In medicine and medical anthropology, a culture-bound syndrome, culture-specific syndrome, or folk illness is a combination of psychiatric and somatic symptoms that are considered to be a recognisable disease only within a specific society or culture.
There are no objective biochemical or structural alterations of body organs or functions, and the disease is not recognized in other cultures. The term culture-bound syndrome was included in the fourth version of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 1994) which also includes a list of the most common culture-bound conditions (DSM-IV: Appendix I). Counterpart within the framework of ICD-10 (Chapter V) are the culture-specific disorders defined in Annex 2 of the Diagnostic criteria for research.
More broadly, an endemic that can be attributed to certain behaviour patterns within a specific culture by suggestion may be referred to as a potential behavioural epidemic. As in the cases of drug use, or alcohol and smoking abuses, transmission can be determined by communal reinforcement and person-to-person interactions. On etiological grounds, it can be difficult to distinguish the causal contribution of culture upon disease from other environmental factors such as toxicity.
A culture-specific syndrome is characterised by:
Categorisation as a disease in the culture (i.e. not a voluntary behaviour or false claim);
Widespread familiarity in the culture;
Complete lack of familiarity or misunderstanding of the condition to people in other cultures;
No objectively demonstrable biochemical or tissue abnormalities (signs); and
The condition is usually recognised and treated by the folk medicine of the culture.
Some culture-specific syndromes involve somatic symptoms (pain or disturbed function of a body part), while others are purely behavioural. Some culture-bound syndromes appear with similar features in several cultures, but with locally specific traits, such as penis panics.
A culture-specific syndrome is not the same as a geographically localised disease with specific, identifiable, causal tissue abnormalities, such as kuru or sleeping sickness, or genetic conditions limited to certain populations. It is possible that a condition originally assumed to be a culture-bound behavioural syndrome is found to have a biological cause; from a medical perspective it would then be redefined into another nosological category.
The American Psychiatric Association states the following:
The term culture-bound syndrome denotes recurrent, locality-specific patterns of aberrant behavior and troubling experience that may or may not be linked to a particular DSM-IV diagnostic category. Many of these patterns are indigenously considered to be “illnesses,” or at least afflictions, and most have local names. Although presentations conforming to the major DSM-IV categories can be found throughout the world, the particular symptoms, course, and social response are very often influenced by local cultural factors. In contrast, culture-bound syndromes are generally limited to specific societies or culture areas and are localized, folk, diagnostic categories that frame coherent meanings for certain repetitive, patterned, and troubling sets of experiences and observations.
The term culture-bound syndrome is controversial since it reflects the different opinions of anthropologists and psychiatrists. Anthropologists have a tendency to emphasize the relativistic and culture-specific dimensions of the syndromes, while physicians tend to emphasize the universal and neuropsychological dimensions. Guarnaccia & Rogler (1999) have argued in favour of investigating culture-bound syndromes on their own terms, and believe that the syndromes have enough cultural integrity to be treated as independent objects of research.
Guarnaccia and Rogler demonstrate the issues that occur when diagnosing cultural bound disorders using the DSM-IV. One of the key problems that arise is the “subsumption of culture bound syndromes into psychiatric categories”, which ultimately creates a medical hegemony and places the western perspective above that of other cultural and epistemological explanations of disease. The urgency for further investigation or reconsideration of the DSM-IV’s authoritative power is emphasized, as the DSM becomes an international document for research and medical systems abroad. Guarnaccia and Rogler provide two research questions that must be considered, “firstly, how much do we know about the culture-bound syndromes for us to be able to fit them into standard classification; and secondly, whether such a standard and exhaustive classification in fact exists”.
It is suggested that the problematic nature of the DSM becomes evident when we view it as definitively conclusive. Questions are raised to whether culture-bound syndromes can be treated as discrete entities, or whether their symptoms are generalised and perceived as an amalgamation of previously diagnosed illnesses. If this is the case, then the DSM may be what Bruno Latour would defined as “particular universalism”. In that the Western medical system views itself to have a privileged insight into the true intelligence of nature, in contrast to the model provided by other cultural perspectives.
Some studies suggest that culture-bound syndromes represent an acceptable way within a specific culture (and cultural context) among certain vulnerable individuals (i.e. an ataque de nervios at a funeral in Puerto Rico) to express distress in the wake of a traumatic experience. A similar manifestation of distress when displaced into a North American medical culture may lead to a very different, even adverse outcome for a given individual and his or her family. The history and etymology of some syndromes such as Brain-Fog Syndrome, have also been reattributed to 19th century Victorian Britain rather than West Africa.
In 2013, the DSM 5, dropped the term culture-bound syndrome, preferring the new name “Cultural Concepts of Distress”.
Cultural Collusion Between Medical Perspectives
Within the traditional Hmong culture, epilepsy (qaug dab peg) directly translates to “the spirit catches you and you fall down” which is said to be an evil spirit called a dab that captures your soul and makes you ill. In this culture, individuals with seizures are seen to be blessed with a gift; an access point into the spiritual realm which no one else has been given. In westernised society, epilepsy is considered a serious long-term brain condition, that can have a major impairment on an individual’s life. The way the illness is dealt with in Hmong culture is vastly different due to the high-status epilepsy has amongst the culture, compared to individuals who have the condition in westernised societies. Individuals with epilepsy within the Hmong culture are a source of pride for their family.
Another culture bound illness is neurasthenia which is a vaguely described medical ailment in Chinese culture that presents as lassitude, weariness, headaches, and irritability and is mostly linked to emotional disturbance. A report done in 1942 showed that 87% of patients diagnosed by Chinese psychiatrists as having neurasthenia could be reclassified as having major depression according to the DSM-3 criteria. Another study conducted in Hong Kong showed that most patients selectively presented their symptoms according to what they perceived as appropriate and tended to only focus on somatic suffering, rather than the emotional problems they were facing.
Globalisation is a process whereby information, cultures, jobs, goods, and services are spread across national borders. This has had a powerful impact on the 21st century in many ways including through enriching cultural awareness across the globe. Greater level of cultural integration is occurring due to rapid industrialisation and globalisation, with cultures absorbing more influences from each other. As cultural awareness begins to increase between countries, there is a consideration into whether cultural bound syndromes will slowly lose their geographically bound nature and become commonly known syndromes that will then become internationally recognised. Anthropologist and psychiatrist Roland Littlewood makes the observation that these diseases are likely to vanish in an increasingly homogenous global culture in the face of globalisation (and industrialisation). Depression for example, was once only accepted in western societies, however it is now recognised as a mental disorder in all parts of the world. In contrast to Eastern civilisations such as Taiwan, depression is still much more common in Western cultures like the United States. This could indicate that globalisation may have an impact on allowing disorders to be spread across borders, however these disorders may remain predominant in certain cultures.
The fourth edition of Diagnostic and Statistical Manual of Mental Disorders classifies the below syndromes as culture-bound syndromes.
Brunei, Singapore, Malaysia, Indonesia, Philippines, Timor-Leste
Ataque de Nervios
Hispanophone, as well as in the Philippines where it is known as “nervous breakdown”
France and French-speaking countries
Brain Fag Syndrome
West African students
Falling-Out, Blacking Out
Southern United States and Caribbean
Native American (Navajo, Muscogee/Creek)
Chinese, Malaysian and Indonesian populations in Southeast Asia; Assam; occasionally in the West
Malaysia and Indonesia, as well as the Philippines (as mali-mali, particularly among Tagalogs)
Latinos in the United States and Latin America
Mal de Pelea
Latin America, Latinos in the United States, Philippines
Mediterranean; Hispanic populations and Ethiopia
Arctic and subarctic Inuit populations
Zou huo ru mo (Qigong Psychotic Reaction)
Southern United States, Caribbean nations
Portuguese populations in Cape Verde
African American, White populations in the southern United States and Ethiopia
Latinos in the United States; Mexico, Central America and South America
Ethiopia, Somalia, Egypt, Sudan, Iran, and other North African and Middle Eastern societies
The fifth edition of Diagnostic and Statistical Manual of Mental Disorders classifies the below syndromes as cultural concepts of distress, a closely related concept.
Ataque de Nervios
Hispanophone, as well as in the Philippines
Latin America, Latinos in the US
Latinos in the US, Mexico, Central America and South America
Southeast Asian Austronesians
Dhat Syndrome (Dhātu), Shen-kʼuei, Jiryan
India and Taiwan
Koro, Suk Yeong, Jinjin Bemar
Southeast Asia, India, and China
Malaysia and Indonesia
Nervios, Nerfiza, Nerves, Nevra
Egypt; Greece; northern Europe; Mexico, Central and South America
Taiwan and Southeast Asia
Pibloktoq (Arctic Hysteria)
Inuit living within the Arctic Circle
Mexico, Central and South America
Taijin Kyofusho, Shinkeishitsu (Anthropophobia)
Kenya, Southern Africa (among Bantu, Zulu, and affiliated groups)
Inuit living within the Arctic Circle
Fear of Windigo
Indigenous people of Northeast America
Though “the ethnocentric bias of Euro-American psychiatrists has led to the idea that culture-bound syndromes are confined to non-Western cultures”, a prominent example of a Western culture-bound syndrome is anorexia nervosa.
Within the contiguous US, the consumption of kaolin, a type of clay, has been proposed as a culture-bound syndrome observed in African Americans in the rural south, particularly in areas in which the mining of kaolin is common.
In South Africa, among the Xhosa people, the syndrome of amafufunyana is commonly used to describe those believed to be possessed by demons or other malevolent spirits. Traditional healers in the culture usually perform exorcisms in order to drive off these spirits. Upon investigating the phenomenon, researchers found that many of the people claimed to be affected by the syndrome exhibited the traits and characteristics of schizophrenia.
Some researchers have suggested that both premenstrual syndrome (PMS) and the more severe premenstrual dysphoric disorder (PMDD), which have currently unknown physical mechanisms, are Western culture-bound syndromes. However, this is controversial.
Morgellons is a rare self-diagnosed skin condition reported primarily in white populations in the US. It has been described by a journalist as “a socially transmitted disease over the Internet”.
Vegetative-vascular dystonia can be considered an example of somatic condition formally recognised by local medical communities in former Soviet Union countries, but not in Western classification systems. Its umbrella term nature as neurological condition also results in diagnosing neurotic patients as neurological ones, in effect substituting possible psychiatric stigma with culture-bound syndrome disguised as a neurological condition.
Refugee children in Sweden have been known to fall into coma-like states on learning their families will be deported. The condition, known in Swedish as uppgivenhetssyndrom, or resignation syndrome, is believed to only exist among the refugee population in Sweden, where it has been prevalent since the early part of the 21st century. In a 130-page report on the condition commissioned by the government and published in 2006, a team of psychologists, political scientists, and sociologists hypothesized that it was a culture-bound syndrome.
A startle disorder similar to latah, called imu (sometimes spelled imu:), is found among Ainu people, both Sakhalin Ainu and Hokkaido Ainu.
A condition similar to piblokto, called menerik (sometimes meryachenie), is found among Yakuts, Yukaghirs, and Evenks living in Siberia.
The trance-like violent behaviour of the Viking age berserkers – behaviour that disappeared with the arrival of Christianity – has been described as a culture-bound syndrome.
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Mass psychogenic illness (MPI) – also called mass sociogenic illness, mass psychogenic disorder, epidemic hysteria, or mass hysteria – involves the spread of illness symptoms through a population where there is no infectious agent responsible for contagion.
It is the rapid spread of illness signs and symptoms affecting members of a cohesive group, originating from a nervous system disturbance involving excitation, loss, or alteration of function, whereby physical complaints that are exhibited unconsciously have no corresponding organic causes.
MPI is distinct from other types of collective delusions by involving physical symptoms. It is not well understood and its causes are uncertain. Features of MPI outbreaks often include:
Symptoms that have no plausible organic basis;
Symptoms that are transient and benign;
Symptoms with rapid onset and recovery;
Occurrence in a segregated group;
The presence of extraordinary anxiety;
Symptoms that are spread via sight, sound or oral communication;
A spread that moves down the age scale, beginning with older or higher-status people;
A preponderance of female participants.
British psychiatrist Simon Wessely distinguishes between two forms of MPI:
Mass anxiety hysteria “consists of episodes of acute anxiety, occurring mainly in schoolchildren. Prior tension is absent and the rapid spread is by visual contact.”
Mass motor hysteria “consists of abnormalities in motor behaviour. It occurs in any age group and prior tension is present. Initial cases can be identified and the spread is gradual. … [T]he outbreak may be prolonged.”
While his definition is sometimes adhered to, others such as Ali-Gombe et al. of the University of Maiduguri, Nigeria contest Wessely’s definition and describe outbreaks with qualities of both mass motor hysteria and mass anxiety hysteria.
The DSM-IV-TR does not have specific diagnosis for this condition but the text describing conversion disorder states that “In ‘epidemic hysteria’, shared symptoms develop in a circumscribed group of people following ‘exposure’ to a common precipitant.”
Timothy F. Jones of the Tennessee Department of Health compiles the following symptoms based on their commonality in outbreaks occurring in 1980-1990:
Dizziness or Light-Headedness
Abdominal Cramps or Pain
Fatigue, Drowsiness or Weakness
Sore or Burning Throat
Hyperventilation or Difficulty Breathing
Watery or Irritated Eyes
Chest Tightness/Chest Pain
Inability to Concentrate/Trouble Thinking
Tingling, Numbness or Paralysis
Anxiety or Nervousness
Trouble with Vision
Loss of Consciousness/Syncope
Prevalence and Intensity
Adolescents and children are frequently affected in cases of MPI. The hypothesis that those prone to extraversion or neuroticism, or those with low IQ scores, are more likely to be affected in an outbreak of hysterical epidemic has not been consistently supported by research. Bartholomew and Wessely state that it “seems clear that there is no particular predisposition to mass sociogenic illness and it is a behavioural reaction that anyone can show in the right circumstances.”
Intense media coverage seems to exacerbate outbreaks. The illness may also recur after the initial outbreak. John Waller advises that once it is determined that the illness is psychogenic, it should not be given credence by authorities. For example, in the Singapore factory case study, calling in a medicine man to perform an exorcism seemed to perpetuate the outbreak.
Besides the difficulties common to all research involving the social sciences, including a lack of opportunity for controlled experiments, mass sociogenic illness presents special difficulties to researchers in this field. Balaratnasingam and Janca report that the methods for “diagnosis of mass hysteria remain contentious.” According to Jones, the effects resulting from MPI “can be difficult to differentiate from [those of] bioterrorism, rapidly spreading infection or acute toxic exposure.”
These troubles result from the residual diagnosis of MPI. There is a lack of logic in an argument that proceeds: “There isn’t anything, so it must be MPI.” It precludes the notion that an organic factor could have been overlooked. Nevertheless, running an extensive number of tests extends the probability of false positives. Singer, of the Uniformed Schools of Medicine, has summarized the problems with such a diagnosis:
“[Y]ou find a group of people getting sick, you investigate, you measure everything you can measure … and when you still can’t find any physical reason, you say ‘well, there’s nothing else here, so let’s call it a case of MPI.'”
The earliest studied cases linked with epidemic hysteria are the dancing manias of the Middle Ages, including St. John’s dance and tarantism. These were supposed to be associated with spirit possession or the bite of the tarantula. Those with dancing mania would dance in large groups, sometimes for weeks at a time. The dancing was sometimes accompanied by stripping, howling, the making of obscene gestures, or even (reportedly) laughing or crying to the point of death. Dancing mania was widespread over Europe.
Between the 15th and 19th centuries, instances of motor hysteria were common in nunneries. The young ladies that made up these convents were sometimes forced there by family. Once accepted, they took vows of chastity and poverty. Their lives were highly regimented and often marked by strict disciplinary action. The nuns would exhibit a variety of behaviours, usually attributed to demonic possession. They would often use crude language and exhibit suggestive behaviours. One convent’s nuns would regularly meow like cats. Priests were often called in to exorcise demons.
18th to 21st Centuries
MPI outbreaks occurred in factories following the industrial revolution in England, France, Germany, Italy and Russia as well as the United States and Singapore.
W.H. Phoon, Ministry of Labour in Singapore, gives a case study of six outbreaks of MPI in Singapore factories between 1973 and 1978. They were characterised by:
Hysterical seizures of screaming and general violence, wherein tranquilizers were ineffective;
Trance states, where a worker would claim to be speaking under the influence of a spirit or jinn; and
Frightened spells: some workers complained of unprecedented fear, or of being cold, numb, or dizzy. Outbreaks would subside in about a week.
Often a bomoh (medicine man) would be called in to do a ritual exorcism. This technique was not effective and sometimes seemed to exacerbate the MPI outbreak. Females and Malay people were affected disproportionately.
Especially notable is the “June Bug” outbreak: In June 1962, a peak month in factory production, 62 workers at a dressmaking factory in a textile town in the Southern US experienced symptoms including severe nausea and breaking out on the skin. Most outbreaks occurred during the first shift, where four fifths of the workers were female. Of 62 total outbreaks, 59 were women, some of whom believed they were bitten by bugs from a fabric shipment, so entomologists and others were called in to discover the pathogen, but none was found. Kerchoff coordinated the interview of affected and unaffected workers at the factory and summarizes his findings:
Strain – those affected were more likely to work overtime frequently and provide the majority of the family income. Many were married with children.
Affected persons tended to deny their difficulties. Kerchoff postulates that such were “less likely to cope successfully under conditions of strain.”
Results seemed consistent with a model of social contagion. Groups of affected persons tended to have strong social ties.
Kerchoff also links the rapid rate of contagion with the apparent reasonableness of the bug infestation theory and the credence given to it in accompanying news stories.
Stahl and Lebedun describe an outbreak of mass sociogenic illness in the data centre of a university town in the United States Midwest in 1974. Ten of 39 workers smelling an unconfirmed “mystery gas” were rushed to a hospital with symptoms of dizziness, fainting, nausea and vomiting. They report that most workers were young women either putting their husbands through school or supplementing the family income. Those affected were found to have high levels of job dissatisfaction. Those with strong social ties tended to have similar reactions to the supposed gas, which only one unaffected woman reported smelling. No gas was detected in subsequent tests of the data centre.
Mass hysteria affected schools in Berry, Alabama, and Miami Beach in 1974, with the former episode taking the form of recurring pruritus, and the latter initially triggering fears of poison gas (it was traced back to a popular student who happened to be sick with a virus).
Thousands were affected by the spread of a supposed illness in a province of Kosovo in March to June 1990, exclusively affecting ethnic Albanians, most of whom were young adolescents. A wide variety of symptoms were manifested, including headache, dizziness, impeded respiration, weakness/adynamia, burning sensations, cramps, retrosternal/chest pain, dry mouth and nausea. After the illness had subsided, a bipartisan Federal Commission released a document, offering the explanation of psychogenic illness. Radovanovic of the Department of Community Medicine and Behavioural Sciences Faculty of Medicine in Safat, Kuwait reports:
This document did not satisfy either of the two ethnic groups. Many Albanian doctors believed that what they had witnessed was an unusual epidemic of poisoning. The majority of their Serbian colleagues also ignored any explanation in terms of psychopathology. They suggested that the incident was faked with the intention of showing Serbs in a bad light but that it failed due to poor organization.
Rodovanovic expects that this reported instance of mass sociogenic illness was precipitated by the demonstrated volatile and culturally tense situation in the province.
The Tanganyika laughter epidemic of 1962 was an outbreak of laughing attacks rumoured to have occurred in or near the village of Kanshasa on the western coast of Lake Victoria, Tanzania, eventually affecting 14 different schools and over 1,000 people.
On the morning of Thursday 07 October 1965, at a girls’ school in Blackburn in England, several girls complained of dizziness. Some fainted. Within a couple of hours, 85 girls from the school were rushed by ambulance to a nearby hospital after fainting. Symptoms included swooning, moaning, chattering of teeth, hyperpnea, and tetany. Moss and McEvedy published their analysis of the event about one year later. Their conclusions follow. Note that their conclusion about the above-average extraversion and neuroticism of those affected is not necessarily typical of MPI:
Clinical and laboratory findings were essentially negative.
Investigations by the public health authorities did not uncover any evidence of pollution of food or air.
The epidemiology of the outbreak was investigated by means of questionnaires administered to the whole school population. It was established that the outbreaks began among the 14-year-olds, but that the heaviest incidence moved to the youngest age groups.
By using the Eysenck Personality Inventory, it was established that, in all age groups, the mean E [extraversion] and N [neuroticism] scores of the affected were higher than those of the unaffected.
The younger girls proved more susceptible, but disturbance was more severe and lasted longer in the older girls.
It was considered that the epidemic was hysterical, that a previous polio epidemic had rendered the population emotionally vulnerable, and that a three-hour parade, producing 20 faints on the day before the first outbreak, had been the specific trigger.
The data collected were thought to be incompatible with organic theories and with the compromise theory of an organic nucleus.
Another possible case occurred in Belgium in June 1999 when people, mainly schoolchildren, became ill after drinking Coca-Cola. In the end, scientists were divided over the scale of the outbreak, whether it fully explains the many different symptoms and the scale to which sociogenic illness affected those involved.
A possible outbreak of mass psychogenic illness occurred at Le Roy Junior-Senior High School in 2011, in upstate New York, US, in which multiple students began having symptoms similar to Tourette syndrome. Various health professionals ruled out such factors as Gardasil, drinking water contamination, illegal drugs, carbon monoxide poisoning and various other potential environmental or infectious causes, before diagnosing the students with a conversion disorder and mass psychogenic illness.
Starting around 2009, a spate of apparent poisonings at girls’ schools across Afghanistan began to be reported; symptoms included dizziness, fainting and vomiting. The United Nations, World Health Organisation and NATO’s International Security Assistance Force carried out investigations of the incidents over multiple years, but never found any evidence of toxins or poisoning in the hundreds of blood, urine and water samples they tested. The conclusion of the investigators was that the girls were experiencing a mass psychogenic illness.
In August 2019 the BBC reported that schoolgirls at the Ketereh national secondary school (SMK Ketereh) in Kelantan, Malaysia, started screaming, with some claiming to have seen ‘a face of pure evil’. Dr Simon Wessely of King’s College Hospital, London suggested it was a form of ‘collective behaviour’. Robert Bartholomew, an American medical sociologist and author, said, “It is no coincidence that Kelantan, the most religiously conservative of all Malaysian states, is also the one most prone to outbreaks.” This view is supported by Afiq Noor, an academic, who argues that the stricter implementation of Islamic law in school in states such as Kelantan is linked to the outbreaks. He suggested that the screaming outbreak was caused by the constricted environment. In Malaysian culture burial sites and trees are common settings for supernatural tales about the spirits of dead infants (toyol), vampiric ghosts (pontianak) and vengeful female spirits (penanggalan). Authorities responded to the Kelantan outbreak by cutting down trees around the school.
Outbreaks of MPI “have been reported in Catholic convents and monasteries across Mexico, Italy and France, in schools in Kosovo and even among cheerleaders in a rural North Carolina town”.
Episodes of mass hysteria has been observed in schools of Nepal frequently, even leading to closure of schools temporarily. A unique phenomenon of “recurrent epidemic of mass hysteria” was reported from a school of Pyuthan district of western Nepal in 2018. After a 9-year-old school girl developed crying and shouting episodes, quickly other children of the same school were also affected resulting in 47 affected students (37 females, 10 males) in the same day. Since 2016 similar episodes of mass psychogenic illness has been occurring in the same school every year. This is thought to be a unique case of recurrent mass hysteria.
In July 2022 reports of up to 15 girls showing unusual symptoms such as screaming, trembling, and banging their heads came up from a government school in Bageshwar, Uttarakhand. Mass psychological illness has been suggested as a possible cause.
Terrorism and Biological Warfare
Bartholomew and Wessely anticipate the “concern that after a chemical, biological or nuclear attack, public health facilities may be rapidly overwhelmed by the anxious and not just the medical and psychological casualties.” Additionally, early symptoms of those affected by MPI are difficult to differentiate from those actually exposed to the dangerous agent.
The first Iraqi missile hitting Israel during the Persian Gulf War was believed to contain chemical or biological weapons. Though this was not the case, 40% of those in the vicinity of the blast reported breathing problems.
Right after the 2001 anthrax attacks in the first two weeks of October 2001, there were over 2,300 false anthrax alarms in the US. Some reported physical symptoms of what they believed to be anthrax.
Also in 2001, a man sprayed what was later found to be a window cleaner into a subway station in Maryland. Thirty-five people were treated for nausea, headaches and sore throats.
In 2017, some employees of the US embassy in Cuba reported symptoms (nicknamed the “Havana syndrome”) attributed to “sonic attacks”. The following year, some US government employees in China reported similar symptoms. Some scientists have suggested the alleged symptoms were psychogenic in nature. However, one study using neuroimaging suggest at least some organic, non-psychogenic cause.
Children in Recent Refugee Families
Refugee children in Sweden have been reported to fall into coma-like states on learning their families will be deported. The condition, known as resignation syndrome (Swedish: uppgivenhetssyndrom), is believed to only exist among the refugee population in the Scandinavian country, where it has been prevalent since the early part of the 21st century. Commentators state “a degree of psychological contagion” is inherent to the condition, by which young friends and relatives of the affected individual can also come to have the condition.
In a 130-page report on the condition, commissioned by the government and published in 2006, a team of psychologists, political scientists and sociologists hypothesized that it was a culture-bound syndrome, a psychological illness endemic to a specific society.
This phenomenon has later been called into question, with children witnessing that they were forced, by their parents, to act in a certain way in order to increase chances of being granted residence permits. As evidenced by medical records, healthcare professionals were aware of this scam, and witnessed parents who actively refused aid for their children, but remained silent. Later, Sveriges Television, Sweden’s national public television broadcaster, were severely critiqued by investigative journalist Janne Josefsson for failing to uncover the truth.
After the rise of a popular breakthrough YouTube channel in 2019 where the presenter exhibits extensive Tourette’s-like behaviour, there was a sharp rise in young people referred to clinics specialising in tics, thought to be related to social contagion spread via the internet, and also to stress from eco-anxiety and the COVID-19 pandemic. The authors of an August 2021 report found evidence that social media was the primary vector for transmission, declaring the phenomenon the first recorded instance of “mass social media–induced illness” (MSMI).
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Boredom boreout syndrome is a psychological disorder that causes physical illness, mainly caused by mental underload at the workplace due to lack of either adequate quantitative or qualitative workload. One reason for boreout could be that the initial job description does not match the actual work.
This theory was first expounded in 2007 in Diagnose Boreout, a book by Peter Werder and Philippe Rothlin, two Swiss business consultants.
Symptoms and Consequences
Symptoms of the bore-out syndrome are described by the Frankfurt psychotherapist Wolfgang Merkle as similar to the burnout syndrome. These include depression, listlessness and insomnia, but also tinnitus, susceptibility to infection, stomach upset, headache and dizziness.
The consequences of boreout for employees are numerous both psychologically and physically and more or less serious. On the psychological level, boredom, dissatisfaction, and permanent frustration gradually lead the victim of a boreout into a vicious circle. They gradually lose the will to act at the professional level and at the personal level. To the loss of self-esteem is added the constant anxiety of being discovered. The boreout victim lives with the constant fear that their supervisor, colleagues, or friends will discover their inactivity and duplicity. The confrontation with and enduring the unsatisfactory situation leads to further stress that paralyses and strains. Being constantly confronted with the emptiness of their professional life and their apparent uselessness in society, the employee may experience significant stress. The suffering all the more accentuated because it cannot be shared and if it is, is not understood. This is also the reason that this syndrome is relatively unknown:
This has to do with the fact that everyone prefers to have disorders that are socially considered. Someone who says, ‘I have so much to do, my God, the job is banging up at work’, is much more respected than someone who says he’s bored, has no responsibilities, and that’s what gets him done. Everyone says: ‘I want to trade with you, that’s great! Interview: Wolfgang Merkle Frankfurter Allgemeinen Zeitung, 2010.
This can lead to serious mental disorders such as personality destruction or even depression or suicide. Boreout is also a trigger for physical diseases such as certain types of epilepsy caused by stress or exhaustion, severe sleep disorders, hand and voice tremors, shingles, and ulcers.
On the physical side, according to the British “Bored to death” study, employees who are bored at work are two to three times more likely to be victims of cardiovascular events than those whose employment is stimulating. The permanent anxiety in which the employee lives exhausts him/her physically. Fatigue is constant despite physical inactivity. Boreout can lead to eating disorders such as untimely nibbling or loss of appetite. Some people may use alcohol or drugs to overcome their discomfort and thus develop a harmful addiction.
According to Peter Werder and Philippe Rothlin, the absence of meaningful tasks, rather than the presence of stress, is many workers’ chief problem. Ruth Stock-Homburg defines boreout as a negative psychological state with low work-related arousal.
Boreout has been studied in terms of its key dimensions. In their practitioners book, Werder and Rothlin suggest elements: boredom, lack of challenge, and lack of interest. These authors disagree with the common perceptions that a demotivated employee is lazy; instead, they claim that the employee has lost interest in work tasks. Those suffering from boreout are “dissatisfied with their professional situation” in that they are frustrated at being prevented, by institutional mechanisms or obstacles as opposed to by their own lack of aptitude, from fulfilling their potential (as by using their skills, knowledge, and abilities to contribute to their company’s development) and/or from receiving official recognition for their efforts.
Relying on empirical data from service employees, Stock-Homburg identifies three components of boreout: job boredom, crisis of meaning and crisis of growth, which arise from a loss of resources due to a lack of challenges.
Peter Werder and Philippe Rothlin suggest that the reason for researchers’ and employers’ overlooking the magnitude of boreout-related problems is that they are underreported because revealing them exposes a worker to the risk of social stigma and adverse economic effects (By the same token, many managers and co-workers consider an employee’s level of workplace stress to be indicative of that employee’s status in the workplace).
There are several reasons boreout might occur. The authors note that boreout is unlikely to occur in many non-office jobs where the employee must focus on finishing a specific task (e.g. a surgeon) or helping people in need (e.g. a childcare worker or nanny). In terms of group processes, it may well be that the boss or certain forceful or ambitious individuals with the team take all the interesting work leaving only a little of the most boring tasks for the others. Alternatively, the structure of the organization may simply promote this inefficiency. Of course, few if any employees (even among those who would prefer to leave) want to be fired or laid off, so the vast majority are unwilling and unlikely to call attention to the dispensable nature of their role.
As such, even if an employee has very little work to do or would only expect to be given qualitative inadequate work, they give the appearance of “looking busy” (e.g. ensuring that a work-related document is open on one’s computer, covering one’s desk with file folders, and carrying briefcases (whether empty or loaded) from work to one’s home and vice versa).
The symptoms of boreout lead employees to adopt coping or work-avoidance strategies that create the appearance that they are already under stress, suggesting to management both that they are heavily “in demand” as workers and that they should not be given additional work: “The boreout sufferer’s aim is to look busy, to not be given any new work by the boss and, certainly, not to lose the job.”
Boreout strategies include:
Stretching work strategy: This involves drawing out tasks so they take much longer than necessary. For example, if an employee’s sole assignment during a work week is a report that takes three work days, the employee will “stretch” this three days of work over the entire work week. Stretching strategies vary from employee to employee. Some employees may do the entire report in the first three days, and then spend the remaining days surfing the Internet, planning their holiday, browsing online shopping websites, sending personal e-mails, and so on (all the while ensuring that their workstation is filled with the evidence of “hard work”, by having work documents ready to be switched-to on the screen). Alternatively, some employees may “stretch” the work over the entire work week by breaking up the process with a number of pauses to send personal e-mails, go outside for a cigarette, get a coffee, chat with friends in other parts of the company, or even go to the washroom for a 10-minute nap.
Pseudo-commitment strategy: The pretence of commitment to the job by attending work and sitting at the desk, sometimes after work hours. As well, demotivated employees may stay at their desks to eat their lunch to give the impression that they are working through the lunch hour; in fact, they may be sending personal e-mails or reading online articles unrelated to work. An employee who spends the afternoon on personal phone calls may learn how to mask this by sounding serious and professional during their responses, to give the impression that it is a work-related call. For example, if a bureaucrat is chatting with a friend to set up a dinner date, when the friend suggests a time, the bureaucrat can respond that “we can probably fit that meeting time in.”
Consequences for Employees
Consequences of boreout for employees include dissatisfaction, fatigue as well as ennui and low self-esteem. The paradox of boreout is that despite hating the situation, employees feel unable to ask for more challenging tasks, to raise the situation with superiors or even look for a new job. The authors do, however, propose a solution: first, one must analyse one’s personal job situation, then look for a solution within the company and finally if that does not help, look for a new job. If all else fails, turning to friends, family, or other co-workers for support can be extremely beneficial until any of the previously listed options become viable.
Consequences for Businesses
Stock-Homburg empirically investigated the impact of the three boreout dimensions among service employees – showing that a crisis of meaning as well as a crisis of growth had a negative impact on the innovative work behaviour. Another study showed that boreout negatively affects customer orientation of service employees.
Prammer studied a variety of boreout effects on businesses:
Whereabouts of dissatisfied employees, who do not work because they have internally terminated, cost the company money.
If employees actively quit internally, they can damage the operation by demonstrating their ability to mentally restore the employment contract.
The qualification of the employee is not recognised (the company can not use its potential).
The qualified employee changes jobs (and takes their experience), which can endanger entire business locations.
As long as a recession continues, the affected employee remains in the company and leaves the company at the appropriate opportunity. In-house, a problem of distribution of work orders arises.
Tabooing causes real problems to go undetected.
Whole generations of employees are lost (because they have no opportunity to fully realise their potential).
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Dissociative disorders (DD) are conditions that involve disruptions or breakdowns of memory, awareness, identity, or perception.
People with dissociative disorders use dissociation as a defence mechanism, pathologically and involuntarily. The individual experiences these dissociations to protect themselves. Some dissociative disorders are triggered by psychological trauma, but depersonalisation–derealisation disorder may be preceded only by stress, psychoactive substances, or no identifiable trigger at all.
The dissociative disorders listed in the American Psychiatric Association’s DSM-5 are as follows:
Dissociative identity disorder (formerly multiple personality disorder): the alternation of two or more distinct personality states with impaired recall among personality states. In extreme cases, the host personality is unaware of the other, alternating personalities; however, the alternate personalities can be aware of all the existing personalities.
Dissociative amnesia (formerly psychogenic amnesia): the temporary loss of recall memory, specifically episodic memory, due to a traumatic or stressful event. It is considered the most common dissociative disorder amongst those documented. This disorder can occur abruptly or gradually and may last minutes to years depending on the severity of the trauma and the patient. Dissociative fugue was previously a separate category but is now treated as a specifier for dissociative amnesia.
Depersonalisation-derealisation disorder: periods of detachment from self or surrounding which may be experienced as “unreal” (lacking in control of or “outside” self) while retaining awareness that this is only a feeling and not a reality.
The old category of dissociative disorder not otherwise specified is now split into two: other specified dissociative disorder, and unspecified dissociative disorder. These categories are used for forms of pathological dissociation that do not fully meet the criteria of the other specified dissociative disorders; or if the correct category has not been determined; or the disorder is transient.
Dissociative identity disorder is caused by ongoing childhood trauma that occurs before the ages of six to nine. People with dissociative identity disorder usually have close relatives who have also had similar experiences.
Long-term psychotherapy to improve the patient’s quality of life.
A way to cope with trauma.
Psychotherapy (e.g. talk therapy) counselling or psychosocial therapy which involves talking about your disorder and related issues with a mental health provider. Psychotherapy often involves hypnosis (help you remember and work through the trauma); creative art therapy (using creative process to help a person who cannot express his or her thoughts); cognitive therapy (talk therapy to identify unhealthy and negative beliefs/behaviours); and medications (antidepressants, anti-anxiety medications, or sedatives). These medications help control the symptoms associated with the dissociative disorders, but there are no medications yet that specifically treat dissociative disorders. However, the medication pentothal can sometimes help to restore the memories. The length of an event of dissociative amnesia may be a few minutes or several years. If an episode is associated with a traumatic event, the amnesia may clear up when the person is removed from the traumatic situation. Dissociative fugue was a separate category but is now listed as a specifier for dissociative amnesia.
Dissociative disorders usually develop as a way to cope with trauma. The disorders most often form in children subjected to chronic physical, sexual or emotional abuse or, less frequently, a home environment that is otherwise frightening or highly unpredictable; however, this disorder can also acutely form due to severe traumas such as war or the death of a loved one.
Same treatment as dissociative amnesia. An episode of depersonalisation–derealisation disorder can be as brief as a few seconds or continue for several years.
Dissociative disorders, especially dissociative identity disorder (DID), while being the result of extraordinary abuse and trauma in childhood, it should not be attributed exotic status. DID would be better examined through a more holistic lens, taking into considering the social, cognitive, and neural components, and how they interact with one another.
There are no medications to treat dissociative disorders, however, drugs to treat anxiety and depression that may accompany the disorders can be given.
Diagnosis and Prevalence
The lifetime prevalence of dissociative disorders varies from 10% in the general population to 46% in psychiatric inpatients. Diagnosis can be made with the help of structured clinical interviews such as the Dissociative Disorders Interview Schedule (DDIS) and the Structured Clinical Interview for DSM-IV Dissociative Disorders (SCID-D-R), and behavioural observation of dissociative signs during the interview. Additional information can be helpful in diagnosis, including the Dissociative Experiences Scale or other questionnaires, performance-based measures, records from doctors or academic records, and information from partners, parents, or friends. A dissociative disorder cannot be ruled out in a single session and it is common for patients diagnosed with a dissociative disorder to not have a previous dissociative disorder diagnosis due to a lack of clinician training. Some diagnostic tests have also been adapted or developed for use with children and adolescents such as the Adolescent Dissociative Experiences Scale, Children’s Version of the Response Evaluation Measure (REM-Y-71), Child Interview for Subjective Dissociative Experiences, Child Dissociative Checklist (CDC), Child Behaviour Checklist (CBCL) Dissociation Subscale, and the Trauma Symptom Checklist for Children Dissociation Subscale.
Dissociative disorders have been found to be quite prevalent in outpatient populations, as well as within low-income communities. One study found that in a population of poor inner-city outpatients, there was a 29% prevalence of dissociative disorders.
There are problems with classification, diagnosis and therapeutic strategies of dissociative and conversion disorders which can be understood by the historic context of hysteria. Even current systems used to diagnose DD such as the DSM-IV and ICD-10 differ in the way the classification is determined. In most cases mental health professionals are still hesitant to diagnose patients with Dissociative Disorder, because before they are considered to be diagnosed with Dissociative Disorder these patients have more than likely been diagnosed with major depressive disorder, anxiety disorder, and most often post-traumatic stress disorder (PTSD). It has been found from interviews with those who may be afflicted with dissociative disorders may be more effective at getting an accurate diagnosis than self-scoring assessments and scales.
The prevalence of dissociative disorders is not completely understood due to the many difficulties in diagnosing dissociative disorders. Many of these difficulties stem from a misunderstanding of dissociative disorders, from an unfamiliarity diagnosis or symptoms to disbelief in some dissociative disorders entirely. Due to this it has been found that only 28% to 48% of people diagnosed with a dissociative disorder receive treatment for their mental health. Patients who are misdiagnosed are often those more likely to be hospitalised repeatedly, and lack of treatment can result in intensive outpatient treatment and higher rates of disability.
An important concern in the diagnosis of dissociative disorders in forensic interviews is the possibility that the patient may be feigning symptoms in order to escape negative consequences. Young criminal offenders report much higher levels of dissociative disorders, such as amnesia. In one study it was found that 1% of young offenders reported complete amnesia for a violent crime, while 19% claimed partial amnesia. There have also been cases in which people with dissociative identity disorder provide conflicting testimonies in court, depending on the personality that is present. The world-wide prevalence of dissociative disorders is not well understood due to different cultural beliefs surrounding human emotions and the human brain
Children and Adolescents
Dissociative disorders (DD) are widely believed to have roots in adverse childhood experiences including abuse and loss, but the symptoms often go unrecognised or are misdiagnosed in children and adolescents. However, a recent western Chinese study showed an increase in awareness of dissociative disorders present in children These studies show that DD’s have an intricate relationship with the patient’s mental, physical and socio-cultural environments. This study suggested that dissociative disorders are more common in Western, or developing countries, however, some cases have been seen in both clinical and non-clinical Chinese populations. There are several reasons why recognising symptoms of dissociation in children is challenging: it may be difficult for children to describe their internal experiences; caregivers may miss signals or attempt to conceal their own abusive or neglectful behaviours; symptoms can be subtle or fleeting; disturbances of memory, mood, or concentration associated with dissociation may be misinterpreted as symptoms of other disorders.
Another resource, Beacon House, informs us of dissociative disorder in children, suggesting that it is a survival mechanism that often goes unnoticed in children that have been traumatised. Dr. Shoshanah Lyons suggests that traumatised children often continue to dissociate even though they might not be in any danger, and that they are often unaware that they are dissociating. In addition to developing diagnostic tests for children and adolescents (see above), a number of approaches have been developed to improve recognition and understanding of dissociation in children. Recent research has focused on clarifying the neurological basis of symptoms associated with dissociation by studying neurochemical, functional and structural brain abnormalities that can result from childhood trauma. Others in the field have argued that recognising disorganised attachment (DA) in children can help alert clinicians to the possibility of dissociative disorders. In their 2008 article, Rebecca Seligman and Laurence Kirmayer suggest the existence of evidence of linkages between trauma experienced in childhood and the capacity for dissociation or depersonalisation. They also suggest that individuals who are able to utilise dissociative techniques are able to keep this as an extended strategy to cope with stressful situations.
Clinicians and researchers stress the importance of using a developmental model to understand both symptoms and the future course of DDs. In other words, symptoms of dissociation may manifest differently at different stages of child and adolescent development and individuals may be more or less susceptible to developing dissociative symptoms at different ages. Further research into the manifestation of dissociative symptoms and vulnerability throughout development is needed. Related to this developmental approach, more research is required to establish whether a young patient’s recovery will remain stable over time.
Current Debates and the DSM-5
A number of controversies surround DD in adults as well as children. First, there is ongoing debate surrounding the aetiology of dissociative identity disorder (DID). The crux of this debate is if DID is the result of childhood trauma and disorganized attachment. A proposed view is that dissociation has a physiological basis, in that it involves automatically triggered mechanisms such as increased blood pressure and alertness, that would, as Lynn contends, imply its existence as a cross-species disorder. A second area of controversy surrounds the question of whether or not dissociation as a defence versus pathological dissociation are qualitatively or quantitatively different. Experiences and symptoms of dissociation can range from the more mundane to those associated with PTSD or acute stress disorder (ASD) to dissociative disorders. Mirroring this complexity, the DSM-5 workgroup considered grouping dissociative disorders with other trauma/stress disorders, but instead decided to put them in the following chapter to emphasize the close relationship. The DSM-5 also introduced a dissociative subtype of PTSD.
A 2012 review article supports the hypothesis that current or recent trauma may affect an individual’s assessment of the more distant past, changing the experience of the past and resulting in dissociative states. However, experimental research in cognitive science continues to challenge claims concerning the validity of the dissociation construct, which is still based on Janetian notions of structural dissociation. Even the claimed etiological link between trauma/abuse and dissociation has been questioned. Links observed between trauma/abuse and DD are largely only present from a Western cultural context. For non-Western cultures dissociation “may constitute a “normal” psychological capacity”. An alternative model proposes a perspective on dissociation based on a recently established link between a labile sleep-wake cycle and memory errors, cognitive failures, problems in attentional control, and difficulties in distinguishing fantasy from reality.
Debates around DD also stem from Western versus non-Western lenses of viewing the disorder, and associated views of causes of DD. DID was initially believed to be specific to the West, until cross-cultural studies indicated its occurrence worldwide. Conversely, anthropologists have largely done little work on DD in the West relating to its perceptions of possession syndromes that would be present in non-Western societies. While dissociation has been viewed and catalogued by anthropologists differently in the West and non-Western societies, there are aspects of each that show DD has universal characteristics. For example, while shamanic and rituals of non-Western societies may hold dissociative aspects, this is not exclusive as many Christian sects, such as “possession by the Holy Ghost” share similar qualities to those of non-Western trances.
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Delusional parasitosis (DP) is a mental disorder in which individuals have a persistent belief that they are infested with living or non-living pathogens such as parasites, insects, or bugs, when no such infestation is present.
They usually report tactile hallucinations known as formication, a sensation resembling insects crawling on or under the skin. Morgellons is considered to be a subtype of this condition, in which individuals have sores that they believe contain harmful fibres.
Delusional parasitosis is classified as a delusional disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM5). The cause is unknown, but is thought to be related to excess dopamine in the brain. Delusional parasitosis is diagnosed when the delusion is the only symptom of psychosis and the delusion – that cannot be better explained by another condition – has lasted a month or longer. Few individuals with the condition willingly accept treatment, because they do not recognise the illness as a delusion. Antipsychotic medications offer a cure, while cognitive behavioural therapy and antidepressants can be used to help alleviate symptoms.
The condition is rare, and is observed twice as often in women as men. The average age of people with the disorder is 57. An alternative name, Ekbom’s syndrome, refers to the neurologist Karl-Axel Ekbom, who published seminal accounts of the disease in 1937 and 1938.
Delusional infestation is classified as a delusional disorder of the somatic subtype in the Diagnostic and Statistical Manual of Mental Disorders (DSM5). The name delusional parasitosis has been the most common name since 2015, but the condition has also been called delusional infestation, delusory parasitosis, delusional ectoparasitosis, psychogenic parasitosis, Ekbom syndrome, dermatophobia, parasitophobia, formication and “cocaine bugs”.
Morgellons is a form of delusional parasitosis in which people have painful skin sensations that they believe contain fibres of various kinds; its presentation is very similar to other delusional infestations, but people with this self-diagnosed condition also believe that strings or fibres are present in their skin lesions.
Delusory cleptoparasitosis is a form of delusion of parasitosis where the person believes the infestation is in their dwelling, rather than on or in their body.
While a rare disorder, delusional parasitosis is the most common of the hypochondriacal psychoses, after other types of delusions such as body odour or halitosis. It may be undetected because those who have it do not see a psychiatrist because they do not recognise the condition as a delusion. A population-based study in Olmsted County, Minnesota found a prevalence of 27 per 100,000 person-years and an incidence of almost 2 cases per 100,000 person-years. The majority of dermatologists will see at least one person with DP during their career.
It is observed twice as often in women than men. The highest incidence occurs in people in their 60s, but there is also a higher occurrence in people in their 30s, associated with substance use. It occurs most often in “socially isolated” women with an average age of 57.
Since the early 2000s, a strong internet presence has led to increasing self-diagnosis of Morgellons.
Karl-Axel Ekbom, a Swedish neurologist, first described delusional parasitosis as “pre-senile delusion of infestation” in 1937. The common name has changed many times since then. Ekbom originally used the German word dermatozoenwahn, but other countries used the term Ekbom’s syndrome. That term fell out of favour because it also referred to restless legs syndrome. Other names that referenced “phobia” were rejected because anxiety disorder was not typical of the symptoms. The eponymous Ekbom’s disease was changed to “delusions of parasitosis” in 1946 in the English literature, when researchers J Wilson and H Miller described a series of cases, and to “delusional infestation” in 2009. The most common name since 2015 has been “delusional parasitosis”.
Ekbom’s original was translated to English in 2003; the authors hypothesized that James Harrington (1611-1677) may have been the “first recorded person to suffer from such delusions when he ‘began to imagine that his sweat turned to flies, and sometimes to bees and other insects’.”
Mary Leitao, the founder of the Morgellons Research Foundation, coined the name Morgellons in 2002, reviving it from a letter written by a physician in the mid-1600s. Leitao and others involved in her foundation (who self-identified as having Morgellons) successfully lobbied members of the US Congress and the US Centres for Disease Control and Prevention (CDC) to investigate the condition in 2006. The CDC published the results of its multi-year study in January 2012. The study found no underlying infectious condition and few disease organisms were present in people with Morgellons; the fibres found were likely cotton, and the condition was “similar to more commonly recognized conditions such as delusional infestation”.
An active online community has supported the notion that Morgellons is an infectious disease, and propose an association with Lyme disease. Publications “largely from a single group of investigators” describe findings of spirochetes, keratin and collagen in skin samples of a small number of individuals; these findings are contradicted by the much larger studies conducted by the CDC.
Signs and Symptoms
People with delusional parasitosis believe that “parasites, worms, mites, bacteria, fungus” or some other living organism has infected them, and reasoning or logic will not dissuade them from this belief. Details vary among those who have the condition, though it typically manifests as a crawling and pin-pricking sensation that is most commonly described as involving perceived parasites crawling upon or burrowing into the skin, sometimes accompanied by an actual physical sensation (known as formication). Affected people may injure themselves in attempts to be rid of the “parasites”; resulting skin damage includes excoriation, bruising and cuts, as well as damage caused from using chemical substances and obsessive cleansing routines.
A “preceding event such as a bug bite, travel, sharing clothes, or contact with an infected person” is often identified by individuals with DP; such events may lead the individual to misattribute symptoms because of more awareness of symptoms they were previously able to ignore. Nearly any marking upon the skin, or small object or particle found on the person or their clothing, can be interpreted as evidence for the parasitic infestation, and individuals with the condition commonly compulsively gather such “evidence” to present to medical professionals. This presentation is known as the “matchbox sign”, “Ziploc bag sign” or “specimen sign”, because the “evidence” is frequently presented in a small container, such as a matchbox. The matchbox sign is present in five to eight out of every ten people with DP. Related is a “digital specimen sign”, in which individuals bring collections of photographs to document their condition.
Similar delusions may be present in close relatives – a shared condition known as a folie à deux – that occurs in 5 to 15% of cases and is considered a shared psychotic disorder. Because the internet and the media contribute to furthering shared delusions, DP has also been called folie à Internet; when affected people are separated, their symptoms typically subside, but most still require treatment.
Approximately eight out of ten individuals with DP have co-occurring conditions – mainly depression, followed by substance abuse and anxiety; their personal and professional lives are frequently disrupted as they are extremely distressed about their symptoms.
A 2011 Mayo Clinic study of 108 patients failed to find evidence of skin infestation in skin biopsies and patient-provided specimens; the study concluded that the feeling of skin infestation was DP.
The cause of delusional parasitosis is unknown. It may be related to excess dopamine in the brain’s striatum, resulting from diminished dopamine transporter (DAT) function, which regulates dopamine reuptake in the brain. Evidence supporting the dopamine theory is that medications that inhibit dopamine reuptake (for example cocaine and amphetamines) are known to induce symptoms such as formication. Other conditions that also demonstrate reduced DAT functioning are known to cause secondary DP; these conditions include “schizophrenia, depression, traumatic brain injury, alcoholism, Parkinson’s and Huntington’s diseases, human immunodeficiency virus infection, and iron deficiency”. Further evidence is that antipsychotics improve DP symptoms, which may be because they affect dopamine transmission.
Delusional parasitosis is diagnosed when the delusion is the only symptom of psychosis, the delusion has lasted a month or longer, behaviour is otherwise not markedly odd or impaired, mood disorders – if present at any time – have been comparatively brief, and the delusion cannot be better explained by another medical condition, mental disorder, or the effects of a substance. For diagnosis, the individual must attribute abnormal skin sensations to the belief that they have an infestation, and be convinced that they have an infestation even when evidence shows they do not.
The condition is recognised in two forms:
Primary delusional parasitosis: The delusions are the only manifestation of a psychiatric disorder.
Secondary delusional parasitosis: This occurs when another psychiatric condition, medical illness or substance (medical or recreational) use causes the symptoms; in these cases, the delusion is a symptom of another condition rather than the disorder itself.
Secondary forms of DP can be functional (due to mainly psychiatric disorders) or organic (due to other medical illness or organic disease.
The secondary organic form may be related to vitamin B12 deficiency, hypothyroidism, anaemia, hepatitis, diabetes, HIV/AIDS, syphilis, or abuse of cocaine.
Examination to rule out other causes is key to diagnosis. Parasitic infestations are ruled out via skin examination and laboratory analyses. Bacterial infections may be present as a result of the individual constantly manipulating their skin. Other conditions that can cause itching skin are also ruled out; this includes a review of medications that may lead to similar symptoms. Testing to rule out other conditions helps build a trusting relationship with the physician; this can include laboratory analysis such as a complete blood count, comprehensive metabolic panel, erythrocyte sedimentation rate, C-reactive protein, urinalysis for toxicology and thyroid-stimulating hormone, in addition to skin biopsies and dermatological tests to detect or rule out parasitic infestations. Depending on symptoms, tests may be done for “human immunodeficiency virus, syphilis, viral hepatitis, B12 or folate deficiency,” and allergies.
Delusional parasitosis must be distinguished from scabies, mites, and other psychiatric conditions that may occur along with the delusion; these include schizophrenia, dementia, anxiety disorders, obsessive-compulsive disorder, and affective or substance-induced psychoses or other conditions such as anaemia that may cause psychosis.
Pruritus and other skin conditions are most commonly caused by mites, but may also be caused by “grocer’s itch” from agricultural products, pet-induced dermatitis, caterpillar/moth dermatitis, or exposure to fiberglass. Several drugs, legal or illegal, such as amphetamines, dopamine agonists, opioids, and cocaine may also cause the skin sensations reported. Diseases that must be ruled out in differential diagnosis include hypothyroidism, and kidney or liver disease. Many of these physiological factors, as well as environmental factors such as airborne irritants, are capable of inducing a “crawling” sensation in otherwise healthy individuals; some people become fixated on the sensation and its possible meaning, and this fixation may then develop into DP.
As of 2019, there have not been any studies that compare available treatments to placebo. The only treatment that provides a cure, and the most effective treatment, is low doses of antipsychotic medication. Cognitive behavioural therapy (CBT) can also be useful. Risperidone is the treatment of choice. For many years, the treatment of choice was pimozide, but it has a higher side effect profile than the newer antipsychotics. Aripiprazole and ziprasidone are effective but have not been well studied for delusional parasitosis. Olanzapine is also effective. All are used at the lowest possible dosage, and increased gradually until symptoms remit.
People with the condition often reject the professional medical diagnosis of delusional parasitosis, and few willingly undergo treatment, despite demonstrable efficacy, making the condition difficult to manage. Reassuring the individual with DP that there is no evidence of infestation is usually ineffective, as the patient may reject that. Because individuals with DP typically see many physicians with different specialties, and feel a sense of isolation and depression, gaining the patient’s trust, and collaborating with other physicians, are key parts of the treatment approach. Dermatologists may have more success introducing the use of medication as a way to alleviate the distress of itching. Directly confronting individuals about delusions is unhelpful because by definition, the delusions are not likely to change; confrontation of beliefs via CBT is accomplished in those who are open to psychotherapy. A five-phase approach to treatment is outlined by Heller et al. (2013) that seeks to establish rapport and trust between physician and patient.
The average duration of the condition is about three years. The condition leads to social isolation and affects employment. Cure may be achieved with antipsychotics or by treating underlying psychiatric conditions.
Society and Culture
Jay Traver (1894-1974), a University of Massachusetts entomologist, was known for “one of the most remarkable mistakes ever published in a scientific entomological journal”, after publishing a 1951 account of what she called a mite infestation which was later shown to be incorrect, and that has been described by others as a classic case of delusional parasitosis as evidenced by her own detailed description. Matan Shelomi argues that the historical paper should be retracted because it has misled people about their delusion. He says the paper has done “permanent and lasting damage” to people with delusional parasitosis, “who widely circulate and cite articles such as Traver’s and other pseudoscientific or false reports” via the internet, making treatment and cure more difficult.
Shelomi published another study in 2013 of what he called scientific misconduct when a 2004 article in the Journal of the New York Entomological Society included what he says is photo manipulation of a matchbox specimen to support the claim that individuals with DP are infested with collembola.
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Paraphrenia is a mental disorder characterised by an organised system of paranoid delusions with or without hallucinations (the positive symptoms of schizophrenia) and without deterioration of intellect or personality (its negative symptom).
This disorder is also distinguished from schizophrenia by a lower hereditary occurrence, less premorbid maladjustment, and a slower rate of progression. Onset of symptoms generally occurs later in life, near the age of 60. The prevalence of the disorder among the elderly is between 0.1% and 4%.
In the Russian psychiatric manuals, paraphrenia (or paraphrenic syndrome) is the last stage of development of paranoid schizophrenia. “Systematised paraphrenia” (with systematised delusions i. e. delusions with complex logical structure) and “expansive-paranoid paraphrenia” (with expansive/grandiose delusions and persecutory delusions) are the variants of paranoid schizophrenia (F20.0). Sometimes systematised paraphrenia can be seen with delusional disorder (F22.0). The word is from Ancient Greek: παρά – beside, near + φρήν – intellect, mind.
The term paraphrenia was originally popularised by Karl Ludwig Kahlbaum in 1863 to describe the tendency of certain psychiatric disorders to occur during certain transitional periods in life (describing paraphrenia hebetica as the insanity of the adolescence and paraphrenia senilis as the insanity of the elders.
The term was also used by Sigmund Freud for a short time starting in 1911 as an alternative to the terms schizophrenia and dementia praecox, which in his estimation did not correctly identify the underlying condition, and by Emil Kraepelin in 1912/1913, who changed its meaning to describe paraphrenia as it is understood today, as a small group of individuals that have many of the symptoms of schizophrenia with a lack of deterioration and thought disorder. Kraepelin’s study was discredited by Wilhelm Mayer in 1921 when he conducted a follow-up study using Kraepelin’s data. His study suggested that there was little to no discrimination between schizophrenia and paraphrenia; given enough time, patients presenting with paraphrenia will merge into the schizophrenic pool. However, Meyer’s data are open to various interpretations. In 1952, Roth and Morrissey conducted a large study in which they surveyed the mental hospital admissions of older patients. They characterised patients as having:
“paraphrenic delusions which… occurred in each case in the setting of a well-preserved intellect and personality, were often ‘primary’ in character, and were usually associated with the passivity failings or other volitional disturbances and hallucinations in clear consciousness pathognomonic of schizophrenia”.
In recent medicine, the term paraphrenia has been replaced by the diagnosis of “very late-onset schizophrenia-like psychosis” and has also been called “atypical psychoses, delusional disorder, psychoses not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults” by psychotherapists. Current studies, however, recognize the condition as “a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients.”
Signs and Symptoms
The main symptoms of paraphrenia are paranoid delusions and hallucinations. The delusions often involve the individual being the subject of persecution, although they can also be erotic, hypochondriacal, or grandiose in nature. The majority of hallucinations associated with paraphrenia are auditory, with 75% of patients reporting such an experience; however, visual, tactile, and olfactory hallucinations have also been reported. The paranoia and hallucinations can combine in the form of “threatening or accusatory voices coming from neighbouring houses [and] are frequently reported by the patients as disturbing and undeserved”. Patients also present with a lack of symptoms commonly found in other mental disorders similar to paraphrenia. There is no significant deterioration of intellect, personality, or habits and patients often remain clean and mostly self-sufficient. Patients also remain oriented well in time and space.
Paraphrenia is different from schizophrenia because, while both disorders result in delusions and hallucinations, individuals with schizophrenia exhibit changes and deterioration of personality whereas individuals with paraphrenia maintain a well-preserved personality and affective response.
Paraphrenia is often associated with a physical change in the brain, such as a tumour, stroke, ventricular enlargement, or neurodegenerative process. Research that reviewed the relationship between organic brain lesions and the development of delusions suggested that “brain lesions which lead to subcortical dysfunction could produce delusions when elaborated by an intact cortex”.
Many patients who present with paraphrenia have significant auditory or visual loss, are socially isolated with a lack of social contact, do not have a permanent home, are unmarried and without children, and have maladaptive personality traits. While these factors do not cause paraphrenia, they do make individuals more likely to develop the disorder later in life.
While the diagnosis of paraphrenia is absent from recent revisions of the DSM and the ICD, many studies have recognised the condition as “a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients.” As such, paraphrenia is seen as being distinct from both schizophrenia and progressive dementia in old age. Ravindran (1999) developed a list of criteria for the diagnosis of paraphrenia, which agrees with much of the research done up to the time it was published.
A delusional disorder of at least six months duration characterized by the following:
Preoccupation with one or more semi-systematised delusions, often accompanied by auditory hallucinations.
Affect notably well-preserved and appropriate. Ability to maintain rapport with others.
Flat or grossly inappropriate affect.
Grossly disorganised behaviour at times other than during the acute episode.
Disturbance of behaviour understandable in relation to the content of the delusions and hallucinations.
Only partly meets criterion A for schizophrenia. No significant organic brain disorder.
Research suggests that paraphrenics respond well to antipsychotic drug therapy if doctors can successfully achieve sufficient compliance. Herbert found that Stelazine combined with Disipal was an effective treatment. It promoted the discharging of patients and kept discharged patients from being readmitted later. While behaviour therapy may help patients reduce their preoccupation with delusions, psychotherapy is not currently of primary value.
Individuals who develop paraphrenia have a life expectancy similar to the normal population. Recovery from the psychotic symptoms seems to be rare, and in most cases paraphrenia results in in-patient status for the remainder of the life of the patient. Patients experience a slow deterioration of cognitive functions and the disorder can lead to dementia in some cases, but this development is no greater than the normal population.
Studies suggest that the prevalence of paraphrenia in the elderly population is around 2-4%.
While paraphrenia can occur in both men and women, it is more common in women, even after the difference has been adjusted for life expectancies. The ratio of women with paraphrenia to men with paraphrenia is anywhere from 3:1 to 45:2.
It is seen mainly in patients over the age of 60, but has been known to occur in patients in their 40s and 50s.
Personality Type and Living Situation
It is suggested that individuals who develop paraphrenia later in life have premorbid personalities, and can be described as “quarrelsome, religious, suspicious or sensitive, unsociable and cold-hearted.” Many patients were also described as being solitary, eccentric, isolated and difficult individuals; these characteristics were also long-standing rather than introduced by the disorder. Most of the traits recognised prior to the onset of paraphrenia in individuals can be grouped as either paranoid or schizoid. Patients presenting with paraphrenia were most often found to be living by themselves (either single, widowed, or divorced). There have also been reports of low marriage rate among paraphrenics and these individuals also have few or no children (possibly because of this premorbid personality).
The development of paranoia and hallucinations in old age have been related to both auditory and visual impairment, and individuals with paraphrenia often present with one or both of these impairments. Hearing loss in paraphrenics is associated with early age of onset, long duration, and profound auditory loss.
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Folie à deux (‘folly of two’, or ‘madness [shared] by two’), also known as shared psychosis or shared delusional disorder (SDD), is a psychiatric syndrome in which symptoms of a delusional belief, and sometimes hallucinations, are transmitted from one individual to another.
The same syndrome shared by more than two people may be called folie à… trois (‘three’) or quatre (‘four’); and further, folie en famille (‘family madness’) or even folie à plusieurs (‘madness of several’).
The disorder was first conceptualised in 19th-century French psychiatry by Charles Lasègue and Jules Falret and is also known as Lasègue-Falret syndrome.
Recent psychiatric classifications refer to the syndrome as shared psychotic disorder (DSM-4 – 297.3) and induced delusional disorder (ICD-10 – F24), although the research literature largely uses the original name.
This disorder is not in the current DSM (DSM-5), which considers the criteria to be insufficient or inadequate. DSM-5 does not consider Shared Psychotic Disorder (Folie à Deux) as a separate entity, but rather, the physician should classify it as “Delusional Disorder” or in the “Other Specified Schizophrenia Spectrum and Other Psychotic Disorder”.
Signs and Symptoms
This syndrome is most commonly diagnosed when the two or more individuals of concern live in proximity, may be socially or physically isolated, and have little interaction with other people.
Various sub-classifications of folie à deux have been proposed to describe how the delusional belief comes to be held by more than one person:
Where a dominant person (known as the ‘primary’, ‘inducer’ or ‘principal’) initially forms a delusional belief during a psychotic episode and imposes it on another person or persons (the ‘secondary’, ‘acceptor’, or ‘associate’), with the assumption that the secondary person might not have become deluded if left to his or her own devices.
If the parties are admitted to hospital separately, then the delusions in the person with the induced beliefs usually resolve without the need of medication.
Either the situation where two people considered to suffer independently from psychosis influence the content of each other’s delusions so they become identical or strikingly similar, or one in which two people “morbidly predisposed” to delusional psychosis mutually trigger symptoms in each other.
Folie à deux and its more populous derivatives are in many ways a psychiatric curiosity. The current Diagnostic and Statistical Manual of Mental Disorders states that a person cannot be diagnosed as being delusional if the belief in question is one “ordinarily accepted by other members of the person’s culture or subculture.” It is not clear at what point a belief considered to be delusional escapes from the folie à… diagnostic category and becomes legitimate because of the number of people holding it. When a large number of people may come to believe obviously false and potentially distressing things based purely on hearsay, these beliefs are not considered to be clinical delusions by the psychiatric profession, and are instead labelled as mass hysteria.
As with most psychological disorders, the extent and type of delusion varies, but the non-dominant person’s delusional symptoms usually resemble those of the inducer. Prior to therapeutic interventions, the inducer typically does not realise that they are causing harm, but instead believe they are helping the second person to become aware of vital or otherwise notable information.
Types of Delusion
Psychology Today magazine defines delusions as “fixed beliefs that do not change, even when a person is presented with conflicting evidence.” Types of delusion include:
Those which are clearly implausible and not understood by peers within the same culture, even those with psychological disorders; for example, if one thought that all of their organs had been taken out and replaced by someone else’s while they were asleep without leaving any scar and without their waking up. It would be impossible to survive such a procedure, and even surgery involving transplantation of multiple organs would leave the person with severe pain, visible scars, etc.
Common among those with personality disorders and are understood by people within the same culture. For example, unsubstantiated or unverifiable claims of being followed by the FBI in unmarked cars and watched via security cameras would be classified as a non-bizarre delusion; while it would be unlikely for the average person to experience such a predicament, it is possible, and therefore understood by those around them.
These correspond to a person’s emotions within a given timeframe, especially during an episode of mania or depression. For example, someone with this type of delusion may believe with certainty that they will win $1 million at the casino on a specific night, despite lacking any way to see the future or influence the probability of such an event. Similarly, someone in a depressive state may feel certain that their mother will get hit by lightning the next day, again in spite of having no means of predicting or controlling future events.
These are unaffected by mood, and can be bizarre or non-bizarre; the formal definition provided by Mental Health Daily is “a false belief that isn’t directly related to the person’s emotional state.” An example would be a person who is convinced that somebody has switched bodies with their neighbour, the belief persisting irrespective of changes in emotional status.
As with many psychiatric disorders, shared delusional disorder can negatively impact the psychological and social aspects of a person’s wellbeing. Unresolved stress resulting from a delusional disorder will eventually contribute to or increase the risk of other negative health outcomes, such as cardiovascular disease, diabetes, obesity, immunological problems, and others. These health risks increase with the severity of the disease, especially if an affected person does not receive or comply with adequate treatment.
Persons with a delusional disorder have a significantly high risk of developing psychiatric comorbidities such as depression and anxiety. This may be attributable to a genetic pattern shared by 55% of SDD patients.
Shared delusional disorder can have a profoundly negative impact on a person’s quality of life. Persons diagnosed with a mental health disorder commonly experience social isolation, which is detrimental to psychological health. This is especially problematic with SDD, as social isolation contributes to the onset of the disorder; in particular, relapse is likely if returning to an isolated living situation, in which shared delusions can be reinstated.
While the exact causes of SDD are unknown, the main two contributors are stress and social isolation.
People who are socially isolated together tend to become dependent on those they are with, leading to an inducers influence on those around them. Additionally, people developing shared delusional disorder do not have others reminding them that their delusions are either impossible or unlikely. As a result, treatment for shared delusional disorder includes those affected be removed from the inducer.
Stress is also a factor, as it is a common factor in mental illness developing or worsening. The majority of people that develop shared delusional disorder are genetically predisposed to mental illness, but this predisposition is not enough to develop a mental disorder. However, stress can increase the risk of this disorder. When stressed, an individual’s adrenal gland releases the “stress hormone” cortisol into the body, increasing the brain’s level of dopamine; this change can be linked to the development of a mental illness, such as a shared delusional disorder.
SDD is often difficult to diagnose. Usually, the person with the condition does not seek out treatment, as they do not realise that their delusion is abnormal, as it comes from someone in a dominant position who they trust. Furthermore, since their delusion comes on gradually and grows in strength over time, their doubt is slowly weakened during this time. SDD is diagnosed using the DSM-5, and according to this, the patient must meet three criteria:
They must have a delusion that develops in the context of a close relationship with an individual with an already established delusion.
The delusion must be very similar or even identical to the one already established one that the primary case has.
The delusion cannot be better explained by any other psychological disorder, mood disorder with psychological features, a direct result of physiological effects of substance abuse or any general medical condition.
Reports have stated that a phenomenon similar to folie à deux was induced by the military incapacitating agent BZ in the late 1960s.
SDD is most commonly found in women with slightly above-average IQs, who are isolated from their family, and who are in relationships with a dominant person who has delusions. The majority of secondary cases (people who develop the shared delusion) also meet the criteria for Dependent Personality Disorder, which is characterised by a pervasive fear that leads them to need constant reassurance, support, and guidance. Additionally, 55% of secondary cases had a relative with a psychological disorder that included delusions and, as a result, the secondary cases are usually susceptible to mental illness.
After a person has been diagnosed, the next step is to determine the proper course of treatment. The first step is to separate the formerly healthy person from the inducer, and see if the delusion goes away or lessens over time. If this is not enough to stop the delusions, there are two possible courses of action: Medication or therapy, which is then broken down into personal therapy and/or family therapy.
With treatment, the delusions, and therefore the disease, will eventually lessen so much so, that it will practically disappear in most cases. However, if left untreated, it can become chronic and lead to anxiety, depression, aggressive behaviour, and further social isolation. Unfortunately, there are not many statistics about the prognosis of shared delusional disorder, as it is a rare disease, and it is expected that the majority of cases go unreported; however, with treatment, the prognosis is very good.
If the separation alone is not working, antipsychotics are often prescribed for a short time to prevent the delusions. Antipsychotics are medications that reduce or relieve symptoms of psychosis such as delusions or hallucinations (seeing or hearing something that is not there). Other uses of antipsychotics include stabilising moods for people with mood swings and mood disorders (i.e. in bipolar patients), reducing anxiety in anxiety disorders, and lessening tics in people with Tourettes. Antipsychotics do not cure psychosis, but they do help reduce symptoms; when paired with therapy, the person with the condition has the best chance of recovering. While antipsychotics are powerful, and often effective, they do have side effects, such as inducing involuntary movements. They should only be taken if absolutely required, and under the supervision of a psychiatrist.
The two most common forms of therapy for people with shared delusional disorder are personal and family therapy.
Is one-on-one counselling that focuses on building a relationship between the counsellor and the patient, and aims to create a positive environment where the patient feels that they can speak freely and truthfully.
This is advantageous, as the counsellor can usually get more information out of the patient to get a better idea of how to help them.
Additionally, if the patient trusts what the counsellor says, disproving the delusion will be easier.
Is a technique in which the entire family comes into therapy together to work on their relationships, and to find ways to eliminate the delusion within the family dynamic.
For example, if someone’s sister is the inducer, the family will have to get involved to ensure the two stay apart, and to sort out how the family dynamic will work around that.
The more support a patient has, the more likely they are to recover, especially since SDD usually occurs due to social isolation.
In May 2008, in the case of twin sisters Ursula and Sabina Eriksson, Ursula ran into the path of an oncoming articulated lorry, sustaining severe injuries.
Sabina then immediately duplicated her twin’s actions by stepping into the path of an oncoming car; both sisters survived the incident with severe but non-life-threatening injuries.
It was later claimed that Sabina Eriksson was a ‘secondary’ sufferer of folie à deux, influenced by the presence or perceived presence of her twin sister, Ursula – the ‘primary’. Sabina later told an officer at the police station, “We say in Sweden that an accident rarely comes alone. Usually at least one more follows—maybe two.”
However, upon her release from hospital, Sabina behaved erratically before stabbing a man to death.
Another case involved a married couple by the name of Margaret and Michael, both aged 34 years, who were discovered to have folie à deux when they were both found to be sharing similar persecutory delusions.
They believed that certain persons were entering their house, spreading dust and fluff, and “wearing down their shoes.”
Both had, in addition, other symptoms supporting a diagnosis of emotional contagion, which could be made independently in either case.
Psychiatrist Reginald Medlicott published an article about the Parker-Hulme murder case, called “Paranoia of the Exalted Type in a Setting of Folie a Deux – A Study of Two Adolescent Homicides”, arguing that the intense relationship and shared fantasy world of the two teenaged friends reinforced and exacerbated the mental illness that led to the murder: “each acted on the other as a resonator, increasing the pitch of their narcissism.”
In 2016, a case involving a family of five from Melbourne, Australia made headlines when they abruptly fled their home and travelled more than 1,600 km (1,000 mi) across the state of Victoria, because some of the family had become convinced someone was out to kill and rob them.
No such evidence was found by the police, and the symptoms of those involved resolved on their own once the family returned to their home.
The book Bad Blood: Secrets and Lies in a Silicon Valley Startup suggests that this ailment plagued the founder of Theranos, Elizabeth Holmes, and her boyfriend and business partner, Ramesh Balwani.
It was suspected a family of eleven members from Burari, India had this condition.
On 30 June 2018, the family died by mass suicide due to the shared belief of one of its members.
Psychologists H. O’Connell and P.G. Doyle believe folie à plusieurs to have been at least a partial factor in the murder of Bridget Cleary.
In 1895, Michael Cleary convinced several friends and relatives that his wife, Bridget Cleary, was a changeling who had been replaced by a fairy.
They assisted him in physically abusing her to “cast the fairies” out, before he ultimately burned her to death shortly afterwards.
Christine and Léa Papin were two French sisters who, as live-in maids, were convicted of murdering their employer’s wife and daughter in Le Mans, France on 02 February 1933.
In Popular Culture
“Folie à Deux” is the title of the nineteenth episode in the fifth season of The X-Files (1998). The episode details a story of a man who believes his boss is an insect monster, a delusion that Fox Mulder begins to share after investigation.
Bug (2006) is a film that depicts a couple with a shared delusion that aphids are living under their skin.
In Season 2, Episode 3 of Criminal Minds, “The Perfect Storm” (2006), Dr. Reid mentions that the rapists had this condition.
In 2008, American rock band Fall Out Boy released their fourth album, Folie à Deux.
The independent film Apart (2011) depicts two lovers affected and diagnosed with induced delusional disorder, trying to uncover a mysterious and tragic past they share. In a 2011 interview, director Aaron Rottinghaus stated the film was based on research from actual case studies.
In 2011, in CSI: Miami (Season 9, Episode 15 “Blood Lust”), it was revealed the killer couple had this condition.
The 2011 horror film Intruders contains characters who suffer from folie à deux.
In 2012, in Criminal Minds (Season 7, Episode 19 “Heathridge Manor”), it was revealed the killer family had this condition.
2013’s horror game “Slender: The Arrival” centres around the shared hallucination by the main character Lauren, and her friend Kate, of the monster known as “Slender Man”.
In 2017, in Chance (Season 2, Episode 9 “A Madness of Two”), it was revealed the villains are having this condition.
The Vanished (2020) shows a couple who lost a child continuing to hold on to the delusional thought of their existence.
Nine Perfect Strangers (miniseries) shows a couple who lost one of their two children. The couple and the surviving child have shared hallucinations of the dead child.
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Disruptive mood dysregulation disorder (DMDD) is a mental disorder in children and adolescents characterised by a persistently irritable or angry mood and frequent temper outbursts that are disproportionate to the situation and significantly more severe than the typical reaction of same-aged peers.
DMDD was added to the DSM-5 as a type of depressive disorder diagnosis for youths. The symptoms of DMDD resemble those of attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), anxiety disorders, and childhood bipolar disorder.
DMDD first appeared as a disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) in 2013 and is classified as a mood disorder. Treatments include medication to manage mood symptoms as well as individual and family therapy to address emotion-regulation skills. Children with DMDD are at risk for developing depression and anxiety later in life.
Beginning in the 1990s, some clinicians began observing children with hyperactivity, irritability, and severe temper outbursts. These symptoms greatly interfered with their lives at home, school, and with friends. Because other diagnoses, like ADHD and ODD, did not capture the severity of children’s irritability and anger, many of these children were diagnosed with bipolar disorder. Longitudinal studies showed that children with chronic irritability and temper outbursts often developed later problems with anxiety and depression, and rarely developed bipolar disorder in adolescence or adulthood. Consequently, the developers of DSM-5 created a new diagnostic label, DMDD, to describe children with persistent irritability and angry outbursts. In 2013, the American Psychiatric Association (APA) added DMDD to the DSM-5 and classified it as a depressive disorder.
Signs and Symptoms
Children with DMDD show severe and recurrent temper outbursts three or more times per week. These outbursts can be verbal or behavioural. Verbal outbursts often are described by observers as “rages”, “fits”, or “tantrums”. Children may scream, yell, and cry for excessively long periods of time, sometimes with little provocation. Physical outbursts may be directed toward people or property. Children may throw objects; hit, slap, or bite others; destroy toys or furniture; or otherwise act in a harmful or destructive manner.
Children with DMDD also display persistently irritable or angry mood that is observable by others. Parents, teachers, and classmates describe these children as habitually angry, touchy, grouchy, or easily “set off”. Unlike the irritability that can be a symptom of other childhood disorders, such as ODD, anxiety disorders, and major depressive disorder (MDD), the irritability displayed by children with DMDD is not episodic or situation-dependent. In DMDD, the irritability or anger is severe and is shown most of the day, nearly every day in multiple settings, lasting for one or more years.
The DSM-5 includes several additional diagnostic criteria which describe the duration, setting, and onset of the disorder: the outbursts must be present for at least 12 months and occur in at least two settings (e.g. home and school), and it must be severe in at least one setting. Symptoms appear before the age of 10, and diagnosis must be made between ages 6 and 18.
The core features of DMDD – temper outbursts and chronic irritability – are sometimes seen in children and adolescents with other psychiatric conditions. Differentiating DMDD from these other conditions can be difficult. Three disorders that most closely resemble DMDD are ADHD, oppositional defiant disorder (ODD), and bipolar disorder in children.
ADHD is a neurodevelopmental disorder characterised by problems with inattention and/or hyperactivity-impulsivity.
ODD is a disruptive behaviour disorder characterised by oppositional, defiant, and sometimes hostile actions directed towards others.
One of the main differences between DMDD and bipolar disorder is that the irritability and anger outbursts associated with DMDD are not episodic; symptoms of DMDD are chronic and displayed constantly on an almost daily basis. On the other hand, bipolar disorder is characterised by distinct manic or hypomanic episodes usually lasting a few days, or a few weeks at most, that parents should be able to differentiate from their child’s typical mood and behaviour in between episodes. The DSM precludes a dual diagnosis of DMDD and bipolar disorder. Bipolar disorder alone should be used for youths who show classic symptoms of episodic mania or hypomania.
Prior to adolescence, DMDD is much more common than bipolar disorder. Most children with DMDD see a decrease in symptoms as they enter adulthood, whereas individuals with bipolar disorder typically display symptoms for the first time as teenagers and young adults. Children with DMDD are more at risk for developing MDD or generalised anxiety disorder when they are older rather than bipolar disorder.
Youth with DMDD have difficulty attending, processing, and responding to negative emotional stimuli and social experiences in their everyday lives. For example, some studies have shown youths with DMDD to have problems interpreting the social cues and emotional expressions of others. These youths may be especially bad at judging others’ negative emotional displays, such as feelings of sadness, fearfulness, and anger. Functional MRI studies suggest that under-activity of the amygdala, the brain area that plays a role in the interpretation and expression of emotions and novel stimuli, is associated with these deficits. Deficits in interpreting social cues may predispose children to instances of anger and aggression in social settings with little provocation. For examples, youths with DMDD may selectively attend to negative social cues (e.g. others scowling, teasing) and minimize all other information about the social events. They may also misinterpret the emotional displays of others, believing others’ benign actions to be hostile or threatening. Consequently, they may be more likely than their peers to act in impulsive and angry ways.
Children with DMDD may also have difficulty regulating negative emotions once they are elicited. To study these problems with emotion regulation, researchers asked children with DMDD to play computer games that are rigged so that children will lose. While playing these games, children with DMDD report more agitation and negative emotional arousal than their typically-developing peers. Furthermore, youths with DMDD showed markedly greater activity in the medial frontal gyrus and anterior cingulate cortex compared to other youths. These brain regions are important because they are involved in evaluating and processing negative emotions, monitoring one’s own emotional state, and selecting an effective response when upset, angry, or frustrated. Altogether, these findings suggest that youths with DMDD are more strongly influenced by negative events than other youths. They may become more upset and select less effective and socially acceptable ways to deal with negative emotions when they arise.
Evidence for treatment is weak, and treatment is determined based on the physician’s response to the symptoms that people with DMDD present. Because the mood stabilizing medication, lithium, is effective in treating adults with bipolar disorder, some physicians have used it to treat DMDD although it has not been shown to be better than placebo in alleviating the signs and symptoms of DMDD. DMDD is treated with a combination of medications that target the child’s symptom presentation. For youths with DMDD alone, antidepressant medication is sometimes used to treat underlying problems with irritability or sadness. For youths with unusually strong temper outbursts, an atypical antipsychotic medication, such as risperidone, may be warranted. Both medications, however, are associated with significant side effects in children. Finally, for children with both DMDD and ADHD, stimulant medication is sometimes used to reduce symptoms of impulsivity.
Several cognitive-behavioural interventions have been developed to help youths with chronic irritability and temper outbursts. Because many youths with DMDD show problems with ADHD and oppositional-defiant behaviour, experts initially tried to treat these children using contingency management. This type of intervention involves teaching parents to reinforce children’s appropriate behaviour and extinguish (usually through systematic ignoring or time out) inappropriate behaviour. Although contingency management can be helpful for ADHD and ODD symptoms, it does not seem to reduce the most salient features of DMDD, namely, irritability and anger.
There are not good estimates of the prevalence of DMDD, but primary studies have found a rate of 0.8 to 3.3%. Epidemiological studies show that approximately 3.2% of children in the community have chronic problems with irritability and temper, the essential features of DMDD. These problems are probably more common among clinic-referred youths. Parents report that approximately 30% of children hospitalised for psychiatric problems meet diagnostic criteria for DMDD; 15% meet criteria based on the observations of hospital staff.
Combat stress reaction (CSR) is a term used within the military to describe acute behavioural disorganisation as a direct result of the trauma of war.
Also known as “combat fatigue”, “battle fatigue”, or “battle neurosis”, it has some overlap with the diagnosis of acute stress reaction used in civilian psychiatry. It is historically linked to shell shock and can sometimes precede post-traumatic stress disorder (PTSD).
Combat stress reaction is an acute reaction that includes a range of behaviours resulting from the stress of battle that decrease the combatant’s fighting efficiency. The most common symptoms are fatigue, slower reaction times, indecision, disconnection from one’s surroundings, and the inability to prioritise. Combat stress reaction is generally short-term and should not be confused with acute stress disorder, PTSD, or other long-term disorders attributable to combat stress, although any of these may commence as a combat stress reaction. The US Army uses the term/acronym COSR (Combat Stress Reaction) in official medical reports. This term can be applied to any stress reaction in the military unit environment. Many reactions look like symptoms of mental illness (such as panic, extreme anxiety, depression, and hallucinations), but they are only transient reactions to the traumatic stress of combat and the cumulative stresses of military operations.
In World War I, shell shock was considered a psychiatric illness resulting from injury to the nerves during combat. The horrors of trench warfare meant that about 10% of the fighting soldiers were killed (compared to 4.5% during World War II) and the total proportion of troops who became casualties (killed or wounded) was about 57%. Whether a shell-shock sufferer was considered “wounded” or “sick” depended on the circumstances. When faced with the phenomenon of a minority of soldiers mentally breaking down, there was an expectation that the root of this problem lay in character of the individual soldier, not because of what they experienced on the front lines during the war. The large proportion of World War I veterans in the European population meant that the symptoms were common to the culture.
Combat stress reaction symptoms align with the symptoms also found in psychological trauma, which is closely related to PTSD. CSR differs from PTSD (among other things) in that a PTSD diagnosis requires a duration of symptoms over one month, which CSR does not.
The most common stress reactions include:
The slowing of reaction time.
Slowness of thought.
Difficulty prioritising tasks.
Difficulty initiating routine tasks.
Preoccupation with minor issues and familiar tasks.
Indecision and lack of concentration.
Loss of initiative with fatigue.
Autonomic Nervous System – Autonomic Arousal
Inability to relax.
Shaking and tremors.
Nausea and vomiting.
Loss of appetite.
Frequency of urination.
Heightened sense of threat.
Loss of adaptability.
Mistrust of others.
Extreme feeling of losing control.
Battle Casualty Rates
The ratio of stress casualties to battle casualties varies with the intensity of the fighting. With intense fighting, it can be as high as 1:1. In low-level conflicts, it can drop to 1:10 (or less). Modern warfare embodies the principles of continuous operations with an expectation of higher combat stress casualties.
The World War II European Army rate of stress casualties of 1 in 10 (101:1,000) troops per annum is skewed downward from both its norm and peak by data by low rates during the last years of the war.
The following PIE principles were in place for the “not yet diagnosed nervous” (NYDN) cases:
Proximity: Treat the casualties close to the front and within sound of the fighting.
Immediacy: Treat them without delay and not wait until the wounded were all dealt with.
Expectancy: Ensure that everyone had the expectation of their return to the front after a rest and replenishment.
United States medical officer Thomas W. Salmon is often quoted as the originator of these PIE principles. However, his real strength came from going to Europe and learning from the Allies and then instituting the lessons. By the end of the war, Salmon had set up a complete system of units and procedures that was then the “world’s best practice”. After the war, he maintained his efforts in educating society and the military. He was awarded the Distinguished Service Medal for his contributions.
Effectiveness of the PIE approach has not been confirmed by studies of CSR, and there is some evidence that it is not effective in preventing PTSD.
US services now use the more recently developed BICEPS principles:
Centrality or contact.
Between the Wars
The British government produced a Report of the War Office Committee of Inquiry 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 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.
World War II
At the outbreak of World War II, most in the United States military had forgotten the treatment lessons of World War I. Screening of applicants was initially rigorous, but experience eventually showed it to lack great predictive power.
The US entered the war in December 1941. Only in November 1943 was a psychiatrist added to the table of organisation of each division, and this policy was not implemented in the Mediterranean Theatre of Operations until March 1944. By 1943, the US Army was using the term “exhaustion” as the initial diagnosis of psychiatric cases, and the general principles of military psychiatry were being used. General Patton’s slapping incident was in part the spur to institute forward treatment for the Italian invasion of September 1943. The importance of unit cohesion and membership of a group as a protective factor emerged.
John Appel found that the average American infantryman in Italy was “worn out” in 200 to 240 days and concluded that the American soldier “fights for his buddies or because his self respect won’t let him quit”. After several months in combat, the soldier lacked reasons to continue to fight because he had proven his bravery in battle and was no longer with most of the fellow soldiers he trained with. Appel helped implement a 180-day limit for soldiers in active combat and suggested that the war be made more meaningful, emphasizing their enemies’ plans to conquer the United States, encouraging soldiers to fight to prevent what they had seen happen in other countries happen to their families. Other psychiatrists believed that letters from home discouraged soldiers by increasing nostalgia and needlessly mentioning problems soldiers could not solve. William Menninger said after the war, “It might have been wise to have had a nation-wide educational course in letter writing to soldiers”, and Edward Strecker criticised “moms” (as opposed to mothers) who, after failing to “wean” their sons, damaged morale through letters.
Airmen flew far more often in the Southwest Pacific than in Europe, and although rest time in Australia was scheduled, there was no fixed number of missions that would produce transfer out of combat, as was the case in Europe. Coupled with the monotonous, hot, sickly environment, the result was bad morale that jaded veterans quickly passed along to newcomers. After a few months, epidemics of combat fatigue would drastically reduce the efficiency of units. Flight surgeons reported that the men who had been at jungle airfields longest were in bad shape:
Many have chronic dysentery or other disease, and almost all show chronic fatigue states. . . .They appear listless, unkempt, careless, and apathetic with almost mask-like facial expression. Speech is slow, thought content is poor, they complain of chronic headaches, insomnia, memory defect, feel forgotten, worry about themselves, are afraid of new assignments, have no sense of responsibility, and are hopeless about the future.
Unlike the Americans, the British leaders firmly held the lessons of World War I. It was estimated that aerial bombardment would kill up to 35,000 a day, but the Blitz killed only 40,000 in total. The expected torrent of civilian mental breakdown did not occur. The Government turned to World War I doctors for advice on those who did have problems. The PIE principles were generally used. However, in the British Army, since most of the World War I doctors were too old for the job, young, analytically trained psychiatrists were employed. Army doctors “appeared to have no conception of breakdown in war and its treatment, though many of them had served in the 1914–1918 war.” The first Middle East Force psychiatric hospital was set up in 1942. With D-Day for the first month there was a policy of holding casualties for only 48 hours before they were sent back over the Channel. This went firmly against the expectancy principle of PIE.
Appel believed that British soldiers were able to continue to fight almost twice as long as their American counterparts because the British had better rotation schedules and because they, unlike the Americans, “fight for survival” – for the British soldiers, the threat from the Axis powers was much more real, given Britain’s proximity to mainland Europe, and the fact that Germany was concurrently conducting air raids and bombarding British industrial cities. Like the Americans, British doctors believed that letters from home often needlessly damaged soldiers’ morale.
The Canadian Army recognised combat stress reaction as “Battle Exhaustion” during the Second World War and classified it as a separate type of combat wound. Historian Terry Copp has written extensively on the subject. In Normandy, “The infantry units engaged in the battle also experienced a rapid rise in the number of battle exhaustion cases with several hundred men evacuated due to the stress of combat. Regimental Medical Officers were learning that neither elaborate selection methods nor extensive training could prevent a considerable number of combat soldiers from breaking down.”
In his history of the pre-Nazi Freikorps paramilitary organisations, Vanguard of Nazism, historian Robert G.L. Waite describes some of the emotional effects of World War I on German troops, and refers to a phrase he attributes to Göring: men who could not become “de-brutalized”.
In an interview, Dr Rudolf Brickenstein stated that:
… he believed that there were no important problems due to stress breakdown since it was prevented by the high quality of leadership. But, he added, that if a soldier did break down and could not continue fighting, it was a leadership problem, not one for medical personnel or psychiatrists. Breakdown (he said) usually took the form of unwillingness to fight or cowardice.
However, as World War II progressed there was a profound rise in stress casualties from 1% of hospitalizations in 1935 to 6% in 1942. Another German psychiatrist reported after the war that during the last two years, about a third of all hospitalisations at Ensen were due to war neurosis. It is probable that there was both less of a true problem and less perception of a problem.
The Finnish attitudes to “war neurosis” were especially tough. Psychiatrist Harry Federley, who was the head of the Military Medicine, considered shell shock as a sign of weak character and lack of moral fibre. His treatment for war neurosis was simple: the patients were to be bullied and harassed until they returned to front line service.
Earlier, during the Winter War, several Finnish machine gun operators on the Karelian Isthmus theatre became mentally unstable after repelling several unsuccessful Soviet human wave assaults on fortified Finnish positions.
Post-World War II Developments
Simplicity was added to the PIE principles by the Israelis: in their view, treatment should be brief, supportive, and could be provided by those without sophisticated training.
Peacekeeping provides its own stresses because its emphasis on rules of engagement contains the roles for which soldiers are trained. Causes include witnessing or experiencing the following:
Constant tension and threat of conflict.
Threat of land mines and booby traps.
Close contact with severely injured and dead people.
Deliberate maltreatment and atrocities, possibly involving civilians.
Cultural issues, e.g. male dominant attitudes towards women in different cultures.
Separation and home issues.
Risk of disease including HIV.
Threat of exposure to toxic agents.
Return to service.
Many of the symptoms initially experienced by CSR sufferers are effects of an extended activation of the human body’s fight-or-flight response. The fight-or-flight response involves a general sympathetic nervous system discharge in reaction to a perceived stressor and prepares the body to fight or run from the threat causing the stress. Catecholamine hormones, such as adrenaline or noradrenaline, facilitate immediate physical reactions associated with a preparation for violent muscular action. Although the flight-or-fight-response normally ends with the removal of the threat, the constant mortal danger in combat zones likewise constantly and acutely stresses soldiers.
General Adaptation Syndrome
The process whereby the human body responds to extended stress is known as general adaptation syndrome (GAS). After the initial fight-or-flight response, the body becomes more resistant to stress in an attempt to dampen the sympathetic nervous response and return to homeostasis. During this period of resistance, physical and mental symptoms of CSR may be drastically reduced as the body attempts to cope with the stress. Long combat involvement, however, may keep the body from homeostasis and thereby deplete its resources and render it unable to normally function, sending it into the third stage of GAS: exhaustion. Sympathetic nervous activation remains in the exhaustion phase and reactions to stress are markedly sensitised as fight-or-flight symptoms return. If the body remains in a state of stress, then such more severe symptoms of CSR as cardiovascular and digestive involvement may present themselves. Extended exhaustion can permanently damage the body.
The British Army treated Operational Stress Reaction according to the 7 R’s:
Recognition: Identify that the individual is suffering from an Operational Stress Reaction.
Respite: Provide a short period of relief from the front line.
Rest: Allow rest and recovery.
Recall: Give the individual the chance to recall and discuss the experiences that have led to the reaction.
Reassurance: Inform the sufferer that their reaction is normal and they will recover.
Rehabilitation: Improve the physical and mental health of the patient until they no longer show symptoms.
Return: Allow the soldier to return to their unit.
Modern front-line combat stress treatment techniques are designed to mimic the historically used PIE techniques with some modification. BICEPS is the current treatment route employed by the US military and stresses differential treatment by the severity of CSR symptoms present in the service member. BICEPS is employed as a means to treat CSR symptoms and return soldiers quickly to combat.
The following BICEPS program is taken from the USMC combat stress handbook:
Critical Event Debriefing should take 2 to 3 hours. Initial rest and replenishment at medical CSC (Combat Stress Control) facilities should last no more than 3 or 4 days. Those requiring further treatment are moved to the next level of care. Since many require no further treatment, military commanders expect their service members to return to duty rapidly.
CSC should be done as soon as possible when operations permit. Intervention is provided as soon as symptoms appear.
Service members requiring observation or care beyond the unit level are evacuated to facilities in close proximity to, but separate from the medical or surgical patients at the BAS, surgical support company in a central location (Marines) or forward support/division support or area support medical companies (Army) nearest the service members’ unit. It is best to send Service members who cannot continue their mission and require more extensive respite to a central facility other than a hospital, unless no other alternative is possible. The Service member must be encouraged to continue to think of himself as a war fighter, rather than a patient or a sick person. The chain of command remains directly involved in the Service member’s recovery and return to duty. The CSC team coordinates with the unit’s leaders to learn whether the over-stressed individual was a good performer prior to the combat stress reaction, or whether he was always a marginal or problem performer whom the team would rather see replaced than returned. Whenever possible, representatives of the unit, or messages from the unit, tell the casualty that he is needed and wanted back. The CSC team coordinates with the unit leaders, through unit medical personnel or chaplains, any special advice on how to assure quick reintegration when the Service member returns to his unit.
The individual is explicitly told that he is reacting normally to extreme stress and is expected to recover and return to full duty in a few hours or days. A military leader is extremely effective in this area of treatment. Of all the things said to a Service member suffering from combat stress, the words of his small-unit leader have the greatest impact due to the positive bonding process that occurs during combat. Simple statements from the small-unit leader to the Service member that he is reacting normally to combat stress and is expected back soon have positive impact. Small-unit leaders should tell Service members that their comrades need and expect them to return. When they do return, the unit treats them as every other Service member and expects them to perform well. Service members suffering and recovering from combat stress disorder are no more likely to become overloaded again than are those who have not yet been overloaded. In fact, they are less likely to become overloaded than inexperienced replacements.
In mobile war requiring rapid and frequent movement, treatment of many combat stress cases takes place at various battalion or regimental headquarters or logistical units, on light duty, rather than in medical units, whenever possible. This is a key factor and another area where the small-unit leader helps in the treatment. CSC and follow-up care for combat stress casualties are held as close as possible to and maintain close association with the member’s unit, and are an integral part of the entire healing process. A visit from a member of the individual’s unit during restoration is very effective in keeping a bond with the organization. A Service member suffering from combat stress reaction is having a crisis, and there are two basic elements to that crisis working in opposite directions. On the one hand, the Service member is driven by a strong desire to seek safety and to get out of an intolerable environment. On the other hand, the Service member does not want to let his comrades down. He wants to return to his unit. If a Service member starts to lose contact with his unit when he enters treatment, the impulse to get out of the war and return to safety takes over. He feels that he has failed his comrades and they have already rejected him as unworthy. The potential is for the Service member to become more and more emotionally invested in keeping his symptoms so he can stay in a safe environment. Much of this is done outside the Service member’s conscious awareness, but the result is the same. The more out of touch the Service member is with his unit, the less likely he will recover. He is more likely to develop a chronic psychiatric illness and get evacuated from the war. This is one of the essential principles of CSC.
Treatment is kept very simple. CSC is not therapy. Psychotherapy is not done. The goal is to rapidly restore the Service member’s coping skills so that he functions and returns to duty again. Sleep, food, water, hygiene, encouragement, work details, and confidence-restoring talk are often all that is needed to restore a Service member to full operational readiness. This can be done in units in reserve positions, logistical units or at medical companies. Every effort is made to reinforce Service members’ identity. They are required to wear their uniforms and to keep their helmets, equipment, chemical protective gear, and flak jackets with them. When possible, they are allowed to keep their weapons after the weapons have been cleared. They may serve on guard duty or as members of a standby quick reaction force.
Historically, screening programs that have attempted to preclude soldiers exhibiting personality traits thought to predispose them to CSR have been a total failure. Part of this failure stems from the inability to base CSR morbidity on one or two personality traits. Full psychological work-ups are expensive and inconclusive, while pen and paper tests are ineffective and easily faked. In addition, studies conducted following WWII screening programs showed that psychological disorders present during military training did not accurately predict stress disorders during combat.
While it is difficult to measure the effectiveness of such a subjective term, soldiers who reported in a WWII study that they had a “higher than average” sense of camaraderie and pride in their unit were more likely to report themselves ready for combat and less likely to fall victim to CSR or other stress disorders. Soldiers with a “lower than average” sense of cohesion with their unit were more susceptible to stress illness.
Stress exposure training or SET is a common component of most modern military training. There are three steps to an effective stress exposure programme.
Providing Knowledge of the Stress Environment
Soldiers with a knowledge of both the emotional and physical signs and symptoms of CSR are much less likely to have a critical event that reduces them below fighting capability. Instrumental information, such as breathing exercises that can reduce stress and suggestions not to look at the faces of enemy dead, is also effective at reducing the chance of a breakdown.
Cognitive control strategies can be taught to soldiers to help them recognise stressful and situationally detrimental thoughts and repress those thoughts in combat situations. Such skills have been shown to reduce anxiety and improve task performance.
Confidence Building through Application and Practice
Soldiers who feel confident in their own abilities and those of their squad are far less likely to suffer from combat stress reaction. Training in stressful conditions that mimic those of an actual combat situation builds confidence in the abilities of themselves and the squad. As this training can actually induce some of the stress symptoms it seeks to prevent, stress levels should be increased incrementally as to allow the soldiers time to adapt.
Figures from the 1982 Lebanon war showed that with proximal treatment, 90% of CSR casualties returned to their unit, usually within 72 hours. With rearward treatment, only 40% returned to their unit. It was also found that treatment efficacy went up with the application of a variety of front line treatment principles versus just one treatment. In Korea, similar statistics were seen, with 85% of US battle fatigue casualties returned to duty within three days and 10% returned to limited duties after several weeks.
Though these numbers seem to promote the claims that proximal PIE or BICEPS treatment is generally effective at reducing the effects of combat stress reaction, other data suggests that long term PTSD effects may result from the hasty return of affected individuals to combat. Both PIE and BICEPS are meant to return as many soldiers as possible to combat, and may actually have adverse effects on the long term health of service members who are rapidly returned to the front-line after combat stress control treatment. Although the PIE principles were used extensively in the Vietnam War, the post traumatic stress disorder lifetime rate for Vietnam veterans was 30% in a 1989 US study and 21% in a 1996 Australian study. In a study of Israeli Veterans of the 1973 Yom Kippur War, 37% of veterans diagnosed with CSR during combat were later diagnosed with PTSD, compared with 14% of control veterans.
There is significant controversy with the PIE and BICEPS principles. Throughout a number of wars, but notably during the Vietnam War, there has been a conflict among doctors about sending distressed soldiers back to combat. During the Vietnam War this reached a peak with much discussion about the ethics of this process. Proponents of the PIE and BICEPS principles argue that it leads to a reduction of long-term disability but opponents argue that combat stress reactions lead to long-term problems such as post-traumatic stress disorder.
The use of psychiatric drugs to treat victims of CSR has also attracted criticism, as some military psychiatrists have come to question the efficacy of such drugs on the long-term health of veterans. Concerns have been expressed as to the effect of pharmaceutical treatment on an already elevated substance abuse rate among former CSR sufferers.
Recent research has caused an increasing number of scientists to believe that there may be a physical (i.e. neurocerebral damage) rather than psychological basis for blast trauma. As traumatic brain injury and combat stress reaction have very different causes yet result in similar neurologic symptoms, researchers emphasize the need for greater diagnostic care.
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The term “acute stress disorder” was first used to describe the symptoms of soldiers during World War I and II, and it was therefore also termed “combat stress reaction” (CSR). Approximately 20% of US troops displayed symptoms of CSR during WWII. It was assumed to be a temporary response of healthy individuals to witnessing or experiencing traumatic events. Symptoms include depression, anxiety, withdrawal, confusion, paranoia, and sympathetic hyperactivity.
The American Psychological Association (APA) officially included the term ASD in the DSM-IV in 1994. Before that, symptomatic individuals within the first month of trauma were diagnosed with adjustment disorder. According to the DSM-IV, acute stress reaction refers to the symptoms experienced immediately to 48 hours after exposure to a traumatic event. In contrast, acute stress disorder is defined by symptoms experienced 48 hours to one month following the event. Symptoms experienced for longer than one month are consistent with a diagnosis of PTSD.
Initially, being able to describe different ASRs was one of the goals of introducing ASD. Some criticisms surrounding ASD’s focal point include issues with ASD recognising other distressing emotional reactions, like depression and shame. Emotional reactions similar to these may then be diagnosed as adjustment disorder under the current system of trying to diagnose ASD.
Since its addition to the DSM-IV, questions about the efficacy and purpose of the ASD diagnosis have been raised. The diagnosis of ASD was criticised as an unnecessary addition to the progress of diagnosing PTSD, as some considered it more akin to a sign of PTSD than an independent issue requiring diagnosis. Also, the terms ASD and ASR have been criticised for not fully covering the range of stress reactions.
Types of ASD
Sympathetic (also known as “Fight or Flight” Response)
Sympathetic acute stress disorder is caused by the release of excessive adrenaline and norepinephrine into the nervous system. These hormones may speed up a person’s pulse and respiratory rate, dilate pupils, or temporarily mask pain. This type of ASD developed as an evolutionary advantage to help humans survive dangerous situations. The “fight or flight” response may allow for temporarily-enhanced physical output, even in the face of severe injury. However, other physical illnesses become more difficult to diagnose, as ASD masks the pain and other vital signs that would otherwise be symptomatic.
Parasympathetic acute stress disorder is characterised by feeling faint and nauseous. This response is fairly often triggered by the sight of blood. In this stress response, the body releases acetylcholine. In many ways, this reaction is the opposite of the sympathetic response, in that it slows the heart rate and can cause the patient to either regurgitate or temporarily lose consciousness. The evolutionary value of this is unclear, although it may have allowed for prey to appear dead to avoid being eaten.
Signs and Symptoms
The DSM-IV specifies that acute stress disorder must be accompanied by the presence of dissociative symptoms, which largely differentiates it from PTSD.
Dissociative symptoms include a sense of numbing or detachment from emotional reactions, a sense of physical detachment – such as seeing oneself from another perspective – decreased awareness of one’s surroundings, the perception that one’s environment is unreal or dreamlike, and the inability to recall critical aspects of the traumatic event (dissociative amnesia).
In addition to these characteristics, ASD can be present in the following four distinct symptom clusters;
Intrusion symptom cluster:
Recurring and distressing dreams, flashbacks, and/or memories related to the traumatic event.
Intense/prolonged psychological distress or somatic reactions to internal or external traumatic cues.
Negative mood cluster:
A persistent inability to experience positive emotions such as happiness, loving feelings, or satisfaction.
Avoidance symptom cluster:
The avoidance of distressing memories, thoughts, feelings (or external reminders of them) that are closely associated with the traumatic event.
Arousal symptom cluster:
Sleep disturbances, hyper-vigilance, difficulties with concentration, easily startled, and irritability/anger/aggression.
There are a number of issues that can arise from acute stress. Depression, anxiety, mood disorders, and substance abuse problems can develop from acute stress. Untreated ASD can also lead to the development of PTSD.
There are several theoretical perspectives on trauma response, including cognitive, biological, and psycho-biological. While PTSD-specific, these theories are still useful in understanding acute stress disorder, as the two disorders share many symptoms. A recent study found that even a single stressful event may have long-term consequences on cognitive function. This result calls the traditional distinction between the effects of acute and chronic stress into question.
Stress is characterised by specific physiological responses to adverse or noxious stimuli.
Hans Selye was the first to coin the term “general adaptation syndrome” to suggest that stress-induced physiological responses proceed through the stages of alarm, resistance, and exhaustion.
The sympathetic branch of the autonomic nervous system gives rise to a specific set of physiological responses to physical or psychological stress. The body’s response to stress is also termed a “fight or flight” response, and it is characterised by an increase in blood flow to the skeletal muscles, heart, and brain, a rise in heart rate and blood pressure, dilation of pupils, and an increase in the amount of glucose released by the liver.
The onset of an acute stress response is associated with specific physiological actions in the sympathetic nervous system, both directly and indirectly through the release of adrenaline and, to a lesser extent, noradrenaline from the medulla of the adrenal glands. These catecholamine hormones facilitate immediate physical reactions by triggering increases in heart rate and breathing, constricting blood vessels. An abundance of catecholamines at neuroreceptor sites facilitates reliance on spontaneous or intuitive behaviours often related to combat or escape.
Normally, when a person is in a serene, non-stimulated state, the firing of neurons in the locus ceruleus is minimal. A novel stimulus, once perceived, is relayed from the sensory cortex of the brain through the thalamus to the brain stem. That route of signalling increases the rate of noradrenergic activity in the locus ceruleus, and the person becomes more alert and attentive to their environment.
If a stimulus is perceived as a threat, a more intense and prolonged discharge of the locus ceruleus activates the sympathetic division of the autonomic nervous system. The activation of the sympathetic nervous system leads to the release of norepinephrine from nerve endings acting on the heart, blood vessels, respiratory centres, and other sites. The ensuing physiological changes constitute a major part of the acute stress response. The other major player in the acute stress response is the hypothalamic-pituitary-adrenal axis. Stress activates this axis and produces neuro-biological changes. These chemical changes increase the chances of survival by bringing the physiological system back to homeostasis.
The autonomic nervous system controls all automatic functions in the body and contains two subsections within it that aid the response to an acute stress reaction. These two subunits are the sympathetic nervous system and the parasympathetic nervous system. The sympathetic response is colloquially known as the “fight or flight” response, indicated by accelerated pulse and respiration rates, pupil dilation, and a general feeling of anxiety and hyper-awareness. This is caused by the release of epinephrine and norepinephrine from the adrenal glands. The epinephrine and norepinephrine strike the beta receptors of the heart, which feeds the heart’s sympathetic nerve fibres to increase the strength of heart muscle contraction; as a result, more blood gets circulated, increasing the heart rate and respiratory rate. The sympathetic nervous system also stimulates the skeletal system and muscular system to pump more blood to those areas to handle the acute stress. Simultaneously, the sympathetic nervous system inhibits the digestive system and the urinary system to optimise blood flow to the heart, lungs, and skeletal muscles. This plays a role in the alarm reaction stage. The parasympathetic response is colloquially known as the “rest and digest” response, indicated by reduced heart and respiration rates, and, more obviously, by a temporary loss of consciousness if the system is fired at a rapid rate. The parasympathetic nervous system stimulates the digestive system and urinary system to send more blood to those systems to increase the process of digestion. To do this, it must inhibit the cardiovascular system and respiratory system to optimise blood flow to the digestive tract, causing low heart and respiratory rates. The parasympathetic nervous system plays no role in acute stress response.
Studies have shown that patients with acute stress disorder have overactive right amygdalae and prefrontal cortices; both structures are involved in the fear-processing pathway.
According to the DSM-V, symptom presentation must last for three consecutive days to be classified as acute stress disorder. If symptoms persist past one month, the diagnosis of PTSD is explored. There must be a clear temporal connection between the impact of an exceptional stressor and the onset of symptoms; onset is usually within a few minutes or days but may occur up to one month after the stressor. Also, the symptoms show a mixed and rapidly changing picture; although “daze” depression, anxiety, anger, despair, hyper-activity, and withdrawal may all be seen, no one symptom dominates for long. The symptoms usually resolve rapidly where removal from the stressful environment is possible. In cases where the stress continues, the symptoms usually begin to diminish after 24-48 hours and are usually minimal after about three days.
Evaluation of patients is done through close examination of emotional response. Using self-report from patients is a large part of diagnosing ASD, as acute stress is the result of reactions to stressful situations.
The DSM-V specifies that there is a higher prevalence rate of ASD among females compared to males due to higher risk of experiencing traumatic events and neurobiological gender differences in stress response.
This disorder may resolve itself with time or may develop into a more severe disorder, such as PTSD. However, results of Creamer, O’Donnell, and Pattison’s (2004) study of 363 patients suggests that a diagnosis of acute stress disorder had only limited predictive validity for PTSD. Creamer et al. found that re-experiences of the traumatic event and arousal were better predictors of PTSD. Early pharmacotherapy may prevent the development of post-traumatic symptoms. Additionally, early trauma-focused cognitive behavioural therapy (TF-CBT) for those with a diagnosis of ASD can protect an individual from developing chronic PTSD.
Studies have been conducted to assess the efficacy of counselling and psychotherapy for people with acute stress disorder. Cognitive behavioural therapy, which includes exposure and cognitive restructuring, was found to be effective in preventing PTSD in patients diagnosed with acute stress disorder with clinically significant results at six-month follow-up appointments. A combination of relaxation, cognitive restructuring, imaginal exposure, and in-vivo exposure was superior to supportive counselling. Mindfulness-based stress reduction programmes also appear to be effective for stress management.
The pharmacological approach has made some progress in lessening the effects of ASD. To relax patients and allow for better sleep, Prazosin can be given to patients, which regulates their sympathetic response. Hydrocortisone has shown some success as an early preventative measure following a traumatic event, typically in the treatment of PTSD.
In a wilderness context where counselling, psychotherapy, and cognitive behavioural therapy is unlikely to be available, the treatment for acute stress reaction is very similar to the treatment of cardiogenic shock, vascular shock, and hypovolemic shock; that is, allowing the patient to lie down, providing reassurance, and removing the stimulus that prompted the reaction. In traditional shock cases, this generally means relieving injury pain or stopping blood loss. In an acute stress reaction, this may mean pulling a rescuer away from the emergency to calm down or blocking the sight of an injured friend from a patient.
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