Schizophrenia

Question 1

What is schizophrenia?

Answer 1

A major psychotic disorder that causes a variety of psychological symptoms but is characterised by a lack of contact with reality.

Question 2

Schizophrenia statistics.

Answer 2

About 25% of people with schizophrenia exhibit physical changes in their brains that can be seen on CT scans.

Modern medication is very effective and reduces the risk of relapse to about 10%

Schizophrenia runs in families. If you have a parent/sibling with it you are more likely to suffer yourself.

On average people with schizophrenia die 10-20 years earlier due to the higher risk of suicide.

Question 3

What is classification?

Answer 3

The process of organising symptoms into categories based on which symptoms cluster together in patients. This then allows us to distinguish one disorder from another.

Question 4

Medical model approach.

Answer 4

Classification and diagnosis.

A diagnosis of a disorder is possible by classification of the symptoms because then we can identify the symptoms a patient has and decide what disorder they have based on their symptoms.

Question 5

Categorising symptoms of schizophrenia.

Answer 5

Kurt Schneider (1959) suggested that categorising the symptoms of schizophrenia as either positive or negative.

Question 6

Positive symptoms.

Answer 6

Behaviours that the person is exhibiting in addition to ‘normal’ behaviours.
Hallucinations
Delusions
Disordered thinking
Disorganised behaviour

Question 7

Hallucinations

Answer 7

Perceptions that are not real
Many people report auditory hallucinations, but they can present in any sensory modality.
Kathryn Lewandowski et al (2009) estimated that 20% of people with schizophrenia have tactile hallucinations - formication (sensations of insects in and under the skin)

Question 8

Delusions

Answer 8

Beliefs that are unreal
Commonly held delusions are of persecution and of grandiosity (the belief that the individual is special in some way- superior).

Question 9

Disordered thinking

Answer 9

Evident through examining speech.
Sometimes described as derailment or knights move thinking.

Question 10

Disordered behaviour

Answer 10

Wandering in circles, fast repetitive movements, useless movements.
Unexpected gestures and loud utterances.
Echopraxia - mimicking someone else’s moments which can be unpredictable and cause observer discomfort.

Question 11

Negative symptoms.

Answer 11

Behaviours that are inhibiting people with schizophrenia from demonstrating ‘normal’ behaviour.
Alogia
Avolition
Anhedonia
Flatness of affect
Catatonic behaviour

Question 12

Alogia

Answer 12

Poverty of speech, lack meaning in what they are saying even simple short answers can be a problem.

Question 13

Avolition

Answer 13

Lack of goal directed behaviour, which may be perceived as disinterest.

Question 14

Anhedonia

Answer 14

An individual does not react appropriately to pleasurable experiences.

Question 15

Flatness of affect

Answer 15

Show little or no facial emotional expression, may be interpreted as apathetic, speech patterns are very monotonous.

Question 16

Catatonic behaviour

Answer 16

Remaining immobile for prolonged periods of time in seemingly uncomfortable postures.
Demonstrate waxy flexibility if moved (staying in the position that they are moved to)

Question 17

What is used to classify schizophrenia?

Answer 17

DSM-5 and ICD-10

Question 18

What does the DSM-5 say about schizophrenia?

Answer 18

At least 2 symptoms must be present for at least a month and one of the symptoms must be a positive symptom.

Question 19

What does the ICD-10 say about schizophrenia?

Answer 19

One of these symptoms (delusions, delusions of control, hallucinatory voices, bizarre delusions) is enough. It also says that 2 negative symptoms are sufficient for diagnosis.

Question 20

Reliability of diagnosing schizophrenia

Answer 20

A psychiatric diagnosis is reliable when different diagnosing clinicians reach the same diagnosis for the same individual and when the same clinician reaches the same diagnosis for the same individual on 2 occasions.
Inter-rated reliability and test-retest reliability.

Not reliable if clinicians are using different diagnostic tools.

Question 21

Reliability as a strength for diagnosing schizophrenia

Answer 21

Osorio et al (2019) reported excellent reliability for the diagnosis of schizophrenia in 180 individuals using the DSM-5.
There was a correlation coefficient of +0.97 for inter-rater reliability and +0.92 for test re-test reliability. Showing a strong positive = very reliable.

Question 22

Validity of diagnosing schizophrenia

Answer 22

Criterion validity (asking if the criteria we are using the diagnose schizophrenia are actually accurate)

Question 23

Validity as a limitation of diagnosing schizophrenia

Answer 23

Cheniaux et al (2009) found that when 100 patients were assessed using ICD-10, 68 were diagnosed with schizophrenia. When the same 100 patients were assessed using DSM-4, only 39 were diagnosing with schizophrenia. Criterion validity is low. The research suggests that sch is either over diagnosed or under diagnosed depending on the diagnostic system used, meaning diagnosing using the set out criteria in the classification systems are not accurate.

Question 24

Validity as a strength of diagnosing schizophrenia

Answer 24

Osorio study showed that there was excellent agreement when the same classification system is used, suggesting that criterion validity is actually good when it takes place within a single diagnostic system. (Could be as a result of improved DSM - DSM-4 for Cheniaux, DSM-5 for Osorio)

Question 25

Co-morbidity.

Answer 25

Occurrence of 2 disorders or conditions together.
Buckley et al (2009) 50% of patients with schizophrenia also have depression, 47% substance abuse, 29% PTSD, 23% OCD

Question 26

Co-morbidity as a limitation of diagnosing schizophrenia

Answer 26

Where 2 conditions are frequently diagnosed together it questions the validity of the classification of both illnesses. Some people may not have schizophrenia at all but instead have unusual cases of other conditions such as depressions.

Question 27

Gender bias in diagnosis

Answer 27

More commonly diagnosed in men. In 2017 the ratio was 1.4:1
Maybe women are just less likely to develop schizophrenia, but research shows this is not the case.
Women are just able to function better because they have closer social support networks compared to men.

Question 28

Gender bias as a limitation of diagnosing schizophrenia

Answer 28

Women are under diagnosed, meaning they are unable to get help. This is because women are able to function better due to their social support network.
Alpha gender bias - differences between men and women are exaggerated

Question 29

Culture bias in diagnosis (limitation)

Answer 29

A higher percentage of individuals of Afro-Caribbean descent are diagnosed with schizophrenia. Cochrane et al (1995) found that black Afro-Caribbean immigrants in the UK are up to 7 times are more likely to be diagnosed with schizophrenia than white British people.
This data cannot be explained by genetics because the increased risk is not apparent in studies conducted in the Caribbean.
Additional stress induced through migration to a different culture was suggested as being a reasonable explanation.
Increased risk and diagnosis was not only found in the first generation migrants but higher rates of schizophrenia were alone notched in the children of the Afro-Caribbean migrants in the UK (Harrison et al, 1988).

Question 30

Symptom overlap as a limitation of diagnosing schizophrenia

Answer 30

Difficult to distinguish schizophrenia from other disorders.
For example, dissociative identity disorder and schizophrenia both have symptoms of feeling disconnected, forgetting about certain time periods, events and periods information and delusions

Question 31

Biological expiations of schizophrenia

Answer 31

Family studies, candidate genes, the role of mutation, neural correlates

Question 32

Family studies

Answer 32

Schizophrenia has a genetic basis, suggesting it can be inherited. The closer the relation to the family member with schizophrenia, the higher risk of developing it.
Gottesman (1991) Cousins = 2%, nephews/nieces = 4%, parents = 6%, identical twins = 48%.

Question 33

Candidate genes

Answer 33

A number of different genes cause schizophrenia (polygenic). Thought that genes that code for neurotransmitters such as dopamine are involved.

2014 Schizophrenia Working Group of the Psychiatric Genomics Consortium reported that there were over 108 genetic loci associated with schizophrenia - used meta analysis which increases population validity.

Question 34

Polygenic

Answer 34

Caused by multiple different genes

Question 35

Aetiologically heterogenous

Answer 35

Schizophrenia is caused my multiple different factors, including genetic variations.

Question 36

The role of mutation

Answer 36

Could be a mutation in parental DNA, which could be caused by radiation, poison or viral infection.

The season of birth influence.
People who develop schizophrenia in North America and Europe are more likely to be born in winter and early spring. This may be related to the exposure to sunlight (lack of vitamin D could alter the development of a child’s brain.

Mutation could also be caused by an autoimmune reaction after contracting influenza

Question 37

Strengths of the genetic explanation

Answer 37

Strong evidence base - Gottesman study, increases validity because it shows that people are more vulnerable.

Practical applications - genetic counselling (people with schizophrenia are told the risks of passing it on to their children and specific information about the genetic contribution to the illness.

Question 38

Limitations of the genetic explanation

Answer 38

Difficult to separate nature and nurture (twins generally raised together) - Genain quadruplets, 4 identical daughters all diagnosed with schizophrenia before the age of 25 (genetics) also raised in a house where there father was an alcoholic and sexually abused his children (environment).
Further research in 2017 found 67% of people with schizophrenia reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues.

Question 39

Neural correlates

Answer 39

Schizophrenia is caused by abnormalities in the brain structure and function. Looking at the role of the neurotransmitter dopamine.

Initial hypothesis - individuals with schizophrenia had too much of the neurotransmitter dopamine. Supporting research - Griffith (1968) induced psychosis in non-schizophrenic volunteers with the administration of dextroamphetamine (increases dopamine in brain). They demonstrated a generally abrupt onset of paranoid delusions and a cold detached emotional response.

Initial hypothesis criticised for being too simple because administering drugs that reduce the levels of dopamine had litter or no effect on those who suffered with mainly negative symptoms.

Also complicated by the discovery of several subtypes of dopamine receptor sites D1-D5. Research shows that D2 receptor is blocked by antipsychotics.

Mesolimbic pathway and mesocortical pathway

Question 40

Mesolimbic pathway

Answer 40

Too much dopamine (hyper function) due to neurotransmitters firing too often or too quickly, causing overstimulation and positive symptoms such as hallucinations or delusions. Involving D2 receptors.

Question 41

Mesocortical pathway

Answer 41

Carries signals from the ventral regimental area to the frontal lobe which is vital in emotional response (flatness of effect), motivation (avolition) and motor function (catatonic behaviour). Too little dopamine (hypofunction) in D1 receptors causing cognitive impairments and negative symptoms.

Question 42

Strengths of neural correlates

Answer 42

Supporting evidence - Griffith study, increases internal validity because it suggests that the dopamine hypothesis is true.

Practical applications - development of anti-psychotic drug therapies. Ben Thornley et al (2003) comparing the effects of chlorpromazine and control conditions. 13 trials, 1121 participants. Showed that it was associated with better overall functioning and reduced symptom severity compared to placebo.
Herbert Meltzer (2012) concluded clozapine is more effective that typical antipsychotics and other atypical antipsychotics. Effective in 30-50% of treatment resistant cases where typical antipsychotics have failed.
Not fully reliable because only some successful trials have been published so the size of the evidence base for positive effects is exaggerated.

Question 43

Limitations of neural correlates

Answer 43

Biologically reductionist - doesn’t consider other factors. Genian quadruplets and 2017 study.

Whether dopamine imbalances cause schizophrenia or schizophrenia causes dopamine imbalances. PET scans have not been able to detect differences in dopamine activity. We cannot establish cause and effect relationship, the only way of overcoming this is with a perspective study which is effective and time consuming and there is no guarantee that the Persian the researcher is following will develop schizophrenia

Question 44

Biological therapy for schizophrenia

Answer 44

Anti-psychotics

Question 45

How do antipsychotics work

Answer 45

Action potential reaches the presynaptic terminal.
Triggers a release of neurotransmitters from vesicles across the synapse via exocytosis.
Neurotransmitters diffuse across the synapse (chemical transmission).
Neurotransmitters bind to receptors on the postsynaptic membrane.

Used to rebalance neurotransmitter activity- either increase or decease activity to restore normal levels.

Question 46

What do antipsychotics used for?

Answer 46

To reduce the intensity of symptoms (especially positive).

Question 47

Two types of antipsychotics

Answer 47

Typical - first generation, used since 1950s, typically target dopamine

Atypical - second generation, used since 1970s , target a range of neurotransmitters, overall more effective and have fewer side effects.

Question 48

Typical antipsychotics

Answer 48

Administered daily at around 400-800mg.

Chlorpromazine works by acting as antagonists in the dopamine system (chemicals which reduce the action of neurotransmitter). They block dopamine receptors in the synapse of the brain, reducing the action. Helps to reduce symptoms such as hallucinations.

Question 49

Atypical antipsychotics

Answer 49

Clozapine - people taking it must have regular blood tests because previously (1970s) patients developed blood conditions which killed them. Due to potentially fatal side effects it is not available as an injection. Typical dosage is 300-450mg/day. Binds to do spine receptors and acts on serotonin receptors which helps improve mood and reduce depression and anxiety, therefore it is sometimes prescribed when a patient is at high risk of attempting suicide.

Risperidone - recently developed to make a drug which is as effective as clozapine but less serious side effects. Typical dosage of 4-8mg per day. Binds to dopamine and serotonin receptors. Binds more strongly to dopamine receptors that clozapine, so is effective in much smaller dosages, this is potentially why there is less side effects.

Question 50

Strength of antipsychotics

Answer 50

Lots of scientific evidence. Cole et al (1964) study on effectiveness of conventional antipsychotics, 75% given the drugs were ‘much improved’ compared to 25% of those given a placebo. Shows that schizophrenia can be treated as it was previously considered untreatable.

Number of controlled double blind placebo trials. Meltzer (2012) found that the atypical antipsychotic clozapine is more effective than typical antipsychotics and can help in 30-50% of cases where typical psychotics have failed. Shows that atypical antipsychotics work and can help people have a better quality of life.

Question 51

Limitations of antipsychotics.

Answer 51

Problems with the supporting studies. Healy (2012) suggested flaws in some studies, most are for short term effects and some successful trails have their data published multiple times, exaggerating the evidence base for positive results. Antipsychotics have a powerful calming effects, is it easy to demonstrate that they have some positive effect, this is not the same as reducing the symptoms of psychosis.

Negative side effects. Cause dizziness, agitation, drowsiness and weight gain , longer term use can cause involuntary facial movements and tremors. Most serious side effect is neuroleptic malignant syndrome which can result in coma or death (0.1-2%).

Question 52

Psychological explanations for schizophrenia

Answer 52

Family dysfunction (schizophrenogenic mother, double bind theory, expressed emotion)

Question 53

Schizophrenogenic mother description.

Answer 53

Suggests childhood experiences are key to our future behaviours, the mother-child relationship is one of the crucial factors in development of schizophrenia.

Developed by Freida Fromm-Reichmann 1940s, based on the accounts she heard from her patients about their childhood. She states that the mothers of those with schizophrenia are controlling and overprotective whilst also being rejecting and distant.
She said mothers with their own psychological problems ‘give birth to healthy children then literally drive them mad’.

Question 54

Strength of theory of schizophrenogenic mother

Answer 54

Supporting research. Kasain et al (1934) examined hospital records and reported that evidence of maternal overprotection was found in 33 of 45 cases of schizophrenia.

Question 55

Limitation of the idea of the schizophrenogenic mother.

Answer 55

Research is tedious. Kasain study shows that almost 1/3 of cases didn’t have an overprotective mother and judgements may have been biased as the researchers were not blind to the hypothesis, so it may have lacked objectivity causing them to be more likely to categorise normal behaviour of concerned parents as overprotective.
Not until mid 1970s when a review of schizophrenogenic mother research was published concluding that there was no evidence that they were more likely than anyone else to have a schizophrenic child.

Question 56

Double bind theory description.

Answer 56

Risk factor for schizophrenia.
Bateson et al (1956). Schizophrenia was the result of communication difficulties in the family, especially between parents and children. Children who receive contradictory messages from their parents are more likely to develop schizophrenia.
Long term exposure to these communications caused the child to perceive the world in terms of contradictory inout from their environment and that they are unable to discriminate between the contradictory messages. This would eventually lead to the manifestation of symptoms of schizophrenia as a means of escaping the contradictory demands of the double bind situation.
Delusions and hallucinations allow people to experience there own world where they understand what is going on.

Question 57

Strength of double bind theory.

Answer 57

Supporting research evidence - Berger (1965) retrospective study, questionnaire given to 20 individuals with schizophrenia and control group of 40 college students. 30 double bind statements were given, participants had to rate on a 4 point scale how frequently they recalled their mothers using such statements. Schizophrenia group consistently reported a higher incidence of recall of such statements.
Increases validity.

Question 58

Limitation of the double bind theory.

Answer 58

Contradicting research - Liem (1974) found the communications offered in a structured task by parents of 11 sons with schizophrenia were no more disordered than parents of the sons without schizophrenia.
Decreased validity.

Liem suggested that those studies that found a difference may be detecting parents who have to adapt their communication styles when communication with a child with schizophrenia.

Question 59

Expressed emotion description.

Answer 59

1956, antipsychotic chlorpromazine used to treat schizophrenia, but many patients soon re admitted due to relapse of symptoms.
Brown (1959), 156 ,en with schizophrenia after they had been discharged. Interviewed and observed patients and their families and their communications. He said adverse home environment that have high levels of expressed emotion are negative and produce stress which exceeds the patients coping mechanism, triggering a relapse. (Lack of population validity, gender bias).

High EE communication includes:
Critical comments about behaviour
Hostility from carers as they get angry or irritated with the individual with schizophrenia as they feel they can control their behaviour.
Emotional over involvement where parents and caters blame themselves, so show severe sadness or being over protective.
Lack of warmth
Lack of unconditional positive regard (humanistic approach)

Question 60

Strength of expressed emotion theory.

Answer 60

Supporting research (for the role of expressed emotion in relapse rate - Vaughn and Leff (1976), 53% of those with schizophrenia who had high EE relatives relapsed wishing 9 months compared to 12% of those with low EE relatives.

Question 61

Limitation of expressed emotion theory.

Answer 61

Contradicting research - McCreadle and Philips (1998) failed to find higher relapse rates among those individuals with schizophrenia living in high EE homes.
Unreliable.

Question 62

General limitations for family dysfunction explanations.

Answer 62

Ethical concerns - unfair to blame the family for causing schizophrenia.

Difficult to separate nature and nurture - Genain quadruplets.

Question 63

Psychological therapy for schizophrenia

Answer 63

Family therapy

Question 64

What is family therapy?

Answer 64

Takes place with the family and the patient.
NICE guidance for family therapy states that: should include the person with schizophrenia, carried out between 3 months and 1 year, include 10 planned sessions, include negotiated problem solving or crisis management.

Aim is to improve the quality of communication and interaction between family members, using family intervention (Burbach’s (2018) model of practice).

Question 65

Family intervention.

Answer 65

Aims to reduce the levels of negative expressed emotion in the family and to develop and trusting and cooperative relationship.

Reducing negative emotions - family encouraged to share their experiences of living with the illness. The family learn more constructive ways of interacting with each other.

Improving the family’s ability to help - involved educational element where the therapist provides information about the cause and symptoms of schizophrenia and ways of managing and coping with the everyday difficulties that arise. The family are also trained to recognise early signs of a relapse, to help reduce its severity. Achieves a balance between caring for up the individual with schizophrenia and maintaining their own lives.

Question 66

Barbach’s (2018) model of practice.

Answer 66

1) sharing basic information. Providing practical and emotional support.
2) identifying resources, including what a family can/cannot offer.
3) creating a safe space for all family members to express their emotions. Encourage mutual understanding.
4) identifying unhelpful patterns of interaction.
5) skills training (learning stress management techniques)
6) relapse prevention training.
7) maintenance fir the future.

Question 67

Strength of family therapy for schizophrenia.

Answer 67

Evidence showing it’s effectiveness - Anderson et al (1991) found relapse rate of 40% when patients had drugs only, 20% with family therapy, 5% with both. Beneficial especially in reducing relapses.

Benefits the whole family - Lobban (2013) reported that other family members felt they were able to cope better. Shows that family therapy has wider benefits.

Tarrier et al (1991) concluded that family intervention was significantly less costly compared to standard care.

Question 68

Cognitive explanations for schizophrenia.

Answer 68

Dysfunctional thinking, metapresentation dysfunction, central control dysfunction.

Cannot provide a complete explanation, no explanation which can account for all of the behaviours seen in individuals with schizophrenia.

Question 69

Dysfunctional thinking.

Answer 69

Cognitive neuroscience explanation.
Lower than usual level of information processing, suggesting cognition is impaired which can be seen in the symptoms (positive - hallucinations, negative - avolition)
Negative symptoms are associated with reduced thought processing in the ventral striatum, part of the mesocortical pathway - backing up the dopamine hypothesis.

Question 70

Metapresentation dysfunction.

Answer 70

Frith et al (1992) 2 kinds of dysfunctional thought processes in people with schizophrenia.

Meta-representation - the cognitive ability to reflect on thoughts and behaviour allowing us insight into own thought processes and also allows us to interpret the actions of others.

Dysfunction in meta representation of our own thoughts are ‘disorders of self-monitoring’ this distrusts the ability to recognise our own thoughts and actions as being carried out by ourselves, which can explain positive symptoms such as hallucinations.

Dysfunction in meta representation of the thoughts of others are ‘disorders of monitoring other people’s thoughts and intentions’ which can explain positive symptoms such as delusions of persecution.

Question 71

Central control dysfunction.

Answer 71

Second dysfunction thought process by Frith et al (1992).
Central control is the ability to suppress out automatic responses to stimuli while performing actions that reflect our intentions. Frith argued that central control is sometimes faulty in patients with schizophrenia. For example speech derailment can be explained. U the inability to resist expressing automatic thoughts.

Question 72

Strengths of cognitive explanations of schizophrenia.

Answer 72

Lots of scientific research - Baruch et al (1999) compared performance on stroop test of people with and without schizophrenia and found that those with schizophrenia were slower and made more mistakes. Highlights impaired cognitive processes specifically central control dysfunction. Increases reliability.

Useful applications - use of CBT, Kuipers et al (1997) 50% of patients with positive symptoms who were ‘medically resistant’ experienced a reduction in symptoms when treated with CBT. Helps people who do not respond to drug therapies. Increasing validity because it suggests that by modifying gysfunctional thinking symptoms are reduced.

Question 73

Limitations of cognitive explanations of schizophrenia.

Answer 73

Some researchers criticise Frith’s cognitive explanations for only describing the cognitive deficits but do not always explain the origin of these deficits. Descriptive rather than explanatory.

Commentary point - suggestions that schizophrenia needs to be viewed in a more holistic way, which can include cognitive factors. Biological predisposition (genetic vulnerability), social stressors (negative life events and dysfunctional families), dopamines system.

Question 74

Cognitive therapy for schizophrenia.

Answer 74

15-20 sessions which is longer than other conditions, this can be I’m groups or individually. CBT helps patients to become aware of the linked between their thought processes and their illness.
The aim of CBT is to reduce the positive symptoms, help the patient become more self reliant, reduce chances of relapse.

5 main components
Engagement strategies - discuss any worries they may have about CBT.
Psycho-education - educates the patient on their symptoms and aims to normalise symptoms, therapist will try and identify reasons they occur and try to help decatastrophise them.
Cognitive strategies - teach patients strategies to challenge their disordered thoughts, empirical disputation where the Laurent will be asked to find evidence for their delusions or hallucinations.
Behavioural skills training - help manage their symptoms eg activity planning and distraction techniques.
Relapse prevention strategies to identify early signs of relapse and make a plan of action if symptoms return.

Question 75

Strengths of cognitive therapy for schizophrenia.

Answer 75

Supporting evidence - Kuipers et al (1997), 60 individuals with schizophrenia who had a positive symptom which was medication resistant were randomly allocated to either CBT plus standard care or standard care only condition, after 9 months, CBT group had 50% of patients who were considered improved with only one individual becoming worse, in the standard care only condition, 33% considered to have improved with 3 people becoming worse and 1 committing suicide.

Cost effective - Kuipers et al (1998) analysed the eco minix impact of offering CBT, reported that the cost involved in delivering CBT weee likely to be offset by the reduced utilisation of service colts in the future.

Question 76

Limitations of cognitive therapy for schizophrenia.

Answer 76

Lack of consistent findings - Jauhar et al (2014) reported a ‘small therapeutic effect’ from using CBT with clients with schizophrenia. Other studies reported that CBT significantly reduced psychiatric symptoms.

NHS in England and Wales is organised into various trusts. In the National Audit of Schizophrenia conducted by the Royal College of Psychiatrists (2014) significant variations in number of those offered CBT, ranging from 67% to 14% with an average of 50% reported that their trust offered them CBT. This contradicts the NICE guidance who recommend that every adult with psychosis or schizophrenia be offered CBT.

Question 77

Management of schizophrenia.

Answer 77

Token economies.

Question 78

What is a token economy?

Answer 78

A physical token which is given to someone when they carry out desirable behaviour. They should be given as soon as possible after the desirable behaviour is carried out.
Tokens can then be swapped for a reward.
This is a form of behaviour modification and it comes from the behavioural approach.
Tokens are removed as punishment to discourage bad behaviour this is operant conditioning.

The primary reinforcer is the reward.
The secondary reinforcer is the token.

Question 79

Managing schizophrenia before token economies.

Answer 79

Today care is provided in the community - NHS Community Care Act 1990.

In the 1960s and 1970s the norm for treating schizophrenia was long term hospitalisation. Institutionalisation can develop under circumstances of prolonged hospitalisation, this can result in maladaptive behaviours. 3 categories of institutionalised behaviour includes personal care, condition related behaviours, social behaviours.
If these behaviours could be modified with a token economy system the benefits would be, improving quality of life in hospital and making it easier to adapt back into life in the community.

Question 80

Study looking at token economies for schizophrenia.

Answer 80

Ayllon and Arzrin (1968) trialled a token economy for female patients with schizophrenia who had been hospitalised for an average of 16 years. When patients completed basic activities they were rewarded with a plastic token which could be exchanged for pleasure activities.
The number of actions patients performed each day rose 8x from 5 to over 40.

Question 81

Strengths of token economy.

Answer 81

Supporting evidence - Paul and Lentz, hospitalised patients with long term schizophrenia , patients developed various social and work related skills and after 4.5, 98% of patients had been released compared to 45% of those who were not in the programme. However there are ethical concerns be cause not all patients were able to access to the programme. There is also a lack of follow up data, we do not know if anyone was readmitted.
Dickerson et al (2005), meta analysis on 13 studies and beneficial results were reported in 11 of these studies. However, the use of secondary data may not have the same standard of research.

Question 82

Limitations of token economy.

Answer 82

Effectiveness is limited as token economies require a very structured environment to work - today most people with schizophrenia live in the community which does not have the same level of structure, so a person cannot constantly be rewarded, when we’re are no tokens available behaviour can relapse. This could mean that token economies are not effective in the real world.

Only focuses on a few of the behavioural symptoms of schizophrenia and institutionalisation - cognitive symptoms are not addressed such as hallucinations and delusions.

Questions over its overall effectiveness - however it is a management strategy not a treatment.

More ethical and pleasant alternatives - Mathew Chiang et al (2019), art therapy maybe a good alternative, evidence has is relatively small, but it has a high gain low risk approach to managing schizophrenia. Art therapy is a pleasant experience without major side effects or ethical abuses. NICE guidelines recommend art therapy. Token economies can be seen as unfair because they take away basic pleasures and can be patronising.

Question 83

The interactionist approach to schizophrenia.

Answer 83

Acknowledges that biological (genes, dopamine abnormalities), psychological (cognitive dysfunction) and social (dysfunctional families, abuse) factors are involved in the development of a condition like schizophrenia.
Diathesis stress model.

Question 84

Diathesis stress model.

Answer 84

Vulnerability and negative experiences cause schizophrenia.
Low vulnerability (pre-disposition) requires high levels of stress to trigger schizophrenia.
Hugh vulnerability (pre-disposition) requires low levels of stress to trigger schizophrenia.

Question 85

Diathesis stress model - Meehl’s 1962 model

Answer 85

Suggested that Diathesis (vulnerability) was entirely genetic and the result of a single ‘schizogene’. Without the gene a person would not be able to develop schizophrenia. If they had the gene they have a biologically based schizotypic personality. So experiencing stress through childhood and adolescence would trigger the gene and result in the development of schizophrenia.

Question 86

Diathesis stress model - modern understanding of Diathesis.

Answer 86

There is no single ‘schizogene’ and schizophrenia is polygenic. The schizophrenia working group of the psychiatric genomics consortium found that there was 108 genetic loci associated with schizophrenia.
We also know that there are other pre-disposing vulnerability factors beyond genetics. Read et al (2001) suggested early severe trauma can seriously affect many aspects of brain development. In 2017, 67% of people with psychotic disorders reported at least one childhood trauma. This can also be shown in the Genain quadruplets.
Today, ‘stress’ refers to anything that risks triggering schizophrenia. One example of a stressor today is cannabis as it can increase the risk of schizophrenia up to 7 times, possibly because it interferes with the dopamine system. Another stressor could be living in an urban area, as it can be seen as more stressful compared to rural areas.

Question 87

Treatment for schizophrenia from the interactionist approach.

Answer 87

Medication and CBT.

Question 88

Strength of the basic Diathesis stress model.

Answer 88

Supporting evidence - Tienari et al (2004), 155 adopted children who had mothers with schizophrenia (genetic high risk) compared to 155 adopted children with non schizophrenic biological parents (genetic low risk). Adoptive parents were assessed and found that high levels of criticism, hostility and low levels of empathy were strongly associated with the development of schizophrenia, but only in the high genetic risk group.

Question 89

Limitation of the basic diathesis stress model.

Answer 89

Too simplistic - diathesis is not a just a single gene and stress is not just dysfunctional parenting. Houston et al (2008) found that those who had been sexually abused and used cannabis under the age of 16 were 12x more likely to have schizophrenia. Meaning Meehl’s model is outdated but there is support for the understanding.

Question 90

Strength of the interactionist approach.

Answer 90

Real world applications - Tarrier et al (2004) randomly allocated 315 patients with schizophrenia to 1 of 3 groups, medication and CBT, medication and counselling, medication only. Participants in groups 1 and 2 showed lower symptoms following the trial compared to the medication only group. Shows that there is a clear practical advantage to adopting an interactionist approach to schizophrenia in terms of superior treatment outcomes. However we cannot automatically assume that the success of combined therapies means interactionist explanations are correct (treatment causation fallacy).