Shell shock

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Shell_shock

Shell shock
Other names	Bullet air, soldier's heart, battle fatigue, operational exhaustion
A soldier displaying the characteristic thousand-yard stare associated with shell shock.
Specialty	Psychiatry

Shell shock is a word that originated during World War I to describe the type of post-traumatic stress disorder (PTSD) that many soldiers experienced during the war, before PTSD was officially recognized. It is a reaction to the intensity of the bombardment and fighting that produced a helplessness, which could manifest as panic, fear, flight, or an inability to reason, sleep, walk or talk.

During the war, the concept of shell shock was poorly defined. Cases of "shell shock" could be interpreted as either a physical or psychological injury, or as a lack of moral fibre. Although the United States’ Department of Veterans Affairs still uses the term shell shock to describe certain aspects of PTSD, it is mostly a historical term, and is often considered to be the signature injury of the war.

In World War II and beyond, the diagnosis of "shell shock" was replaced by that of combat stress reaction, which is a similar but not identical response to the trauma of warfare and bombardment.

Origin

During the early stages of World War I in 1914, soldiers from the British Expeditionary Force began to report medical symptoms after combat, including tinnitus, amnesia, headaches, dizziness, tremors, and hypersensitivity to noise. While these symptoms resembled those that would be expected after a physical wound to the brain, many of those reporting sick showed no signs of head wounds. By December 1914, as many as 10% of British officers and 4% of enlisted men were experiencing "nervous and mental shock".

The term "shell shock" was coined during the Battle of Loos to reflect an assumed link between the symptoms and the effects of explosions from artillery shells. The term was first published in 1915 in an article in The Lancet by Charles Myers. Some 60–80% of shell shock cases displayed acute neurasthenia, while 10% displayed what would now be termed symptoms of conversion disorder, including mutism and fugue.

The number of shell shock cases grew during 1915 and 1916 but it remained poorly understood medically and psychologically. Some physicians held the view that it was a result of hidden physical damage to the brain, with the shock waves from bursting shells creating a cerebral lesion that caused the symptoms and could potentially prove fatal. Another explanation was that shell shock resulted from poisoning by the carbon monoxide formed by explosions.

At the same time, an alternative view developed describing shell shock as an emotional, rather than a physical, injury. Evidence for this point of view was provided by the fact that an increasing proportion of men with shell shock symptoms had not been exposed to artillery fire. Since the symptoms appeared in men who had no proximity to an exploding shell, the physical explanation was clearly unsatisfactory.

In spite of this evidence, the British Army continued to try to differentiate those whose symptoms followed explosive exposure from others. In 1915 the British Army in France was instructed that:

Shell-shock and shell concussion cases should have the letter 'W' prefixed to the report of the casualty, if it was due to the enemy; in that case the patient would be entitled to rank as 'wounded' and to wear on his arm a 'wound stripe'. If, however, the man's breakdown did not follow a shell explosion, it was not thought to be 'due to the enemy', and he was to [be] labelled 'Shell-shock' or 'S' (for sickness) and was not entitled to a wound stripe or a pension.

However, it often proved difficult to identify which cases were which, as the information on whether a casualty had been close to a shell explosion or not was rarely provided.

Management

Acute

At first, shell-shock casualties were rapidly evacuated from the front line – in part because of fear over their frequently dangerous and unpredictable behaviour. As the size of the British Expeditionary Force increased, and manpower became in shorter supply, the number of shell shock cases became a growing problem for the military authorities. At the Battle of the Somme in 1916, as many as 40% of casualties were shell-shocked, resulting in concern about an epidemic of psychiatric casualties, which could not be afforded in either military or financial terms.

Among the consequences of this were an increasing official preference for the psychological interpretation of shell shock, and a deliberate attempt to avoid the medicalisation of shell shock. If men were 'uninjured' it was easier to return them to the front to continue fighting. Another consequence was an increasing amount of time and effort devoted to understanding and treating shell shock symptoms. Soldiers who returned with shell shock generally could not remember much because their brain would shut out all the traumatic memories.

By the Battle of Passchendaele in 1917, the British Army had developed methods to reduce shell shock. A man who began to show shell-shock symptoms was best given a few days' rest by his local medical officer. Col. Rogers, Regimental Medical Officer, 4th Battalion Black Watch wrote:

You must send your commotional cases down the line. But when you get these emotional cases, unless they are very bad, if you have a hold of the men and they know you and you know them (and there is a good deal more in the man knowing you than in you knowing the man) … you are able to explain to him that there is really nothing wrong with him, give him a rest at the aid post if necessary and a day or two’s sleep, go up with him to the front line, and, when there, see him often, sit down beside him and talk to him about the war and look through his periscope and let the man see you are taking an interest in him.

If symptoms persisted after a few weeks at a local Casualty Clearing Station, which would normally be close enough to the front line to hear artillery fire, a casualty might be evacuated to one of four dedicated psychiatric centres which had been set up further behind the lines, and were labelled as "NYDN – Not Yet Diagnosed Nervous" pending further investigation by medical specialists.

Although the Battle of Passchendaele generally became a byword for horror, the number of cases of shell shock were relatively few. 5,346 shell shock cases reached the Casualty Clearing Station, or roughly 1% of the British forces engaged. 3,963 (or just under 75%) of these men returned to active service without being referred to a hospital for specialist treatment. The number of shell shock cases reduced throughout the battle, and the epidemic of illness was ended.

During 1917, "shell shock" was entirely banned as a diagnosis in the British Army, and mentions of it were censored, even in medical journals.

Chronic treatment

The treatment of chronic shell shock varied widely according to the details of the symptoms, the views of the doctors involved, and other factors including the rank and class of the patient.

There were so many officers and men with shell shock that 19 British military hospitals were wholly devoted to the treatment of cases. Ten years after the war, 65,000 veterans of the war were still receiving treatment for it in Britain. In France it was possible to visit aged shell shock victims in hospital in 1960.

Physical causes

Research by Johns Hopkins University in 2015 found that the brain tissue of combat veterans who had been exposed to improvised explosive devices (IEDs) exhibited a pattern of injury in the areas responsible for decision making, memory and reasoning. This evidence has led the researchers to conclude that shell shock may not only be a psychological disorder, since the symptoms exhibited by affected individuals from the First World War are very similar to these injuries. Immense pressure changes are involved in shell shock. Even mild changes in air pressure from weather have been linked to changes in behavior.

There is also evidence to suggest that the type of warfare faced by soldiers would affect the probability of shell shock symptoms developing. First-hand reports from medical doctors at the time note that rates of such conditions decreased once the war was mobilized again during the 1918 German offensive, following the 1916–1917 period where the highest rates of shell shock can be found. This could suggest that it was trench warfare, and the experience of siege warfare specifically, that led to the development of these symptoms.

Cowardice

See also: British Army during World War I

Some men with shell shock were put on trial, and even executed, for military crimes including desertion and cowardice. While it was recognised that the stresses of war could cause men to break down, a lasting episode was likely to be seen as symptomatic of an underlying lack of character. For instance, in his testimony to the post-war Royal Commission examining shell shock, Lord Gort said that shell shock was a weakness and was not found in "good" units. The continued pressure to avoid medical recognition of shell shock meant that it was not, in itself, considered an admissible defence. Although some doctors or medics did take procedure to try to cure soldiers' shell shock, it was first done in a brutal way. Doctors would provide electric shock to soldiers in hopes that it would shock them back to their normal, heroic, pre-war self. While illustrating cases of mutism in his book Hysterical Disorders of Warfare, therapist Lewis Yealland describes a patient who had over the course of 9 months been subjected unsuccessfully to numerous treatments for his mutism. These included strong application of electricity to his throat, lit cigarette ends had been applied to the tip of his tongue, and "hot plates" had been placed in the back of his mouth.

Executions of soldiers in the British Army were not commonplace. While there were 240,000 Courts Martial and 3080 death sentences handed down, in only 346 cases was the sentence carried out. 266 British soldiers were executed for "Desertion", 18 for "Cowardice", 7 for "Quitting a post without authority", 5 for "Disobedience to a lawful command" and 2 for "Casting away arms". On 7 November 2006, the government of the United Kingdom gave them all a posthumous conditional pardon.

Committee of Enquiry report

The British government produced a Report of the War Office Committee of Enquiry into "Shell-Shock" which was published in 1922. Recommendations from this included:

In forward areas

No soldier should be allowed to think that loss of nervous or mental control provides an honourable avenue of escape from the battlefield, and every endeavour should be made to prevent slight cases leaving the battalion or divisional area, where treatment should be confined to provision of rest and comfort for those who need it and to heartening them for return to the front line.

In neurological centres

When cases are sufficiently severe to necessitate more scientific and elaborate treatment they should be sent to special Neurological Centres as near the front as possible, to be under the care of an expert in nervous disorders. No such case should, however, be so labelled on evacuation as to fix the idea of nervous breakdown in the patient’s mind.

In base hospitals

When evacuation to the base hospital is necessary, cases should be treated in a separate hospital or separate sections of a hospital, and not with the ordinary sick and wounded patients. Only in exceptional circumstances should cases be sent to the United Kingdom, as, for instance, men likely to be unfit for further service of any kind with the forces in the field. This policy should be widely known throughout the Force.

Forms of treatment

The establishment of an atmosphere of cure is the basis of all successful treatment, the personality of the physician is, therefore, of the greatest importance. While recognising that each individual case of war neurosis must be treated on its merits, the Committee are of opinion that good results will be obtained in the majority by the simplest forms of psycho-therapy, i.e., explanation, persuasion and suggestion, aided by such physical methods as baths, electricity and massage. Rest of mind and body is essential in all cases.

The committee are of opinion that the production of hypnoidal state and deep hypnotic sleep, while beneficial as a means of conveying suggestions or eliciting forgotten experiences are useful in selected cases, but in the majority they are unnecessary and may even aggravate the symptoms for a time.

They do not recommend psycho-analysis in the Freudian sense.

In the state of convalescence, re-education and suitable occupation of an interesting nature are of great importance. If the patient is unfit for further military service, it is considered that every endeavour should be made to obtain for him suitable employment on his return to active life.

Return to the fighting line

Soldiers should not be returned to the fighting line under the following conditions:

(1) If the symptoms of neurosis are of such a character that the soldier cannot be treated overseas with a view to subsequent useful employment.

(2) If the breakdown is of such severity as to necessitate a long period of rest and treatment in the United Kingdom.

(3) If the disability is anxiety neurosis of a severe type.

(4) If the disability is a mental breakdown or psychosis requiring treatment in a mental hospital.

It is, however, considered that many of such cases could, after recovery, be usefully employed in some form of auxiliary military duty.

Part of the concern was that many British veterans were receiving pensions and had long-term disabilities.

By 1939, some 120,000 British ex-servicemen had received final awards for primary psychiatric disability or were still drawing pensions – about 15% of all pensioned disabilities – and another 44,000 or so … were getting pensions for ‘soldier’s heart’ or Effort Syndrome. There is, though, much that statistics do not show, because in terms of psychiatric effects, pensioners were just the tip of a huge iceberg.

War correspondent Philip Gibbs wrote:

Something was wrong. They put on civilian clothes again and looked to their mothers and wives very much like the young men who had gone to business in the peaceful days before August 1914. But they had not come back the same men. Something had altered in them. They were subject to sudden moods, and queer tempers, fits of profound depression alternating with a restless desire for pleasure. Many were easily moved to passion where they lost control of themselves, many were bitter in their speech, violent in opinion, frightening.

One British writer between the wars wrote:

There should be no excuse given for the establishment of a belief that a functional nervous disability constitutes a right to compensation. This is hard saying. It may seem cruel that those whose sufferings are real, whose illness has been brought on by enemy action and very likely in the course of patriotic service, should be treated with such apparent callousness. But there can be no doubt that in an overwhelming proportion of cases, these patients succumb to ‘shock’ because they get something out of it. To give them this reward is not ultimately a benefit to them because it encourages the weaker tendencies in their character. The nation cannot call on its citizens for courage and sacrifice and, at the same time, state by implication that an unconscious cowardice or an unconscious dishonesty will be rewarded.

Development of psychiatry

At the beginning of World War II, the term "shell shock" was banned by the British Army, though the phrase "postconcussional syndrome" was used to describe similar traumatic responses.

Society and culture

Shell shock has had a profound impact in British culture and the popular memory of World War I. At the time, war writers like the poets Siegfried Sassoon and Wilfred Owen dealt with shell shock in their work. Sassoon and Owen spent time at Craiglockhart War Hospital, which treated shell shock casualties. Author Pat Barker explored the causes and effects of shell shock in her Regeneration Trilogy, basing many of her characters on real historical figures and drawing on the writings of the first world war poets and the army doctor W. H. R. Rivers.

Modern cases of shell shock

Although the term "shell shocked" is typically used in discussion of WWI to describe early forms of PTSD, its high-impact explosives-related nature provides modern applications as well. During their deployment in Iraq and Afghanistan, approximately 380,000 U.S. troops, about 19% of those deployed, were estimated to have sustained brain injuries from explosive weapons and devices. This prompted the U.S. Defense Advanced Research Projects Agency (DARPA) to open up a $10 million study of the blast effects on the human brain. The study revealed that, while the brain remains initially intact immediately after low level blast effects, the chronic inflammation afterwards is what ultimately leads to many cases of shell shock and PTSD.

Conversion disorder

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Conversion_disorder 

 

Conversion disorder
Jean-Martin Charcot demonstrating hypnosis in a hysterical patient to his students. Hysteria as a clinical diagnosis was later replaced by conversion disorder.
Specialty	Psychiatry, Neurology
Symptoms	Numbness, weakness, paralysis, seizures, tremor, fainting, impaired hearing, swallowing and vision
Causes	Long term stress
Treatment	Cognitive behavioral therapy, antidepressants, physical/occupational therapy

Conversion disorder (CD), or functional neurologic symptom disorder, is a diagnostic category used in some psychiatric classification systems. It is sometimes applied to patients who present with neurological symptoms, such as numbness, blindness, paralysis, or fits, which are not consistent with a well-established organic cause, which cause significant distress, and can be traced back to a psychological trigger. It is thought that these symptoms arise in response to stressful situations affecting a patient's mental health or an ongoing mental health condition such as depression. Conversion disorder was retained in DSM-5, but given the subtitle functional neurological symptom disorder. The new criteria cover the same range of symptoms, but remove the requirements for a psychological stressor to be present and for feigning to be disproved. The ICD-10 classifies conversion disorder as a dissociative disorder, and the ICD-11 as a dissociative disorder with unspecified neurological symptoms.However, the DSM-IV classifies conversion disorder as a somatoform disorder.

Signs and symptoms

Conversion disorder begins with some stressor, trauma, or psychological distress. Usually the physical symptoms of the syndrome affect the senses or movement. Common symptoms include blindness, partial or total paralysis, inability to speak, deafness, numbness, difficulty swallowing, incontinence, balance problems, seizures, tremors, and difficulty walking. The symptom of feeling unable to breathe, but where the lips are not turning blue, can indicate conversion disorder or sleep paralysis. Sleep paralysis and narcolepsy can be ruled out with sleep tests. These symptoms are attributed to conversion disorder when a medical explanation for the conditions cannot be found. Symptoms of conversion disorder usually occur suddenly. Conversion disorder is typically seen in people aged 10 to 35, and affects between 0.011% and 0.5% of the general population.

Conversion disorder can present with motor or sensory symptoms including any of the following:

Motor symptoms or deficits:

• Impaired coordination or balance
• Weakness/paralysis of a limb or the entire body (hysterical paralysis or motor conversion disorders)
• Impairment or loss of speech (hysterical aphonia)
• Difficulty swallowing (dysphagia) or a sensation of a lump in the throat
• Urinary retention
• Psychogenic non-epileptic seizures or convulsions
• Persistent dystonia
• Tremor, myoclonus or other movement disorders
• Gait problems (astasia-abasia)
• Loss of consciousness (fainting)

Sensory symptoms or deficits:

• Impaired vision (hysterical blindness), double vision
• Impaired hearing (deafness)
• Loss or disturbance of touch or pain sensation

Conversion symptoms typically do not conform to known anatomical pathways and physiological mechanisms. It has sometimes been stated that the presenting symptoms tend to reflect the patient's own understanding of anatomy and that the less medical knowledge a person has, the more implausible are the presenting symptoms. However, no systematic studies have yet been performed to substantiate this statement.

Diagnosis

Definition

Conversion disorder is now contained under the umbrella term functional neurological symptom disorder. In cases of conversion disorder, there is a psychological stressor.

The diagnostic criteria for functional neurological symptom disorder, as set out in DSM-5, are:

1. The patient has at least one symptom of altered voluntary motor or sensory function.
2. Clinical findings provide evidence of incompatibility between the symptom and recognised neurological or medical conditions.
3. The symptom or deficit is not better explained by another medical or mental disorder.
4. The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.

Specify type of symptom or deficit as:

• With weakness or paralysis
• With abnormal movement (e.g. tremor, dystonic movement, myoclonus, gait disorder)
• With swallowing symptoms
• With speech symptoms (e.g. dysphonia, slurred speech)
• With attacks or seizures
• With amnesia or memory loss
• With special sensory loss symptoms (e.g. visual blindness, olfactory loss, or hearing disturbance)
• With mixed symptoms.

Specify if:

• Acute episode: symptoms present for less than six months
• Persistent: symptoms present for six months or more.

Specify if:

• Psychological stressor (conversion disorder)
• No psychological stressor (functional neurological symptom disorder)

Exclusion of neurological disease

Conversion disorder presents with symptoms that typically resemble a neurological disorder such as stroke, multiple sclerosis, epilepsy, hypokalemic periodic paralysis or narcolepsy. The neurologist must carefully exclude neurological disease, through examination and appropriate investigations. However, it is not uncommon for patients with neurological disease to also have conversion disorder.

In excluding neurological disease, the neurologist has traditionally relied partly on the presence of positive signs of conversion disorder, i.e. certain aspects of the presentation that were thought to be rare in neurological disease but common in conversion. The validity of many of these signs has been questioned, however, by a study showing they also occur in neurological disease. One such symptom, for example, is la belle indifférence, described in DSM-IV as "a relative lack of concern about the nature or implications of the symptoms". In a later study, no evidence was found that patients with functional symptoms are any more likely to exhibit this than patients with a confirmed organic disease. In DSM-V, la belle indifférence was removed as a diagnostic criterion.

Another feature thought to be important was that symptoms tended to be more severe on the non-dominant (usually left) side of the body. There have been a number of theories about this, such as the relative involvement of cerebral hemispheres in emotional processing, or more simply, that it was "easier" to live with a functional deficit on the non-dominant side. However, a literature review of 121 studies established that this was not true, with publication bias the most likely explanation for this commonly held view. Although agitation is often assumed to be a positive sign of conversion disorder, release of epinephrine is a well-demonstrated cause of paralysis from hypokalemic periodic paralysis.

Misdiagnosis does sometimes occur. In a highly influential study from the 1960s, Eliot Slater demonstrated that misdiagnoses had occurred in one third of his 112 patients with conversion disorder. Later authors have argued that the paper was flawed, however, and a meta-analysis has shown that misdiagnosis rates since that paper was published are around four percent, the same as for other neurological diseases.

Deliberate feigning

Conversion disorder, by its nature, is more prone to deliberate feigning. One neuroimaging study suggested that feigning may be distinguished from conversion by the pattern of frontal lobe activation.

Psychological mechanism

The psychological mechanism of conversion can be the most difficult aspect of a conversion diagnosis. Even if there is a clear antecedent trauma or other possible psychological trigger, it is still not clear exactly how this gives rise to the symptoms observed. Patients with medically unexplained neurological symptoms may not have any psychological stressor, hence the use of the term "functional neurological symptom disorder" in DSM-5 as opposed to "conversion disorder", and DSM-5's removal of the need for a psychological trigger.

Treatment

There are a number of different treatments available to treat and manage conversion syndrome. Treatments for conversion syndrome include hypnosis, psychotherapy, physical therapy, stress management, and transcranial magnetic stimulation. Treatment plans will consider duration and presentation of symptoms and may include one or multiple of the above treatments. This may include the following:

1. Occupational therapy to maintain autonomy in activities of daily living;
2. Physiotherapy where appropriate.
3. Treatment of comorbid depression or anxiety if present.
4. Educating patients on the causes of their symptoms might help them learn to manage both the psychiatric and physical aspects of their condition. Psychological counseling is often warranted given the known relationship between conversion disorder and emotional trauma. This approach ideally takes place alongside other types of treatment.

There is little evidence-based treatment of conversion disorder. Other treatments such as cognitive behavioral therapy, hypnosis, EMDR, and psychodynamic psychotherapy, EEG brain biofeedback need further trials. Psychoanalytic treatment may possibly be helpful. However, most studies assessing the efficacy of these treatments are of poor quality and larger, better controlled studies are urgently needed. Cognitive Behavioural Therapy is the most common treatment, however boasts a mere 13% improvement rate.

Prognosis

Empirical studies have found that the prognosis for conversion disorder varies widely, with some cases resolving in weeks, and others enduring for years or decades. There is also evidence that there is no cure for conversion disorder, and that although patients may go into remission they can relapse at any point. Furthermore, many patients can get rid of their symptoms with time, treatments and reassurance.

Epidemiology

Frequency

Information on the frequency of conversion disorder in the West is limited, in part due to the complexities of the diagnostic process. In neurology clinics, the reported prevalence of unexplained symptoms among new patients is very high (between 30 and 60%). However, diagnosis of conversion typically requires an additional psychiatric evaluation, and since few patients will see a psychiatrist it is unclear what proportion of the unexplained symptoms are actually due to conversion. Large scale psychiatric registers in the US and Iceland found incidence rates of 22 and 11 newly diagnosed cases per 100,000 person-years, respectively. Some estimates claim that in the general population, between 0.011% and 0.5% of the population have conversion disorder.

Culture

Although it is often thought that the frequency of conversion may be higher outside of the West, perhaps in relation to cultural and medical attitudes, evidence of this is limited. A community survey of urban Turkey found a prevalence of 5.6%. Many authors have found occurrence of conversion to be more frequent in rural, lower socio-economic groups, where technological investigation of patients is limited and people may know less about medical and psychological concepts.

Gender

Historically, the concept of 'hysteria' was originally understood to be a condition exclusively affecting women, though the concept was eventually extended to men. In recent surveys of conversion disorder (formerly classified as "hysterical neurosis, conversion type"), females predominate, with between two and six female patients for every male but some research suggests this gender disparity may be confounded by higher rates of violence against women.

Age

Conversion disorder may present at any age but is rare in children younger than ten or in the elderly. Studies suggest a peak onset in the mid-to-late 30s.

History

The first evidence of functional neurological symptom disorder dates back to 1900 BC, when the symptoms were blamed on the uterus moving within the female body. The treatment varied "depending on the position of the uterus, which must be forced to return to its natural position. If the uterus had moved upwards, this could be done by placing malodorous and acrid substances near the woman's mouth and nostrils, while scented ones were placed near her vagina; on the contrary, if the uterus had lowered, the document recommends placing the acrid substances near her vagina and the perfumed ones near her mouth and nostrils."

In Greek mythology, hysteria, the original name for functional neurological symptom disorder, was thought to be caused by a lack of orgasms, uterine melancholy and not procreating. Plato, Aristotle and Hippocrates believed a lack of sex upsets the uterus. The Greeks believed it could be prevented and cured with wine and orgies. Hippocrates argued that a lack of regular sexual intercourse led to the uterus producing toxic fumes and caused it to move in the body, and that this meant all women should be married and enjoy a satisfactory sexual life.

From the 13th century, women with hysteria were exorcised, as it was believed that they were possessed by the devil. It was believed that if doctors could not find the cause of a disease or illness, it must be caused by the devil.

At the beginning of the 16th century, women were sexually stimulated by midwives in order to relieve their symptoms. Gerolamo Cardano and Giambattista della Porta believed polluted water and fumes caused the symptoms of hysteria. Towards the end of the century, however, the role of the uterus was no longer thought central to the disorder, with Thomas Willis discovering that the brain and central nervous system were the cause of the symptoms. Thomas Sydenham argued that the symptoms of hysteria may have an organic cause. He also proved the uterus is not the cause of symptom.

In 1692, in the US town of Salem, Massachusetts, there was an outbreak of hysteria. This led to the Salem witch trials, where the women accused of being witches had symptoms such as sudden movements, staring eyes and uncontrollable jumping.

During the 18th century, there was a move from the idea of hysteria being caused by the uterus to it being caused by the brain. This led to an understanding that it could affect both sexes. Jean-Martin Charcot argued that hysteria was caused by "a hereditary degeneration of the nervous system, namely a neurological disorder".

In the 19th century, hysteria moved from being considered a neurological disorder to being considered a psychological disorder, when Pierre Janet argued that "dissociation appears autonomously for neurotic reasons, and in such a way as to adversely disturb the individual's everyday life". However, as early as 1874, doctors including W. B. Carpenter and J. A. Omerod began to speak out against the hysteria phenomenon as there was no evidence to prove its existence.

Sigmund Freud referred to the condition as both hysteria and conversion disorder throughout his career. He believed those with the condition could not live in a mature relationship, and that those with the condition were unwell in order to achieve a "secondary gain", in that they are able to manipulate their situation to fit their needs or desires. He also found that both men and women could have the disorder.

Freud's model suggested the emotional charge deriving from painful experiences would be consciously repressed as a way of managing the pain, but that the emotional charge would be somehow "converted" into neurological symptoms. Freud later argued that the repressed experiences were of a sexual nature. As Peter Halligan comments, conversion has "the doubtful distinction among psychiatric diagnoses of still invoking Freudian mechanisms".

Pierre Janet, the other great theoretician of hysteria, argued that symptoms arose through the power of suggestion, acting on a personality vulnerable to dissociation. In this hypothetical process, the subject's experience of their leg, for example, is split off from the rest of their consciousness, resulting in paralysis or numbness in that leg.

Later authors have attempted to combine elements of these various models, but none of them has a firm empirical basis. In 1908, Steyerthal predicted that: "Within a few years the concept of hysteria will belong to history ... there is no such disease and there never has been. What Charcot called hysteria is a tissue woven of a thousand threads, a cohort of the most varied diseases, with nothing in common but the so-called stigmata, which in fact may accompany any disease." However, the term "hysteria" was still being used well into the 20th century.

Some support for the Freudian model comes from findings of high rates of childhood sexual abuse in conversion patients. Support for the dissociation model comes from studies showing heightened suggestibility in conversion patients. However, critics argue that it can be challenging to find organic pathologies for all symptoms, and so the practice of diagnosing patients with such symptoms as having hysteria led to the disorder being meaningless, vague and a sham diagnosis, as it does not refer to any definable disease. Furthermore, throughout its history, many patients have been misdiagnosed with hysteria or conversion disorder when they had organic disorders such as tumours or epilepsy or vascular diseases. This has led to patient deaths, a lack of appropriate care and suffering for the patients. Eliot Slater, after studying the condition in the 1950s, stated: "The diagnosis of 'hysteria' is all too often a way of avoiding a confrontation with our own ignorance. This is especially dangerous when there is an underlying organic pathology, not yet recognised. In this penumbra we find patients who know themselves to be ill but, coming up against the blank faces of doctors who refuse to believe in the reality of their illness, proceed by way of emotional lability, overstatement and demands for attention ... Here is an area where catastrophic errors can be made. In fact it is often possible to recognise the presence though not the nature of the unrecognisable, to know that a man must be ill or in pain when all the tests are negative. But it is only possible to those who come to their task in a spirit of humility. In the main the diagnosis of 'hysteria' applies to a disorder of the doctor–patient relationship. It is evidence of non-communication, of a mutual misunderstanding ... We are, often, unwilling to tell the full truth or to admit to ignorance ... Evasions, even untruths, on the doctor's side are among the most powerful and frequently used methods he has for bringing about an efflorescence of 'hysteria'".

Much recent work has been done to identify the underlying causes of conversion and related disorders and to better understand why conversion disorder and hysteria appear more commonly in women. Current theoreticians tend to believe there is no single cause for these disorders. Instead, the emphasis tends to be on the patient's understanding and a variety of psychotherapeutic techniques. In some cases, the onset of conversion disorder correlates to a traumatic or stressful event. There are also certain populations that are considered at risk for conversion disorder, including people with a medical illness or condition, people with personality disorders or dissociative identity disorder. However, no biomarkers have yet been found to support the idea that conversion disorder is caused by a psychiatric condition.

There has been much recent interest in using functional neuroimaging to study conversion. As researchers identify the mechanisms which underlie conversion symptoms, it is hoped they will enable the development of a neuropsychological model. A number of such studies have been performed, including some which suggest the blood-flow in patients' brains may be abnormal while they are unwell. However, the studies have all been too small to be confident of the generalisability of their findings, so no neuropsychological model has been clearly established.

An evolutionary psychology explanation for conversion disorder is that the symptoms may have been evolutionarily advantageous during warfare. A non-combatant with these symptoms signals non-verbally, possibly to someone speaking a different language, that she or he is not dangerous as a combatant and also may be carrying some form of dangerous infectious disease. This can explain that conversion disorder may develop following a threatening situation, that there may be a group effect with many people simultaneously developing similar symptoms (as in mass psychogenic illness), and the gender difference in prevalence.

The Lacanian model accepts conversion disorder as a common phenomenon inherent in specific psychical structures. The higher prevalence of it among women is based on somewhat different intrapsychic relations to the body from those of typical males, which allows the formation of conversion symptoms.

A Beautiful Mind (film)

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/A_Beautiful_Mind_(film) 

 

A Beautiful Mind
Theatrical release poster
Directed by	Ron Howard
Written by	Akiva Goldsman
Based on	A Beautiful Mind by Sylvia Nasar
Produced by	Brian Grazer Ron Howard
Starring	Russell Crowe Ed Harris Jennifer Connelly Paul Bettany Adam Goldberg Judd Hirsch Josh Lucas Anthony Rapp Christopher Plummer
Cinematography	Roger Deakins
Edited by	Daniel P. Hanley Mike Hill
Music by	James Horner
Production companies	Universal Pictures DreamWorks Pictures Imagine Entertainment
Distributed by	Universal Pictures (North America) DreamWorks Pictures (International)
Release dates	December 13, 2001 (Beverly Hills premiere) December 21, 2001 (United States)
Running time	135 minutes
Country	United States
Language	English
Budget	$58 million
Box office	$316.8 million

A Beautiful Mind is a 2001 American biographical drama film directed by Ron Howard. Written by Akiva Goldsman, its screenplay was inspired by Sylvia Nasar's 1998 biography of the mathematician John Nash, a Nobel Laureate in Economics. A Beautiful Mind stars Russell Crowe as Nash, along with Ed Harris, Jennifer Connelly, Paul Bettany, Adam Goldberg, Judd Hirsch, Josh Lucas, Anthony Rapp, and Christopher Plummer in supporting roles. The story begins in Nash's days as a brilliant but asocial mathematics graduate student at Princeton University. After Nash accepts secret work in cryptography, his life takes a turn for the nightmarish.

A Beautiful Mind was released theatrically in the United States on December 21, 2001. It went on to gross over $313 million worldwide and won four Academy Awards, for Best Picture, Best Director, Best Adapted Screenplay and Best Supporting Actress for Connelly. It was also nominated for Best Actor, Best Film Editing, Best Makeup, and Best Original Score.

Plot

In 1947, John Nash arrives at Princeton University as a co-recipient, with Martin Hansen, of the Carnegie Scholarship for Mathematics. He meets fellow math and science graduate students Sol, Ainsley, and Bender, as well as his roommate Charles Herman, a literature student.

Determined to publish his own original idea, Nash is inspired when he and his classmates discuss how to approach a group of women at a bar. Hansen quotes Adam Smith advocating "every man for himself", but Nash argues that a cooperative approach would lead to better chances of success in developing a new concept of governing dynamics. Publishing an article on his theory, he earns an appointment at MIT where he chooses Sol and Bender over Hansen to join him.

In 1953, Nash is invited to the Pentagon to study encrypted enemy telecommunications, which he deciphers mentally. Bored with his regular duties at MIT, including teaching, he is recruited by the mysterious William Parcher of the United States Department of Defense with a classified assignment: to look for hidden patterns in magazines and newspapers to thwart a Soviet plot. Nash becomes increasingly obsessive in his search for these patterns, delivering his results to a secret mailbox, and comes to believe he is being followed.

One of his students, Alicia Larde, asks him to dinner, and they fall in love. On a return visit to Princeton, Nash runs into Charles and his niece, Marcee. With Charles' encouragement, he proposes to Alicia and they marry. Nash fears for his life after surviving a shootout between Parcher and Soviet agents, and learns Alicia is pregnant, but he is forced to continue his assignment. While delivering a guest lecture at Harvard University, Nash tries to flee from people he thinks are Soviet agents, led by a psychiatrist named Dr. Rosen, but is forcibly sedated and committed to a psychiatric facility.

Dr. Rosen tells Alicia that Nash has schizophrenia and that Charles, Marcee, and Parcher exist only in his imagination. Alicia backs up the doctor, telling Nash that no "William Parcher" is in the Defense Department and takes out the unopened documents he delivered to the secret mailbox. Nash is given a course of insulin shock therapy and eventually released. Frustrated with the side effects of his antipsychotic medication, he secretly stops taking it and starts seeing Parcher and Charles again.

In 1956, Alicia discovers Nash has resumed his "assignment" in a shed near their home. Realizing he has relapsed, Alicia rushes to the house to find Nash had left their infant son in the running bathtub, believing "Charles" was watching the baby. Alicia calls Dr. Rosen, but Nash accidentally knocks her and the baby to the ground, believing he's fighting Parcher.

As Alicia flees with the baby, Nash fights with his visions and realizes that all of them have looked the same ever since he first saw them. He stops Alicia's car and tells her he realizes that "Marcee" isn't real because she doesn't age, finally accepting that Parcher and other figures are hallucinations. Against Dr. Rosen's advice, Nash chooses not to restart his medication, believing he can deal with his symptoms himself, and Alicia decides to stay and support him.

Nash returns to Princeton, approaching his old rival Hansen, now head of the mathematics department, who allows him to work out of the library and audit classes. Over the next two decades, Nash learns to ignore his hallucinations and, by the late 1970s, is allowed to teach again.

In 1994, Nash is awarded the Nobel Memorial Prize in Economic Sciences for his revolutionary work on game theory, and is honored by his fellow professors. At the ceremony, he dedicates the prize to his wife. As Nash, Alicia, and their son leave the auditorium in Stockholm, Nash sees Charles, Marcee, and Parcher watching him, but merely glances at them before departing.

Cast

• Russell Crowe as John Nash
• Jennifer Connelly as Alicia Nash
• Ed Harris as William Parcher
• Christopher Plummer as Dr. Rosen
• Paul Bettany as Charles Herman
• Adam Goldberg as Richard Sol
• Josh Lucas as Martin Hansen
• Anthony Rapp as Bender
• Jason Gray-Stanford as Ainsley Neilson
• Judd Hirsch as Hellinger
• Austin Pendleton as Thomas King
• Vivien Cardone as Marcee Herman
• Killian, Christian, and Daniel Coffinet-Crean as Baby

Production

Development

A Beautiful Mind was the second schizophrenia-themed film that Ron Howard had planned to direct. The first, Laws of Madness, would have been based on the true story of schizophrenic Michael Laudor, who overcame difficult odds to successfully graduate from Yale Law School. Howard purchased the rights to Laudor's life story for $1.5 million in 1995 and had Brad Pitt slated to play the lead role. However, after Laudor killed his fiancée in 1998 in the midst of a psychotic episode, plans for the movie were cancelled.

After producer Brian Grazer first read an excerpt of Sylvia Nasar's 1998 book A Beautiful Mind in Vanity Fair magazine, he immediately purchased the rights to the film. Grazer later said that many A-list directors were calling with their point of view on the project. He eventually brought the project to Ron Howard, his long time partner.

Grazer met with a number of screenwriters, mostly consisting of "serious dramatists", but he chose Akiva Goldsman because of his strong passion and desire for the project. Goldsman's creative take on the project was to avoid having viewers understand they are viewing an alternative reality until a specific point in the film. This was done to rob the viewers of their understanding, to mimic how Nash comprehended his experiences. Howard agreed to direct the film based on the first draft. He asked Goldsman to emphasize the love story of Nash and his wife; she was critical to his being able to continue living at home.

Dave Bayer, a professor of mathematics at Barnard College, Columbia University, was consulted on the mathematical equations that appear in the film. For the scene where Nash has to teach a calculus class and gives them a complicated problem to keep them busy, Bayer chose a problem physically unrealistic but mathematically very rich, in keeping with Nash as "someone who really doesn't want to teach the mundane details, who will home in on what's really interesting". Bayer received a cameo role in the film as a professor who lays his pen down for Nash in the pen ceremony near the end of the film.

Greg Cannom was chosen to create the makeup effects for A Beautiful Mind, specifically the age progression of the characters. Crowe had previously worked with Cannom on The Insider. Howard had also worked with Cannom on Cocoon. Each character's stages of makeup were broken down by the number of years that would pass between levels. Cannom stressed subtlety between the stages, but worked toward the ultimate stage of "Older Nash". The production team originally decided that the makeup department would age Russell Crowe throughout the film; however, at Crowe's request, the makeup was used to push his look to resemble the facial features of John Nash. Cannom developed a new silicone-type makeup that could simulate skin and be used for overlapping applications; this shortened make-up application time from eight to four hours. Crowe was also fitted with a number of dentures to give him a slight overbite in the film.

Howard and Grazer chose frequent collaborator James Horner to score the film because they knew of his ability to communicate. Howard said, regarding Horner, "it's like having a conversation with a writer or an actor or another director". A running discussion between the director and the composer was the concept of high-level mathematics being less about numbers and solutions, and more akin to a kaleidoscope, in that the ideas evolve and change. After the first screening of the film, Horner told Howard: "I see changes occurring like fast-moving weather systems". He chose it as another theme to connect to Nash's ever-changing character. Horner chose Welsh singer Charlotte Church to sing the soprano vocals after deciding that he needed a balance between a child and adult singing voice. He wanted a "purity, clarity and brightness of an instrument" but also a vibrato to maintain the humanity of the voice.

The film was shot 90% chronologically. Three separate trips were made to the Princeton University campus. During filming, Howard decided that Nash's delusions should always be introduced first audibly and then visually. This provides a clue for the audience and establishes the delusions from Nash's point of view. The historic John Nash had only auditory delusions. The filmmakers developed a technique to represent Nash's mental epiphanies. Mathematicians described to them such moments as a sense of "the smoke clearing", "flashes of light" and "everything coming together", so the filmmakers used a flash of light appearing over an object or person to signify Nash's creativity at work. Two night shots were done at Fairleigh Dickinson University's campus in Florham Park, New Jersey, in the Vanderbilt Mansion ballroom. Portions of the film set at Harvard were filmed at Manhattan College. (Harvard has turned down most requests for on-location filming ever since the filming of Love Story (1970), which caused significant physical damage to trees on campus.)

Tom Cruise was considered for the lead role. Howard ultimately cast Russell Crowe. For the role of Alicia Nash, Rachel Weisz was offered the role but turned it down. Charlize Theron and Julia Ormond auditioned for the role. According to Ron Howard, the four finalists for the role of Alicia were Ashley Judd, Claire Forlani, Mary McCormack and Jennifer Connelly, with Connelly winning the role. Before the casting of Connelly, Hilary Swank and Salma Hayek were also candidates for the part.

Writing

The narrative of the film differs considerably from the events of Nash's life, as filmmakers made choices for the sense of the story. The film has been criticized for this aspect, but the filmmakers said they never intended a literal representation of his life.

One difficulty was the portrayal of his mental illness and trying to find a visual film language for this. As a matter of fact, Nash never had visual hallucinations: Charles Herman (the "roommate"), Marcee Herman and William Parcher (the Defense agent) are a scriptwriter's invention. Sylvia Nasar said that the filmmakers "invented a narrative that, while far from a literal telling, is true to the spirit of Nash's story". Nash spent his years between Princeton and MIT as a consultant for the RAND Corporation in California, but in the film he is portrayed as having worked for the Department of Defense at the Pentagon instead. His handlers, both from faculty and administration, had to introduce him to assistants and strangers. The PBS documentary A Brilliant Madness tried to portray his life more accurately.

Few of the characters in the film, besides John and Alicia Nash, correspond directly to actual people. The discussion of the Nash equilibrium was criticized as over-simplified. In the film, Nash has schizophrenic hallucinations while he is in graduate school, but in his life he did not have this experience until some years later. No mention is made of Nash's homosexual experiences at RAND, which are noted in the biography, though both Nash and his wife deny this occurred. Nash fathered a son, John David Stier (born June 19, 1953), by Eleanor Agnes Stier (1921–2005), a nurse whom he abandoned when she told him of her pregnancy. The film did not include Alicia's divorce of John in 1963. It was not until after Nash won the Nobel Memorial Prize in 1994 that they renewed their relationship. Beginning in 1970, Alicia allowed him to live with her as a boarder. They remarried in 2001.

Nash is shown to join Wheeler Laboratory at MIT, but there is no such lab. Instead, he was appointed as C. L. E. Moore instructor at MIT, and later as a professor. The film furthermore does not touch on the revolutionary work of John Nash in differential geometry and partial differential equations, such as the Nash embedding theorem or his proof of Hilbert's nineteenth problem, work which he did in his time at MIT and for which he was given the Abel Prize in 2015. The so-called pen ceremony tradition at Princeton shown in the film is completely fictitious. The film has Nash saying in 1994: "I take the newer medications", but in fact, he did not take any medication from 1970 onwards, something highlighted in Nasar's biography. Howard later stated that they added the line of dialogue because they worried that the film would be criticized for suggesting that all people with schizophrenia can overcome their illness without medication. In addition, Nash never gave an acceptance speech for his Nobel prize.

Release and response

A Beautiful Mind received a limited release on December 21, 2001, receiving positive reviews, with Crowe receiving wide acclaim for his performance. It was later released in the United States on January 4, 2002.

Critical response

On Rotten Tomatoes, A Beautiful Mind holds an approval rating of 74% based on 213 reviews and an average score of 7.20/10. The website's critical consensus states: "The well-acted A Beautiful Mind is both a moving love story and a revealing look at mental illness." On Metacritic, the film has a weighted average score of 72 out of 100 based on 33 reviews, indicating "generally favorable reviews". Audiences polled by CinemaScore gave the film an average grade of "A-" on an A+ to F scale.

Roger Ebert of Chicago Sun-Times gave the film four out of four stars. Mike Clark of USA Today gave three-and-a-half out of four stars and also praised Crowe's performance, calling it a welcome follow-up to Howard's previous film, 2001's How the Grinch Stole Christmas. Desson Thomson of The Washington Post found the film to be "one of those formulaically rendered Important Subject movies". The portrayal of mathematics in the film was praised by the mathematics community, including John Nash himself.

John Sutherland of The Guardian noted the film's biopic distortions, but said:

Howard pulls off an extraordinary trick in A Beautiful Mind by seducing the audience into Nash's paranoid world. We may not leave the cinema with A-level competence in game theory, but we do get a glimpse into what it feels like to be mad - and not know it.

Some writers such as Shailee Koranne argue that the film presents an unrealistic or inappropriate depiction of the disorder schizophrenia, which the protagonist John Nash suffers from, stating that places too much emphasis on “fixing” the disorder.

Writing in the Los Angeles Times, Lisa Navarrette criticized the casting of Jennifer Connelly as Alicia Nash as an example of whitewashing. Alicia Nash was born in El Salvador and had an accent not portrayed in the film.

Box office

During the five-day weekend of the limited release, A Beautiful Mind opened at the #12 spot at the box office, peaking at the #2 spot following the wide release. The film went on to gross $170,742,341 in the United States and Canada and $313,542,341 worldwide.

Insulin shock therapy

From Wikipedia, the free encyclopedia

 

Insulin shock therapy
Insulin shock therapy administered in Långbro Hospital, Stockholm in the 1930s
ICD-9-CM	94.24
MeSH	D003295

Insulin shock therapy or insulin coma therapy was a form of psychiatric treatment in which patients were repeatedly injected with large doses of insulin in order to produce daily comas over several weeks. It was introduced in 1927 by Austrian-American psychiatrist Manfred Sakel and used extensively in the 1940s and 1950s, mainly for schizophrenia, before falling out of favour and being replaced by neuroleptic drugs in the 1960s.

It was one of a number of physical treatments introduced into psychiatry in the first four decades of the 20th century. These included the convulsive therapies (cardiazol/metrazol therapy and electroconvulsive therapy), deep sleep therapy, and psychosurgery. Insulin coma therapy and the convulsive therapies are collectively known as the shock therapies.

Origins

In 1927, Sakel, who had recently qualified as a medical doctor in Vienna and was working in a psychiatric clinic in Berlin, began to use low (sub-coma) doses of insulin to treat drug addicts and psychopaths, and after one of the patients experienced improved mental clarity after having slipped into an accidental coma, Sakel reasoned the treatment might work for mentally ill patients. Having returned to Vienna, he treated schizophrenic patients with larger doses of insulin in order to deliberately produce coma and sometimes convulsions. Sakel made his results public in 1933, and his methods were soon taken up by other psychiatrists.

Joseph Wortis, after seeing Sakel practice it in 1935, introduced it to the US. British psychiatrists from the Board of Control visited Vienna in 1935 and 1936, and by 1938, 31 hospitals in England and Wales had insulin treatment units. In 1936, Sakel moved to New York and promoted the use of insulin coma treatment in US psychiatric hospitals. By the late 1940s, the majority of psychiatric hospitals in the US were using insulin coma treatment.

Technique

An insulin treatment ward, circa 1951, Roundway Hospital, Devizes, England

Insulin coma therapy was a labour-intensive treatment that required trained staff and a special unit. Patients, who were almost invariably diagnosed with schizophrenia, were selected on the basis of having a good prognosis and the physical strength to withstand an arduous treatment. There were no standard guidelines for treatment. Different hospitals and psychiatrists developed their own protocols. Typically, injections were administered six days a week for about two months.

The daily insulin dose was gradually increased to 100–150 units (1 unit = 34.7 μg) until comas were produced, at which point the dose would be levelled out. Occasionally doses of up to 450 units were used. After about 50 or 60 comas, or earlier if the psychiatrist thought that maximum benefit had been achieved, the dose of insulin was rapidly reduced before treatment was stopped. Courses of up to 2 years have been documented.

After the insulin injection patients would experience various symptoms of decreased blood glucose: flushing, pallor, perspiration, salivation, drowsiness or restlessness. Sopor and coma—if the dose was high enough—would follow. Each coma would last for up to an hour and be terminated by intravenous glucose or via naso-gastric tube. Seizures occurred before or during the coma. Many would be tossing, rolling, moaning, twitching, spasming or thrashing around.

Some psychiatrists regarded seizures as therapeutic and patients were sometimes also given electroconvulsive therapy or cardiazol/metrazol convulsive therapy during the coma, or on the day of the week when they didn't have insulin treatment. When they were not in a coma, insulin coma patients were kept together in a group and given special treatment and attention. One handbook for psychiatric nurses, written by British psychiatrist Eric Cunningham Dax, instructs nurses to take their insulin patients out walking and occupy them with games and competitions, flower-picking and map-reading, etc. Patients required continuous supervision as there was a danger of hypoglycemic aftershocks after the coma.

In "modified insulin therapy", used in the treatment of neurosis, patients were given lower (sub-coma) doses of insulin.

Effects

A patient subjected to the practice in Lapinlahti Hospital, Helsinki in the 1950s

A few psychiatrists (including Sakel) claimed success rates for insulin coma therapy of over 80% in the treatment of schizophrenia. A few others argued that it merely accelerated remission in those patients who would undergo remission anyway. The consensus at the time was somewhere in between, claiming a success rate of about 50% in patients who had been ill for less than a year (about double the spontaneous remission rate) with no influence on relapse.

Sakel suggested the therapy worked by "causing an intensification of the tonus of the parasympathetic end of the autonomic nervous system, by blockading the nerve cell, and by strengthening the anabolic force which induces the restoration of the normal function of the nerve cell and the recovery of the patient." The shock therapies in general had developed on the erroneous premise that epilepsy and schizophrenia rarely occurred in the same patient. The premise was supported by neuropathologic studies that found a dearth of glia in the brains of schizophrenic patients and a surplus of glia in epileptic brains. These observations led the Hungarian neuropsychiatrist Ladislas Meduna to induce seizures in schizophrenic patients with injections of camphor, soon replaced by pentylenetetrazol (Metrazole). Another theory was that patients were somehow "jolted" out of their mental illness.

The hypoglycemia (pathologically low glucose levels) that resulted from insulin coma therapy made patients extremely restless, sweaty, and liable to further convulsions and "after-shocks". In addition, patients invariably emerged from the long course of treatment "grossly obese", probably due to glucose rescue-induced glycogen storage disease. The most severe risks of insulin coma therapy were death and brain damage, resulting from irreversible or prolonged coma respectively. A study at the time claimed that many of the cases of brain damage were actually therapeutic improvement because they showed "loss of tension and hostility". Mortality risk estimates varied from about one percent to 4.9 percent.

Respected singer-songwriter Townes Van Zandt was said to have lost much of his long-term memory from this treatment, performed on him for bipolar disorder, preceding a life of substance abuse and depression.

Decline

Insulin coma therapy was used in most hospitals in the US and the UK during the 1940s and 1950s. The numbers of patients were restricted by the requirement for intensive medical and nursing supervision and the length of time it took to complete a course of treatment. For example, at one typical large British psychiatric hospital, Severalls Hospital in Essex, insulin coma treatment was given to 39 patients in 1956. In the same year, 18 patients received modified insulin treatment, while 432 patients were given electroconvulsive treatment.

In 1953, British psychiatrist Harold Bourne published a paper entitled "The insulin myth" in the Lancet, in which he argued that there was no sound basis for believing that insulin coma therapy counteracted the schizophrenic process in a specific way. If treatment worked, he said, it was because patients were chosen for their good prognosis and were given special treatment: "insulin patients tend to be an elite group sharing common privileges and perils". Prior to publishing "The insulin myth" in The Lancet, Bourne had tried to submit the article to the Journal of Mental Science; after a 12-month delay, the Journal informed Bourne they had rejected the article, telling him to "get more experience".

In 1957, when insulin coma treatment use was declining, The Lancet published the results of a randomized, controlled trial where patients were either given insulin coma treatment or identical treatment but with unconsciousness produced by barbiturates. There was no difference in outcome between the groups and the authors concluded that, whatever the benefits of the coma regimen, insulin was not the specific therapeutic agent.

In 1958, American neuropsychiatrist Max Fink published in the Journal of the American Medical Association the results of a random controlled comparison in 60 patients treated with 50 iatrogenic insulin-induced comas or chlorpromazine in doses from 300 mg to 2000 mg/day. The results were essentially the same in relief and discharge ratings but chlorpromazine was safer with fewer side-effects, easier to administer, and better suited to long-term care.

In 1958, Bourne published a paper on increasing disillusionment in the psychiatric literature about insulin coma therapy for schizophrenia. He suggested there were several reasons it had received almost universal uncritical acceptance by reviews and textbooks for several decades despite the occasional disquieting negative finding, including that, by the 1930s when it all started, schizophrenics were considered inherently unable to engage in psychotherapy, and insulin coma therapy "provided a personal approach to the schizophrenic, suitably disguised as a physical treatment so as to slip past the prejudices of the age."

Although coma therapy had largely fallen out of use in the US by the 1970s, it was still being practiced and researched in some hospitals, and may have continued for longer in countries such as China and the Soviet Union.

Recent writing

Recent articles about insulin coma treatment have attempted to explain why it was given such uncritical acceptance. In the US, Deborah Doroshow wrote that insulin coma therapy secured its foothold in psychiatry not because of scientific evidence or knowledge of any mechanism of therapeutic action, but due to the impressions it made on the minds of the medical practitioners within the local world in which it was administered and the dramatic recoveries observed in some patients. Today, she writes, those who were involved are often ashamed, recalling it as unscientific and inhumane. Administering insulin coma therapy made psychiatry seem a more legitimate medical field. Harold Bourne, who questioned the treatment at the time, said: "It meant that psychiatrists had something to do. It made them feel like real doctors instead of just institutional attendants".

One retired psychiatrist who was interviewed by Doroshow "described being won over because his patients were so sick and alternative treatments did not exist". Doroshow argues that "psychiatrists used complications to exert their practical and intellectual expertise in a hospital setting" and that collective risk-taking established "especially tight bonds among unit staff members". She finds it ironic that psychiatrists "who were willing to take large therapeutic risks were extremely careful in their handling of adverse effects". Psychiatrists interviewed by Doroshow recalled how insulin coma patients were provided with various routines and recreational and group-therapeutic activities, to a much greater extent than most psychiatric patients. Insulin coma specialists often chose patients whose problems were the most recent and who had the best prognosis; in one case discussed by Doroshow a patient had already started to show improvement before insulin coma treatment, and after the treatment denied that it had helped, but the psychiatrists nevertheless argued that it had.

A Beautiful Mind

The 1994 Nobel Prize winner in Economics John Nash became psychotic and was first treated at McLean Hospital. When he relapsed he was admitted to Trenton NJ State hospital. His associates at Princeton University pleaded with the hospital director to have Nash treated in the insulin coma unit, recognizing that it was better staffed than other hospital units. He responded to treatment and treatment was continued with neuroleptics.

Nash's life story was presented in the film A Beautiful Mind, which accurately portrayed the seizures associated with his treatments. In a review of the Nash history, Fink ascribed the success of coma treatments to the 10% of associated seizures, noting that physicians often augmented the comas by convulsions induced by ECT. He envisioned insulin coma treatment as a weak form of convulsive therapy.

Other explanations

In the UK, psychiatrist Kingsley Jones sees the support of the Board of Control as important in persuading psychiatrists to use insulin coma therapy. The treatment then acquired the privileged status of a standard procedure, protected by professional organizational interests. He also notes that it has been suggested that the Mental Treatment Act 1930 encouraged psychiatrists to experiment with physical treatments.

British lawyer Phil Fennell notes that patients "must have been terrified" by the insulin coma therapy procedures and the effects of the massive overdoses of insulin, and were often rendered more compliant and easier to manage after a course.

Leonard Roy Frank, an American activist from the psychiatric survivors movement who underwent 50 forced insulin coma treatments combined with ECT, described the treatment as "the most devastating, painful and humiliating experience of my life", a "flat-out atrocity" glossed over by psychiatric euphemism, and a violation of basic human rights.

In 2013, French physician-and-novelist Laurent Seksik wrote an historical novel about the tragic life of Eduard Einstein: Le cas Eduard Einstein. He related the encounter between Dr Sakel and Mileva Maric, Albert Einstein's first wife (and Eduard's mother), and the way Sakel's therapy had been given to Eduard, who had schizophrenia.

Representation in media

Like many new medical treatments for diseases previously considered incurable, depictions of insulin coma therapy in the media were initially favorable. In the 1940 film Dr. Kildare's Strange Case, young Kildare uses the new "insulin shock cure for schizophrenia" to bring a man back from insanity. The film dramatically shows a five-hour treatment that ends with a patient eating jelly sandwiches and reconnecting with his wife. Other films of the era began to show a more sinister approach, beginning with the 1946 film Shock, in which actor Vincent Price plays a doctor who plots to murder a patient using an overdose of insulin in order to keep the fact that he was a murderer a secret. More recent films include Frances (1982) in which actress Frances Farmer undergoes insulin coma treatment, and A Beautiful Mind, which depicted genius John Nash undergoing insulin treatment. In an episode of the medical drama House M.D., House puts himself in an insulin shock to try to make his hallucinations disappear. Sylvia Plath's The Bell Jar refers to insulin coma therapy in chapter 15.