What is Double Depression?

Introduction

Double depression refers to the co-existence of major depressive disorder (MDD) and persistent depressive disorder (PDD), the latter previously referred to as dysthymia. Research has shown that double depression tends to be more severe than either MDD or PDD alone and that individuals with double depression experience relapse more often than those with either MDD or PDD alone. However, there is some research that indicates few differences exist between double depression, MDD, and PDD; as a result, those researchers conclude that double depression is not a distinct disorder.

The literature that details the pharmaceutical treatment of double depression is sparse. Although there are studies that demonstrate that certain medications, such as selective serotonin reuptake inhibitors (SSRIs), are effective methods of treatment, those studies lack placebo controls; therefore, the studies’ conclusions are questionable.

Research has found that, as is the case with other depressive disorders, pharmaceutical and therapeutic treatments combined are more effective than the use of either form of treatment alone. Individuals with double depression tend to experience more functional impairment than those with either MDD or PDD alone. As a result, researchers emphasize the need for unique treatments for double depression to be developed and implemented.

Presentation

Individuals with double depression meet the DSM-5 classification criteria for both MDD and PDD. Goldney and Fisher (2004) determined that, in a sample of 3,010 individuals from southern portions of Australia calculated a prevalence rate of double depression of 2.2%. Jonas et al. (2003) reported a prevalence rate of double depression in the United States of 3.4%—based upon an assessment of 7,667 Americans. The prevalence rate of double depression can be compared to rates of PDD at 6.2%, major depressive episode (MDE) at 8.6%, and major depressive episode with severity (MDE-s) at 7.7%. Keller and Shapiro (1982) found that 26% of patients within a sample of 101 met the criteria for both MDD and PDD; however, the aforementioned sample is much smaller—and much more inclined to inaccuracies—than the samples (3,010 and 7,667) described above. Thus, double depression is less common than other forms of depression, but it is still a form of depression that warrants medical attention in the form of behavioral therapies; pharmaceutical treatments; or, both (Miller, Norman, and Keitner, 1999).

The characteristics of those with double depression tend to be more severe in nature than those associated with those who have either MDD or PDD. Levitt, Joffe, and MacDonald (1991) found that those with double depression experience fluctuations in mood at an earlier point in life, a more substantial number of depressive episodes, as well as co-morbid disorders of anxieties more often than their MDD-alone counterparts. Goldney and Fisher (2004) reported that individuals with double depression seek medical attention more often than those with either MDD or PDD alone. Leader and Klein (1996) found that individuals with double depression experience a more substantial level of social impairment, which includes factors such as leisure pursuits and relationship characteristics, than those with either MDD or PDD. Dixon and Thyer (1998) concluded that individuals with double depression experiences recoveries on a more frequent basis than their counterparts who have MDD alone (88% to 69%); however, individuals with double depression experience the most substantial rates of relapse of all of those who suffer from chronic depression. In addition, remission from MDD tends to happen faster than remission from PDD (Dixon & Thyer, 1998).

Miller, Norman, and Dow (1986) reported that individuals with double depression endure a more severe path of illness, but experience few differences with respect to social impairment compared to their MDD-alone counterparts. In addition, McCullough et al. (2000) found that, with the exception that patients with double depression tended to experience of more severe illness, few differences were apparent. Therefore, the conclusions drawn in previous research that are associated with the nature of the clinical presentation of double depression are mixed. Multiple scientists emphasize the need for additional research to determine adequate treatments for those with double depression, as depression is a disease that places a considerable burden upon communities and societies; furthermore, those researchers predict depression will be, in an economic sense, the second-most burdensome disease on societies come 2020.

Treatment

Research on pharmaceutical treatment of double depression in particular is sparse. Certain medications, such as fluoxetine, were found in numerous studies to be effective at reducing symptom severity; however, these studies involved open-label trials, double-blind randomised trials that lack placebo conditions, and small sample sizes. Thus, placebo-controlled trials are needed in order to determine adequate and unique treatments for double depression. In addition, the considerable burden depression places upon communities and societies (Goldney & Fisher, 2004) emphasizes the need for additional research into the treatment of chronic depression.

Hellerstein et al. (1994) theorised that antidepressant medications could be used to ameliorate both MDD and PDD; a pharmaceutical trial found that fluoxetine facilitated remission in 57.1% of patients after five months of treatment. In addition, Miller, Norman, and Keitner (1999) conducted an intervention in which one cohort received pharmaceutical treatment while another cohort received both pharmaceutical and therapeutic treatment. Their results indicated that those who received the combined intervention were more functional—in a social sense—as well as relieved of their depression than those who received the pharmaceutical intervention alone (Miller, Norman, & Keitner, 1999). However, the researchers found that the effect disappeared at both the 6 and 12-month follow-up assessments.

Vasile et al. (2012) conducted a pharmaceutical trial with 16 patients with double depression (who had comorbid alcohol dependence) who were treated and monitored for six months. Results showed that three antidepressantsvenlafaxine, duloxetine, and milnacipran – were associated with substantial improvement; venlafaxine was the most effective of the three antidepressants.

Koran, Aboujaoude, and Gamel (2007) conducted a pharmaceutical trial with 24 adults who received duloxetine over the course of a 12-week period. Results showed that duloxetine was successful in the treatment of both PDD as well as double depression. However, the researchers’ trial was an open-label trial; as a result, the researchers called for a double-blind and placebo-controlled trial to be conducted in order to further validate the benefits the medication seems to provide.

In addition, Waslick et al. (1999) used duloxetine to treat 19 children and adolescents with either PDD or double depression; after eight weeks of pharmaceutical treatment, 11 of the patients failed to meet the classification criteria for one of the two disorders, which led to the conclusion that duloxetine was a medication that appeared to provide relief from PDD and double depression in children and adolescents. However, the aforementioned trial (in addition to Koran et al.’s (2007) trial) was an open-label trial, which the authors noted as a limitation.

Hirschfield et al. (1998) conducted a 12-week randomised controlled trial (RCT) that involved the administration of sertraline or imipramine, after which 324 of 623 patients either qualified for remission or experienced a substantive improvement in clinical presentation. In a double-blind, fixed-dose trial that involved the use of either the monoamine oxidase inhibitor (MAOI) moclobemide or the SSRI fluoxetine, Duarte, Mikkelsen, and DeliniStula (1996) were able to facilitate a minimum of a 50% score reduction on the Hamilton Depression Rating Scale (HDRS). 71% of cases that involved moclobemide – versus 38% of cases that involved fluoxetine – were determined to achieve the aforementioned desired outcome. As a result, the researchers concluded that both antidepressants were similar in their abilities to treat double depression in an effective fashion. However, the lack of a placebo control undermines the extent to which the results can be applied.

Marin, Kocsis, Frances, and Parides (1994) conducted an eight-week open trial that entailed the administration of desipramine to 42 individuals with double depression and 33 individuals with PDD. The researchers found that 70% of the PDD patients experienced a substantial improvement in clinical presentation; the proportion associated with the double depression-cohort was said to be similar. However, the lack of blindness as well as a placebo control notes a considerable limitation of the aforementioned research.

Goldney and Bain (2006) found that those who have double depression receive some form of treatment on a more substantial basis than their MDD-alone and PDD-alone counterparts. To elaborate, the authors measured that, in Australia, 41.4% of those evaluated with double depression received treatment three or more times over the course of the previous month, whereas 34.5% of those with MDD alone; 23.2% of those with PDD alone; and 10.3% of those who were not depressed received treatment three or more times over the course of the previous month (Goldney & Bain, 2006). In addition, the researchers concluded that those with double depression acquire a more substantial number of treatment visits per month (a mean of 4.3) when compared to their MDD-alone counterparts (a mean of 3.0); their PDD-alone counterparts (a mean of 2.6); and their non-depressed counterparts (a mean of 1.5).

Prognosis

Although double depression is less prevalent than either MDD or PDD, it is still a form of depression that warrants medical attention in the form of behavioural therapies; pharmaceutical treatments; or, both. Miller, Norman, and Keitner (1999) found that the use of both behavioural and pharmaceutical treatments was more effective on a short-term basis in the reduction of depression than the use of pharmaceutical treatments alone.

Klein, Shankman, and Rose (2008) determined that poor maternal-child relationship, histories of sexual abuse, co-morbid disorders of anxieties, and lower educational attainment predicted an increased HAM-D score after a decade; the researchers also determined that those same factors predicted, after a decade, increased functional impairment. In addition, the results showed that the life course of depression did not differ to a substantial extent between individuals with MDD-alone and double depression.

Hirschfield et al. (1998) conducted a 12-week RCT that involved the administration of sertraline or imipramine, in which the most notable predictors of treatment response were educational attainment and relationship status; in addition, the authors noted the apparent influence of intrinsic personal traits. However, Hirschfield et al. noted the limitation of a lack of a placebo control.

Klein, Taylor, Harding, and Dickstein (1988) reported that, via their assessment of clinical, familial, and socio-environmental characteristics of those with chronic depression, at a six-month follow-up, individuals with double depression experienced decreased rates of remission, increased manifestations of clinical depressive phenomena, increased functional impairment, and increased likelihood of the development and onset of a hypomanic episode than their MDD-alone counterparts; as a result, the authors underscore the importance of the creation of a distinct classification of double depression due to its unique episodic path.

Controversies

Previous research on the clinical presentation of double depression tends to be mixed. Numerous studies indicate that the course of double depression tends to be more severe in nature. In addition, numerous studies demonstrate that individuals with double depression seek medical attention to a more substantial extent than those with either MDD or PDD. However, Miller, Norman, and Dow (1986) determined that individuals with MDD or PDD versus individuals with double depression experienced similar levels of social impairment. In addition, McCullough and colleagues found that there were few additional differences overall between the characteristics of those with double depression versus those with either MDD or PDD.

Research on the course of double depression is also mixed. Klein, Taylor, Harding, and Dickstein (1988) found that remission in individuals with double depression is less probable than it is in individuals with either MDD or PDD; the researchers also noted that those with double depression are more prone to the development and onset of a hypomanic episode than those with either MDD or PDD. In addition, Klein, Shankman, and Rose (2008) and Hirschfield et al. (1998) both concluded that educational status predicted treatment outcome. However, Levitt, Joffe, and MacDonald (1991) demonstrated that the courses of the respective depressive disorders did not differ to a substantial extent. While Klein, Shankman, and Rose (2008) advocate for the creation of a distinct classification of double depression in the future edition(s) of the DSM, Levitt and colleagues (as well as McCullough and colleagues) seem to indicate that, due to the numerous similarities as well as limited differences between double depression and either MDD or PDD, the creation of such a classification would be inappropriate and incorrect. Remick, Sadovnick, Lam, Zis, and Yee (1996) determine that the heritable bases of MDD, PDD, and double depression are similar and that, as a result, the three disorders are unable to be differentiated.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Double_depression >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

An Overview of Externalising Disorders

Introduction

Externalising disorders are mental disorders characterised by externalising behaviours, maladaptive behaviours directed toward an individual’s environment, which cause impairment or interference in life functioning. In contrast to individuals with internalising disorders who internalise (keep inside) their maladaptive emotions and cognitions, such feelings and thoughts are externalised (manifested outside) in behaviour in individuals with externalising disorders. Externalising disorders are often specifically referred to as disruptive behaviour disorders (attention-deficit/hyperactivity disorder, oppositional defiant disorder, and conduct disorder) or conduct problems which occur in childhood. Externalising disorders, however, are also manifested in adulthood. For example, alcohol- and substance-related disorders and antisocial personality disorder are adult externalising disorders. Externalising psychopathology is associated with antisocial behaviour, which is different from and often confused for asociality.

Brief History

The classification for several externalising disorders changed from DSM-IV to DSM-5. ADHD, ODD, and CD were previously classified in the Attention-deficit and Disruptive Behaviour Disorders section in DSM-IV. Pyromania, kleptomania, and IED were previously classified in the Impulse-Control Disorders Not Otherwise Specified Section of DSM-IV. ADHD is now categorised in the Neurodevelopmental Disorders section in DSM-5. ODD, CD, pyromania, kleptomania, and IED are now categorised in the new Disruptive, Impulse-Control, and Conduct Disorders chapter of DSM-5. Overall, there were many changes made to the DSM from the transition of DSM-IV-TR to DSM-5, which was somewhat controversial.

Signs and Symptoms

Externalising disorders often involve emotion dysregulation problems and impulsivity that are manifested as antisocial behaviour and aggression in opposition to authority, societal norms, and often violate the rights of others. Some examples of externalising disorder symptoms include, often losing one’s temper, excessive verbal aggression, physical aggression to people and animals, destruction of property, theft, and deliberate fire setting. As with all DSM-5 mental disorders, an individual must have functional impairment in at least one domain (e.g. academic, occupational, social relationships, or family functioning) in order to meet diagnostic criteria for an externalising disorder. Moreover, an individual’s symptoms should be atypical for their cultural and environmental context and physical medical conditions should be ruled out before an externalising disorder diagnosis is considered. Diagnoses must be made by qualified mental health professionals. DSM-5 classifications of externalising disorders are listed herein, however, ICD-10 can also be used to classify externalising disorders. More specific criteria and examples of symptoms for various externalising disorders can be found in the DSM-5.

DSM-5 Classification

There are no specific criteria for “externalising behaviour” or “externalising disorders”. Thus, there is no clear classification of what constitutes an externalizing disorder in the DSM-5. Attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), conduct disorder (CD), antisocial personality disorder (ASPD), pyromania, kleptomania, intermittent explosive disorder (IED), and substance-related disorders are frequently referred to as externalising disorders. Disruptive mood dysregulation disorder has also been posited as an externalising disorder, but little research has examined and validated it to date given its recent addition to the DSM-5, and thus, it is not included further herein.

Attention-Deficit/Hyperactivity Disorder

Inattention ADHD symptoms include: “often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or during other activities,” “often has difficulty sustaining attention in tasks or play activities,” “often does not seem to listen when spoken to directly,” “often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace,” “often has difficulty organizing tasks and activities,” “often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort,” “often loses things necessary for tasks or activities,” “is often easily distracted by extraneous stimuli (for older adolescents and adults, may include unrelated thoughts),” and “is often forgetful in daily activities.”

Hyperactivity and impulsivity ADHD symptoms include: “often fidgets with or taps hands or feet or squirms in seat,” “often leaves seat in situations when remaining seated is expected,” “often runs about or climbs in situations where it is inappropriate,” “is often unable to play or engage in leisure activities quietly,” “is often “on the go,” acting as if “driven by a motor,” “often talks excessively,” “often blurts out an answer before a question has been completed,” “often has difficulty waiting his or her turn,” and “often interrupts or intrudes on others.”

In order to meet criteria for an ADHD diagnosis, an individual must have at least six symptoms of inattention and/or hyperactivity/impulsivity, have an onset of several symptoms prior to age 12 years, have symptoms present in at least two settings, have functional impairment, and have symptoms that are not better explained by another mental disorder.

Oppositional Defiant Disorder

ODD symptoms include: “often loses temper,” “is often touchy or easily annoyed,” “is often angry and resentful,” “often argues with authority figures, or for children and adolescents, with adults,” “often actively defies or refuses to comply with requests from authority figures or with rules,” “often deliberately annoys others,” and “often blames others for his or her mistakes or misbehavior.” In order to receive an ODD diagnosis, individuals must have at least four symptoms from above for at least six months (most days for youth younger than five years) with at least one individual who is not a sibling, which causes impairment in at least one setting. Rule outs for a diagnosis include symptoms occurring concurrently during an episode of another disorder.

Conduct Disorder

CD symptoms include “often bullies, threatens, or intimidates others,” “often initiates physical fights,” “has used a weapon that can cause serious physical harm to others,” “has been physically cruel to people,” “has been physically cruel to animals,” “has stolen while confronting a victim,” “has forced someone into sexual activity,” “has deliberately engaged in fire setting with the intention of causing serious damage,” “has deliberately destroyed others’ property (other than by fire setting),” “has broken into someone else’s house, building, or car,” “often lies to obtain goods or favors or to avoid obligations,” “has stolen items of nontrivial value without confronting a victim,” “often stays out at night despite parental prohibitions, beginning before age 13 years,” “has run away from home overnight at least twice while living in the parental or parental surrogate home, or once without returning for a lengthy period,” and “is often truant from school, beginning before age 13 years.” In order to receive a CD diagnosis, individuals must have three of these symptoms for at least one year, at least two symptoms for at least six months, be impaired in at least one setting, and not have an antisocial personality disorder diagnosis if 18 years or older

Antisocial Personality Disorder

ASPD symptoms include: “failure to conform to social norms with respect to lawful behaviors, as indicated by repeatedly performing acts that are grounds for arrest,” “deceitfulness, as indicated by repeated lying, use of aliases, or conning others for personal profit or pleasure,” “impulsivity or failure to plan ahead,” “irritability and aggressiveness, as indicated by repeated physical fights or assaults,” “reckless disregard for safety of self or others,” “consistent irresponsibility, as indicated by repeated failure to sustain consistent work behavior or honor financial obligations,” and “lack of remorse, as indicated by being indifferent to or rationalizing having hurt, mistreated, or stolen from another.” In order to meet diagnostic criteria for ASPD, an individual must have “a pervasive pattern of disregard for and violation of the rights of others, occurring since age 15 years,” three or more of the above symptoms, be at least age 18 years, have a conduct disorder onset before age 15 years, and not have antisocial behaviour exclusively during schizophrenia or bipolar disorder.

Pyromania

Pyromania symptoms include: “deliberate and purposeful fire setting on more than one occasion,” “tension or affective arousal before the act,” “fascination with, interest in, curiosity about, or attraction to fire and its situational contexts,” and “pleasure, gratification, or relief when setting fires or when witnessing or participating in their aftermath.” In order to receive a pyromania diagnosis, “the fire setting is not done for monetary gain, as an expression of sociopolitical ideology, to conceal criminal activity, to express anger or vengeance, to improve one’s living circumstances, in response to a delusion or hallucination, or as a result of impaired judgment.” A conduct disorder diagnosis, manic episode, or antisocial personality disorder diagnosis must not better account for the fire setting in order to receive a pyromania diagnosis.

Kleptomania

Kleptomania symptoms include: “recurrent failure to resist impulses to steal objects that are not needed for personal use or for their monetary value,” “increasing sense of tension immediately before committing the theft,” and “pleasure, gratification, or relief at the time of committing the theft.” In order to receive a kleptomania diagnosis, “the stealing is not committed to express anger or vengeance and is not in response to a delusion or a hallucination.” Additionally, in order to receive a diagnosis, “the stealing is not better explained by conduct disorder, a manic episode, or antisocial personality disorder.”

Intermittent Explosive Disorder

IED symptoms include:

“recurrent behavioral outbursts representing a failure to control aggressive impulses as manifested by either of the following: 1) Verbal aggression (e.g., temper tantrums, tirades, verbal arguments or fights) or physical aggression toward property, animals, or other individuals, occurring twice weekly, on average, for a period of 3 months. The physical aggression does not result in damage or destruction of property and does not result in physical injury to animals or other individuals. 2) Three behavioral outbursts involving damage or destruction of property and/or physical assault involving physical injury against animals or other individuals occurring within a 12-month period.”

In order to receive an IED diagnosis, “the magnitude of aggressiveness expressed during the recurrent outbursts is grossly out of proportion to the provocation or to any precipitating psychosocial stressors,” “the recurrent aggressive outbursts are not premeditated” and “are not committed to achieve some tangible objective.” Additionally, to receive an IED diagnosis, an individual must be six years or older (chronologically or developmentally), have functional impairment, and not have symptoms better explained by another mental disorder, medical condition, or substance.

Substance Use Disorders

According to the DSM-5, “the essential feature of a substance use disorder is a cluster of cognitive, behavioral, and physiological symptoms indicating that the individual continues using the substance despite significant substance-related problems.” Given that at least 10 separate classes of drugs are covered in the DSM-5 Substance-Related and Addictive Disorders section, it is outside the scope of this article. Refer to the DSM-5 for more information on signs and symptoms.

Comorbidity

Externalising disorders are frequently comorbid or co-occurring with other disorders. Individuals who have the co-occurrence of more than one externalising disorder have homotypic comorbidity, whereas individuals who have co-occurring externalising and internalising disorders have heterotypic comorbidity. It is not uncommon for children with early externalising problems to develop both internalising and further externalising problems across the lifespan. Additionally, the complex interplay between externalising and internalising symptoms across development could explain the association between these problems and other risk behaviours, that typically initiate in adolescence (such as antisocial behaviours and substance use).

Stigma

Consistent with many mental disorders, individuals with externalising disorders are subject to significant implicit and explicit forms of stigma. Because externalising behaviours are salient and difficult to conceal, individuals with externalising disorders may be more susceptible to stigmatisation relative to individuals with other disorders. Parents of youth with childhood mental disorders, such as ADHD and ODD, are frequently stigmatised when parenting practices are strongly implicated in the aetiology or cause of the disorder. Educational and policy-related initiatives have been proposed as potential mechanisms to reduce stigmatisation of mental disorders.

Psychopathic Traits

Individuals with psychopathic traits, including callous-unemotional (CU) traits, represent a phenomenologically and etiologically distinct group with severe externalising problems. Psychopathic traits have been measured in children as young as two-years-old, are moderately stable, are heritable, and associated with atypical affective, cognitive, personality, and social characteristics. Individuals with psychopathic traits are at risk for poor response to treatment, however, some data suggest that parent management training interventions for youth with psychopathic traits early in development may have promise.

Developmental Course

ADHD often precedes the onset of ODD, and approximately half of children with ADHD, combined type also have ODD. ODD is a risk factor for CD and frequently precedes the onset of CD symptoms. Children with an early onset of CD symptoms, with at least one symptom before age 10 years, are at risk for more severe and persistent antisocial behaviour continuing into adulthood. Youth with early-onset conduct problems are particularly at risk for ASPD (note that an onset of CD prior to age 15 is part of the diagnostic criteria for ASPD), whereas CD is typically limited to adolescence when youth’s CD symptoms begin during adolescence.

Treatment

Despite recent initiatives to study psychopathology along dimensions of behaviour and neurobiological indices, which would help refine a clearer picture of the development and treatment of externalising disorders, the majority of research has examined specific mental disorders. Thus, best practices for many externalising disorders are disorder-specific. For example, substance use disorders themselves are very heterogeneous and their best-evidenced treatment typically includes cognitive behavioural therapy, motivational interviewing, and a substance disorder-specific detoxification or psychotropic medication treatment component. The best-evidenced treatment for childhood conduct and externalising problems more broadly, including youth with ADHD, ODD, and CD, is parent management training, a form of cognitive behavioural therapy. Additionally, individuals with ADHD, both youth and adults, are frequently treated with stimulant medications (or alternative psychotropic medications), especially if psychotherapy alone has not been effective in managing symptoms and impairment. Psychotherapy and medication interventions for individuals with severe, adult forms of antisocial behaviour, such as antisocial personality disorder, have been mostly ineffective. An individual’s comorbid psychopathology may also influences the course of treatment for an individual.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Externalizing_disorder >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Intermittent Explosive Disorder?

Introduction

Intermittent explosive disorder (sometimes abbreviated as IED) is a behavioural disorder characterised by explosive outbursts of anger and/or violence, often to the point of rage, that are disproportionate to the situation at hand (e.g. impulsive shouting, screaming or excessive reprimanding triggered by relatively inconsequential events). Impulsive aggression is not premeditated, and is defined by a disproportionate reaction to any provocation, real or perceived. Some individuals have reported affective changes prior to an outburst, such as tension, mood changes, energy changes, etc.

The disorder is currently categorised in the American Psychiatric Association’s (APA’s) Diagnostic and Statistical Manual of Mental Disorders (DSM-5) under the “Disruptive, Impulse-Control, and Conduct Disorders” category. The disorder itself is not easily characterised and often exhibits comorbidity with other mood disorders, particularly bipolar disorder. Individuals diagnosed with IED report their outbursts as being brief (lasting less than an hour), with a variety of bodily symptoms (sweating, stuttering, chest tightness, twitching, palpitations) reported by a third of one sample. Aggressive acts are frequently reported to be accompanied by a sensation of relief and in some cases pleasure, but often followed by later remorse.

Also known as Episodic Dyscontrol Syndrome or dyscontrol.

Brief History

In the first edition of the APA’s DSM-I, a disorder of impulsive aggression was referred to as a passive-aggressive personality type (aggressive type). This construct was characterised by a “persistent reaction to frustration are “generally excitable, aggressive, and over-responsive to environmental pressures” with “gross outbursts of rage or of verbal or physical aggressiveness different from their usual behavior”.

In the third edition (DSM-III), this was for the first time codified as intermittent explosive disorder and assigned clinical disorder status under Axis I. However, some researchers saw the criteria as poorly operationalised. About 80% of individuals who would now be diagnosed with the disorder would have been excluded.

In the DSM-IV, the criteria were improved but still lacked objective criteria for the intensity, frequency, and nature of aggressive acts to meet criteria for IED. This led some researchers to adopt alternate criteria set with which to conduct research, known as the IED-IR (Integrated Research). The severity and frequency of aggressive behaviour required for the diagnosis were clearly operationalized, the aggressive acts were required to be impulsive in nature, subjective distress was required to precede the explosive outbursts, and the criteria allowed for comorbid diagnoses with borderline personality disorder and antisocial personality disorder. These research criteria became the basis for the DSM-5 diagnosis.

In the current version of the DSM (DSM-5), the disorder appears under the “Disruptive, Impulse-Control, and Conduct Disorders” category. In the DSM-IV, physical aggression was required to meet the criteria for the disorder, but these criteria were modified in the DSM-5 to include verbal aggression and non-destructive/non-injurious physical aggression. The listing was also updated to specify frequency criteria. Further, aggressive outbursts are now required to be impulsive in nature and must cause marked distress, impairment, or negative consequences for the individual. Individuals must be at least six years old to receive the diagnosis. The text also clarified the disorder’s relationship to other disorders such as ADHD and disruptive mood dysregulation disorder.

Epidemiology

Two epidemiological studies of community samples approximated the lifetime prevalence of IED to be 4–6%, depending on the criteria set used. A Ukrainian study found comparable rates of lifetime IED (4.2%), suggesting that a lifetime prevalence of IED of 4–6% is not limited to American samples. One-month and one-year point prevalence of IED in these studies were reported as 2.0% and 2.7%, respectively. Extrapolating to the national level, 16.2 million Americans would have IED during their lifetimes and as many as 10.5 million in any year and 6 million in any month.

Among a clinical population, a 2005 study found the lifetime prevalence of IED to be 6.3%.

Prevalence appears to be higher in men than in women.

Of US subjects with IED, 67.8% had engaged in direct interpersonal aggression, 20.9% in threatened interpersonal aggression, and 11.4% in aggression against objects. Subjects reported engaging in 27.8 high-severity aggressive acts during their worst year, with 2–3 outbursts requiring medical attention. Across the lifespan, the mean value of property damage due to aggressive outbursts was $1603.

A study in the March 2016 Journal of Clinical Psychiatry suggests a relationship between infection with the parasite Toxoplasma gondii and psychiatric aggression such as IED.

Pathophysiology

Impulsive behaviour, and especially impulsive violence predisposition, have been correlated to a low brain serotonin turnover rate, indicated by a low concentration of 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF). This substrate appears to act on the suprachiasmatic nucleus in the hypothalamus, which is the target for serotonergic output from the dorsal and median raphe nuclei playing a role in maintaining the circadian rhythm and regulation of blood sugar. A tendency towards low 5-HIAA may be hereditary. A putative hereditary component to low CSF 5-HIAA and concordantly possibly to impulsive violence has been proposed. Other traits that correlate with IED are low vagal tone and increased insulin secretion. A suggested explanation for IED is a polymorphism of the gene for tryptophan hydroxylase, which produces a serotonin precursor; this genotype is found more commonly in individuals with impulsive behaviour.

IED may also be associated with damage or lesions in the prefrontal cortex, with damage to these areas, including the amygdala and hippocampus, increasing the incidences of impulsive and aggressive behaviour and the inability to predict the outcomes of an individual’s own actions. Lesions in these areas are also associated with improper blood sugar control, leading to decreased brain function in these areas, which are associated with planning and decision making. A national sample in the United States estimated that 16 million Americans may fit the criteria for IED.

Diagnosis

DSM-5 Diagnosis

The current DSM-5 criteria for IED include:

  • Recurrent outbursts that demonstrate an inability to control impulses, including either of the following:
    • Verbal aggression (tantrums, verbal arguments, or fights) or physical aggression that occurs twice in a week-long period for at least three months and does not lead to the destruction of property or physical injury (Criterion A1)
    • Three outbursts that involve injury or destruction within a year-long period (Criterion A2)
  • Aggressive behaviour is grossly disproportionate to the magnitude of the psychosocial stressors (Criterion B)
  • The outbursts are not premeditated and serve no premeditated purpose (Criterion C)
  • The outbursts cause distress or impairment of functioning or lead to financial or legal consequences (Criterion D)
  • The individual must be at least six years old (Criterion E)
  • The recurrent outbursts cannot be explained by another mental disorder and are not the result of another medical disorder or substance use (Criterion F)

It is important to note that DSM-5 now includes two separate criteria for types of aggressive outbursts (A1 and A2) which have empirical support:

CriterionOutline
A11. Episodes of verbal and/or non-damaging, non-destructive, or non-injurious physical assault that occur, on average, twice weekly for three months.
2. These could include temper tantrums, tirades, verbal arguments/fights, or assault without damage.
3. This criterion includes high frequency/low-intensity outbursts.
A21. More severe destructive/assaultive episodes which are more infrequent and occur, on average, three times within a twelve-month period.
2. These could be destroying an object without regard to value, assaulting an animal or individual.
3. This criterion includes high-intensity/low-frequency outbursts.

DSM-IV Diagnosis

The past DSM-IV criteria for IED were similar to the current criteria, however, verbal aggression was not considered as part of the diagnostic criteria. The DSM-IV diagnosis was characterised by the occurrence of discrete episodes of failure to resist aggressive impulses that result in violent assault or destruction of property. Additionally, the degree of aggressiveness expressed during an episode should be grossly disproportionate to provocation or precipitating psychosocial stressor, and, as previously stated, diagnosis is made when certain other mental disorders have been ruled out, e.g. a head injury, Alzheimer’s disease, etc., or due to substance use or medication. Diagnosis is made using a psychiatric interview to affective and behavioural symptoms to the criteria listed in the DSM-IV.

The DSM-IV-TR was very specific in its definition of Intermittent Explosive Disorder which was defined, essentially, by the exclusion of other conditions. The diagnosis required:

  • Several episodes of impulsive behaviour that result in serious damage to either persons or property, wherein
  • The degree of the aggressiveness is grossly disproportionate to the circumstances or provocation, and
  • The episodic violence cannot be better accounted for by another mental or physical medical condition.

Differential Diagnosis

Many psychiatric disorders and some substance use disorders are associated with increased aggression and are frequently comorbid with IED, often making differential diagnosis difficult. Individuals with IED are, on average, four times more likely to develop depression or anxiety disorders, and three times more likely to develop substance use disorders. Bipolar disorder has been linked to increased agitation and aggressive behaviour in some individuals, but for these individuals, aggressiveness is limited to manic and/or depressive episodes, whereas individuals with IED experience aggressive behaviour even during periods with a neutral or positive mood.

In one clinical study, the two disorders co-occurred 60% of the time. Patients report manic-like symptoms occurring just before outbursts and continuing throughout. According to a study, the average onset age of IED was around five years earlier than the onset age of bipolar disorder, indicating a possible correlation between the two.

Similarly, alcoholism and other substance use disorders may exhibit increased aggressiveness, but unless this aggression is experienced outside of periods of acute intoxication and withdrawal, no diagnosis of IED is given. For chronic disorders, such as PTSD, it is important to assess whether the level of aggression met IED criteria before the development of another disorder. In antisocial personality disorder, interpersonal aggression is usually instrumental in nature (i.e. motivated by tangible rewards), whereas IED is more of an impulsive, unpremeditated reaction to situational stress.

Treatment

Although there is no cure, treatment is attempted through cognitive behavioural therapy and psychotropic medication regimens, though the pharmaceutical options have shown limited success. Therapy aids in helping the patient recognise the impulses in hopes of achieving a level of awareness and control of the outbursts, along with treating the emotional stress that accompanies these episodes. Multiple drug regimens are frequently indicated for IED patients. Cognitive Relaxation and Coping Skills Therapy (CRCST) has shown preliminary success in both group and individual settings compared to waitlist control groups. This therapy consists of 12 sessions, the first three focusing on relaxation training, then cognitive restructuring, then exposure therapy. The final sessions focus on resisting aggressive impulses and other preventative measures.

In France, antipsychotics such as cyamemazine, levomepromazine and loxapine are sometimes used.

Tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs, including fluoxetine, fluvoxamine, and sertraline) appear to alleviate some pathopsychological symptoms. GABAergic mood stabilisers and anticonvulsive drugs such as gabapentin, lithium, carbamazepine, and divalproex seem to aid in controlling the incidence of outbursts. Anxiolytics help alleviate tension and may help reduce explosive outbursts by increasing the provocative stimulus tolerance threshold, and are especially indicated in patients with comorbid obsessive-compulsive or other anxiety disorders.

This page is based on the copyrighted Wikipedia articles < https://en.wikipedia.org/wiki/Episodic_dyscontrol_syndrome > AND < https://en.wikipedia.org/wiki/Intermittent_explosive_disorder >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Dissociative Identity Disorder?

Introduction

Dissociative identity disorder (DID), formerly known as multiple personality disorder, and commonly referred to as split personality disorder or dissociative personality disorder, is a member of the family of dissociative disorders classified by the DSM-5, DSM-5-TR, ICD-10, ICD-11, and Merck Manual for diagnosis. It remains a controversial diagnosis.

Dissociative identity disorder is characterised by the presence of at least two distinct and relatively enduring personality states. The disorder is accompanied by memory gaps more severe than could be explained by ordinary forgetfulness. The personality states alternately show in a person’s behaviour; however, presentations of the disorder vary. Other conditions that often occur in people with DID include post-traumatic stress disorder, personality disorders (especially borderline, Schizotypal and avoidant), depression, substance use disorders, conversion disorder, somatic symptom disorder, eating disorders, obsessive–compulsive disorder, and sleep disorders. Self-harm, non-epileptic seizures, flashbacks with amnesia for content of flashbacks, anxiety disorders, and suicidality are also common.

DID requires an unintegrated mind to form. Genetic and biological factors are also believed to play a role. The diagnosis should not be made if the person’s condition is better accounted for by substance use disorder, seizures, other medical problems, imaginative play in children, or religious practices.

According to the DSM-5-TR, early life trauma, typically before the age of 10, can place someone at risk of developing dissociative identity disorder. Across diverse geographic regions, 90% of individuals diagnosed with dissociative identity disorder report experiencing multiple forms of childhood abuse, such as neglect or severe bullying. Other traumatic childhood experiences that have been reported include painful medical or surgical procedures, war, terrorism, attachment disturbance, natural disaster, cult, and occult abuse, loss of a loved one or loved ones, human trafficking, and dysfunctional family dynamics.

There is no medication to treat DID directly. Medications can be used for comorbid disorders or targeted symptom relief, for example antidepressants or treatments to improve sleep, however. Treatment generally involves supportive care and psychotherapy. The condition usually persists without treatment. It is believed to affect about 1.5% of the general population (based on a small US community sample) and 3% of those admitted to hospitals with mental health issues in Europe and North America. DID is diagnosed about six times more often in women than in men. The number of recorded cases increased significantly in the latter half of the 20th century, along with the number of identities reported by those affected.

It is unclear whether increased rates of the disorder are due to better recognition or sociocultural factors such as mass media portrayals. The typical presenting symptoms in different regions of the world may also vary depending on culture, such as alter identities taking the form of possessing spirits, deities, ghosts, or mythical creatures and figures in cultures where normative possession states are common. The possession form of dissociative identity disorder is involuntary and distressing, and occurs in a way that violates cultural or religious norms.

Definitions

Dissociation, the term that underlies dissociative disorders including DID, lacks a precise, empirical, and generally agreed upon definition.

A large number of diverse experiences have been termed dissociative, ranging from normal failures in attention to the breakdowns in memory processes characterized by the dissociative disorders. It is therefore unknown if there is a commonality between all dissociative experiences, or if the range of mild to severe symptoms is a result of different aetiologies and biological structures. Other terms used in the literature, including personality, personality state, identity, ego state, and amnesia, also have no agreed upon definitions. Multiple competing models exist that incorporate some non-dissociative symptoms while excluding dissociative ones.

Due to the lack of consensus regarding terminology in the study of DID, several terms have been proposed. One is ego state (behaviours and experiences possessing permeable boundaries with other such states but united by a common sense of self), while the other term is alters (each of which may have a separate autobiographical memory, independent initiative and a sense of ownership over individual behaviour).

Ellert Nijenhuis and colleagues suggest a distinction between personalities responsible for day-to-day functioning (associated with blunted physiological responses and reduced emotional reactivity, referred to as the “apparently normal part of the personality” or ANP) and those emerging in survival situations (involving fight-or-flight responses, vivid traumatic memories and strong, painful emotions – the “emotional part of the personality” or EP). “Structural dissociation of the personality” is used by Onno van der Hart and colleagues to distinguish dissociation they attribute to traumatic or pathological causes, which in turn is divided into primary, secondary and tertiary dissociation. According to this theory, primary dissociation prototypically involves one ANP and one EP, while secondary dissociation prototypically involves an ANP and at least two EPs, and tertiary dissociation, typically characterised in DID, is described as having at least two ANPs and at least two EPs. Others have suggested dissociation can be separated into two distinct forms, detachment and compartmentalisation, the latter of which, involving a failure to control normally controllable processes or actions, is most evident in DID. Efforts to psychometrically distinguish between normal and pathological dissociation have been made.

Signs and Symptoms

The full presentation of dissociative identity disorder can onset at any age, although symptoms typically begin at ages 5-10. According to DSM-5, symptoms of DID include “the presence of two or more distinct personality states” accompanied by the inability to recall personal information beyond what is expected through normal memory issues. Other DSM-5 symptoms include a loss of identity as related to individual distinct personality states, loss of one’s subjective experience of the passage of time, and degradation of a sense of self and consciousness. In each individual, the clinical presentation varies and the level of functioning can change from severe impairment to minimal impairment. The symptoms of dissociative amnesia are subsumed under a DID diagnosis, and thus should not be diagnosed separately if DID criteria are met. Individuals with DID may experience distress from both the symptoms of DID (intrusive thoughts or emotions) and the consequences of the accompanying symptoms (dissociation rendering them unable to remember specific information). The majority of patients with DID report childhood sexual or physical abuse. Amnesia between identities may be asymmetrical; identities may or may not be aware of what is known by another. Individuals with DID may be reluctant to discuss symptoms due to associations with abuse, shame, and fear. DID patients may also frequently and intensely experience time disturbances.

Around half of people with DID have fewer than 10 identities and most have fewer than 100; although as many as 4,500 have been reported. The average number of identities has increased over the past few decades, from two or three to now an average of approximately 16. However, it is unclear whether this is due to an actual increase in identities, or simply that the psychiatric community has become more accepting of a high number of compartmentalised memory components.

Comorbid Disorders

The psychiatric history frequently contains multiple previous diagnoses of various disorders and treatment failures. The most common presenting complaint of DID is depression, with headaches being a common neurological symptom. Comorbid disorders can include substance use disorder, eating disorders, anxiety disorders, bipolar disorder, and personality disorders. A significant percentage of those diagnosed with DID have histories of borderline personality disorder and post-traumatic stress disorder (PTSD). Presentations of dissociation in people with schizophrenia differ from those with DID as not being rooted in trauma, and this distinction can be effectively tested, although both conditions share a high rate of dissociative auditory hallucinations. Other disorders that have been found to be comorbid with DID are somatization disorders, major depressive disorder, as well as history of a past suicide attempt, in comparison to those without a DID diagnosis. Disturbed and altered sleep has also been suggested as having a role in dissociative disorders in general and specifically in DID, alterations in environments also largely affecting the DID patient. Individuals diagnosed with DID demonstrate the highest hypnotisability of any clinical population. Although DID has high comorbidity and its development is related to trauma, there exists evidence to suggest that DID merits a separate diagnosis from other conditions like PTSD.

Causes

General

There are two competing theories on what causes dissociative identity disorder to develop. The trauma-related model suggests that trauma or severe adversity in childhood, also known as developmental trauma, increases the risk of someone developing dissociative identity disorder. The non-trauma related model, also referred to as the Sociocognitive model or the fantasy model, suggests that dissociative identity disorder is developed through high fantasy-proneness or suggestibility, roleplaying, or sociocultural influences.

The DSM-5-TR states that “early life trauma (e.g. neglect and physical, sexual, and emotional abuse, usually before ages 5-6 years) represents a risk factor for dissociative identity disorder.” Other risk factors reported include painful medical procedures, war, terrorism, or being trafficked in childhood. Dissociative disorders frequently occur after trauma, and the DSM-5-TR places them after the trauma- and stressor-related disorders to reflect this close relationship.

Trauma-Related Model

Dissociative identity disorder is often conceptualised as “the most severe form of a childhood onset post-traumatic stress disorder.” According to many researchers, the aetiology of dissociative identity is multifactorial, involving a complex interaction between developmental trauma, sociocultural influences, and biological factors.

People diagnosed with dissociative identity disorder often report that they have experienced physical or sexual abuse during childhood (although the accuracy of these reports has been disputed); others report overwhelming stress, serious medical illness, or other traumatic events during childhood. They also report more historical psychological trauma than those diagnosed with any other mental illness.

Severe sexual, physical, or psychological trauma in childhood has been proposed as an explanation for its development; awareness, memories, and emotions of harmful actions or events caused by the trauma are removed from consciousness, and alternate personalities or subpersonalities form with differing memories, emotions and behaviour. Dissociative identity disorder is attributed to extremes of stress or disorders of attachment. What may be expressed as post-traumatic stress disorder (PTSD) in adults may become dissociative identity disorder when occurring in children, possibly due to their greater use of imagination as a form of coping.

Possibly due to developmental changes and a more coherent sense of self past the age of six, the experience of extreme trauma may result in different, though also complex, dissociative symptoms and identity disturbances. A specific relationship between childhood abuse, disorganized attachment, and lack of social support are thought to be a necessary component of dissociative identity disorder. Although what role a child’s biological capacity to dissociate to an extreme level remains unclear, some evidence indicates a neurobiological impact of developmental stress.

Delinking early trauma from the aetiology of dissociation has been explicitly rejected by those supporting the early trauma model. However, 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. Giesbrecht et al. have suggested there is no actual empirical evidence linking early trauma to dissociation, and instead suggest that problems with neuropsychological functioning, such as increased distractibility in response to certain emotions and contexts, account for dissociative features. A middle position hypothesizes that trauma, in some situations, alters neuronal mechanisms related to memory. Evidence is increasing that dissociative disorders are related both to a trauma history and to “specific neural mechanisms”. It has also been suggested that there may be a genuine but more modest link between trauma and dissociative identity disorder, with early trauma causing increased fantasy-proneness, which may in turn render individuals more vulnerable to socio-cognitive influences surrounding the development of dissociative identity disorder. Another suggestion made by Hart indicates that there are triggers in the brain that can be the catalyst for different self-states, and that victims of trauma are more susceptible to these triggers than non-victims of trauma; these triggers are said to be related to dissociative identity disorder.

Paris states that the trauma model of dissociative identity disorder increased the appeal of the diagnosis among health care providers, patients and the public as it validated the idea that child abuse had lifelong, serious effects. Paris asserts that there is very little experimental evidence supporting the trauma-dissociation hypothesis, and no research showing that dissociation consistently links to long-term memory disruption.

Non-Trauma-Related Model

The prevailing trauma-related model of dissociation and dissociative disorders is contested. It has been hypothesized that symptoms of dissociative identity disorder may be created by therapists using techniques to “recover” memories (such as the use of hypnosis to “access” alter identities, facilitate age regression or retrieve memories) on suggestible individuals. Referred to as the non-trauma-related model, or the sociocognitive model or fantasy model, it proposes that dissociative identity disorder is due to a person consciously or unconsciously behaving in certain ways promoted by cultural stereotypes, with unwitting therapists providing cues through improper therapeutic techniques. This model posits that behaviour is enhanced by media portrayals of dissociative identity disorder.

Proponents of the non-trauma-related model note that the dissociative symptoms are rarely present before intensive therapy by specialists in the treatment of dissociative identity disorder who, through the process of eliciting, conversing with, and identifying alters, shape or possibly create the diagnosis. While proponents note that dissociative identity disorder is accompanied by genuine suffering and the distressing symptoms, and can be diagnosed reliably using the DSM criteria, they are sceptical of the trauma-related aetiology suggested by proponents of the trauma-related model. Proponents of non-trauma-related dissociative identity disorder are concerned about the possibility of hypnotisability, suggestibility, frequent fantasisation and mental absorption predisposing individuals to dissociation. They note that a small subset of doctors are responsible for diagnosing the majority of individuals with dissociative identity disorder.

Psychologist Nicholas Spanos and others have suggested that in addition to therapy caused cases, dissociative identity disorder may be the result of role-playing, though others disagree, pointing to a lack of incentive to manufacture or maintain separate identities and point to the claimed histories of abuse. Other arguments that therapy can cause dissociative identity disorder include the lack of children diagnosed with DID, the sudden spike in rates of diagnosis after 1980 (although dissociative identity disorder was not a diagnosis until DSM-IV, published in 1994), the absence of evidence of increased rates of child abuse, the appearance of the disorder almost exclusively in individuals undergoing psychotherapy, particularly involving hypnosis, the presences of bizarre alternate identities (such as those claiming to be animals or mythological creatures) and an increase in the number of alternate identities over time (as well as an initial increase in their number as psychotherapy begins in DID-oriented therapy). These various cultural and therapeutic causes occur within a context of pre-existing psychopathology, notably borderline personality disorder, which is commonly comorbid with dissociative identity disorder. In addition, presentations can vary across cultures, such as Indian patients who only switch alters after a period of sleep – which is commonly how dissociative identity disorder is presented by the media within that country.

Proponents of non-trauma-related dissociative identity disorder state that the disorder is strongly linked to (possibly suggestive) psychotherapy, often involving recovered memories (memories that the person previously had amnesia for) or false memories, and that such therapy could cause additional identities. Such memories could be used to make an allegation of child sexual abuse. There is little agreement between those who see therapy as a cause and trauma as a cause. Supporters of therapy as a cause of dissociative identity disorder suggest that a small number of clinicians diagnosing a disproportionate number of cases would provide evidence for their position though it has also been claimed that higher rates of diagnosis in specific countries like the United States may be due to greater awareness of DID. Lower rates in other countries may be due to artificially low recognition of the diagnosis. However, false memory syndrome per se is not regarded by mental health experts as a valid diagnosis, and has been described as “a non-psychological term originated by a private foundation whose stated purpose is to support accused parents,” and critics argue that the concept has no empirical support, and further describe the False Memory Syndrome Foundation as an advocacy group that has distorted and misrepresented memory research.

Children

The rarity of dissociative identity disorder diagnosis in children is cited as a reason to doubt the validity of the disorder, and proponents of both aetiologies believe that the discovery of dissociative identity disorder in a child who had never undergone treatment would critically undermine the non-trauma related model. Conversely, if children are found to develop dissociative identity disorder only after undergoing treatment it would challenge the trauma-related model. As of 2011, approximately 250 cases of dissociative identity disorder in children have been identified, though the data does not offer unequivocal support for either theory. While children have been diagnosed with dissociative identity disorder before therapy, several were presented to clinicians by parents who were themselves diagnosed with dissociative identity disorder; others were influenced by the appearance of dissociative identity disorder in popular culture or due to a diagnosis of psychosis due to hearing voices – a symptom also found in dissociative identity disorder. No studies have looked for children with dissociative identity disorder in the general population, and the single study that attempted to look for children with dissociative identity disorder not already in therapy did so by examining siblings of those already in therapy for dissociative identity disorder. An analysis of diagnosis of children reported in scientific publications, 44 case studies of single patients were found to be evenly distributed (i.e. each case study was reported by a different author) but in articles regarding groups of patients, four researchers were responsible for the majority of the reports.

The initial theoretical description of dissociative identity disorder was that dissociative symptoms were a means of coping with extreme stress (particularly childhood sexual and physical abuse), but this belief has been challenged by the data of multiple research studies. Proponents of the trauma-related model claim the high correlation of child sexual and physical abuse reported by adults with dissociative identity disorder corroborates the link between trauma and dissociative identity disorder. However, the link between dissociative identity disorder and maltreatment has been questioned for several reasons. The studies reporting the links often rely on self-report rather than independent corroborations, and these results may be worsened by selection and referral bias. Most studies of trauma and dissociation are cross-sectional rather than longitudinal, which means researchers can not attribute causation, and studies avoiding recall bias have failed to corroborate such a causal link. In addition, studies rarely control for the many disorders comorbid with dissociative identity disorder, or family maladjustment (which is itself highly correlated with dissociative identity disorder). The popular association of dissociative identity disorder with childhood abuse is relatively recent, occurring only after the publication of Sybil in 1973. Most previous examples of “multiples” such as Chris Costner Sizemore, whose life was depicted in the book and film The Three Faces of Eve, disclosed no history of child abuse.

Pathophysiology

Despite research on DID including structural and functional magnetic resonance imaging, positron emission tomography, single-photon emission computed tomography, event-related potential, and electroencephalography, no convergent neuroimaging findings have been identified regarding DID, making it difficult to hypothesize a biological basis for DID. In addition, many of the studies that do exist were performed from an explicitly trauma-based position, and did not consider the possibility of therapy as a cause of DID. There is no research to date regarding the neuroimaging and introduction of false memories in DID patients, though there is evidence of changes in visual parameters and support for amnesia between alters. DID patients also appear to show deficiencies in tests of conscious control of attention and memorisation (which also showed signs of compartmentalisation for implicit memory between alters but no such compartmentalization for verbal memory) and increased and persistent vigilance and startle responses to sound. DID patients may also demonstrate altered neuroanatomy. Experimental tests of memory suggest that patients with DID may have improved memory for certain tasks, which has been used to criticise the hypothesis that DID is a means of forgetting or suppressing memory. Patients also show experimental evidence of being more fantasy-prone, which in turn is related to a tendency to over-report false memories of painful events.

Diagnosis

General

DSM-5 diagnoses DID according to the diagnostic criteria found under code 300.14 (dissociative disorders). DID is often initially misdiagnosed because clinicians receive little training about dissociative disorders or DID, and often use standard diagnostic interviews that do not include questions about trauma, dissociation, or post-traumatic symptoms. This contributes to difficulties diagnosing the disorder, and clinician bias.

DID is rarely diagnosed in children, despite the average age of appearance of the first alter being three years old. The criteria require that an individual be recurrently controlled by two or more discrete identities or personality states, accompanied by memory lapses for important information that is not caused by alcohol, drugs or medications and other medical conditions such as complex partial seizures. In children the symptoms must not be better explained by “imaginary playmates or other fantasy play”. Diagnosis is normally performed by a clinically trained mental health professional such as a psychiatrist or psychologist through clinical evaluation, interviews with family and friends, and consideration of other ancillary material. Specially designed interviews (such as the SCID-D) and personality assessment tools may be used in the evaluation as well. Since most of the symptoms depend on self-report and are not concrete and observable, there is a degree of subjectivity in making the diagnosis. People are often disinclined to seek treatment, especially since their symptoms may not be taken seriously; thus dissociative disorders have been referred to as “diseases of hiddenness”.

The diagnosis has been criticized by supporters of therapy as a cause or the sociocognitive hypothesis as they believe it is a culture-bound and often health care induced condition. The social cues involved in diagnosis may be instrumental in shaping patient behaviour or attribution, such that symptoms within one context may be linked to DID, while in another time or place the diagnosis could have been something other than DID. Other researchers disagree and argue that the existence of the condition and its inclusion in the DSM is supported by multiple lines of reliable evidence, with diagnostic criteria allowing it to be clearly discriminated from conditions it is often mistaken for (schizophrenia, borderline personality disorder, and seizure disorder). That a large proportion of cases are diagnosed by specific health care providers, and that symptoms have been created in nonclinical research subjects given appropriate cueing has been suggested as evidence that a small number of clinicians who specialise in DID are responsible for the creation of alters through therapy. The condition may be under-diagnosed due to scepticism and lack of awareness from mental health professionals, made difficult due to the lack of specific and reliable criteria for diagnosing DID as well as a lack of prevalence rates due to the failure to examine systematically selected and representative populations.

Differential Diagnoses

People with DID are diagnosed with five to seven comorbid disorders on average – much higher than other mental illnesses.

Due to overlapping symptoms, the differential diagnosis includes schizophrenia, normal and rapid-cycling bipolar disorder, epilepsy, borderline personality disorder, and autism spectrum disorder. Delusions or auditory hallucinations can be mistaken for speech by other personalities. Persistence and consistency of identities and behavior, amnesia, measures of dissociation or hypnotisability and reports from family members or other associates indicating a history of such changes can help distinguish DID from other conditions. A diagnosis of DID takes precedence over any other dissociative disorders. Distinguishing DID from malingering is a concern when financial or legal gains are an issue, and factitious disorder may also be considered if the person has a history of help or attention-seeking. Individuals who state that their symptoms are due to external spirits or entities entering their bodies are generally diagnosed with dissociative disorder not otherwise specified rather than DID due to the lack of identities or personality states. Most individuals who enter an emergency department and are unaware of their names are generally in a psychotic state. Although auditory hallucinations are common in DID, complex visual hallucinations may also occur. Those with DID generally have adequate reality testing; they may have positive Schneiderian symptoms of schizophrenia but lack the negative symptoms. They perceive any voices heard as coming from inside their heads (patients with schizophrenia experience them as external). In addition, individuals with psychosis are much less susceptible to hypnosis than those with DID. Difficulties in differential diagnosis are increased in children.

DID must be distinguished from, or determined if comorbid with, a variety of disorders including mood disorders, psychosis, anxiety disorders, PTSD, personality disorders, cognitive disorders, neurological disorders, epilepsy, somatoform disorder, factitious disorder, malingering, other dissociative disorders, and trance states. An additional aspect of the controversy of diagnosis is that there are many forms of dissociation and memory lapses, which can be common in both stressful and non-stressful situations and can be attributed to much less controversial diagnoses. Individuals faking or mimicking DID due to factitious disorder will typically exaggerate symptoms (particularly when observed), lie, blame bad behaviour on symptoms and often show little distress regarding their apparent diagnosis. In contrast, genuine people with DID typically exhibit confusion, distress, and shame regarding their symptoms and history.

A relationship between DID and borderline personality disorder has been posited, with various clinicians noting overlap between symptoms and behaviours and it has been suggested that some cases of DID may arise “from a substrate of borderline traits”. Reviews of DID patients and their medical records concluded that the majority of those diagnosed with DID would also meet the criteria for either borderline personality disorder or more generally borderline personality.

The DSM-5 elaborates on cultural background as an influence for some presentations of DID:

Many features of dissociative identity disorder can be influenced by the individual’s cultural background. Individuals with this disorder may present with prominent medically unexplained neurological symptoms, such as non-epileptic seizures, paralyses, or sensory loss, in cultural settings where such symptoms are common. Similarly, in settings where normative possession is common (e.g., rural areas in the developing world, among certain religious groups in the United States and Europe), the fragmented identities may take the form of possessing spirits, deities, demons, animals, or mythical figures. Acculturation or prolonged intercultural contact may shape the characteristics of other identities (e.g., identities in India may speak English exclusively and wear Western clothes). Possession-form dissociative identity disorder can be distinguished from culturally accepted possession states in that the former is involuntary, distressing, uncontrollable, and often recurrent or persistent; involves conflict between the individual and his or her surrounding family, social, or work milieu; and is manifested at times and in places that violate the norms of the culture or religion.

Controversy

DID is among the most controversial of the dissociative disorders and among the most controversial disorders found in the DSM-5. The primary dispute is between those who believe DID is caused by traumatic stresses forcing the mind to split into multiple identities, each with a separate set of memories, and the belief that the symptoms of DID are produced artificially by certain psychotherapeutic practices or patients playing a role they believe appropriate for a person with DID. The debate between the two positions is characterized by intense disagreement. Research into this hypothesis has been characterized by poor methodology. Psychiatrist Joel Paris notes that the idea that a personality is capable of splitting into independent alters is an unproven assertion that is at odds with research in cognitive psychology.

Some people, such as Russell A. Powell and Travis L. Gee, believe that DID is caused by health care, i.e. symptoms of DID are created by therapists themselves via hypnosis. This belief also implies that those with DID are more susceptible to manipulation by hypnosis and suggestion than others. The iatrogenic model also sometimes states that treatment for DID is harmful. According to Brand, Loewenstein, and Spiegel, “[t]he claims that DID treatment is harmful are based on anecdotal cases, opinion pieces, reports of damage that are not substantiated in the scientific literature, misrepresentations of the data, and misunderstandings about DID treatment and the phenomenology of DID”. Their claim is evidenced by the fact that only 5%–10% of people receiving treatment worsen in their symptoms.

Psychiatrists August Piper and Harold Merskey have challenged the trauma hypothesis, arguing that correlation does not imply causation – the fact that people with DID report childhood trauma does not mean trauma causes DID – and point to the rareness of the diagnosis before 1980 as well as a failure to find DID as an outcome in longitudinal studies of traumatised children. They assert that DID cannot be accurately diagnosed because of vague and unclear diagnostic criteria in the DSM and undefined concepts such as “personality state” and “identities”, and question the evidence for childhood abuse beyond self-reports, the lack of definition of what would indicate a threshold of abuse sufficient to induce DID and the extremely small number of cases of children diagnosed with DID despite an average age of appearance of the first alter of three years. Psychiatrist Colin Ross disagrees with Piper and Merskey’s conclusion that DID cannot be accurately diagnosed, pointing to internal consistency between different structured dissociative disorder interviews (including the Dissociative Experiences Scale, Dissociative Disorders Interview Schedule and Structured Clinical Interview for Dissociative Disorders) that are in the internal validity range of widely accepted mental illnesses such as schizophrenia and major depressive disorder. In his opinion, Piper and Merskey are setting the standard of proof higher than they are for other diagnoses. He also asserts that Piper and Merskey have cherry-picked data and not incorporated all relevant scientific literature available, such as independent corroborating evidence of trauma.

A study in 2018 revealed that the phenomena of pathological dissociation (including identity alteration) had been portrayed in the ancient Chinese medicine literature, suggesting that pathological dissociation is a cross-cultural condition.

A paper published in 2022 in the journal Comprehensive Psychiatry described how prolonged social media use, especially on video-sharing platforms including TikTok, has exposed young people, largely adolescent females, a core user group of TikTok, to a growing number of content creators making videos about their self-diagnosed disorders.

“An increasing number of reports from the US, UK, Germany, Canada, and Australia have noted an increase in functional tic-like behaviors prior to and during the Covid-19 pandemic, coinciding with an increase in social media content related to[…]dissociative identity disorder.”

The paper concluded by saying there:

“is an urgent need for focused empirical research investigation into this concerning phenomenon that is related to the broader research and discourse examining social media influences on mental health”.

Screening

Perhaps due to their perceived rarity, the dissociative disorders (including DID) were not initially included in the Structured Clinical Interview for DSM-IV (SCID), which is designed to make psychiatric diagnoses more rigorous and reliable. Instead, shortly after the publication of the initial SCID a freestanding protocol for dissociative disorders (SCID-D) was published. This interview takes about 30 to 90 minutes depending on the subject’s experiences. An alternative diagnostic instrument, the Dissociative Disorders Interview Schedule, also exists but the SCID-D is generally considered superior. The Dissociative Disorders Interview Schedule (DDIS) is a highly structured interview that discriminates among various DSM-IV diagnoses. The DDIS can usually be administered in 30–45 minutes.

Other questionnaires include the Dissociative Experiences Scale (DES), Perceptual Alterations Scale, Questionnaire on Experiences of Dissociation, Dissociation Questionnaire, and the Mini-SCIDD. All are strongly intercorrelated and except the Mini-SCIDD, all incorporate absorption, a normal part of personality involving narrowing or broadening of attention. The DES is a simple, quick, and validated questionnaire that has been widely used to screen for dissociative symptoms, with variations for children and adolescents. Tests such as the DES provide a quick method of screening subjects so that the more time-consuming structured clinical interview can be used in the group with high DES scores. Depending on where the cut-off is set, people who would subsequently be diagnosed can be missed. An early recommended cut-off was 15-20. The reliability of the DES in non-clinical samples has been questioned.

Treatment

Treatment aims to increase integrated functioning. The International Society for the Study of Trauma and Dissociation has published guidelines for phase-oriented treatment in adults as well as children and adolescents that are widely used in the field of DID treatment. The guidelines state that “a desirable treatment outcome is a workable form of integration or harmony among alternate identities”. Some experts in treating people with DID use the techniques recommended in the 2011 treatment guidelines. The empirical research includes the longitudinal TOP DD treatment study, which found that patients showed “statistically significant reductions in dissociation, PTSD, distress, depression, hospitalisations, suicide attempts, self-harm, dangerous behaviours, drug use, and physical pain” and improved overall functioning. Treatment effects have been studied for over thirty years, with some studies having a follow-up of ten years. Adult and child treatment guidelines exist that suggest a three-phased approach, and are based on expert consensus. Highly experienced therapists have few patients that achieve a unified identity.

Common treatment methods include an eclectic mix of psychotherapy techniques, including cognitive behavioural therapy (CBT), insight-oriented therapy, dialectical behavioural therapy (DBT), hypnotherapy, and eye movement desensitisation and reprocessing (EMDR).

Hypnosis should be carefully considered when choosing both treatment and provider practitioners because of its dangers. For example, hypnosis can sometimes lead to false memories and false accusations of abuse by family, loved ones, friends, providers, and community members. Those who suffer from dissociative identity disorder have commonly been subject to actual abuse (sexual, physical, emotional, financial) by therapists, family, friends, loved ones, and community members.

Some behaviour therapists initially use behavioural treatments such as only responding to a single identity, and then use more traditional therapy once a consistent response is established. Brief treatment due to managed care may be difficult, as individuals diagnosed with DID may have unusual difficulties in trusting a therapist and take a prolonged period to form a comfortable therapeutic alliance. Regular contact (at least weekly) is recommended, and treatment generally lasts years – not weeks or months. Sleep hygiene has been suggested as a treatment option, but has not been tested. In general there are very few clinical trials on the treatment of DID, none of which were randomised controlled trials.

Therapy for DID is generally phase oriented. Different alters may appear based on their greater ability to deal with specific situational stresses or threats. While some patients may initially present with a large number of alters, this number may reduce during treatment – though it is considered important for the therapist to become familiar with at least the more prominent personality states as the “host” personality may not be the “true” identity of the patient. Specific alters may react negatively to therapy, fearing the therapist’s goal is to eliminate the alter (particularly those associated with illegal or violent activities). A more realistic and appropriate goal of treatment is to integrate adaptive responses to abuse, injury, or other threats into the overall personality structure. There is debate over issues such as whether exposure therapy (reliving traumatic memories, also known as abreaction), engagement with alters and physical contact during therapy are appropriate and there are clinical opinions both for and against each option with little high-quality evidence for any position.

Brandt et al., commenting on the lack of empirical studies of treatment effectiveness, conducted a survey of 36 clinicians expert in treating dissociative disorder (DD) who recommended a three-stage treatment. They agreed that skill building in the first stage is important so the patient can learn to handle high risk, potentially dangerous behaviour, as well as emotional regulation, interpersonal effectiveness and other practical behaviours. In addition, they recommended “trauma-based cognitive therapy” to reduce cognitive distortions related to trauma; they also recommended that the therapist deal with the dissociated identities early in treatment. In the middle stage, they recommended graded exposure techniques, along with appropriate interventions as needed. The treatment in the last stage was more individualized; few with DD [sic] became integrated into one identity.

The first phase of therapy focuses on symptoms and relieving the distressing aspects of the condition, ensuring the safety of the individual, improving the patient’s capacity to form and maintain healthy relationships, and improving general daily life functioning. Comorbid disorders such as substance use disorder and eating disorders are addressed in this phase of treatment. The second phase focuses on stepwise exposure to traumatic memories and prevention of re-dissociation. The final phase focuses on reconnecting the identities of disparate alters into a single functioning identity with all its memories and experiences intact.

A study was conducted to develop an “expertise-based prognostic model for the treatment of complex post-traumatic stress disorder (PTSD) and dissociative identity disorder (DID)”. Researchers constructed a two-stage survey and factor analyses performed on the survey elements found 51 factors common to complex PTSD and DID. The authors concluded from their findings:

“The model is supportive of the current phase-oriented treatment model, emphasizing the strengthening of the therapeutic relationship and the patient’s resources in the initial stabilization phase. Further research is needed to test the model’s statistical and clinical validity.”

Prognosis

Little is known about prognosis of untreated DID. It rarely, if ever, goes away without treatment, but symptoms may resolve from time to time or wax and wane spontaneously. Patients with mainly dissociative and post-traumatic symptoms face a better prognosis than those with comorbid disorders or those still in contact with abusers, and the latter groups often face lengthier and more difficult treatment. Suicidal ideation, suicide attempts, and self-harm also may occur. Duration of treatment can vary depending on patient goals, which can range from merely improving inter-alter communication and cooperation, to reducing inter-alter amnesia, to integration of all alters, but generally takes years.

Epidemiology

General

According to the American Psychiatric Association, the 12-month prevalence of DID among adults in the US is 1.5%, with similar prevalence between women and men. Population prevalence estimates have been described to widely vary, with some estimates of DID in inpatient settings suggesting 1-9.6%.” Reported rates in the community vary from 1% to 3% with higher rates among psychiatric patients. As of 2017, evidence suggested a prevalence of DID of 2–5% among psychiatric inpatients, 2–3% among outpatients, and 1% in the general population, with rates reported as high as 16.4% for teenagers in psychiatric outpatient services. Dissociative disorders in general have a prevalence of 12.0%–13.8% for psychiatric outpatients.

As of 2012, DID was diagnosed 5 to 9 times more common in women than men during young adulthood, although this may have been due to selection bias as men meeting DID diagnostic criteria were suspected to end up in the criminal justice system rather than hospitals. In children, rates among men and women are approximately the same (5:4). DID diagnoses are extremely rare in children; much of the research on childhood DID occurred in the 1980s and 1990s and does not address ongoing controversies surrounding the diagnosis. DID occurs more commonly in young adults and declines in prevalence with age.

There is a poor awareness of DID in the clinical settings and the general public. Poor clinical education (or lack thereof) for DID and other dissociative disorders has been described in literature: “most clinicians have been taught (or assume) that DID is a rare disorder with a florid, dramatic presentation.” Symptoms in patients are often not easily visible, which complicates diagnosis. DID has a high correlation with, and has been described as a form of, complex post-traumatic stress disorder. There is a significant overlap of symptoms between borderline personality disorder and DID, although symptoms are understood to originate from different underlying causes.

Historical Prevalence

Rates of diagnosed DID were increasing in the late 20th century, reaching a peak of diagnoses at approximately 40,000 cases by the end of the 20th century, up from less than 200 diagnoses before 1970. Initially DID along with the rest of the dissociative disorders were considered the rarest of psychological conditions, diagnosed in less than 100 by 1944, with only one further case reported in the next two decades. In the late 1970s and ’80s, the number of diagnoses rose sharply. An estimate from the 1980s placed the incidence at 0.01%. Accompanying this rise was an increase in the number of alters, rising from only the primary and one alter personality in most cases, to an average of 13 in the mid-1980s (the increase in both number of cases and number of alters within each case are both factors in professional scepticism regarding the diagnosis). Others explain the increase as being due to the use of inappropriate therapeutic techniques in highly suggestible individuals, though this is itself controversial while proponents of DID claim the increase in incidence is due to increased recognition of and ability to recognize the disorder. Figures from psychiatric populations (inpatients and outpatients) show a wide diversity from different countries.

A 1996 essay suggested three possible causes for the sudden increase of DID diagnoses, among which the author suspects the first being most likely:

  • The result of therapist suggestions to suggestible people, much as Charcot’s hysterics acted in accordance with his expectations.
  • Psychiatrists’ past failure to recognise dissociation being redressed by new training and knowledge.
  • Dissociative phenomena are actually increasing, but this increase only represents a new form of an old and protean entity: “hysteria”.

Dissociative disorders were excluded from the Epidemiological Catchment Area Project.

North America

DID is considered a controversial diagnosis and condition, with much of the literature on DID still being generated and published in North America, to the extent that it was once regarded as a phenomenon confined to that continent. Although research has appeared discussing the appearance of DID in other countries and cultures and the condition has been described in non-English speaking nations and non-Western cultures, these reports all occur in English-language journals authored by international researchers who cite Western scientific literature and are therefore not isolated from Western influences. Etzel Cardeña and David Gleaves believed the overrepresentation of DID in North America was the result of increased awareness and training about the condition.

Brief History

Early References

In the 19th century, “dédoublement”, or “double consciousness”, the historical precursor to DID, was frequently described as a state of sleepwalking, with scholars hypothesizing that the patients were switching between a normal consciousness and a “somnambulistic state”.

An intense interest in spiritualism, parapsychology and hypnosis continued throughout the 19th and early 20th centuries, running in parallel with John Locke’s views that there was an association of ideas requiring the coexistence of feelings with awareness of the feelings. Hypnosis, which was pioneered in the late 18th century by Franz Mesmer and Armand-Marie Jacques de Chastenet, Marques de Puységur, challenged Locke’s association of ideas. Hypnotists reported what they thought were second personalities emerging during hypnosis and wondered how two minds could coexist.

In the 19th century, there were a number of reported cases of multiple personalities which Rieber estimated would be close to 100. Epilepsy was seen as a factor in some cases, and discussion of this connection continues into the present era.

By the late 19th century, there was a general acceptance that emotionally traumatic experiences could cause long-term disorders which might display a variety of symptoms. These conversion disorders were found to occur in even the most resilient individuals, but with profound effect in someone with emotional instability like Louis Vivet (1863–?), who had a traumatic experience as a 17-year-old when he encountered a viper. Vivet was the subject of countless medical papers and became the most studied case of dissociation in the 19th century.

Between 1880 and 1920, various international medical conferences devoted time to sessions on dissociation. It was in this climate that Jean-Martin Charcot introduced his ideas of the impact of nervous shocks as a cause for a variety of neurological conditions. One of Charcot’s students, Pierre Janet, took these ideas and went on to develop his own theories of dissociation. One of the first individuals diagnosed with multiple personalities to be scientifically studied was Clara Norton Fowler, under the pseudonym Christine Beauchamp; American neurologist Morton Prince studied Fowler between 1898 and 1904, describing her case study in his 1906 monograph, Dissociation of a Personality.

20th Century

In the early 20th century, interest in dissociation and multiple personalities waned for several reasons. After Charcot’s death in 1893, many of his so-called hysterical patients were exposed as frauds, and Janet’s association with Charcot tarnished his theories of dissociation. Sigmund Freud recanted his earlier emphasis on dissociation and childhood trauma.

In 1908, Eugen Bleuler introduced the term “schizophrenia” to represent a revised disease concept for Emil Kraepelin’s dementia praecox. Whereas Kraepelin’s natural disease entity was anchored in the metaphor of progressive deterioration and mental weakness and defect, Bleuler offered a reinterpretation based on dissociation or “splitting” (Spaltung) and widely broadened the inclusion criteria for the diagnosis. A review of the Index medicus from 1903 through 1978 showed a dramatic decline in the number of reports of multiple personality after the diagnosis of schizophrenia became popular, especially in the United States. The rise of the broad diagnostic category of dementia praecox has also been posited in the disappearance of “hysteria” (the usual diagnostic designation for cases of multiple personalities) by 1910. A number of factors helped create a large climate of scepticism and disbelief; paralleling the increased suspicion of DID was the decline of interest in dissociation as a laboratory and clinical phenomenon.

Starting in about 1927, there was a large increase in the number of reported cases of schizophrenia, which was matched by an equally large decrease in the number of multiple personality reports. With the rise of a uniquely American reframing of dementia praecox/schizophrenia as a functional disorder or “reaction” to psychobiological stressors – a theory first put forth by Adolf Meyer in 1906—many trauma-induced conditions associated with dissociation, including “shell shock” or “war neuroses” during World War I, were subsumed under these diagnoses. It was argued in the 1980s that DID patients were often misdiagnosed with schizophrenia.

The public, however, was exposed to psychological ideas which took their interest. Mary Shelley’s Frankenstein, Robert Louis Stevenson’s Strange Case of Dr Jekyll and Mr Hyde, and many short stories by Edgar Allan Poe had a formidable impact.

The Three Faces of Eve

In 1957, with the publication of the bestselling book The Three Faces of Eve by psychiatrists Corbett H. Thigpen and Hervey M. Cleckley, based on a case study of their patient Chris Costner Sizemore, and the subsequent popular movie of the same name, the American public’s interest in multiple personality was revived. More cases of dissociative identity disorder were diagnosed in the following years. The cause of the sudden increase of cases is indefinite, but it may be attributed to the increased awareness, which revealed previously undiagnosed cases or new cases may have been induced by the influence of the media on the behaviour of individuals and the judgement of therapists. During the 1970s an initially small number of clinicians campaigned to have it considered a legitimate diagnosis.

History in the DSM

The DSM-II used the term hysterical neurosis, dissociative type. It described the possible occurrence of alterations in the patient’s state of consciousness or identity, and included the symptoms of “amnesia, somnambulism, fugue, and multiple personality”. The DSM-III grouped the diagnosis with the other four major dissociative disorders using the term “multiple personality disorder”. The DSM-IV made more changes to DID than any other dissociative disorder, and renamed it DID. The name was changed for two reasons: First, the change emphasizes the main problem is not a multitude of personalities, but rather a lack of a single, unified identity and an emphasis on “the identities as centers of information processing”. Second, the term “personality” is used to refer to “characteristic patterns of thoughts, feelings, moods, and behaviors of the whole individual”, while for a patient with DID, the switches between identities and behaviour patterns is the personality. It is, for this reason, the DSM-IV-TR referred to “distinct identities or personality states” instead of personalities. The diagnostic criteria also changed to indicate that while the patient may name and personalise alters, they lack independent, objective existence. The changes also included the addition of amnesia as a symptom, which was not included in the DSM-III-R because despite being a core symptom of the condition, patients may experience “amnesia for the amnesia” and fail to report it. Amnesia was replaced when it became clear that the risk of false negative diagnoses was low because amnesia was central to DID.

The ICD-10 places the diagnosis in the category of “dissociative disorders”, within the subcategory of “other dissociative (conversion) disorders”, but continues to list the condition as multiple personality disorder.

The DSM-IV-TR criteria for DID have been criticised for failing to capture the clinical complexity of DID, lacking usefulness in diagnosing individuals with DID (for instance, by focusing on the two least frequent and most subtle symptoms of DID) producing a high rate of false negatives and an excessive number of DDNOS diagnoses, for excluding possession (seen as a cross-cultural form of DID), and for including only two “core” symptoms of DID (amnesia and self-alteration) while failing to discuss hallucinations, trance-like states, somatoform, depersonalisation, and derealisation symptoms. Arguments have been made for allowing diagnosis through the presence of some, but not all of the characteristics of DID rather than the current exclusive focus on the two least common and noticeable features. The DSM-IV-TR criteria have also been criticised] for being tautological, using imprecise and undefined language and for the use of instruments that give a false sense of validity and empirical certainty to the diagnosis.

The DSM-5 updated the definition of DID in 2013, summarizing the changes as:

Several changes to the criteria for dissociative identity disorder have been made in DSM-5. First, Criterion A has been expanded to include certain possession-form phenomena and functional neurological symptoms to account for more diverse presentations of the disorder. Second, Criterion A now specifically states that transitions in identity may be observable by others or self-reported. Third, according to Criterion B, individuals with dissociative identity disorder may have recurrent gaps in recall for everyday events, not just for traumatic experiences. Other text modifications clarify the nature and course of identity disruptions.

Between 1968 and 1980, the term that was used for dissociative identity disorder was “Hysterical neurosis, dissociative type”. The APA wrote in the second edition of the DSM: “In the dissociative type, alterations may occur in the patient’s state of consciousness or in his identity, to produce such symptoms as amnesia, somnambulism, fugue, and multiple personality.” The number of cases sharply increased in the late 1970s and throughout the 80s, and the first scholarly monographs on the topic appeared in 1986.

Book and Film Sybil

In 1974, the highly influential book Sybil was published, and later made into a miniseries in 1976 and again in 2007. Describing what Robert Rieber called “the third most famous of multiple personality cases,” it presented a detailed discussion of the problems of treatment of “Sybil Isabel Dorsett”, a pseudonym for Shirley Ardell Mason.

Though the book and subsequent films helped popularize the diagnosis and trigger an epidemic of the diagnosis, later analysis of the case suggested different interpretations, ranging from Mason’s problems having been caused by the therapeutic methods and sodium pentathol injections used by her psychiatrist, C.B. Wilbur, or an inadvertent hoax due in part to the lucrative publishing rights, though this conclusion has itself been challenged.

David Spiegel, a Stanford psychiatrist whose father treated Shirley Ardell Mason on occasion, says that his father described Mason as “a brilliant hysteric. He felt that Wilbur tended to pressure her to exaggerate on the dissociation she already had.” As media attention on DID increased, so too did the controversy surrounding the diagnosis.

Re-Classifications

With the publication of the DSM-III, which omitted the terms “hysteria” and “neurosis” (and thus the former categories for dissociative disorders). There was no category eliminated, it was renamed to Anxiety disorders. The DSM-III also created the controversial PTSD diagnosis -controversial due to Vietnam vets.}} dissociative diagnoses became “orphans” with their own categories with dissociative identity disorder appearing as “multiple personality disorder”.

In the opinion of McGill University psychiatrist Joel Paris, this inadvertently legitimized them by forcing textbooks, which mimicked the structure of the DSM, to include a separate chapter on them and resulted in an increase in diagnosis of dissociative conditions. Once a rarely occurring spontaneous phenomenon (research in 1944 showed only 76 cases), the diagnosis became “an artifact of bad (or naïve) psychotherapy” as patients capable of dissociating were accidentally encouraged to express their symptoms by “overly fascinated” therapists.

In a 1986 book chapter (later reprinted in another volume), philosopher of science Ian Hacking focused on multiple personality disorder as an example of “making up people” through the untoward effects on individuals of the “dynamic nominalism” in medicine and psychiatry. With the invention of new terms, entire new categories of “natural kinds” of people are assumed to be created, and those thus diagnosed respond by re-creating their identity in light of the new cultural, medical, scientific, political and moral expectations. Hacking argued that the process of “making up people” is historically contingent, hence it is not surprising to find the rise, fall, and resurrection of such categories over time. Hacking revisited his concept of “making up people” in a 2006.

“Interpersonality amnesia” was removed as a diagnostic feature from the DSM III in 1987, which may have contributed to the increasing frequency of the diagnosis. There were 200 reported cases of DID as of 1980, and 20,000 from 1980 to 1990. Joan Acocella reports that 40,000 cases were diagnosed from 1985 to 1995. Scientific publications regarding DID peaked in the mid-1990s then rapidly declined.

There were several contributing factors to the rapid decline of reports of multiple personality disorder/dissociative identity disorder. One was the discontinuation in December 1997 of Dissociation: Progress in the Dissociative Disorders, the journal of The International Society for the Study of Multiple Personality and Dissociation.[151] The society and its journal were perceived as uncritical sources of legitimacy for the extraordinary claims of the existence of intergenerational satanic cults responsible for a “hidden holocaust” of Satanic ritual abuse that was linked to the rise of MPD reports. In an effort to distance itself from the increasing scepticism regarding the clinical validity of MPD, the organisation dropped “multiple personality” from its official name in 1993, and then in 1997 changed its name again to the International Society for the Study of Trauma and Dissociation.

In 1994, the fourth edition of the DSM replaced the criteria again and changed the name of the condition from “multiple personality disorder” to the current “dissociative identity disorder” to emphasize the importance of changes to consciousness and identity rather than personality. The inclusion of interpersonality amnesia helped to distinguish DID from dissociative disorder not otherwise specified (DDNOS), but the condition retains an inherent subjectivity due to difficulty in defining terms such as personality, identity, ego-state, and even amnesia. The ICD-10 classified DID as a “Dissociative [conversion] disorder” and used the name “multiple personality disorder” with the classification number of F44.81. In the ICD-11, the World Health Organisation have classified DID under the name “dissociative identity disorder” (code 6B64), and most cases formerly diagnosed as DDNOS are classified as “partial dissociative identity disorder” (code 6B65).

21st Century

A 2006 study compared scholarly research and publications on DID and dissociative amnesia to other mental health conditions, such as anorexia nervosa, alcohol use disorder, and schizophrenia from 1984 to 2003. The results were found to be unusually distributed, with a very low level of publications in the 1980s followed by a significant rise that peaked in the mid-1990s and subsequently rapidly declined in the decade following. Compared to 25 other diagnosis, the mid-1990s “bubble” of publications regarding DID was unique. In the opinion of the authors of the review, the publication results suggest a period of “fashion” that waned, and that the two diagnoses “[did] not command widespread scientific acceptance.”

Society and Culture

General

The public’s long fascination with DID has led to a number of different books and films, with many representations described as increasing stigma by perpetuating the myth that people with mental illness are usually dangerous. Movies about DID have been also criticised for poor representation of both DID and its treatment, including “greatly overrepresenting” the role of hypnosis in therapy, showing a significantly smaller number of personalities than many people with DID have, and misrepresenting people with DID as having flamboyant and obvious personalities. Some movies are parodies and ridicule DID, for instance, Me, Myself & Irene, which also incorrectly states that DID is schizophrenia. In some stories DID is used as a plot device, e.g. in Fight Club, and in whodunnit stories like Secret Window.

United States of Tara was reported to be the first US television series with DID as its focus, and a professional commentary on each episode was published by the International Society for the Study of Trauma and Dissociation. More recently, the award winning Korean TV series Kill Me, Heal Me (Korean: 킬미, 힐미; RR: Kilmi, Hilmi) featured a wealthy young man with seven identities, one of whom falls in love with the beautiful psychiatry resident who tries to help him.

In a Dissociative Identity Disorder documentary by A&E named, Many Sides Of Jane, it follows a young mom struggling to be a single mom with Dissociative Identity Disorder. Jane wants to bring awareness to the disorder.

Most people with DID are believed to downplay or minimise their symptoms rather than seeking fame, often due to shame or fear of the effects of stigma. Therapists may discourage people with DID from media work due to concerns that they may feel exploited or traumatised, for example as a result of demonstrating switching between personality states to entertain others.

However, a number of people with DID have publicly spoken about their experiences, including comedian and talk show host Roseanne Barr, who interviewed Truddi Chase, author of When Rabbit Howls; Chris Costner Sizemore, the subject of The Three Faces of Eve, Cameron West, author of First Person Plural: My life as a multiple, and NFL player Herschel Walker, author of Breaking Free: My life with dissociative identity disorder.

In The Three Faces of Eve (1957) hypnosis is used to identify a childhood trauma which then allows her to fuse from three identities into just one. However, Sizemore’s own books I’m Eve and A Mind of My Own revealed that this did not last; she later attempted suicide, sought further treatment, and actually had twenty-two personalities rather than three. Sizemore re-entered therapy and by 1974 had achieved a lasting recovery. Voices Within: The Lives of Truddi Chase portrays many of the 92 personalities Chase described in her book When Rabbit Howls, and is unusual in breaking away from the typical ending of integrating into one. Frankie & Alice (2010), starring Halle Berry; and the TV mini-series Sybil were also based on real people with DID. In popular culture dissociative identity disorder is often confused with schizophrenia, and some movies advertised as representing dissociative identity disorder may be more representative of psychosis or schizophrenia, for example Psycho (1960).

In his book The C.I.A. Doctors: Human Rights Violations by American Psychiatrists, psychiatrist Colin A. Ross states that based on documents obtained through freedom of information legislation, a psychiatrist linked to Project MKULTRA reported being able to deliberately induce dissociative identity disorder using a variety of aversive or abusive techniques, creating a Manchurian Candidate for military purposes.

A DID community exists on social media, including YouTube, Reddit, Discord, and TikTok. However, numerous high-profile members of this community have been criticised for faking their condition for views, or for portraying the disorder lightheartedly. Conversely, psychologist Naomi Torres-Mackie, head of research at The Mental Health Coalition, has stated “All of a sudden, all of my adolescent patients think that they have this, and they don’t … Folks start attaching clinical meaning and feeling like, ‘I should be diagnosed with this. I need medication for this’, when actually a lot of these experiences are normative and don’t need to be pathologized or treated.”

In the USA Network television production Mr. Robot, the protagonist Elliot Alderson was created using anecdotal experiences of DID of the show’s creator’s friends. Sam Esmail said he consulted with a psychologist who “concretized” the character’s mental health conditions, especially his plurality.

In M. Night Shyamalan’s Unbreakable superhero film series (specifically the films, Split and Glass), one character is diagnosed with DID, and that some of the personalities have super-human powers. Some advocates believe that the films are a negative portrayal and promote the stigmatization of the disorder.

Bollywood thriller Bhool Bhulaiyaa (2007) featured Vidya Balan as Avni, an individual diagnosed with DID who associated herself with Manjulika, a deceased dancer in a royal palace. Although the movie was criticised for being insensitive, it was also lauded for spreading awareness about DID and contributing towards removing stigma around mental health.

In Marvel Comics, the character of Moon Knight is shown to have DID. In the TV series Moon Knight based on the comic book character, protagonist Marc Spector is depicted with DID; the website for the National Alliance on Mental Illness appears in the series’ end credits. Another Marvel character, Legion, has DID in the comics, although he has schizophrenia in the TV show version.

Legal Issues

People with dissociative identity disorder may be involved in legal cases as a witness, defendant, or as the victim/injured party. Claims of DID have been used only rarely to argue criminal insanity in court. In the United States dissociative identity disorder has previously been found to meet the Frye test as a generally accepted medical condition, and the newer Daubert standard. Within legal circles, DID has been described as one of the most disputed psychiatric diagnoses and forensic assessments are needed. For defendants whose defence states they have a diagnosis of DID, courts must distinguish between those who genuinely have DID and those who are malingering to avoid responsibility. Expert witnesses are typically used to assess defendants in such cases, although some of the standard assessments like the MMPI-2 were not developed for people with a trauma history and the validity scales may incorrectly suggest malingering. The Multiscale Dissociation Inventory (Briere, 2002) is well suited to assessing malingering and dissociative disorders, unlike the self-report Dissociative Experiences Scale. In DID, evidence about the altered states of consciousness, actions of alter identities and episodes of amnesia may be excluded from a court if they not considered relevant, although different countries and regions have different laws. A diagnosis of DID may be used to claim a defence of not guilty by reason of insanity, but this very rarely succeeds, or of diminished capacity, which may reduce the length of a sentence. DID may also affect competency to stand trial. A not guilty by reason of insanity plea was first used successfully in an American court in 1978, in the State of Ohio v. Milligan case. However, a DID diagnosis is not automatically considered a justification for an insanity verdict, and since Milligan the few cases claiming insanity have largely been unsuccessful.

Advocacy Movement

In the context of neurodiversity, the experience of dissociative identities has been called multiplicity and has led to advocacy for the recognition of ‘positive plurality’ and the use of plural pronouns such as “we” and “our”. Liz Fong-Jones states those with this condition might have fear in regard to “coming out” about their DID, as it could put them in a vulnerable position.

In particular, advocates have challenged the necessity of integration. Timothy Baynes argues that alters have full moral status, just as their host does. He states that as integration may entail the (involuntary) elimination of such an entity, forcing people to undergo it as a therapeutic treatment is “seriously immoral”.

A DID (or Dissociative Identities) Awareness Day takes place on 05 March annually, and a multicoloured awareness ribbon is used, based on the idea of a “crazy quilt”.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Dissociative_identity_disorder >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Culture-Bound Syndrome?

Introduction

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.

Identification

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.

Medical Perspectives

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

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.

DSM-IV-TR List

The fourth edition of Diagnostic and Statistical Manual of Mental Disorders classifies the below syndromes as culture-bound syndromes.

NameGeographical Localisation/Population(s)
Running AmokBrunei, Singapore, Malaysia, Indonesia, Philippines, Timor-Leste
Ataque de NerviosHispanophone, as well as in the Philippines where it is known as “nervous breakdown”
Bilis, CóleraLatinos
Bouffée DéliranteFrance and French-speaking countries
Brain Fag SyndromeWest African students
Dhat SyndromeIndia
Falling-Out, Blacking OutSouthern United States and Caribbean
Ghost SicknessNative American (Navajo, Muscogee/Creek)
HwabyeongKorean
KoroChinese, Malaysian and Indonesian populations in Southeast Asia; Assam; occasionally in the West
LatahMalaysia and Indonesia, as well as the Philippines (as mali-mali, particularly among Tagalogs)
LocuraLatinos in the United States and Latin America
Mal de PeleaPuerto Rico
NerviosLatin America, Latinos in the United States, Philippines
Evil EyeMediterranean; Hispanic populations and Ethiopia
PibloktoArctic and subarctic Inuit populations
Zou huo ru mo
(Qigong Psychotic Reaction)
Han Chinese
RootworkSouthern United States, Caribbean nations
Sangue DormidoPortuguese populations in Cape Verde
Shenjing ShuairuoHan Chinese
Shenkui, shen-kʼueiHan Chinese
ShinbyeongKorean
SpellAfrican American, White populations in the southern United States and Ethiopia
SustoLatinos in the United States; Mexico, Central America and South America
Taijin KyofushoJapanese
ZārEthiopia, Somalia, Egypt, Sudan, Iran, and other North African and Middle Eastern societies

DSM-5 List

The fifth edition of Diagnostic and Statistical Manual of Mental Disorders classifies the below syndromes as cultural concepts of distress, a closely related concept.

NameGeographical Localisation/Population(s)
Ataque de NerviosHispanophone, as well as in the Philippines
Dhat SyndromeIndia
Khyâl CapCambodian
Ghost SicknessNative American
KufungisisaZimbabwe
Maladi MounHaiti
NerviosLatin America, Latinos in the US
Shenjing ShuairuoHan Chinese
SustoLatinos in the US, Mexico, Central America and South America
Taijin KyofushoJapanese

ICD-10 List

NameGeographical Localisation/Population(s)
AmokSoutheast Asian Austronesians
Dhat Syndrome (Dhātu), Shen-kʼuei, JiryanIndia and Taiwan
Koro, Suk Yeong, Jinjin BemarSoutheast Asia, India, and China
LatahMalaysia and Indonesia
Nervios, Nerfiza, Nerves, NevraEgypt; Greece; northern Europe; Mexico, Central and South America
Pa-leng (Frigophobia)Taiwan and Southeast Asia
Pibloktoq (Arctic Hysteria)Inuit living within the Arctic Circle
Susto, EspantoMexico, Central and South America
Taijin Kyofusho, Shinkeishitsu (Anthropophobia)Japan
Ufufuyane, SakaKenya, Southern Africa (among Bantu, Zulu, and affiliated groups)
UqamairineqInuit living within the Arctic Circle
Fear of WindigoIndigenous people of Northeast America

Other Examples

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.

Tarantism is an expression of mass psychogenic illness documented in Southern Italy since the 11th century.

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.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Culture-bound_syndrome >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Mass Psychogenic Illness?

Introduction

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.

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.”

Common Symptoms

Timothy F. Jones of the Tennessee Department of Health compiles the following symptoms based on their commonality in outbreaks occurring in 1980-1990:

SymptomPercent Reporting
Headache67
Dizziness or Light-Headedness46
Nausea41
Abdominal Cramps or Pain39
Cough31
Fatigue, Drowsiness or Weakness31
Sore or Burning Throat30
Hyperventilation or Difficulty Breathing19
Watery or Irritated Eyes13
Chest Tightness/Chest Pain12
Inability to Concentrate/Trouble Thinking11
Vomiting10
Tingling, Numbness or Paralysis10
Anxiety or Nervousness8
Diarrhoea7
Trouble with Vision7
Rash4
Loss of Consciousness/Syncope4
Itching3

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.

Research

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.'”

Brief History

Middle Ages

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

Factories

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:

  1. Hysterical seizures of screaming and general violence, wherein tranquilizers were ineffective;
  2. Trance states, where a worker would claim to be speaking under the influence of a spirit or jinn; and
  3. 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.

Schools

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.

Internet

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).

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Mass_psychogenic_illness >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Boredom Boreout Syndrome?

Introduction

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.

Elements

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).

Coping Strategies

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).

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Boreout >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Dissociative Disorder?

Introduction

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 depersonalisationderealisation 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.

The ICD 11 lists dissociative disorders as:

  • Dissociative neurological symptom disorder.
  • Dissociative amnesia.
  • Dissociative amnesia with dissociative fugue.
  • Trance disorder.
  • Possession trance disorder.
  • Dissociative identity disorder.
  • Partial dissociative identity disorder.
  • Depersonalisation-derealisation disorder.

Cause and Treatment

Dissociative Identity Disorder

Cause

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.

Treatment

Long-term psychotherapy to improve the patient’s quality of life.

Dissociative Amnesia

Cause

A way to cope with trauma.

Treatment

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.

Depersonalisation-Derealisation Disorder

Cause

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.

Treatment

Same treatment as dissociative amnesia. An episode of depersonalisationderealisation 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.

Medications

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.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Dissociative_disorder >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Delusional Parasitosis?

Introduction

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.

Classification

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.

Epidemiology

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.

Brief History

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’.”

Morgellons

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.

Cause

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.

Diagnosis

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.

Differential Diagnosis

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.

Treatment

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.

Prognosis

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.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Delusional_parasitosis >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Paraphrenia?

Introduction

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%.

Paraphrenia is not included in the DSM-5; psychiatrists often diagnose patients presenting with paraphrenia as having atypical psychosis, delusional disorder, psychosis not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults. Recently, mental health professionals have also been classifying paraphrenia as very late-onset schizophrenia-like psychosis.

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.

Brief History

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.[4] 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.”[4]

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.

Causes

Neurological

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”.

Predisposing Factors

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.

Diagnosis

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.

  1. A delusional disorder of at least six months duration characterized by the following:
    1. Preoccupation with one or more semi-systematised delusions, often accompanied by auditory hallucinations.
    2. Affect notably well-preserved and appropriate. Ability to maintain rapport with others.
    3. None of:
      1. Intellectual deterioration.
      2. Visual hallucinations.
      3. Incoherence.
      4. Flat or grossly inappropriate affect.
      5. Grossly disorganised behaviour at times other than during the acute episode.
    4. Disturbance of behaviour understandable in relation to the content of the delusions and hallucinations.
    5. Only partly meets criterion A for schizophrenia. No significant organic brain disorder.

Management

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.

Prognosis

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.

Epidemiology

Studies suggest that the prevalence of paraphrenia in the elderly population is around 2-4%.

Sex Differences

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.

Age

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).

Physical Factors

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.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Paraphrenia >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.