Schizophrenia Flashcards
(91 cards)
1
Q
What is schizophrenia?
A
A major psychotic disorder that causes a variety of psychological symptoms but is characterised by a lack of contact with reality.
2
Q
Schizophrenia statistics.
A
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.
3
Q
What is classification?
A
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.
4
Q
Medical model approach.
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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.
5
Q
Categorising symptoms of schizophrenia.
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Kurt Schneider (1959) suggested that categorising the symptoms of schizophrenia as either positive or negative.
6
Q
Positive symptoms.
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Behaviours that the person is exhibiting in addition to ‘normal’ behaviours.
Hallucinations
Delusions
Disordered thinking
Disorganised behaviour
7
Q
Hallucinations
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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)
8
Q
Delusions
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Beliefs that are unreal
Commonly held delusions are of persecution and of grandiosity (the belief that the individual is special in some way- superior).
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Q
Disordered thinking
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Evident through examining speech.
Sometimes described as derailment or knights move thinking.
10
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Disordered behaviour
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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.
11
Q
Negative symptoms.
A
Behaviours that are inhibiting people with schizophrenia from demonstrating ‘normal’ behaviour.
Alogia
Avolition
Anhedonia
Flatness of affect
Catatonic behaviour
12
Q
Alogia
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Poverty of speech, lack meaning in what they are saying even simple short answers can be a problem.
13
Q
Avolition
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Lack of goal directed behaviour, which may be perceived as disinterest.
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Anhedonia
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An individual does not react appropriately to pleasurable experiences.
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Q
Flatness of affect
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Show little or no facial emotional expression, may be interpreted as apathetic, speech patterns are very monotonous.
16
Q
Catatonic behaviour
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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)
17
Q
What is used to classify schizophrenia?
A
DSM-5 and ICD-10
18
Q
What does the DSM-5 say about schizophrenia?
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At least 2 symptoms must be present for at least a month and one of the symptoms must be a positive symptom.
19
Q
What does the ICD-10 say about schizophrenia?
A
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.
20
Q
Reliability of diagnosing schizophrenia
A
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.
21
Q
Reliability as a strength for diagnosing schizophrenia
A
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.
22
Q
Validity of diagnosing schizophrenia
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Criterion validity (asking if the criteria we are using the diagnose schizophrenia are actually accurate)
23
Q
Validity as a limitation of diagnosing schizophrenia
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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.
24
Q
Validity as a strength of diagnosing schizophrenia
A
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)
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Co-morbidity.
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
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Co-morbidity as a limitation of diagnosing schizophrenia
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.
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Gender bias in diagnosis
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.
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Gender bias as a limitation of diagnosing schizophrenia
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
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Culture bias in diagnosis (limitation)
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).
Misunderstanding or disregarding cultural specific symptoms - not sure what to diagnose causing clinician to ignore symptoms.
Clinician does not account for culture - using Western medical model to diagnose non western individuals causing over diagnosis due to lack of understanding - ethnocentricism.
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Symptom overlap as a limitation of diagnosing schizophrenia
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
Depression - lethargy and lack of motivation and unable to maintain routine.
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Biological expiations of schizophrenia
Family studies, candidate genes, the role of mutation, neural correlates
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Family studies
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%.
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Candidate genes
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.
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Polygenic
Caused by multiple different genes
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Aetiologically heterogenous
Schizophrenia is caused my multiple different factors, including genetic variations.
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The role of mutation
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
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Strengths of the genetic explanation
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.
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Limitations of the genetic explanation
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.
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Neural correlates
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
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Mesolimbic pathway
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.
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Mesocortical pathway
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.
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Strengths of neural correlates
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.
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Limitations of neural correlates
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
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Biological therapy for schizophrenia
Anti-psychotics
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How do antipsychotics work
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.
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What do antipsychotics used for?
To reduce the intensity of symptoms (especially positive).
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Two types of antipsychotics
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.
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Typical antipsychotics
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.
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Atypical antipsychotics
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.
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Strength of antipsychotics
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.
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Limitations of antipsychotics.
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%).
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Psychological explanations for schizophrenia
Family dysfunction (schizophrenogenic mother, double bind theory, expressed emotion)
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Schizophrenogenic mother description.
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’.
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Strength of theory of schizophrenogenic mother
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.
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Limitation of the idea of the schizophrenogenic mother.
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.
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Double bind theory description.
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.
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Strength of double bind theory.
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.
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Limitation of the double bind theory.
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.
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Expressed emotion description.
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)
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Strength of expressed emotion theory.
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.
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Limitation of expressed emotion theory.
Contradicting research - McCreadle and Philips (1998) failed to find higher relapse rates among those individuals with schizophrenia living in high EE homes.
Unreliable.
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General limitations for family dysfunction explanations.
Ethical concerns - unfair to blame the family for causing schizophrenia.
Difficult to separate nature and nurture - Genain quadruplets.
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Psychological therapy for schizophrenia
Family therapy
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What is family therapy?
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).
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Family intervention.
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.
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Barbach’s (2018) model of practice.
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.
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Strength of family therapy for schizophrenia.
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.
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Cognitive explanations for schizophrenia.
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.
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Dysfunctional thinking.
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.
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Metapresentation dysfunction.
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.
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Central control dysfunction.
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.
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Strengths of cognitive explanations of schizophrenia.
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.
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Limitations of cognitive explanations of schizophrenia.
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.
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Cognitive therapy for schizophrenia.
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.
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Strengths of cognitive therapy for schizophrenia.
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.
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Limitations of cognitive therapy for schizophrenia.
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.
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Management of schizophrenia.
Token economies.
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What is a token economy?
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.
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Managing schizophrenia before token economies.
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.
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Study looking at token economies for schizophrenia.
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.
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Strengths of token economy.
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.
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Limitations of token economy.
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.
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The interactionist approach to schizophrenia.
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.
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Diathesis stress model.
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.
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Diathesis stress model - Meehl’s 1962 model
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.
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Diathesis stress model - modern understanding of Diathesis.
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.
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Treatment for schizophrenia from the interactionist approach.
Medication and CBT.
Taking antipsychotics to control their symptoms which allows them to engage better in CBT.
Research has found reduced symptoms when combining the 2 compared to just one or the other, making it cost effective.
Could make side effects of the drugs worse because they emphasise challenging dysfunction thought processes
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Strength of the basic Diathesis stress model.
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.
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Limitation of the basic diathesis stress model.
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.
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Strength of the interactionist approach.
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).
Revised understanding for the Diathesis stress model - previously suggested schizophrenia was caused by a single ‘schizogene’ now understood to be polygenic. Allows better access to treatment because it is understood that there is not just one cause. Also improved understanding of stress. Schizophrenia could be caused by childhood trauma (67%) and risk factors - cannabis use can increase the risk of developing schizophrenia by up to 7x
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Limitations of interactionist approach.
Does not acknowledge other factors such as the file of neurotransmitters - only a partial explanation.
