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.

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On This Day … 26 July [2022]

Events

  • 1990 – The Americans with Disabilities Act of 1990 is signed into law by President George H.W. Bush.

People (Births)

Americans with Disabilities Act of 1990

The Americans with Disabilities Act of 1990 or ADA (42 U.S.C. § 12101) is a civil rights law that prohibits discrimination based on disability.

It affords similar protections against discrimination to Americans with disabilities as the Civil Rights Act of 1964, which made discrimination based on race, religion, sex, national origin, and other characteristics illegal, and later sexual orientation and gender identity. In addition, unlike the Civil Rights Act, the ADA also requires covered employers to provide reasonable accommodations to employees with disabilities, and imposes accessibility requirements on public accommodations.

In 1986, the National Council on Disability had recommended the enactment of an Americans with Disabilities Act (ADA) and drafted the first version of the bill which was introduced in the House and Senate in 1988. The final version of the bill was signed into law on 26 July 1990, by President George H.W. Bush. It was later amended in 2008 and signed by President George W. Bush with changes effective as of 01 January 2009.

Disabilities Included

ADA disabilities include both mental and physical medical conditions. A condition does not need to be severe or permanent to be a disability. Equal Employment Opportunity Commission regulations provide a list of conditions that should easily be concluded to be disabilities:

Other mental or physical health conditions also may be disabilities, depending on what the individual’s symptoms would be in the absence of “mitigating measures” (medication, therapy, assistive devices, or other means of restoring function), during an “active episode” of the condition (if the condition is episodic).

Certain specific conditions that are widely considered anti-social, or tend to result in illegal activity, such as kleptomania, paedophilia, exhibitionism, voyeurism, etc. are excluded under the definition of “disability” in order to prevent abuse of the statute’s purpose. Additionally, gender identity or orientation is no longer considered a disorder and is also excluded under the definition of “disability”.

Carl Jung

Carl Gustav Jung (26 July 1875 to 06 June 1961) was a Swiss psychiatrist and psychoanalyst who founded analytical psychology. Jung’s work has been influential in the fields of psychiatry, anthropology, archaeology, literature, philosophy, psychology, and religious studies.

Jung worked as a research scientist at the famous Burghölzli hospital, under Eugen Bleuler. During this time, he came to the attention of Sigmund Freud, the founder of psychoanalysis. The two men conducted a lengthy correspondence and collaborated, for a while, on a joint vision of human psychology.

Freud saw the younger Jung as the heir he had been seeking to take forward his “new science” of psychoanalysis and to this end secured his appointment as president of his newly founded International Psychoanalytical Association. Jung’s research and personal vision, however, made it impossible for him to follow his older colleague’s doctrine and a schism became inevitable. This division was personally painful for Jung and resulted in the establishment of Jung’s analytical psychology as a comprehensive system separate from psychoanalysis.

Among the central concepts of analytical psychology is individuation – the lifelong psychological process of differentiation of the self out of each individual’s conscious and unconscious elements. Jung considered it to be the main task of human development. He created some of the best known psychological concepts, including synchronicity, archetypal phenomena, the collective unconscious, the psychological complex and extraversion and introversion.

Jung was also an artist, craftsman, builder and a prolific writer. Many of his works were not published until after his death and some are still awaiting publication.

Glynis Breakwell

Dame Glynis Marie Breakwell DBE DL FRSA FAcSS (born West Bromwich, 26 July 1952) is a social psychologist and an active public policy adviser and researcher specialising in leadership, identity process and risk management. In January 2014 she was listed in the Science Council’s list of ‘100 leading UK practising scientists’. Her achievements as Vice-Chancellor of the University of Bath in Bath were marred by controversy culminating in her dismissal in a dispute regarding her remuneration.

Breakwell has been a Fellow of the British Psychological Society since 1987 and an Honorary Fellow since 2006. She is a chartered health psychologist and in 2002 was elected an Academician of the Academy of Social Sciences.

Breakwell was appointed Dame Commander of the Order of the British Empire in the 2012 New Year Honours for services to higher education. She is also a Deputy Lieutenant of the County of Somerset.

What is Organic Personality Disorder?

Introduction

Organic personality disorder (OPD), irrespective of the apparent nomenclature, is not included in the group of personality disorders.

For this reason, the symptoms and diagnostic criteria of the organic personality disorder are different from those of the other mental health disorders included in this various group. According to the Tenth Revision of the International Classification of Diseases (ICD-10) organic personality disorder is associated with a “significant alteration of the habitual patterns of premorbid behaviour”. There are crucial influences on emotions, impulses and personal needs because of this disorder.

Thus, all these definitions about the organic personality disorder support that this type of disorder is associated with changes in personality and behaviour.

Causes

Organic personality disorder is associated with “personality change due to general medical condition”. The organic personality disorder is included in a wide group of personality and behavioural disorders. This mental health disorder can be caused by disease, brain damages or dysfunctions in specific brain areas in frontal lobe. The most common reason for this profound change in personality is the traumatic brain injury (TBI). Children, whose brain areas have been injured or damaged, may present attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD) and organic personality disorder. Moreover, this disorder is characterised as “frontal lobe syndrome”. This characteristic name shows that the organic personality disorder can usually be caused by lesions in three brain areas of frontal lobe. Specifically, the symptoms of organic personality disorder can also be caused by traumatic brain injuries in orbitofrontal cortex, anterior cingulate cortex and dorsolateral prefrontal cortex. It is worth mention that organic personality disorder may also be caused by lesions in other circumscribed brain areas.

Diagnosis and Symptoms

The ICD-10 includes a diagnostic guideline for the wide group of personality and behavioural disorders. However, every disorder has its own diagnostic criteria. In case of the organic personality disorder, patient has to show at least three of the following diagnostic criteria over a six or more months period. Organic personality disorder is associated with a large variety of symptoms, such as deficits in cognitive function, dysfunctional behaviours, psychosis, neurosis, emotional changes, alterations in expression function and irritability. Patients with organic personality disorder can present emotional lability that means their emotional expressions are unstable and fluctuating. In addition, patients show reduction in ability of perseverance with their goals and they express disinhibited behaviours, which are characterised by inappropriate sexual and antisocial actions. For instance, patients can show dissocial behaviours, like stealing. Moreover, according to diagnostic guideline of ICD-10, patients can suffer from cognitive disturbances and they present signs of suspiciousness and paranoid ideas. Additionally, patients may present alteration in process of language production that means there are changes in language rate and flow. Furthermore, patients may show changes in their sexual preference and hyposexuality symptoms.

Another common feature of personality of patients with organic personality disorder is their dysfunctional and maladaptive behaviour that causes serious problems in these patients, because they face problems with pursuit and achievement of their goals. It is worth to be mentioned that patients with organic personality disorder express a feeling of unreasonable satisfaction and euphoria. Also, the patients show aggressive behaviours sometimes and these serious dysfunctions in their behaviour can have effects on their life and their relationships with other people. Specifically patients show intense signs of anger and aggression because of their inability to handle their impulses. The type of this aggression is called “impulsive aggression”. Furthermore, it is worth to be mentioned that the pattern of organic personality disorder presents some similarities with pattern of temporal lobe epilepsy (TLE). Specifically patients who suffer from this chronic disorder type of epilepsy, express aggressive behaviours, likewise it happens to patients with organic personality disorder. Another similar symptom between Temporal lobe epilepsy and organic personality disorder is the epileptic seizure. The symptom of epileptic seizure has influence on patients’ personality that means it causes behavioural alterations”. The Temporal lobe epilepsy (TLE) is associated with the hyperexcitability of the medial temporal lobe (MTL) of patients. Finally, patients with organic personality disorder may present similar symptoms with patients, who suffer from the Huntington’s disease as well. The symptoms of apathy and irritability are common between these two groups of patients.

Treatment

As it has already been mentioned, patients with organic personality disorder show a wide variety of sudden behavioural changes and dysfunctions. There are not a lot of information about the treatment of this mental health disorder. The pharmacological approach is the most common therapy among patients with organic personality disorder. However, the choice of drug therapy relies on the seriousness of patient’s situation and what symptoms are shown. The choice and administration of specific drugs contribute to the reduction of symptoms of organic personality disorder. For this reason, it is crucial for patients’ treatment to be assessed by clinical psychologists and psychiatrists before the administration of drugs.

Additionally, the dysfunctions in expression of behaviour of patients with organic personality disorder and the development of symptom of irritability, which are caused by aggressive and self-injurious behaviours, can be dealt with the administration of carbamazepine. Moreover, the symptoms of this disorder can be decreased by the administration of valproic acid. Also, emotional irritability and signs of depression can be dealt with the use of nortriptyline and low-dose thioridazine. Except from the symptom of irritability, patients express aggressive behaviours. At the onset of drug therapy for effective treatment of anger and aggression, the drug of carbamazepine, phenobarbital, benztropine (or benzatropine) and haloperidol can be administrated in order to reduce the symptoms of patients with organic personality disorder. In addition, the use of propranolol may decrease the frequent behaviours of rage attacks.

Finally, it is important for patients to take part in psychotherapy during drug therapy. In this way, many of the adverse effects of the medications, both physiological and behavioural, can be lessened or avoided entirely. Furthermore, the clinicians can provide useful and helpful support to patients during these psychotherapy sessions. Thus, the combination of drug therapy with psychotherapy can lead to the reduction of symptoms of this disorder and the improvement of patients’ situation.

What is a Mental Health Consumer?

Introduction

A mental health consumer (or mental health patient) is a person who is obtaining treatment or support for a mental disorder, also known as psychiatric or mental illness.

The term was coined by people who use mental health services in an attempt to empower those with mental health issues, historically considered a marginalised segment of society. The term suggests that there is a reciprocal contract between those who provide a service and those who use a service and that individuals have a choice in their treatment and that without them there could not exist mental health providers.

Brief History

In the 1970s the term “patient” was most commonly used. Mental Health activists of the civil rights times recognised, as did many other groups seeking self-definition, that such labels are metaphors that reflect how identities are perceived and constructed. In particular, in the mental health field they shape the nature of the relationship between the giver and receiver of psychiatric services, be it one with an emphasis on reciprocity or hierarchy. Users of psychiatric services repulsed the efforts of experts to define them and sought to develop ways to define themselves. In Australia, informal support groups of people who had recovered from episodes of mental ill health were formed during the first wave of moving patients out of psychiatric hospitals into the community in the 1960s. In the USA and other countries, radical movements to change service delivery and legislation began to be driven by consumers during the 1980s. Activists, such as Judi Chamberlain, pressed for alternatives to psychiatrist dominated and controlled systems of mental health provision. Chamberlain’s On Our Own: Patient Controlled Alternatives to the Mental Health System helped guide others intent on a more collaborative form of mental health healing.

In the 1980s with some funding from NIMH, small experimental groups flourished. In 1985 at the First Alternatives Conference attendees agreed upon the term “consumer” reflecting the patients’ choice of services. The term also implied assumptions of rationality and ability to make choices in one’s own best interests rather than be a passive incapacitated recipient of “expert” attention. In the 1990s many consumer groups were formed, such as Self Help Clearing House and the National Empowerment Centre. They continued to press for more peer involvement in alternatives treatments, pointing out that peers support and comfort, which may be in contrast to some therapists who just attempt to change the behaviour and thinking patterns.

Contemporary Usage

Today, the word mental health consumer has expanded in the popular usage of consumers themselves to include anyone who has received mental health services in the past, anyone who has a behavioural health diagnosis, or simply anyone who has experienced a mental or behavioural disorder. Other terms sometimes used by members of this community for empowerment through positive self-identification include “peers,” “people with mental health disabilities,” “psychiatric survivors,” “users,” individuals with “lived experience” and “ex-patients.” The term “service users,” is commonly used in the UK. In the US “consumer” is most frequently used by ex-patients and users of psychiatric and alternative services.

One can view this term, “consumer,” neutrally as a person who receives psychological services, perhaps from a psychologist, a psychiatrist or a social worker. It can be impersonal term relating to the use in the health sector of a large economy. It suggests that the consumer expects to have some influence on service delivery and provides feedback to the provider. Used in its more activist sense, consumer groups aim to correct perceived problems in mental health services and to promote consultation with consumers. Consumer theory was devised to interpret the special relationship between a service provider and service user in the context of mental health. Consumer theory examines the consequences and sociological meaning of the relationship.

What is Mental Health Denial?

Introduction

Mental illness denial or mental disorder denial is a form of denialism in which a person denies the existence of mental disorders.

Both serious analysts, as well as pseudoscientific movements question the existence of certain disorders.

A minority of professional researchers see disorders such as depression from a sociocultural perspective and argue that the solution to it is fixing a dysfunction in the society not in the person’s brain.

Certain analysts argue this denialism is usually fuelled by narcissistic injury. Anti-psychiatry movements such as Scientology promote mental illness denial by having alternative practices to psychiatry.

Views

Views of Thomas Szasz

According to Thomas Szasz there is no such thing as mental illness. He views psychiatry as a mechanism for political oppression. Szasz wrote a book on the subject in 1961, which is called The Myth of Mental Illness. There are also “Szasz followers”, people who agree with ideas of Thomas Szasz.

Views of Elyn Saks

Probing patient’s denial may lead to better ways to help them overcome their denial and provide insight into other issues. Major reasons for denial are narcissistic injury and denialism. In denialism, a person tries to deny psychologically uncomfortable truth and tries to rationalise it. This urge for denialism is fuelled further by narcissistic injury. Narcissism gets injured when a person feels vulnerable (or weak or overwhelmed) for some reason like mental illness.

Denialism in India

Mental illness denial in Republic of India is a common problem. Many Indians view mental illnesses as, quote: “touchy-feely, new-age hogwash”, even though 1 in every 10 Indians have a mental health condition in India.

Athletes

Studies show that Overtrained (OT) athletes suffer from Major Depressive Disorder but many athletic trainers and psychologists deny this and as a result athletes are not getting proper medical treatment. Patients deny existence of depression and blame themselves for their inadequacies and try to overcome their inadequacies which can make the symptoms more severe. Their denial also acts as an obstacle for biopsychological approach towards OT.

TV Series

In the animated TV series South Park, in the episode titled City Sushi there is a scene where Butters Stotch is wondering whether Dr. William Janus is having an incident of his multiple personality disorder, to which Dr. William Janus replies: “Come on, you think multiple personality disorder is real? I’ve been using that to scam this town for seven years.”

What is Body Dysmorphic Disorder?

Introduction

Body dysmorphic disorder (BDD), occasionally still called dysmorphophobia, is a mental disorder characterized by the obsessive idea that some aspect of one’s own body part or appearance is severely flawed and therefore warrants exceptional measures to hide or fix it.

A cartoon of a patient with body dysmorphia looking in a mirror, seeing a distorted image of himself.

In BDD’s delusional variant, the flaw is imagined. If the flaw is actual, its importance is severely exaggerated. Either way, thoughts about it are pervasive and intrusive, and may occupy several hours a day, causing severe distress and impairing one’s otherwise normal activities. BDD is classified as a somatoform disorder, and the DSM-5 categorises BDD in the obsessive-compulsive spectrum, and distinguishes it from anorexia nervosa.

BDD is estimated to affect from 0.7% to 2.4% of the population. It usually starts during adolescence and affects both men and women. The BDD subtype muscle dysmorphia, perceiving the body as too small, affects mostly males. Besides thinking about it, one repetitively checks and compares the perceived flaw, and can adopt unusual routines to avoid social contact that exposes it. Fearing the stigma of vanity, one usually hides the preoccupation. Commonly unsuspected even by psychiatrists, BDD has been underdiagnosed. Severely impairing quality of life via educational and occupational dysfunction and social isolation, BDD has high rates of suicidal thoughts and attempts at suicide.

Brief History

In 1886, Enrico Morselli reported a disorder that he termed dysmorphophobia, which described the disorder as a feeling of being ugly even though there does not appear to be anything wrong with the person’s appearance. In 1980, the American Psychiatric Association recognised the disorder, while categorising it as an atypical somatoform disorder, in the third edition of its Diagnostic and Statistical Manual of Mental Disorders (DSM). Classifying it as a distinct somatoform disorder, the DSM-III’s 1987 revision switched the term to body dysmorphic disorder.

Published in 1994, DSM-IV defines BDD as a preoccupation with an imagined or trivial defect in appearance, a preoccupation causing social or occupational dysfunction, and not better explained as another disorder, such as anorexia nervosa. Published in 2013, the DSM-5 shifts BDD to a new category (obsessive-compulsive spectrum), adds operational criteria (such as repetitive behaviours or intrusive thoughts), and notes the subtype muscle dysmorphia (preoccupation that one’s body is too small or insufficiently muscular or lean).

Signs and Symptoms

Dislike of one’s appearance is common, but individuals who suffer from BDD have extreme misperceptions about their physical appearance. Whereas vanity involves a quest to aggrandise the appearance, BDD is experienced as a quest to normalise the appearance merely. Although delusional in about one of three cases, the appearance concern is usually non-delusional, an overvalued idea.

The bodily area of focus can be nearly any and is commonly face, hair, and skin. In addition, multiple areas can be focused on simultaneously. A subtype of body dysmorphic disorder is bigorexia (anorexia reverse or muscle dysphoria). In muscular dysphoria, patients perceive their body as excessively thin despite being muscular and trained. Many seek dermatological treatment or cosmetic surgery, which typically do not resolve the distress. On the other hand, attempts at self-treatment, as by skin picking, can create lesions where none previously existed.

BDD is an obsessive-compulsive disorder but involves more depression and social avoidance despite DOC. BDD often associates with social anxiety disorder. Some experience delusions that others are covertly pointing out their flaws. Cognitive testing and neuroimaging suggest both a bias toward detailed visual analysis and a tendency toward emotional hyper-arousal.

Most generally, one experiencing BDD ruminates over the perceived bodily defect several hours daily or longer, uses either social avoidance or camouflaging with cosmetics or apparel, repetitively checks the appearance, compares it to that of other people, and might often seek verbal reassurances. One might sometimes avoid mirrors, repetitively change outfits, groom excessively, or restrict eating.

BDD’s severity can wax and wane, and flareups tend to yield absences from school, work, or socializing, sometimes leading to protracted social isolation, with some becoming housebound for extended periods. Social impairment is usually greatest, sometimes approaching avoidance of all social activities. Poor concentration and motivation impair academic and occupational performance. The distress of BDD tends to exceed that of either major depressive disorder or diabetes, and rates of suicidal ideation and attempts are especially high.

Causal Factors

As with most mental disorders, BDD’s cause is likely intricate, altogether biopsychosocial, through an interaction of multiple factors, including genetic, developmental, psychological, social, and cultural. BDD usually develops during early adolescence, although many patients note earlier trauma, abuse, neglect, teasing, or bullying. In many cases, social anxiety earlier in life precedes BDD. Though twin studies on BDD are few, one estimated its heritability at 43%. Yet other factors may be introversion, negative body image, perfectionism, heightened aesthetic sensitivity, and childhood abuse and neglect.

Social Media

Constant use of social media and “selfie taking” may translate into low self-esteem and body dysmorphic tendencies. The sociocultural theory of self-esteem states that the messages given by media and peers about the importance of appearance are internalised by individuals who adopt others’ standards of beauty as their own. Due to excessive social media use and selfie taking, individuals may become preoccupied about presenting an ideal photograph for the public. Specifically, females’ mental health has been the most affected by persistent exposure to social media. Girls with BDD present symptoms of low self-esteem and negative self-evaluation. Researchers in Istanbul Bilgi University and Bogazici University in Turkey found that individuals who have low self-esteem participate more often in trends of taking selfies along with using social media to mediate their interpersonal interaction in order to fulfil their self-esteem needs. The self-verification theory, explains how individuals use selfies to gain verification from others through likes and comments. Social media may therefore trigger one’s misconception about their physical look. Similar to those with body dysmorphic tendencies, such behaviour may lead to constant seeking of approval, self-evaluation and even depression.

In 2019 systematic review using Web of Science, PsycINFO, and PubMed databases was used to identify social networking site patterns. In particular appearance focused social media use was found to be significantly associated with greater body image dissatisfaction. It is highlighted that comparisons appear between body image dissatisfaction and BDD symptomatology. They concluded that heavy social media use may mediate the onset of sub-threshold BDD.

Individuals with BDD tend to engage in heavy plastic surgery use. Mayank Vats from Rashid Hospital in the UAE, indicated that selfies may be the reason why young people seek plastic surgery with a 10% increase in nose jobs, a 7% increase in hair transplants and a 6% increase in eyelid surgery in 2013. In 2018, the term “Snapchat Dysmorphia” was brought to life after several plastic surgeons reported that some of their patients were seeking plastic surgeries to mimic “filtered” pictures. Filtered photos, such as those on Instagram and Snapchat, often present unrealistic and unattainable looks that may be a causal factor in triggering BDD.

Diagnosis

Estimates of prevalence and gender distribution have varied widely via discrepancies in diagnosis and reporting. In American psychiatry, BDD gained diagnostic criteria in the DSM-IV, having been historically unrecognised, only making its first appearance in the DSM in 1987, but clinicians’ knowledge of it, especially among general practitioners, is constricted. Meanwhile, shame about having the bodily concern, and fear of the stigma of vanity, makes many hide even having the concern.

Via shared symptoms, BDD is commonly misdiagnosed as social anxiety disorder, obsessive-compulsive disorder, major depressive disorder, or social phobia. Social anxiety disorder and BDD are highly comorbid (within those with BDD, 12-68.8% also have SAD; within those with SAD, 4.8-12% also have BDD), developing similarly in patients -BDD is even classified as a subset of SAD by some researchers. Correct diagnosis can depend on specialized questioning and correlation with emotional distress or social dysfunction. Estimates place the Body Dysmorphic Disorder Questionnaire’s sensitivity at 100% (0% false negatives) and specificity at 92.5% (7.5% false positives). BDD is also comorbid with eating disorders, up to 12% comorbidity in one study. Both eating and body dysmorphic disorders are concerned with physical appearance, but eating disorders tend to focus more on weight rather than one’s general appearance.

BDD is classified as an obsessive-compulsive disorder in DSM-5. It is important to treat people suffering from BDD as soon as possible because the person may have already been suffering for an extended period of time and as BDD has a high suicide rate, at 2-12 times higher than the national average.

Treatment

Medication and Psychotherapy

Antidepressant medication, such as selective serotonin reuptake inhibitors (SSRIs), and cognitive-behavioural therapy (CBT) are considered effective. SSRIs can help relieve obsessive-compulsive and delusional traits, while CBT can help patients recognise faulty thought patterns. Before treatment, it can help to provide psychoeducation, as with self-help books and support websites.

Self-Improvement

For many people with BDD cosmetic surgery does not work to alleviate the symptoms of BDD as their opinion of their appearance is not grounded in reality. It is recommended that cosmetic surgeons and psychiatrists work together in order to screen surgery patients to see if they suffer from BDD, as the results of the surgery could be harmful for them.

What is a Spectrum Disorder?

Introduction

A spectrum disorder is a mental disorder that includes a range of linked conditions, sometimes also extending to include singular symptoms and traits.

The different elements of a spectrum either have a similar appearance or are thought to be caused by the same underlying mechanism. In either case, a spectrum approach is taken because there appears to be “not a unitary disorder but rather a syndrome composed of subgroups”. The spectrum may represent a range of severity, comprising relatively “severe” mental disorders through to relatively “mild and nonclinical deficits”.

In some cases, a spectrum approach joins together conditions that were previously considered separately. A notable example of this trend is the autism spectrum, where conditions on this spectrum may now all be referred to as autism spectrum disorders. A spectrum approach may also expand the type or the severity of issues which are included, which may lessen the gap with other diagnoses or with what is considered “normal”. Proponents of this approach argue that it is in line with evidence of gradations in the type or severity of symptoms in the general population.

Origin

The term spectrum was originally used in physics to indicate an apparent qualitative distinction arising from a quantitative continuum (i.e. a series of distinct colours experienced when a beam of white light is dispersed by a prism according to wavelength). Isaac Newton first used the word spectrum (Latin for “appearance” or “apparition”) in print in 1671, in describing his experiments in optics.

The term was first used by analogy in psychiatry with a slightly different connotation, to identify a group of conditions that is qualitatively distinct in appearance but believed to be related from an underlying pathogenic point of view. It has been noted that for clinicians trained after the publication of DSM-III (1980), the spectrum concept in psychiatry may be relatively new, but that it has a long and distinguished history that dates back to Emil Kraepelin and beyond. A dimensional concept was proposed by Ernst Kretschmer in 1921 for schizophrenia (schizothymic – schizoid – schizophrenic) and for affective disorders (cyclothymic temperament – cycloid ‘psychopathy’ – manic-depressive disorder), as well as by Eugen Bleuler in 1922. The term “spectrum” was first used in psychiatry in 1968 in regard to a postulated schizophrenia spectrum, at that time meaning a linking together of what were then called “schizoid personalities”, in people diagnosed with schizophrenia and their genetic relatives (refer to Seymour S. Kety).

For different investigators, the hypothetical common disease-causing link has been of a different nature.

A spectrum approach generally overlays or extends a categorical approach, which today is most associated with the Diagnostic and Statistical Manual of Mental Disorders (DSM) and International Statistical Classification of Diseases (ICD). In these diagnostic guides, disorders are considered present if there is a certain combination and number of symptoms. Gradations of present versus absent are not allowed, although there may be subtypes of severity within a category. The categories are also polythetic, because a constellation of symptoms is laid out and different patterns of them can qualify for the same diagnosis. These categories are aids important for our practical purposes such as providing specific labels to facilitate payments for mental health professionals. They have been described as clearly worded, with observable criteria, and therefore an advance over some previous models for research purposes.

A spectrum approach sometimes starts with the nuclear, classic DSM diagnostic criteria for a disorder (or may join together several disorders), and then include an additional broad range of issues such as temperaments or traits, lifestyle, behavioural patterns, and personality characteristics.

In addition, the term ‘spectrum’ may be used interchangeably with continuum, although the latter goes further in suggesting a direct straight line with no significant discontinuities. Under some continuum models, there are no set types or categories at all, only different dimensions along which everyone varies (hence a dimensional approach).

An example can be found in personality or temperament models. For example, a model that was derived from linguistic expressions of individual differences is subdivided into the Big Five personality traits, where everyone can be assigned a score along each of the five dimensions. This is by contrast to models of ‘personality types’ or temperament, where some have a certain type and some do not. Similarly, in the classification of mental disorders, a dimensional approach, which is being considered for the DSM-V, would involve everyone having a score on personality trait measures. A categorical approach would only look for the presence or absence of certain clusters of symptoms, perhaps with some cut-off points for severity for some symptoms only, and as a result diagnose some people with personality disorders.

A spectrum approach, by comparison, suggests that although there is a common underlying link, which could be continuous, particular sets of individuals present with particular patterns of symptoms (i.e. syndrome or subtype), reminiscent of the visible spectrum of distinct colours after refraction of light by a prism.

It has been argued that within the data used to develop the DSM system there is a large literature leading to the conclusion that a spectrum classification provides a better perspective on phenomenology (appearance and experience) of psychopathology (mental difficulties) than a categorical classification system. However, the term has a varied history, meaning one thing when referring to a schizophrenia spectrum and another when referring to bipolar or obsessive-compulsive disorder spectrum, for example.

Types of Spectrum

The widely used DSM and ICD manuals are generally limited to categorical diagnoses. However, some categories include a range of subtypes which vary from the main diagnosis in clinical presentation or typical severity. Some categories could be considered subsyndromal (not meeting criteria for the full diagnosis) subtypes. In addition, many of the categories include a ‘not otherwise specified’ subtype, where enough symptoms are present but not in the main recognized pattern; in some categories this is the most common diagnosis.

Spectrum concepts used in research or clinical practice include the following.

Anxiety, Stress, and Dissociation

Several types of spectrum are in use in these areas, some of which are being considered in the DSM-5.

NameOutline
Generalised Anxiety SpectrumThis spectrum has been defined by duration of symptoms: a type lasting over six months (a DSM-IV criterion), over one month (DSM-III), or lasting two weeks or less (though may recur), and also isolated anxiety symptoms not meeting criteria for any type.
Social Anxiety SpectrumThis has been defined to span shyness to social anxiety disorder, including typical and atypical presentations, isolated signs and symptoms, and elements of avoidant personality disorder.
Panic-Agoraphobia SpectrumDue to the heterogeneity (diversity) found in individual clinical presentations of panic disorder and agoraphobia, attempts have been made to identify symptom clusters in addition to those included in the DSM diagnoses, including through the development of a dimensional questionnaire measure.
Post-Traumatic Stress Spectrum (or Trauma and Loss Spectrum)Work in this area has sought to go beyond the DSM category and consider in more detail a spectrum of severity of symptoms (rather than just presence or absence for diagnostic purposes), as well as a spectrum in terms of the nature of the stressor (e.g. the traumatic incident) and a spectrum of how people respond to trauma. This identifies a significant amount of symptoms and impairment below threshold for DSM diagnosis but nevertheless important, and potentially also present in other disorders a person might be diagnosed with.
Depersonalisation-Derealisation SpectrumAlthough the DSM identifies only a chronic and severe form of depersonalisation disorder, and the ICD a ‘depersonalisation-derealisation syndrome’, a spectrum of severity has long been identified, including short-lasting episodes commonly experienced in the general population and often associated with other disorders.

Obsessions and Compulsions

An obsessive-compulsive spectrum: This can include a wide range of disorders from Tourette syndrome to the hypochondrias, as well as forms of eating disorder, itself a spectrum of related conditions.

General Developmental Disorders

An autistic spectrum: In its simplest form this joins together autism and Asperger syndrome, and can additionally include other pervasive developmental disorders (PDD). These include PDD ‘not otherwise specified’ (including ‘atypical autism’), as well as Rett syndrome and childhood disintegrative disorder (CDD). The first three of these disorders are commonly called the autism spectrum disorders; the last two disorders are much rarer, and are sometimes placed in the autism spectrum and sometimes not. The merging of these disorders is based on findings that the symptom profiles are similar, such that individuals are better differentiated by clinical specifiers (i.e. dimensions of severity, such as extent of social communication difficulties or how fixed or restricted behaviours or interests are) and associated features (e.g. known genetic disorders, epilepsy, intellectual disabilities). The term specific developmental disorders is reserved for categorising particular specific learning disabilities and developmental disorders affecting coordination.

Psychosis

Refer to Psychosis.

The schizophrenia spectrum or psychotic spectrum: There are numerous psychotic spectrum disorders already in the DSM, many involving reality distortion. These include:

There are also traits identified in first degree relatives of those diagnosed with schizophrenia associated with the spectrum. Other spectrum approaches include more specific individual phenomena which may also occur in non-clinical forms in the general population, such as some paranoid beliefs or hearing voices. Some researchers have also proposed that avoidant personality disorder and related social anxiety traits should be considered part of a schizophrenia spectrum. Psychosis accompanied by mood disorder may be included as a schizophrenia spectrum disorder, or may be classed separately as below.

Schizoaffective Disorders

A schizoaffective spectrum: This spectrum refers to features of both psychosis (hallucinations, delusions, thought disorder etc.) and mood disorder (see below). The DSM has, on the one hand, a category of schizoaffective disorder (which may be more affective (mood) or more schizophrenic), and on the other hand psychotic bipolar disorder and psychotic depression categories. A spectrum approach joins these together and may additionally include specific clinical variables and outcomes, which initial research suggested may not be particularly well captured by the different diagnostic categories except at the extremes.

Schizophrenia-Like Personality Disorders

Schizoid personality disorder, schizotypal personality disorder and paranoid personality disorder can be considered ‘schizophrenia-like personality disorders’ because of their links to the schizophrenia spectrum.

Mood

A mood disorder (affective) spectrum or bipolar spectrum or depressive spectrum. These approaches have expanded out in different directions. On the one hand, work on major depressive disorder has identified a spectrum of subcategories and sub-threshold symptoms that are prevalent, recurrent and associated with treatment needs. People are found to move between the subtypes and the main diagnostic type over time, suggesting a spectrum. This spectrum can include already recognised categories of minor depressive disorder, ‘melancholic depression‘ and various kinds of atypical depression.

In another direction, numerous links and overlaps have been found between major depressive disorder and bipolar syndromes, including mixed states (simultaneous depression and mania or hypomania). Hypomanic (‘below manic’) and more rarely manic signs and symptoms have been found in a significant number of cases of major depressive disorder, suggesting not a categorical distinction but a dimension of frequency that is higher in bipolar II and higher again in bipolar I. In addition, numerous subtypes of bipolar have been proposed beyond the types already in the DSM (which includes a milder form called cyclothymia). These extra subgroups have been defined in terms of more detailed gradations of mood severity, or the rapidity of cycling, or the extent or nature of psychotic symptoms. Furthermore, due to shared characteristics between some types of bipolar disorder and borderline personality disorder, some researchers have suggested they may both lie on a spectrum of affective disorders, although others see more links to post-trauma syndromes.

Substance Use

A spectrum of drug use, drug abuse and substance dependence: One spectrum of this type, adopted by the Health Officers Council of British Columbia in 2005, does not employ loaded terms and distinctions such as “use” vs. “abuse”, but explicitly recognises a spectrum ranging from potentially beneficial to chronic dependence. The model includes the role not just of the individual but of society, culture and availability of substances. In concert with the identified spectrum of drug use, a spectrum of policy approaches was identified which depended partly on whether the drug in question was available in a legal, for-profit commercial economy, or at the other of the spectrum only in a criminal/prohibition, black-market economy. In addition, a standardised questionnaire has been developed in psychiatry based on a spectrum concept of substance use.

Paraphilias and Obsessions

The interpretative key of ‘spectrum,’ developed from the concept of ‘related disorders,’ has been considered also in paraphilias.

Paraphilic behaviour is triggered by thoughts or urges that are psychopathologically close to obsessive impulsive area. Hollander (1996) includes in the obsessive-compulsive spectrum, neurological obsessive disorders, body-perception-related disorders and impulsivity-compulsivity disorders. In this continuum from impulsivity to compulsivity it is particularly hard to find a clear borderline between the two entities.

On this point of view, paraphilias represent such as sexual behaviours due to a high impulsivity-compulsivity drive. It is difficult to distinguish impulsivity from compulsivity: sometimes paraphilic behaviours are prone to achieve pleasure (desire or fantasy), in some other cases these attitudes are merely expressions of anxiety, and the behavioural perversion is an attempt to reduce anxiety. In the last case, the pleasure gained is short in time and is followed by a new increase in anxiety levels, such as it can be seen in an obsessive patient after he performs his compulsion.

Eibl-Eibelsfeldt (1984) underlines a female sexual arousal condition during flight and fear reactions. Some women, with masochistic traits, can reach orgasm in such conditions.

Broad Spectrum Approach

Various higher-level types of spectrum have also been proposed, that subsume conditions into fewer but broader overarching groups.

One psychological model based on factor analysis, originating from developmental studies but also applied to adults, posits that many disorders fall on either an “internalising” spectrum (characterised by negative affectivity; subdivides into a “distress” subspectrum and a “fear” subspectrum) or an “externalising” spectrum (characterised by negative affectivity plus disinhibition). These spectra are hypothetically linked to underlying variation in some of the big five personality traits. Another theoretical model proposes that the dimensions of fear and anger, defined in a broad sense, underlie a broad spectrum of mood, behavioural and personality disorders. In this model, different combinations of excessive or deficient fear and anger correspond to different neuropsychological temperament types hypothesized to underlie the spectrum of disorders.

Similar approaches refer to the overall ‘architecture’ or ‘meta-structure’, particularly in relation to the development of the DSM or ICD systems. Five proposed meta-structure groupings were recently proposed in this way, based on views and evidence relating to risk factors and clinical presentation. The clusters of disorder that emerged were described as:

  • Neurocognitive (identified mainly by neural substrate abnormalities);
  • Neurodevelopmental (identified mainly by early and continuing cognitive deficits);
  • Psychosis (identified mainly by clinical features and biomarkers for information processing deficits);
  • Emotional (identified mainly by being preceded by a temperament of negative emotionality); and
  • Externalising (identified mainly be being preceded by disinhibition).

However, the analysis was not necessarily able to validate one arrangement over others. From a psychological point of view, it has been suggested that the underlying phenomena are too complex, inter-related and continuous – with too poorly understood a biological or environmental basis – to expect that everything can be mapped into a set of categories for all purposes. In this context the overall system of classification is to some extent arbitrary, and could be thought of as a user interface which may need to satisfy different purposes.

What is Mania?

Introduction

Mania, also known as manic syndrome, is a mental and behavioural disorder defined as a state of abnormally elevated arousal, affect, and energy level, or “a state of heightened overall activation with enhanced affective expression together with lability of affect.”

During a manic episode, an individual will experience rapidly changing emotions and moods, highly influenced by surrounding stimuli. Although mania is often conceived as a “mirror image” to depression, the heightened mood can be either euphoric or dysphoric. As the mania intensifies, irritability can be more pronounced and result in anxiety or anger.

The symptoms of mania include elevated mood (either euphoric or irritable), flight of ideas and pressure of speech, increased energy, decreased need and desire for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states. However, in full-blown mania, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behaviour.

Refer to Bipolar I Disorder, Bipolar II Disorder, and Mixed Affective State.

Etymology

The nosology of the various stages of a manic episode has changed over the decades. The word derives from the Ancient Greek μανία (manía), “madness, frenzy” and the verb μαίνομαι (maínomai), “to be mad, to rage, to be furious”.

Causes and Diagnosis

Mania is a syndrome with multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (such as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, such as multiple sclerosis; certain medications may perpetuate a manic state, for example prednisone; or substances prone to abuse, especially stimulants, such as caffeine and cocaine. In the current DSM-5, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterised as either mild, moderate, or severe, with certain diagnostic criteria (e.g. catatonia, psychosis). Mania is divided into three stages:

  • Hypomania, or stage I;
  • Acute mania, or stage II; and
  • Delirious mania (delirium), or stage III.

This “staging” of a manic episode is useful from a descriptive and differential diagnostic point of view.

Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardised tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic/hypomanic bipolar patient needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have “gone manic” severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.

Classification

Mixed States

Refer to Mixed Affective State.

In a mixed affective state, the individual, though meeting the general criteria for a hypomanic (discussed below) or manic episode, experiences three or more concurrent depressive symptoms. This has caused some speculation, among clinicians, that mania and depression, rather than constituting “true” polar opposites, are, rather, two independent axes in a unipolar – bipolar spectrum.

A mixed affective state, especially with prominent manic symptoms, places the patient at a greater risk for suicide. Depression on its own is a risk factor but, when coupled with an increase in energy and goal-directed activity, the patient is far more likely to act with violence on suicidal impulses.

Hypomania

Refer to Hypomania.

Hypomania, which means “less than mania”, is a lowered state of mania that does little to impair function or decrease quality of life. It may, in fact, increase productivity and creativity. In hypomania, there is less need for sleep and both goal-motivated behaviour and metabolism increase. Some studies exploring brain metabolism in subjects with hypomania, however, did not find any conclusive link; while there are studies that reported abnormalities, some failed to detect differences. Though the elevated mood and energy level typical of hypomania could be seen as a benefit, true mania itself generally has many undesirable consequences including suicidal tendencies, and hypomania can, if the prominent mood is irritable as opposed to euphoric, be a rather unpleasant experience. In addition, the exaggerated case of hypomania can lead to problems. For instance, trait-based positivity for a person could make them more engaging and outgoing, and cause them to have a positive outlook in life. When exaggerated in hypomania, however, such a person can display excessive optimism, grandiosity, and poor decision making, often with little regard to the consequences.

Associated Disorders

A single manic episode, in the absence of secondary causes, (i.e. substance use disorders, pharmacologics, or general medical conditions) is often sufficient to diagnose bipolar I disorder. Hypomania may be indicative of bipolar II disorder. Manic episodes are often complicated by delusions and/or hallucinations; and if the psychotic features persist for a duration significantly longer than the episode of typical mania (two weeks or more), a diagnosis of schizoaffective disorder is more appropriate. Certain obsessive-compulsive spectrum disorders as well as impulse control disorders share the suffix “-mania,” namely, kleptomania, pyromania, and trichotillomania. Despite the unfortunate association implied by the name, however, no connection exists between mania or bipolar disorder and these disorders. Furthermore, evidence indicates a B12 deficiency can also cause symptoms characteristic of mania and psychosis.

Hyperthyroidism can produce similar symptoms to those of mania, such as agitation, elevated mood, increased energy, hyperactivity, sleep disturbances and sometimes, especially in severe cases, psychosis.

Signs and Symptoms

A manic episode is defined in the American Psychiatric Association’s diagnostic manual as a “distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration, if hospitalisation is necessary),” where the mood is not caused by drugs/medication or a non-mental medical illness (e.g. hyperthyroidism), and: (a) is causing obvious difficulties at work or in social relationships and activities, or (b) requires admission to hospital to protect the person or others, or (c) the person is suffering psychosis.

To be classified as a manic episode, while the disturbed mood and an increase in goal-directed activity or energy is present, at least three (or four, if only irritability is present) of the following must have been consistently present:

  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep (e.g. feels rested after 3 hours of sleep).
  • More talkative than usual, or acts pressured to keep talking.
  • Flights of ideas or subjective experience that thoughts are racing.
  • Increase in goal-directed activity, or psychomotor acceleration.
  • Distractibility (too easily drawn to unimportant or irrelevant external stimuli).
  • Excessive involvement in activities with a high likelihood of painful consequences.(e.g. extravagant shopping, improbable commercial schemes, hypersexuality).

Though the activities one participates in while in a manic state are not always negative, those with the potential to have negative outcomes are far more likely.

If the person is concurrently depressed, they are said to be having a mixed episode.

The World Health Organisation’s classification system defines a manic episode as one where mood is higher than the person’s situation warrants and may vary from relaxed high spirits to barely controllable exuberance, is accompanied by hyperactivity, a compulsion to speak, a reduced sleep requirement, difficulty sustaining attention, and/or often increased distractibility. Frequently, confidence and self-esteem are excessively enlarged, and grand, extravagant ideas are expressed. Behaviour that is out-of-character and risky, foolish or inappropriate may result from a loss of normal social restraint.

Some people also have physical symptoms, such as sweating, pacing, and weight loss. In full-blown mania, often the manic person will feel as though their goal(s) are of paramount importance, that there are no consequences, or that negative consequences would be minimal, and that they need not exercise restraint in the pursuit of what they are after. Hypomania is different, as it may cause little or no impairment in function. The hypomanic person’s connection with the external world, and its standards of interaction, remain intact, although intensity of moods is heightened. But those who suffer from prolonged unresolved hypomania do run the risk of developing full mania, and may cross that “line” without even realising they have done so.

One of the signature symptoms of mania (and to a lesser extent, hypomania) is what many have described as racing thoughts. These are usually instances in which the manic person is excessively distracted by objectively unimportant stimuli. This experience creates an absent-mindedness where the manic individual’s thoughts totally preoccupy them, making them unable to keep track of time, or be aware of anything besides the flow of thoughts. Racing thoughts also interfere with the ability to fall asleep.

Manic states are always relative to the normal state of intensity of the afflicted individual; thus, already irritable patients may find themselves losing their tempers even more quickly, and an academically gifted person may, during the hypomanic stage, adopt seemingly “genius” characteristics and an ability to perform and articulate at a level far beyond that which they would be capable of during euthymia. A very simple indicator of a manic state would be if a heretofore clinically depressed patient suddenly becomes inordinately energetic, enthusiastic, cheerful, aggressive, or “over-happy”. Other, often less obvious, elements of mania include delusions (generally of either grandeur or persecution, according to whether the predominant mood is euphoric or irritable), hypersensitivity, hypervigilance, hypersexuality, hyper-religiosity, hyperactivity and impulsivity, a compulsion to over explain (typically accompanied by pressure of speech), grandiose schemes and ideas, and a decreased need for sleep (for example, feeling rested after only 3 or 4 hours of sleep). In the case of the latter, the eyes of such patients may both look and seem abnormally “wide open”, rarely blinking, and may contribute to some clinicians’ erroneous belief that these patients are under the influence of a stimulant drug, when the patient, in fact, is either not on any mind-altering substances or is actually on a depressant drug. Individuals may also engage in out-of-character behaviour during the episode, such as questionable business transactions, wasteful expenditures of money (e.g. spending sprees), risky sexual activity, abuse of recreational substances, excessive gambling, reckless behaviour (such as extreme speeding or other daredevil activity), abnormal social interaction (e.g. over-familiarity and conversing with strangers), or highly vocal arguments. These behaviours may increase stress in personal relationships, lead to problems at work, and increase the risk of altercations with law enforcement. There is a high risk of impulsively taking part in activities potentially harmful to the self and others.

Although “severely elevated mood” sounds somewhat desirable and enjoyable, the experience of mania is ultimately often quite unpleasant and sometimes disturbing, if not frightening, for the person involved and for those close to them, and it may lead to impulsive behaviour that may later be regretted. It can also often be complicated by the sufferer’s lack of judgment and insight regarding periods of exacerbation of characteristic states. Manic patients are frequently grandiose, obsessive, impulsive, irritable, belligerent, and frequently deny anything is wrong with them. Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprived psychosis may appear, further complicating the ability to think clearly. Racing thoughts and misperceptions lead to frustration and decreased ability to communicate with others.

Mania may also, as earlier mentioned, be divided into three “stages”. Stage I corresponds with hypomania and may feature typical hypomanic characteristics, such as gregariousness and euphoria. In stages II and III mania, however, the patient may be extraordinarily irritable, psychotic or even delirious. These latter two stages are referred to as acute and delirious (or Bell’s), respectively.

Cause

Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69%. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medication possibly include glutaminergic agents and drugs that alter the hypothalamic-pituitary-adrenal (HPA) axis. Lifestyle triggers include irregular sleep-wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.

Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioural changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behaviour. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behaviour in preclinical models.

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.

Deep brain stimulation of the subthalamic nucleus in Parkinson’s disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.

Mania can also be caused by physical trauma or illness. When the causes are physical, it is called secondary mania.

Mechanism

Refer to Biology of Bipolar Disorder.

The mechanism underlying mania is unknown, but the neurocognitive profile of mania is highly consistent with dysfunction in the right prefrontal cortex, a common finding in neuroimaging studies. Various lines of evidence from post-mortem studies and the putative mechanisms of anti-manic agents point to abnormalities in GSK-3, dopamine, Protein kinase C and Inositol monophosphatase.

Meta analysis of neuroimaging studies demonstrate increased thalamic activity, and bilaterally reduced inferior frontal gyrus activation. Activity in the amygdala and other subcortical structures such as the ventral striatum tend to be increased, although results are inconsistent and likely dependent upon task characteristics such as valence. Reduced functional connectivity between the ventral prefrontal cortex and amygdala along with variable findings supports a hypothesis of general dysregulation of subcortical structures by the prefrontal cortex. A bias towards positively valenced stimuli, and increased responsiveness in reward circuitry may predispose towards mania. Mania tends to be associated with right hemisphere lesions, while depression tends to be associated with left hemisphere lesions.

Post-mortem examinations of bipolar disorder demonstrate increased expression of Protein Kinase C (PKC). While limited, some studies demonstrate manipulation of PKC in animals produces behavioural changes mirroring mania, and treatment with PKC inhibitor tamoxifen (also an anti-oestrogen drug) demonstrates antimanic effects. Traditional antimanic drugs also demonstrate PKC inhibiting properties, among other effects such as GSK3 inhibition.

Manic episodes may be triggered by dopamine receptor agonists, and this combined with tentative reports of increased VMAT2 activity, measured via PET scans of radioligand binding, suggests a role of dopamine in mania. Decreased cerebrospinal fluid levels of the serotonin metabolite 5-HIAA have been found in manic patients too, which may be explained by a failure of serotonergic regulation and dopaminergic hyperactivity.

Limited evidence suggests that mania is associated with behavioural reward hypersensitivity, as well as with neural reward hypersensitivity. Electrophysiological evidence supporting this comes from studies associating left frontal EEG activity with mania. As left frontal EEG activity is generally thought to be a reflection of behavioural activation system activity, this is thought to support a role for reward hypersensitivity in mania. Tentative evidence also comes from one study that reported an association between manic traits and feedback negativity during receipt of monetary reward or loss. Neuroimaging evidence during acute mania is sparse, but one study reported elevated orbitofrontal cortex activity to monetary reward, and another study reported elevated striatal activity to reward omission. The latter finding was interpreted in the context of either elevated baseline activity (resulting in a null finding of reward hypersensitivity), or reduced ability to discriminate between reward and punishment, still supporting reward hyperactivity in mania. Punishment hyposensitivity, as reflected in a number of neuroimaging studies as reduced lateral orbitofrontal response to punishment, has been proposed as a mechanism of reward hypersensitivity in mania.

Diagnosis

In the ICD-10 there are several disorders with the manic syndrome:

  • Organic manic disorder (F06.30).
  • Mania without psychotic symptoms (F30.1).
  • Mania with psychotic symptoms (F30.2).
  • Other manic episodes (F30.8).
  • Unspecified manic episode (F30.9).
  • Manic type of schizoaffective disorder (F25.0).
  • Bipolar affective disorder, current episode manic without psychotic symptoms (F31.1).
  • Bipolar affective disorder, current episode manic with psychotic symptoms (F31.2).

Treatment

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.

The acute treatment of a manic episode of bipolar disorder involves the utilisation of either a mood stabiliser (Carbamazepine, valproate, lithium, or lamotrigine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, or aripiprazole). The use of antipsychotic agents in the treatment of acute mania was reviewed by Tohen and Vieta in 2009.

When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilise the patient’s mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.

Lithium is the classic mood stabiliser to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine and topiramate, both anticonvulsants as well.

In some cases, long-acting benzodiazepines, particularly clonazepam, are used after other options are exhausted. In more urgent circumstances, such as in emergency rooms, lorazepam, combined with haloperidol, is used to promptly alleviate symptoms of agitation, aggression, and psychosis.

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilisers in these patients. Some atypical antidepressants, however, such as mirtazepine and trazodone have been occasionally used after other options have failed.

Society and Culture

In Electroboy: A Memoir of Mania by Andy Behrman, he describes his experience of mania as “the most perfect prescription glasses with which to see the world… life appears in front of you like an oversized movie screen”. Behrman indicates early in his memoir that he sees himself not as a person suffering from an uncontrollable disabling illness, but as a director of the movie that is his vivid and emotionally alive life. There is some evidence that people in the creative industries suffer from bipolar disorder more often than those in other occupations. Winston Churchill had periods of manic symptoms that may have been both an asset and a liability.

English actor Stephen Fry, who suffers from bipolar disorder, recounts manic behaviour during his adolescence: “When I was about 17 … going around London on two stolen credit cards, it was a sort of fantastic reinvention of myself, an attempt to. I bought ridiculous suits with stiff collars and silk ties from the 1920s, and would go to the Savoy and Ritz and drink cocktails.” While he has experienced suicidal thoughts, he says the manic side of his condition has had positive contributions on his life.

What is Hypomania?

Introduction

Hypomania (literally “under mania” or “less than mania”) is a mental and behavioural disorder, characterised essentially by an apparently non-contextual elevation of mood (euphoria) which contributes to persistently disinhibited behaviour.

The individual afflicted may suffer with irritability, not necessarily less severe than full mania; in fact, the presence of marked irritability is a documented feature of hypomanic and mixed episodes in Bipolar type II. According to DSM-5 criteria, hypomania is distinct from mania in that there is no significant functional impairment; mania, by DSM-5 definition, does include significant functional impairment and may have psychotic features.

Characteristic behaviours of persons experiencing hypomania are a notable decrease in the need for sleep, an overall increase in energy, unusual behaviours and actions, and a markedly distinctive increase in talkativeness and confidence, commonly exhibited with a flight of creative ideas. Other symptoms related to this may include feelings of grandiosity, distractibility, and hypersexuality. While hypomanic behaviour often generates productivity and excitement, it can become troublesome if the subject engages in risky or otherwise inadvisable behaviours, and/or the symptoms manifest themselves in trouble with everyday life events. When manic episodes are separated into stages of a progression according to symptomatic severity and associated features, hypomania constitutes the first stage of the syndrome, wherein the cardinal features (euphoria or heightened irritability, pressure of speech and activity, increased energy, decreased need for sleep, and flight of ideas) are most plainly evident.

Refer to Bipolar I Disorder, Bipolar II Disorder, and Mixed Affective State.

Etymology

The Ancient Greek physician Hippocrates called one personality type ‘hypomanic’ (Greek: ὑπομαινόμενοι, hypomainómenoi). In 19th century psychiatry, when mania had a broad meaning of insanity, hypomania was equated by some to concepts of ‘partial insanity’ or monomania. A more specific usage was advanced by the German neuro-psychiatrist Emanuel Ernst Mendel in 1881, who wrote, “I recommend, taking into consideration the word used by Hippocrates, to name those types of mania that show a less severe phenomenological picture, ‘hypomania'”. Narrower operational definitions of hypomania were developed in the 1960s and 1970s.

Signs and Symptoms

Individuals in a hypomanic state have a decreased need for sleep, are extremely gregarious and competitive, and have a great deal of energy. They are, otherwise, often fully functioning (unlike individuals suffering from a full manic episode).

Distinctive Markers

Specifically, hypomania is distinguished from mania by the absence of psychotic symptoms, and by its lesser degree of impact on functioning.

Hypomania is a feature of bipolar II disorder and cyclothymia, but can also occur in schizoaffective disorder. Hypomania is also a feature of bipolar I disorder; it arises in sequential procession as the mood disorder fluctuates between normal mood (euthymia) and mania. Some individuals with bipolar I disorder have hypomanic as well as manic episodes. Hypomania can also occur when moods progress downwards from a manic mood state to a normal mood. Hypomania is sometimes credited with increasing creativity and productive energy. Numerous people with bipolar disorder have credited hypomania with giving them an edge in their theatre of work.

People who experience hyperthymia, or “chronic hypomania”, encounter the same symptoms as hypomania but on a longer-term basis.

Associated Disorders

Cyclothymia, a condition of continuous mood fluctuations, is characterised by oscillating experiences of hypomania and depression that fail to meet the diagnostic criteria for either manic or major depressive episodes. These periods are often interspersed with periods of relatively normal (euthymic) functioning.

When a patient presents with a history of at least one episode of both hypomania and major depression, each of which meet the diagnostic criteria, bipolar II disorder is diagnosed. In some cases, depressive episodes routinely occur during the fall or winter and hypomanic ones in the spring or summer. In such cases, one speaks of a “seasonal pattern”.

If left untreated, and in those so predisposed, hypomania may transition into mania, which may be psychotic, in which case bipolar I disorder is the correct diagnosis.

Causes

Often in those who have experienced their first episode of hypomania – generally without psychotic features – there may be a long or recent history of depression or a mix of hypomania combined with depression (known as mixed-state) prior to the emergence of manic symptoms. This commonly surfaces in the mid to late teens. Because the teenage years are typically an emotionally charged time of life, it is not unusual for mood swings to be passed off as normal hormonal teen behaviour and for a diagnosis of bipolar disorder to be missed until there is evidence of an obvious manic or hypomanic phase.

In cases of drug-induced hypomanic episodes in unipolar depressives, the hypomania can almost invariably be eliminated by lowering medication dosage, withdrawing the drug entirely, or changing to a different medication if discontinuation of treatment is not possible.

Hypomania can be associated with narcissistic personality disorder.

Psychopathology

Mania and hypomania are usually studied together as components of bipolar disorders, and the pathophysiology is usually assumed to be the same. Given that norepinephrine and dopaminergic drugs are capable of triggering hypomania, theories relating to monoamine hyperactivity have been proposed. A theory unifying depression and mania in bipolar individuals proposes that decreased serotonergic regulation of other monoamines can result in either depressive or manic symptoms. Lesions on the right side frontal and temporal lobes have further been associated with mania.

Diagnosis

The DSM-IV-TR defines a hypomanic episode as including, over the course of at least four days, elevated mood plus three of the following symptoms OR irritable mood plus four of the following symptoms, when the behaviours are clearly different from how the person typically acts when not depressed:

  • Pressured speech.
  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep.
  • Flight of ideas or the subjective experience that thoughts are racing.
  • Easily distracted.
  • Increase in goal-directed activity (e.g. social activity, at work, or hypersexuality), or psychomotor agitation.
  • Involvement in pleasurable activities that may have a high potential for negative psycho-social or physical consequences (e.g. the person engages in unrestrained buying sprees, sexual indiscretions, reckless driving, physical and verbal conflicts, foolish business investments, quitting a job to pursue some grandiose goal, etc.).

Treatment

Medications

Antimanic drugs are used to control acute attacks and prevent recurring episodes of hypomania combined with a range of psychological therapies. The recommended length of treatment ranges from 2 years to 5 years. Anti-depressants may also be required for existing treatments but are avoided in patients who have had a recent history with hypomania. Sertraline has often been debated to have side effects that can trigger hypomania.

What was the National Survey of Mental Health and Wellbeing?

Introduction

The 2007 National Survey of Mental Health and Wellbeing (NSMHWB) was designed to provide lifetime prevalence estimates for mental disorders.

Purpose

To gain statistics on key mental health issues including the prevalence of mental disorders, the associated disability, and the use of services.

As such the NSMHWB was a national epidemiological survey of mental disorders that used similar methodology to the NCS. It aimed to answer three main questions:

  1. How many people meet DSM-IV and ICD-10 diagnostic criteria for the major mental disorders?
  2. How disabled are they by their mental disorders? and
  3. How many have seen a health professional for their mental disorder?

Background

Respondents were asked about experiences throughout their lifetime. In this survey, 12-month diagnoses were derived based on lifetime diagnosis and the presence of symptoms of that disorder in the 12 months prior to the survey interview. Assessment of mental disorders presented in this publication are based on the definitions and criteria of the World Health Organisation’s (WHO) International Classification of Diseases, Tenth Revision (ICD-10). Prevalence rates are presented with hierarchy rules applied (i.e. a person will not meet the criteria for particular disorders because the symptoms are believed to be accounted for by the presence of another disorder).

Results

  • Among the 16,015,300 people aged 16-85 years, 45% (or 7,286,600 people) had a lifetime mental disorder (i.e. a mental disorder at some point in their life).
  • More than half (55% or 8,728,700 people) of people had no lifetime mental disorders.
  • Of people who had a lifetime mental disorder:
    • 20% (or 3,197,800 people) had a 12-month mental disorder and had symptoms in the 12 months prior to the survey interview; and
    • 25% (or 4,088,800 people) had experienced a lifetime mental disorder but did not have symptoms in the 12 months prior to the survey interview.

Prevalence of 12-Month Mental Health Disorders

Prevalence of mental disorders is the proportion of people in a given population who met the criteria for diagnosis of a mental disorder at a point in time

  • Among the 3,197,800 people (or 20% of people) who had a 12-month mental disorder and had symptoms in the 12 months prior to interview:
    • 14.4% had a 12-month Anxiety disorder (includes Panic disorder (2.6%); Agoraphobia (2.8%); Social Phobia (4.7%); Generalised Anxiety Disorder (2.7%); Obsessive-Compulsive Disorder (1.9%); and Post-Traumatic Stress Disorder (6.4%))
    • 6.2% had a 12-month Affective disorder (includes Depressive Episode (4.1%) (includes severe, moderate and mild depressive episodes); Dysthymia (1.3%); and Bipolar Affective Disorder (1.8%)), and
    • 5.1% had a 12-month Substance Use Disorder (includes Alcohol Harmful Use (2.9%); Alcohol Dependence (1.4%); and Drug Use Disorders (includes harmful use and dependence) (1.4%)).
  • Note that a person may have had more than one mental disorder.
    • The components when added may therefore not add to the total shown.
    • Includes Severe Depressive Episode, Moderate Depressive Episode, and Mild Depressive Episode.
    • Includes Harmful Use and Dependence.

There were 3.2 million people who had a 12-month mental disorder. In total, 14.4% (2.3 million) of Australians aged 16-85 years had a 12-month Anxiety disorder, 6.2% (995,900) had a 12-month Affective disorder and 5.1% (819,800) had a 12-month Substance Use disorder.

Women experienced higher rates of 12-month mental disorders than men (22% compared with 18%). Women experienced higher rates than men of Anxiety (18% and 11% respectively) and Affective disorders (7.1% and 5.3% respectively). However, men had twice the rate of Substance Use disorders (7.0% compared with 3.3% for women).

The prevalence of 12-month mental disorders varies across age groups, with people in younger age groups experiencing higher rates of disorder. More than a quarter (26%) of people aged 16-24 years and a similar proportion (25%) of people aged 25-34 years had a 12-month mental disorder compared with 5.9% of those aged 75-85 years old.

You can read the full survey results here and a shorter analysis can be found here.