biology Laboratory in Coral Gables, Florida. Sperry went back to The University of Chicago in 1952 and became an Associate Professor of Psychology. He was not offered tenure at Chicago and planned to move to Bethesda, Maryland but was held up by a delay in construction at the National Institutes of Health. During this time Sperry’s friend Victor Hepburn invited him to lecture about his research at a symposium. There were professors from the California Institute of Technology in the audience of the symposium who, after listening to Sperry’s lecture, were so impressed with him they offered him a job as the Hixson Professor of Psychobiology. In 1954, he accepted the position as a professor at the California Institute of Technology (Caltech as Hixson Professor of Psychobiology) where he performed his most famous experiments with Joseph Bogen, MD and many students including Michael Gazzaniga.

Under the supervision of Paul Weiss while earning his Ph.D. at the University of Chicago, Sperry became interested in neuronal specificity and brain circuitry and began questioning the existing concepts about these two topics. He asked the simple question first asked in his Introduction to Psychology class at Oberlin: Nature or nurture? He began a series of experiments in an attempt to answer this question. Sperry crosswired the motor nerves of rats’ legs so the left nerve controlled the right leg and vice versa. He would then place the rats in a cage that had an electric grid on the bottom separated into four sections. Each leg of the rat was placed into one of the four sections of the electric grid. A shock was administered to a specific section of the grid, for example the grid where the rat’s left back leg was located would receive a shock. Every time the left paw was shocked the rat would lift his right paw and vice versa. Sperry wanted to know how long it would take the rat to realize he was lifting the wrong paw. After repeated tests Sperry found that the rats never learned to lift up the correct paw, leading him to the conclusion that some things are just hardwired and cannot be relearned. In Sperry’s words, “no adaptive functioning of the nervous system took place.” During Sperry’s postdoctoral years with Karl Lashley at Harvard and at the Yerkes Laboratories of Primate Biology in Orange Park, Florida, he continued his work on neuronal specificity that he had begun as a doctoral student and initiated a new series of studies involving salamanders. The optic nerves were sectioned and the eyes rotated 180 degrees. The question was whether vision would be normal after regeneration or would the animal forever view the world as “upside down” and right-left reversed. Should the latter prove to be the case, it would mean that the nerves were somehow “guided” back to their original sites of termination. Restoration of normal vision (i.e. “seeing” the world in a “right-side-up” orientation) would mean that the regenerating nerves had terminated in new sites, quite different from the original ones. The animals reacted as though the world was upside down and reversed from right to left. Furthermore, no amount of training could change the response. These studies, which provided strong evidence for nerve guidance by “intricate chemical codes under genetic control” (1963) culminated in Sperry’s chemoaffinity hypothesis (1951).

Sperry later served on the Board of Trustees and as Professor of Psychobiology Emeritus at California Institute of Technology. The Sperry Neuroscience Building at Oberlin College was named in his honour in 1990.

Donald O. Hebb

Donald Olding Hebb FRS (22 July 1904 to 20 August 1985) was a Canadian psychologist who was influential in the area of neuropsychology, where he sought to understand how the function of neurons contributed to psychological processes such as learning. He is best known for his theory of Hebbian learning, which he introduced in his classic 1949 work The Organisation of Behaviour. He has been described as the father of neuropsychology and neural networks. A Review of General Psychology survey, published in 2002, ranked Hebb as the 19th most cited psychologist of the 20th century. His views on learning described behaviour and thought in terms of brain function, explaining cognitive processes in terms of connections between neuron assemblies.