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What is Personality Disorder Not Otherwise Specified?

Published on by Andrew Marshall3 Comments

Introduction

Personality disorder not otherwise specified (PDNOS) is a diagnostic classification for some DSM-IV Axis II personality disorders not otherwise listed in DSM-IV.

The DSM-5 does not have an equivalent to Personality Disorder NOS. However Personality disorder-trait specified (PD-TS) remains under consideration for future revisions. The DSM 5 “Unspecified Disorder” is not a personality disorder, it is used to enhance specificity of an existing disorder or it is an emergency diagnosis unto itself (i.e. Unspecified Mental Disorder, 300.9), without being attached to another disorder.

Not to be confused with PDD-NOS (Pervasive Developmental Disorder Not Otherwise Specified).

Diagnostic Criteria

DSM-IV-TR

This diagnosis may be given when no other personality disorder defined in the DSM fits the patient’s symptoms.

Four personality disorders were excluded from the main body of the DSM-IV-TR but this diagnosis may be used instead. The four excluded personality disorders are:

It is a requirement of DSM-IV that a diagnosis of any personality disorder also satisfies a set of Diagnostic criteria.

ICD-10

The World Health Organisation’s ICD-10 defines a conceptually similar disorder to “personality disorder not otherwise specified” called (F60.9) Personality disorder, unspecified.

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

Epidemiology

In one study, PDNOS was found to be the third most frequent personality disorder diagnosis.

On This Day … 20 October

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People (Births)

  • 1859 – John Dewey, American psychologist and philosopher (d. 1952).
  • 1927 – Joyce Brothers, American psychologist, author, and actress (d. 2013).

People (Deaths)

  • 2015 – Arno Gruen, German-Swiss psychologist and psychoanalyst (b. 1923).

John Dewey

John Dewey (20 October 1859 to 01 June 1952) was an American philosopher, psychologist, and educational reformer whose ideas have been influential in education and social reform. He was one of the most prominent American scholars in the first half of the twentieth century.

The overriding theme of Dewey’s works was his profound belief in democracy, be it in politics, education, or communication and journalism. As Dewey himself stated in 1888, while still at the University of Michigan, “Democracy and the one, ultimate, ethical ideal of humanity are to my mind synonymous.” Dewey considered two fundamental elements – schools and civil society – to be major topics needing attention and reconstruction to encourage experimental intelligence and plurality. He asserted that complete democracy was to be obtained not just by extending voting rights but also by ensuring that there exists a fully formed public opinion, accomplished by communication among citizens, experts and politicians, with the latter being accountable for the policies they adopt.

Dewey was one of the primary figures associated with the philosophy of pragmatism and is considered one of the fathers of functional psychology. His paper “The Reflex Arc Concept in Psychology,” published in 1896, is regarded as the first major work in the (Chicago) functionalist school. A Review of General Psychology survey, published in 2002, ranked Dewey as the 93rd-most-cited psychologist of the 20th century.

Dewey was also a major educational reformer for the 20th century. A well-known public intellectual, he was a major voice of progressive education and liberalism. While a professor at the University of Chicago, he founded the University of Chicago Laboratory Schools, where he was able to apply and test his progressive ideas on pedagogical method. Although Dewey is known best for his publications about education, he also wrote about many other topics, including epistemology, metaphysics, aesthetics, art, logic, social theory, and ethics.

Joyce Brothers

Joyce Diane Brothers (20 October 1927 to 13 May 2013) was an American psychologist, television personality, advice columnist, and writer. She first became famous in 1955 for winning the top prize on the American game show The $64,000 Question. Her fame from the game show allowed her to go on to host various advice columns and television shows, which established her as a pioneer in the field of “pop (popular) psychology”.

Brothers is often credited as the first to normalise psychological concepts to the American mainstream. Her syndicated columns were featured in newspapers and magazines, including a monthly column for Good Housekeeping, in which she contributed for nearly 40 years. As Brothers quickly became the “face of psychology” for American audiences, she often appeared in various television roles, usually as herself. From the 1970s onward, she also began to accept fictional roles that parodied her “woman psychologist” persona. She is noted for working continuously for five decades across various genres. Numerous groups recognised Brothers for her strong leadership as a woman in the psychological field and for helping to destigmatise the profession overall.

Arno Gruen

Gruen was born in Berlin in 1923, and emigrated to the United States as a child in 1936 when his parents, James and Rosa Gruen, fled Germany to save their lives.

He studied at the City College of New York. Then, after completing his graduate studies in psychology at New York University, he trained in psychoanalysis under Theodor Reik at one of the first psychoanalytic training centres for psychologists, the National Psychological Association for Psychoanalysis in New York City.

Gruen held many teaching posts, including seventeen years as professor of psychology at Rutgers University. From 1979 on, he lived and practiced in Switzerland. Widely published in German, his groundbreaking first book to be released in English, The Betrayal of the Self, was published by Grove Press in 1988.

What is Carbamazepine?

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Introduction

Carbamazepine (CBZ), sold under the trade name Tegretol among others, is an anticonvulsant medication used primarily in the treatment of epilepsy and neuropathic pain.

It is used as an adjunctive treatment in schizophrenia along with other medications and as a second-line agent in bipolar disorder. Carbamazepine appears to work as well as phenytoin and valproate for focal and generalised seizures. It is not effective for absence or myoclonic seizures.

Common side effects include nausea and drowsiness. Serious side effects may include skin rashes, decreased bone marrow function, suicidal thoughts, or confusion. It should not be used in those with a history of bone marrow problems. Use during pregnancy may cause harm to the baby; however, stopping the medication in pregnant women with seizures is not recommended. Its use during breastfeeding is not recommended. Care should be taken in those with either kidney or liver problems.

Carbamazepine was discovered in 1953 by Swiss chemist Walter Schindler. It was first marketed in 1962. It is available as a generic medication. It is on the World Health Organisation’s List of Essential Medicines. In 2018, it was the 204th most commonly prescribed medication in the United States, with more than 2 million prescriptions. The newer but structurally related drugs, Oxcarbazepine and eslicarbazepine acetate, both show similar interactions, adverse events, and mechanism of action profiles.

Brief History

Carbamazepine was discovered by chemist Walter Schindler at J.R. Geigy AG (now part of Novartis) in Basel, Switzerland, in 1953. It was first marketed as a drug to treat epilepsy in Switzerland in 1963 under the brand name “Tegretol”; its use for trigeminal neuralgia (formerly known as tic douloureux) was introduced at the same time. It has been used as an anticonvulsant and antiepileptic in the UK since 1965, and has been approved in the US since 1968.

In 1971, Drs. Takezaki and Hanaoka first used carbamazepine to control mania in patients refractory to antipsychotics (lithium was not available in Japan at that time). Dr. Okuma, working independently, did the same thing with success. As they were also epileptologists, they had some familiarity with the anti-aggression effects of this drug. Carbamazepine was studied for bipolar disorder throughout the 1970s.

Medical Uses

Carbamazepine is typically used for the treatment of seizure disorders and neuropathic pain. It is used off-label as a second-line treatment for bipolar disorder and in combination with an antipsychotic in some cases of schizophrenia when treatment with a conventional antipsychotic alone has failed. However, evidence does not support this usage. It is not effective for absence seizures or myoclonic seizures. Although carbamazepine may have a similar effectiveness (people continue on medication) and efficacy (medicine reduces seizure recurrence and improves remission) when compared to phenytoin and valproate the choice of medications should be considered for each person individually as further research is needed to determine which medication is most helpful for people with newly-onset seizures.

In the United States, the FDA-approved medical uses are epilepsy (including partial seizures, generalised tonic-clonic seizures and mixed seizures), trigeminal neuralgia, and manic and mixed episodes of bipolar I disorder.

The drug is also claimed to be effective for ADHD.

As of 2014, a controlled release formulation was available for which there is tentative evidence showing fewer side effects and unclear evidence with regard to whether there is a difference in efficacy.

Adverse Effects

In the US, the label for carbamazepine contains warnings concerning:

  • Effects on the body’s production of red blood cells, white blood cells, and platelets: rarely, there are major effects of aplastic anaemia and agranulocytosis reported and more commonly, there are minor changes such as decreased white blood cell or platelet counts, but these do not progress to more serious problems.
  • Increased risks of suicide.
  • Increased risks of hyponatremia and syndrome of inappropriate antidiuretic hormone secretion (SIADH).
  • Risk of seizures, if the person stops taking the drug abruptly.
  • Risks to the foetus in women who are pregnant, specifically congenital malformations like spina bifida, and developmental disorders.

Common adverse effects may include drowsiness, dizziness, headaches and migraines, motor coordination impairment, nausea, vomiting, and/or constipation. Alcohol use while taking carbamazepine may lead to enhanced depression of the central nervous system.[2] Less common side effects may include increased risk of seizures in people with mixed seizure disorders,[21] abnormal heart rhythms, blurry or double vision.[2] Also, rare case reports of an auditory side effect have been made, whereby patients perceive sounds about a semitone lower than previously; this unusual side effect is usually not noticed by most people, and disappears after the person stops taking carbamazepine.

Pharmacogenetics

Serious skin reactions such as Stevens–Johnson syndrome or toxic epidermal necrolysis due to carbamazepine therapy are more common in people with a particular human leukocyte antigen allele, HLA-B1502. Odds ratios for the development of Stevens-Johnson syndrome or toxic epidermal necrolysis (SJS/TEN) in people who carry the allele can be in the double, triple or even quadruple digits, depending on the population studied. HLA-B1502 occurs almost exclusively in people with ancestry across broad areas of Asia, but has a very low or absent frequency in European, Japanese, Korean and African populations. However, the HLA-A31:01 allele has been shown to be a strong predictor of both mild and severe adverse reactions, such as the DRESS form of severe cutaneous reactions, to carbamazepine among Japanese, Chinese, Korean, and Europeans. It is suggested that carbamazepine acts as a potent antigen that binds to the antigen-presenting area of HLA-B1502 alike, triggering an everlasting activation signal on immature CD8-T cells, thus resulting in widespread cytotoxic reactions like SJS/TEN.

Interactions

Carbamazepine has a potential for drug interactions. Drugs that decrease breaking down of carbamazepine or otherwise increase its levels include erythromycin, cimetidine, propoxyphene, and calcium channel blockers. Grapefruit juice raises the bioavailability of carbamazepine by inhibiting the enzyme CYP3A4 in the gut wall and in the liver. Lower levels of carbamazepine are seen when administrated with phenobarbital, phenytoin, or primidone, which can result in breakthrough seizure activity.

Valproic acid and valnoctamide both inhibit microsomal epoxide hydrolase (mEH), the enzyme responsible for the breakdown of the active metabolite carbamazepine-10,11-epoxide into inactive metabolites. By inhibiting mEH, valproic acid and valnoctamide cause a build-up of the active metabolite, prolonging the effects of carbamazepine and delaying its excretion.

Carbamazepine, as an inducer of cytochrome P450 enzymes, may increase clearance of many drugs, decreasing their concentration in the blood to subtherapeutic levels and reducing their desired effects. Drugs that are more rapidly metabolized with carbamazepine include warfarin, lamotrigine, phenytoin, theophylline, valproic acid, many benzodiazepines, and methadone. Carbamazepine also increases the metabolism of the hormones in birth control pills and can reduce their effectiveness, potentially leading to unexpected pregnancies.

Pharmacology

Mechanism of Action

Carbamazepine is a sodium channel blocker. It binds preferentially to voltage-gated sodium channels in their inactive conformation, which prevents repetitive and sustained firing of an action potential. Carbamazepine has effects on serotonin systems but the relevance to its anti-seizure effects is uncertain. There is evidence that it is a serotonin releasing agent and possibly even a serotonin reuptake inhibitor.

Pharmacokinetics

Carbamazepine is relatively slowly but practically completely absorbed after administration by mouth. Highest concentrations in the blood plasma are reached after 4 to 24 hours depending on the dosage form. Slow release tablets result in about 15% lower absorption and 25% lower peak plasma concentrations than ordinary tablets, as well as in less fluctuation of the concentration, but not in significantly lower minimum concentrations.

20 to 30% of the substance are circulating in form of carbamazepine itself, the rest are metabolites. 70 to 80% are bound to plasma proteins. Concentrations in the breast milk are 25 to 60% of those in the blood plasma.

Carbamazepine itself is not pharmacologically active. It is activated, mainly by CYP3A4, to carbamazepine-10,11-epoxide, which is solely responsible for the drug’s anticonvulsant effects. The epoxide is then inactivated by microsomal epoxide hydrolase (mEH) to carbamazepine-trans-10,11-diol and further to its glucuronides. Other metabolites include various hydroxyl derivatives and carbamazepine-N-glucuronide.

The plasma half-life is about 35 to 40 hours when carbamazepine is given as single dose, but it is a strong inducer of liver enzymes, and the plasma half-life shortens to about 12 to 17 hours when it is given repeatedly. The half-life can be further shortened to 9-10 hours by other enzyme inducers such as phenytoin or phenobarbital. About 70% are excreted via the urine, almost exclusively in form of its metabolites, and 30% via the faeces.

Society and Culture

Environmental Impact

Carbamazepine and its (bio-)transformation products have been detected in wastewater treatment plant effluent  and in streams receiving treated wastewater. Field and laboratory studies have been conducted to understand the accumulation of carbamazepine in food plants grown in soil treated with sludge, which vary with respect to the concentrations of carbamazepine present in sludge and in the concentrations of sludge in the soil. Taking into account only studies that used concentrations commonly found in the environment, a 2014 review concluded that “the accumulation of carbamazepine into plants grown in soil amended with biosolids poses a de minimis risk to human health according to the approach.” 

Brand Names

Carbamazepine is available worldwide under many brand names including Tegretol.

Who was Hans Asperger?

Published on by Andrew Marshall2 Comments

Introduction

Johann Friedrich Karl Asperger (18 February 1906 to 21 October 1980) was an Austrian physician.

Noted for his early studies on atypical neurology, specifically in children, he is the namesake of the autism spectrum disorder Asperger syndrome. He wrote over 300 publications on psychological disorders that posthumously acquired international renown in the 1980s. His diagnosis of autism, which he termed “autistic psychopathy”, has also garnished controversy. Further controversy arose during the late 2010s over allegations that Asperger referred children to a Nazi German clinic responsible for murdering disabled patients, although his knowledge and involvement remains unknown.

Hans Asperger with a young patient, University Paediatric Clinic, Vienna c. 1940.

Personal Life

Hans Asperger was born in Hausbrunn, Austria, and raised on a farm not far from the city. The eldest of three sons, Asperger had difficulty finding friends and was considered a lonely, remote child. He was talented in language; in particular, he was interested in the Austrian poet Franz Grillparzer, whose poetry he would frequently quote to his uninterested classmates. He also liked to quote himself and often referred to himself from a third-person perspective.

As a youth, he joined the Wandering Scholars of the Bund Neuland, a conservative Catholic organisation within the German Youth Movement. He considered this a formative experience, later stating: “I was molded by the spirit of the German youth movement, which was one of the noblest blossoms of the German spirit.”

Asperger studied medicine at the University of Vienna under Franz Hamburger and practiced at the University Children’s Hospital in Vienna. He earned his medical degree in 1931 and became director of the special education section at the university children’s clinic in Vienna in 1932. He joined the Austrofascist Fatherland Front on 10 May 1934, nine days after Chancellor Engelbert Dollfuss passed a new constitution making himself dictator. Asperger married in 1935 and had five children.

Career

During World War II, he was a medical officer, serving in the Axis occupation of Yugoslavia; his younger brother died at Stalingrad. Near the end of the war, Asperger opened a school for children with Sister Viktorine Zak. The school was bombed and destroyed, Viktorine was killed, and much of Asperger’s early work was lost.

Georg Frankl was Asperger’s chief diagnostician until he moved from Austria to America and was hired by Leo Kanner in 1937.

Asperger published a definition of autistic psychopathy in 1944 that resembled the definition published earlier by a Russian neurologist named Grunya Sukhareva in 1926. Asperger identified in four boys a pattern of behaviour and abilities that included “a lack of empathy, little ability to form friendships, one-sided conversations, intense absorption in a special interest, and clumsy movements”. Asperger noticed that some of the children he identified as being autistic used their special talents in adulthood and had successful careers. One of them became a professor of astronomy and solved an error in Newton’s work he had originally noticed as a student.  Another one of Asperger’s patients was the Austrian writer and Nobel Prize in Literature laureate, Elfriede Jelinek.

In 1944, after the publication of his landmark paper describing autistic symptoms, Hans Asperger found a permanent tenured post at the University of Vienna. Shortly after the war ended, he became director of a children’s clinic in the city. It was there that he was appointed chair of pediatrics at the University of Vienna, a post he held for twenty years. He later held a post at Innsbruck. Beginning in 1964, he headed the SOS-Kinderdorf in Hinterbrühl. He became professor emeritus in 1977, and died three years later. AS was named after Hans Asperger and officially recognised in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1994; it was removed from DSM-5 in 2013.

Posthumous Developments

Asperger Syndrome Diagnosis

Asperger died before his identification of this pattern of behaviour became widely recognised. This was in part due to his work being exclusively in German and as such it was little-translated; medical academics, then as now, also disregarded Asperger’s work based on its merits or lack thereof. English researcher Lorna Wing proposed the condition Asperger’s syndrome in a 1981 paper, Asperger’s syndrome: a clinical account, that challenged the previously accepted model of autism presented by Leo Kanner in 1943. It was not until 1991 that an authoritative translation of Asperger’s work was made by Uta Frith; before this AS had still been “virtually unknown”. Frith said that fundamental questions regarding the diagnosis had not been answered, and the necessary scientific data to address this did not exist. Unlike Kanner, who overshadowed Asperger, the latter’s findings were ignored and disregarded in the English-speaking world in his lifetime.

In the early 1990s, Asperger’s work gained some notice due to Wing’s research on the subject and Frith’s recent translation, leading to the inclusion of the eponymous condition in the International Statistical Classification of Diseases and Related Health Problems 10th revision (ICD-10) in 1993, and the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders 4th revision (DSM-IV) in 1994, some half a century after Asperger’s original research.

Despite this brief resurgence of interest in his work in the 1990s, AS remains a controversial and contentious diagnosis due to its unclear relationship to the autism spectrum. In 2010 there was a majority consensus to subsume AS into the diagnosis “Autistic Spectrum Disorder” in the 2013 DSM-5 diagnostic manual. The World Health Organisation’s ICD-10 Version 2015 describes AS as “a disorder of uncertain nosological validity”.

In his 1944 paper, as Uta Frith translated from the German in 1991, Asperger wrote, “We are convinced, then, that autistic people have their place in the organism of the social community. They fulfil their role well, perhaps better than anyone else could, and we are talking of people who as children had the greatest difficulties and caused untold worries to their care-givers.” Based on Frith’s translation, however, Asperger initially stated: “Unfortunately, in the majority of cases the positive aspects of autism do not outweigh the negative ones.” Psychologist Eric Schopler wrote in 1998:

Asperger’s own publications did not inspire research, replication, or scientific interest prior to 1980. Instead, he laid the fertile groundwork for the diagnostic confusion that has grown since 1980.

Since 2009, Asperger’s birthday, 18 February, has been declared International Asperger’s Day by various governments.

Nazi Involvement

Edith Sheffer, a modern European history scholar, wrote in 2018 that Asperger cooperated with the Nazi regime, including sending children to the Spiegelgrund clinic which participated in the euthanasia programme. Sheffer wrote a book further elaborating on her research called Asperger’s Children: The Origins of Autism in Nazi Vienna (2018).

Another scholar and historian from the Medical University of Vienna, Herwig Czech concluded in a 2017 article in the journal Molecular Autism, which was published in April 2018:

Asperger managed to accommodate himself to the Nazi regime and was rewarded for his affirmations of loyalty with career opportunities. He joined several organisations affiliated with the NSDAP (although not the Nazi party itself), publicly legitimised ‘race hygiene’ policies including forced sterilisations and, on several occasions, actively cooperated with the child ‘euthanasia’ programme.

Dean Falk, American anthropologist from Florida State University, questioned Herwig Czech’s and Edith Sheffer’s allegations against Hans Asperger in a paper in Journal of Autism and Developmental Disorders. Czech’s reply was published in the same journal. Falk defended her paper against Czech’s reply in a second paper.

In May 2019, Ketil Slagstad, a Norwegian doctor and historical scholar, added his interpretation of both Sheffer’s and Czech’s work, in his article “Asperger, the Nazis and the children – the history of the birth of a diagnosis”, in which he describes the nuances of the situation. He offers an alternative explanation of Asperger’s involvement: citing the challenges of war, a desire to protect his career, and protection of the children for whom he was caring. Slagstad concludes:

The story of Hans Asperger, Nazism, murdered children, post-war oblivion, the birth of the diagnosis in the 1980s, the gradual expansion of the diagnostic criteria and the huge recent interest in autism spectrum disorders exemplify the historical and volatile nature of diagnoses: they are historic constructs that reflect the times and societies where they exert their effect.

Critically, Slagstad noted “Historical research has now shown that he [Asperger] was…a well-adapted cog in the machine of a deadly regime. He deliberately referred disabled children to the clinic Am Spiegelgrund, where he knew that they were at risk of being killed. The eponym Asperger’s syndrome ought to be used with awareness of its historical origin.”

What is Bretazenil?

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Introduction

Bretazenil (Ro16-6028) is an imidazopyrrolobenzodiazepine anxiolytic drug which is derived from the benzodiazepine family, and was invented in 1988.

It is most closely related in structure to the GABA antagonist flumazenil, although its effects are somewhat different. It is classified as a high-potency benzodiazepine due to its high affinity binding to benzodiazepine binding sites where it acts as a partial agonist. Its profile as a partial agonist and preclinical trial data suggests that it may have a reduced adverse effect profile. In particular bretazenil has been proposed to cause a less strong development of tolerance and withdrawal syndrome. Bretazenil differs from traditional 1,4-benzodiazepines by being a partial agonist and because it binds to α1, α2, α3, α4, α5 and α6 subunit containing GABAA receptor benzodiazepine receptor complexes. 1,4-benzodiazepines bind only to α1, α2, α3 and α5 GABAA benzodiazepine receptor complexes.

Brief History

Bretazenil was originally developed as an anti-anxiety drug and has been studied for its use as an anticonvulsant but has never commercialised. It is a partial agonist for GABAA receptors in the brain. David Nutt from the University of Bristol has suggested bretazenil as a possible base from which to make a better social drug, as it displays several of the positive effects of alcohol intoxication such as relaxation and sociability, but without the bad effects such as aggression, amnesia, nausea, loss of coordination, liver disease and brain damage. The effects of bretazenil can also be quickly reversed by the action of flumazenil, which is used as an antidote to benzodiazepine overdose, in contrast to alcohol for which there is no effective and reliable antidote.

Traditional benzodiazepines are associated with side effects such as drowsiness, physical dependence and abuse potential. It was hoped that bretazenil and other partial agonists would be an improvement on traditional benzodiazepines which are full agonists due to preclinical evidence that their side effect profile was less than that of full agonist benzodiazepines. For a variety of reasons however, bretazenil and other partial agonists such as pazinaclone and abecarnil were not clinically successful. However, research continues into other compounds with partial agonist and compounds which are selective for certain GABAA benzodiazepine receptor subtypes.

Tolerance and Dependence

In a study in rats, cross-tolerance between the benzodiazepine drug chlordiazepoxide and bretazenil has been demonstrated. In a primate study bretazenil was found to be able to replace the full agonist diazepam in diazepam dependent primates without precipitating withdrawal effects, demonstrating cross tolerance between bretazenil and benzodiazepine agonists, whereas other partial agonists precipitated a withdrawal syndrome. The differences are likely due to differences in intrinsic properties between different benzodiazepine partial agonists. Cross-tolerance has also been shown between bretazenil and full agonist benzodiazepines in rats. In rats tolerance is slower to develop to the anticonvulsant effects compared to the benzodiazepine site full agonist diazepam. However, tolerance developed to the anticonvulsant effects of bretazenil partial agonist more quickly than they developed to imidazenil.

Pharmacology

Bretazenil has a more broad spectrum of action than traditional benzodiazepines as it has been shown to have low affinity binding to α4 and α6 GABAA receptors in addition to acting on α1, α2, α3 and α5 subunits which traditional benzodiazepine drugs work on. The partial agonist imidazenil does not, however, act at these subunits. 0.5mg of bretazenil is approximately equivalent in its psychomotor-impairing effect to 10 mg of diazepam. Bretazenil produces marked sedative-hypnotic effects when taken alone and when combined with alcohol. This human study also indicates that bretazenil is possibly more sedative than diazepam. The reason is unknown, but the study suggests the possibility that a full-agonist metabolite may be generated in humans but not animals previously tested or else that there are significant differences in benzodiazepine receptor population in animals and humans.

In a study of monkeys bretazenil has been found to antagonize the effects of full agonist benzodiazepines. However, bretazenil has been found to enhance the effects of neurosteroids acting on the neurosteroid binding site of the GABAA receptor. Another study found that bretazenil acted as an antagonist provoking withdrawal symptoms in monkeys who were physically dependent on the full agonist benzodiazepine triazolam.

Partial agonists of benzodiazepine receptors have been proposed as a possible alternative to full agonists of the benzodiazepine site to overcome the problems of tolerance, dependence and withdrawal which limits the role of benzodiazepines in the treatment of anxiety, insomnia and epilepsy. Such adverse effects appear to be less problematic with bretazenil than full agonists. Bretazenil has also been found to have less abuse potential than benzodiazepine full agonists such as diazepam and alprazolam, however long-term use of bretazenil would still be expected to result in dependence and addiction.

Bretazenil alters the sleep EEG profile and causes a reduction in cortisol secretion and increases significantly the release of prolactin. Bretazenil has effective hypnotic properties but impairs cognitive ability in humans. Bretazenil causes a reduction in the number of movements between sleep stages and delays movement into REM sleep. At a dosage of 0.5 mg of bretazenil REM sleep is decreased and stage 2 sleep is lengthened.

On This Day … 18 October

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People (Births)

People (Deaths)

  • 1911 – Alfred Binet, French psychologist and author (b. 1857).

Martha Burk

Martha Gertrude Burk (born 18 October 1941) is an American political psychologist, feminist, and former Chair of the National Council of Women’s Organisations.

Alfred Binet

Alfred Binet (08 July 1857 to 18 October 1911), born Alfredo Binetti, was a French psychologist who invented the first practical IQ test, the Binet–Simon test.

In 1904, the French Ministry of Education asked psychologist Alfred Binet to devise a method that would determine which students did not learn effectively from regular classroom instruction so they could be given remedial work. Along with his collaborator Théodore Simon, Binet published revisions of his test in 1908 and 1911, the last of which appeared just before his death.

On This Day … 16 October

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People (Births)

  • 1888 – Paul Popenoe, American founder of relationship counselling (d. 1979).

People (Deaths)

  • 2015 – James W. Fowler, American psychologist and academic (b. 1940).

Paul Popenoe

Paul Bowman Popenoe (16 October 1888 to 19 June 1979) was an American agricultural explorer and eugenicist. He was an influential advocate of the compulsory sterilisation of the mentally ill and the mentally disabled, and the father of marriage counselling in the United States.

James W. Fowler

James William Fowler III (12 October 1940 to 16 October 2015) was an American theologian who was Professor of Theology and Human Development at Emory University. He was director of both the Centre for Research on Faith and Moral Development, and the Centre for Ethics until he retired in 2005. He was a minister in the United Methodist Church. Fowler is best known for his book Stages of Faith, published in 1981, in which he sought to develop the idea of a developmental process in “human faith”.

What is Experiential Avoidance?

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Introduction

Experiential avoidance (EA) has been broadly defined as attempts to avoid thoughts, feelings, memories, physical sensations, and other internal experiences – even when doing so creates harm in the long-run.

The process of EA is thought to be maintained through negative reinforcement – that is, short-term relief of discomfort is achieved through avoidance, thereby increasing the likelihood that the behaviour will persist. Importantly, the current conceptualisation of EA suggests that it is not negative thoughts, emotions, and sensations that are problematic, but how one responds to them that can cause difficulties. In particular, a habitual and persistent unwillingness to experience uncomfortable thoughts and feelings (and the associated avoidance and inhibition of these experiences) is thought to be linked to a wide range of problems.

Background

EA has been popularised by recent third-wave cognitive-behavioural theories such as acceptance and commitment therapy (ACT). However, the general concept has roots in many other theories of psychopathology and intervention.

Psychodynamic

Defence mechanisms were originally conceptualised as ways to avoid unpleasant affect and discomfort that resulted from conflicting motivations. These processes were thought to contribute to the expression of various types of psychopathology. Gradual removal of these defensive processes are thought to be a key aspect of treatment and eventually return to psychological health.

Process-Experiential

Process-experiential therapy merges client-centred, existential, and Gestalt approaches. Gestalt theory outlines the benefits of being fully aware of and open to one’s entire experience. One job of the psychotherapist is to:

“explore and become fully aware of [the patient’s] grounds for avoidance” and to “[lead] the patient back to that which he wishes to avoid”.

Similar ideas are expressed by early humanistic theory:

“Whether the stimulus was the impact of a configuration of form, color, or sound in the environment on the sensory nerves, or a memory trace from the past, or a visceral sensation of fear or pleasure or disgust, the person would be ‘living’ it, would have it completely available to awareness…he is more open to his feelings of fear and discouragement and pain…he is more able fully to live the experiences of his organism rather than shutting them out of awareness.”

Behavioural

Traditional behaviour therapy utilises exposure to habituate the patient to various types of fears and anxieties, eventually resulting in a marked reduction in psychopathology. In this way, exposure can be thought of as “counter-acting” avoidance, in that it involves individuals repeatedly encountering and remaining in contact with that which causes distress and discomfort.

Cognitive

In cognitive theory, avoidance interferes with reappraisals of negative thought patterns and schema, thereby perpetuating distorted beliefs. These distorted beliefs are thought to contribute and maintain many types of psychopathology.

Third-Wave Cognitive-Behavioural

The concept of EA is explicitly described and targeted in more recent CBT modalities including acceptance and commitment therapy (ACT), dialectical behaviour therapy (DBT), functional analytic psychotherapy (FAP), and behavioural activation (BA).

Associated Problems

  • Distress is an inextricable part of life; therefore, avoidance is often only a temporary solution.
  • Avoidance reinforces the notion that discomfort, distress and anxiety are bad, or dangerous.
  • Sustaining avoidance often requires effort and energy.
  • Avoidance limits one’s focus at the expense of fully experiencing what is going on in the present.
  • Avoidance may get in the way of other important, valued aspects of life.

Empirical Evidence

  • Laboratory-based thought suppression studies suggest avoidance is paradoxical, in that concerted attempts at suppression of a particular thought often leads to an increase of that thought.
  • Studies examining emotional suppression and pain suppression suggest that avoidance is ineffective in the long-run. Conversely, expressing unpleasant emotion results in short-term increases in arousal, but long-term decreases in arousal.
  • Exposure-based therapy techniques have been shown to be effective in treating a wide range of psychiatric disorders.
  • Numerous self-report studies have linked EA and related constructs (avoidance coping, thought suppression) to psychopathology and other forms of dysfunction.

Relevance to Psychopathology

Seemingly disparate forms of pathological behaviour can be understood by their common function (i.e., attempts to avoid distress). Some examples can be seen in the Table below.

DiagnosisExample BehavioursTarget of Avoidance
Major Depressive DisorderIsolation/suicideFeelings of sadness, guilt, and/or low self-worth.
PTSDAvoiding trauma reminders, hypervigilanceMemories, anxiety, concerns of safety.
Social PhobiaAvoiding social situationsAnxiety, concerns of judgement from others.
Panic DisorderAvoiding situations that might induce panicFear, physiological sensations.
AgoraphobiaRestricting travel outside of home or other ‘safe areas’Anxiety, fear of having symptoms of panic.
Obsessive-Compulsive DisorderChecking/ritualsWorry of consequences (e.g. contamination).
Substance Use DisordersAbusing alcohol/drugsEmotions, memories, withdrawal symptoms
Eating DisordersRestricting food intake, purgingWorry about becoming ‘overweight’, fear of losing control.
Borderline Personality DisorderSelf-harm (e.g. cutting)High emotional arousal.

Relevance to Quality of Life

Perhaps the most significant impact of EA is its potential to disrupt and interfere with important, valued aspects of an individual’s life. That is, EA is seen as particularly problematic when it occurs at the expense of a person’s deeply held values. Some examples include:

  • Putting off an important task because of the discomfort it evokes.
  • Not taking advantage of an important opportunity due to attempts to avoid worries of failure or disappointment.
  • Not engaging in physical activity/exercise, meaningful hobbies, or other recreational activities due to the effort they demand.
  • Avoiding social gatherings or interactions with others because of the anxiety and negative thoughts they evoke.
  • Not being a full participant in social gatherings due to attempts to regulate anxiety relating to how others are perceiving you.
  • Being unable to fully engage in meaningful conversations with others because one is scanning for signs of danger in the environment (attempting to avoid feeling “unsafe”).
  • Inability to “connect” and sustain a close relationship because of attempts to avoid feelings of vulnerability.
  • Staying in a “bad” relationship to try to avoid discomfort, guilt, and potential feelings of loneliness a break-up might entail.
  • Losing a marriage or contact with children due to an unwillingness to experience uncomfortable feelings (e.g. achieved through drug or alcohol abuse) or symptoms of withdrawal.
  • Not attending an important graduation, wedding, funeral, or other family event to try to avoid anxiety or symptoms of panic.
  • Engaging in self-destructive behaviours in an attempt to avoid feelings of boredom, emptiness, worthlessness.
  • Not functioning or taking care of basic responsibilities (e.g. personal hygiene, waking up, showing up to work, shopping for food) because of the effort they demand and/or distress they evoke.
  • Spending so much time attempting to avoid discomfort that one has little time for anyone or anything else in life.

Measurement

Self-Report

The Acceptance and Action Questionnaire (AAQ) was the first self-report measure explicitly designed to measure EA, but has since been re-conceptualised as a measure of “psychological flexibility”. The 62-item Multidimensional Experiential Avoidance Questionnaire (MEAQ) was developed to measure different aspects of EA. The Brief Experiential Avoidance Questionnaire (BEAQ) is a 15-item measure developed using MEAQ items, which has become the most widely used measure of experiential avoidance.

What is Avoidance Coping?

Published on by Andrew MarshallLeave a comment

Introduction

In psychology, avoidance coping is a coping mechanism and form of experiential avoidance.

It is characterized by a person’s efforts, conscious or unconscious, to avoid dealing with a stressor in order to protect oneself from the difficulties the stressor presents. Avoidance coping can lead to substance abuse, social withdrawal, and other forms of escapism. High levels of avoidance behaviours may lead to a diagnosis of avoidant personality disorder, though not everyone who displays such behaviours meets the definition of having this disorder. Avoidance coping is also a symptom of post-traumatic stress disorder (PTSD) and related to symptoms of depression and anxiety. Additionally, avoidance coping is part of the approach-avoidance conflict theory introduced by psychologist Kurt Lewin.

Literature on coping often classifies coping strategies into two broad categories: approach/active coping and avoidance/passive coping. Approach coping includes behaviours that attempt to reduce stress by alleviating the problem directly, and avoidance coping includes behaviours that reduce stress by distancing oneself from the problem. Traditionally, approach coping has been seen as the healthiest and most beneficial way to reduce stress, while avoidance coping has been associated with negative personality traits, potentially harmful activities, and generally poorer outcomes. However, avoidance coping can reduce stress when nothing can be done to address the stressor.

Measurement

Avoidance coping is measured via a self-reported questionnaire. Initially, the Multidimensional Experiential Avoidance Questionnaire (MEAQ) was used, which is a 62-item questionnaire that assesses experiential avoidance, and thus avoidance coping, by measuring how many avoidant behaviours a person exhibits and how strongly they agree with each statement on a scale of 1-6. Today, the Brief Experiential Avoidance Questionnaire (BEAQ) is used instead, containing 15 of the original 62 items from the MEAQ.

Treatment

Cognitive behavioural and psychoanalytic therapy are used to help those coping by avoidance to acknowledge, comprehend, and express their emotions. Acceptance and commitment therapy, a behavioural therapy that focuses on breaking down avoidance coping and showing it to be an unhealthy method for dealing with traumatic experiences, is also sometimes used.

Both active-cognitive and active-behavioural coping are used as replacement techniques for avoidance coping. Active-cognitive coping includes changing one’s attitude towards a stressful event and looking for any positive impacts. Active-behavioural coping refers taking positive actions after finding out more about the situation.