Schizophrenia Flashcards
What is Sz
best described as a condition where personality loses its unity
classification of mental disorder
The process of organising symptoms into categories based on which symptoms frequently cluster together
What did stafford-clark say about sz
Sz is a generic name for a group of disorders characterised by a progressive disintegration of emotional stability, judgement, contact with and appreciation of reality
What are the classification systems used for sz
-ICD-10
-DSM-5
How do the Diagnostic manuals differ
the manuals differ in their classification of Sz
-DSM-5 patients must have a positive symptom
-ICD-10 patients must have 2+ negative
Positive symptoms
Atypical symptoms experienced in addition to normal experiences
What are positive symptoms
-Hallucinations: unusual sensory experiences that can be related to the environment or have no relationship to what the senses are picking up
-Delusions: irrational beliefs that can take any form and make a person behave in ways that make sense to them but seem bizarre to others
Negative symptoms
Atypical experiences that represent the loss of a usual experience such as clear thinking
What are negative symptoms
-speech poverty: involves reduced frequency and quality of speech
-Avolition: loss of motivation to carry out tasks and results in lowered activity levels
What are different subtypes of sz
-paranoid sz
-hebephrenic sz- involves negative symptoms
-catatonic sz
Which manual recognises different subtypes of sz
ICD-10
What is the prevalence of sz
overall just less than 1% of the world suffer from sz
What age does sz occur
onset of sz mostly occurs between 15 and 45
Who has a higher prevalence rate
males, cities, working class
What is a strength of the diagnosis of Sz (reliability)
-test-retest occurs when a practitioner makes the same diagnosis on separate occasions from the same information
-inter-rater occurs when several practitioners make the same diagnosis of the same patient
-Making a diagnosis with most mental disorders can be a problem as often there are no physical symptoms therefore the practitioner has to diagnose with the patients report
-In 180 cases inter-rater reliability was +0.97 and test-retest reliability was +0.92
What is a limitation of diagnosis of sz (validity)
-concerns how accurate, meaningful and useful diagnosis is
-Validity of a psychotic diagnosis can be assessed by criterion validity
-If someone is diagnosed with sz they should show symptoms of sz
-Cheniaux had 2 psychiatrists independently assess the same 100 clients using ICD and DSM
68 were diagnosed using ICD and only 39 using DSM
-This suggests that sz is either under or over diagnosed and therefore has low criterion validity
What is a counterpoint to low validity of diagnosis of sz
Criterion validity is good for diagnosis as long as the same diagnostic manual is used
What is a limitation of diagnosis of sz (comorbidity)
-Its co-morbidity with other conditions
-if conditions occur together then this calls into question the validity of their diagnosis because they might actually be a single condition
-Sz is commonly diagnosed with other conditions
-a review found that about half of those diagnosed with sz also had a diagnosis of depression or substance abuse
-This is a problem because sz may not exists as a distinct condition
What is a limitation of diagnosis of sz (gender bias)
-after the 1980s more men appear to have been diagnosed with sz than women.
-men may be genetically more vulnerable than women or there is a gender bias in the diagnosis of sz
-Women seem to function better than men with sz which may mean they are being under diagnosed
-this means women may not therefore be receiving treatment and services that might benefit them
What is a limitation of diagnosis of sz (culture bias)
-African americans and english people of afro-caribbean origin are more likely to be diagnosed with sz
-not due to a genetic vulnerability but due to a cultural bias
-African cultures may be more accepting of symptoms such as hearing voices and therefore speak more freely about it to their psychiatrist, leading to more diagnosis
-incidence in the west indies and in great britain is about 1% but afro- caribbean living in GB are 7x more likely to be diagnosed sz.
-This suggest either the stress of living in GB causes sz or invalid diagnosis
What is a limitation of diagnosis of sz (symptom overlap )
there is a considerable overlap of the symptoms in sz and in other conditions.
-I.E bipolar disorder
-This is an issue as Sz is a cluster of different symptoms
what was Gottesman study on
Genetic basis of Sz
what did Gottesman find
Ran a controlled study and found that the risk of an individual developing sz increased in line with genetic similarities to a relative with the disorder
Dz twins and siblings share the same amount of DNA but have a different risk of developing Sz, why
-different shared environments due to age and other social factors
Why can’t sz be 100% down to nature (Gottesman)
identical twins would have a 100% risk of developing sz. however it’s only 48% suggesting other factors influence sz such as the environment
polygenetic
Sz is caused by more than one gene. Most likely those coding for neurotransmitters like dopamine
aetiologically heterogeneous
different combinations of factors can cause it
Ripke et al (study on candidate genes)
-Gathered data from genome wide study of sz
-37,000 sz patients genetic make up was compared to 113,000 controls
-108 separate genetic variations were associated with increased risk of sz
-genes associated with the risk included those coding the functioning of a number of neurotransmitters
What is the role of mutation
-Sz can also have a genetic origin in the form of mutated parental DNA
-This could be caused radiation, poison or viral infection
What evidence is there for mutation
Brown 2002 evidence carries from positive correlation between parental age (sperm mutation) and risk of sz
neural correlates
Patterns of structure or activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience.
Dopamine
A neurotransmitter that generally has an excitatory effect and is linked to the sensation of pleasure. Unusually high levels are associated with schizophrenia and unusually low levels are associated with Parkinson’s disease.
What is the original dopamine (DA) hypotheses
schizophrenia might be the result of high levels of DA (hyperdopaminergia, ‘hyper’ means ‘high’) in subcortical areas of the brain
What is the original DA hypotheses based on
the discovery that drugs used to treat schizophrenia (antipsychotics, which reduce DA) caused symptoms similar to those in people with Parkinson’s disease, a condition associated with low DA levels
What is the updated DA hypotheses
low DA in the prefrontal cortex (responsible for thinking) could explain cognitive problems i.e. negative symptoms of schizophrenia. It has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia - so both high and low levels of DA in different brain regions
What is a strength of the genetic explanation (research support)
-strength of the genetic explanation is the strong evidence base.
-Family studies such as Gottesman show that risk increases with genetic similarity to a family member with schizophrenia. -Adoption studies such as Tienari et al. (2004), show that biological children of parents with schizophrenia are at heightened risk even if they grow up in an adoptive family.
-A recent twin study by Hilker et al. (2018) showed a concordance rate of 33% for identical twins and 7% for non-identical twins.
-This shows that some people are more vulnerable to schizophrenia as a result of their genetic make-up.
What is a limitation of the genetic explanation (environmental factors)
-limitation of the genetic explanation is there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia.
-These include both biological and psychological influences.
-Biological risk factors include birth complications (Morgan et al. 2017) and smoking THC-rich cannabis in teenage years (Di Forti et al. 2015).
-Psychological risk factors include childhood trauma which leaves people more vulnerable to adult mental health problems in general but there is now evidence for a particular link with schizophrenia.
-In one study by Morkved et al. (2017), 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues.
-This means that genetic factors alone cannot provide a complete explanation for schizophrenia.
What is a strength of the neural explanation (evidence for dopamine)
-strength is support for the idea that dopamine (DA) is involved in schizophrenia. -First, amphetamines increase DA and worsen symptoms in people with schizophrenia and induce symptoms in people without (Curran et al. 2004).
- Second, antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms (Tauscher et al. 2014).
-Third, some candidate genes act on the production of DA or DA receptors.
-This strongly suggests that dopamine is involved in the symptoms of schizophrenia.
What is a limitation of the neural explanation (glutamate)
-limitation of the dopamine hypothesis is evidence for a central role of glutamate. -Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia (McCutcheon et al. 2020).
-In addition, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing.
-This means that an equally strong case can be made for a role for other neurotransmitters.
Family dysfunction
Psychologists have attempted to link SZ to childhood and adult experiences of living in a dysfunctional family.
what are the three theories to do with family dysfunction
The schizophrenogenic mother
Double-bind theory
Expressed emotion
The schizophrenogenic mother
Psychodynamic explanation based on childhood accounts by Fromm- Reichmann who said a particular type of parenting reoccurred ‘schizophrenogenic mother’
Attributes of the schizophrenogenic mother
Cold
Rejecting
Critical
Controlling
What does the schizophrenogenic mother cause
Creates a family environment of tension and secrecy
This parenting style leads to distrust that later develops into paranoid
delusions and ultimately SZ
Who developed double bind theory
Bateson et al (1972)
Double bind theory
Expanded on Fromm-Reichmanns work, and added to the idea of the
Family environment causing SZ. He emphasised the role of communication
style within a family.
How is Sz developed according to double bind theory
Developing child fears doing wrong, but gets mixed messages about what
‘wrong’ is. They are unable to comment on unfairness of the situation or seek
clarification.
What happens when a child is wrong according to the double bind theory
When they get it ‘wrong’ (frequently) child is punished by withdrawal of
love.
Impact of the double bind theory
Child is confused, finds the world a frightening and dangerous place.
Results in paranoid delusions and disorganised thinking
What does Bateson recognise
But, Bateson said this was a risk factor, and didn’t always exist in SZ
families.
Expressed emotion
EE is the level of negative emotion expressed towards a SZ patient by
their family/carers.
What are the elements of EE
Verbal Criticism – some time accompanied by violence
Hostility - anger and rejection
Emotional overinvolvement, needless self-sacrifice.
What are high levels of EE are source of
Stress
What is high EE an explanation for
This is an explanation of relapse rather than cause of SZ.
How can high EE be an explanation for onset of sz
in vulnerable people this could trigger the onset of SZ.
cognitive explanations of sz
These are explanations that focus on mental processes such as thinking, language and attention.
What are the cognitive explanations for sz
-Dysfunctional thinking
-Metarepresentation dysfunction
-Central control dysfunction
Dysfunctional thinking
-A cognitive explanation focuses on the role of mental processes.
-SZ is associated with several types of dysfunctional thought processing and this can provide a full explanation for SZ.
-SZ ‘s can have information processing that doesn’t accurately represent reality.
What did Simon say about dysfunctional thinking
-SZ is characterised by disruption to normal thought processing.
-Reduced thought processing in the ventral striatum is associated with negative symptoms.
-Reduced processing of info in temporal and cingulate gyri are associated with hallucinations.
Metarepresentation dysfunction
The inability to reflect on thoughts and behaviours
What did Frith et al identify about metarepresentation dyfunction
Frith et al (1992) – identifies an inability to use meta representation in SZ patients. Therefore they cannot recognise their own actions and thoughts, and believe these are being carried out by someone other than themselves.
This explains auditory hallucinations and delusions like thought insertion.
Central control dysfunction
-Frith also identifies inability to stop automatic responses while performing deliberate actions in SZ patients.
-Speech poverty and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts.
What is an example of central control dysfunction
SZ patients can have derailment of thought because each word triggers associations, and the person cannot suppress automatic responses.
What is a strength of family dysfunction (research support)
One strength of these explanations is evidence linking family dysfunction to schizophrenia. Indicators of family dysfunction include insecure attachment and exposure to childhood trauma, especially abuse. According to a review by Read et al. (2005) adults with schizophrenia are disproportionately likely to have insecure attachment, particularly Type C or D. Read et al. also reported that 69% of women and 59% of men with schizophrenia have a history of physical and/or sexual abuse. In the Merkved et al. (2017) study, on the previous spread, most adults with schizophrenia reported at least one childhood trauma, mostly abuse. This strongly suggests that family dysfunction makes people more vulnerable to schizophrenia.
What is a limitation of family dysfunction (explanations lack support)
One limitation of family explanations is the poor evidence base for any of the explanations. Although there is plenty of evidence supporting the idea that childhood family-based stress is associated with adult schizophrenia, there is almost none to support the importance of traditional family-based theories such as the schizophrenogenic mother and double bind. Both these theories are based on clinical observation of people with schizophrenia and also informal assessment of their mothers’ personalities, but not systematic evidence. This means that family explanations have not been able to account for the link between childhood trauma and schizophrenia.
What is a strength of cognitive explanations of Sz (Research support)
One strength of cognitive explanations is evidence for dysfunctional thought processing. Stirling et al. (2006) compared performance on a range of cognitive tasks in 30 people with schizophrenia and a control group of 30 people without schizophrenia. Tasks included the Stroop task , in which participants have to name the font-colours of colour-words, so have to suppress the tendency to read the words aloud. As predicted by Frith et alis central control theory, people with schizophrenia took longer - over twice as long on average - to name the font-colours.This means that the cognitive processes of people with schizophrenia are impaired.
What is a limitation of cognitive explanations of Sz (a proximal explanation)
One limitation of cognitive explanations is that they only explain the proximal origins of symptoms.
Cognitive explanations for schizophrenia are proximal explanations because they explain what is happening now to produce symptoms - as distinct from distal explanations which focus on what initially caused the condition. Possible distal explanations are genetic and family dysfunction explanations. What is currently unclear and not well-addressed is how genetic variation or childhood trauma might lead to problems with metarepresentation or central control. This means that cognitive theories on their own only provide partial explanations for schizophrenia.
What are the therapies for Sz
-Biological – Psychosurgery, drugs (chemotherapy), ECT.
-Psychological – CBT, Family therapy, Token economies
What are antisychotics for
Short term or long term use
What are the two types of antipsychotic drugs
-typical
-atypical
typical antipsychotics
around since 1950’s, e.g. Chlorpromazine, thought to work on the neurotransmitter dopamine system, by reducing the action of dopamine, blocks the receptor sites, can reduce symptoms like hallucinations, and also is a sedative.
How does chlorpromazine work
acts as a dopamine antagonist. It acts against dopamine in this case blocking dopamine receptors at the postsynaptic receptor sites. This reduces the action of dopamine. Initially levels of dopamine build up in the synapse, but then production is reduced.
What type of symptoms does chlorpromazine reduce
This dopamine antagonist effect normalises neurotransmission, reducing positive symptoms like hallucinations.
Sedative effects of drug therapy (chlorpromazine)
As well as antipsychotic effects, Chlorpromazine is also a sedative. This is linked to its effects on histamine receptors. The drug is used to calm SZ patients and others.
When is chlorpromazine usually administered
Used on initial admittance to hospital if very anxious.
Atypical antipsychotics
around since 1960’s-80’s. Made to improve the effectiveness of drugs in supressing the symptoms of psychosis and minimise the side effects.
Examples of Atypical antipsychotics
-Clozapine, taken if typical drugs fail, thought to work on dopamine, serotonin and glutamine receptors, improves mood so can reduce suicide risk.
-Risperidone, less side effects than Clozapine, binds to dopamine and serotonin sites.
Ways to administer typical antipsychotics
tablets, syrups or injections
Dosage of typical typical antipsychotics
-taken orally the maximum daily dosage is 1000mg
-initial dosage is smaller and for most people the dosage is increased to 400-800mg
side effects of typical antipsychotics
dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin.
More serious side effects include tardive dyskinesia.
The most serious side effects include neuroleptic malignant syndrome which can lead to death
side effects of clozapine
agranulocytosis-blood condition
ways to administer clozapine
tablet or syrup
dosage of clozapine
300-450mg
ways to administer risperidone
tablet, syrup or injection (last up to 2 weeks)
dosage of risperidone
-small dose is initially given and build up to a typical dose of 4-8mg
-maximum is 12mg
A strength of biological therapies of sz (evidence of effectiveness)
One strength of antipsychotics is evidence to support their effectiveness. There is a large body of evidence to support the idea that both typical and atypical antipsychotics are at least moderately effective in tackling the symptoms of schizophrenia.Thornley et al. (2003) reviewed studies comparing the effects of chlorpromazine to control conditions. Data from 13 trials with a total of 1121 participants showed that chlorpromazine was associated with better overall functioning and reduced symptom severity as compared to placebo. There is also evidence for the benefits of atypical antipsychotics. In a review Meltzer (2012) concluded that clozapine is more effective than typical antipsychotics and other atypical antipsychotics, and that it is effective in 30-50% of treatment-resistant cases where typical antipsychotics have failed. This means that, as far as we can tell, antipsychotics work.
Counterpoint of evidence for effectiveness of biological therapies
Healy (2012) has suggested serious flaws with evidence for effectiveness. For example most studies are of short-term effects only and some successful trials have had their data published multiple times, exaggerating the size of the evidence base for positive effects. Also, because antipsychotics have powerful calming effects, it is easy to demonstrate that they have some positive effect on people experiencing the symptoms of schizophrenia. This is not the same as saying they really reduce the severity of psychosis. This means that the evidence base for antipsychotic effectiveness is less impressive than it first appears.
A limitation of biological therapies (serious side effects)
One limitation of antipsychotic drugs is the likelihood of side effects. Typical antipsychotics are associated with a range of side effects including dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin. Long-term use can result in tardive dyskinesia, which is caused by dopamine supersensitivity and causes involuntary facial movements such as grimacing, blinking and lip-smacking. The most serious side effect of antipsychotics (particularly typical antipsychotics) is neuroleptic malignant syndrome (NMS). This is believed to be caused when the drug blocks dopamine action in the hypothalamus, an area in the brain associated with the regulation of a number of body systems. NMS results in high temperature, delirium and coma, and can be fatal. Estimates of its frequency range from less than 0.1% to just over 2%. This means that antipsychotics can do harm as well as good and individuals who experience these may avoid such treatments (which makes the treatment ineffective).
A limitation of biological therapies for sz (mechanism unclear)
A further limitation of antipsychotics (typical and at least some atypical) is that we do not know why they work.
Our understanding of the mechanism by which antipsychotic drugs work is strongly tied up with the original dopamine hypothesis - the idea that symptoms of schizophrenia are linked to high levels of dopamine activity in the subcortex of the brain. However we now know that this original dopamine hypothesis is not a complete explanation for schizophrenia, and that in fact dopamine levels in other parts of the brain are too low rather than too high. If this is true then most antipsychotics should not work. Given that there are questions over the effectiveness of antipsychotics anyway this adds to the argument that in fact they are ineffective. This means that at least some of the antipsychotics may not be the best treatment to opt for - perhaps some other factor is involved in their apparent success.
Cognitive behaviour therapy
CBT aims to deal with both thoughts (cognitions) and behaviour.
how many CBT sessions do individuals usually take
It usually takes place over a period of 5-20 sessions (this is longer than for other conditions), either in groups or on an individual basis.
How cognitive behaviour therapy helps
-Help a client make sense of how their irrational cognitions (such as delusions and hallucinations) impact on their feelings and behaviour.
-Just understanding where symptoms come from can be hugely helpful for those with symptoms like auditory hallucinations.
-This will not eliminate the symptoms of schizophrenia but it can make people better able to cope with them. This in turn reduces their distress and improves their ability to function adequately.
Example of how CBT helps
For example, a client hears voices and believes the voices represent demonic forces, they will naturally be very afraid. If a therapist can convince them that the voice actually comes from the malfunctioning speech centre in their own brain and that it cannot hurt them if they ignore it, this is much less frightening and hence less debilitating.
Normalisation
People hearing voices can also be helped by teaching them that voice-hearing is an extension of the ordinary experience of thinking in words
How can delusions be challenged using CBT
a process of reality testing in which the person with schizophrenia and their therapist jointly examine the likelihood that beliefs are true. In some cases where delusions are resistant to reality testing CBT can still be used to tackle the anxiety and depression that result from living with schizophrenia.
Family therapy
Takes place with families as well as the identified patient. The therapy aims to improve the quality of communication and interaction between family members. There is a range of approaches to family therapy for schizophrenia.
identified patient
a term used in family therapy which describes one member of a dysfunctional family who expresses the family’s conflicts
How family therapy helps
Pharoah et al. (2010) identified a range of strategies that family therapists use to try to improve the functioning of a family that has a member with schizophrenia.
What are the strategies that family therapists use to improve family functioning
-Reduces negative emotions: Family therapy aims to reduce levels of expressed emotion (EE),Reducing stress is important to reduce the likelihood of relapse.
-Improves the family’s ability to help: The therapist encourages family members to form a therapeutic alliance whereby they all agree on the aims of therapy. A further aim is to ensure that family members achieve a balance between caring for the individual with schizophrenia and maintaining their own lives.
A model of practice for families dealing with Sz
Burbach (2018) has proposed a model for working with families dealing with schizophrenia.
Begins with sharing basic information and providing emotional and practical support.
Phase 2 involves identifying resources including what different family members can (and cannot) offer.
Phase 3 aims to encourage mutual understanding, creating a safe space for all family members to express their feelings.
Phase 4 involves identifying unhelpful patterns of interaction.
Phase 5 is about skills training such as learning stress management techniques.
Phase 6 looks at relapse prevention planning.
Phase 7 is maintenance for the future.
How many phases are their in the model of practice for working with families dealing with Sz
7
A strength of CBT (evidence for effectiveness)
One strength of CBT is the evidence for effectiveness. Jauhar (2014) reviewed 34 studies of using CBT with SZ, concluding there is small significant changes in both positive and negative symptoms.
Pontillo (2016)also found a reduction in frequency and severity of auditory hallucinations.
NICE (National Institute for Health and Care Excellent), recommends CBT for SZ.
Therefore both research and clinical experience support the benefits of CBT for SZ.
A limitation of CBT (Quality of evidence)
One limitation of CBT for SZ is the wide range of techniques and symptoms included in studies. These vary widely from one case to another.
Thomas (2015) different studies have involved the use of different CBT techniques and people with different combinations of positive and negative symptoms.
The overall modest benefits of CBT for SZ probably conceal a wide variety of effects of different CBT techniques on different symptoms.
This therefore makes it hard to say how effective CBT for a particular patient with SZ will be.
A strength of family therapy (evidence of effectiveness)
One strength of family therapy is the evidence for effectiveness. McFarlane (2016) reviewed studies and concluded that family therapy was one of the most consistently effective treatments for SZ. Relapse rates were found to be reduced typically by 50-60%.
He also concluded that using family therapy as mental health initially starts to decline is particularly promising.
Clinical trials from NICE recommends family therapy for everyone with a diagnosis of SZ.
This means that family therapy is likely to be beneficial to people with both early and ‘full-blown’ SZ.
a strength of family therapy (benefits to whole family)
A further strength of family therapy is the benefits it brings to the whole family.
Lobban & Barrowclough (2016) concluded that these effects are important because families provide the bulk of the care for the SZ patient.
By strengthening the functioning of the whole family, family therapy lessens the negative impact of SZ on other family members and strengthens the ability of the family to support the person with SZ.
This therefore means that family therapy has wider benefits beyond the obvious positive impact on the SZ patient.
Token economies
are reward systems used to manage the behaviour of people with schizophrenia, in particular those who have developed patterns of maladaptive behaviour through spending long periods in psychiatric hospitals.
What are token economies based on
operant conditioning
What type of reinforcers are tokens
Tokens are secondary reinforcers because they only have value once the person receiving them has learned that they can be used to obtain meaningful rewards, such as sweets or a walk outside
What type of reinforcers are rewards
meaningful rewards are primary reinforcers. Those tokens that can be exchanged for a range of different primary reinforcers are particularly powerful secondary reinforcers.
What is involved in a token economy?
-The idea is that tokens - in the form of coloured discs - are given immediately to individuals when they have carried out a desirable behaviour. Target behaviours are decided on an individual basis and it is important to know the person in order to identify the most appropriate target behaviours for them (Cooper et al. 2007).
-Although the tokens have no value in themselves they are swapped later for more tangible rewards. Having some form of immediate reward for target behaviour is important because delayed rewards are less effective. Tokens are therefore administered as soon as possible after a target behaviour.
-Rewards in a hospital setting might include objects like sweets or magazines, or access to activities like a film or a walk outside, or perhaps an appointment with a social worker to plan for life after hospitalisation.
Institutionalisation
develops under circumstances of prolonged hospitalisation.
Outcome of institutionalisation
One outcome is that people often develop bad habits,e.g. they might cease to maintain good hygiene or perhaps stop socialising with others. This is an understandable response to living without the kind of routine and small pleasures we experience in everyday life.
What categories of behaviour did Matson identify were commonly tackled in Token economies
Matson et al. (2016) identify three categories of institutional behaviour commonly tackled by means of token economies: personal care, condition-related behaviours (e.g. apathy) and social behaviour.
how are Matsons behaviours modified to benefit individuals with Sz
-Improves the person’s quality of life within the hospital setting,e.g. make-up for someone who usually takes a lot of pride in their appearance or social interaction for a usually sociable person.
-‘Normalises’ behaviour and this makes it easier for people who have spent a time in hospital to adapt back into life in the community,e.g. getting dressed in the morning or making their bed.
demonstration of a token economy carried out by Ayllon and Azrin
-They trialled a token economy system in a ward of women with a diagnosis of schizophrenia.
-Every time the participants carried out a task such as making their bed or cleaning up they were given a plastic token embossed with the words ‘one gift’.
-These tokens could then be swapped for ward privileges, for example being able to watch a film. The number of tasks carried out increased significantly.
Why are token economies not commonly used now in the UK
Their use has now declined in the UK, partly because of the growth of community-based care and the closure of many psychiatric hospitals, but also because of the complex ethical issues raised by restricting rewards to people with mental disorders.
However token economies still remain a standard approach to managing schizophrenia in many parts of the world.
A strength of token economies in treating Sz (evidence of effectiveness)
One strength of token economies for the management of schizophrenia is evidence for their effectiveness. Glowacki et al. (2016) identified 7 high quality studies published between 1999 and 2013 that examined the effectiveness of token economies for people with chronic mental health issues such as schizophrenia and involved patients living in a hospital setting. All the studies showed a reduction in negative symptoms and a decline in the frequency of unwanted behaviours.This supports the value of token economies.
A counterpoint of evidence of effectiveness for token economies in treating Sz
However, 7 studies is quite a small evidence base to support the effectiveness of a technique. One issue with a small number of studies is the file drawer problem. This phenomenon leads to a bias towards positive published findings because undesirable results have been filed away. This is a particular problem in reviews that only include a small number of studies. This means that there is a serious question over the evidence for the effectiveness of token economies.
A limitation of token economies in treating Sz (ethical issues)
One limitation with the use of token economies to manage schizophrenia is the ethical issues raised.
The use of token economies raises ethical issues because it gives professionals considerable power to control the behaviour of people in the role of patient. This inevitably involves imposing one person’s (or institution’s) norms on others, which is especially problematic if target behaviours are not identified sensitively. For example, someone who likes to look scruffy and get up late might have these personal freedoms curtailed. Perhaps more seriously, restricting the availability of pleasures (e.g. having sweets or seeing films) to people who don’t behave as desired means that seriously ill people, who are already experiencing distressing symptoms, have an even worse time. Legal action by families who see their relatives in this position has been a major factor in the decline in the use of token economies. This means that the benefits of token economies may be outweighed by their impact on personal freedom and short-term reduction in quality of life.
The interactionist approach
Otherwise known as the biosocial approach.
This approach acknowledges that there are biological, psychological and societal factors in the development of SZ.
Can you give any examples of what may be included as biological, psychological or societal factors
-genetic vulnerability
-stress
–poor quality interactions in the family
Explaining the interactionist approach: the diathesis stress model.
Diathesis means vulnerability.
In this context stress simply means negative psychological experience.
The diathesis stress model says that both a vulnerability to SZ and a stress-trigger are necessary in order to develop the condition.
Meehls model
In the original diathesis-stress model the diathesis was entirely genetic, the result of a ‘schizogene’.
Which led to which type of personality?
led to the idea of a biologically based schizotypical personality
What were these people with schizotypical personality sensitive to?
stress
A person who is a carrier of the gene could develop SZ, what childhood stressor could cause this to develop?
-chronic stress in childhood and adolescence
-presence of sz mother
The modern understanding of diathesis
It is now clear that many genes each appear to increase the genetic vulnerability slightly, there is no ‘schizogene’.
What do modern views of diathesis include?
a range of factors beyond the genetic
What does this modern theory suggest is the diatheses instead of stress?
trauma
What did Read (2001) propose about trauma and developing SZ?
a neurodevelopmental model in which early trauma alters the developing brain
Which part of the brain may be responsible in making the person more vulnerable to later stress?
The hypothalamic pituitary adrenal system
The modern understanding of stress
In the original model stress was seen as psychological in nature, and related to parenting. Although this may be important, a more modern definition of stress (in relation to diatheses stress) includes anything that risks triggering SZ.
Where has recent research focussed its concerns on in terms of developing SZ?
cannabis use
Why is cannabis deemed as a stressor for SZ?
it increases the risk of sz by up to 7 times according to dose
What does cannabis do to the body that could cause SZ?
interferes with the dopamine system
Is this cannabis use fully proven?
most people don’t develop sz after smoking cannabis presumably because they lack the vulnerability factors so it’s not fully proven
Treatments according to the interactionists approach
The model acknowledges both the bio’ and psych’ explanations so logically both bio’ and psych’ treatments are compatible.
The model best combines both antipsychotic and CBT treatments.
What does Turkington (2006) believe regards the treatment of SZ?
points out that it’s perfectly possible to believe in biological causes of sz and still practise CBT to relieve psychological symptoms
What is the most common treatment for SZ IN the UK?
combination of antipsychotic drugs and CBT
What is the most common treatment for SZ IN the US?
medication without accompanying psychological treatment
What is a strength for the interactionist approach( support for vulnerability and triggers)
One strength of the interactionist approach to schizophrenia is evidence supporting the role of both vulnerability and triggers. In a large-scale study, Tienari et al. (2004) investigated the impact of both genetic vulnerability and a psychological trigger (dysfunctional parenting). The study followed 19,000 Finnish children whose biological mothers had been diagnosed with schizophrenia. In adulthood this high genetic risk group were compared to a control group of adoptees without a family history of schizophrenia (low genetic risk). Adoptive parents had been assessed for child-rearing style and it was 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. This shows that a combination of genetic vulnerability and family stress can lead to greatly increased risk of schizophrenia.
What is a limitation of the interactionist approach (diathesis and stress are complex)
One limitation of the original diathesis-stress model is over simplicity. It is now clear that the original model that portrayed diathesis as a single schizogene and portrayed stress as schizophrenogenic parenting is hopelessly simplistic. Multiple genes in multiple combinations influence diathesis. Stress also comes in many forms, including but not limited to dysfunctional parenting. In fact diathesis can also be influenced by psychological factors and stress can be biological as well as psychological. This is shown in a study by Houston et al. (2008), in which childhood sexual abuse emerged as the major influence on underlying vulnerability to schizophrenia and cannabis use as the major trigger. This means that there are multiple factors, both biological and psychological, affecting both diathesis and stress, supporting the modern understanding of both diathesis and stress.
What is a strength of the interactionist approach (real world application)
One further strength of the interactionist approach is in the combination of biological and psychological treatments. A practical application of acknowledging biological and psychological factors in schizophrenia has been the combination of drug treatment and psychological therapies. Studies show that combining treatments enhances their effectiveness. For example Tarrier et al. (2004) randomly allocated 315 participants to
(1) medication + CBT, (2) medication + counselling, or (3) control group (medication only). Participants in the two combination groups showed lower symptoms following the trial than the medication-only group, though there was no difference in hospital readmission. This means that there is a clear practical advantage to adopting an interactionist approach to schizophrenia in terms of superior treatment outcomes.
What is a counterpoint to real world application of the interactionist approach
Jarvis and Okami (2019) point out that saying that a successful treatment for mental disorder justifies a particular explanation is the logical equivalent of saying that because alcohol reduces shyness, shyness is caused by lack of alcohol. This logical error is called the treatment-causation fallacy. Therefore we cannot automatically assume that the success of combined therapies means interactionist explanations are correct.
