What are Hallucinations in Psychosis?

Introduction

Visual hallucinations in psychosis are hallucinations accompanied by delusions, which are abnormal beliefs that are endorsed by patients as real, that persist in spite of evidence to the contrary, and that are not part of a patient’s culture or subculture.

Presentation

Visual hallucinations in psychoses are reported to have physical properties similar to real perceptions. They are often life-sized, detailed, and solid, and are projected into the external world. They typically appear anchored in external space, just beyond the reach of individuals, or further away. They can have three-dimensional shapes, with depth and shadows, and distinct edges. They can be colourful or in black and white and can be static or have movement.

Simple versus Complex

Visual hallucinations may be simple, or non-formed visual hallucinations, or complex, or formed visual hallucinations.

Simple visual hallucinations are also referred to as non-formed or elementary visual hallucinations. They can take the form of multicoloured lights, colours, geometric shapes, indiscrete objects. Simple visual hallucinations without structure are known as phosphenes and those with geometric structure are known as photopsias. These hallucinations are caused by irritation to the primary visual cortex (Brodmann’s area 17).

Complex visual hallucinations are also referred to as formed visual hallucinations. They tend to be clear, lifelike images or scenes, such as faces of animals or people. Sometimes, hallucinations are ‘Lilliputian’, i.e. patients experience visual hallucinations where there are miniature people, often undertaking unusual actions. Lilliputian hallucinations may be accompanied by wonder, rather than terror.

Content

The frequency of hallucinations varies widely from rare to frequent, as does duration (seconds to minutes). The content of hallucinations varies as well. Complex (formed) visual hallucinations are more common than Simple (non-formed) visual hallucinations. In contrast to hallucinations experienced in organic conditions, hallucinations experienced as symptoms of psychoses tend to be more frightening. An example of this would be hallucinations that have imagery of bugs, dogs, snakes, distorted faces. Visual hallucinations may also be present in those with Parkinson’s, where visions of dead individuals can be present. In psychoses, this is relatively rare, although visions of God, angels, the devil, saints, and fairies are common. Individuals often report being surprised when hallucinations occur and are generally helpless to change or stop them. In general, individuals believe that visions are experienced only by themselves.

Causes

Two neurotransmitters are particularly important in visual hallucinations – serotonin and acetylcholine. They are concentrated in the visual thalamic nuclei and visual cortex.

The similarity of visual hallucinations that stem from diverse conditions suggest a common pathway for visual hallucinations. Three pathophysiologic mechanisms are thought to explain this.

The first mechanism has to do with cortical centres responsible for visual processing. Irritation of visual association cortices (Brodmann’s areas 18 and 19) cause complex visual hallucinations.

The second mechanism is deafferentation, the interruption or destruction of the afferent connections of nerve cells, of the visual system, caused by lesions, leading to the removal of normal inhibitory processes on cortical input to visual association areas, leading to complex hallucinations as a release phenomenon.

The third mechanism has to do with the reticular activating system, which plays a role in the maintenance of arousal. Lesions in the brain stem can cause visual hallucinations. Visual hallucinations are frequent in those with certain sleep disorders, occurring more often when drowsy. This suggests that the reticular activating system plays a part in visual hallucinations, although the precise mechanism has still not fully been established.

Prevalence

Hallucinations in those with psychoses are often experienced in colour, and most often are multi-modal, consisting of visual and auditory components. They frequently accompany paranoia or other thought disorders, and tend to occur during the daytime and are associated with episodes of excess excitability. The DSM-V lists visual hallucinations as a primary diagnostic criterion for several psychotic disorders, including schizophrenia and schizoaffective disorder.

The lifetime prevalence of all psychotic disorders is 3.48% and that of the different diagnostic groups are as follows:

  • 0.87% for schizophrenia.
  • 0.32% for schizoaffective disorder.
  • 0.07% for schizophreniform disorder.
  • 0.18% for delusional disorder.
  • 0.24% for bipolar I disorder.
  • 0.35% for major depressive disorder with psychotic features.
  • 0.42% for substance-induced psychotic disorders.
  • 0.21% for psychotic disorders due to a general medical condition.

Visual hallucinations can occur as a symptom of the above psychotic disorders in 24% to 72% of patients at some point in the course of their illness. Not all individuals who experience hallucinations have a psychotic disorder. Many physical and psychiatric disorders can manifest with hallucinations, and some individuals may have more than one disorder that could cause different types of hallucinations.

What is Schizoid Avoidant Behaviour?

Introduction

The relationship between schizoid personality disorder (SPD) and avoidant personality disorder (AvPD) has been a subject of controversy for decades.

Today it is still unclear and remains to be seen if these two personality disorders are linked to genetically distinct, but overlapping, personality disorders or if these two personality disorders are merely two different phenotypic expressions of the same genetic disorder.

Background

Both have been associated with a shared genetic risk factor and the same polymorphism within the ANKK1 gene. There is also some evidence that AvPD (like SPD) is a personality disorder of the schizophrenia spectrum.

Originally, schizoid personality disorder involved social avoidance combined with marked ambivalence regarding the desirability of social contact. It included indifference or even cold disdain oscillating with longing for normal relationships. Through the efforts of Theodore Millon, this complex idea was later divided across two disorders with the emergence of a separate AvPD construct and the idea of ambivalence was lost.

According to the differential diagnosis guidelines provided in the text of the DSM-IV the two conditions are distinguished by the extent to which the individual desires social contact versus being indifferent to it. But such distinctions are often difficult to apply in practice, as patients often have unclear, marginal, or shifting status on those elements thought most crucial for differential diagnosis. In the case of the avoidant and schizoid personality disorders, however, both the problem and its solution may be more academic than real.

  • First, research indicates that all of the avoidant symptoms except social withdrawal correlate negatively with the schizoid symptom list and that differential diagnosis is not difficult.
  • Second, schizoid personality disorder is exceedingly rare and the diagnostic quandary may never occur in practice.

However, new research shows that both personality disorders are linked to hypersensitivity.

On This Day … 19 April

People (Births)

  • 1874 – Ernst Rüdin, Swiss psychiatrist, geneticist, and eugenicist (d. 1952).

Ernst Rudin

Ernst Rüdin (19 April 1874 to 22 October 1952) was a Swiss-born German psychiatrist, geneticist, eugenicist and Nazi. Rising to prominence under Emil Kraepelin and assuming his directorship at what is now called the Max Planck Institute of Psychiatry in Munich. While he has been credited as a pioneer of psychiatric inheritance studies, he also argued for, designed, justified and funded the mass sterilisation and clinical killing of adults and children.

Early Career

Commencing in 1893, Rüdin studied medicine at universities in several countries, graduating in 1898. At the Burghölzli in Zurich, he worked as assistant to Eugen Bleuler who coined the term ‘schizophrenia‘. He completed his PhD, then a psychiatric residency at a Berlin prison. From 1907, he worked at the University of Munich as assistant to Emil Kraepelin, the highly influential psychiatrist who had developed the diagnostic split between ‘dementia praecox’ (‘early dementia’ – reflecting his pessimistic prognosis – renamed schizophrenia) and ‘manic-depressive illness’ (including unipolar depression), and who is considered by many to be the father of modern psychiatric classification. Rüdin became senior lecturer in 1909, as well as senior physician at the Munich Psychiatric Hospital, succeeding Alois Alzheimer.

Kraepelin and Rüdin were both ardent advocates of a theory that the German race was becoming overly ‘domesticated’ and thus degenerating into higher rates of mental illness and other conditions. Fears of degeneration were somewhat common internationally at the time, but the extent to which Rüdin took them may have been unique, and from the very beginning of his career he made continuous efforts to have his research translate into political action. He also repeatedly drew attention to the financial burden of the sick and disabled.

Rüdin developed the concept of “empirical genetic prognosis” of mental disorders. He published influential initial results on the genetics of schizophrenia (known as dementia praecox) in 1916. Rüdin’s data did not show a high enough risk in siblings for schizophrenia to be due to a simple recessive gene as he and Kraepelin thought, but he put forward a two-recessive-gene theory to try to account for this. This has been attributed to a “mistaken belief” that just one or a small number of gene variations caused such conditions. Similarly his own large study on Mood disorders correctly disproved his own theory of simple Mendelian inheritance and also showed environmental causes, but Rüdin simply neglected to publish and continued to advance his eugenic theories. Nevertheless, Rüdin pioneered and refined complex techniques for conducting studies of inheritance, was widely cited in the international literature for decades, and is still regarded as “the father of psychiatric genetics”.

Rüdin was influenced by his then brother-in-law, and long-time friend and colleague, Alfred Ploetz, who was considered the ‘father’ of racial hygiene and indeed had coined the term in 1895. This was a form of eugenics, inspired by social darwinism, which had gained some popularity internationally, as would the voluntary or compulsory sterilization of psychiatric patients, initially in America. Rüdin campaigned for this early on. At a conference on alcoholism in 1903, he argued for the sterilisation of ‘incurable alcoholics’, but his proposal was roundly defeated. In 1904, he was appointed co-editor in chief of the newly founded Archive for Racial Hygiene and Social Biology, and in 1905 was among the co-founders of the German Society for Racial Hygiene (which soon became International), along with Ploetz. He published an article of his own in Archives in 1910, in which he argued that medical care for the mentally ill, alcoholics, epileptics and others was a distortion of natural laws of natural selection, and medicine should help to clean the genetic pool.

Increasing Influence

In 1917, a new German Institute for Psychiatric Research was established in Munich (known as the DFA in German; renamed the Max Planck Institute of Psychiatry after World War II), designed and driven forward by Emil Kraepelin. The Institute incorporated a Department of Genealogical and Demographic Studies (known as the GDA in German) – the first in the world specialising in psychiatric genetics – and Rüdin was put in charge by overall director Kraepelin. In 1924, the Institute came under the umbrella of the prestigious Kaiser Wilhelm Society. From 1925, Rüdin spent three years as full Professor of Psychology at Basel, Switzerland. He returned to the Institute in 1928, with an expanded departmental budget and new building at 2 Kraepelinstrasse, financed primarily by the American Rockefeller Foundation. The institute soon gained an international reputation as leading psychiatric research, including in hereditary genetics. In 1931, a few years after Kraepelin’s death, Rüdin took over the directorship of the entire Institute as well as remaining head of his department.

Rüdin was among the first to attempt to educate the public about the “dangers” of hereditary defectives and the value of the Nordic race as “culture creators”. By 1920, his colleague Alfred Hoche published, with lawyer Karl Binding, the influential “Allowing the Destruction of Life Unworthy of Living”.

In 1930, Rüdin was a leading German representative at the First International Congress for Mental Hygiene, held in Washington, US, arguing for eugenics. In 1932, he became President of the International Federation of Eugenics Organisations. He was in contact with Carlos Blacker of the British Eugenics Society, and sent him a copy of pre-Nazi voluntary sterilisation laws enacted in Prussia; a precursor to the Nazi forced sterilisation laws that Rüdin is said to have already prepared in his desk drawer.

From 1935 to 1945, he was President of the Society of German Neurologists and Psychiatrists (GDNP), later renamed the German Association for Psychiatry, Psychotherapy and Neurology (DGPPN).

The American Rockefeller Foundation funded numerous international researchers to visit and work at Rüdin’s psychiatric genetics department, even as late as 1939. These included Eliot Slater and Erik Stromgren, considered the founding fathers of psychiatric genetics in Britain and Scandinavia respectively, as well as Franz Josef Kallmann who became a leading figure in twins research in the US after emigrating in 1936.[4] Kallmann had claimed in 1935 that ‘minor anomalies’ in otherwise unaffected relatives of schizophrenics should be grounds for compulsory sterilisation.

Rüdin’s research was also supported with manpower and financing from the German National Socialists.

Nazi Expert

In 1933, Ernst Rüdin, Alfred Ploetz, and several other experts on racial hygiene were brought together to form the Expert Committee on Questions of Population and Racial Policy under Reich Interior Minister Wilhelm Frick. The committee’s ideas were used as a scientific basis to justify the racial policy of Nazi Germany and its “Law for the Prevention of Hereditarily Diseased Offspring” was passed by the German government on 01 January 1934. Rüdin was such an avid proponent that colleagues nicknamed him the “Reichsfuhrer for Sterilization”

In a speech to the German Society for Rassenhygiene published in 1934, Rüdin recalled the early days of trying to alert the public to the special value of the Nordic race and the dangers of defectives. He stated: “The significance of Rassenhygiene racial hygiene did not become evident to all aware Germans until the political activity of Adolf Hitler and only through his work has our 30-year-long dream of translating Rassenhygiene into action finally become a reality.” Describing it as a ‘duty of honour’ for society to help implement the Nazi policies, Rüdin declared: “Whoever is not physically or mentally fit must not pass on his defects to his children. The state must take care that only the fit produce children. Conversely, it must be regarded as reprehensible to withhold healthy children from the state.”

From early on, Rüdin had been a ‘racial fanatic’ for the purity of the ‘German people’. However, he was also described in 1988 as “not so much a fanatical Nazi as a fanatical geneticist”. His ideas for reducing new cases of schizophrenia would prove a total failure, despite between 73% and 100% of the diagnosed being sterilised or killed.

Rüdin joined the Nazi party in 1937. In 1939, on his 65th birthday, he was awarded a ‘Goethe medal for art and science’ handed to him personally by Hitler, who honoured him as the ‘pioneer of the racial-hygienic measures of the Third Reich’. In 1944, he received a bronze Nazi eagle medal (Adlerschild des Deutschen Reiches), with Hitler calling him the ‘pathfinder in the field of hereditary hygiene’.

In 1942, speaking about ‘euthanasia’, Rüdin emphasised “the value of eliminating young children of clearly inferior quality”. He supported and financially aided the work of Julius Duessen at Heidelberg University with Carl Schneider, clinical research which from the beginning involving killing children.

Post-War

At the end of the war in 1945, Rüdin claimed he had only ever engaged in academic science, only ever heard rumours of killings at the nearby insane asylums, and that he hated the Nazis. However, some of his Nazi political activities, scientific justifications, and awards from Hitler were already uncovered in 1945 (as were his lecture handouts praising Nordics and disparaging Jews). Investigative journalist Victor H. Bernstein concluded: “I am sure that Prof. Rüdin never so much as killed a fly in his 74 years. I am also sure he is one of the most evil men in Germany.” Rüdin was stripped of his Swiss citizenship which he had held jointly with German, and two months later was placed under house arrest by the Munich Military Government. However, interned in the US, he was released in 1947 after a ‘denazification’ trial where he was supported by former colleague Kallmann (a eugenicist himself) and famous quantum physicist Max Planck[verification needed]; his only punishment was a 500-mark fine.

Speculation about the reasons for his early release, despite having been considered as a potential criminal defendant for the Nuremberg trials, include the need to restore confidence and order in the German medical profession; his personal and financial connections to prestigious American and British researchers, funding bodies and others; and the fact that he repeatedly cited American eugenic sterilization initiatives to justify his own as legal (indeed the Nuremberg trials carefully avoided highlighting such links in general). Nevertheless, Rüdin has been cited as a more senior and influential architect of Nazi crimes than the physician who was sentenced to death, Karl Brandt, or the infamous Josef Mengele who had attended his lectures and been employed by his Institute.

After Rüdin’s death in 1952, the funeral eulogy was held by Kurt Pohlisch, a close friend who had been professor of psychiatry at Bonn University, director of the second-largest genetics research institute in Germany, and expert Nazi advisor on Action T4.

Rüdin’s connections to the Nazis were a major reason for criticisms of psychiatric genetics in Germany after 1945.

He was survived by his daughter, Edith Zerbin-Rüdin, who became a psychiatric geneticist and eugenicist herself. In 1996, Zerbin-Rüdin, along with Kenneth S. Kendler, published a series of articles on his work which were criticised by others for whitewashing his racist and later Nazi ideologies and activities (Elliot S. Gershon also notes that Zerbin-Rüdin acted as defender and apologist for her father in private conversation and in a transcribed interview published in 1988). Kendler and other leading psychiatric genetic authors have been accused as recently as 2013 of producing revisionist historical accounts of Rüdin and his ‘Munich School’. Three types of account have been identified: “(A) those who write about German psychiatric genetics in the Nazi period, but either fail to mention Rüdin at all, or cast him in a favorable light; (B) those who acknowledge that Rüdin helped promote eugenic sterilization and/or may have worked with the Nazis, but generally paint a positive picture of Rüdin’s research and fail to mention his participation in the “euthanasia” killing program; and (C) those who have written that Rüdin committed and supported unspeakable atrocities.”

On This Day … 18 April

People (Deaths)

  • 1917 – Vladimir Serbsky, Russian psychiatrist and academic (b. 1858).

Vladimir Serbsky

Vladimir Petrovich Serbsky (Russian: Влади́мир Петро́вич Се́рбский, 26 February 1858 to 18 April 1917 in Moscow) was a Russian psychiatrist and one of the founders of forensic psychiatry in Russia. The author of The Forensic Psychopathology, Serbsky thought delinquency to have no congenital basis, considering it to be caused by social reasons.

The Central Institute of Forensic Psychiatry was named after Serbsky in 1921. Now the facility is known as the Serbsky Centre (Serbsky State Scientific Centre for Social and Forensic Psychiatry).

Biography

Vladimir Petrovich Serbsky was born in 1858 in Bogorodsk (now Noginsk, Moscow Region) in the family of a zemstvo doctor.

After Serbsky grew up, his family moved to Moscow, where he studied at the Second Moscow Gymnasium. After graduation he entered the Physics and Mathematics Department of Moscow University, graduating in 1880 with a candidate’s degree. In the same year, he entered the Medical Department of Moscow University. Since he already had a higher education, he was immediately placed into the third year. Serbsky was fascinated by the study of nervous and mental diseases and became one of the students of S.S. Korsakov. In 1883 Serbsky defended his thesis on “The clinical importance of albuminuria”, for which he received a silver medal.

After graduating from the medical department, Serbsky began medical work under the direction of S.S. Korsakov in the private psychiatric hospital M.F. Bekker. In 1885, Vladimir Petrovich Serbsky was offered to manage a zemstvo psychiatric clinic in the Tambov province; he accepted the offer, leading the clinic until 1887. The local zemstvo offered him a trip to Austria, where he worked for almost a year at the Vienna Psychiatric Clinic under the direction of T. Meinert.

After returning from Austria, Serbsky worked for several months in the Tambov Clinic for the mentally ill, and then returned to Moscow, where he was elected to the position of senior assistant of the Moscow University psychiatric clinic. In 1891, Serbsky defended his thesis, “Forms of mental disorders described under the name of catatonia” for the degree of Doctor of Medicine and in 1892 received the title of privat-docent.

After the death of S.S. Korsakov, Serbsky in actuality became the chief psychiatrist in Russia. In 1902 he was appointed extraordinary professor and director of the psychiatric clinic, and in 1903 he headed the Department of Psychiatry of Moscow University, which he directed until 1911.

In 1905, Serbsky made a report in which he showed that the situation created in the country promotes the growth of mental illnesses. After the congress, he published a book in which he considered the role of revolution as a factor influencing the change in the consciousness of a large number of people. Such a position had a negative effect on his relations with the authorities. In 1911, as a sign of protest against the reactionary policy of the Minister of Education L.A. Kasso, Serbsky resigned and in the same year at the First Congress of Russian Psychiatrists and Neuropathologists he spoke against the government’s policy of suppressing rights and freedoms that resulted in the closing of the congress.

In 1913, the English and Scottish societies of psychiatrists elected the scientist their honorary member and were invited to visit Britain. Serbsky accepted the invitation. He was accepted as a famous scientist and public figure. He gave lectures, visited clinics, and advised patients. The University of Edinburgh offered him the position of a professor. He declined it and returned to Russia.

In 1913 Serbsky publicly denounced unsound examination of government-inspired anti-Semitic case M. Bayliss, who was unjustly accused of murdering a boy for ritual purposes.

After the Provisional Government came to power, the new Minister of Education, A.A. Manuilov, sent a letter to Serbsky, in which he invited him to return to Moscow University. The letter came too late, the scientist was already terminally ill. Vladimir Petrovich lived out his last days in poverty, since he retired without earning his pension. Renal failure due to chronic nephritis was gradually aggravated, and on 23 March 1917, Serbsky died. He was buried at the Novodevichy Cemetery.

Scientific Activity

Under the supervision of Serbsky, the Tambov hospital became one of the most advanced institutions of its type in Russia. Straight jackets and leather sleeves were banned in the patients clinic. There was a widespread use of work and entertainment for patients and the main contingent of workers who took part in walks and other festivities consisted of chronic patients.

Serbsky always advocated that patients were treated primarily as people. He repeatedly engaged in arguments with psychiatrist E. Krepelin, who fell back on a formalised diagnosis of mental illness. Considering the big picture of the disease, Serbsky took into account not only mental, but also physical ailments of patients, trying to recreate a picture of their relationships.

Serbsky was the first teacher at Moscow University in 1892 who lectured on forensic psychiatry to students of the law and medical departments.

Serbsky worked on issues of diagnosing the main forms of psychosis. He was the first one to find that some of the painful manifestations observed in adult patients are consequences of their childhood intellectual disorders. Gradually, Serbsky formulated the basic principles of the methodology by which psychiatrists could now determine the degree of the patient’s sanity, that is, the ability to critically evaluate his actions.

Serbsky supported and developed A.W. Freze’s and V.X. Kandinsky’s positions on the significance of the psychological understanding of mental disorders for the correct solution to forensic psychiatric questions. He pointed to the merits of V.X. Kandinsky: “V. X. Kandinsky developed the need to establish the psychological criterion of insanity by law with the greatest conviction- I can only align myself with the views of this talented psychologist.”

Serbsky first proved the inconsistency of K. Kalbaums’s doctrine of catatonia as an independent disease. In 1890 Serbsky found that the catatonic symptom complex can be a consequence of schizophrenia and other psychoses.

In 1895, Serbsky released the first volume of “The Guide to Forensic Psychopathology,” devoted to general theoretical questions and legislation on forensic psychiatry. This covered issues of forensic psychiatric theory and practice, as well as legislation for mental patients. The second volume of the “Guide” was published in 1900. For many decades the book was the desk guide for psychiatrists around the world. In this book, for the first time in the history of science, a description of various forms of malignant schizophrenia was presented. Serbsky succeeded in showing that an accurate diagnosis can be made only on the basis of a comprehensive examination of the patient.

Serbsky proved that from the point of view of psychiatry even a dangerous criminal can be a sick person. In this case, he should be isolated from society and be allowed to heal. The scientist was deeply convinced that in many crimes the environment that influenced the formation of his personality is to blame. He suggested introducing mandatory psychiatric examination for those accused of committing serious crimes. Usually in such cases, death sentences were imposed.

In 1912, Serbsky organised and headed the “Moscow Psychiatric Circle of Small Fridays,” which became one of the first organisational structures composed and led by psychoanalysts (M.M. Asatiani, E.N. Dovbnya, N.Ye. Osipov, O.B. Feltsman and others). He criticized a number of provisions of Freud’s teachings and the works of Russian psychoanalysts, including his students. At the same time encouraged the discussion of psychoanalytic problems. The discussions were carried out from the first day of the work of the circle.

Serbsky developed a modern form of sponsorship for psychiatric patients, was one of the founders of the Journal of Neuropathology and Psychiatry after S.S. Kosakov and the Russian Union of Psychiatrists and Neuropathologists, he was an active participant in all psychiatric and Pirogov congresses, delivering program papers on problems of forensic psychiatry, participated in many complex and forensically responsible psychiatric examinations in cases that caused great public outcry, boldly defending his own-always clinically sound- opinion.

Memory

Since 1912 the name of Vladimir Petrovich Serbsky has been carried by the Central Institute of Forensic Psychiatry in Moscow.

Major Works

  • The Forensic Psychopathology (1896-1900).
  • On Dementia praecox (1902).
  • Manual of Study of Mental Diseases (1906).

Is there an Association between Metabolic Disorder & Cognitive Impairment in Patients with Early-Stage Schizophrenia?

Research Paper Title

The Association Between Metabolic Disturbance and Cognitive Impairments in Early-Stage Schizophrenia.

Background

Cognitive impairment is one of the core symptoms of schizophrenia, which is considered to be significantly correlated to prognosis. In recent years, many studies have suggested that metabolic disorders could be related to a higher risk of cognitive defects in a general setting. However, there has been limited evidence on the association between metabolism and cognitive function in patients with early-stage schizophrenia.

Methods

In this study, the researchers recruited 172 patients with early-stage schizophrenia. Relevant metabolic parameters were examined and cognitive function was evaluated by using the MATRICS Consensus Cognitive Battery (MCCB) to investigate the relationship between metabolic disorder and cognitive impairment.

Results

Generally, the prevalence of cognitive impairment among patients in our study was 84.7% (144/170), which was much higher than that in the general population. Compared with the general Chinese setting, the study population presented a higher proportion of metabolic disturbance. Patients who had metabolic disturbance showed no significant differences on cognitive function compared with the other patients. Correlation analysis showed that metabolic status was significantly correlated with cognitive function as assessed by the cognitive domain scores (p < 0.05), while such association was not found in further multiple regression analysis.

Conclusions

Therefore, there may be no association between metabolic disorder and cognitive impairment in patients with early-stage schizophrenia.

Reference

Peng, X-J., Hei, G-R., Li, R-R., Yang, Y., Liu, C-C., Xiao, J-M., Long, Y-J., Shao, P., Huang, J., Zhao, J-P. & Wu, R-R. (2021) The Association Between Metabolic Disturbance and Cognitive Impairments in Early-Stage Schizophrenia. Frontiers in Human Neuroscience. doi: 10.3389/fnhum.2020.599720. eCollection 2020.

On This Day … 07 April

People (Deaths)

  • 1999 – Heinz Lehmann, German-Canadian psychiatrist and academic (b. 1911).

Heinz Lehmann

Heinz Edgar Lehmann, OC FRSC (17 July 17 1911 to 07 April 1999) was a German-born Canadian psychiatrist best known for his use of chlorpromazine for the treatment of schizophrenia in 1950s and “truly the father of modern psychopharmacology.”

Early Life

Born in Berlin, Germany, he was educated at the University of Freiburg, the University of Marburg, the University of Vienna, and the University of Berlin. He emigrated to Canada in 1937.

Hospital Work in Canada

In 1947, he was appointed the clinical director of Montreal’s Douglas Hospital. From 1971 to 1975, he was the chair of the McGill University Department of Psychiatry. He was also a humane lecturer in psychiatry in 1952, and was able to give empathetic lectures on the plight of people suffering from anxiety, depression obsessions, paranoia etc. No one to that time had been able to understand or help schizophrenic patients, who filled mental hospitals around the world, so when chlorpromazine showed some promise he helped to promote it in North America and start the drug revolution. He was ahead of his time in that he supported research in the use of the active ingredient psilocybin to alleviate anxiety.

Le Dain Commission

From 1969 to 1972, he was one of the five members of the Le Dain Commission, a royal commission appointed in Canada to study the non-medical use of drugs. He was an advocate for decriminalisation of marijuana.

DSM Work

In 1973, he was a member of the Nomenclature Committee of the American Psychiatric Association that decided to drop homosexuality from the Diagnostic and Statistical Manual of Mental Disorders, i.e. to depathologise it.

Honours and Awards

In 1970 he was made a Fellow of the Royal Society of Canada and, in 1976, he was made an Officer of the Order of Canada. He was inducted into the Canadian Medical Hall of Fame in 1998.

Heinz Lehmann Award

In 1999, the Canadian College of Neuropsychopharmacology established the Heinz Lehmann Award in his honour, given in recognition of outstanding contributions to research in neuropsychopharmacology in Canada.

What is Family Therapy?

Introduction

Family therapy, also referred to as couple and family therapy, marriage and family therapy, family systems therapy, and family counselling, is a branch of psychotherapy that works with families and couples in intimate relationships to nurture change and development. It tends to view change in terms of the systems of interaction between family members.

The different schools of family therapy have in common a belief that, regardless of the origin of the problem, and regardless of whether the clients consider it an “individual” or “family” issue, involving families in solutions often benefits clients. This involvement of families is commonly accomplished by their direct participation in the therapy session. The skills of the family therapist thus include the ability to influence conversations in a way that catalyses the strengths, wisdom, and support of the wider system.

In the field’s early years, many clinicians defined the family in a narrow, traditional manner usually including parents and children. As the field has evolved, the concept of the family is more commonly defined in terms of strongly supportive, long-term roles and relationships between people who may or may not be related by blood or marriage.

The conceptual frameworks developed by family therapists, especially those of family systems theorists, have been applied to a wide range of human behaviour, including organisational dynamics and the study of greatness.

Brief History and Theoretical Frameworks

Formal interventions with families to help individuals and families experiencing various kinds of problems have been a part of many cultures, probably throughout history. These interventions have sometimes involved formal procedures or rituals, and often included the extended family as well as non-kin members of the community (see for example Ho’oponopono). Following the emergence of specialisation in various societies, these interventions were often conducted by particular members of a community – for example, a chief, priest, physician, and so on – usually as an ancillary function.

Family therapy as a distinct professional practice within Western cultures can be argued to have had its origins in the social work movements of the 19th century in the United Kingdom and the United States. As a branch of psychotherapy, its roots can be traced somewhat later to the early 20th century with the emergence of the child guidance movement and marriage counselling. The formal development of family therapy dates from the 1940s and early 1950s with the founding in 1942 of the American Association of Marriage Counsellors (the precursor of the AAMFT), and through the work of various independent clinicians and groups – in the United Kingdom (John Bowlby at the Tavistock Clinic), the United States (Donald deAvila Jackson, John Elderkin Bell, Nathan Ackerman, Christian Midelfort, Theodore Lidz, Lyman Wynne, Murray Bowen, Carl Whitaker, Virginia Satir, Ivan Boszormenyi-Nagy), and in Hungary, D.L.P. Liebermann – who began seeing family members together for observation or therapy sessions. There was initially a strong influence from psychoanalysis (most of the early founders of the field had psychoanalytic backgrounds) and social psychiatry, and later from learning theory and behaviour therapy – and significantly, these clinicians began to articulate various theories about the nature and functioning of the family as an entity that was more than a mere aggregation of individuals.

The movement received an important boost starting in the early 1950s through the work of anthropologist Gregory Bateson and colleagues – Jay Haley, Donald D. Jackson, John Weakland, William Fry, and later, Virginia Satir, Ivan Boszormenyi-Nagy, Paul Watzlawick and others – at Palo Alto in the United States, who introduced ideas from cybernetics and general systems theory into social psychology and psychotherapy, focusing in particular on the role of communication (refer to Bateson Project). This approach eschewed the traditional focus on individual psychology and historical factors – that involve so-called linear causation and content – and emphasized instead feedback and homeostatic mechanisms and “rules” in here-and-now interactions – so-called circular causation and process – that were thought to maintain or exacerbate problems, whatever the original cause(s). This group was also influenced significantly by the work of US psychiatrist, hypnotherapist, and brief therapist, Milton H. Erickson – especially his innovative use of strategies for change, such as paradoxical directives. The members of the Bateson Project (like the founders of a number of other schools of family therapy, including Carl Whitaker, Murray Bowen, and Ivan Boszormenyi-Nagy) had a particular interest in the possible psychosocial causes and treatment of schizophrenia, especially in terms of the putative “meaning” and “function” of signs and symptoms within the family system. The research of psychiatrists and psychoanalysts Lyman Wynne and Theodore Lidz on communication deviance and roles (e.g. pseudo-mutuality, pseudo-hostility, schism and skew) in families of people with schizophrenia also became influential with systems-communications-oriented theorists and therapists. A related theme, applying to dysfunction and psychopathology more generally, was that of the “identified patient” or “presenting problem” as a manifestation of or surrogate for the family’s, or even society’s, problems (refer to Double Bind).

By the mid-1960s, a number of distinct schools of family therapy had emerged. From those groups that were most strongly influenced by cybernetics and systems theory, there came MRI Brief Therapy, and slightly later, strategic therapy, Salvador Minuchin’s Structural Family Therapy and the Milan systems model. Partly in reaction to some aspects of these systemic models, came the experiential approaches of Virginia Satir and Carl Whitaker, which downplayed theoretical constructs, and emphasized subjective experience and unexpressed feelings (including the subconscious), authentic communication, spontaneity, creativity, total therapist engagement, and often included the extended family. Concurrently and somewhat independently, there emerged the various intergenerational therapies of Murray Bowen, Ivan Boszormenyi-Nagy, James Framo, and Norman Paul, which present different theories about the intergenerational transmission of health and dysfunction, but which all deal usually with at least three generations of a family (in person or conceptually), either directly in therapy sessions, or via “homework”, “journeys home”, etc. Psychodynamic family therapy – which, more than any other school of family therapy, deals directly with individual psychology and the unconscious in the context of current relationships – continued to develop through a number of groups that were influenced by the ideas and methods of Nathan Ackerman, and also by the British School of Object Relations and John Bowlby’s work on attachment. Multiple-family group therapy, a precursor of psychoeducational family intervention, emerged, in part, as a pragmatic alternative form of intervention – especially as an adjunct to the treatment of serious mental disorders with a significant biological basis, such as schizophrenia – and represented something of a conceptual challenge to some of the “systemic” (and thus potentially “family-blaming”) paradigms of pathogenesis that were implicit in many of the dominant models of family therapy. The late-1960s and early-1970s saw the development of network therapy (which bears some resemblance to traditional practices such as Ho’oponopono) by Ross Speck and Carolyn Attneave, and the emergence of behavioural marital therapy (renamed behavioural couples therapy in the 1990s; see also relationship counselling) and behavioural family therapy as models in their own right.

By the late-1970s, the weight of clinical experience – especially in relation to the treatment of serious mental disorders – had led to some revision of a number of the original models and a moderation of some of the earlier stridency and theoretical purism. There were the beginnings of a general softening of the strict demarcations between schools, with moves toward rapprochement, integration, and eclecticism – although there was, nevertheless, some hardening of positions within some schools. These trends were reflected in and influenced by lively debates within the field and critiques from various sources, including feminism and post-modernism, that reflected in part the cultural and political tenor of the times, and which foreshadowed the emergence (in the 1980s and 1990s) of the various “post-systems” constructivist and social constructionist approaches. While there was still debate within the field about whether, or to what degree, the systemic-constructivist and medical-biological paradigms were necessarily antithetical to each other (refer to Anti-psychiatry; Biopsychosocial model), there was a growing willingness and tendency on the part of family therapists to work in multi-modal clinical partnerships with other members of the helping and medical professions.

From the mid-1980s to the present, the field has been marked by a diversity of approaches that partly reflect the original schools, but which also draw on other theories and methods from individual psychotherapy and elsewhere – these approaches and sources include: brief therapy, structural therapy, constructivist approaches (e.g. Milan systems, post-Milan/collaborative/conversational, reflective), Bring forthism approach (e.g. Dr. Karl Tomm’s IPscope model and Interventive interviewing), solution-focused therapy, narrative therapy, a range of cognitive and behavioural approaches, psychodynamic and object relations approaches, attachment and emotionally focused therapy, intergenerational approaches, network therapy, and multi-systemic therapy (MST). Multicultural, intercultural, and integrative approaches are being developed, with Vincenzo Di Nicola weaving a synthesis of family therapy and transcultural psychiatry in his model of cultural family therapy, A Stranger in the Family: Culture, Families, and Therapy. Many practitioners claim to be “eclectic”, using techniques from several areas, depending upon their own inclinations and/or the needs of the client(s), and there is a growing movement toward a single “generic” family therapy that seeks to incorporate the best of the accumulated knowledge in the field and which can be adapted to many different contexts; however, there are still a significant number of therapists who adhere more or less strictly to a particular, or limited number of, approach(es).

The Liberation Based Healing framework for family therapy offers a complete paradigm shift for working with families while addressing the intersections of race, class, gender identity, sexual orientation and other socio-political identity markers. This theoretical approach and praxis is informed by Critical Pedagogy, Feminism, Critical Race Theory, and Decolonising Theory. This framework necessitates an understanding of the ways Colonisation, Cis-Heteronormativity, Patriarchy, White Supremacy and other systems of domination impact individuals, families and communities and centres the need to disrupt the status quo in how power operates. Traditional Western models of family therapy have historically ignored these dimensions and when white, male privilege has been critiqued, largely by feminist theory practitioners, it has often been to the benefit of middle class, white women’s experiences. While an understanding of intersectionality is of particular significance in working with families with violence, a liberatory framework examines how power, privilege and oppression operate within and across all relationships. Liberatory practices are based on the principles of Critical-Consciousness, Accountability and Empowerment. These principles guide not only the content of the therapeutic work with clients but also the supervisory and training process of therapists. Dr. Rhea Almeida, developed the Cultural Context Model as a way to operationalize these concepts into practice through the integration of culture circles, sponsors, and a socio-educational process within the therapeutic work.

Ideas and methods from family therapy have been influential in psychotherapy generally: a survey of over 2,500 US therapists in 2006 revealed that of the 10 most influential therapists of the previous quarter-century, three were prominent family therapists and that the marital and family systems model was the second most utilised model after cognitive behavioural therapy.

Techniques

Family therapy uses a range of counselling and other techniques including:

  • Structural therapy – identifies and re-orders the organisation of the family system.
  • Strategic therapy – looks at patterns of interactions between family members.
  • Systemic/Milan therapy – focuses on belief systems.
  • Narrative therapy – restoring of dominant problem-saturated narrative, emphasis on context, separation of the problem from the person.
  • Transgenerational therapy – transgenerational transmission of unhelpful patterns of belief and behaviour.
  • IPscope model and Interventive Interviewing.
  • Communication theory.
  • Psychoeducation.
  • Psychotherapy.
  • Relationship counselling.
  • Relationship education.
  • Systemic coaching.
  • Systems theory.
  • Reality therapy.
  • The genogram.

The number of sessions depends on the situation, but the average is 5-20 sessions. A family therapist usually meets several members of the family at the same time. This has the advantage of making differences between the ways family members perceive mutual relations as well as interaction patterns in the session apparent both for the therapist and the family. These patterns frequently mirror habitual interaction patterns at home, even though the therapist is now incorporated into the family system. Therapy interventions usually focus on relationship patterns rather than on analysing impulses of the unconscious mind or early childhood trauma of individuals as a Freudian therapist would do – although some schools of family therapy, for example psychodynamic and intergenerational, do consider such individual and historical factors (thus embracing both linear and circular causation) and they may use instruments such as the genogram to help to elucidate the patterns of relationship across generations.

The distinctive feature of family therapy is its perspective and analytical framework rather than the number of people present at a therapy session. Specifically, family therapists are relational therapists: They are generally more interested in what goes on between individuals rather than within one or more individuals, although some family therapists – in particular those who identify as psychodynamic, object relations, intergenerational, or experiential family therapists (EFTs) – tend to be as interested in individuals as in the systems those individuals and their relationships constitute. Depending on the conflicts at issue and the progress of therapy to date, a therapist may focus on analysing specific previous instances of conflict, as by reviewing a past incident and suggesting alternative ways family members might have responded to one another during it, or instead proceed directly to addressing the sources of conflict at a more abstract level, as by pointing out patterns of interaction that the family might have not noticed.

Family therapists tend to be more interested in the maintenance and/or solving of problems rather than in trying to identify a single cause. Some families may perceive cause-effect analyses as attempts to allocate blame to one or more individuals, with the effect that for many families a focus on causation is of little or no clinical utility. It is important to note that a circular way of problem evaluation is used as opposed to a linear route. Using this method, families can be helped by finding patterns of behaviour, what the causes are, and what can be done to better their situation.

Summary of Theories and Techniques

Theoretical ModelTheoristsSummaryTechniques
Adlerian family therapyAlfred AdlerAlso known as “individual psychology”. Sees the person as a whole. Ideas include compensation for feelings of inferiority leading to striving for significance toward a fictional final goal with a private logic. Birth order and mistaken goals are explored to examine mistaken motivations of children and adults in the family constellation.Psychoanalysis, typical day, reorienting, re-educating
Attachment theoryJohn Bowlby, Mary Ainsworth, Douglas HaldaneIndividuals are shaped by their experiences with caregivers in the first three years of life. Used as a foundation for Object Relations Theory. The Strange Situation experiment with infants involves a systematic process of leaving a child alone in a room in order to assess the quality of their parental bond.Psychoanalysis, play therapy
Bowenian family systems therapyMurray Bowen, Betty Carter, Philip Guerin, Michael Kerr, Thomas Fogarty, Monica McGoldrick, Edwin Friedman, Daniel PaperoAlso known as “intergenerational family therapy” (although there are also other schools of intergenerational family therapy). Family members are driven to achieve a balance of internal and external differentiation, causing anxiety, triangulation, and emotional cutoff. Families are affected by nuclear family emotional processes, sibling positions and multigenerational transmission patterns resulting in an undifferentiated family ego mass.Detriangulation, non-anxious presence, genograms, coaching
Cognitive behavioural family therapyJohn Gottman, Albert Ellis, Albert BanduraProblems are the result of operant conditioning that reinforces negative behaviours within the family’s interpersonal social exchanges that extinguish desired behaviour and promote incentives toward unwanted behaviours. This can lead to irrational beliefs and a faulty family schema.Therapeutic contracts, modelling, systematic desensitisation, shaping, charting, examining irrational beliefs
Collaborative language systems therapyHarry Goolishian, Harlene Anderson, Tom Andersen, Lynn Hoffman, Peggy PennIndividuals form meanings about their experiences within the context of social relationship on a personal and organisational level. Collaborative therapists help families reorganise and dis-solve their perceived problems through a transparent dialogue about inner thoughts with a “not-knowing” stance intended to illicit new meaning through conversation. Collaborative therapy is an approach that avoids a particular theoretical perspective in favour of a client-centred philosophical process.Dialogical conversation, not knowing, curiosity, being public, reflecting teams
Communications approachesVirginia Satir, John Banmen, Jane Gerber, Maria GomoriAll people are born into a primary survival triad between themselves and their parents where they adopt survival stances to protect their self-worth from threats communicated by words and behaviours of their family members. Experiential therapists are interested in altering the overt and covert messages between family members that affect their body, mind and feelings in order to promote congruence and to validate each person’s inherent self-worth.Equality, modelling communication, family life chronology, family sculpting, metaphors, family reconstruction
Contextual therapyIvan Boszormenyi-NagyFamilies are built upon an unconscious network of implicit loyalties between parents and children that can be damaged when these “relational ethics” of fairness, trust, entitlement, mutuality and merit are breached.Rebalancing, family negotiations, validation, filial debt repayment
Cultural family therapyVincenzo Di Nicola
Key influences: Celia Falicov, Antonio Ferreira, James Framo, Edwin Friedman, Mara Selvini Palazzoli, Carlos Sluzki, Victor Turner, Michael White
A synthesis of systemic family therapy with cultural psychiatry to create cultural family therapy (CFT). CFT is an interweaving of stories (family predicaments expressed in narratives of family life) and tools (clinical methods for working with and making sense of these stories in cultural context). Integrates and synthesizes systemic therapy and cultural and medical anthropology with narrative therapy.Conceptual tools for working across cultures – spirals, masks, roles, codes, cultural strategies, bridges, stories, multiple codes (metaphor and somatics), therapy as “story repair”
Emotion-focused therapySue Johnson, Les GreenbergCouples and families can develop rigid patterns of interaction based on powerful emotional experiences that hinder emotional engagement and trust. Treatment aims to enhance empathic capabilities of family members by exploring deep-seated habits and modifying emotional cues.Reflecting, validation, heightening, reframing, restructuring
Experiential family therapyCarl Whitaker, David Keith, Laura Roberto, Walter Kempler, John Warkentin, Thomas Malone, August NapierStemming from Gestalt foundations, change and growth occurs through an existential encounter with a therapist who is intentionally “real” and authentic with clients without pretence, often in a playful and sometimes absurd way as a means to foster flexibility in the family and promote individuation.Battling, constructive anxiety, redefining symptoms, affective confrontation, co-therapy, humour
Family mode deactivation therapy (FMDT)Jack A. ApscheTarget population adolescents with conduct and behavioural problems. Based on schema theory. Integrate mindfulness to focus family on the present. Validate core beliefs based on past experiences. Offer viable alternative responses. Treatment is based on case conceptualisation process; validate and clarify core beliefs, fears, triggers, and behaviours. Redirect behaviour by anticipating triggers and realigning beliefs and fears.Cognitive behavioural therapy, mindfulness, acceptance and commitment therapy, dialectical behaviour therapy, defusion, validate-clarify-redirect
Family-of-origin therapyJames FramoHe developed an object relations approach to intergenerational and family-of-origin therapy.Working with several generations of the family, family-of-origin approach with families in therapy and with trainees
Feminist family therapySandra Bem Marianne WaltersComplications from social and political disparity between genders are identified as underlying causes of conflict within a family system. Therapists are encouraged to be aware of these influences in order to avoid perpetuating hidden oppression, biases and cultural stereotypes and to model an egalitarian perspective of healthy family relationships.Demystifying, modelling, equality, personal accountability
Milan systemic family therapyLuigi Boscolo, Gianfranco Cecchin, Mara Selvini Palazzoli, Giuliana PrataA practical attempt by the “Milan Group” to establish therapeutic techniques based on Gregory Bateson’s cybernetics that disrupts unseen systemic patterns of control and games between family members by challenging erroneous family beliefs and reworking the family’s linguistic assumptions.Hypothesizing, circular questioning, neutrality, counter-paradox
MRI brief therapyGregory Bateson, Milton Erickson, Heinz von FoersterEstablished by the Mental Research Institute (MRI) as a synthesis of ideas from multiple theorists in order to interrupt misguided attempts by families to create first and second order change by persisting with “more of the same”, mixed signals from unclear metacommunication and paradoxical double-bind messages.Reframing, prescribing the symptom, relabelling, restraining (going slow), Bellac Ploy
Narrative therapyMichael White, David EpstonPeople use stories to make sense of their experience and to establish their identity as a social and political constructs based on local knowledge. Narrative therapists avoid marginalising their clients by positioning themselves as a co-editor of their reality with the idea that “the person is not the problem, but the problem is the problem.”Deconstruction, externalising problems, mapping, asking permission
Object relations therapyHazan & Shaver, David Scharff & Jill Scharff, James FramoIndividuals choose relationships that attempt to heal insecure attachments from childhood. Negative patterns established by their parents (object) are projected onto their partners.Detriangulation, co-therapy, psychoanalysis, holding environment
Psychoanalytic family therapyNathan AckermanBy applying the strategies of Freudian psychoanalysis to the family system therapists can gain insight into the interlocking psychopathologies of the family members and seek to improve complementarity.Psychoanalysis, authenticity, joining, confrontation
Solution focused therapyKim Insoo Berg, Steve de Shazer, William O’Hanlon, Michelle Weiner-Davis, Paul WatzlawickThe inevitable onset of constant change leads to negative interpretations of the past and language that shapes the meaning of an individual’s situation, diminishing their hope and causing them to overlook their own strengths and resources.Future focus, beginner’s mind, miracle question, goal setting, scaling
Strategic therapyJay Haley, Cloe MadanesSymptoms of dysfunction are purposeful in maintaining homeostasis in the family hierarchy as it transitions through various stages in the family life cycle.Directives, paradoxical injunctions, positioning, metaphoric tasks, restraining (going slow)
Structural family therapySalvador Minuchin, Harry Aponte, Charles Fishman, Braulio MontalvoFamily problems arise from maladaptive boundaries and subsystems that are created within the overall family system of rules and rituals that governs their interactions.Joining, family mapping, hypothesizing, re-enactments, reframing, unbalancing

Evidence Base

Family therapy has an evolving evidence base. A summary of current evidence is available via the UK’s Association of Family Therapy. Evaluation and outcome studies can also be found on the Family Therapy and Systemic Research Centre website. The website also includes quantitative and qualitative research studies of many aspects of family therapy.

According to a 2004 French government study conducted by French Institute of Health and Medical Research, family and couples therapy was the second most effective therapy after Cognitive behavioural therapy. The study used meta-analysis of over a hundred secondary studies to find some level of effectiveness that was either “proven” or “presumed” to exist. Of the treatments studied, family therapy was presumed or proven effective at treating schizophrenia, bipolar disorder, anorexia and alcohol dependency.

Concerns and Criticism

In a 1999 address to the Coalition of Marriage, Family and Couples Education conference in Washington, D.C., University of Minnesota Professor William Doherty said:

“I take no joy in being a whistle blower, but it’s time. I am a committed marriage and family therapist, having practiced this form of therapy since 1977. I train marriage and family therapists. I believe that marriage therapy can be very helpful in the hands of therapists who are committed to the profession and the practice. But there are a lot of problems out there with the practice of therapy – a lot of problems.”

Doherty suggested questions prospective clients should ask a therapist before beginning treatment:

  1. “Can you describe your background and training in marital therapy?”
  2. “What is your attitude toward salvaging a troubled marriage versus helping couples break up?”
  3. “What is your approach when one partner is seriously considering ending the marriage and the other wants to save it?”
  4. “What percentage of your practice is marital therapy?”
  5. “Of the couples you treat, what percentage would you say work out enough of their problems to stay married with a reasonable amount of satisfaction with the relationship.” “What percentage break up while they are seeing you?” “What percentage do not improve?” “What do you think makes the differences in these results?”

Licensing and Degrees

Family therapy practitioners come from a range of professional backgrounds, and some are specifically qualified or licensed/registered in family therapy (licensing is not required in some jurisdictions and requirements vary from place to place). In the United Kingdom, family therapists will have a prior relevant professional training in one of the helping professions usually psychologists, psychotherapists, or counsellors who have done further training in family therapy, either a diploma or an M.Sc. In the United States there is a specific degree and license as a marriage and family therapist; however, psychologists, nurses, psychotherapists, social workers, or counsellors, and other licensed mental health professionals may practice family therapy. In the UK, family therapists who have completed a four-year qualifying programme of study (MSc) are eligible to register with the professional body the Association of Family Therapy (AFT), and with the UK Council for Psychotherapy (UKCP).

A master’s degree is required to work as a Marriage and Family Therapist (MFT) in some American states. Most commonly, MFTs will first earn a M.S. or M.A. degree in marriage and family therapy, counselling, psychology, family studies, or social work. After graduation, prospective MFTs work as interns under the supervision of a licensed professional and are referred to as an MFTi.

Prior to 1999 in California, counsellors who specialised in this area were called Marriage, Family and Child Counsellors. Today, they are known as Marriage and Family Therapists (MFT), and work variously in private practice, in clinical settings such as hospitals, institutions, or counselling organisations.

Marriage and family therapists in the United States and Canada often seek degrees from accredited Masters or Doctoral programmes recognised by the Commission on Accreditation for Marriage and Family Therapy Education (COAMFTE), a division of the American Association of Marriage and Family Therapy.

Requirements vary, but in most states about 3,000 hours of supervised work as an intern are needed to sit for a licensing exam. MFTs must be licensed by the state to practice. Only after completing their education and internship and passing the state licensing exam can a person call themselves a Marital and Family Therapist and work unsupervised.

License restrictions can vary considerably from state to state. Contact information about licensing boards in the United States are provided by the Association of Marital and Family Regulatory Boards.

There have been concerns raised within the profession about the fact that specialist training in couples therapy – as distinct from family therapy in general – is not required to gain a license as an MFT or membership of the main professional body, the AAMFT.

Values and Ethics

Since issues of interpersonal conflict, power, control, values, and ethics are often more pronounced in relationship therapy than in individual therapy, there has been debate within the profession about the different values that are implicit in the various theoretical models of therapy and the role of the therapist’s own values in the therapeutic process, and how prospective clients should best go about finding a therapist whose values and objectives are most consistent with their own. An early paper on ethics in family therapy written by Vincenzo Di Nicola in consultation with a bioethicist asked basic questions about whether strategic interventions “mean what they say” and if it is ethical to invent opinions offered to families about the treatment process, such as statements saying that half of the treatment team believes one thing and half believes another. Specific issues that have emerged have included an increasing questioning of the longstanding notion of therapeutic neutrality, a concern with questions of justice and self-determination, connectedness and independence, “functioning” versus “authenticity”, and questions about the degree of the therapist’s “pro-marriage/family” versus “pro-individual” commitment.

The American Association for Marriage and Family Therapy requires members to adhere to a “Code of Ethics”, including a commitment to “continue therapeutic relationships only so long as it is reasonably clear that clients are benefiting from the relationship.”

Founders and Key Influences

Some key developers of family therapy are:

  • Alfred Adler (individual psychology).
  • Nathan Ackerman (psychoanalytic).
  • Tom Andersen (reflecting practices and dialogues about dialogues).
  • Harlene Anderson (postmodern collaborative therapy and Collaborative Language Systems).
  • Maurizio Andolfi (interactional, integrative, multigenerational, and relational family therapy).
  • Harry J Aponte (Person-of-the-Therapist).
  • Jack A. Apsche (family mode deactivation therapy, FMDT).
  • Gregory Bateson (1904–1980) (cybernetics, systems theory).
  • Ivan Boszormenyi-Nagy (contextual therapy, intergenerational, relational ethics).
  • Murray Bowen (systems theory, intergenerational).
  • Steve de Shazer (solution focused therapy).
  • Vincenzo Di Nicola (cultural family therapy).
  • Milton H. Erickson (hypnotherapy, strategic therapy, brief therapy).
  • Richard Fisch (brief therapy, strategic therapy).
  • James Framo (object relations theory, intergenerational, family-of-origin therapy).
  • Edwin Friedman (family process in religious congregations).
  • Harry Goolishian (postmodern collaborative therapy and collaborative language systems).
  • John Gottman (marriage).
  • Robert-Jay Green (LGBT, cross-cultural issues).
  • Douglas Haldane (Attachment-based couple therapist).
  • Jay Haley (strategic therapy, communications).
  • Lynn Hoffman (strategic, post-systems, collaborative).
  • Don D. Jackson (systems theory).
  • Sue Johnson (emotionally focused therapy, attachment theory).
  • Walter Kempler (Gestalt psychology).
  • Cloe Madanes (strategic therapy).
  • Salvador Minuchin (structural family therapy).
  • Braulio Montalvo (structural family therapy).
  • Virginia Satir (communications, experiential, conjoint and co-therapy).
  • Mara Selvini Palazzoli (Milan family systems therapy).
  • Karl Tomm (IPscope model and interventive interviewing, Bringforthism).
  • Robin Skynner (group analysis).
  • Paul Watzlawick (brief therapy, systems theory).
  • John Weakland (brief therapy, strategic therapy, systems theory).
  • Carl Whitaker (family systems, experiential, co-therapy).
  • Michael White (narrative therapy).
  • Lyman Wynne (schizophrenia, pseudomutuality).

What is a Double Bind?

Introduction

A double bind is a dilemma in communication in which an individual (or group) receives two or more conflicting messages, with one negating the other. In some circumstances (particularly families and relationships) this might be emotionally distressing. This creates a situation in which a successful response to one message results in a failed response to the other (and vice versa), so that the person will automatically be wrong regardless of response. The double bind occurs when the person cannot confront the inherent dilemma, and therefore can neither resolve it nor opt out of the situation.

Double bind theory was first described by Gregory Bateson and his colleagues in the 1950s.

Double binds are often utilised as a form of control without open coercion – the use of confusion makes them difficult both to respond to and to resist.

A double bind generally includes different levels of abstraction in the order of messages and these messages can either be stated explicitly or implicitly within the context of the situation, or they can be conveyed by tone of voice or body language. Further complications arise when frequent double binds are part of an ongoing relationship to which the person or group is committed.

Refer to Family Therapy and the Bateson Project (1953-1963).

Explanation

The double bind is often misunderstood to be a simple contradictory situation, where the subject is trapped by two conflicting demands. While it is true that the core of the double bind is two conflicting demands, the difference lies in how they are imposed upon the subject, what the subject’s understanding of the situation is, and who (or what) imposes these demands upon the subject. Unlike the usual no-win situation, the subject has difficulty in defining the exact nature of the paradoxical situation in which they are caught. The contradiction may be unexpressed in its immediate context and therefore invisible to external observers, only becoming evident when a prior communication is considered. Typically, a demand is imposed upon the subject by someone whom they respect (such as a parent, teacher, or doctor) but the demand itself is inherently impossible to fulfil because some broader context forbids it. For example, this situation arises when a person in a position of authority imposes two contradictory conditions but there exists an unspoken rule that one must never question authority.

Gregory Bateson and his colleagues defined the double bind as follows:

  1. The situation involves two or more people, one of whom (for the purpose of the definition), is designated as the “subject”. The others are people who are considered the subject’s superiors: figures of authority (such as parents), whom the subject respects.
  2. Repeated experience: the double bind is a recurrent theme in the experience of the subject, and as such, cannot be resolved as a single traumatic experience.
  3. A ‘primary injunction’ is imposed on the subject by the others generally in one of two forms:
    • (a) “Do X, or I will punish you”; or
    • (b) “Do not do X, or I will punish you.”
    • The punishment may include the withdrawing of love, the expression of hate and anger, or abandonment resulting from the authority figure’s expression of helplessness.
  4. A ‘secondary injunction’ is imposed on the subject, conflicting with the first at a higher and more abstract level. For example: “You must do X, but only do it because you want to.” It is unnecessary for this injunction to be expressed verbally.
  5. If necessary, a ‘tertiary injunction’ is imposed on the subject to prevent them from escaping the dilemma.
    • See phrase examples below for clarification.
  6. Finally, Bateson states that the complete list of the previous requirements may be unnecessary, in the event that the subject is already viewing their world in double bind patterns. Bateson goes on to give the general characteristics of such a relationship:
    • When the subject is involved in an intense relationship; that is, a relationship in which he feels it is vitally important that he discriminate accurately what sort of message is being communicated so that he may respond appropriately;
    • And, the subject is caught in a situation in which the other person in the relationship is expressing two orders of message and one of these denies the other;
    • And, the subject is unable to comment on the messages being expressed to correct his discrimination of what order of message to respond to: i.e., he cannot make a metacommunicative statement.

Thus, the essence of a double bind is two conflicting demands, each on a different logical level, neither of which can be ignored or escaped. This leaves the subject torn both ways, so that whichever demand they try to meet, the other demand cannot be met. “I must do it, but I can’t do it” is a typical description of the double-bind experience.

For a double bind to be effective, the subject must be unable to confront or resolve the conflict between the demand placed by the primary injunction and that of the secondary injunction. In this sense, the double bind differentiates itself from a simple contradiction to a more inexpressible internal conflict, where the subject really wants to meet the demands of the primary injunction, but fails each time through an inability to address the situation’s incompatibility with the demands of the secondary injunction. Thus, subjects may express feelings of extreme anxiety in such a situation, as they attempt to fulfil the demands of the primary injunction albeit with obvious contradictions in their actions.

This was a problem in United States legal circles prior to the Fifth Amendment to the United States Constitution being applied to state action. A person could be subpoenaed to testify in a federal case and given Fifth Amendment immunity for testimony in that case. However, since the immunity did not apply to a state prosecution, the person could refuse to testify at the Federal level despite being given immunity, thus subjecting the person to imprisonment for contempt of court, or the person could testify, and the information they were forced to give in the Federal proceeding could then be used to convict the person in a state proceeding.

Brief History

The term double bind was first used by the anthropologist Gregory Bateson and his colleagues (including Don D. Jackson, Jay Haley and John H. Weakland) in the mid-1950s in their discussions on complexity of communication in relation to schizophrenia. Bateson made clear that such complexities are common in normal circumstances, especially in “play, humour, poetry, ritual and fiction” (see Logical Types below). Their findings indicated that the tangles in communication often diagnosed as schizophrenia are not necessarily the result of an organic brain dysfunction. Instead, they found that destructive double binds were a frequent pattern of communication among families of patients, and they proposed that growing up amidst perpetual double binds could lead to learned patterns of confusion in thinking and communication.

Complexity in Communication

Human communication is complex, and context is an essential part of it. Communication consists of the words said, tone of voice, and body language. It also includes how these relate to what has been said in the past; what is not said, but is implied; how these are modified by other nonverbal cues, such as the environment in which it is said, and so forth. For example, if someone says “I love you”, one takes into account who is saying it, their tone of voice and body language, and the context in which it is said. It may be a declaration of passion or a serene reaffirmation, insincere and/or manipulative, an implied demand for a response, a joke, its public or private context may affect its meaning, and so forth.

Conflicts in communication are common and often we ask “What do you mean?” or seek clarification in other ways. This is called meta-communication: communication about the communication. Sometimes, asking for clarification is impossible. Communication difficulties in ordinary life often occur when meta-communication and feedback systems are lacking or inadequate or there is not enough time for clarification.

Double binds can be extremely stressful and become destructive when one is trapped in a dilemma and punished for finding a way out. But making the effort to find the way out of the trap can lead to emotional growth.

Examples

The classic example given of a negative double bind is of a mother telling her child that she loves them, while at the same time turning away in disgust, or inflicting corporal punishment as discipline: the words are socially acceptable; the body language is in conflict with it. The child does not know how to respond to the conflict between the words and the body language and, because the child is dependent on the mother for basic needs, they are in a quandary. Small children have difficulty articulating contradictions verbally and can neither ignore them nor leave the relationship.

Another example is when one is commanded to “be spontaneous”. The very command contradicts spontaneity, but it only becomes a double bind when one can neither ignore the command nor comment on the contradiction. Often, the contradiction in communication is not apparent to bystanders unfamiliar with previous communications.

Phrase Examples

  • An example from Gerald M. Weinberg in a non-family situation…. “I suggest you find someone who you feel is more capable in this role”.
    • This requires the recipient to either confirm that the current incumbent in the role is sufficiently capable, or accept that they choose someone else based on their feelings – not an objective assessment of whether the incumbent is capable.
  • Mother telling her child: “You must love me”.
  • The primary injunction here is the command itself: “you must”; the secondary injunction is the unspoken reality that love is spontaneous, that for the child to love the mother genuinely, it can only be of their own accord.
  • Child-abuser to child: “You should have escaped from me earlier, now it’s too late—because now, nobody will believe that you didn’t want what I have done”, while at the same time blocking all of the child’s attempts to escape.
  • Child-abusers often start the double-bind relationship by “grooming” the child, giving little concessions, or gifts or privileges to them, thus the primary injunction is: “You should like what you are getting from me!”
  • When the child begins to go along (i.e. begins to like what they are receiving from the person), then the interaction goes to the next level and small victimisation occurs, with the secondary injunction being: “I am punishing you! (for whatever reason the child-abuser is coming up with, e.g. “because you were bad/naughty/messy”, or “because you deserve it”, or “because you made me do it”, etc.).
  • If child shows any resistance (or tries to escape) from the abuser, then the words: “You should have escaped from me earlier (…)” serve as the third level or tertiary injunction.
  • Then the loop starts to feed on itself, allowing for ever worse victimisation to occur.
  • Mother to son: “Leave your sister alone!”, while the son knows his sister will approach and antagonize him to get him into trouble.
  • The primary injunction is the command, which he will be punished for breaking.
    • The secondary injunction is the knowledge that his sister will get into conflict with him, but his mother will not know the difference and will default to punishing him.
    • He may be under the impression that if he argues with his mother, he may be punished.
    • One possibility for the son to escape this double bind is to realise that his sister only antagonises him to make him feel anxious (if indeed it is the reason behind his sister’s behaviour).
  • If he were not bothered about punishment, his sister might not bother him.
    • He could also leave the situation entirely, avoiding both the mother and the sister.
    • The sister can not claim to be bothered by a non-present brother, and the mother can not punish (or scapegoat) a non-present son.
    • Other solutions exist too, which are based on the creative application of logic and reasoning.
  • An apt reply would be: “Please tell sis the same”. If mother wants to ‘scapegoat’ him, her response will be negative.
    • The command has a negative undertone towards the son.

Positive Double Binds

Bateson also described positive double binds, both in relation to Zen Buddhism with its path of spiritual growth, and the use of therapeutic double binds by psychiatrists to confront their patients with the contradictions in their life in such a way that would help them heal. One of Bateson’s consultants, Milton H. Erickson (5 volumes, edited by Rossi) eloquently demonstrated the productive possibilities of double binds through his own life, showing the technique in a brighter light.

The Science

One of the causes of double binds is the loss of feedback systems. Gregory Bateson and Lawrence S. Bale describe double binds that have arisen in science that have caused decades-long delays of progress in science because the scientific community had defined something as outside of its scope (or as “not science”) – see Bateson in his Introduction to Steps to an Ecology of Mind (1972, 2000), pp.xv–xxvi; and Bale in his article, Gregory Bateson, Cybernetics and the Social/Behavioural Sciences (esp. pp.1-8) on the paradigm of classical science vs. that of systems theory/cybernetics. (See also Bateson’s description in his Forward of how the double bind hypothesis fell into place).

Work by Bateson

Schizophrenia

The Double Bind Theory was first articulated in relationship to schizophrenia, but Bateson and his colleagues hypothesized that schizophrenic thinking was not necessarily an inborn mental disorder but a learned confusion in thinking.

It is helpful to remember the context in which these ideas were developed. Bateson and his colleagues were working in the Veteran’s Administration Hospital (1949-1962) with World War II veterans. As soldiers they’d been able to function well in combat, but the effects of life-threatening stress had affected them. At that time, 18 years before Post-Traumatic Stress Disorder was officially recognised, the veterans had been saddled with the catch-all diagnosis of schizophrenia. Bateson did not challenge the diagnosis but he did maintain that the seeming nonsense the patients said at times did make sense within context, and he gives numerous examples in section III of Steps to an Ecology of Mind, “Pathology in Relationship”. For example, a patient misses an appointment, and when Bateson finds him later the patient says ‘the judge disapproves’; Bateson responds, “You need a defense lawyer”. Bateson also surmised that people habitually caught in double binds in childhood would have greater problems – that in the case of the schizophrenic, the double bind is presented continually and habitually within the family context from infancy on. By the time the child is old enough to have identified the double bind situation, it has already been internalised, and the child is unable to confront it. The solution then is to create an escape from the conflicting logical demands of the double bind, in the world of the delusional system.

One solution to a double bind is to place the problem in a larger context, a state Bateson identified as Learning III, a step up from Learning II (which requires only learned responses to reward/consequence situations). In Learning III, the double bind is contextualized and understood as an impossible no-win scenario so that ways around it can be found.

Bateson’s double bind theory was never followed up by research into whether family systems imposing systematic double binds might be a cause of schizophrenia. This complex theory has been only partly tested, and there are gaps in the current psychological and experimental evidence required to establish causation. The current understanding of schizophrenia emphasizes the robust scientific evidence for a genetic predisposition to the disorder, with psychosocial stressors, including dysfunctional family interaction patterns, as secondary causative factors in some instances.

Evolution

After many years of research into schizophrenia, Bateson continued to explore problems of communication and learning, first with dolphins, and then with the more abstract processes of evolution. Bateson emphasised that any communicative system characterized by different logical levels might be subject to double bind problems. Especially including the communication of characteristics from one generation to another (genetics and evolution).

“…evolution always followed the pathways of viability. As Lewis Carroll has pointed out, the theory [of natural selection] explains quite satisfactorily why there are no bread-and-butter-flies today.”

Bateson used the fictional Bread and Butter Fly (from Through the Looking Glass, and What Alice Found There) to illustrate the double bind in terms of natural selection. The gnat points out that the insect would be doomed if he found his food (which would dissolve his own head, since this insect’s head is made of sugar, and his only food is tea), and starve if he did not. Alice suggests that this must happen quite often, to which the gnat replies: “It always happens.”

The pressures that drive evolution therefore represent a genuine double bind. And there is truly no escape: “It always happens.” No species can escape natural selection, including our own.

Bateson suggested that all evolution is driven by the double bind, whenever circumstances change: If any environment becomes toxic to any species, that species will die out unless it transforms into another species, in which case, the species becomes extinct anyway.

Most significant here is Bateson’s exploration of what he later came to call ‘the pattern that connects’ – that problems of communication which span more than one level (e.g. the relationship between the individual and the family) should also be expected to be found spanning other pairs of levels in the hierarchy (e.g. the relationship between the genotype and the phenotype):

“We are very far, then, from being able to pose specific questions for the geneticist; but I believe that the wider implications of what I have been saying modify somewhat the philosophy of genetics. Our approach to the problems of schizophrenia by way of a theory of levels or logical types has disclosed first that the problems of adaptation and learning and their pathologies must be considered in terms of a hierarchic system in which stochastic change occurs at the boundary points between the segments of the hierarchy. We have considered three such regions of stochastic change—the level of genetic mutation, the level of learning, and the level of change in family organization. We have disclosed the possibility of a relationship of these levels which orthodox genetics would deny, and we have disclosed that at least in human societies the evolutionary system consists not merely in the selective survival of those persons who happen to select appropriate environments but also in the modification of family environment in a direction which might enhance the phenotypic and genotypic characteristics of the individual members.”

Girard’s Mimetic Double Bind

René Girard, in his literary theory of mimetic desire, proposes what he calls a “model-obstacle”, a role model who demonstrates an object of desire and yet, in possessing that object, becomes a rival who obstructs fulfilment of the desire. According to Girard, the “internal mediation” of this mimetic dynamic “operates along the same lines as what Gregory Bateson called the ‘double bind’.” Girard found in Sigmund Freud’s psychoanalytic theory, a precursor to mimetic desire. “The individual who ‘adjusts’ has managed to relegate the two contradictory injunctions of the double bind—to imitate and not to imitate—to two different domains of application. This is, he divides reality in such a way as to neutralize the double bind.” While critical of Freud’s doctrine of the unconscious mind, Girard sees the ancient Greek tragedy, Oedipus Rex, and key elements of Freud’s Oedipus complex, patricidal and incestuous desire, to serve as prototypes for his own analysis of the mimetic double bind.

Far from being restricted to a limited number of pathological cases, as American theoreticians suggest, the double bind – a contradictory double imperative, or rather a whole network of contradictory imperatives – is an extremely common phenomenon. In fact, it is so common that it might be said to form the basis of all human relationships.

Bateson is undoubtedly correct in believing that the effects of the double bind on the child are particularly devastating. All the grown-up voices around him, beginning with those of the father and mother (voices which, in our society at least, speak for the culture with the force of established authority) exclaim in a variety of accents, “Imitate us!” “Imitate me!” “I bear the secret of life, of true being!” The more attentive the child is to these seductive words, and the more earnestly he responds to the suggestions emanating from all sides, the more devastating will be the eventual conflicts. The child possesses no perspective that will allow him to see things as they are. He has no basis for reasoned judgements, no means of foreseeing the metamorphosis of his model into a rival. This model’s opposition reverberates in his mind like a terrible condemnation; he can only regard it as an act of excommunication. The future orientation of his desires – that is, the choice of his future models – will be significantly affected by the dichotomies of his childhood. In fact, these models will determine the shape of his personality.

If desire is allowed its own bent, its mimetic nature will almost always lead it into a double bind. The unchanneled mimetic impulse hurls itself blindly against the obstacle of a conflicting desire. It invites its own rebuffs and these rebuffs will in turn strengthen the mimetic inclination. We have, then, a self-perpetuating process, constantly increasing in simplicity and fervor. Whenever the disciple borrows from his model what he believes to be the “true” object, he tries to possess that truth by desiring precisely what this model desires. Whenever he sees himself closest to the supreme goal, he comes into violent conflict with a rival. By a mental shortcut that is both eminently logical and self-defeating, he convinces himself that the violence itself is the most distinctive attribute of this supreme goal! Ever afterward, violence will invariably awaken desire… (René Girard, Violence and the Sacred: “From Mimetic Desire to the Monstrous Double”, pp.156-157).

Neuro-Linguistic Programming

The field of Neuro-Linguistic Programming (NLP) also makes use of the expression “double bind”. Grinder and Bandler (both of whom had personal contact with Bateson and Erickson) asserted that a message could be constructed with multiple messages, whereby the recipient of the message is given the impression of choice – although both options have the same outcome at a higher level of intention. This is called a “double bind” in NLP terminology, and has applications in both sales and therapy. In therapy, the practitioner may seek to challenge destructive double binds that limit the client in some way and may also construct double binds in which both options have therapeutic consequences. In a sales context, the speaker may give the respondent the illusion of choice between two possibilities. For example, a salesperson might ask: “Would you like to pay cash or by credit card?”, with both outcomes presupposing that the person will make the purchase; whereas the third option (that of not buying) is intentionally excluded from the spoken choices.

Note that in the NLP context, the use of the phrase “double bind” does not carry the primary definition of two conflicting messages; it is about creating a false sense of choice which ultimately binds to the intended outcome. In the “cash or credit card?” example, this is not a “Bateson double bind” since there is no contradiction, although it still is an “NLP double bind”. Similarly if a salesman were selling a book about the evils of commerce, it could perhaps be a “Bateson double bind” if the buyer happened to believe that commerce was evil, yet felt compelled or obliged to buy the book.

What was the Bateson Project?

Introduction

The Bateson Project (1953-1963) was the name given to a ground-breaking collaboration organised by Gregory Bateson which was responsible for some of the most important papers and innovations in communication and psychotherapy in the 1950s and early 1960s. Its other members were Donald deAvila Jackson, Jay Haley, John Weakland, and Bill Fry.

Background

Perhaps their most famous and influential publication was Towards a Theory of Schizophrenia (1956), which introduced the concept of the Double Bind, and helped found Family Therapy.

One of the project’s first locations was the Menlo Park VA Hospital, which was chosen because of Bateson’s previous work there as an ethnologist. The initial research, which was funded by a Rockefeller grant, focused on “strange communication” and nonsensical language among the patients of the institution who were suffering from schizophrenia. The group studied this within the context of double bind communication in family dynamics.

Refer to Double Bind and Family Therapy.

What is Catatonia?

Introduction

Catatonia is a neuropsychiatric behavioural syndrome that is characterised by abnormal movements, immobility, abnormal behaviours, and withdrawal. The onset of catatonia can be acute or subtle and symptoms can wax, wane, or change during episodes. There are several subtypes of catatonia: akinetic catatonia, excited catatonia, malignant catatonia, and other forms.

Although catatonia has historically been related to schizophrenia (catatonic schizophrenia), catatonia is most often seen in mood disorders. It is now known that catatonic symptoms are nonspecific and may be observed in other mental, neurologic, and medical conditions. Catatonia is not a stand-alone diagnosis (although some experts disagree), and the term is used to describe a feature of the underlying disorder.

Recognising and treating catatonia is very important as failure to do this can lead to poor outcomes and can be potentially fatal. Treatment with benzodiazepines or ECT can lead to remission of catatonia. There is growing evidence of the effectiveness of the NMDA receptor antagonists amantadine and memantine for benzodiazepine-resistant catatonia. Antipsychotics are sometimes employed, but they can worsen symptoms and have serious adverse effects.

Brief History

It was first described in 1874 by Karl Ludwig Kahlbaum as Die Katatonie oder das Spannungsirresein (Catatonia or Tension Insanity).

Aetiology/Causes

Catatonia is almost always secondary to another underlying illness, often a psychiatric disorder. Mood disorders such as a bipolar disorder and depression are the most common aetiologies to progress to catatonia. Other psychiatric associations include schizophrenia and other primary psychotic disorders. It also is related to autism spectrum disorders.

Catatonia is also seen in many medical disorders, including infections (such as encephalitis), autoimmune disorders, meningitis, focal neurological lesions (including strokes), alcohol withdrawal, abrupt or overly rapid benzodiazepine withdrawal, cerebrovascular disease, neoplasms, head injury, and some metabolic conditions (homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcaemia).

Epidemiology

Catatonia has been mostly studied in acutely ill psychiatric patients. Catatonia frequently goes unrecognised, leading to the belief that the syndrome is rare, however, this is not true and prevalence has been reported to be as high as 10% in patients with acute psychiatric illnesses. 21-46% of all catatonia cases can be attributed to a general medical condition.

Pathogenesis/Mechanism

The pathophysiology that leads to catatonia is still poorly understood and a definite mechanism remains unknown. Neurologic studies have implicated several pathways, however, it remains unclear whether these findings are the cause or the consequence of the disorder.

Abnormalities in GABA, glutamate signalling, serotonin, and dopamine transmission are believed to be implicated in catatonia.

Furthermore, it has also been hypothesized that pathways that connect the basal ganglia with the cortex and thalamus is involved in the development of catatonia.

Signs and Symptoms

The presentation of a patient with catatonia varies greatly depending on the subtype, underlying cause and it can be acute or subtle.

Because most patients with catatonia have an underlying psychiatric illness, the majority will present with worsening depression, mania, or psychosis followed by catatonia symptoms. Catatonia presents as a motor disturbance in which patients will display marked reduction in movement, marked agitation, or a mixture of both despite having the physical capacity to move normally. These patients may be unable to start an action or stop one. Movements and mannerisms may be repetitive, or purposeless.

The most common signs of catatonia are immobility, mutism, withdrawal and refusal to eat, staring, negativism, posturing (rigidity), rigidity, waxy flexibility/catalepsy, stereotypy (purposeless, repetitive movements), echolalia or echopraxia, verbigeration (repeat meaningless phrases). It should not be assumed that patients presenting with catatonia are unaware of their surroundings as some patients can recall in detail their catatonic state and their actions.

There are several subtypes of catatonia and they are characterised by the specific movement disturbance and associated features. Although catatonia can be divided into various subtypes, the natural history of catatonia is often fluctuant and different states can exist within the same individual.

Subtypes

  • Retarded/Withdrawn Catatonia:
    • This form of catatonia is characterised by decreased response to external stimuli, immobility or inhibited movement, mutism, staring, posturing, and negativism.
    • Patients may sit or stand in the same position for hours, may hold odd positions, and may resist movement of their extremities.
  • Excited Catatonia:
    • Excited catatonia is characterised by odd mannerisms/gestures, performing purposeless or inappropriate actions, excessive motor activity restlessness, stereotypy, impulsivity, agitation, combativeness.
    • Speech and actions may be repetitive or mimic another person’s.
    • People in this state are extremely hyperactive and may have delusions and hallucinations.
    • Catatonic excitement is commonly cited as one of the most dangerous mental states in psychiatry.
  • Malignant Catatonia:
    • Malignant catatonia is a life-threatening condition that may progress rapidly within a few days. It is characterised by fever, abnormalities in blood pressure, heart rate, respiratory rate, diaphoresis (sweating), and delirium.
    • Certain lab findings are common with this presentation, however, they are nonspecific which means that they are also present in other conditions and do not diagnose catatonia.
    • These lab findings include: leukocytosis, elevated creatine kinase, low serum iron.
    • The signs and symptoms of malignant catatonia overlap significantly with neuroleptic malignant syndrome (NMS) and so a careful history, review of medications, and physical exam are critical to properly differentiate these conditions.
    • For example, if the patient has waxy flexibility and holds a position against gravity when passively moved into that position, then it is likely catatonia.
    • If the patient has a “lead-pipe rigidity” then NMS should be the prime suspect.

Diagnosis

There is not yet a definitive consensus regarding diagnostic criteria of catatonia. In the American Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the World Health Organisation’s eleventh edition of the International Classification of Disease (ICD-11) the classification is more homogeneous than in earlier editions. Prominent researchers in the field have other suggestions for diagnostic criteria.

DSM-5 Classification

The DSM-5 does not classify catatonia as an independent disorder, but rather it classifies it as catatonia associated with another mental disorder, due to another medical condition, or as unspecified catatonia. Catatonia is diagnosed by the presence of three or more of the following 12 psychomotor symptoms in association with the above mentioned mental disorder, medical condition, or unspecified.

  • Stupor: no psycho-motor activity; not actively relating to environment.
  • Catalepsy: passive induction of a posture held against gravity.
  • Waxy flexibility: allowing positioning by examiner and maintaining that position.
  • Mutism: no, or very little, verbal response (exclude if known aphasia).
  • Negativism: opposition or no response to instructions or external stimuli.
  • Posturing: spontaneous and active maintenance of a posture against gravity.
  • Mannerisms that are odd, circumstantial caricatures of normal actions.
  • Stereotypy: repetitive, abnormally frequent, non-goal-directed movements.
  • Agitation, not influenced by external stimuli.
  • Grimacing: keeping a fixed facial expression.
  • Echolalia: mimicking another’s speech.
  • Echopraxia: mimicking another’s movements.

Other disorders (additional code 293.89 [F06.1] to indicate the presence of the co-morbid catatonia):

  • Catatonia associated with autism spectrum disorder.
  • Catatonia associated with schizophrenia spectrum and other psychotic disorders.
  • Catatonia associated with brief psychotic disorder.
  • Catatonia associated with schizophreniform disorder.
  • Catatonia associated with schizoaffective disorder.
  • Catatonia associated with substance-induced psychotic disorder.
  • Catatonia associated with bipolar and related disorders.
  • Catatonia associated with major depressive disorder.
  • Catatonic disorder due to another medical condition.
  • If catatonic symptoms are present but do not form the catatonic syndrome, a medication- or substance-induced aetiology should first be considered.

ICD-11 Classification

In ICD-11 catatonia is defined as a syndrome of primarily psychomotor disturbances that is characterised by the simultaneous occurrence of several symptoms such as stupor; catalepsy; waxy flexibility; mutism; negativism; posturing; mannerisms; stereotypies; psychomotor agitation; grimacing; echolalia and echopraxia. Catatonia may occur in the context of specific mental disorders, including mood disorders, schizophrenia or other primary psychotic disorders, and Neurodevelopmental disorders, and may be induced by psychoactive substances, including medications. Catatonia may also be caused by a medical condition not classified under mental, behavioural, or neurodevelopmental disorders.

Assessment/Physical

Catatonia is often overlooked and under-diagnosed. Patients with catatonia most commonly have an underlying psychiatric disorder, for this reason, physicians may overlook signs of catatonia due to the severity of the psychosis the patient is presenting with. Furthermore, the patient may not be presenting with the common signs of catatonia such as mutism and posturing. Additionally, the motor abnormalities seen in catatonia are also present in psychiatric disorders. For example, a patient with mania will show increased motor activity that may progress to excited catatonia. One way in which physicians can differentiate between the two is to observe the motor abnormality. Patients with mania present with increased goal-directed activity. On the other hand, the increased activity in catatonia is not goal-directed and often repetitive.

Catatonia is a clinical diagnosis and there is no specific laboratory test to diagnose it. However, certain testing can help determine what is causing the catatonia. An EEG will likely show diffuse slowing. If a seizure activity is driving the syndrome, then an EEG would also be helpful in detecting this. CT or MRI will not show catatonia; however, they might reveal abnormalities that might be leading to the syndrome. Metabolic screens, inflammatory markers, or autoantibodies may reveal reversible medical causes of catatonia.

Vital signs should be frequently monitored as catatonia can progress to malignant catatonia which is life-threatening. Malignant catatonia is characterised by fever, hypertension, tachycardia, and tachypnoea.

Rating Scale

Various rating scales for catatonia have been developed, however, their utility for clinical care has not been well established. The most commonly used scale is the Bush-Francis Catatonia Rating Scale (BFCRS) (downloadable PDF). The scale is composed of 23 items with the first 14 items being used as the screening tool. If 2 of the 14 are positive, this prompts for further evaluation and completion of the remaining 9 items.

A diagnosis can be supported by the lorazepam challenge or the zolpidem challenge. While proven useful in the past, barbiturates are no longer commonly used in psychiatry; thus the option of either benzodiazepines or ECT.

Differential Diagnosis

The differential diagnosis of catatonia is extensive as signs and symptoms of catatonia may overlap significantly with those of other conditions. Therefore, a careful and detailed history, medication review, and physical exam are key to diagnosing catatonia and differentiating it from other conditions. Furthermore, some of these conditions can themselves lead to catatonia. The differential diagnosis is as follows:

  • Neuroleptic malignant syndrome (NMS):
    • Malignant catatonia and NMS are both life-threatening conditions that share many of the same characteristics including fever, autonomic instability, rigidity, and delirium.
    • Lab values of low serum iron, elevated creatine kinase, and white blood cell count are also shared by the two disorders further complicating the diagnosis.
    • Some experts consider NMS a drug-induced form of catatonia, however, it has not been established as a subtype.
    • There are features of malignant catatonia (posturing, impulsivity, etc) that are absent from NSM and the lab results are not as consistent in malignant catatonia as they are in NMS.
    • NMS is a drug-induced condition associated with antipsychotics, particularly, first generation antipsychotics.
    • Therefore, discontinuing antipsychotics and starting benzodiazepines is a treatment for this condition, and similarly it is helpful in catatonia as well.
  • Anti-NMDA receptor encephalitis:
    • Anti-NMDA receptor encephalitis is an autoimmune disorder characterised by neuropsychiatric features and the presence of IgG antibodies.
    • The presentation of anti-NMDAR encephalitis has been categorized into 5 phases: prodromal phase, psychotic phase, unresponsive phase, hyperkinetic phase, and recovery phase.
    • The psychotic phase progresses into the unresponsive phase characterized by mutism, decreased motor activity, and catatonia.
  • Serotonin syndrome:
    • Both serotonin syndrome and malignant catatonia may present with signs and symptoms of delirium, autonomic instability, hyperthermia, and rigidity.
    • Again, similar to the presentation in NSM. However, patients with Serotonin syndrome have a history of ingestion of serotonergic drugs (Ex: SSRI).
    • These patients will also present with hyperreflexia, myoclonus, nausea, vomiting, and diarrhoea.
  • Malignant hyperthermia:
    • Malignant hyperthermia and malignant catatonia share features of autonomic instability, hyperthermia, and rigidity.
    • However, malignant hyperthermia is a hereditary disorder of skeletal muscle that makes these patients susceptible to exposure to halogenated anaesthetics and/or depolarising muscle relaxants like succinylcholine.
    • Malignant hyperthermia most commonly occurs in the intraoperative or postoperative periods. Other signs and symptoms of malignant hyperthermia include metabolic and respiratory acidosis, hyperkalaemia, and cardiac arrhythmias.
  • Akinetic mutism:
    • Akinetic mutism is a neurological disorder characterised by a decrease in goal-directed behaviour and motivation, however, the patient has an intact level of consciousness.
    • Patients may present with apathy, and may seem indifferent to pain, hunger, or thirst.
    • Akinetic mutism has been associated with structural damage in a variety of brain areas.
    • Akinetic mutism and catatonia may both manifest with immobility, mutism, and waxy flexibility.
    • Differentiating both disorders is the fact that akinetic mutism does not present with echolalia, echopraxia, or posturing.
    • Furthermore, it is not responsive to benzodiazepines as is the case for catatonia.
  • Elective mutism:
    • Elective mutism has an anxious aetiology but has also been associated with personality disorders.
    • Patients with this disorder fail to speak with some individuals but will speak with others.
    • Likewise, they may refuse to speak in certain situations, for example, a child who refuses to speak at school but is conversational at home.
    • This disorder is distinguished from catatonia by the absence of any other signs/symptoms.
  • Non-convulsive status epilepticus:
    • Non-convulsive status epilepticus is seizure activity with no accompanying tonic-clonic movements.
    • It can present with stupor, similar to catatonia, and they both respond to benzodiazepines.
    • Non-convulsive status epilepticus is diagnosed by the presence of seizure activity seen on electroencephalogram (EEG).
    • Catatonia on the other hand, is associated with normal EEG or diffuse slowing.
  • Delirium:
    • Delirium is characterised by fluctuating disturbed perception and consciousness in the ill individual.
    • It has hypoactive and hyperactive or mixed forms. People with hyperactive delirium present similarly to those with excited catatonia and have symptoms of restlessness, agitation and aggression.
    • Those with hypoactive delirium present with similarly to retarded catatonia, withdrawn and quiet.
    • However, catatonia also includes other distinguishing features including posturing and rigidity as well as a positive response to benzodiazepines.
  • Locked-in syndrome:
    • Patients with locked-in syndrome present with immobility and mutism, however, unlike patients with catatonia who are unmotivated to communicate, patients with locked-in syndrome try to communicate with eye movements and blinking.
    • Furthermore, locked-in syndrome is caused by damage to the brainstem.
  • Stiff-person syndrome:
    • Catatonia and stiff-person syndrome are similar in that they may both present with rigidity, autonomic instability and a positive response to benzodiazepines.
    • However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies and other catatonic signs such as mutism and posturing are not part of the syndrome.
  • Parkinson’s disease:
    • Untreated late-stage Parkinson’s disease may present similarly to retarded catatonia with symptoms of immobility, rigidity, and difficulty speaking.
    • Further complicating the diagnosis is the fact that many patients with Parkinson’s disease will have major depressive disorder which may be the underlying cause of catatonia.
    • Parkinson’s disease can be distinguished from catatonia by a positive response to levodopa.
    • Catatonia on the other hand will show a positive response to benzodiazepines.

Treatment

The initial treatment of catatonia is to stop medication that could be potentially leading to the syndrome. These may include steroids, stimulants, anticonvulsants, neuroleptics, dopamine blockers, etc. The next step is to provide a “lorazepam challenge,” in which patients are given 2 mg of IV lorazepam (or another benzodiazepine). Most patients with catatonia will respond significantly to this within the first 15-30 minutes. If no change is observed during the first dose, then a second dose is given and the patient is re-examined. If the patient responds to the lorazepam challenge, then lorazepam can be scheduled at interval doses until the catatonia resolves. The lorazepam must be tapered slowly, otherwise, the catatonia symptoms may return. The underlying cause of the catatonia should also be treated during this time. If within a week the catatonia is not resolved, then ECT can be used to reverse the symptoms. ECT in combination with benzodiazepines is used to treat malignant catatonia. In France, zolpidem has also been used in diagnosis, and response may occur within the same time period. Ultimately the underlying cause needs to be treated.

Electroconvulsive therapy (ECT) is an effective treatment for catatonia that is well acknowledged. ECT has also shown favourable outcomes in patients with chronic catatonia. However, it has been pointed out that further high quality randomised controlled trials are needed to evaluate the efficacy, tolerance, and protocols of ECT in catatonia.

Antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic.

Excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, NMDA antagonists such as amantadine or memantine may be used. Amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. Memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. Topiramate is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of AMPA receptors.

Complications, Outcomes, and Recurrence

Patients may suffer several complications from being in a catatonic state. The nature of these complications will depend on the type of catatonia being experienced by the patient. For example, patients presenting with retarded catatonia may have refusal to eat which will in turn lead to malnutrition and dehydration. Furthermore, if immobility is a symptom the patient is presenting with, then they may develop pressure ulcers, muscle contractions, and are at risk of developing deep vein thrombosis (DVT) and pulmonary embolus (PE). Patients with excited catatonia may be aggressive and violent, and physical trauma may result from this. Catatonia may progress to the malignant type which will present with autonomic instability and may be life threatening. Other complications also include the development of pneumonia and neuroleptic malignant syndrome.[2]

Patients who experience an episode of catatonia are more likely to suffer recurrence. Treatment response for patients with catatonia is 50-70% and these patients have a good prognosis. However, failure to respond to medication is a very poor prognosis. Many of these patients will require long-term and continuous mental health care. For patients with catatonia with underlying schizophrenia, the prognosis is much poorer.