Schizophrenia Flashcards
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. This affects a person’s language, thought, perception, emotions and even their sense of self.
2
Q
How common is schizophrenia?
A
Affects 1% of the population at some point in their lifetime
3
Q
What type of disorder is schizophrenia?
A
Psychotic disorder
4
Q
When does schizophrenic symptoms typically begin to show?
A
It can occur any time in life, but usually occurs late in adolescence or early adulthood. The peak of incidence onset is 25-30 years.
5
Q
What do we mean by classification in the context of schizophrenia?
A
Organising symptoms into categories based on which symptoms cluster together in sufferers i.e. what are the symptoms of schizophrenia?
6
Q
What do we mean by diagnosis in the context of schizophrenia?
A
Deciding whether someone has a particular mental illness using the classifications. (does someone have the symptoms)
7
Q
Define positive symptoms
A
Atypical symptoms that are in addition to regular sensory experience
8
Q
Define negative symptoms
A
Atypical symptoms that represent a loss compared to regular sensory experience
9
Q
Define hallucinations
A
Disturbances of perception in any of the senses. They are false sensory perceptions that have no basis in reality or are a distorted perception of things that are (positive)
10
Q
Define delusions
A
False (irrational) beliefs not based in reality or are a distorted perception of things that are (positive)
11
Q
Define speech poverty
A
Limited speech output with limited, often repetitive content. It involves reduced frequency (amount) and quality of speech (negative)
12
Q
Define 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. (negative)
13
Q
Give examples of different kinds of hallucinations
A
Visual - see something that isn’t there
Auditory - hear something that isn’t real
14
Q
Give examples of different kinds of delusions
A
Delusions of persecution – the belief that others want to harm, threaten or manipulate you e.g. the government, aliens.
Delusions of grandeur – the belief that they are an important individual, even god-like and have extraordinary powers e.g. the belief that they are Jesus Christ.
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).
15
Q
What do we mean by a classification system of schizophrenia?
A
A cluster of symptoms
16
Q
There are two classification systems used to classify and diagnose schizophrenia. For each one, name it and explain what combination of symptoms are required for a diagnosis of schizophrenia.
A
DSM-5 - America - two of the positive symptoms must be present for diagnosis, but only one if delusions are bizarre or hallucinations consist of 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 the 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.
ICD-10 - Europe - two or more negative symptoms are sufficient for diagnosis or one positive symptom.
17
Q
What do we mean by reliability in the context of classifying and diagnosing schizophrenia?
A
The level of agreement (consistency) on the diagnosis of schizophrenia by different psychiatrists (inter-rater reliability) across time (test-retest reliability) and cultures. It is also the stability of diagnosis over time given no change in symptoms.
18
Q
What do we mean by validity in the context of classifying and diagnosing schizophrenia?
A
The extent to which schizophrenia is a unique syndrome with unique characteristics, signs and symptoms (so whether it measures what it intends to measure). Miss Maiden’s note: this includes whether we can tell the difference between schizophrenia and other mental illnesses and whether we can accurately diagnose someone has having schizophrenia when they do and not diagnose them when they don’t.
19
Q
Describe evidence that the DSM5 is reliable.
A
Osario et al. (2019) found inter-rater reliability of +0.97 and test-retest reliability of +0.92 for the DSM5 suggesting the diagnosis of schizophrenia is consistently applied.
20
Q
Define symptom overlap.
A
When two or more conditions share symptoms.
21
Q
Give an example of symptom overlap in the classification and/or diagnosis of schizophrenia
A
Hallucinations, difficulty concentrating and delusions are a part of bipolar disorder
22
Q
Explain how this impacts the validity of the classification and/or diagnosis of schizophrenia.
A
Validity of classification - it seems that schizophrenia does not have enough unique characteristics, signs and symptoms to be distinguishable from other mental health problems.
Validity of diagnosis - therefore there may be misdiagnoses as people may not be accurately diagnosed with schizophrenia when they have it, and not diagnosed when they don’t have it.
23
Q
Describe evidence that supports the symptom overlap is an issue in the validity of the classification and/or diagnosis of schizophrenia.
A
Ketter (2005) points out that misdiagnosis due to symptom overlap can lead to years of delay in receiving relevant treatment, during which time suffering and further degeneration can occur, as well as high levels of suicide- so symptom overlap can have serious consequences. Focusing on fixing this issue could save money and lives.
24
Q
Describe evidence that supports that symptom overlap is not a significant issue in the validity of the classification and/or diagnosis of schizophrenia.
A
Serper et al. (1999) assessed patients with co-morbid schizophrenia and cocaine abuse, cocaine intoxication on its own and schizophrenia on its own. They found that despite there being considerable symptom overlap in patients with schizophrenia and cocaine abuse, it was actually possible to make accurate diagnoses.
25
Define co-morbidity.
When one person has more than one mental illness at the same time e.g. Schizophrenia and personality disorders
26
Explain how this impacts the validity of the classification and/or diagnosis of schizophrenia.
Validity of classification - if schizophrenia tends to occur with another mental illness, it doesn't seem to have enough unique characteristics as a mental health problem to be distinguished from others. Also, if two illnesses tend to occur together, it may be better to class them as one overall illness.
Validity of diagnosis - therefore it's unlikely that we will be able to accurately diagnose someone with schizophrenia when they have it and as not having it when they don't.
27
Describe evidence that supports the co-morbidity is an issue in the validity of the classification and/or diagnosis of schizophrenia.
Buckley et al. (2009) concluded that around half of patients with a diagnosis of schizophrenia also have a diagnosis of depression (50%) or substance abuse (47%). PTSD also occurred in 29% of cases and OCD in 23%.
28
What is cultural bias?
A tendency to interpret all phenomena through the lens of one's own culture, ignoring the effects that cultural differences might have on behaviour.
29
What makes researchers think that diagnoses of schizophrenia may be culturally biased?
African-Americans and English people of Afro-Caribbean origin are up to 10 times more likely to be diagnosed with schizophrenia. Given that rates in Africa and the West Indies aren’t high (ruling out a genetic vulnerability), the diagnosis seems to be the result of cultural bias.
Positive symptoms of hearing voices may be more acceptable in African cultures because of cultural beliefs in communication with ancestors.
30
Why might this cultural bias occur?
When reported to a psychiatrist from a different cultural tradition, hearing voices etc is more likely to be seen as bizarre and irrational.
31
Explain how this impacts the validity and/or reliability of diagnoses of schizophrenia.
This calls into question the validity of diagnoses of schizophrenia as psychiatrists may impose their own cultural standards for schizophrenia onto those from other cultures and so are biased towards what is ‘normal’ in their culture (ethnocentric). Therefore, the diagnoses may not be valid across cultures as any deviation from what is normal in their culture is misinterpreted and mislabelled as a symptom of schizophrenia.
It also calls into question the reliability of diagnoses of schizophrenia as it suggests that there may not be agreement on the diagnosis by psychiatrists across cultures and so the methods may not be suitable for use across all cultures as there wouldn’t be consistent diagnoses/classifications. It suggests that patients can display the same symptoms but receive different diagnoses because of their ethnic background; i.e. a patient’s ethnicity makes it more or less likely that they will be diagnosed with schizophrenia.
32
Describe two pieces of evidence that support that cultural bias is a significant issue in the reliability and/or validity of the diagnosis of schizophrenia.
Copeland et al. (1971) gave a description of a patient (who is described as being from an ethnic minority) to 134 US and 194 British psychiatrists. 69% of the US psychiatrists diagnosed schizophrenia but only 2% of the British gave the diagnosis of schizophrenia. No research has found any cause for this, so it suggests that the symptoms of ethnic minorities are misinterpreted.
Escobar (2012) has 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 patients 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.
33
What is gender bias in the diagnosis of schizophrenia?
A tendency to treat one individual or group in a different way from others (it may not present the experience or behaviour of one of the genders)
34
What makes researchers think that diagnoses of schizophrenia may be gender biased?
Longenecker et al. (2010) reviewed studies of the prevalence of schizophrenia and concluded that since the 1980s, men have been diagnosed with schizophrenia more often than women. Prior to this, there had been no difference.
35
Why might this gender bias occur?
Female patients typically function better than men, being more likely to work and have good family relationships
36
Explain how this impacts the validity and/or reliability of the diagnoses of schizophrenia.
This calls into question the reliability of the diagnosis of schizophrenia because if patients are seen by different clinicians, they may receive different 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 it is present.
37
Describe evidence that supports that gender bias is a significant issue in the reliability and/or validity of the diagnosis of schizophrenia.
Loring and Powell (1988) randomly selected 290 male and female psychiatrists to read two case articles of patients’ behaviour and then asked them to offer their judgment on these individuals using standard diagnostic criteria. When the patients were described as ‘male’ or no information was given about their gender, 56% were given a diagnosis of schizophrenia. However, when the patients were described as ‘female’, only 20% were given a diagnosis of schizophrenia. 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 the female psychiatrists.
38
What do we mean by 'biological explanations' of schizophrenia?
Biological explanations emphasise the role of inherited factors and dysfunction of brain activity in the development of schizophrenia.
Two explanations are genetics and neural correlates
39
What do we mean when we say that schizophrenia is genetic?
Inherited
40
Describe Gottesman's (1991) study.
Gottesman (1991) conducted a large-scale family and found much higher concordance rates in MZ twins (48%) in comparison to DZ twins (17%). This suggests that individuals with identical genetic make-up (MZ twins) have an increased risk of developing schizophrenia compared to those who share fewer genes, suggesting that there is an association between the degree of genetic similarity and shared risks of schizophrenia.
41
Explain how this suggests that schizophrenia is genetic using the concordance rates and % of genes the family members share.
MZ twin concordance rate is higher than DZ twin concordance rate and MZ twins more likely to have schizophrenia in common - more genes shared (MZ share 100% and DZ share 50%), more schiz in common
42
What does the genetic explanation suggest about schizophrenia being polygenic?
Schizophrenia is 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. Research suggests that there are 108 genetic variations associated with increased risk of schizophrenia.
43
What does the genetic explanation suggest about schizophrenia potentially being the result of a mutation?
Schizophrenia can also have a genetic origin through the mutation of parental DNA by radiation, poison or viral infection. Brown et al. (2002) found a positive correlation between paternal 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.
44
What are neural correlates?
Neural correlates are measurements of the structure or function of the brain (including neurotransmitters) that occur in conjunction with (correlate with) the characteristic symptoms of schizophrenia, and so may be implicated in the origins of schizophrenia.
45
Describe the (revised) dopamine hypothesis.
Dopamine is a neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure.
In the original hypothesis, they suggested that the positive symptoms of schizophrenia are caused by higher levels or activity 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.
In the revised version, it was added that the negative symptoms of schizophrenia are thought to arise from lower levels of dopamine in the pre-frontal cortex (e.g. cognitive problems, avolition).
It has been suggested that low levels of dopamine in the cortex may lead to the high levels of dopamine in the subcortical areas of the brain. Therefore, it may be that both high and low levels of dopamine in different brain regions are involved in schizophrenia.
46
Describe one other neural correlate of schizophrenia.
Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus have been found in those experiencing auditory hallucinations. Therefore, reduced activity in these two areas is a neural correlate of auditory hallucinations (positive symptom).
47
Describe evidence to support that schizophrenia is genetic. Remember to explain exactly how it supports that schizophrenia is genetic.
Gottesman (1991) conducted a large-scale family and found much higher concordance rates in MZ twins (48%) in comparison to DZ twins (17%). This suggests that individuals with identical genetic make-up (MZ twins) have an increased risk of developing schizophrenia compared to those who share fewer genes, suggesting that there is an association between the degree of genetic similarity and shared risks of schizophrenia.
This supports the idea that genetic factors make some people much more vulnerable to developing schizophrenia than others [remember that you need to explain how exactly]. This does not mean that schizophrenia is entirely genetic, as there are a number of environmental factors associated with risk of schizophrenia, but the available evidence suggests that genetic susceptibility is very important.
48
Supporting evidence for the genetic explanation can come from twin studies. Why are twin studies not very strong support for the biological explanations of schizophrenia?
The assumption that the greater concordance for schizophrenia between MZ twins is a product of greater genetic similarity rather than greater environmental similarity. However, MZ twins are treated more similarly, encounter more similar environments (e.g. are more likely to do things together) and are frequently treated ‘as twins’ rather than as two distinct individuals than DZ twins.
As a result, the differences in concordance rates between MZ twins and DZ twins may reflect nothing more than the environmental differences that distinguish the two types of twin. As such, the results from twin studies may not provide as strong support for the biological explanations of schizophrenia as previously suggested.
49
Describe evidence to both support and undermine the dopamine hypothesis. Remember to explain exactly how it supports the hypothesis.
There is evidence to support the dopamine hypothesis from drug treatments. For example Leucht et al. (2013) found that anti-psychotic drugs were significantly more effective than placebos in the treatment of positive and negative symptoms. Dopamine agonists that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers (Curran et al., 2004). However, 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. Therefore overall, this suggests that rather than dopamine being the sole cause of positive symptoms in the sub cortex, other neurotransmitter systems, acting independently of the dopamine system may also produce the positive symptoms associated with schizophrenia, undermining the dopamine hypothesis as a neural correlate of schizophrenia.
50
Neural correlates are exactly that - correlates. Why is that a problem when it comes to explaining schizophrenia?
Correlations don't show cause and effect (Although studies of neural correlates are useful in flagging up particular brain systems that may not be working properly, this kind of evidence does not prove that the activity in the brain region causes the symptom. For example, whilst it may be that something wrong in the ventral striatum causes the negative symptoms, it is possible that the negative symptoms themselves mean that less information passes through the striatum resulting in its reduced activity. It’s also possible that another factor influences both.
51
Describe evidence to support that schizophrenia is not entirely biological?
Many researchers now accept that the fact that schizophrenia appears to run in families may be more to do with common rearing patterns or other factors that have nothing to do with heredity. After all, the probability of developing schizophrenia even if your identical twin has it is less than 50%. For example, childhood trauma may make people more vulnerable to schizophrenia. Morkved et al. (2017) found that 67% of people with schizophrenia and related psychotic conditions reported at least one childhood trauma compared to 38% of a matched group with non-psychotic mental health problems.
This suggests that whilst a genetic vulnerability for schizophrenia may be important, psychological factors beyond genetics are also important and so the biological explanations alone cannot be considered to be complete explanations of schizophrenia. It may be better to take an interactionist approach, combining biological and psychological factors.
52
What is drug therapy?
Drug therapy involves the treatment of schizophrenia through the use of antipsychotic medication to reduce the symptoms of the disorder. They help the person with schizophrenia to function as well as possible whilst also increasing their feelings of subjective wellbeing.
53
How can drugs be taken?
Tablets, syrup or injections
54
Do dosages typically start high and get lower or lower and get higher?
Low and get higher
55
All antipsychotics work by doing what?
By reducing dopaminergic transmission i.e. reducing the actions of the neurotransmitter dopamine in areas of the brain associated with the symptoms of schizophrenia.
56
When were typical antipsychotics developed?
1950s
57
Describe how typical antipsychotics work at a biological level, making sure to make it clear which symptoms of schizophrenia they therefore treat.
They are dopamine antagonists – they bind to (and so block) dopamine receptors but don’t stimulate them, reducing the action of dopamine. Initially dopamine levels build up but then production is reduced. This normalises neurotransmission in key areas of the brain, by reducing stimulation of the dopamine system, reducing positive symptoms such as hallucinations.
Hallucinations and delusions usually diminish within a few days of beginning medication, although other symptoms may take several weeks before a significant improvement is noted.
58
Which typical antipsychotic is also an effective sedative?
Chlorpromazine
59
When were atypical antipsychotics developed?
1970s
60
Describe how atypical antipsychotics work at a biological level, making sure to make it clear which parts of the process treat which symptoms of schizophrenia.
Atypical antipsychotics also block dopamine receptors like typical antipsychotics. However, they only temporarily occupy the receptors and then rapidly dissociate to allow normal dopamine transmission. This is thought to be the reason for the fewer side effects associated with atypical antipsychotics.
Atypical antipsychotics also act on other neurotransmitters, particularly 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 and reduce depression and anxiety in patients, as well as potentially improving cognitive functioning. Therefore they are prescribed for patients with a higher risk of suicide (as 30-50% of people with schizophrenia attempt suicide at some point).
61
Which atypical antipsychotic is newer and so doesn't have the most serious side effects?
Risperidone
62
Which type of antipsychotic is more likely to be prescribed to people who have a higher risk of suicide? Why?
Atypical - they address negative symptoms such as avolition
It is believed that this action helps to improve mood and reduce depression and anxiety in patients, as well as potentially improving cognitive functioning. Therefore they are prescribed for patients with a higher risk of suicide (as 30-50% of people with schizophrenia attempt suicide at some point).
63
Name (and define where technical terms are used) two-three side effects for each type of antipsychotic.
Chlorpromazine - dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin. Long-term use can result in tardive dyskinesia (involuntary muscle movements of the tongue, face and jaw).
Clozapine and risperidone - agranulocytosis (an autoimmune disorder affecting white blood cells) - have to have regular blood tests
64
How are typical antipsychotics different from atypical antipsychotics?
Typical occupy the receptor permanently and only effect positive symptoms whereas atypical only temporarily affect it and affect both positive and negative symptoms
65
How can we argue that antipsychotics are an appropriate treatment of schizophrenia?
They treat the symptoms
66
Describe two studies to support that antipsychotics are an effective treatment of schizophrenia.
Thornley et al. (2003) reviewed studies comparing the effects of Chlorpromazine (typical antipsychotic) and a placebo. Data from 13 trials of 1121 participants found that Chlorpromazine was associated with better overall functioning and reduced symptom severity.
Meltzer et al. (2012) concluded that Clozapine (atypical antipsychotic) 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.
67
Why might antipsychotics not be an appropriate treatment for all patients with schizophrenia?
A problem with antipsychotics drugs is the likelihood of side effects, ranging from the mild to the serious to the fatal. 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. The most serious side effect of typical antipsychotics is neuroleptic malignant syndrome (NMS), which results in high temperature, delirium and coma, and can be fatal. Atypical antipsychotics have fewer side effects because of their mechanism of action, but do still have side effects such as agranulocytosis.
68
Explain how a cost-benefit analysis of antipsychotics would be negative.
Critics argue that if side effects, deaths and psychosocial consequences 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 the Human Rights Act that no one should be subjected to inhuman or degrading treatment or punishment. Additionally, it is widely believed that antipsychotics have been used in hospital situations to make patients calmer and easier to deal with, rather than for the benefits to the patients themselves. Furthermore, patients with severe symptoms may not be able to give fully informed consent.
69
How might the effectiveness of antipsychotics have been exaggerated?
Healy (2012) argued that some successful trials 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 for positive effects. As antipsychotics have calming effects, it is easy to demonstrate that they have some positive effects on patients. This is not the same as saying they really reduce the severity of symptoms.
70
Generally, what are the psychological explanations of schizophrenia?
Childhood trauma e.g. Schizophrenogenic mother
71
What do we mean by family dysfunction explanations of schizophrenia?
Family dysfunction explanations suggest that schizophrenia is due to family experiences of interpersonal conflict, communication problems, criticism and control
72
There are three family dysfunction explanations of schizophrenia. Name them.
Schizophrenogenic mother
Double-bind theory
Expressed emotion
73
Describe the researchers who proposed it, the characteristics of family, impact on the individual and the symptoms of schizophrenia it's associated with for the schizophrenogenic mother
Fromm-Reichmann (1948)
Mother is cold, controlling and rejecting; father is often passive
Leads to excessive stress and distrust as the family climate is characterised by tension and secrecy
This triggers psychotic thinking and paranoid delusions and ultimately schizophrenia
74
Describe the researchers who proposed it, the characteristics of family, impact on the individual and the symptoms of schizophrenia it's associated with for the double-bind theory
Bateson et al (1972)
The child receives mixed messages and cannot do the right thing. When they get it wrong, they are punished with withdrawal of love
Leads to understanding the world as confusing and dangerous
This triggers disorganised thinking and paranoid delusions and ultimately schizophrenia
75
Describe the researchers who proposed it, the characteristics of family, impact on the individual and the symptoms of schizophrenia it's associated with for expressed emotion
The family shows exaggerated involvement in the life of the patient (including needless self-sacrifice), control, verbal criticism of the patient (occasionally including violence) and hostility towards the patient (including anger and rejection)
High levels leads to excessive stress beyond impaired copying mechanisms
This triggers relapse in patients with schizophrenia and may trigger the onset in a person who is already vunerable due to their genetic makeup (diathesis stress model)
76
What do we mean by a cognitive explanation of schizophrenia.
Dysfunctional thought processing
77
The cognitive explanation of schizophrenia argues that schizophrenia is due to dysfunctional thought processing. What is this?
Cogntive beliefs that mean we evaluate info inappropriately
78
Frith et al. (1992) identified two kinds of dysfunctional thought processing that could underlie some of the symptoms of schizophrenia. Name them both, define them and explain which symptoms of schizophrenia they may lead to.
Central control - ability to express (squash) automatic thoughts to make deliberate actions --> Cannot suppress automatic thoughts --> disorganised speech and speech poverty
Metarepresentation - reflection on our thoughts anf feelings and know they occured becuase we intended them to --> disrupts ability to recognise that we did it becuase we wanted to --> auditory hallucinations and delusions
79
Describe evidence to support the family dysfunction explanation. Identify which family dysfunction explanation it supports and explain exactly how it supports it.
Garety et al. (2008) estimate that relapse rates for individuals who receive family therapy as 25% compared to 50% for those who receive standard care alone. The effectiveness of family therapy based on reducing expressed emotion supports a family dysfunction approach because by changing the expressed emotion, the rate of relapse reduces. This implies that the expressed emotion plays a role in the return of symptoms of schizophrenia and so may be a valid explanation of this.
80
Family dysfunction explanations can be supported by family therapy working. Describe evidence which supports that this is the case and explain exactly how this supports the family dysfunction explanations of schizophrenia.
McFarlane (2016) concluded that family therapy was one of the most consistently effective treatments available for schizophrenia. In particular, relapse rates were found to be reduced, typically by 50-60%. McFarlane also concluded that using family therapy as mental health initially starts to decline is particularly promising. Clinical advice from NICE recommends family therapy for everyone with a diagnosis of schizophrenia.
81
Describe evidence to undermine the family dysfunction explanation. Identify which family dysfunction explanation it undermines and explain exactly how it undermines it.
Altorfer et al. (1998) found that ¼ of the patients they studied showed no physiological responses to stressful comments from their relatives. This suggests that not all patients who live in high EE families relapse. Therefore, there are individual differences in response to high EE-like behaviours and so we cannot consider the EE explanation to be completely Valid as it may not apply to all schizophrenia sufferers
82
How can family dysfunction explanations be seen as parent blaming? Why is this a problem?
Historically, family-based explanations have led to parent-blaming. Parents, who have already suffered at seeing their child’s descent into schizophrenia and who are likely to bear the lifelong responsibility for their care, feel responsible for their child’s illness causing even greater stress and anxiety. Out-dated views that were once accepted are no longer tolerated by families and are now seen as destructive rather than productive. This is highly Unethical and literally adds insult to injury. It has ethical implications as it could cause stress to the parents which could then compromise their own mental health. The shift in the 1980s from hospital to community care (often involving parental care) may be one of the factors leading to the decline of the schizophrenogenic mother and double-bind theories – parents no longer tolerated them.
83
Describe evidence to support the cognitive explanations. Explain exactly how it supports the cognitive explanations of schizophrenia.
Stirling et al. (2006) compared 30 patients with a diagnosis of schizophrenia with 18 non-patient controls on a range of cognitive tasks, including the Stroop test. Patients took over twice as long to name the ink colours as the control group. This supports Frith et al.’s suggestion of a relationship between Central control dysfunction and symptoms of schizophrenia. However, whilst the link between symptoms and faulty cognitions is clear, this does not tell us about the origins of those cognitions and therefore the origins of schizophrenia. Therefore, from the research, we can’t strongly support the Internal validity of the cognitive explanation because we cannot determine that that the dysfunctional thought processing caused the symptoms of schizophrenia as it could be the other way around.
84
Cognitive explanations can be supported by CBTp working. Describe evidence which supports that this is the case and explain exactly how this supports the cognitive explanations of schizophrenia.
CBTp (cognitive behavioural therapy for psychosis) has been demonstrated to be effective in the NICE review of treatments for schizophrenia (NICE, 2014). When compared to antipsychotic medication, CBTp was more effective in reducing symptoms severity and improving levels of social functioning. This supports that the origin of schizophrenia may be in faulty cognitions as changing these cognitions reduces the symptoms of schizophrenia. As such, it seems that the cognitive explanations have some validity in explaining schizophrenia.
85
Cognitive explanations only explain what is happening now to produce symptoms. Why is this a problem?
Cognitive explanations of schizophrenia only explain what is happening now to produce symptoms rather than what initially caused the condition. It may be that genetics and/or family dysfunction cause schizophrenia. What is currently unclear is how genetic variation or childhood trauma might lead to problems with meta-representation or central control. This means that the cognitive explanations only provide partial explanations of schizophrenia and may not explain the root cause of the condition. This also means that any therapies that are based on the cognitive explanations are unlikely to treat the root cause of schizophrenia and so won't be able to treat all symptoms.
86
Both psychological explanations have a direction of causality issue. Explain what this means in the context of each explanation and why this is a problem for both explanations of schizophrenia.
Ignore
The family dysfunction explanations propose the family problems lead to schizophrenia. The cognitive explanations propose that dysfunctional thought processing leads to schizophrenia. However, it is possible that it may be the opposite way around and schizophrenia leads to family problems and/or dysfunctional thought processing. Alternatively, a third variable could cause both. As such, it is difficult to strongly support the Internal validity of the explanations as it is not certain that family dysfunction/dysfunctional thought processing causes schizophrenia.
87
What is CBTp?
Cognitive behavioural therapy for psychosis
88
What are the aims of CBTp?
CBTp aims to help patients to identify irrational thoughts and challenge them (including the origin of ‘voices’) and reality testing them to reduce distress.
89
How many sessions of CBTp do people with schizophrenia typically have?
5-20 (NICE recommending at least 16)
90
Describe the ABCDE model with examples of schizophrenia for each one.
A - activating events
B - beliefs
C - emotional and behavioural consequences
D - disputing (critical collaborative analysis)
E - effect
For example, a patient might believe that the Mafia are observing them and trying to determine how to kill them (delusion), and that members of the mafia are speaking to them about how they plan to do this (auditory hallucination). This may lead the patient to withdraw from society, hiding from friends and family and take steps to defend themselves physically (e.g. arming themselves).
The therapist uses gentle questioning to help the patient to understand and challenge illogical deductions and conclusions e.g. ‘if your voices are real, why can no one else hear them?’ and ‘It’s possible that it’s the Mafia, but there are also other possibilities. How do you know it’s the Mafia?’. Through this, the patient develops alternative explanations for their previously unhealthy assumptions (e.g. That the voices could be theirs and so aren't real). Therefore, the effect (E) is restructured (more rational) beliefs (e.g. Viewing voices as interesting rather than threatening). The patient also becomes much better at identifying delusional thoughts.
Additionally, delusions can be challenged through reality testing. This where the person with schizophrenia and the therapist jointly examine the likelihood that beliefs are true. Through this, the patient develops alternative (more rational) explanations for their previously unhealthy assumptions. Therefore, the effect (E) is restructured beliefs.
91
What is critical collaborative analysis? What effect does this have?
The therapist uses gentle questioning to help the patient to understand and challenge illogical deductions and conclusions e.g. ‘if your voices are real, why can no one else hear them?’ and ‘It’s possible that it’s the Mafia, but there are also other possibilities. How do you know it’s the Mafia?’. Through this, the patient develops alternative explanations for their previously unhealthy assumptions (e.g. That the voices could be theirs and so aren't real). Therefore, the effect (E) is restructured (more rational) beliefs (e.g. Viewing voices as interesting rather than threatening). The patient also becomes much better at identifying delusional thoughts.
92
What is reality testing? What effect does this have?
This where the person with schizophrenia and the therapist jointly examine the likelihood that beliefs are true. Through this, the patient develops alternative (more rational) explanations for their previously unhealthy assumptions. Therefore, the effect (E) is restructured beliefs.
93
What is normalisation? What effect does this have?
The therapist shares with the patient that many people have unusual experiences such as hallucinations and delusions in many different circumstances (e.g. in situations of extreme stress). They reassure the patient that people hearing voices is an extension of the ordinary experience of thinking in words. This reduces anxiety (distress) and the sense of isolation by making the patient feel less alienated and stigmatised. This makes the possibility of recovery seem more likely and improves their ability to function adequately.
94
What are behavioural assignments?
Assignments to improve their general level of functioning, such as to shower every day or to go out and socialise with friends once between now and the next session. It may also include relaxation techniques.
95
Explain the difference between the effectiveness of a treatment and the appropriateness of a treatment.
Effectiveness - how well it treats schiz
Appropriateness - whether it is suited for the person or not
96
Does CBTp cure schizophrenia? Why or why not?
No as it does not get rid of the symptoms it just helps someone manage them
97
What does this tell us about the effectiveness of CBTp?
Whilst CBTp may provide patients with strategies that they can use to manage their current and future symptoms, it does not effectively cure schizophrenia.
98
Describe evidence to support that CBTp is modestly effective alone and that it is probably more effective long-term when combined with drug therapy.
The NICE review of treatments for schizophrenia (NICE, 2014) found consistent evidence that when compared with standard care (antipsychotics alone), CBTp was effective in reduction rehospitalisation rates up to 18 months following the end of treatment. CBTp was also shown to be effective in reducing symptom severity and improving social functioning. Jauhar et al. (2014) reviewed 34 studies of using CBTp to treat schizophrenia and concluded that there is evidence for small but significant effects on positive and negative symptoms. However, most studies of the effectiveness of CBTp have been conducted with patients treated at the same time with antipsychotic medication. It is therefore difficult to assess the effectiveness of CBTp independent of antipsychotics. Additionally, the studies involve different CBTp techniques and patients with different combinations of symptoms.
99
CBTp is thought to be more effective at certain stages of disorder that others. Which ones and why? How does this impact our thoughts about its effectiveness and appropriateness?
Addington and Addington (2005) claim that self-reflection is not particularly appropriate during the initial acute phase of schizophrenia. Following stabilisation of the psychotic symptoms with antipsychotics, individuals may then benefit more from group-based CBTp.
This can help to normalise their experience by meeting others with similar issues. Research has found that it is those with more experience of their schizophrenia and a greater realisation of their symptoms that benefit more from individual CBTp. This suggests that CBTp is effective, but may be more appropriate in the latter stages of treatment rather than initially.
100
CBTp requires motivation that the patient may not have. How? How does this impact what we think of its appropriateness of a treatment for schizophrenia?
The length of the therapy means that patients have to be motivated and committed to multiple sessions. The therapy itself also requires self-awareness and a willingness to engage with the process. However, the positive symptoms of schizophrenia lead to a lack of awareness and the negative symptoms lead to a reluctance or inability to engage. The length of the therapy also leads patients to drop out at times of severe episodes. Overall, this suggests that CBTp may not be an appropriate treatment for all patients with schizophrenia.
101
CBTp is difficult to access. How difficult? How does this impact what we think of its effectiveness?
Despite being recommended by NICE as a treatment for people with schizophrenia, it is estimated that only 1 in 10 people in the UK who could benefit from CBTp can get access to it. Haddock et al. (2013) found that in NW England, only 6.9% of patients had been offered CBTp. This limits the effectiveness of CBTp as patients are unable to participate in the therapy. Of those who are offered CBTp, a significant number either refuse or fail to attend the therapy sessions, thus limiting its effectiveness even more.
102
CBTp raises ethical issues. How? How does this impact what we think of it as a treatment for schizophrenia?
Ignore
CBTp may involve, for example, challenging a person’s paranoia. At what point does this interfere with an individual’s freedom of thought? If, for example, CBTp challenged a patient’s beliefs in a highly controlling government, this can easily stray into modifying their politics. This is a weakness of CBTp as a treatment for schizophrenia (appropriateness).
103
What is family therapy?
Family therapy is a range of interventions aimed at the family (e.g. parents, siblings, partners) of someone with schizophrenia. It should also involve the person with schizophrenia if practical.
104
What are the aims of family therapy?
It aims to reduce the anger, frustration and expressed emotion within the family to reduce the stress of living as a family.
It also aims to improve the communication and interaction between family members. It does this by the therapist meeting family members and the patient for an open, productive discussion. The family members are educated about the disorder and what to expect.
Overall, it aims to reduce the stress of living as a family and so reduce rehospitalisation.
105
What happens during family therapy sessions?
During sessions, the individual with schizophrenia is encouraged to talk to their family and explain what sort of support they do and do not find helpful. It improves relationships within the household because the therapist encourages family members to listen to each other, discuss problems and negotiate potential solutions together i.e. It helps the family to develop problem-solving and communication skills to help to support the patient.
106
Describe at least three strategies used during family therapy.
Helping the patient and their family to understand and be better able to deal with the illness.
Improving the ability of the family to anticipate and solve problems.
Reduction of anger and guilt in family members.
107
What impact do these strategies have according to Pharoah et al. (2010)?
Pharoah et al. (2010) suggest that these strategies reduce stress and expressed emotion (particularly negative emotions such as anger and guilt which create stress), whilst increasing the chances of patients complying with medication. This tends to result in a reduced likelihood of relapse and readmission to hospital.
108
Describe Pharoah et al.'s (2010) procedure and findings. Explain what this tell us about the effectiveness of family therapy.
Pharoah et al. (2010) reviewed the evidence for the effectiveness of family therapy (compared to antipsychotics alone). They found that:
There was a reduction in the risk of relapse and a reduction in hospital readmission during treatment and in the 24 months after.
Some studies reported an improvement in the overall mental state of patients whereas others didn’t.
There was an increased compliance with medication.
Family therapy did not appear to have much of an effect on more concrete outcomes such as living independently or employment
109
Does family therapy cure schizophrenia? Why or why not? What does this tell us about family therapy as a treatment for schizophrenia?
Whilst family therapy may provide patients with strategies that they can use to manage their current and future symptoms, it does not effectively cure schizophrenia.
110
Describe McFarlane's (2016) study of family therapy. What does this tell us about the effectiveness of family therapy as a treatment for schizophrenia?
McFarlane (2016) concluded that family therapy was one of the most consistently effective treatments available for schizophrenia. In particular, relapse rates were found to be reduced, typically by 50-60%. McFarlane also concluded that using family therapy as mental health initially starts to decline is particularly promising. Clinical advice from NICE recommends family therapy for everyone with a diagnosis of schizophrenia. This suggests that family therapy is likely to be of benefit to people with both early signs of schizophrenia and diagnosed schizophrenia, implying that it is an effective therapy.
111
Explain at least one way in which we can consider family therapy to an appropriate treatment for schizophrenia.
Family therapy benefits all family members, not just the patient. Lobban and Barrowclough (2016) concluded that these effects on family members are important because families provide the bulk of the care for the patient with schizophrenia. By strengthening the functioning of a whole family, family therapy lessens the negative impact of schizophrenia on other family members and strengthens the ability of the family to support the person with schizophrenia.
112
What is token economy?
A form of behavioural modification, where desirable behaviours are encourages by the use of selective reinforcement. For example, people are given rewards (tokens) when they engage in socially desirable behaviours. The tokens are secondary reinforcers and can then be exchanged for primary reinforcers - food or privileges
113
Does token economy manage or treat schizophrenia? Why is this a problem?
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 not effectively cure schizophrenia.
114
What is selective reinforcement?
Token economy is a form of behavioural therapy used in the management of schizophrenia. It is used to shape and manage behaviour so that patients in long stay hospitals are easier to manage.
115
Describe the process of token economy, using the terms primary reinforcers, secondary reinforcers, repeated, association
Rewards (tokens) are given immediately as secondary reinforcers when patients engage in desirable behaviours e.g. getting dressed in the morning, making a bed, taking medication etc.
Although these tokens have no value in themselves, they can be swapped later for more tangible rewards (primary reinforcers). For example, sweets, magazines, privileges such as a walk outside the hospital. Therefore, this encourages the desirable behaviour to be repeated because they have become associated with rewards and privileges.
To ensure the tokens become effective secondary reinforcers, initially they are administered at the same time as the primary reinforcer.
116
Token economy raises ethical issues. How? Why is this a problem with using it as a way of managing schizophrenia?
Token economy raises ethical issues as it gives professionals considerable power to control the behaviour of patients. For example, in order to make reinforcement effective, clinicians may 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 rights to food, privacy etc. that cannot be violated regardless of the positive consequences 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 severe 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. 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.
117
Describe evidence to support that token economy is effective.
Dickerson et al. (2005) reviewed 13 studies of the use of token economy systems in the treatment of schizophrenia. 11 of these studies reported beneficial effects that were directly attributable to the use of token economies. Glowacki et al. (2016) reviewed 7 studies and found that all studies showed a reduction in negative symptoms and a decline in the frequency of unwanted behaviours. This supports the effectiveness of token economy in increasing the adaptive behaviours of those with schizophrenia. However, 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. Key note: again, you could then link back to how this still isn't addressing the symptoms and so isn't treating schizophrenia.
118
How do token economy studies tend to lack control. How? Why is this a problem? What does this tell us about token economy as a way of managing schizophrenia?
A major problem in 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. This means that patients’ improvements can only be compared with their past behaviours 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 token economy as previously thought.
119
Token economy is thought to only really work in a hospital setting. Why is this? Why is this a problem?
Token economy has only really been shown to work in a hospital setting. There are problems administering the token economy method with outpatients who live in the community. Within a psychiatric ward setting, inpatients receive 24 hour care and so there is better control for staff to monitor and reward patients appropriately. In the community, outpatients only receive day treatment for a few hours a day and so the token economy method can only be used for part of the day. Therefore, even if token economy did produce positive results within the ward setting, these results may not be maintained beyond that environment, limiting the long-term effectiveness of token economy as a method to manage schizophrenia. It also means that it is not appropriate beyond the hospital setting.
120
For each of the combinations of treatments of schizophrenia, suggest three ways that they can be compared (similarities or differences):
Antipsychotics and CBTp - one treats one doesn't, one only effective at certain times the other always effective, one has bad side affects the other doesn't
Antipsychotics and family therapy - same as above
Antipsychotics and token economy - treat doesn't treat, can be used outside hospital and can't, effective and not effective
CBTp and family therapy - both therapies, both don't treat, one does whole family one doesn't
CBTp and token economy - both don't treat, both can be abused, one less effective at one times the other not as much
Family therapy and token economy -
121
What is the interactionist approach to schizophrenia?
A way to explain the development of behaviour in terms of a range of factors, including both biological and psychological ones (biological – genes causing it, psychological – external factors like schizophrenogenic mother) and social ones. Most importantly such factors don't simply add together but combine in a way that can't be predicated by each separately i.e. They interact
122
A diathesis-stress model is an interactionist approach to schizophrenia. What is the diathesis-stress model?
A diathesis-stress model is an interactionist approach to schizophrenia. Schizophrenia is argued to be the result of both an underlying (internal) vulnerability (diathesis) and any negative psychological experience (external) trigger (stress). Both are necessary for the onset of schizophrenia. One or more underlying factors make a person particularly vulnerable to developing schizophrenia, but the onset of the condition is triggered by stress.
123
In Meehl's original model, what was the diathesis and what was the stress?
Diathesis - Genetic ('schizogene')--> neural chemical abnormalities (dopamine)
Stress - Chronic stress in childhood --> schizophrenogenic mother
124
How did Meehl expand diathesis and stress in the revised model?
Diathesis - Any psychological experience that impacts brain development e.g. Child abuse --> HPA pathway (chronic stress response)
Stress - Any negative psychological experience e.g. Family dysfunction, stressful life events
Cannabis use (substance abuse)
125
What treatment is recommended based on an interactionist approach? Describe how they treat schizophrenia.
As the interactionist model acknowledges both biological and psychological factors in schizophrenia, it is associated with combining antipsychotic medication and psychological therapies (most commonly CBTp).
126
Describe Tienari et al.'s (2004) procedure and results. Explain exactly how the study supports the interactionist approach.
There is evidence to support the dual role of genetic vulnerability and stress in the development of schizophrenia. Tienari et al. (2004) studied 19000 Finnish children who had at least one biological parent with schizophrenia and were adopted into a new family and compared them with adoptees without this genetic risk. The adopted parents were assessed for child-rearing style and the rates of schizophrenia across the two groups was compared. They found that a child-rearing style characterised by high levels of criticism and conflict and low levels of empathy were implicated in the development of schizophrenia (dysfunctional parenting - psychological trigger), but only for those in the high-genetic-risk group. High-genetic-risk adoptees reared in families with low scores on this child-rearing style scale were significantly less likely to have developed schizophrenia than high genetic risk adoptees reared in families with high scores on the child-rearing style scale. This suggests that both genetic vulnerability and family-related stress are important in the development of schizophrenia - genetically vulnerable children are more sensitive to parenting behaviour. This is strong direct support for the importance of adopting an interactionist approach to schizophrenia, including that poor parenting is a possible source of stress that triggers schizophrenia in those who are vulnerable.
127
The original diathesis-stress model was criticised for being too simplistic. How? Why is this a problem? How can this also be spun into a strength?
It is now 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 diathesis, as well as brain damage caused by environmental factors. For example, Verdoux et al. (1998) estimated that the risk of developing schizophrenia later in life was four times greater for those who had experienced prolonged labour and oxygen deprivation than those who hadn’t experienced such complications. Stress has also been found to come in many forms, not just dysfunctional parenting. For example, Houston et al. (2008) found that childhood sexual abuse emerged as the major influence on underlying vulnerability to schizophrenia and cannabis use as the major trigger. This suggests that the old idea of diathesis-stress may be overly simple. However, it supports a modern interactionist approach to schizophrenia is important in that vulnerabilities and triggers seem to interact together in some way to produce schizophrenia. Although, most people do not develop schizophrenia after smoking cannabis and so it seems there must also be one or more triggering stressful factors, which means that from the model it is difficult to predict exactly who will develop schizophrenia.
128
Why is it so difficult to determine which stressor triggered schizophrenia? Why is this a problem for both the explanation and treatment?
It is possible that stressors earlier in life can also influence how people respond to later stressful events, and increase their susceptibility to the disorder. Maladaptive methods of coping with stress in childhood and throughout development means that the individual fails to develop effective coping skills, which in turn compromises their resilience and increases vulnerability. This may make life generally more stressful for the individual and so trigger schizophrenia. Therefore, it is extremely difficult to determine the causal stress that triggered schizophrenia, which may negatively impact the effectiveness of treatment.
