What is the Taylor Manifest Anxiety Scale?

Introduction

The Taylor Manifest Anxiety Scale, often shortened to TMAS, is a test of anxiety as a personality trait, and was created by Janet Taylor in 1953 to identify subjects who would be useful in the study of anxiety disorders. The TMAS originally consisted of 50 true or false questions a person answers by reflecting on themselves, in order to determine their anxiety level. Janet Taylor spent her career in the field of psychology studying anxiety and gender development.

Her scale has often been used to separate normal participants from those who would be considered to have pathological anxiety levels. The TMAS has been shown to have high test-retest reliability. The test is for adults but in 1956 a children’s form was developed. The test was very popular for many years after its development but is now used infrequently.

Refer to Zung Self-Rating Anxiety Scale.

Development and Validation

The TMAS has been proven reliable using test-retest reliability. O’Connor, Lorr, and Stafford found there were five general factors in the scale: chronic anxiety or worry, increased physiological reactivity, sleep disturbances associated with inner strain, sense of personal inadequacy, and motor tension. This study showed that persons administered the test could be display different anxiety levels across these areas. O’Connor, Lorr, and Stafford’s realisation allows patients and their doctors to better understand which dimension of anxiety needs to be addressed.

Childhood and Adolescence

The Children’s Manifest Anxiety Scale, sometimes shortened to the CMAS, was created in 1956.

This scale was closely modelled after the Taylor Manifest Anxiety Scale. It was developed so that the TMAS could be applied to a broader range of people, specifically children.

Kitano tested the validity of the CMAS by comparing students who were placed in special education classes versus those placed in regular classrooms. Kitano proposed the idea that children who were in special education classes were more likely to have higher anxiety than those in regular classrooms. Using the CMAS, Kitano found boys tested in the special education classes had higher anxiety scores than their regular classroom counterparts.

Hafner tested the reliability of the CMAS with the knowledge that the TMAS had a feminine bias. Hafner found that the CMAS did not have a female bias. He only found two questions that females always scored higher on than their male counterparts.

As the test stands now, the suggestion is to compare the female and male participants separately. Castaneda found significant differences across different grade levels, indicating that as students develop they are affected differentially by various stressors.

Gender Differences

Although the CMAS proved to not have a feminine bias, Quarter and Laxer found that females tend to score higher on the TMAS than their male counterparts. An example of these questions endorsed more frequently by females is, “I cry easily”. Similarly, Goodstein and Goldberger found that 17 of the 38 questions were more likely to be endorsed by females than males. Gall found that when she tested the femininity versus masculinity qualities of men and women, then compared them to the TMAS score, the people that were more feminine, either male or female, were more likely to have a positive correlation with their anxiety level score. Based on this, Gall agreed with previous research that stated the TMAS is more strongly female based. Hafner, however, found that the CMAS does not reflect the gender difference as the girls that took the children’s test only scored higher than the boys consistently on two of the questions.

Cultural Differences

Since the TMAS was introduced in 1953, comprehensive research has been done regarding the validity of the scale. across different cultures. In 1967, a study of cross-cultural differences in the scale was done between 9 year-old Japanese, French, and American students. The data concluded that Japanese and French students tested significantly lower on anxiety scores compared to the American students. Thus, there are strong cross-cultural differences related to the scores on the TMAS. Additional studies of the validity of the TMAS include a study between South African Natives and South African Europeans in 1979. Both groups included individuals with varying levels of education. This study found that the TMAS is sensitive to certain cross-cultural differences, but precautions should be taken when interpreting scores from the scale in non-Western cultures, regardless of the individual’s education level.

The Adult Manifest Anxiety Scale

In 2003, the Adult Manifest Anxiety Scale (AMAS) was introduced. It was made for three different age groups. The AMAS takes into account age-related situations that affect an individual’s anxiety. The divisions include:

  • One scale for adults (AMA-A);
  • One scale for college students (AMAS-C), and
  • The other for the elderly population (AMAS-E).

Each scale is geared towards examining situations specific to that age group. For example, the AMAS-C has items pertaining specifically to college students, such as questions about anxiety of the future.

The AMAS-A is geared more toward mid-life issues, and the AMAS-E has specific anxieties the older population deals with, such as fear of aging and dying. The AMAS-A contains 36 items. It has 14 questions relating to worry/oversensitivity, nine questions about physiological anxiety, seven questions about social concerns/stress, and six questions about lies. An example of an age appropriate item for this scale is, “I am worried about my job performance”. The AMAS-C contains 49 items about the same topics, but incorporates 15 items related specifically to test anxiety. Questions relating to the items on this scale include, “I worry too much about tests and exams”. This scale is similar in structure to the CMAS discussed above. The AMAS-E contains 44 items related to worry/oversensitivity, physiological anxiety, lying, and the fear of aging. Twenty-three of the questions on the AMAS-E are related to worry/oversensitivity, but The Fear of Aging category of this scale includes items such as, “I worry about becoming senile”. Similar to the TMAS, the AMAS can be given in a group or individual setting, and the person responds either yes or no to each item listed according to if it pertains to themselves or not. The more items that are answered yes, suggest a higher level of anxiety. The scale has been said to be easy to complete and practical, because it takes only about 10 minutes to complete and just a few minutes to score.

Applications and Limitations of AMAS

The AMAS has a broad range of applications, but also a number of limitations. The AMAS can be used in clinical settings, career counselling centres on campuses, hospices, nursing homes, and to monitor the progress and effectiveness of psychotherapy and drug treatment. Effective psychotherapy is indicated by a decrease in AMAS. Almost all college students will experience some type of stress in their academic career. Examples of their stress range from text anxiety to worry of the future after graduation. The AMAS-C items can provide psychologists with a statistical reference point to judge the student’s level of anxiety compared to other college students. A limitation of the AMAS-C is that it does not lend insight into the factors that are influencing the students anxiety, such as lack of studying and social factors. A more formal and extensive level of testing is necessary to resolve this limitation.

Utility

The utility of the TMAS is that it is a way to relate anxiety directly to performance in a certain area. The scale is able to measure anxiety levels and use the scores to determine performance on certain tasks. In some studies, researchers found that high anxiety (high drive) participants would make a greater number of mistakes, therefore taking longer for the participants to reach the learned criterion, whereas participants with low anxiety (low drive) would reach the learned criterion quicker. The TMAS was able to measure that anxiety, so the researchers could make inclusions or exclusions of the participants for their specific studies. This would allow them to achieve the results they want. The TMAS was also a way to relate intelligence to anxiety. Studies have shown there is a possible correlation between anxiety and academic achievement, but they do not recommend it be the sole predictor of achievement. It should be paired with other tests in order to make an accurate prediction.

Decline

The TMAS scale was frequently used in the past, however, its use has declined over the years due to problems with the validity of this self-report measure. Participants use their own judgement when answering questions, which causes internal and construct validity issues, which makes the interpretation of results difficult. Another possible reason this scale has declined in its use over the years is that researchers seemed to only get results of anxiety from participants under threat conditions and not under non-threat conditions, which again questioned the scale’s validity.

Awards

The Association for Psychological Science established an award in honour of Janet Taylor Spence for her contributions to psychology. Receiving this award means that the psychologist made honourable, new, creative, and cutting edge contributions to research and impact in the early years of their career, as Janet Taylor did during her career. The award is named the Janet Taylor Spence Award for Transformative Early Career Contributions.

Reference

Taylor, J. (1953). A Personality Scale of Manifest Anxiety. The Journal of Abnormal and Social Psychology. 48(2), pp.285-290. doi:10.1037/h0056264.

What is the Zung Self-Rating Anxiety Scale?

Introduction

The Zung Self-Rating Anxiety Scale (SAS) was designed by William W. K. Zung M.D, (1929-1992) a professor of psychiatry from Duke University, to quantify a patient’s level of anxiety.

Background

The SAS is a 20-item self-report assessment device built to measure anxiety levels, based on scoring in 4 groups of manifestations: cognitive, autonomic, motor and central nervous system symptoms. Answering the statements a person should indicate how much each statement applies to him or her within a period of one or two weeks prior to taking the test. Each question is scored on a Likert-type scale of 1-4 (based on these replies: “a little of the time,” “some of the time,” “good part of the time,” “most of the time”). Some questions are negatively worded to avoid the problem of set response. Overall assessment is done by total score.

The Anxiety Index

The total raw scores range from 20-80. The raw score then needs to be converted to an “Anxiety Index” score using the chart on the paper version of the test that can be found on the link below. The “Anxiety Index” score can then be used on this scale below to determine the clinical interpretation of one’s level of anxiety:

  • 20-44: Normal Range.
  • 45-59: Mild to Moderate Anxiety Levels.
  • 60-74: Marked to Severe Anxiety Levels.
  • 75 and above: Extreme Anxiety Levels.

You can find an online version of the SAS here.

Refer to Zung Self-Rating Depression Scale and Taylor Manifest Anxiety Scale (TMAS).

PDF version of test with Raw Score-Index Score Conversion Table.

References

Zung, W.A.K. (1974). The Measurement of Affects: Depression and Anxiety. Modern Problems of Pharmacopsychiatry. 7(0), pp.170-188. doi: 10.1159/000395075.

Zung, W.A.K. (1971) A Rating Instrument for Anxiety Disorders. Psychosomatics. 12(6), pp.371-379. doi: 10.1016/S0033-3182(71)71479-0.

What is Schizophrenia?

Introduction

Schizophrenia is a psychiatric disorder characterised by continuous or relapsing episodes of psychosis. Major symptoms include hallucinations (typically hearing voices), delusions, and disorganised thinking. Other symptoms include social withdrawal, decreased emotional expression, and apathy. Symptoms typically come on gradually, begin in young adulthood, and in many cases never resolve. There is no objective diagnostic test; diagnosis is based on:

  • Observed behaviour;
  • A history that includes the person’s reported experiences; and
  • Reports of others familiar with the person.

To be diagnosed with schizophrenia, symptoms and functional impairment need to be present for six months (DSM-5) or one month (ICD-11). Many people with schizophrenia have other mental disorders that often includes an anxiety disorder such as panic disorder, an obsessive compulsive disorder (OCD), or a substance use disorder.

About 0.3% to 0.7% of people are affected by schizophrenia during their lifetime. In 2017, there were an estimated 1.1 million new cases and in 2019 a total of 20 million cases globally. Males are more often affected and on average have an earlier onset. The causes of schizophrenia include genetic and environmental factors. Genetic factors include a variety of common and rare genetic variants. Possible environmental factors include being raised in a city, cannabis use during adolescence, infections, the ages of a person’s mother or father, and poor nutrition during pregnancy.

About half of those diagnosed with schizophrenia will have a significant improvement over the long term with no further relapses, and a small proportion of these will recover completely. The other half will have a lifelong impairment, and severe cases may be repeatedly admitted to hospital. Social problems such as long-term unemployment, poverty, homelessness, exploitation, and victimisation are common consequences of schizophrenia. Compared to the general population, people with schizophrenia have a higher suicide rate (about 5% overall) and more physical health problems, leading to an average decrease in life expectancy by 20 years. In 2015, an estimated 17,000 deaths were caused by schizophrenia.

The mainstay of treatment is antipsychotic medication, along with counselling, job training, and social rehabilitation. Up to a third of people do not respond to initial antipsychotics, in which case the antipsychotic clozapine may be used. In situations where there is a risk of harm to self or others, a short involuntary hospitalisation may be necessary. Long-term hospitalisation may be needed for a small number of people with severe schizophrenia. In countries where supportive services are limited or unavailable, long-term hospital stays are more typical.

Epidemiology

In 2017, the Global Burden of Disease Study estimated there were 1.1 million new cases, and in 2019 the World Health Organisation (WHO) reported a total of 20 million cases globally. Schizophrenia affects around 0.3-0.7% of people at some point in their life. It occurs 1.4 times more frequently in males than females and typically appears earlier in men – the peak ages of onset are 25 years for males and 27 years for females. Onset in childhood, before the age of 13 can sometimes occur. A later onset can occur between the ages of 40 and 60, known as late onset, and also after 60 known as very late onset.

Worldwide, schizophrenia is the most common psychotic disorder. The frequency of schizophrenia varies across the world, within countries, and at the local and neighbourhood level. This variation has been estimated to be fivefold. It causes approximately 1% of worldwide disability adjusted life years and resulted in 17,000 deaths in 2015.

In 2000, the WHO found the percentage of people affected and the number of new cases that develop each year is roughly similar around the world, with age-standardised prevalence per 100,000 ranging from 343 in Africa to 544 in Japan and Oceania for men, and from 378 in Africa to 527 in Southeastern Europe for women. About 1.1% of adults have schizophrenia in the United States. However, in areas of conflict this figure can rise to between 4.0 and 6.5%.

Brief History

Accounts of a schizophrenia-like syndrome are rare in records before the 19th century. The earliest cases detailed were reported in 1797, and 1809. Dementia praecox, meaning premature dementia was used by German psychiatrist Heinrich Schüle in 1886, and then in 1891 by Arnold Pick in a case report of hebephrenia. In 1893 Emil Kraepelin used the term in making a distinction, known as the Kraepelinian dichotomy, between the two psychoses – dementia praecox, and manic depression (now called bipolar disorder). Kraepelin believed that dementia praecox was probably caused by a systemic disease that affected many organs and nerves, affecting the brain after puberty in a final decisive cascade. It was thought to be an early form of dementia, a degenerative disease. When it became evident that the disorder was not degenerative it was renamed schizophrenia by Eugen Bleuler in 1908.

The word schizophrenia translates roughly as “splitting of the mind” and is Modern Latin from the Greek roots schizein (σχίζειν, “to split”) and phrēn, (φρεν, “mind”) Its use was intended to describe the separation of function between personality, thinking, memory, and perception.

The term schizophrenia used to be associated with split personality by the general population but that usage went into decline when split personality became known as a separate disorder, first as multiple identity disorder , and later as dissociative identity disorder. In 2002 in Japan the name was changed to integration disorder, and in 2012 in South Korea, the name was changed to attunement disorder to reduce the stigma, both with good results.

In the early 20th century, the psychiatrist Kurt Schneider listed the psychotic symptoms of schizophrenia into two groups of hallucinations, and delusions. The hallucinations were listed as specific to auditory, and the delusional included thought disorders. These were seen as the symptoms of first-rank importance and were termed first-rank symptoms. Whilst these were also sometimes seen to be relevant to the psychosis in manic-depression, they were highly suggestive of schizophrenia and typically referred to as first-rank symptoms of schizophrenia. The most common first-rank symptom was found to belong to thought disorders. In 2013 the first-rank symptoms were excluded from the DSM-5 criteria. First-rank symptoms are seen to be of limited use in detecting schizophrenia but may be of help in differential diagnosis.]

The earliest attempts to treat schizophrenia were psychosurgical, involving either the removal of brain tissue from different regions or the severing of pathways. These were notably frontal lobotomies and cingulotomies which were carried out from the 1930s. In the 1930s a number of shock therapies were introduced which induced seizures (convulsions) or comas. Insulin shock therapy involved the injecting of large doses of insulin in order to induce comas, which in turn produced hypoglycaemia and convulsions. The use of electricity to induce seizures was developed, and in use as electroconvulsive therapy (ECT) by 1938. Stereotactic surgeries were developed in the 1940s. Treatment was revolutionized in the mid-1950s with the development and introduction of the first typical antipsychotic, chlorpromazine. In the 1970s the first atypical antipsychotic clozapine, was introduced followed by the introduction of others.

In the early 1970s in the US, the diagnostic model used for schizophrenia was broad and clinically-based using DSM II. It had been noted that schizophrenia was diagnosed far more in the US than in Europe which had been using the ICD-9 criteria. The US model was criticised for failing to demarcate clearly those people with a mental illness, and those without. In 1980 DSM III was published and showed a shift in focus from the clinically-based biopsychosocial model to a reason-based medical model. DSM IV showed an increased focus to an evidence-based medical model.

Subtypes of schizophrenia classified as paranoid, disorganized, catatonic, undifferentiated, and residual type were difficult to distinguish between and are no longer recognised as separate conditions by DSM-5 (2013) or ICD-11.

Signs and Symptoms

Schizophrenia is a mental disorder characterized by significant alterations in perception, thoughts, mood, and behaviour. Symptoms are described in terms of positive, and negative, and cognitive symptoms. The positive symptoms of schizophrenia are the same for any psychosis and are sometimes referred to as psychotic symptoms. These may be present in any of the different psychoses, and are often transient making early diagnosis of schizophrenia problematic. Psychosis noted for the first time in a person who is later diagnosed with schizophrenia is referred to as a first-episode psychosis (FEP).

Positive Symptoms

Positive symptoms are those symptoms that are not normally experienced, but are present in people during a psychotic episode in schizophrenia. They include delusions, hallucinations, and disorganised thoughts and speech, typically regarded as manifestations of psychosis. Hallucinations most commonly involve the sense of hearing as hearing voices but can sometimes involve any of the other senses of taste, sight, smell, and touch. They are also typically related to the content of the delusional theme. Delusions are bizarre or persecutory in nature. Distortions of self-experience such as feeling as if one’s thoughts or feelings are not really one’s own, to believing that thoughts are being inserted into one’s mind, sometimes termed passivity phenomena, are also common. Thought disorders can include thought blocking, and disorganised speech – speech that is not understandable is known as word salad. Positive symptoms generally respond well to medication, and become reduced over the course of the illness, perhaps related to the age-related decline in dopamine activity.

Negative Symptoms

Negative symptoms are deficits of normal emotional responses, or of other thought processes. The five recognised domains of negative symptoms are:

  • Blunted affect: showing flat expressions or little emotion;
  • Alogia: a poverty of speech;
  • Anhedonia: an inability to feel pleasure;
  • Asociality: the lack of desire to form relationships; and
  • Avolition: a lack of motivation and apathy.

Avolition and anhedonia are seen as motivational deficits resulting from impaired reward processing. Reward is the main driver of motivation and this is mostly mediated by dopamine. It has been suggested that negative symptoms are multidimensional and they have been categorised into two subdomains of apathy or lack of motivation, and diminished expression. Apathy includes avolition, anhedonia, and social withdrawal; diminished expression includes blunt effect, and alogia. Sometimes diminished expression is treated as both verbal and non-verbal. Apathy accounts for around 50% of the most often found negative symptoms and affects functional outcome and subsequent quality of life. Apathy is related to disrupted cognitive processing affecting memory and planning including goal-directed behaviour. The two subdomains has suggested a need for separate treatment approaches. A lack of distress – relating to a reduced experience of depression and anxiety is another noted negative symptom. A distinction is often made between those negative symptoms that are inherent to schizophrenia, termed primary; and those that result from positive symptoms, from the side effects of antipsychotics, substance abuse, and social deprivation – termed secondary negative symptoms. Negative symptoms are less responsive to medication and the most difficult to treat. However if properly assessed, secondary negative symptoms are amenable to treatment.

Scales for specifically assessing the presence of negative symptoms, and for measuring their severity, and their changes have been introduced since the earlier scales such as the PANNS that deals with all types of symptoms. These scales are the Clinical Assessment Interview for Negative Symptoms (CAINS), and the Brief Negative Symptom Scale (BNSS) also known as second-generation scales. In 2020, ten years after its introduction a cross-cultural study of the use of BNSS found valid and reliable psychometric evidence for the five-domain structure cross-culturally. The BNSS is designed to assess both the presence and severity and change of negative symptoms of the five recognised domains, and the additional item of reduced normal distress. BNSS can register changes in negative symptoms in relation to psychosocial and pharmacological intervention trials. BNSS has also been used to study a proposed non-D2 treatment called SEP-363856. Findings supported the favouring of five domains over the two-dimensional proposition.

Cognitive Symptoms

Cognitive deficits are the earliest and most constantly found symptoms in schizophrenia. They are often evident long before the onset of illness in the prodromal stage, and may be present in early adolescence, or childhood. They are a core feature but not considered to be core symptoms, as are positive and negative symptoms. However, their presence and degree of dysfunction is taken as a better indicator of functionality than the presentation of core symptoms. Cognitive deficits become worse at first episode psychosis but then return to baseline, and remain fairly stable over the course of the illness.

The deficits in cognition are seen to drive the negative psychosocial outcome in schizophrenia, and are claimed to equate to a possible reduction in IQ from the norm of 100 to 70-85. Cognitive deficits may be of neurocognition (non-social) or of social cognition. Neurocognition is the ability to receive and remember information, and includes verbal fluency, memory, reasoning, problem solving, speed of processing, and auditory and visual perception. Verbal memory and attention are seen to be the most affected. Verbal memory impairment is associated with a decreased level of semantic processing (relating meaning to words). Another memory impairment is that of episodic memory. An impairment in visual perception that is consistently found in schizophrenia is that of visual backward masking. Visual processing impairments include an inability to perceive complex visual illusions. Social cognition is concerned with the mental operations needed to interpret, and understand the self and others in the social world. This is also an associated impairment, and facial emotion perception is often found to be difficult. Facial perception is critical for ordinary social interaction. Cognitive impairments do not usually respond to antipsychotics, and there are a number of interventions that are used to try to improve them; cognitive remediation therapy has been found to be of particular help.

Onset

Onset typically occurs between the late teens and early 30s, with the peak incidence occurring in males in the early to mid twenties, and in females in the late twenties. Onset before the age of 17 is known as early-onset, and before the age of 13, as can sometimes occur, is known as childhood schizophrenia or very early-onset. A later stage of onset can occur between the ages of 40 and 60, known as late-onset schizophrenia. A later onset over the age of 60, which may be difficult to differentiate as schizophrenia, is known as very-late-onset schizophrenia-like psychosis. Late onset has shown that a higher rate of females are affected; they have less severe symptoms and need lower doses of antipsychotics. The tendency for earlier onset in males is later seen to be balanced by a post-menopausal increase in the development in females. Oestrogen produced pre-menopause has a dampening effect on dopamine receptors but its protection can be overridden by a genetic overload. There has been a dramatic increase in the numbers of older adults with schizophrenia. An estimated 70% of those with schizophrenia have cognitive deficits, and these are most pronounced in early onset and late-onset illness.

Onset may happen suddenly or may occur after the slow and gradual development of a number of signs and symptoms, a period known as the prodromal stage. Up to 75% of those with schizophrenia go through a prodromal stage. The negative and cognitive symptoms in the prodrome stage can precede FEP by many months and up to five years. The period from FEP and treatment is known as the duration of untreated psychosis (DUP) which is seen to be a factor in functional outcome. The prodromal stage is the high-risk stage for the development of psychosis. Since the progression to first episode psychosis is not inevitable, an alternative term is often preferred of at risk mental state Cognitive dysfunction at an early age impact a young person’s usual cognitive development. Recognition and early intervention at the prodromal stage would minimize the associated disruption to educational and social development and has been the focus of many studies. It is suggested that the use of anti-inflammatory compounds such as D-serine may prevent the transition to schizophrenia. Cognitive symptoms are not secondary to positive symptoms or to the side effects of antipsychotics.

Cognitive impairments in the prodromal stage become worse after first episode psychosis (after which they return to baseline and then remain fairly stable), making early intervention to prevent such transition of prime importance. Early treatment with cognitive behavioural therapies are the gold standard. Neurological soft signs of clumsiness and loss of fine motor movement are often found in schizophrenia, which may resolve with effective treatment of FEP.

Risk Factors

Schizophrenia is described as a neurodevelopmental disorder with no precise boundary, or single cause, and is thought to develop from gene-environment interactions with involved vulnerability factors. The interactions of these risk factors are complex, as numerous and diverse insults from conception to adulthood can be involved. A genetic predisposition on its own, without interacting environmental factors, will not give rise to the development of schizophrenia. The genetic component means that prenatally brain development is disturbed, and environmental influence affects the postnatal development of the brain. Evidence suggests that genetically susceptible children are more likely to be vulnerable to the effects of environmental risk factors.

Genetic

Estimates of the heritability of schizophrenia are between 70% and 80%, which implies that 70% to 80% of the individual differences in risk to schizophrenia is associated with genetics. These estimates vary because of the difficulty in separating genetic and environmental influences, and their accuracy has been queried. The greatest risk factor for developing schizophrenia is having a first-degree relative with the disease (risk is 6.5%); more than 40% of identical twins of those with schizophrenia are also affected. If one parent is affected the risk is about 13% and if both are affected the risk is nearly 50%. However, DSM-5 points out that most people with schizophrenia have no family history of psychosis. Results of candidate gene studies of schizophrenia have generally failed to find consistent associations, and the genetic loci identified by genome-wide association studies explain only a small fraction of the variation in the disease.

Many genes are known to be involved in schizophrenia, each with small effect and unknown transmission and expression. The summation of these effect sizes into a polygenic risk score can explain at least 7% of the variability in liability for schizophrenia. Around 5% of cases of schizophrenia are understood to be at least partially attributable to rare copy-number variations (CNVs); these structural variations are associated with known genomic disorders involving deletions at 22q11.2 (DiGeorge syndrome), duplications at 16p11.2 16p11.2 duplication (most frequently found) and deletions at 15q11.2 (Burnside-Butler syndrome). Some of these CNVs increase the risk of developing schizophrenia by as much as 20-fold, and are frequently comorbid with autism and intellectual disabilities.

The genes CRHR1 and CRHBP have been shown to be associated with a severity of suicidal behaviour. These genes code for stress response proteins needed in the control of the HPA axis, and their interaction can affect this axis. Response to stress can cause lasting changes in the function of the HPA axis possibly disrupting the negative feedback mechanism, homeostasis, and the regulation of emotion leading to altered behaviours.

The question of how schizophrenia could be primarily genetically influenced, given that people with schizophrenia have lower fertility rates, is a paradox. It is expected that genetic variants that increase the risk of schizophrenia would be selected against due to their negative effects on reproductive fitness. A number of potential explanations have been proposed, including that alleles associated with schizophrenia risk confers a fitness advantage in unaffected individuals. While some evidence has not supported this idea, others propose that a large number of alleles each contributing a small amount can persist.

Environmental

Environmental factors, each associated with a slight risk of developing schizophrenia in later life include oxygen deprivation, infection, prenatal maternal stress, and malnutrition in the mother during prenatal development. A risk is also associated with maternal obesity, in increasing oxidative stress, and dysregulating the dopamine and serotonin pathways. Both maternal stress and infection have been demonstrated to alter foetal neurodevelopment through an increase of pro-inflammatory cytokines. There is a slighter risk associated with being born in the winter or spring possibly due to vitamin D deficiency or a prenatal viral infection. Other infections during pregnancy or around the time of birth that have been linked to an increased risk include infections by Toxoplasma gondii and Chlamydia. The increased risk is about 5-8%. Viral infections of the brain during childhood are also linked to a risk of schizophrenia during adulthood.

Adverse childhood experiences (ACEs), severe forms of which are classed as childhood trauma, range from being bullied or abused, to the death of a parent. Many adverse childhood experiences can cause toxic stress and increase the risk of psychosis. Chronic trauma can promote lasting inflammatory dysregulation throughout the nervous system. It is suggested that early stress may contribute to the development of schizophrenia through these alterations in the immune system. Schizophrenia was the last diagnosis to benefit from the link made between ACEs and adult mental health outcomes.

Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of schizophrenia by a factor of two, even after taking into account drug use, ethnic group, and size of social group. A possible link between the urban environment and pollution has been suggested to be the cause of the elevated risk of schizophrenia.

Other risk factors of importance include social isolation, immigration related to social adversity and racial discrimination, family dysfunction, unemployment, and poor housing conditions. Having a father older than 40 years, or parents younger than 20 years are also associated with schizophrenia. It has been suggested that apart from gene-environment interactions, environment-environment interactions also be taken into account as each environmental risk factor on its own is not enough.

Substance Use

About half of those with schizophrenia use recreational drugs, including cannabis, tobacco, and alcohol excessively. Use of stimulants such as amphetamine and cocaine can lead to a temporary stimulant psychosis, which presents very similarly to schizophrenia. Rarely, alcohol use can also result in a similar alcohol-related psychosis. Drugs may also be used as coping mechanisms by people who have schizophrenia, to deal with depression, anxiety, boredom, and loneliness. The use of cannabis and tobacco are not associated with the development of cognitive deficits, and sometimes a reverse relationship is found where their use improves these symptoms. However, substance abuse is associated with an increased risk of suicide, and a poor response to treatment.

Cannabis-use may be a contributory factor in the development of schizophrenia, potentially increasing the risk of the disease in those who are already at risk. The increased risk may require the presence of certain genes within an individual. Its use is associated with doubling the rate. The use of more potent strains of cannabis having a high level of its active ingredient tetrahydrocannabinol (THC), increases the risk further. One of these strains is well known as skunk.

Mechanisms

The mechanisms of schizophrenia are unknown, and a number of models have been put forward to explain the link between altered brain function and schizophrenia. The prevailing model of schizophrenia is that of a neurodevelopmental disorder, and the underlying changes that occur before symptoms become evident are seen as arising from the interaction between genes and the environment. Extensive studies support this model. Maternal infections, malnutrition and complications during pregnancy and childbirth are known risk factors for the development of schizophrenia, which usually emerges between the ages of 18-25 a period that overlaps with certain stages of neurodevelopment. Gene-environment interactions lead to deficits in the neural circuitry that affect sensory and cognitive functions.

The common dopamine and glutamate models proposed are not mutually exclusive; each is seen to have a role in the neurobiology of schizophrenia. The most common model put forward was the dopamine hypothesis of schizophrenia, which attributes psychosis to the mind’s faulty interpretation of the misfiring of dopaminergic neurons. This has been directly related to the symptoms of delusions and hallucinations. Abnormal dopamine signalling has been implicated in schizophrenia based on the usefulness of medications that affect the dopamine receptor and the observation that dopamine levels are increased during acute psychosis. A decrease in D1 receptors in the dorsolateral prefrontal cortex may also be responsible for deficits in working memory.

The glutamate hypothesis of schizophrenia links alterations between glutamatergic neurotransmission and the neural oscillations that affect connections between the thalamus and the cortex. Studies have shown that a reduced expression of a glutamate receptor – NMDA receptor, and glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with schizophrenia. Post-mortem studies consistently find that a subset of these neurons fail to express GAD67 (GAD1), in addition to abnormalities in brain morphometry. The subsets of interneurons that are abnormal in schizophrenia are responsible for the synchronising of neural ensembles needed during working memory tasks. These give the neural oscillations produced as gamma waves that have a frequency of between 30 and 80 hertz. Both working memory tasks and gamma waves are impaired in schizophrenia, which may reflect abnormal interneuron functionality.

Deficits in executive functions, such as planning, inhibition, and working memory, are pervasive in schizophrenia. Although these functions are separable, their dysfunction in schizophrenia may reflect an underlying deficit in the ability to represent goal related information in working memory, and to utilize this to direct cognition and behaviour. These impairments have been linked to a number of neuroimaging and neuropathological abnormalities. For example, functional neuroimaging studies report evidence of reduced neural processing efficiency, whereby the dorsolateral prefrontal cortex is activated to a greater degree to achieve a certain level of performance relative to controls on working memory tasks. These abnormalities may be linked to the consistent post-mortem finding of reduced neuropil, evidenced by increased pyramidal cell density and reduced dendritic spine density. These cellular and functional abnormalities may also be reflected in structural neuroimaging studies that find reduced grey matter volume in association with deficits in working memory tasks.

Positive symptoms have been linked to cortical thinning in the superior temporal gyrus. Severity of negative symptoms has been linked to reduced thickness in the left medial orbitofrontal cortex. Anhedonia, traditionally defined as a reduced capacity to experience pleasure, is frequently reported in schizophrenia. However, a large body of evidence suggests that hedonic responses are intact in schizophrenia, and that what is reported to be anhedonia is a reflection of dysfunction in other processes related to reward. Overall, a failure of reward prediction is thought to lead to impairment in the generation of cognition and behaviour required to obtain rewards, despite normal hedonic responses.

It has been hypothesized that in some people, development of schizophrenia is related to intestinal tract dysfunction such as seen with non-celiac gluten sensitivity or abnormalities in the gut microbiota. A subgroup of persons with schizophrenia present an immune response to gluten differently from that found in people with celiac, with elevated levels of certain serum biomarkers of gluten sensitivity such as anti-gliadin IgG or anti-gliadin IgA antibodies.

Another theory links abnormal brain lateralization to the development of being left-handed which is significantly more common in those with schizophrenia. This abnormal development of hemispheric asymmetry is noted in schizophrenia. Studies have concluded that the link is a true and verifiable effect that may reflect a genetic link between lateralisation and schizophrenia.

An important process that may be disrupted in neurodevelopment is astrogenesis – the formation of astrocytes. Astrocytes are crucial in contributing to the formation and maintenance of neural circuits and it is believed that disruption in this role can result in a number of neurodevelopmental disorders including schizophrenia.

Bayesian models of brain functioning have been utilised to link abnormalities in cellular functioning to symptoms. Both hallucinations and delusions have been suggested to reflect improper encoding of prior expectations, thereby causing expectation to excessively influence sensory perception and the formation of beliefs. In approved models of circuits that mediate predictive coding, reduced NMDA receptor activation, could in theory result in the positive symptoms of delusions and hallucinations.

Diagnosis

Refer to Diagnosis of Schizophrenia.

There is no objective test or biomarker to confirm diagnosis. Psychoses can occur in several conditions and are often transient making early diagnosis of schizophrenia difficult. Psychosis noted for the first time in a person that is later diagnosed with schizophrenia is referred to as a first-episode psychosis (FEP).

Criteria

Schizophrenia is diagnosed based on criteria in either the Diagnostic and Statistical Manual of Mental Disorders (DSM) published by the American Psychiatric Association or the International Statistical Classification of Diseases and Related Health Problems (ICD) published by the World Health Organization. These criteria use the self-reported experiences of the person and reported abnormalities in behaviour, followed by a psychiatric assessment. The mental status examination is an important part of the assessment. An established tool for assessing the severity of positive and negative symptoms is the Positive and Negative Syndrome Scale (PANSS). This has been seen to have shortcomings relating to negative symptoms, and other scales – the Clinical Assessment Interview for Negative Symptoms (CAINS), and the Brief Negative Symptoms Scale (BNSS) have been introduced. The DSM-5, published in 2013, gives a Scale to Assess the Severity of Symptom Dimensions outlining eight dimensions of symptoms.

DSM-5 states that to be diagnosed with schizophrenia, two diagnostic criteria have to be met over the period of one month, with a significant impact on social or occupational functioning for at least six months. One of the symptoms needs to be either delusions, hallucinations, or disorganised speech. A second symptom could be one of the negative symptoms, or severely disorganised or catatonic behaviour. A different diagnosis of schizophreniform disorder can be made before the six months needed for the diagnosis of schizophrenia.

In Australia the guideline for diagnosis is for six months or more with symptoms severe enough to affect ordinary functioning. In the UK diagnosis is based on having the symptoms for most of the time for one month, with symptoms that significantly affect the ability to work, study, or to carry on ordinary daily living, and with other similar conditions ruled out.

The ICD criteria are typically used in European countries; the DSM criteria are used predominantly in the United States and Canada, and are prevailing in research studies. In practice, agreement between the two systems is high. The current proposal for the ICD-11 criteria for schizophrenia recommends adding self-disorder as a symptom.

A major unresolved difference between the two diagnostic systems is that of the requirement in DSM of an impaired functional outcome. WHO for ICD argues that not all people with schizophrenia have functional deficits and so these are not specific for the diagnosis.

Changes Made

Both manuals have adopted the chapter heading of Schizophrenia spectrum and other psychotic disorders; ICD modifying this as Schizophrenia spectrum and other primary psychotic disorders. The definition of schizophrenia remains essentially the same as that specified by the 2000 text revised DSM-IV (DSM-IV-TR). However, with the publication of DSM-5, the APA removed all sub-classifications of schizophrenia. ICD-11 has also removed subtypes. The removed subtype from both, of catatonic has been relisted in ICD-11 as a psychomotor disturbance that may be present in schizophrenia.

Another major change was to remove the importance previously given to Schneider’s first-rank symptoms. DSM-5 still uses the listing of schizophreniform disorder but ICD-11 no longer includes it. DSM-5 also recommends that a better distinction be made between a current condition of schizophrenia and its historical progress, to achieve a clearer overall characterisation.

A dimensional assessment has been included in DSM-5 covering eight dimensions of symptoms to be rated (using the Scale to Assess the Severity of Symptom Dimensions) – these include the five diagnostic criteria plus cognitive impairments, mania, and depression. This can add relevant information for the individual in regard to treatment, prognosis, and functional outcome; it also enables the response to treatment to be more accurately described.

Two of the negative symptoms – avolition and diminished emotional expression, have been given more prominence in both manuals.

Comorbidities

Many people with schizophrenia may have one or more other mental disorders, such as panic disorder, OCD, or substance use disorder. These are separate disorders that require treatment. When comorbid with schizophrenia, substance use disorder and antisocial personality disorder both increase the risk for violence. Comorbid substance abuse also increases risk for suicide.

Sleep disorders often co-occur with schizophrenia, and may be an early sign of relapse. Sleep disorders are linked with positive symptoms such as disorganised thinking and can adversely affect cortical plasticity and cognition. The consolidation of memories is disrupted in sleep disorders. They are associated with severity of illness, a poor prognosis, and poor quality of life. Sleep onset and maintenance insomnia is a common symptom, regardless of whether treatment has been received or not. Genetic variations have been found associated with these conditions involving the circadian rhythm, dopamine and histamine metabolism, and signal transduction. Limited positive evidence has been found for the use of acupuncture as an add-on.

Differential Diagnosis

To make a diagnosis of schizophrenia other possible causes of psychosis need to be excluded. Psychotic symptoms lasting less than a month may be diagnosed as brief psychotic disorder, or as schizophreniform disorder. Psychosis is noted in Other specified schizophrenia spectrum and other psychotic disorders as a DSM-5 category. Schizoaffective disorder is diagnosed if symptoms of mood disorder are substantially present alongside psychotic symptoms. Psychosis that results from a general medical condition or substance is termed secondary psychosis. Psychotic symptoms may be present in several other conditions, including bipolar disorder, borderline personality disorder, substance intoxication, substance-induced psychosis, and a number of drug withdrawal syndromes. Non-bizarre delusions are also present in delusional disorder, and social withdrawal in social anxiety disorder, avoidant personality disorder and schizotypal personality disorder. Schizotypal personality disorder has symptoms that are similar but less severe than those of schizophrenia. Schizophrenia occurs along with OCD considerably more often than could be explained by chance, although it can be difficult to distinguish obsessions that occur in OCD from the delusions of schizophrenia. There can be considerable overlap with the symptoms of post-traumatic stress disorder.

A more general medical and neurological examination may be needed to rule out medical illnesses which may rarely produce psychotic schizophrenia-like symptoms, such as metabolic disturbance, systemic infection, syphilis, HIV-associated neurocognitive disorder, epilepsy, limbic encephalitis, and brain lesions. Stroke, multiple sclerosis, hyperthyroidism, hypothyroidism, and dementias such as Alzheimer’s disease, Huntington’s disease, frontotemporal dementia, and the Lewy body dementias may also be associated with schizophrenia-like psychotic symptoms. It may be necessary to rule out a delirium, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, and indicates an underlying medical illness. Investigations are not generally repeated for relapse unless there is a specific medical indication or possible adverse effects from antipsychotic medication. In children hallucinations must be separated from typical childhood fantasies. It is difficult to distinguish childhood schizophrenia from autism.

Prevention

Prevention of schizophrenia is difficult as there are no reliable markers for the later development of the disorder. There is tentative though inconclusive evidence for the effectiveness of early intervention to prevent schizophrenia in the prodrome phase. There is some evidence that early intervention in those with first-episode psychosis may improve short-term outcomes, but there is little benefit from these measures after five years. Cognitive behavioural therapy (CBT) may reduce the risk of psychosis in those at high risk after a year and is recommended in this group, by the National Institute for Health and Care Excellence (NICE). Another preventive measure is to avoid drugs that have been associated with development of the disorder, including cannabis, cocaine, and amphetamines.

Antipsychotics are prescribed following a first-episode psychosis, and following remission a preventive maintenance use is continued to avoid relapse. However, it is recognised that some people do recover following a single episode and that long-term use of antipsychotics will not be needed but there is no way of identifying this group.

Management

The primary treatment of schizophrenia is the use of antipsychotic medications, often in combination with psychosocial interventions and social supports. Community support services including drop-in centres, visits by members of a community mental health team, supported employment, and support groups are common. The time between the onset of psychotic symptoms to being given treatment – the duration of untreated psychosis (DUP) is associated with a poorer outcome in both the short term and the long term.

Voluntary or involuntary admittance to hospital may be needed to treat a severe episode, however, hospital stays are as short as possible. In the UK large mental hospitals termed asylums began to be closed down in the 1950s with the advent of antipsychotics, and with an awareness of the negative impact of long-term hospital stays on recovery. This process was known as deinstitutionalisation, and community and supportive services were developed in order to support this change. Many other countries followed suit with the US starting in the 60s. There will still remain a few people who do not improve enough to be discharged. In those countries that lack the necessary supportive and social services long-term hospital stays are more usual.

Medication

The first-line treatment for schizophrenia is an antipsychotic. The first-generation antipsychotics, now called typical antipsychotics, are dopamine antagonists that block D2 receptors, and affect the neurotransmission of dopamine. Those brought out later, the second-generation antipsychotics known as atypical antipsychotics, can also have effect on another neurotransmitter, serotonin. Antipsychotics can reduce the symptoms of anxiety within hours of their use but for other symptoms they may take several days or weeks to reach their full effect. They have little effect on negative and cognitive symptoms, which may be helped by additional psychotherapies and medications. There is no single antipsychotic suitable for first-line treatment for everyone, as responses and tolerances vary between people. Stopping medication may be considered after a single psychotic episode where there has been a full recovery with no symptoms for twelve months. Repeated relapses worsen the long-term outlook and the risk of relapse following a second episode is high, and long-term treatment is usually recommended.

Tobacco smoking increases the metabolism of some antipsychotics, by strongly activating CYP1A2, the enzyme that breaks them down, and a significant difference is found in these levels between smokers and non-smokers. It is recommended that the dosage for those smokers on clozapine be increased by 50%, and for those on olanzapine by 30%. The result of stopping smoking can lead to an increased concentration of the antipsychotic that may result in toxicity, so that monitoring of effects would need to take place with a view to decreasing the dosage; many symptoms may be noticeably worsened, and extreme fatigue, and seizures are also possible with a risk of relapse. Likewise those who resume smoking may need their dosages adjusted accordingly. The altering effects are due to compounds in tobacco smoke and not to nicotine; the use of nicotine replacement therapy therefore has the equivalent effect of stopping smoking and monitoring would still be needed.

About 30-50% of people with schizophrenia fail to accept that they have an illness or comply with their recommended treatment. For those who are unwilling or unable to take medication regularly, long-acting injections of antipsychotics may be used, which reduce the risk of relapse to a greater degree than oral medications. When used in combination with psychosocial interventions, they may improve long-term adherence to treatment.

Research findings suggested that other neurotransmission systems, including serotonin, glutamate, GABA, and acetycholine, were implicated in the development of schizophrenia, and that a more inclusive medication was needed. A new first-in-class antipsychotic that targets multiple neurotransmitter systems called lumateperone (ITI-007), was trialled and approved by the FDA in December 2019 for the treatment of schizophrenia in adults. Lumateperone is a small molecule agent that shows improved safety, and tolerance. It interacts with dopamine, serotonin, and glutamate in a complex, uniquely selective manner, and is seen to improve negative and positive symptoms, and social functioning. Lumateperone was also found to reduce potential metabolic dysfunction, have lower rates of movement disorders, and have lower cardiovascular side effects such as a fast heart rate.

Side Effects

Typical antipsychotics are associated with a higher rate of movement disorders including akathisia. Some atypicals are associated with considerable weight gain, diabetes and the risk of metabolic syndrome. Risperidone (atypical) has a similar rate of extrapyramidal symptoms to haloperidol (typical). A rare but potentially lethal condition of neuroleptic malignant syndrome (NMS) has been associated with the use of antipsychotics. Through its early recognition, and timely intervention rates have declined. However, an awareness of the syndrome is advised to enable intervention. Another less rare condition of tardive dyskinesia can occur due to long-term use of antipsychotics, developing after many months or years of use. It is more often reported with use of typical antipsychotics.

Clozapine is associated with side effects that include weight gain, tiredness, and hypersalivation. More serious adverse effects include seizures, NMS, neutropenia, and agranulocytosis (lowered white blood cell count) and its use needs careful monitoring. Studies have found that antipsychotic treatment following NMS and neutropenia may sometimes be successfully re-challenged (restarted) with clozapine.

Clozapine is also associated with thromboembolism (including pulmonary embolism), myocarditis, and cardiomyopathy. A systematic review of clozapine-associated pulmonary embolism indicates that this adverse effect can often be fatal, and that it has an early onset, and is dose-dependent. The findings advised the consideration of using a prevention therapy for venous thromboembolism after starting treatment with clozapine, and continuing this for six months. Constipation is three times more likely to occur with the use of clozapine, and severe cases can lead to ileus and bowel ischemia resulting in many fatalities.

However, the risk of serious adverse effects from clozapine is low, and there are the beneficial effects to be gained of a reduced risk of suicide, and aggression. Typical antipsychotics and atypical risperidone can have a side effect of sexual dysfunction. Clozapine, olanzapine, and quetiapine are associated with beneficial effects on sexual functioning helped by various psychotherapies. Unwanted side effects cause people to stop treatment, resulting in relapses.

Treatment Resistant Schizophrenia

About half of those with schizophrenia will respond favourably to antipsychotics, and have a good return of functioning. However, positive symptoms persist in up to a third of people. Following two trials of different antipsychotics over six weeks, that also prove ineffective, they will be classed as having treatment resistant schizophrenia (TRS), and clozapine will be offered. Clozapine is of benefit to around half of this group although it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people. Between 12-20% will not respond to clozapine and this group is said to have ultra treatment resistant schizophrenia. ECT may be offered to treat TRS as an add-on therapy, and is shown to sometimes be of benefit. A review concluded that this use only has an effect on medium-term TRS and that there is not enough evidence to support its use other than for this group.

TRS is often accompanied by a low quality of life, and greater social dysfunction. TRS may be the result of inadequate rather than inefficient treatment; it also may be a false label due to medication not being taken regularly, or at all. About 16% of people who had initially been responsive to treatment later develop resistance. This could relate to the length of time on APs, with treatment becoming less responsive. This finding also supports the involvement of dopamine in the development of schizophrenia. Studies suggest that TRS may be a more heritable form.

TRS may be evident from first episode psychosis, or from a relapse. It can vary in its intensity and response to other therapies. This variation is seen to possibly indicate an underlying neurobiology such as dopamine super-sensitivity (DSS), glutamate or serotonin dysfunction, inflammation and oxidative stress. Studies have found that dopamine super-sensitivity is found in up to 70% of those with TRS. The variation has led to the suggestion that treatment responsive and treatment resistant schizophrenia be considered as two different subtypes. It is further suggested that if the subtypes could be distinguished at an early stage significant implications could follow for treatment considerations, and for research. Neuroimaging studies have found a significant decrease in the volume of grey matter in those with TRS with no such change seen in those who are treatment responsive. In those with ultra treatment resistance the decrease in grey matter volume was larger.

A link has been made between the gut microbiota and the development of TRS. The most prevalent cause put forward for TRS is that of mutation in the genes responsible for drug effectiveness. These include liver enzyme genes that control the availability of a drug to brain targets, and genes responsible for the structure and function of these targets. In the colon the bacteria encode a hundred times more genes than exist in the human genome. Only a fraction of ingested drugs reach the colon, having been already exposed to small intestinal bacteria, and absorbed in the portal circulation. This small fraction is then subject to the metabolic action of many communities of bacteria. Activation of the drug depends on the composition and enzymes of the bacteria and of the specifics of the drug, and therefore a great deal of individual variation can affect both the usefulness of the drug and its tolerability. It is suggested that parenteral administration of antipsychotics would bypass the gut and be more successful in overcoming TRS. The composition of gut microbiota is variable between individuals, but they are seen to remain stable. However, phyla can change in response to many factors including ageing, diet, substance-use, and medications – especially antibiotics, laxatives, and antipsychotics. In FEP, schizophrenia has been linked to significant changes in the gut microbiota that can predict response to treatment.

Psychosocial Interventions

A number of psychosocial interventions that include several types of psychotherapy may be useful in the treatment of schizophrenia such as: family therapy, group therapy, cognitive remediation therapy, CBT, and metacognitive training. Skills training, and help with substance use, and weight management – often needed as a side effect of an antipsychotic, are also offered. In the US, interventions for first episode psychosis have been brought together in an overall approach known as coordinated speciality care (CSC) and also includes support for education. In the UK care across all phases is a similar approach that covers many of the treatment guidelines recommended. The aim is to reduce the number of relapses and stays in hospital.

Other support services for education, employment, and housing are usually offered. For people suffering from severe schizophrenia, and discharged from a stay in hospital, these services are often brought together in an integrated approach to offer support in the community away from the hospital setting. In addition to medicine management, housing, and finances, assistance is given for more routine matters such as help with shopping and using public transport. This approach is known as assertive community treatment (ACT) and has been shown to achieve positive results in symptoms, social functioning and quality of life. Another more intense approach is known as intensive care management (ICM). ICM is a stage further than ACT and emphasises support of high intensity in smaller caseloads, (less than twenty). This approach is to provide long-term care in the community. Studies show that ICM improves many of the relevant outcomes including social functioning.

Some studies have shown little evidence for the effectiveness of CBT in either reducing symptoms or preventing relapse. However, other studies have found that CBT does improve overall psychotic symptoms (when in use with medication) and has been recommended in Canada, but it has been seen here to have no effect on social function, relapse, or quality of life. In the UK it is recommended as an add-on therapy in the treatment of schizophrenia, but is not supported for use in treatment resistant schizophrenia. Arts therapies are seen to improve negative symptoms in some people, and are recommended by NICE in the UK. This approach however, is criticised as having not been well-researched, and arts therapies are not recommended in Australian guidelines for example. Peer support, in which people with personal experience of schizophrenia, provide help to each other, is of unclear benefit.

Other

Exercise including aerobic exercise has been shown to improve positive and negative symptoms, cognition, working memory, and improve quality of life. Exercise has also been shown to increase the volume of the hippocampus in those with schizophrenia. A decrease in hippocampal volume is one of the factors linked to the development of the disease. However, there still remains the problem of increasing motivation for, and maintaining participation in physical activity. Supervised sessions are recommended. In the UK healthy eating advice is offered alongside exercise programmes.

An inadequate diet is often found in schizophrenia, and associated vitamin deficiencies including those of folate, and vitamin D are linked to the risk factors for the development of schizophrenia and for early death including heart disease. Those with schizophrenia possibly have the worst diet of all the mental disorders. Lower levels of folate and vitamin D have been noted as significantly lower in first episode psychosis. The use of supplemental folate is recommended. A zinc deficiency has also been noted. Vitamin B12 is also often deficient and this is linked to worse symptoms. Supplementation with B vitamins has been shown to significantly improve symptoms, and to put in reverse some of the cognitive deficits. It is also suggested that the noted dysfunction in gut microbiota might benefit from the use of probiotics.

Violence

Most people with schizophrenia are not aggressive, and are more likely to be victims of violence rather than perpetrators. However, though the risk of violence in schizophrenia is small the association is consistent, and there are minor subgroups where the risk is high. This risk is usually associated with a comorbid disorder such as a substance use disorder – in particular alcohol, or with antisocial personality disorder. Substance abuse is strongly linked, and other risk factors are linked to deficits in cognition and social cognition including facial perception and insight that are in part included in theory of mind impairments. Poor cognitive functioning, decision-making, and facial perception may contribute to making a wrong judgement of a situation that could result in an inappropriate response such as violence. These associated risk factors are also present in antisocial personality disorder which when present as a comorbid disorder greatly increases the risk of violence.

A review in 2012 showed that schizophrenia was responsible for 6% of homicides in Western countries. Another wider review put the homicide figure at between 5-20%. There was found to be a greater risk of homicide during first episode psychosis that accounted for 38.5% of homicides. The association between schizophrenia and violence is complex. Homicide is linked with young age, male sex, a history of violence, and a stressful event in the preceding year. Clinical risk factors are severe untreated psychotic symptoms – untreated due to either not taking medication or to the condition being treatment resistant. A comorbid substance use disorder or an antisocial personality disorder increases the risk for homicidal behaviour by 8-fold, in contrast to the 2-fold risk in those without the comorbid disorders. Rates of homicide linked to psychosis are similar to those linked to substance misuse, and parallel the overall rate in a region. What role schizophrenia has on violence independent of substance misuse is controversial, but certain aspects of individual histories or mental states may be factors.

Hostility is anger felt and directed at a person or group and has related dimensions of impulsiveness and aggression. When this impulsive-aggression is evident in schizophrenia neuroimaging has suggested the malfunctioning of a neural circuit that modulates hostile thoughts and behaviours that are linked with negative emotions in social interactions. This circuit includes the amygdala, striatum, prefrontal cortex, anterior cingulate cortex, insula, and hippocampus. Hostility has been reported during acute psychosis, and following hospital discharge. There is a known association between low cholesterol levels, and impulsivity, and violence. A review finds that people with schizophrenia, and lower cholesterol levels are four times more likely to instigate violent acts. This association is also linked to the increased number of suicides in schizophrenia. It is suggested that cholesterol levels could serve as a biomarker for violent and suicidal tendencies.

A review found that just under 10% of those with schizophrenia showed violent behaviour compared to 1.6% of the general population. An excessive risk of violence is associated with drugs or alcohol and increases the risk by as much as 4-fold. Violence often leads to imprisonment. Clozapine is an effective medication that can be used in penal settings such as prisons. However, a condition of benign ethnic neutropenia in many African-Americans excludes them from the use of clozapine the most effective medication. Cognitive deficits are recognised as playing an important part in the origin and maintenance of aggression, and cognitive remediation therapy may therefore help to prevent the risk of violence in schizophrenia.

Prognosis

Schizophrenia has great human and economic costs. It results in a decreased life expectancy of 20 years. This is primarily because of its association with obesity, poor diet, a sedentary lifestyle, and smoking, with an increased rate of suicide playing a lesser role. Side effects of antipsychotics may also increase the risk. These differences in life expectancy increased between the 1970s and 1990s. An Australian study puts the rate of early death at 25 years, and views the main cause to be related to heart disease.

Several studies indicate that almost 40% of those with schizophrenia die from complications of cardiovascular disease including heart attacks, and sudden cardiac death which is seen to be increasingly associated. An underlying factor of sudden cardiac death may be Brugada syndrome (BrS) – BrS mutations that overlap with those linked with schizophrenia are the calcium channel mutations. BrS may also be drug-induced from certain antipsychotics and antidepressants. Primary polydipsia, or excessive fluid intake, is relatively common in people with chronic schizophrenia. This may lead to hyponatremia which can be life-threatening. Antipsychotics can lead to a dry mouth, but there are several other factors that may contribute to the disorder. It is suggested to lead to a reduction in life expectancy by 13%. A study has suggested that real barriers to improving the mortality rate in schizophrenia are poverty, overlooking the symptoms of other illnesses, stress, stigma, and medication side effects, and that these need to be changed.

Schizophrenia is a major cause of disability. In 2016 it was classed as the 12th most disabling condition. Approximately 75% of people with schizophrenia have ongoing disability with relapses and 16.7 million people globally are deemed to have moderate or severe disability from the condition. Some people do recover completely and others function well in society. Most people with schizophrenia live independently with community support. About 85% are unemployed. In people with a first episode of psychosis in schizophrenia a good long-term outcome occurs in 31%, an intermediate outcome in 42% and a poor outcome in 31%. Males are affected more often than females, and have a worse outcome. Outcomes for schizophrenia appear better in the developing than the developed world. These conclusions have been questioned. Social problems, such as long-term unemployment, poverty, homelessness, exploitation, stigmatisation and victimisation are common consequences, and lead to social exclusion.

There is a higher than average suicide rate associated with schizophrenia estimated at around 5% to 6%, most often occurring in the period following onset or first hospital admission. Several times more (20 to 40%) attempt suicide at least once. There are a variety of risk factors, including male gender, depression, a high IQ, heavy smoking, and substance abuse. Repeated relapse is linked to an increased risk of suicidal behaviour. The use of clozapine can reduce the risk of suicide and aggression.

A strong association between schizophrenia and tobacco smoking has been shown in worldwide studies. Smoking is especially high in those diagnosed with schizophrenia, with estimates ranging from 80 to 90% being regular smokers, as compared to 20% of the general population. Those who smoke tend to smoke heavily, and additionally smoke cigarettes with high nicotine content. Some propose that this is in an effort to improve symptoms. Among people with schizophrenia use of cannabis is also common.

Society and Culture

In 2002, the term for schizophrenia in Japan was changed from seishin-bunretsu-byō (精神分裂病, lit. “mind-split disease”) to tōgō-shitchō-shō (統合失調症, lit. “integration-dysregulation syndrome”) to reduce stigma. The new name also interpreted as “integration disorder” was inspired by the biopsychosocial model; it increased the percentage of people who were informed of the diagnosis from 37 to 70% over three years. A similar change was made in South Korea in 2012 to attunement disorder. A professor of psychiatry, Jim van Os, has proposed changing the English term to psychosis spectrum syndrome. In 2013 with the reviewed DSM-5, the DSM-5 committee was in favour of giving a new name to schizophrenia but they referred this to WHO.

In the United States, the cost of schizophrenia – including direct costs (outpatient, inpatient, drugs, and long-term care) and non-health care costs (law enforcement, reduced workplace productivity, and unemployment) – was estimated to be $62.7 billion in 2002. In the UK the cost in 2016 was put at £11.8 billion per year with a third of that figure directly attributable to the cost of hospital and social care, and treatment.

The book A Beautiful Mind chronicled the life of John Forbes Nash who had been diagnosed with schizophrenia but who went on to win the Nobel Memorial Prize in Economic Sciences. This was later made into the film with the same name. An earlier documentary was made with the title A Brilliant Madness.

In 1964, a lengthy case study of three males diagnosed with schizophrenia who each had the delusional belief that they were Jesus Christ was published as a book. This has the title of The Three Christs of Ypsilanti, and a film with the title Three Christs was released in 2020. Such religious delusions are a fairly common feature in psychoses including schizophrenia.

Media coverage relating to violent acts by people with schizophrenia reinforces public perception of an association between schizophrenia and violence. Such sensationalist reporting stigmatizes schizophrenia more than any other mental illness. In the UK guidelines are given for the reporting of different conditions. Its campaigns have shown a reduction in negative reporting.

Research Directions

Research into schizophrenia has made use of a number of animal models in particular rats, that have shown to be useful in evaluating the different aspects of its development and pathology. Effects of early intervention is an active area of research, importantly focusing on the early detection of at-risk individuals and the development of risk calculators. Methods for large-scale population screening are also included.

Various agents have been explored for possible effectiveness in treating negative symptoms, for which antipsychotics have been of little benefit. There have been trials on medications with anti-inflammatory activity, based on the premise that inflammation might play a role in the pathology of schizophrenia.

Various brain stimulation techniques are being studied to treat the positive symptoms of schizophrenia, in particular auditory verbal hallucinations (AVHs). A 2015 Cochrane review found unclear evidence of benefit. Most studies focus on transcranial direct-current stimulation (tDCM), and repetitive transcranial magnetic stimulation (rTMS). Techniques based on focused ultrasound for deep brain stimulation could provide insight for the treatment of AVHs.

Another active area of research is the study of a variety of potential biomarkers that would be of invaluable help not only in the diagnosis but also in the treatment and prognosis of schizophrenia. Possible biomarkers include markers of inflammation, neuroimaging, BDNF, genetics, and speech analysis. Some inflammatory markers such as C-reactive protein are useful in detecting levels of inflammation implicated in some psychiatric disorders but they are not disorder-specific. However, other inflammatory cytokines are found to be elevated in first episode psychosis and acute relapse that are normalised after treatment with antipsychotics, and these may be considered as state markers. Deficits in sleep spindles in schizophrenia may serve as a marker of an impaired thalamocortical circuit, and a mechanism for memory impairment. MicroRNAs are highly influential in early neuronal development, and their disruption is implicated in several CNS disorders; circulating microRNAs (cimiRNAs) are found in body fluids such as blood and cerebrospinal fluid, and changes in their levels are seen to relate to changes in microRNA levels in specific regions of brain tissue. These studies suggest that cimiRNAs have the potential to be early and accurate biomarkers in a number of disorders including schizophrenia.

The use of choline as a supplement during pregnancy may have effect in the prevention of the later development of schizophrenia, and is an area of research.

In 2020, over 3,000 clinical trials into drugs, symptom assessment tools, and treatments related to schizophrenia were listed with some recruiting, and some newly completed.

Book: Beating OCD and Anxiety

Book Title:

Beating OCD and Anxiety – 75 Tried and Tested Strategies for Sufferers and their Supporters.

Author(s): Helena Tarrant.

Year: 2020.

Edition: First (1st).

Publisher: Cherish Editions.

Type(s): Paperback and Kindle.

Synopsis:

Does anxiety impact on everything you do, leaving you unable to get through the day or with an inability to make decisions, no matter how small? Has it affected or even destroyed friendships and relationships? Or maybe you know or live with someone with these issues, and feel unable to help them?

Helena Tarrant gets it. She also understands why you may have struggled with text-heavy anxiety guides in the past. This book can help you to start a new fulfilling life, or help you provide invaluable support to someone you care about. The author has recovered from lifelong debilitating obsessive compulsive disorder and generalized anxiety disorder. This book shares the tried and tested techniques that she used to do it, based largely but not entirely on the methods and concepts behind cognitive behavioural therapy.

Written in accessible language, conveniently segmented and illustrated with over 100 original cartoons, the techniques are described clearly and concisely. Beating OCD and Anxiety knows you don’t want to read pages of complex theory on your quest for help.

In this book, Helena will show you how to get your life back.

Book: A Concise Introduction to Existential Counselling

Book Title:

A Concise Introduction to Existential Counselling.

Author(s): Martin Adams.

Year: 2013.

Edition: First (1st).

Publisher: SAGE Publications Ltd.

Type(s): Hardcover, Paperback, and Kindle.

Synopsis:

A Concise Introduction to Existential Counselling is just that: a brief and accessible pocket guide to the underlying theory & practice of the existential approach.

Addressing everything a new trainee needs to know and do in a way that is entirely accessible and jargon-free, this book:

  • Provides a short history of the existential tradition.
  • Puts key concepts into contexts, showing how theory translates into practice.
  • Discusses issues in the therapeutic process.
  • Shows how to work effectively with whatever the client brings to the session.
  • Addresses the significance of existential thought in the wider world.

This book will be the perfect companion to new trainees looking to embark on their path to thinking and practicing existentially.

Martin Adams is a practitioner and supervisor in private practice and a Lecturer at the New School of Psychotherapy and Regents College, both in London.

Linking Anxiety, AUD & GABAB

Research Paper Title

The influence of anxiety symptoms on clinical outcomes during baclofen treatment of alcohol use disorder: A systematic review and meta-analysis.

Background

Given the high coexistence of anxiety symptoms in people with alcohol use disorder (AUD), the researchers aimed to determine the influence of anxiety symptoms on outcomes in patients with AUD treated with GABAB receptor agonist baclofen.

Methods

A meta-analysis of 13 comparisons (published 2010-2020) including baseline and outcome data on alcohol consumption and anxiety after 12 weeks was undertaken.

Results

There were significantly higher rates of abstinent days in patients treated with baclofen compared to placebo (p = 0.004; high certainty evidence); specifically in those with higher baseline anxiety levels (p < 0.00001; high certainty evidence) compared to those with lower baseline anxiety levels (p = 0.20; moderate certainty evidence). The change in anxiety ratings over 12 weeks did not differ between those treated with baclofen or placebo (p = 0.84; moderate certainty evidence).

Conclusions

This may be due to different anxiety constructs being measured by scales not validated in this patient group, or that anxiety is not a biobehavioural mechanism by which baclofen may reduce alcohol drinking. Given the prevalence of anxiety symptoms in AUD all these factors warrant further research.

Reference

Agabio, R., Baldwin, D.S., Amaro, H., Leggio, L. & Sinclair, J.M.A. (2021) The influence of anxiety symptoms on clinical outcomes during baclofen treatment of alcohol use disorder: A systematic review and meta-analysis. Neuroscience and Biobehavioural Reviews. doi: 10.1016/j.neubiorev.2020.12.030. Online ahead of print.

What is Hikikomori?

Introduction

Hikikomori (Japanese: ひきこもり or 引き籠もり, lit. “pulling inward, being confined”), also known as “acute social withdrawal” , is total withdrawal from society and seeking extreme degrees of social isolation and confinement. Hikikomori refers to both the phenomenon in general and the recluses themselves. Hikikomori have been described as loners or “modern-day hermits”. Estimates suggest that half a million Japanese youths have become social recluses, as well as more than half a million middle-aged individuals.

Definition

The Japanese Ministry of Health, Labour, and Welfare defines hikikomori as a condition in which the affected individuals refuse to leave their parents’ house, do not work or go to school and isolate themselves away from society and family in a single room for a period exceeding six months. The psychiatrist Tamaki Saitō defines hikikomori as “a state that has become a problem by the late twenties, that involves cooping oneself up in one’s own home and not participating in society for six months or longer, but that does not seem to have another psychological problem as its principal source”.

More recently, researchers have developed more specific criteria to more accurately identify hikikomori. During a diagnostic interview, trained clinicians evaluate for:

  • Spending most of the day and nearly every day confined to home;
  • Marked and persistent avoidance of social situations, and social relationships;
  • Social withdrawal symptoms causing significant functional impairment;
  • Duration of at least six months; and
  • No apparent physical or mental aetiology to account for the social withdrawal symptoms.

The psychiatrist Alan Teo first characterised hikikomori in Japan as modern-day hermits, while the literary and communication scholar Flavio Rizzo similarly described hikikomori as “post-modern hermits” whose solitude stems from ancestral desires for withdrawal.

While the degree of the phenomenon varies on an individual basis, in the most extreme cases, some people remain in isolation for years or even decades. Often hikikomori start out as school refusers, or futōkō (不登校) in Japanese (an older term is tōkōkyohi (登校拒否)).

Common Traits

While many people feel the pressures of the outside world, hikikomori react by complete social withdrawal. In some more extreme cases, they isolate themselves in their bedrooms for months or years at a time. They usually have few or no friends. In interviews with current or recovering hikikomori, media reports and documentaries have captured the strong levels of psychological distress and angst felt by these individuals.

While hikikomori favour indoor activities, some venture outdoors occasionally. The withdrawal from society usually starts gradually. Affected people may appear unhappy, lose their friends, become insecure and shy, and talk less.

Prevalence

According to Japanese government figures released in 2010, there are 700,000 individuals living as hikikomori within Japan, with an average age of 31. Still, the numbers vary widely among experts. These include the hikikomori who are now in their 40s (as of 2011) and have spent 20 years in isolation. This group is generally referred to as the “first-generation hikikomori.” There is concern about their reintegration into society in what is known as “the 2030 Problem,” when they are in their 60s and their parents begin to die. Additionally, the government estimates that 1.55 million people are on the verge of becoming hikikomori. Tamaki Saitō, who first coined the phrase, originally estimated that there may be over one million hikikomori in Japan, although this was not based on national survey data. Nonetheless, considering that hikikomori adolescents are hidden away and their parents are often reluctant to talk about the problem, it is extremely difficult to gauge the number accurately.

A 2015 Cabinet Office survey estimated that 541,000 recluses aged 15 to 39 existed. In 2019, another survey showed that there are roughly 613,000 people aged 40 to 64 that fall into the category of “adult hikikomori”, which Japan’s welfare minister Takumi Nemoto referred to as a “new social issue.”

While hikikomori is mostly a Japanese phenomenon, cases have been found in the United States, United Kingdom, Oman, Spain, Italy, India, Sweden, South Korea, and France.

Hypotheses on the Cause(s)

Developmental and Psychiatric Conditions

Hikikomori is similar to the social withdrawal exhibited by some people with autism spectrum disorders, a group of developmental disorders that include Asperger syndrome, PDD-NOS and “classic” autism. This has led some psychiatrists to suggest that hikikomori may be affected by autism spectrum disorders and other disorders that affect social integration, but that their disorders are altered from their typical Western presentation because of Japanese sociocultural pressures. Suwa & Hara (2007) discovered that 5 of 27 cases of hikikomori had a high-functioning pervasive developmental disorder (HPDD), and 12 more had other disorders or mental diseases (6 cases of personality disorders, 3 cases of obsessive-compulsive disorder, 2 cases of depression, 1 case of slight mental retardation); 10 out of 27 had primary hikikomori. The researchers used a vignette to illustrate the difference between primary hikikomori (without any obvious mental disorder) and hikikomori with HPDD or other disorder. Alan Teo and colleagues conducted detailed diagnostic evaluations of 22 individuals with hikikomori and found that while the majority of cases fulfilled criteria for multiple psychiatric conditions, about 1 in 5 cases were primary hikikomori. Till date, however, hikikomori is not included in the DSM-5, due to insufficient data.

According to Michael Zielenziger’s book, Shutting Out the Sun: How Japan Created Its Own Lost Generation, the syndrome is more closely related to posttraumatic stress disorder. The author claimed that the hikikomori interviewed for the book had discovered independent thinking and a sense of self that the current Japanese environment could not accommodate.

The syndrome also closely parallels the terms avoidant personality disorder, schizoid personality disorder, schizotypal personality disorder, agoraphobia or social anxiety disorder (also known as “social phobia”).

Social and Cultural Influence

Sometimes referred to as a social problem in Japanese discourse, hikikomori has a number of possible contributing factors. Alan Teo has summarised a number of potential cultural features that may contribute to its predominance in Japan. These include tendencies toward conformity and collectivism, overprotective parenting, and particularities of the educational, housing and economic systems.

Acute social withdrawal in Japan appears to affect both genders equally. However, because of differing social expectations for maturing boys and girls, the most widely reported cases of hikikomori are from middle- and upper-middle-class families; sons, typically their eldest, refuse to leave the home, often after experiencing one or more traumatic episodes of social or academic failure.

In The Anatomy of Dependence, Takeo Doi identifies the symptoms of hikikomori, and explains its prevalence as originating in the Japanese psychological construct of amae (in Freudian terms, “passive object love”, typically of the kind between mother and infant). Other Japanese commentators such as academic Shinji Miyadai and novelist Ryū Murakami, have also offered analysis of the hikikomori phenomenon, and find distinct causal relationships with the modern Japanese social conditions of anomie, amae and atrophying paternal influence in nuclear family child pedagogy. Young adults may feel overwhelmed by modern Japanese society, or be unable to fulfil their expected social roles as they have not yet formulated a sense of personal honne and tatemae – one’s “true self” and one’s “public façade” – necessary to cope with the paradoxes of adulthood.

The dominant nexus of hikikomori centres on the transformation from youth to the responsibilities and expectations of adult life. Indications are that advanced industrialised societies such as modern Japan fail to provide sufficient meaningful transformation rituals for promoting certain susceptible types of youth into mature roles. As do many societies, Japan exerts a great deal of pressure on adolescents to be successful and perpetuate the existing social status quo. A traditionally strong emphasis on complex social conduct, rigid hierarchies and the resulting, potentially intimidating multitude of social expectations, responsibilities and duties in Japanese society contribute to this pressure on young adults. Historically, Confucian teachings de-emphasizing the individual and favouring a conformist stance to ensure social harmony in a rigidly hierarchized society have shaped much of East Asia, possibly explaining the emergence of the hikikomori phenomenon in other East Asian countries.

In general, the prevalence of hikikomori tendencies in Japan may be encouraged and facilitated by three primary factors:

  • Middle class affluence in a post-industrial society such as Japan allows parents to support and feed an adult child in the home indefinitely.
    • Lower-income families do not have hikikomori children because a socially withdrawing youth is forced to work outside the home.
  • The inability of Japanese parents to recognise and act upon the youth’s slide into isolation; soft parenting; or co-dependence between mother and son, known as amae in Japanese.
  • A decade of flat economic indicators and a shaky job market in Japan makes the pre-existing system requiring years of competitive schooling for elite jobs appear like a pointless effort to many.

Role of Modern Technology

Although the connection between modern communication technologies, such as the Internet, social media and video games, and the phenomenon is not conclusively established, it is considered at least an exacerbating factor that can deepen and nurture withdrawal. Previous studies of hikikomori in South Korea and Spain found that some of them showed signs of Internet addiction, though researchers do not consider this to be the main issue. However, according to associate professor of psychiatry at Kyushu University in Fukuoka, Takahiro Kato, video games and social media have reduced the amount of time that people spent outside and in social environments that require direct face to face interaction. The emergence of mobile phones and then smartphones may also have deepened the issue, given that people can continue their addiction to gaming and online surfing anywhere, even in bed.

Japanese Education System

The Japanese education system, like those found in China, Singapore, India, and South Korea, puts great demands upon youth. A multitude of expectations, high emphasis on competition, and the rote memorization of facts and figures for the purpose of passing entrance exams into the next tier of education in what could be termed a rigid pass-or-fail ideology, induce a high level of stress. Echoing the traditional Confucian values of society, the educational system is viewed as playing an important part in society’s overall productivity and success.

In this social frame, students often face significant pressure from parents and the society in general to conform to its dictates and doctrines. These doctrines, while part of modern Japanese society, are increasingly being rejected by Japanese youth in varying ways such as hikikomori, freeter, NEET (Not currently engaged in Employment, Education, or Training), and parasite singles. The term “Hodo-Hodo zoku” (the “So-So tribe”) applies to younger workers who refuse promotion to minimise stress and maximise free time.

Beginning in the 1960s, the pressure on Japanese youth to succeed began successively earlier in their lives, sometimes starting before pre-school, where even toddlers had to compete through an entrance exam for the privilege of attending one of the best pre-schools. This was said to prepare children for the entrance exam of the best kindergarten, which in turn prepared the child for the entrance exam of the best elementary school, junior high school, high school, and eventually for their university entrance exam. Many adolescents take one year off after high school to study exclusively for the university entrance exam, and are known as ronin. More prestigious universities have more difficult exams. The most prestigious university with the most difficult exam is the University of Tokyo.

Since 1996, the Japanese Ministry of Education has taken steps to address this ‘pressure-cooker’ educational environment and instil greater creative thought in Japanese youth by significantly relaxing the school schedule from six-day weeks to five-day weeks and dropping two subjects from the daily schedule, with new academic curricula more comparable to Western educational models. However, Japanese parents are sending their children to private cram schools, known as juku, to ‘make up’ for lost time.

After graduating from high school or university, Japanese youth also have to face a very difficult job market in Japan, often finding only part-time employment and ending up as freeters with little income, unable to start a family.

Another source of pressure is from their co-students, who may harass and bully (ijime) some students for a variety of reasons, including physical appearance, wealth, or educational or athletic performance. Some have been punished for bullying or truancy, bringing shame to their families. Refusal to participate in society makes hikikomori an extreme subset of a much larger group of younger Japanese that includes freeters.

Impact

Japanese Financial Burden

Some organizations such as the non-profit Japanese organisation NPO lila have been trying to combat the financial burden the hikikomori phenomenon has had on Japan’s economy. The Japanese CD and DVD producer Avex Group produces DVD videos of live-action women staring into a camera to help hikikomori learn to cope with eye contact and long spans of human interaction. The goal is to help hikikomori reintegrate into society by personal choice, thereby realising an economic contribution and reducing the financial burden on parents.

“80-50 Problem”

Described in Japanese literature and media, first from the late 2010s, hikikomori of youth from earlier days, as have their parents upon whom they rely. The “80-50 problem” refers to the hikikomori children being in their 50s (or thereabouts), with their only means of support being their ageing parents who are in their 80s (or thereabouts).

A Japanese government Cabinet Office survey counted roughly 540,000 hikikomori people in 2015. However, this survey covers a restricted age group of 15 to 39 years of age. Hikikomori people in their 40s and 50s are consequently not surveyed or otherwise studied.

In 2019, Japanese psychiatrist Dr. Saitō Tamaki held a press briefing at the Foreign Press Centre Japan on the subject of hikikomori. Among addressing ageing, he recommended practical advice to that parents with hikikomori, such as drawing up a lifetime financial plan for hikikomori children, so they can get by after the parents are gone. He also recommended that parents should not fear embarrassment or be concerned about appearances as they look at the options, including disability pensions or other forms of public assistance for their children. Given the Japanese government – failing to see the urgency of the problem – is demonstrating no motion toward developing substantive policies or systems related to the ageing of hikikomori, Dr Tamaki has emphasised the urgency and necessity for families to plan ahead.

Treatment Programmes

When it comes to psychosocial support, it is hard for therapists to attain direct access to hikikomori; research to find different and effective treatment plans to aid hikikomori has been ongoing. One such treatment plan is focused on the families of hikikomori. Such focus primarily includes, educational intervention programmes (e.g. lectures, role-play, etc.) that are geared towards reducing any averse stigma that family members have towards psychiatric disorders like hikikomori. These educational programmes are derived from other established family support programmes, specifically Mental Health First Aid (MFHA) and Community Reinforcement and Family Training (CRAFT). CRAFT specifically trains family members express positive and functional communication, whereas MFHA provides skills to support hikikomori with depression/suicidal like behaviour. Studies so far that have modified the family unit’s behavioural response to a hikikomori has yielded positive results, indicating that family behaviour is essential for recovery, however further research is still needed.

Although there has been a primary emphasis on educating family members, there are still therapy programmes for the hikikomori to participate themselves in. For example, the use of exercise therapy. The individual psychotherapy methods that are being stressed in current research are primarily motivated on cultivating self-confidence within the hikikomori. With that being said, however, studies have delineated that efficacious treatment towards hikikomori requires a multifaceted approach rather than the utilisation of one individual approach, such as individual psychotherapy or family therapy.

Pandemic Impact

Based on prior outbreaks (e.g. SARS, MERS, etc.), studies have shown that quarantined individuals, due to increased loneliness, have heightened stress-related mental disturbances. Considering that political, social, and/or economical challenges already bring people to express hikikomori like behaviour, researchers theorise that since all the aforementioned factors are by-products of a pandemic, many postulate a hikikomori phenomenon common in a post-pandemic world. In fact, people who do experience mental disturbances in Japan generally view seeking the help of a psychiatrist as shameful or a reason for them to be socially shunned. Experts predict an increase in focus on both the youth and also on mental health specifically through effective telemedicine to either the affected individual and/or their respective family unit.

Furthermore, with hikikomori becoming more prevalent amid a pandemic, experts theorise that it will bring out more empathy and constructive attention towards the issue.

What is Agoraphobia?

Introduction

Agoraphobia is an anxiety disorder characterised by symptoms of anxiety in situations where the person perceives their environment to be unsafe with no easy way to escape. These situations can include open spaces, public transit, shopping centres, or simply being outside their home. Being in these situations may result in a panic attack. The symptoms occur nearly every time the situation is encountered and last for more than six months. Those affected will go to great lengths to avoid these situations. In severe cases people may become completely unable to leave their homes.

Agoraphobia is believed to be due to a combination of genetic and environmental factors. The condition often runs in families, and stressful or traumatic events such as the death of a parent or being attacked may be a trigger. In the DSM-5 agoraphobia is classified as a phobia along with specific phobias and social phobia. Other conditions that can produce similar symptoms include separation anxiety, post-traumatic stress disorder, and major depressive disorder. Those affected are at higher risk of depression and substance use disorder.

Without treatment it is uncommon for agoraphobia to resolve. Treatment is typically with a type of counselling called cognitive behavioural therapy (CBT). CBT results in resolution for about half of people. Agoraphobia affects about 1.7% of adults. Women are affected about twice as often as men. The condition often begins in early adulthood and becomes less common in old age. It is rare in children. The term “agoraphobia” is from Greek ἀγορά, agorā́, meaning a “place of assembly” or “market-place” and -φοβία, -phobía, meaning “fear.”

Refer to Hikikomori.

Signs and Symptoms

Agoraphobia is a condition where sufferers become anxious in unfamiliar environments or where they perceive that they have little control. Triggers for this anxiety may include wide-open spaces, crowds (social anxiety), or travelling (even short distances). Agoraphobia is often, but not always, compounded by a fear of social embarrassment, as the agoraphobic fears the onset of a panic attack and appearing distraught in public. Most of the time they avoid these areas and stay in the comfort of their safe haven, usually their home.

Agoraphobia is also defined as “a fear, sometimes terrifying, by those who have experienced one or more panic attacks”. In these cases, the sufferer is fearful of a particular place because they have experienced a panic attack at the same location at a previous time. Fearing the onset of another panic attack, the sufferer is fearful or even avoids a location. Some refuse to leave their homes even in medical emergencies because the fear of being outside of their comfort areas is too great.

The sufferers can sometimes go to great lengths to avoid the locations where they have experienced the onset of a panic attack. Agoraphobia, as described in this manner, is actually a symptom professionals check when making a diagnosis of panic disorder. Other syndromes like obsessive compulsive disorder (OCD) or post-traumatic stress disorder (PTSD) can also cause agoraphobia. Essentially, any irrational fear that keeps one from going outside can cause the syndrome.

Agoraphobics may suffer from temporary separation anxiety disorder when certain other individuals of the household depart from the residence temporarily, such as a parent or spouse, or when the agoraphobic is left home alone. Such temporary conditions can result in an increase in anxiety or a panic attack or feeling the need to separate themselves from family or maybe friends.

People with agoraphobia sometimes fear waiting outside for long periods of time; that symptom can be called “macrophobia.”

Panic Attacks

Agoraphobia patients can experience sudden panic attacks when traveling to places where they fear they are out of control, help would be difficult to obtain, or they could be embarrassed. During a panic attack, epinephrine is released in large amounts, triggering the body’s natural fight-or-flight response. A panic attack typically has an abrupt onset, building to maximum intensity within 10 to 15 minutes, and rarely lasts longer than 30 minutes. Symptoms of a panic attack include palpitations, rapid heartbeat, sweating, trembling, nausea, vomiting, dizziness, tightness in the throat, and shortness of breath. Many patients report a fear of dying, fear of losing control of emotions or fear of losing control of behaviours.

Causes

Agoraphobia is believed to be due to a combination of genetic and environmental factors. The condition often runs in families, and stressful or traumatic events such as the death of a parent or being attacked may be a trigger.

Research has uncovered a link between agoraphobia and difficulties with spatial orientation. Individuals without agoraphobia are able to maintain balance by combining information from their vestibular system, their visual system, and their proprioceptive sense. A disproportionate number of agoraphobics have weak vestibular function and consequently rely more on visual or tactile signals. They may become disoriented when visual cues are sparse (as in wide-open spaces) or overwhelming (as in crowds). Likewise, they may be confused by sloping or irregular surfaces. In a virtual reality study, agoraphobics showed impaired processing of changing audiovisual data in comparison with subjects without agoraphobia.

Substance Induced

Chronic use of tranquilisers and sleeping pills such as benzodiazepines has been linked to onset of agoraphobia. In 10 patients who had developed agoraphobia during benzodiazepine dependence, symptoms abated within the first year of assisted withdrawal. Similarly, alcohol use disorders are associated with panic with or without agoraphobia; this association may be due to the long-term effects of alcohol consumption causing a distortion in brain chemistry. Tobacco smoking has also been associated with the development and emergence of agoraphobia, often with panic disorder; it is uncertain how tobacco smoking results in anxiety-panic with or without agoraphobia symptoms, but the direct effects of nicotine dependence or the effects of tobacco smoke on breathing have been suggested as possible causes. Self-medication or a combination of factors may also explain the association between tobacco smoking and agoraphobia and panic.

Attachment Theory

Some scholars have explained agoraphobia as an attachment deficit, i.e. the temporary loss of the ability to tolerate spatial separations from a secure base. Recent empirical research has also linked attachment and spatial theories of agoraphobia.

Spatial Theory

In the social sciences, a perceived clinical bias exists in agoraphobia research. Branches of the social sciences, especially geography, have increasingly become interested in what may be thought of as a spatial phenomenon. One such approach links the development of agoraphobia with modernity. Factors considered contributing to agoraphobia within modernity are the ubiquity of cars and urbanization. These have helped develop the expansion of public space, on one hand, and the contraction of private space on the other, thus creating in the minds of agoraphobia-prone people a tense, unbridgeable gulf between the two.

Evolutionary Psychology

An evolutionary psychology view is that the more unusual primary agoraphobia without panic attacks may be due to a different mechanism from agoraphobia with panic attacks. Primary agoraphobia without panic attacks may be a specific phobia explained by it once having been evolutionarily advantageous to avoid exposed, large, open spaces without cover or concealment. Agoraphobia with panic attacks may be an avoidance response secondary to the panic attacks, due to fear of the situations in which the panic attacks occurred.

Diagnosis

Most people who present to mental health specialists develop agoraphobia after the onset of panic disorder. Agoraphobia is best understood as an adverse behavioural outcome of repeated panic attacks and subsequent anxiety and preoccupation with these attacks that leads to an avoidance of situations where a panic attack could occur. Early treatment of panic disorder can often prevent agoraphobia. Agoraphobia is typically determined when symptoms are worse than panic disorder, but also do not meet the criteria for other anxiety disorders such as depression. In rare cases where agoraphobics do not meet the criteria used to diagnose panic disorder, the formal diagnosis of agoraphobia without history of panic disorder is used (primary agoraphobia).

Treatments

Therapy

Systematic desensitisation can provide lasting relief to the majority of patients with panic disorder and agoraphobia. The disappearance of residual and sub-clinical agoraphobic avoidance, and not simply of panic attacks, should be the aim of exposure therapy. Many patients can deal with exposure easier if they are in the company of a friend on whom they can rely. Patients must remain in the situation until anxiety has abated because if they leave the situation, the phobic response will not decrease and it may even rise.

A related exposure treatment is in vivo exposure, a CBT method, that gradually exposes patients to the feared situations or objects. This treatment was largely effective with an effect size from d = 0.78 to d = 1.34, and these effects were shown to increase over time, proving that the treatment had long-term efficacy (up to 12 months after treatment).

Psychological interventions in combination with pharmaceutical treatments were overall more effective than treatments simply involving either CBT or pharmaceuticals. Further research showed there was no significant effect between using group CBT versus individual CBT.

Cognitive restructuring has also proved useful in treating agoraphobia. This treatment involves coaching a participant through a dianoetic discussion, with the intent of replacing irrational, counterproductive beliefs with more factual and beneficial ones.

Relaxation techniques are often useful skills for the agoraphobic to develop, as they can be used to stop or prevent symptoms of anxiety and panic.

Medications

Antidepressant medications most commonly used to treat anxiety disorders are mainly selective serotonin reuptake inhibitors. Benzodiazepines, monoamine oxidase inhibitor, and tricyclic antidepressants are also sometimes prescribed for treatment of agoraphobia. Antidepressants are important because some have anxiolytic effects. Antidepressants should be used in conjunction with exposure as a form of self-help or with CBT. A combination of medication and cognitive behaviour therapy is sometimes the most effective treatment for agoraphobia.

Benzodiazepines and other anxiolytic medications such as alprazolam and clonazepam are used to treat anxiety and can also help control the symptoms of a panic attack. If taken for too long, they can cause dependence. Treatment with benzodiazepines should not exceed 4 weeks. Side effects may include confusion, drowsiness, light-headedness, loss of balance, and memory loss.

Alternative Medicine

Eye movement desensitisation and reprocessing (EMDR) has been studied as a possible treatment for agoraphobia, with poor results. As such, EMDR is only recommended in cases where cognitive-behavioural approaches have proven ineffective or in cases where agoraphobia has developed following trauma.

Many people with anxiety disorders benefit from joining a self-help or support group (telephone conference-call support groups or online support groups being of particular help for completely housebound individuals). Sharing problems and achievements with others, as well as sharing various self-help tools, are common activities in these groups. In particular, stress management techniques and various kinds of meditation practices and visualisation techniques can help people with anxiety disorders calm themselves and may enhance the effects of therapy, as can service to others, which can distract from the self-absorption that tends to go with anxiety problems. Also, preliminary evidence suggests aerobic exercise may have a calming effect. Since caffeine, certain illicit drugs, and even some over-the-counter cold medications can aggravate the symptoms of anxiety disorders, they should be avoided.

Epidemiology

Agoraphobia occurs about twice as commonly among women as it does in men. The gender difference may be attributable to several factors: sociocultural traditions that encourage, or permit, the greater expression of avoidance coping strategies by women (including dependent and helpless behaviours), women perhaps being more likely to seek help and therefore be diagnosed, and men being more likely to abuse alcohol in reaction to anxiety and be diagnosed as an alcoholic. Research has not yet produced a single clear explanation for the gender difference in agoraphobia.

Panic disorder with or without agoraphobia affects roughly 5.1% of Americans, and about 1/3 of this population with panic disorder have co-morbid agoraphobia. It is uncommon to have agoraphobia without panic attacks, with only 0.17% of people with agoraphobia not presenting panic disorders as well.

In Popular Culture

Notable Cases

  • Woody Allen (b. 1935), American actor, director, musician.
  • Kim Basinger (b. 1953), American actress.
  • Earl Campbell (b. 1955), American pro football player.
  • Macaulay Culkin (b. 1980), American actor, known for his portrayal of Kevin McCallister in Home Alone and Home Alone 2: Lost in New York, said he had “self-diagnosed” agoraphobia.
  • Paula Deen (b. 1947), American chef, author, and television personality.
  • H.L. Gold (1914-1996), science fiction editor – as a result of trauma during his wartime experiences, his agoraphobia became so severe that for more than two decades he was unable to leave his apartment. Towards the end of his life, he acquired some control over the condition.
  • Daryl Hannah (b. 1960), American actress.
  • Howard Hughes (1905-1976), American aviator, industrialist, film producer and philanthropist.
  • Olivia Hussey (b. 1951), Anglo-Argentine actress.
  • Shirley Jackson (1916-1965), American writer – her agoraphobia is considered to be a primary inspiration for the novel We Have Always Lived in the Castle.
  • Elfriede Jelinek (b. 1946), Austrian writer, Nobel Prize laureate in Literature in 2004.
  • Bolesław Prus (1847-1912), Polish journalist and novelist.
  • Peter Robinson (b. 1962), British musician known as Marilyn.
  • Brian Wilson (b. 1942), American singer and songwriter, primary songwriter of the Beach Boys, a former recluse and agoraphobic who has schizophrenia.

What is Panic Disorder?

Introduction

Panic disorder is an anxiety disorder characterised by reoccurring unexpected panic attacks. Panic attacks are sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling that something terrible is going to happen. The maximum degree of symptoms occurs within minutes. There may be ongoing worries about having further attacks and avoidance of places where attacks have occurred in the past.

The cause of panic disorder is unknown. Panic disorder often runs in families. Risk factors include smoking, psychological stress, and a history of child abuse. Diagnosis involves ruling out other potential causes of anxiety including other mental disorders, medical conditions such as heart disease or hyperthyroidism, and drug use. Screening for the condition may be done using a questionnaire.

Panic disorder is usually treated with counselling and medications. The type of counselling used is typically cognitive behavioural therapy (CBT) which is effective in more than half of people. Medications used include antidepressants and occasionally benzodiazepines or beta blockers. Following stopping treatment up to 30% of people have a recurrence.

Panic disorder affects about 2.5% of people at some point in their life. It usually begins during adolescence or early adulthood but any age can be affected. It is less common in children and older people. Women are more often affected than men.

Signs and Symptoms

Panic disorder sufferers usually have a series of intense episodes of extreme anxiety during panic attacks. These attacks typically last about ten minutes, and can be as short-lived as 1-5 minutes, but can last twenty minutes to more than an hour, or until helpful intervention is made. Panic attacks can wax and wane for a period of hours (panic attacks rolling into one another), and the intensity and specific symptoms of panic may vary over the duration.

In some cases, the attack may continue at unabated high intensity or seem to be increasing in severity. Common symptoms of an attack include rapid heartbeat, perspiration, dizziness, dyspnoea, trembling, uncontrollable fear such as: the fear of losing control and going crazy, the fear of dying and hyperventilation. Other symptoms are a sensation of choking, paralysis, chest pain, nausea, numbness or tingling, chills or hot flashes, faintness, crying and some sense of altered reality. In addition, the person usually has thoughts of impending doom. Individuals suffering from an episode have often a strong wish of escaping from the situation that provoked the attack. The anxiety of panic disorder is particularly severe and noticeably episodic compared to that from generalised anxiety disorder. Panic attacks may be provoked by exposure to certain stimuli (e.g. seeing a mouse) or settings (e.g. the dentist’s office). Nocturnal panic attacks are common in people with panic disorder. Other attacks may appear unprovoked. Some individuals deal with these events on a regular basis, sometimes daily or weekly.

Limited symptom attacks are similar to panic attacks but have fewer symptoms. Most people with PD experience both panic attacks and limited symptom attacks.

Interoceptive

Studies investigating the relationship between interoception and panic disorder have shown that people with panic disorder feel heartbeat sensations more intensely when stimulated by pharmacological agents, suggesting that they experience heightened interoceptive awareness compared to subjects without PD.

Causes

Psychological Models

While there is not just one explanation for the cause of panic disorder, there are certain perspectives researchers use to explain the disorder. The first one is the biological perspective. Past research concluded that there is irregular norepinephrine activity in people who have panic attacks. Current research also supports this perspective as it has been found that those with panic disorder also have a brain circuit that performs improperly. This circuit consists of the amygdala, central gray matter, ventromedial nucleus of the hypothalamus, and the locus ceruleus.

There is also a cognitive perspective. Theorists believe that people with panic disorder may experience panic reactions because they mistake their bodily sensations for life-threatening situations. These bodily sensations cause some people to feel as though are out of control which may lead to feelings of panic. This misconception of bodily sensations is referred to as anxiety sensitivity, and studies suggest that people who score higher on anxiety sensitivity surveys are fives times more likely to be diagnosed with panic disorder.

Panic disorder has been found to run in families, which suggests that inheritance plays a strong role in determining who will get it.

Psychological factors, stressful life events, life transitions, and environment as well as often thinking in a way that exaggerates relatively normal bodily reactions are also believed to play a role in the onset of panic disorder. Often the first attacks are triggered by physical illnesses, major stress, or certain medications. People who tend to take on excessive responsibilities may develop a tendency to suffer panic attacks. Post-traumatic stress disorder (PTSD) patients also show a much higher rate of panic disorder than the general population.

Prepulse inhibition has been found to be reduced in patients with panic disorder.

Substance Misuse

Substance abuse is often correlated with panic attacks. In a study, 39% of people with panic disorder had abused substances. Of those who used alcohol, 63% reported that the alcohol use began prior to the onset of panic, and 59% of those abusing illicit drugs reported that drug use began first. The study that was conducted documented the panic-substance abuse relationship. Substance abuse began prior to the onset of panic and substances were used to self-medicate for panic attacks by only a few subjects.

In another study, 100 methamphetamine-dependent individuals were analysed for co-morbid psychiatric disorders; of the 100 individuals, 36% were categorised as having co-morbid psychiatric disorders. Mood and Psychotic disorders were more prevalent than anxiety disorders, which accounted for 7% of the 100 sampled individuals.

Smoking

Tobacco smoking increases the risk of developing panic disorder with or without agoraphobia and panic attacks; smoking started in adolescence or early adulthood particularly increases this risk of developing panic disorder. While the mechanism of how smoking increases panic attacks is not fully understood, a few hypotheses have been derived. Smoking cigarettes may lead to panic attacks by causing changes in respiratory function (e.g. feeling short of breath). These respiratory changes in turn can lead to the formation of panic attacks, as respiratory symptoms are a prominent feature of panic. Respiratory abnormalities have been found in children with high levels of anxiety, which suggests that a person with these difficulties may be susceptible to panic attacks, and thus more likely to subsequently develop panic disorder. Nicotine, a stimulant, could contribute to panic attacks. However, nicotine withdrawal may also cause significant anxiety which could contribute to panic attacks.

It is also possible that panic disorder patients smoke cigarettes as a form of self-medication to lessen anxiety. Nicotine and other psychoactive compounds with antidepressant properties in tobacco smoke which act as monoamine oxidase inhibitors in the brain can alter mood and have a calming effect, depending on dose.

Stimulants

A number of clinical studies have shown a positive association between caffeine ingestion and panic disorder and/or anxiogenic effects. People who have panic disorder are more sensitive to the anxiety-provoking effects of caffeine. One of the major anxiety-provoking effects of caffeine is an increase in heart rate.

Certain cold and flu medications containing decongestants may also contain pseudoephedrine, ephedrine, phenylephrine, naphazoline and oxymetazoline. These may be avoided by the use of decongestants formulated to prevent causing high blood pressure.

Alcohol and Sedatives

About 30% of people with panic disorder use alcohol and 17% use other psychoactive drugs. This is in comparison with 61% (alcohol) and 7.9% (other psychoactive drugs) of the general population who use alcohol and psychoactive drugs, respectively. Utilisation of recreational drugs or alcohol generally make symptoms worse. Most stimulant drugs (caffeine, nicotine, cocaine) would be expected to worsen the condition, since they directly increase the symptoms of panic, such as heart rate.

Deacon and Valentiner (2000) conducted a study that examined co-morbid panic attacks and substance use in a non-clinical sample of young adults who experienced regular panic attacks. The authors found that compared to healthy controls, sedative use was greater for non-clinical participants who experienced panic attacks. These findings are consistent with the suggestion made by Cox, Norton, Dorward, and Fergusson (1989) that panic disorder patients self-medicate if they believe that certain substances will be successful in alleviating their symptoms. If panic disorder patients are indeed self-medicating, there may be a portion of the population with undiagnosed panic disorder who will not seek professional help as a result of their own self-medication. In fact, for some patients panic disorder is only diagnosed after they seek treatment for their self-medication habit.

While alcohol initially helps ease panic disorder symptoms, medium- or long-term alcohol abuse can cause panic disorder to develop or worsen during alcohol intoxication, especially during alcohol withdrawal syndrome. This effect is not unique to alcohol but can also occur with long-term use of drugs which have a similar mechanism of action to alcohol such as the benzodiazepines which are sometimes prescribed as tranquilisers to people with alcohol problems. The reason chronic alcohol misuse worsens panic disorder is due to distortion of the brain chemistry and function.

Approximately 10% of patients will experience notable protracted withdrawal symptoms, which can include panic disorder, after discontinuation of benzodiazepines. Protracted withdrawal symptoms tend to resemble those seen during the first couple of months of withdrawal but usually are of a subacute level of severity compared to the symptoms seen during the first 2 or 3 months of withdrawal. It is not known definitively whether such symptoms persisting long after withdrawal are related to true pharmacological withdrawal or whether they are due to structural neuronal damage as a result of chronic use of benzodiazepines or withdrawal. Nevertheless, such symptoms do typically lessen as the months and years go by eventually disappearing altogether.

A significant proportion of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia have developed these conditions as a result of alcohol or sedative abuse. Anxiety may pre-exist alcohol or sedative dependence, which then acts to perpetuate or worsen the underlying anxiety disorder. Someone suffering the toxic effects of alcohol abuse or chronic sedative use or abuse will not benefit from other therapies or medications for underlying psychiatric conditions as they do not address the root cause of the symptoms. Recovery from sedative symptoms may temporarily worsen during alcohol withdrawal or benzodiazepine withdrawal.

Mechanism

The neuroanatomy of panic disorder largely overlaps with that of most anxiety disorders. Neuropsychological, neurosurgical, and neuroimaging studies implicate the insula, amygdala, hippocampus, anterior cingulate cortex (ACC), lateral prefrontal cortex, and periaqueductal grey. During acute panic attacks, viewing emotionally charged words, and rest, most studies find elevated blood flow or metabolism. However, the observation of amygdala hyperactivity is not entirely consistent, especially in studies that evoke panic attacks chemically. Hippocampus hyperactivity has been observed during rest and viewing emotionally charged pictures, which has been hypothesized to be related to memory retrieval bias towards anxious memories. Insula hyperactivity during the onset of and over the course of acute panic episodes is thought to be related to abnormal introceptive processes; the perception that bodily sensations are “wrong” is a transdiagnostic finding(i.e. found across multiple anxiety disorders), and may be related to insula dysfunction. Rodent and human studies heavily implicate the periaqueductal grey in generating fear responses, and abnormalities related to the structure and metabolism in the PAG have been reported in panic disorder. The frontal cortex is implicated in panic disorder by multiple lines of evidence. Damage to the dorsal ACC has been reported to lead to panic disorder. Elevated ventral ACC and dorsolateral prefrontal cortex during symptom provocation and viewing emotional stimuli have also been reported, although findings are not consistent.

Researchers studying some individuals with panic disorder propose they may have a chemical imbalance within the limbic system and one of its regulatory chemicals gamma-aminobutyric acid (GABA-A). The reduced production of GABA-A sends false information to the amygdala which regulates the body’s “fight or flight” response mechanism and, in return, produces the physiological symptoms that lead to the disorder. Clonazepam, an anticonvulsant benzodiazepine with a long half-life, has been successful in keeping the condition under control.

Recently, researchers have begun to identify mediators and moderators of aspects of panic disorder. One such mediator is the partial pressure of carbon dioxide, which mediates the relationship between panic disorder patients receiving breathing training and anxiety sensitivity; thus, breathing training affects the partial pressure of carbon dioxide in a patient’s arterial blood, which in turn lowers anxiety sensitivity. Another mediator is hypochondriacal concerns, which mediate the relationship between anxiety sensitivity and panic symptomatology; thus, anxiety sensitivity affects hypochondriacal concerns which, in turn, affect panic symptomatology.

Perceived threat control has been identified as a moderator within panic disorder, moderating the relationship between anxiety sensitivity and agoraphobia; thus, the level of perceived threat control dictates the degree to which anxiety sensitivity results in agoraphobia. Another recently identified moderator of panic disorder is genetic variations in the gene coding for galanin; these genetic variations moderate the relationship between females suffering from panic disorder and the level of severity of panic disorder symptomatology.

Diagnosis

The DSM-IV-TR diagnostic criteria for panic disorder require unexpected, recurrent panic attacks, followed in at least one instance by at least a month of a significant and related behaviour change, a persistent concern of more attacks, or a worry about the attack’s consequences. There are two types, one with and one without agoraphobia. Diagnosis is excluded by attacks due to a drug or medical condition, or by panic attacks that are better accounted for by other mental disorders.

The ICD-10 diagnostic criteria:

  • The essential feature is recurrent attacks of severe anxiety (panic), which are not restricted to any particular situation or set of circumstances and are therefore unpredictable.

The dominant symptoms include:

  • Sudden onset of palpitations.
  • Chest pain.
  • Choking sensations.
  • Dizziness.
  • Feelings of unreality (depersonalisation or derealisation).
  • Secondary fear of dying, losing control, or going mad.
  • Panic disorder should not be given as the main diagnosis if the person has a depressive disorder at the time the attacks start; in these circumstances, the panic attacks are probably secondary to depression.

The Panic Disorder Severity Scale (PDSS) is a questionnaire for measuring the severity of panic disorder.

Treatment

Panic disorder is a serious health problem that in many cases can be successfully treated, although there is no known cure. Identification of treatments that engender as full a response as possible, and can minimise relapse, is imperative. CBT and positive self-talk specific for panic are the treatments of choice for panic disorder. Several studies show that 85% to 90% of panic disorder patients treated with CBT recover completely from their panic attacks within 12 weeks. When CBT is not an option, pharmacotherapy can be used. SSRIs are considered a first-line pharmacotherapeutic option.

Psychotherapy

Panic disorder is not the same as phobic symptoms, although phobias commonly result from panic disorder. CBT and one tested form of psychodynamic psychotherapy have been shown efficacious in treating panic disorder with and without agoraphobia. A number of randomized clinical trials have shown that CBT achieves reported panic-free status in 70-90% of patients about 2 years after treatment.

A 2009 Cochrane review found little evidence concerning the efficacy of psychotherapy in combination with benzodiazepines such that recommendations could not be made.

Symptom inductions generally occur for one minute and may include:

  • Intentional hyperventilation creates lightheadedness, derealisation, blurred vision, and dizziness.
  • Spinning in a chair creates dizziness and disorientation.
  • Straw breathing creates dyspnoea and airway constriction.
  • Breath holding creates sensation of being out of breath.
  • Running in place creates increased heart rate, respiration, and perspiration.
  • Body tensing creates feelings of being tense and vigilant.

Another form of psychotherapy that has shown effectiveness in controlled clinical trials is panic-focused psychodynamic psychotherapy, which focuses on the role of dependency, separation anxiety, and anger in causing panic disorder. The underlying theory posits that due to biochemical vulnerability, traumatic early experiences, or both, people with panic disorder have a fearful dependence on others for their sense of security, which leads to separation anxiety and defensive anger. Therapy involves first exploring the stressors that lead to panic episodes, then probing the psychodynamics of the conflicts underlying panic disorder and the defence mechanisms that contribute to the attacks, with attention to transference and separation anxiety issues implicated in the therapist-patient relationship.

Comparative clinical studies suggest that muscle relaxation techniques and breathing exercises are not efficacious in reducing panic attacks. In fact, breathing exercises may actually increase the risk of relapse.

Appropriate treatment by an experienced professional can prevent panic attacks or at least substantially reduce their severity and frequency – bringing significant relief to 70% to 90% of people with panic disorder. Relapses may occur, but they can often be effectively treated just like the initial episode.

vanApeldoorn, F.J. et al. (2011) demonstrated the additive value of a combined treatment incorporating an SSRI treatment intervention with CBT. Gloster et al. (2011) went on to examine the role of the therapist in CBT. They randomised patients into two groups: one being treated with CBT in a therapist guided environment, and the second receiving CBT through instruction only, with no therapist guided sessions. The findings indicated that the first group had a somewhat better response rate, but that both groups demonstrated a significant improvement in reduction of panic symptomatology. These findings lend credibility to the application of CBT programs to patients who are unable to access therapeutic services due to financial, or geographic inaccessibility. Koszycky et al. (2011) discuss the efficacy of self-administered CBT (SCBT) in situations where patients are unable to retain the services of a therapist. Their study demonstrates that it is possible for SCBT in combination with an SSRI to be as effective as therapist-guided CBT with SSRI. Each of these studies contributes to a new avenue of research that allows effective treatment interventions to be made more easily accessible to the population.

Cognitive Behavioural Therapy (CBT)

CBT encourages patients to confront the triggers that induce their anxiety. By facing the very cause of the anxiety, it is thought to help diminish the irrational fears that are causing the issues to begin with. The therapy begins with calming breathing exercises, followed by noting the changes in physical sensations felt as soon as anxiety begins to enter the body. Many clients are encouraged to keep journals. In other cases, therapists may try and induce feelings of anxiety so that the root of the fear can be identified.

Comorbid clinical depression, personality disorders and alcohol abuse are known risk factors for treatment failure.

As with many disorders, having a support structure of family and friends who understand the condition can help increase the rate of recovery. During an attack, it is not uncommon for the sufferer to develop irrational, immediate fear, which can often be dispelled by a supporter who is familiar with the condition. For more serious or active treatment, there are support groups for anxiety sufferers which can help people understand and deal with the disorder.

Current treatment guidelines American Psychiatric Association and the American Medical Association primarily recommend either CBT or one of a variety of psychopharmacological interventions. Some evidence exists supporting the superiority of combined treatment approaches.

Another option is self-help based on principles of CBT. Using a book or a website, a person does the kinds of exercises that would be used in therapy, but they do it on their own, perhaps with some email or phone support from a therapist. A systematic analysis of trials testing this kind of self-help found that websites, books, and other materials based on CBT could help some people. The best-studied conditions are panic disorder and social phobia.

Interoceptive Techniques

Interoceptive exposure is sometimes used for panic disorder. People’s interoceptive triggers of anxiety are evaluated one-by-one before conducting interoceptive exposures, such as addressing palpitation sensitivity via light exercise. Despite evidence of its clinical efficacy, this practice is reportedly used by only 12-20% of psychotherapists. Potential reasons for this underutilisation include “lack of training sites, logistical hurdles (e.g. occasional need for exposure durations longer than a standard therapy session), policies against conducting exposures outside of the workplace setting, and perhaps most tellingly, negative therapist beliefs (e.g. that interoceptive exposures are unethical, intolerable, or even harmful).”

Medication

Appropriate medications are effective for panic disorder. Selective serotonin reuptake inhibitors are first line treatments rather than benzodiazepines due to concerns with the latter regarding tolerance, dependence and abuse. Although there is little evidence that pharmacological interventions can directly alter phobias, few studies have been performed, and medication treatment of panic makes phobia treatment far easier (an example in Europe where only 8% of patients receive appropriate treatment).

Medications can include:

  • Antidepressants (SSRIs, MAOIs, tricyclic antidepressants and norepinephrine reuptake inhibitors).
  • Antianxiety agents (benzodiazepines):
    • Use of benzodiazepines for panic disorder is controversial.
    • The American Psychiatric Association states that benzodiazepines can be effective for the treatment of panic disorder and recommends that the choice of whether to use benzodiazepines, antidepressants with anti-panic properties or psychotherapy should be based on the individual patient’s history and characteristics.
    • Other experts believe that benzodiazepines are best avoided due to the risks of the development of tolerance and physical dependence.
    • The World Federation of Societies of Biological Psychiatry, say that benzodiazepines should not be used as a first-line treatment option but are an option for treatment-resistant cases of panic disorder.
    • Despite increasing focus on the use of antidepressants and other agents for the treatment of anxiety as recommended best practice, benzodiazepines have remained a commonly used medication for panic disorder.
    • They reported that in their view there is insufficient evidence to recommend one treatment over another for panic disorder.
    • The APA noted that while benzodiazepines have the advantage of a rapid onset of action, that this is offset by the risk of developing a benzodiazepine dependence.
    • The UKs National Institute of Clinical Excellence (NICE) came to a different conclusion, they pointed out the problems of using uncontrolled clinical trials to assess the effectiveness of pharmacotherapy and based on placebo-controlled research they concluded that benzodiazepines were not effective in the long-term for panic disorder and recommended that benzodiazepines not be used for longer than 4 weeks for panic disorder.
    • Instead NICE clinical guidelines recommend alternative pharmacotherapeutic or psychotherapeutic interventions.
    • When compared to placebos, benzodiazepines demonstrate possible superiority in the short term but the evidence is low quality with limited applicability to clinical practice.

Other Treatments

For some people, anxiety can be greatly reduced by discontinuing the use of caffeine. Anxiety can temporarily increase during caffeine withdrawal.

Epidemiology

Panic disorder typically begins during early adulthood; roughly half of all people who have panic disorder develop the condition between the ages of 17 and 24, especially those subjected to traumatic experiences. However, some studies suggest that the majority of young people affected for the first time are between the ages of 25 and 30. Women are twice as likely as men to develop panic disorder and it occurs far more often in people with above average intelligence.

Panic disorder can continue for months or years, depending on how and when treatment is sought. If left untreated, it may worsen to the point where one’s life is seriously affected by panic attacks and by attempts to avoid or conceal the condition. In fact, many people have had problems with personal relationships, education and employment while struggling to cope with panic disorder. Some people with panic disorder may conceal their condition because of the stigma of mental illness. In some individuals, symptoms may occur frequently for a period of months or years, then many years may pass with little or no symptoms. In some cases, the symptoms persist at the same level indefinitely. There is also some evidence that many individuals (especially those who develop symptoms at an early age) may experience symptom cessation later in life (e.g. past age 50).

In 2000, the World Health Organisation found prevalence and incidence rates for panic disorder to be very similar across the globe. Age-standardised prevalence per 100,000 ranged from 309 in Africa to 330 in East Asia for men and from 613 in Africa to 649 in North America, Oceania, and Europe for women.

Children

A retrospective study has shown that 40% of adult panic disorder patients reported that their disorder began before the age of 20. In an article examining the phenomenon of panic disorder in youth, Diler et al. (2004) found that only a few past studies have examined the occurrence of juvenile panic disorder. They report that these studies have found that the symptoms of juvenile panic disorder almost replicate those found in adults (e.g. heart palpitations, sweating, trembling, hot flashes, nausea, abdominal distress, and chills). The anxiety disorders co-exist with staggeringly high numbers of other mental disorders in adults. The same comorbid disorders that are seen in adults are also reported in children with juvenile panic disorder. Last and Strauss (1989) examined a sample of 17 adolescents with panic disorder and found high rates of comorbid anxiety disorders, major depressive disorder, and conduct disorders. Eassau et al. (1999) also found a high number of comorbid disorders in a community-based sample of adolescents with panic attacks or juvenile panic disorder. Within the sample, adolescents were found to have the following comorbid disorders: major depressive disorder (80%), dysthymic disorder (40%), generalised anxiety disorder (40%), somatoform disorders (40%), substance abuse (40%), and specific phobia (20%). Consistent with this previous work, Diler et al. (2004) found similar results in their study in which 42 youths with juvenile panic disorder were examined. Compared to non-panic anxiety disordered youths, children with panic disorder had higher rates of comorbid major depressive disorder and bipolar disorder.

Children differ from adolescents and adults in their interpretation and ability to express their experience. Like adults, children experience physical symptoms including accelerated heart rate, sweating, trembling or shaking, shortness of breath, nausea or stomach pain, dizziness or light-headedness. In addition, children also experience cognitive symptoms like fear of dying, feelings of being detached from oneself, feelings of losing control or going crazy, but they are unable to vocalize these higher-order manifestations of fear. They simply know that something is going wrong and that they are very afraid. Children can only describe physical symptoms. They have not yet developed the constructs to put these symptoms together and label them as fear. Parents often feel helpless when they watch a child suffer. They can help children give a name to their experience, and empower them to overcome the fear they are experiencing.

The role of the parent in treatment and intervention for children diagnosed with panic disorder is discussed by McKay & Starch (2011). They point out that there are several levels at which parental involvement should be considered. The first involves the initial assessment. Parents, as well as the child, should be screened for attitudes and treatment goals, as well as for levels of anxiety or conflict in the home. The second involves the treatment process in which the therapist should meet with the family as a unit as frequently as possible. Ideally, all family members should be aware and trained in the process of CBT in order to encourage the child to rationalize and face fears rather than employ avoidant safety behaviours. McKay & Storch (2011) suggest training/modelling of therapeutic techniques and in-session involvement of the parents in the treatment of children to enhance treatment efficacy.

Despite the evidence pointing to the existence of early-onset panic disorder, the DSM-IV-TR currently only recognizes six anxiety disorders in children: separation anxiety disorder, generalised anxiety disorder, specific phobia, obsessive-compulsive disorder, social anxiety disorder (a.k.a. social phobia), and post-traumatic stress disorder. Panic disorder is notably excluded from this list.

Book: Anxiety and Depression in Children and Adolescents

Book Title:

Anxiety and Depression in Children and Adolescents: Assessment, Intervention, and Prevention.

Author(s): Thomas J. Huberty..

Year: 2012.

Edition: First (1st).

Publisher: Springer.

Type(s): Hardcover and eBook.

Synopsis:

Although generally considered adult disorders, anxiety and depression are widespread among children and adolescents, affecting academic performance, social development, and long-term outcomes. They are also difficult to treat and, especially when they occur in tandem, tend to fly under the diagnostic radar.

Anxiety and Depression in Children and Adolescents offers a developmental psychology perspective for understanding and treating these complex disorders as they manifest in young people. Adding the school environment to well-known developmental contexts such as biology, genetics, social structures, and family, this significant volume provides a rich foundation for study and practice by analyzing the progression of pathology and the critical role of emotion regulation in anxiety disorders, depressive disorders, and in combination. Accurate diagnostic techniques, appropriate intervention methods, and empirically sound prevention strategies are given accessible, clinically relevant coverage. Illustrative case examples and an appendix of forms and checklists help make the book especially useful.

Featured in the text:

  • Developmental psychopathology of anxiety, anxiety disorders, depression, and mood disorders.
  • Differential diagnosis of the anxiety and depressive disorders.
  • Assessment measures for specific conditions.
  • Age-appropriate interventions for anxiety and depression, including CBT and pharmacotherapy.
  • Multitier school-based intervention and community programmes.
  • Building resilience through prevention.

Anxiety and Depression in Children and Adolescents is an essential reference for practitioners, researchers, and graduate students in school and clinical child psychology, mental health and school counselling, family therapy, psychiatry, social work, and education.