Schizophrenia Flashcards
(120 cards)
1
Q
What is schizophrenia?
A
A type of psychosis, a severe mental disorder characterised by a profound disruption of cognition and emotion so that contact with external reality and insight are impaired.
2
Q
How common is schizophrenia?
A
It is the most common psychotic disorder, affecting 1% of the population at some point in their lifetime.
3
Q
Who is most commonly diagnosed with schziophrenia?
A
Mostly commonly diagnosed in males, city-dwellers and lower socio-economic groups.
4
Q
When does schizophrenia usually occur?
A
Can occur at any time in life, but usually occurs late in adolescence or early in adulthood. The peak of incidence onset is 25-30 years.
5
Q
How many people recover?
A
Its been estimated that no more than 1 in 5 individuals recover completely, even with treatments available that can relieve many symptoms.
6
Q
What is classification?
A
Organising symptoms into categories based on which symptoms cluster together in sufferers i.e. what are the symptoms of schizophrenia?
7
Q
What is diagnosis?
A
Deciding whether someone has a particular mental illness using the classifications.
8
Q
How can the characteristics schizophrenia affect someone?
A
Can affect a person’s langauge, thought, perception, emotions and even their sense of self.
9
Q
What are the types of symptoms of schizophrenia?
A
Positive and negative symptoms
10
Q
What are positive symptoms?
A
Atypical symptoms experinced in addition to normal experiences (an excess of normal functioning). These include hallucinations and delusions.
11
Q
What are negative symptoms?
A
Atypical experiences that represent the loss of usual experience (a diminution or loss of normal functioning). These include avolition and speech poverty.
12
Q
What are hallucinations?
A
Disturbances to perceptions in any of the senses. They are false sensory perceptions that either have no basis in reality or are distorted perceptions of things that are.
13
Q
What are the most common type of hallucinations?
A
The most common are auditory hallucinations (hearing voices). Many schizophrenics report hearing voices or seeing people, telling them to do something (e.g. harm themselves or others) or commenting on their behaviour.
14
Q
What are delusions?
A
Firmly held irrational beliefs that have no basis in reality.
15
Q
What is a common type of delusions?
A
Delusions of control- the belief that their body is under external control e.g. being controlled by aliens or the government (e.g. have implanted radio transmitters)
16
Q
What is avolition?
A
A lack of purposeful willed behaviour. It is the reduction, difficulty or inability to start and continue with goal-directed behaviour i.e. actions performed to achieve a result. People with schizophrenia often have a sharply reduced motivation to carry out a range of activities and results in lowered activity levels. E.g. no longer being interested in going out and meeting friends, poor hygiene and grooming, lack of persistence in work or education, siting in the house every day doing nothing.
17
Q
What is speech poverty?
A
Limited speech output with limited, often repetitive content. It involves reduced frequency (amount) and quality of speech. This is sometimes accompanied by the delay in sufferer’s verbal responses during conversation. It’s not that they don’t know the words, but that they have difficulty in spontaneously producing them.
18
Q
What are the two major systems for classifying schizophrenia and where are they used?
A
The World Health Organisation’s International Classification of Disease edition 10 (ICD-10) and the American Psychiatric Association’s Diagnostic and Stastical Manual edition 5 (DSM-5).
The ICD-10 is mainly used in Europe and the DSM-5 is mostly used in the USA.
19
Q
According to the DSM-5 system, what symptoms does someone need to have to be diagnosed with schizophrenia?
A
Two of the positive symptoms must be present for diagnosis, but only if the delusions are bizarre or hallucinations consist if a voice keeping up a running commentary on the person’s behaviour or thoughts, or two or more voices conversing together. There must be continuous signs of disturbance for at least 1 month. For a significant portion of time, one or more major areas of functioning such as work, interpersonal relations or self-care must be markedly below the level achieved prior to onset.
20
Q
According to the ICD-10 system, what symptoms does someone need to have to be diagnosed with schizophrenia?
A
Two or more negative symptoms are sufficient for diagnosis or one positive symptom.
21
Q
Why are there no longer subtypes of schizophrenia recognised in classification systems?
A
The ICD-10 and DSM have both dropped subtypes of schizophrenia (e.g. paranoid schizophrenia, which is characterised by powerful hallucinations and delusions but relatively few other symptoms) because they tended to be inconscient.
22
Q
What is reliability (in terms of diagnosis of schizophrenia)?
A
Reliability is the level of agreement (consistency) on the diagnosis of schizophrenia by different psychiatrists (inter-rate reliability) across time (test-retest reliability) and cultures. It is also the stability of diagnosis over time given no changes in symptoms.
23
Q
What did Osario et al (2019) find about the reliability of diagnosis of schizophrenia?
A
Found that inter-rater reliability of +0.97 and test-retest reliability of +0.92 for the DSM5 suggesting the diagnosis of schziophrenia is consistency applied.
24
Q
What is validity in terms of diagnosis and classifications of schizophrenia?
A
The extent to which schizophrenia is a unqiue syndrome with unique charateristics, signs and symptoms.
Classification- Are the symptoms of schizophrenia unqiue enough that we can distinguish them from other mental health problems?
Diagnosis- If we diagnosis someone with schizophrenia, do they actually have it?
25
What is symptom overlap?
When there is an overlap between symptoms of schziophrenia and other conditions. For example, schziophrenia and bipolar disorder share positive symptoms like hallucinations and delusions. The lack of distinction calls into question the validity of the classification and diagnosis of schizophrenia as a unique syndrome with its own charateristics, signs and symptoms.
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Evaluation: Symptom overlap: What did Ketter (2005) point out?
Points out that misdiagnosis due to symptom overlap can lead to years of delay in recieving relevant treatment, during which time suffering and further degeneration can occur, as well as high levels of suicide- so symptom overlap can have serious consqeunces. Focusing on this issue could save money and lives.
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Evaluation: Symptom overlap: What does Ketter's point suggest about the validity of classification and/or diagnosis of schizophrenia?
This calls into question the validity of classification and diagnosis of schizophrenia. In terms of classification, if a number of mental illnesses share many symptoms, schizophrenia does not have enough unqiue characteristics, signs and symptoms to be easily distinguished from other mental health problems, and so it may lack external validity as a seperate condition. This then impacts the validity of diagnosis as if clinicals cannot easily distinguish between schizophrenia and other mental illnesses, people may be misdiagnosed with other conditions when they have schizophrenia. This then has serious consquences for patients with schziophrenia and so suggests symptom overlap is a significant issue impacting the validity of classification and diagnosis of schizophrenia.
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Evaluation: Symptom overlap: What did Serper et al (1999) do?
Assessed pateints with co-morbid schizophrenia and cocaine abuse, cocaine intoxication on its own and schizophrenia on its own. They found that despite there being a considerable symptom overlap in pateints with schizophrenia and cocaine abuse, it was actually possible to make accurate diagnoses.
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Evaluation: Symptom overlap: What does Serper et al's findings suggest about the validity of classification and/or diagnosis of schizophrenia?
This suggests that symptom overlap did not affect the validity of the diagnosis and clinicians can tell the differnece between the illnesses. Therefore this suggests that symptom overlap may not be as significant an issue as previously thought because schizophrenia has enough unique characteristics, signs and symptoms to be valid as a seperate condition and so be accurately diagnosed.
30
What is co-morbidity?
Refers to the extent that two or more conditions occur together. Co-morbidities are common among patients with schizophrenia e.g. substance abuse, anxiety and depression. Where two conditions are frequently diagnosed together, it calls into question the validity of the classification and diagnosis of both illnesses.
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How does co-morbidity affect classification and diagnosis?
In terms of diagnosis, if many pateints are diagnosed with both conditions, psychiatrists may not be able to tell the difference between the two conditions. In terms of classification, it may be that if one illness (e.g. serve depression) looks a lot like schizophrenia and vice versa, they might be better seen as a single condition.
32
Evaluation: Co-morbidity: What did Buckley et al. (2019) conclude?
They concluded around half of patients with a diagnosis of schizophrenia also have a diagnosis of depression (50%) or substance abuse (47%). PTSD also occured in 29% of cases and OCD in 23%.
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Evaluation: Co-morbidity: What did Buckley et al.'s conclusion suggest about the validity of classification and/or diagnosis of schizophrenia?
This calls into question the validity of classification and diagnosis of both illnesses. In terms of diagnosis, if many pateints are diagnosed with both conditions, psychiatrists may not be able to tell the difference between the two conditions. This suggests that schizophrenia may not be a syndroyme with unqiue symptoms and charcteristics and so it may be that if one illness (e.g. severe depression) looks a lot like schziophrenia and vice versa, they might be better seen as a single condition, implying that they lack validity as seperate conditions. This could have implications such as patients being diagnosed with schizophrenia when they have depression leading to inappropriate treatments, as well as patients being stigmatised due to being labelled as schizophrenic. This may even impact their job prospects and relationships, exacerbating their depression (self-fufilling prophecy).
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What is cultural bias?
The tendency to interpret all phenomena through the lens of one's own culture, ignoring the effects that cultural differences might have on behaviour.
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Why is cultural bias an issue for diagnosis?
Cultural bias is an issue for diagnosing schizophrenia, because psychiatrists may ignore cultural differences between them and their patient, and only consider the symptoms through their own culture. This is a problem for the validity of diagnosing schizophrenia, because they may not be diagnosing people who have schizophrenia correctly.
36
Evaluation: Cultural bias: What did Escobar (2012) point out?
Pointed out that White psychiatrists may tend to over-interpret the symptoms of Black people during diagnosis. Such factors as cultural differences in language and mannerisms, difficulties in relating between black pateints and white therapists, and the myth that black people rarely suffer from affective disorders may be causing this problem. Therefore clinicians and researchers must pay more attention to the effects of cultural differences on diagnosis.
37
Evaluation: Cultural bias: What does Escobar's point suggest about the relaibility of classification and/or diagnosis of schizophrenia?
This calls into question the reliability of the diagnoses of schziophrenia as there doesn't seen to be agreement on the diagnosis of schizophrenia by psychiatrists across cultures as there isn't consistent diagnoses. Additionaly, it questions the validity of diagnoses of schziophrenia as it suggests psychiatrists may be imposing their own cultural standards for schziophrenia when diagnosing patients and so they may be misinterpreting symptoms and mislabelling behaviour as symptoms of schizophrenia.
38
What is gender bias?
A tendency to treat one individual or group in a different way from others (it may not present the experince or behaviour of one of the genders).
39
When does gender bias occur in the diagnosis of schizophrenia?
Said to occur when the accuracy of diagnosis is dependent on the gender of the individual. This may be due to gender-biased diagnostic criteria or clinicians basing their judgements on stereotypical beliefs held about gender.
40
Evaluation: Gender bias: What did Loring and Powell (1988) do?
Randomly selected 290 male and female psychiatrists to read two case articles of patients' behaviour and the asked them to offer their judgement on these individuals using standard diagnostic criteria. When patients were described as 'male' or no information was given about gender, 56% were given a diagnosis of schziophrenia. However, when patients were described as being 'female', only 20% were given a diagnosis of schziophrenia. This suggests that there is a gender bias in the diagnosis of schizophrenia which calls into question its validity. This gender bias did not appear to be evident amongst female psychiatrists.
41
Evaluation: Gender bias: What did Loring and Powell's findings suggest about the reliability and validity of diagnosis of schizophrenia?
Suggests that the diagnosis is influenced not only by gender of the patient but also the gender of the clinician. This calls into question the reliability of the diagnosis of schizophrenia because if patients are seen by different clinicians, they may recieve differnet diagnoses and therefore the diagnoses lack inter-rater reliability. It also questions the validity of the diagnoses of schizophrenia as it suggests that schizophrenia may not accurately be diagnosed when gender bias is present.
42
What do biological explanations emphasise?
The role of inherited factors and dysfunction of brain activity in the development of schizophrenia.
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What are the two main biological explanations of schizophrenia?
Genetics and neural correlates
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Biological explanations: Genetics: What is there considerable evidence of?
That schizophrenia runs in families and is in part genetic (inherited- as genes are transmitted from parent to child).
45
Biological explanations: Genetics: What is an example of schizophrenia being genetic?
For example, Gottesman (1991) conducted a large-scale study and found much higher concordence rates in MZ twins (48%) in comparsion to DZ twins (17%). This suggests that individuals with identical genetic make-up (MZ twins) have an increased chance if developing schizophrenia comapred to those sharing fewer genes, suggesting that there is an association between the degree of genetic similarity and shared risk of schizophrenia.
46
Biological explanations: Genetics: What is schizophrenia thought to be?
Polygenic (it requires a number of different genes to work in combination) and so different combinations of genes can lead to the condition. The most likely genes are those coding for neurotransmitters such as dopamine.
47
Biological explanations: Genetics: How many different genetic variations are associated with the increased risk of schizophrenia?
Reserach suggests 108
48
Biological explanations: Genetics: How else can schizophrenia also have a genetic origin?
Through the mutation of parental DNA by radiation, poison or viral infection.
49
Biological explanations: Genetics: How else can schizophrenia also have a genetic origin?
Through the mutation of parental DNA by radiation, poison or viral infection.
50
Biological explanations: Genetics: What did Brown et al (2002) find?
A positive correlation between parental age (which is associated with increased risk of sperm mutation) and risk of schizophrenia, increasing from around 0.7% in fathers under 25 to over 2% in fathers over 50.
51
Biological explanations: What are neural correlates?
Measurements of the structure or function of the brain that occur in conjunction with (correlate with) the characteristic symptoms of schizophrenia, and so may be implicated in the origins of schizophrenia.
There are thought to be neural correlates of positive and negative symptoms.
52
Biological explanations: Who proposed the revised dopamine hypothesis?
Davis and Khan (1991)
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Biological explanations: What is dopamine?
A neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure.
54
Biological explanations: What did the orginal dopamine hypothesis suggest?
Suggested that positive symptoms of schizophrenia are caused by higher levels of dopamine in the subcortical areas of the brain (central areas of the brain). Messages from neurons that transmit dopamine fire too easily or too often in those with schizophrenia. Schizophrenics are thought to have abnormally high levels of D2 receptors on post-synaptic neurons, resulting in more dopamine binding and therefore more neurons firing. E.g. an excess of dopamine receptors in Broca's area may be associated with speech poverty and/ or auditory hallucinations.
55
Biological explanations: What was added to the revised dopamine hypothesis?
That the negative symptoms of schizophrenia are thought to arise from lower levels of dopamine in the pre-frontal cortex (e.g. cognitive problems).
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Biological explanations: What has it been suggested that low levels of dopamine in the cortex lead to?
May lead to high levels of dopamine in the subcortical areas of the brain. Therefore, it may be both high and low levels of dopamine in different brain regions that are involved in schizophrenia.
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Biological explanations: What did Howes et al (2017) propose?
That genetic variations and early experinces of stress make some people more sensitive to low levels of dopamine in the cortex and therefore high levels of dopamine in the subcortex.
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Evaluation: Biological explanations: Neural explanations: What is supporting evidence?
Much of the evidence supporting the dopamine hypothesis comes from the success of drug treatments that attempt to change the levels of dopamine activity in the brain. The basic method mechanism of anti-psychotic drugs is to reduce dopamine activity and so reduce the effect of schziophrenia. Leucht et al (2013) found that anti-psychotic drugs were significantly more effective than placebos in the treatment of positive & negative symptoms. Dopamine agonists that increase dopamine levels make schziophrenia worse and can produce schziophrenia-like symptoms in non-sufferers (Curran et al., 2004)
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Evaluation: Biological explanations: Neural explanations: What does the supporting evidence tell us about biological explanations of schizophrenia?
Suggests that the normalisation of dopamine activity levels treats schizophrenia and therefore that dopamine levels may cause schizophrenia, supporting the orginal dopamine hypothesis (biological explanation).
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Evaluation: Biological explanations: Neural explanations: What evidence is there to undermine?
Noll (2009) argues that antipsychotic drugs do not alleviate hallucinations and delusions in about 1/3 of people experiencing these symptoms. Also in some people, hallucinations and delusions are present despite levels of dopamine being normal. Blocking the D2 receptors has little or no effect on their symptoms.
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Evaluation: Biological explanations: Neural explanations: What does the undermining evidence tell us about biological explanations of schizophrenia?
This suggests that rather than dopamine being the sole cause of positive symptoms in the subcortex, other neurotransmitters systems, acting independently of the dopamine system may also produce positive symptoms associated with schziophrenia, undermining the dopamine hypothesis as a neural correlate of schziophrenia.
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Evaluation: Biological explanations: Genetic explanations: What evidence is there to support?
There is now strong evidence for genetic vunerability to schziophrenia from a variety of sources e.g. Gottesman's (1991) study. Additionaly, Tienari et al's (2004) adoption study found that children of schizophrenia sufferers are still at a heighted risk of schizophrenia if adopted into families with no history of schizophrenia. A recent twin study from Hilker et al (2018) found a concordence rate of 33% for identical twins and 7% for non-identical twins.
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Evaluation: Biological explanations: Genetic explanations: What does the supporting evidence tell us about biological explanations of schizophrenia?
This supports the idea that genetic factors make some people much more vunerable to developing schziophrenia than others though schziophrenia running in families and being inherited. This does not mean that schizophrenia is entirely genetic, as there are a number of enviornmental factors associated with the risk of schizophrenia, but the available evidence suggests that genetic susceptibility is very important.
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Evaluation: Biological explanations: Genetic explanations: What is a weakness?
There is the assumption that the greater concordence rate for schziophrenia between MZ twins is a product of greater genetic similarity rather than greater enviornmental similarity. However, MZ twins are treated more similarly, encounter more similar environments (e.g. more likely to do things together) and are frequently treated 'as twins' rather than as two distinct individuals than DZ twins.
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Evaluation: Biological explanations: Genetic explanations: What does the weakness tell us about biological explanations of schizophrenia?
As a result, the differences in concordence rates between MZ twins and DZ twins may reflect nothing more than environmental differences that distinguish the two types of twin. As such, the results from the twin studies may not provide as strong support for the biological explanations of schizophrenia as previously suggested.
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How is drug therapy used?
Involves the treatment of schziophrenia through the use of antipsychotic medication to reduce the symptoms of the disorder. These can be taken as tablets, syrup or injections if necessary.
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What do drug therapies do?
They help the person with schziophrenia to function as well as possible whilst also increasing their feelings of subjective wellbeing.
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How do all antipsychotics work?
By reducing dopaminergic transmission i.e. reducing the actions of the neurotransmitter dopamine in areas of the brain asscoiated with the symptoms of schizophrenia.
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What are the two types of antipsychotics?
Typical (older) antipsychotics
Atypical (newer) antipsychotics
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When were typical antipsychotics developed and what is an example?
Developed in the 1950s e.g. chlorpromazine
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How do typical antipsychotics work?
They are dopamine antagonists- they bind to (and so block) dopamine receptors but don't stimulate them, reducing the action of dopamine.
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What effect do typical antipsychotics have initally and then what is the overall effect?
Initally they cause dopamine levels to build up but the production is reduced. This normalises neurotransmission in key areas of the brain, by reducing the stimulation of dopamine system, reducing positive symptoms sch as hallucinations.
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How quickly does it take for typical antipsychotics to have an effect?
Hallucinations and delusions usually diminish within a few days of beginning the medication, although other symptoms may take several weeks before a significant improvement is noted.
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Why do typical antipsychotics lead to undesirable side effects?
There a several dopamine pathways in the barin, and it appears that blocking dopamine receptors in only one of them is useful. Unfortunately, the typical antipsychotics block dopamine receptors in other areas of the brain as well, leading to side effects.
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What are the long term side effects of typical antipsychotics?
Dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin. Long-term use can result in tardive dyskinesia (involuntary movement of the tongue, face and jaw).
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When did atypical antipsychotics start being used?
Since the 1970s.
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What is an example of an atypical antipsychotics?
Clozapine and risperidone
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What was the aim of developing newer antipsychotics?
Was to improve/ maintain upon the effectiveness of drugs in suppressing symptoms and also to minimise side effects.
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How do atypical antipsychotics work?
Also block dopamine receptors like typical antipsychotics. However, they only temporarily occupy the receptors and then rapidly dissociate to allow normal dopamine transmission. Which is thought to be why there are fewer side effects effects associated with them.
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What are the atypical antipsychotics side effects?
Even though they have less side effects, they still have some, the most serious of which is agranulocytosis (an autoimmune disorder affecting white blood cells).
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When are atypical antipsychotics taken?
When other treatments have failed and patients have to have regular blood tests to ensure they are not developing agranulocytosis.
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What else do atypical antipsychotics act on?
Other neurotransmitters, particulary serotonin (and acetylcholine) and they address negative symptoms, e.g. avolition, as well as positive symptoms. It is believed that this action helps to improve mood ad reduce depression and anxiety in patients, as well as potentially improving cognitive function.
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Who are atypical antipsychotics prescribed to?
Patients with a higher risk of suicide (as 30-50% of people with schizophrenia attempt suicide at some point).
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What is effectiveness?
Does the therpay work
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What is appropriateness?
Should we use the therapy/ can it be used by different types of people on different types of schizophrenia?
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Evaluation: Drug therapies- Effectiveness: What is supporting evidence?
Leucht et al (2012) carried out a meta-analysis of 65 studies involving nearly 6000 participants. All had been given antipsychotics. Some of these patients were taken off their antipsychotics and given a placebo instead. Within 12 months, 64% of those on the placebo had relapsed, comapred to the 27% of those who remained on their antipsychotic drugs.
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Evaluation: Drug therapies- Effectiveness: What does the supporting evidence tell us about using drug therapies to treat schizophrenia?
This suggests that antipsychotic drugs are reasonably effective at treating schizophrenia. However, as 36% of patients didn't relapse when on the placebo, this implies that cognitive factors are also important in the treatment of schizophrenia and so drugs may not be entirely necessary in all cases. Although, it could be argued that the lack of relapse is due to partipants having been on antipsychotic medication for a sufficient amount of time before switching to the placebo and that the drugs are therefore effective.
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Evaluation: Drug therapies- Effectiveness: What is undermining evidence?
Healy (2012) argued that some successful trails of the effectiveness of antipsychotics have only studied the short-term effects (rather than long-term effectiveness) and had their data published multiple times, exaggerating the evidence of positive effects. As antipsychotics have calming effects, it is easy to demonstrate they have some positive effects on patients. This is not the same as saying the really reduce the severity of symptoms.
89
Evaluation: Drug therapies- Effectiveness: What does the undermining evidence tell us about using drug therapies to treat schizophrenia?
This suggests that the effectiveness of drug therapies to treat schizophrenia may be overexaggerated and so may not be as effective as we initally thought. It is also often not possible to determine whether drug therapies are effective in the long-term from research.
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Evaluation: Drug therapies- Appropriateness : What is a strength?
Antipsychotics enhance the quality of life for patients as they allow them to live independently/ outside of institutional care. They also enhance the quality of life for family member who are able to live their lives rather than continously care for their relative
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Evaluation: Drug therapies- Appropriatness : What does the strength tell us about using drug therapies to treat schizophrenia?
This supports the appropriatness of drug therapies to treat schizophrenia
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Evaluation: Drug therapies- Appropriateness : What is a weakness?
Critics argue that if side effects, deaths and psychological consquences were taken into account, a cost-benefit analysis of its advantages would probably be negative. In the USA, a large out-of-court settlement was awarded to a tardive dyskinesia sufferer on the basis of Human Rights Act that no one should be subjected to inhumane ore degrading treatment or punishment. Additionaly, it is widely believed that antipsychotics have been used in hospital situations to make patients easier and calmer to deal with, rather than for the benefits if the patient themselves. Furthermore, patients with serve symptoms may not be able to give fully informed consent.
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Evaluation: Drug therapies- Appropriatness : What does the weakness tell us about using drug therapies to treat schizophrenia?
This practice is seen by some as human rights abuse. As cost-benefit analysis may be negative, it suggests that drug therapy is not an appropriate treatment for schizophrenia.
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What is token economy?
A form of behavioural therapy used in the management of schizophrenia.
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What is token economy used for?
Used to shape and manage behaviour so that patients in long stay hospitals are easier to manage.
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What does token economy involve?
Involves desirable behaviours being encouraged through selective reinforcement- a type of behaviour modification which seeks to increase the occurrence of certain behaviours by responding to desired behaviours with a pleasurable stimulus, while seeking to extinguish undesired behaviours by not responding to those.
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Token economy: When are tokens (rewards) given and what do they act as?
Given immediately as secondary reinforcers when patients engage in desirable behaviours e.g. getting dresses in the morning, making a bed, taking medication ect.
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Token economy: What can they do with the tokens?
Although the token in themselves have no value, they can later swapped for more tangible rewards (primary reinforcers). For example, sweets, magazines, privileges such as a walk outside of the hospital. Therefore this encourages the desirable behaviour to be repeated because they have become associated with the rewards and privileges.
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Token economy: How can they ensure tokens become effective secondary reinforcers?
By initially administering them at the same time as the primary reinforcer.
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Token economy: What doe it do for patients?
Whilst modifying the behaviours doesn't cure schizophrenia, it improves patients' quality of life and make it more liekly that they can live outside a hospital setting.
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Token economy: Evaluation: What is supporting evidence?
Dickerson et al. (2005) reviewed 13 studied of the use of token economy systems in the treatment of schziophrenia. 11 of these studies reported beneficial effects that were directly attributed to the use of the token economies. Glowacki et al (2016) reviewed 7 studies and found all studies showed a reduction in negtaive symptoms and a decline in frequently unwanted behaviours.
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Token economy: Evaluation: What does the supporting evidence tell us about token economy as a method to manage schizophrenia?
This supports the effectiveness of token economy in increasing adaptive behaviours of those with schizophrenia. Howver, Dickerson et al. did caution that many of the studies reviewed had significant methodological shortcomings that limited their impact in the overall assessment of token economies, in this context.
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Token economy: Evaluation: What is a weakness (uncontrolled)?
A major problem of assessing the effectiveness of token economies is that studies of their use tend to be uncontrolled. When a token economy system is introduced into a psychiatric ward, typically all patients are put onto the programme rather than having a control group that does not get put on the programme.
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Token economy: Evaluation: What does the weakness suggest about using token economy as a method to manage schizophrenia?
This means that patients' improvements can only be compared with their past behaviour rather than a control group, which may be misleading as other factors (e.g. an increase in staff attention) could be causing the patients' improvement rather than the token economy. Therefore, the research evidence can't provide as strong support for the effectiveness of the token economy as previously thought.
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Token economy: Evaluation: What is a weakness (unethical)?
Token economy raises ethical issues as it gives professionals considerable power to control the behaviour of patients. For example, in order to make reinforcers effective, clinicians may over exercise control over important primary reinforcers such as food, privacy or access to activities that alleviate boredom. However, it is generally accepted that all human beings have basic access to food, privacy ect. that cannot be violated regardless of the positive consquences that might be achieved by manipulating them within a token economy programme. Additionally, primary reinforcers become more available to those with mild symptoms than those with more serve symptoms that prevent them from complying with desirable behaviours. Therefore, the most severely ill patients suffer discrimination and some families have challenged the legality of this.
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Token economy: Evaluation: What does the weakness (unethical) suggest about using token economy as a method to manage schizophrenia?
As such, token economy may not be appropriate for all patients with schizophrenia. The benefits of it may be outweighed by their impact on personal freedom and short-term reduction in quality of life. Legal action by families who see their relatives in such positions has been a major factor in the decline in the use of token economies.
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Token economy: Evaluation: What is a weakness (do not cure)?
Token economies only aim to make schizophrenia more manageable and improve the patients' quality of life. Then help by making patients' behaviour more socially acceptable so that they can reintegrate into society.
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Token economy: Evaluation: What does the weakness (do not cure) suggest about using token economy as a method to manage schizophrenia?
Whilst this is worth doing, it should not be confused with curing schizophrenia. Token economies do not address symptoms of schizophrenia, so they are not a 'treatment'. Therefore, whilst token economies may provide patients with strategies that they can use to manage their current symptoms, they do effectively cure schziophrenia.
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Interactionist approach: What is it?
Acknowledges the combinded effects of biological, psychology and social factors are involved in the development of schizophrenia
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Interactionist approach: What is the diathesis stress model?
An interactionist approach to schizophrenia. Schizophrenia is argues to be the result of both an underlying (internal) vunerability (diathesis) and any negative psychological experince (external) trigger (stress). Both are necessary for the onset of schizophrenia.
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Interactionist approach: Who originally created the diathesis stress model?
Meehl (1962)
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Interactionist approach: Orginal diathesis-stress model, diathesis part?
In orginal model the diathesis for schizophrenia was entirely genetic (inherited). Genes are assumed to cause neurochemical abnormalities (dopamine levels too high in the subcortex, too low in the prefrontal cortex) that in turn, result in an increased risk for schizophrenia.
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Interactionist approach: Revised diathesis-stress model, diathesis part?
Revised to also include vulnerabilities due to childhood trauma which might have affected brain development. For instance, child abuse can alter the developing brain and act as a diathesis.
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Interactionist approach: Orginal diathesis-stress model, stress part?
The stress (trigger) for schizophrenia was chronic stress in childhood and adolescence, in particular schizophrenogenic mother (cold, rejecting and controlling and the father is passive-> leads to tension and secrecy in family -> leads to psychotic thinking and paranoid delusions).
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Interactionist approach: Revised diathesis-stress model, stress part?
Revised to include any negative psychological experince that risk triggering schziophrenia e.g. dysfunctional parents (double bind or expressed emotion) and stressful live events (e.g. going to university, moving house, relationship breakdown, academic pressure, substance abuse ect).
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Interactionist approach: How do they treat schziophrenia?
Combining antipsychotic medications and psychological therapies (mostly CBTp).
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Interactionist approach: Evaluation: It is possible that stressors in earlier life can also infleunce how people respond in later stressful events, and increase their susceptibility to the disorder?
Maladaptive methods of cooping with stress in childhood and throughout development means the individual fails to develop effective coping skills, which in turn compromises their resilience and increases vunerability. This may make like generally more stressful for the individual and so trigger schizophrenia.
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Interactionist approach: Evaluation: It is possible that stressors in earlier life can also infleunce how people respond in later stressful events, and increase their susceptibility to the disorder- What does this suggest
Therefore it is extremely difficult to determine the causal realtionship that triggered schizophrenia, which may negatively impact the effectiveness of treatment.
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Interactionist approach: Evaluation: One limitation of the interactionist approach to explaining schziophrenia is the simplicity of the orginal model.
It is clear that portraying diathesis as a single gene and stress as schizophrenogenic parenting is overly simplistic. Multiple genes in multiple combinations have been found to act as the diathesis, as well as brain damage caused by enviornmental factors. For example Verdoux et al (1998) estimated that the risk of developing schiz in later life was 4x greater for those who had experinced prolonged labour and oxygen deprivation than those who hadn't.
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Interactionist approach: Evaluation: One limitation of the interactionist approach to explaining schziophrenia is the simplicity of the orginal model- what does this suggest?
Suggests that the old idea of the diathesis-stress may be overly simplistic. However, it supports a modern interactionist approach to schziophrenia in that vulnerabilities and triggers seem to interact together in some way to produce schziophrenia. Although, most people do not develop schiz after smoking cannabis and so it seems there must be one or more triggering stressful factors, which means that from the model it is difficult to predict who will develop schiz.
