Psychology-Schizophrenia Flashcards
(148 cards)
1
Q
What is schizophrenia?
A
A type of psychosis, a severe mental disorder in which thoughts and emotions are so impaired that contact is lost with external reality
2
Q
How common is schizophrenia?
A
It is the most common psychotic disorder and affects about 1% of the population at some point in their life
3
Q
When is schizophrenia most often diagnosed?
A
Between ages 15 and 35
4
Q
What is the gender difference in schizophrenia?
A
Men and women are affected equally
5
Q
What are two resources often used to diagnose schizophrenia?
A
The ICD 10 and the DSM V
6
Q
What is the ICD 10?
A
The international classification of diseases version 10 is mostly used in Europe
7
Q
What is the DSM V?
A
The diagnostic and statistical manual of psychiatric disorders version 5 is most often used in USA. It’s a classification and description of over 200 mental disorders, grouped in terms of their common features
8
Q
How does the DSM V diagnose schizophrenia?
A
Must meet criterion A (two or more positive symptoms unless they are bizarre or hallucinations are a running commentary or in conversation with multiple voices), criterion B (social/occupational dysfunction), and criterion C (continuous signs of disturbance persists for at least 6 months)
9
Q
What are the two types of symptoms?
A
Positive (an excess or distortion of normal functions), and negative (a diminution or loss of normal functioning)
10
Q
What are the positive symptoms of schizophrenia?
A
Hallucinations, delusions, disorganised speech, and grossly disorganised or catatonic behaviour
11
Q
What are hallucinations?
A
Distortions or exaggerations of perception in any of the senses, mostly auditory hallucinations, but can be visual, olfactory or tactile
12
Q
What are delusions?
A
Firmly held bizarre beliefs that are caused by distortions of reasoning or misinterpretations of perceptions or experiences. These can sometimes be paranoid delusions or delusions of grandeur or delusions of reference (events in environment appear to be directly related to them)
13
Q
What is disorganised speech?
A
The result of abnormal thought processes, that then shows up in speech
14
Q
What is grossly disorganised or catatonic behaviour
A
Includes inability or motivation to initiate or complete a task leading to difficulty in daily life. Catatonic behaviours are characterised by a reduced reaction to the immediate environment, rigid postures, or aimless motor activity
15
Q
How common are negative symptoms?
A
About one in three schizophrenia patients suffer from significant negative symptoms (Mäkinen et al)
16
Q
What are negative symptoms also known as?
A
Deficit syndrome characterised by the presence of at least two negative symptoms for at least 12 months. These often lead to more pronounced cognitive deficits and poorer outcomes (Milev et al) and they often respond poorly to antipsychotic treatment
17
Q
What are the negative symptoms of schizophrenia?
A
Speech poverty, avolition, affective flattening and anhedonia
18
Q
What is speech poverty?
A
The lessening of speech fluency and productivity, which reflects slowing or blocked thoughts. Often have difficulty in spontaneously producing words at a time. Also maybe less complex syntax eg fewer clauses
19
Q
What is avolition?
A
The reduction, difficulty or inability to initiate and persist in goal-directed behaviour, often mistaken for apparent disinterest
20
Q
What is affective flattening?
A
Reduction in the range and intensity of emotional expression, including facial expression, voice tone, eye contact and body language
21
Q
What is anhedonia?
A
Loss of interest or pleasure in all or almost all activities, or lack or a lack of reactivity to normally pleasurable stimuli. It can be pervasive, physical or social
22
Q
What is reliability?
A
Reliability means consistency therefore in relation to diagnosis of schizophrenia, we should see consistency in diagnosis
23
Q
What is validity?
A
Validity refers to whether an observed effect is a genuine one, so in relation to diagnosis of schizophrenia, it it a true diagnosis?
24
Q
What are the relevant types of reliability?
A
Test-re-test reliability, inter-rater reliability (ICD/DSM should raise this)
25
What are the relevant types of validity?
Symptom overlap (many disorders share symptoms which could lead to the wrong diagnosis), co-morbidity (where a person has more than one disorder it can make it harder to diagnose), and predictive validity (a diagnosis should allow psychiatrists to give a clear prognosis for all sufferers that are diagnosed with the same type of schizophrenia)
26
What are the relevant types of bias?
Cultural bias, gender bias (critics of the DSM say its categories are biased towards diagnosing one gender more than the other), and confirmation bias (sometimes psychiatrists have been criticised for trying to 'find a diagnosis' rather that give a true diagnosis or non diagnosis based on symptoms)
27
What were the research findings in Copeland, and what problem is highlighted?
Compared a group of American and a group of British Psychiatrists diagnosing the same patients, only 2% of British psychiatrists diagnosed schizophrenia compared to 69% of America psychiatrists. This highlights lack of inter rater reliability and culture bias
28
What problem is highlighted where different psychiatrists have used the DSM and found correlation coefficients as low as 0.11 between psychiatrists diagnosing schizophrenia?
Lack of inter rater reliability
29
What problem is highlighted by the used of 'bizarre' as a determinant for whether one or two symptoms are needed, leading to a concordance rate of 0.4 in senior psychologists?
Lack of inter rater reliability
30
What is an example of co-morbidity in diagnosing schizophrenia?
Research shows many schizophrenic patients have medical issues such as asthma, diabetes and hypertension. Other research shows 50% of schizophrenics have another disorder, mostly depression, substance abuse or anxiety. Also high rates of OCD in schizophrenic patients
31
What is the problem highlighted by the DSM being androcentric?
Gender bias as what is classed as mentally healthy for an adult is actually healthy 'male' behaviour
32
What does Rosenhan's study 'being sane in insane places' illustrate?
Lack of reliability in diagnosis, and confirmation bias
33
What are the evaluation points for validity?
Research support for gender bias (Loring and Powell where psychiatrists judged patients labelled as males (56% diagnosed), females (20%) or not labelled (56% diagnosed)). The consequences of co-morbidity and differences in prognosis (predictive validity)
34
What are the evaluation points for reliability?
Lack of inter-rater reliability (Copeland), unreliable symptoms (use of 'bizarre' and senior psychiatrists) and cultural differences in the diagnosis of schizophrenia (America vs Britain)
35
What are the three kinds of biological explanations for schizophrenia?
Genetics, bio-chemistry and a link between the flu virus during pregnancy to the development of schizophrenia
36
What family members share 100% of their genes?
Identical twins
37
What family members share 50% of their genes?
Non-identical twins, brothers and sisters, parents and children
38
What family members share 25% of their genes?
Grandparents and grandchild
39
What does the genetic explanation suggest about schizophrenia?
That it is hereditary as it tends to run in families and you are more likely to develop it if you have a close family member with schizophrenia, however no single 'schizophrenic gene' has been identified-it is different combinations of genes that makes someone more prone to developing the disorder
40
What types of studies are used to investigate the role of genetics in schizophrenia?
Family studies, twin studies and adoption studies
41
Explain family studies into schizophrenia
They look at concordance rates of features with different family members. Those more closely related to someone with schizophrenia are more likely to develop it. Eg Gottesman found that having two schizophrenic parents had a higher concordance rate than someone with one schizophrenic parent
42
Explain twin studies into schizophrenia
Look at difference in concordance rates between MZ and DZ twins and those raised apart or together. If the biological explanation was completely correct that MZ twins should have almost 100% concordance rate. Joseph found that concordance rates were dramatically higher in monozygotic twins
43
Explain adoption studies into schizophrenia?
Look at the concordance rates between biological parents and children, and adopted children and parents. Tienari et al found concordance rate higher between adopted children with biologiscal parents with schizophrenia, than those without schizophrenic biological parents
44
What are the evaluation points for genetic factors?
Common rearing patterns may explain family similarities instead of heredity, MZ twins encounter more similar environments which is why there is a difference between MZ and DZ twins (Joseph), In adoption studies if the adoptive parents know the child's biological parents have schizophrenia then they may look out for signs that aren't actually there to show the child is schizophrenic, leading to a high concordance rate
45
What is the biochemical explanation of schizophrenia?
Neurons transmit messages in the form of neurotransmitters which cross the synapse to another neuron. Once the neurotransmitter is released, it is either locked into the receptor site or broken down or reabsorbed (reuptake). The key neurotransmitter in schizophrenia is dopamine
46
What is the dopamine hypothesis?
In a schizophrenic brain, there is an excess of dopamine activity which is associated with positive symptoms. Neurons transmit dopamine fire too easily, and neurones receiving dopamine have too many receptors
47
What drugs can cause schizophrenic symptoms?
Amphetamines as these increase dopamine. Also L-Dopa is a drug prescribed for Parkinson's disease which is linked to low levels of dopamine however patients that use this medication have reported schizophrenic symptoms such as hallucinations. Symptoms usually go after stopping the medications
48
What drugs decrease schizophrenic symptoms?
Anti-psychotics because they reduce dopamine and so are effective in treating positive symptoms. This strengthens the case for the importance of dopamine in this disorder
49
What is the updated dopamine hypothesis?
Davis and Kahn propsed that positive symptoms of schizophrenia are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway. The negative and cognitive symptoms are thought to arise from a deficit of dopamine in areas of the prefrontal cortex (mesocortical pathway)
50
Where does evidence for the Dopamine Hypothesis come from?
Leucht et al's meta-analysis of studies that compared effectiveness of psychotic in reducing schizophrenic symptoms to a placebo. The found that all the drugs tested were significantly more effective than the placebo
51
What do critics of the dopamine hypothesis argue?
That the effects of adjusting dopamine have been exaggerated. One way this is shown is through negative or inconclusive results of dopamine concentration in post-mortem brain tissue research. Mocrieff points out that confounding sources of dopamine such as stress and smoking are rarely considered. Lack of current evidence of the dopamine hypothesis. Stimulant drugs can also induce schizophrenic episodes (affect many neurotransmitters other than dopamine)
52
What are the evidence points for the dopamine hypothesis?
Evidence from treatment (Leucht et al), inconclusive supporting evidence (Moncrieff), and challenges to the dopamine hypothesis (Noll-strong evidence for both versions of the hypothesis, but anti-psychotic drugs don't work on 1/3 of patients and some people experience symptoms with normal dopamine levels, suggesting other neurotransmitter systems produce positive symptoms)
53
What are the psychological explanations for schizophrenia?
Family dysfunction (double blind theory and expressed emotion) and cognitive explanations
54
What are family dysfunction explanations?
Explanations for schizophrenia that focus on the idea that is is caused by abnormal patterns or communication within the family
55
What is double blind theory based on?
The idea that schizophrenics have regularly received contradictory messages from parents as a child, for example, the verbal message may be of affection but the non verbal message may be of animosity or disgust to the child
56
How do these contradictory messages affect the child?
They don't know how to respond to the parent, they are unsure whether to respond to the verbal or behavioural cue, they are unaware of which cue is the 'real' one
57
How does double blind theory explain the development of schizophrenia from contradictory messages?
The child doesn't know how to respond to the parent. Such contradictions prevent the child from developing a coherent construction of reality-too many contradictory messages do not allow sense to be made. In time, this manifests itself as schizophrenic symptoms such as withdrawal from social situations and a loss of contact with reality
58
How does Tienari et al's adoption study support the role of dysfunctional family life?
Those who developed schizophrenia were the ones that's adopted family was rated as disturbed. Supports family dysfunction as an explanation for schizophrenia over biological/genetic explanations
59
How does Berger's research support double blind theory?
Found that schizophrenic individuals reported having received more contradictory messages from parents than non-schizophrenia individuals suggesting that double blind messages do play a role in the development of schizophrenia
60
What are issues with Berger's research?
Patients recall may not necessarily be trusted as they want an explanation as to why they have schizophrenia and so may think their parents gave contradictory messages. Also time and medication may have affected memory
61
How does Liem et al refute Berger's findings?
Measured patterns of parental communication in families with a schizophrenic child and found no difference when compared to normal families-similar to findings from Hall and Levin
62
What is expressed emotion?
When members of the family talk openly about the patient in a critical or hostile way or in an 'over involved, emotional way'. This type of family have been referred to as 'talk more, listen less', and evidence suggests schizophrenic patients in these families are 4 times more likely to relapse
63
Why do high expressed emotion families cause a more likely chance of relapse?
Families with a negative emotional climate or high levels of EE are more likely to lead to relapse because schizophrenia leads to individuals having a lower tolerance for intense stimuli and the intense emotional climate stimulates the individual too much, causing too much stress for their coping mechanism-triggering a schizophrenic episode
64
What is the main criticism for expressed emotion?
Individual differences (not all patients in high EE families will relapse and not all in low EE families will avoid relapse). Altofer et al found 1/4 of patients studied showed no physiological responses to stressful comments from their relatives. Vulnerability to the influences of high EE may also be psychologically based
65
How does Lebell's research highlight and develop the theory further?
Suggests that how patients perceive the value of the behaviour of their relatives is important. In cases where high EE behaviours are not perceived as negative or stressful, they can do well regardless of how the family environment is objectively rated. Shows that not all patients are equally vulnerable to high levels of EE in the family environment
66
What is the cognitive explanation for schizophrenia?
Cognition refers to thought processes, in relation to schizophrenia, the cognitive approach explains the development of symptoms as due to faulty cognitive processes. This explanation gives key examples for how faulty though processes cause both hallucinations and delusions
67
What does the cognitive approach say causes delusions?
Inadequate information processing, the main issue being egocentric bias where someone thinks everything revolves around them. It is a dysfunctional and faulty thought process that causes schizophrenic symptoms by jumping to conclusions about external events
68
Why does egocentric bias make delusions relatively impervious to reality testing?
Whatever someone says or does can be turned around to fit the delusions so they continue. They are unwilling or unable to consider that they may wrong ('impaired insight') (Beck and Rector)
69
What does the cognitive approach say causes hallucinations?
A hyper vigilance to auditory stimuli
70
How does a hyper vigilance to auditory stimuli explain the manifestation of hearing voices?
Hallucinations (mainly hearing voices) are caused by an individual focussing too much attention on auditory stimuli. Significantly more likely to misattribute 'self-generated' auditory experiences to external sources (Baker and Morrison). These errors aren't picked up as they don't have the same processes of reality testing
71
What is supporting evidence for the idea that both positive and negative symptoms in schizophrenia have their own etiology?
Sarin and Wallin-delusions=jumping to conclusions and lack of reality testing (biases in information processing. Hallucinations=impaired self-monitoring and also tended to experience their own thoughts as voices. Negative symptoms also=dysfunctional thought processes such as low expectations regarding pleasure and success
72
What else is support from the cognitive explanation?
Cognitive behavioural therapy for psychosis (CBTp)
73
How do results of CBTp compare to antipsychotic drugs according to NICE?
NICEs' (national institute for clinical excellence) claim that symptoms of schizophrenia have their origin in faulty cognition is reinforced by the success of cognitive-based therapies for schizophrenia. More effective in reducing symptoms and improving levels of social functioning than antipsychotic drugs
74
When comparing the biological and psychological explanations, what is needed when looking at the cause of schizophrenia?
The diathesis-stress model
75
What is the link between etiology and treatment for drugs?
Drugs reduce dopamine activity to reduce symptoms
76
How were schizophrenic patients treated before drug therapies existed?
Before the discovery of the dopamine hypothesis and subsequent development of specific drugs, schizophrenic patients would be institutionalised
77
What is an anti-psychotic drug?
Drugs that work by reducing the action of dopamine in brain areas associated with symptoms. They work for schizophrenic and bipolar disorder
78
What are the two types of anti-psychotic drug?
Typical (first generation/chlorpromazine) and atypical (second generation/clozapine)
79
What are typical anti-psychotic drugs?
They are used to primarily treat positive symptoms. After taking the drug, hallucinations and delusions usually go within a few days, though other symptoms may last longer
80
How do typical anti-psychotic drugs work?
They are dopamine antagonists-they bind to D2 receptors (without stimulating them) in the mesolimbic pathway, therefore stopping dopamine being received by the post-synaptic neurone, therefore blocking dopamine activity. It has been estimated that 60-75% of D2 receptors need to be blocked for it to work, meaning dopamine pathways in other parts of the brain are also affected
81
What can typical anti-psychotic drugs lead to?
Extrapyramidal side effects. These mimic symptoms of Parkinson's disease (parkinsonian). The other type is Tardive Dyskinesia. These side effects mean that patients may stop taking the drugs and schizophrenic symptoms return
82
What are atypical anti-psychotic drugs?
They have a beneficial effect on negative symptoms and cognitive impairment as well as positive symptoms. They also have a lower risk of side effects
83
How do atypical anti-psychotic drugs work?
They also bind to D2 receptors but they rapidly dissociate to allow normal transmission to resume-this is what reduces side effects. They also work on serotonin receptors
84
What makes second generation anti-psychotic drugs seem better?
They only temporarily bind to D2 receptors so there are less side effects, meaning the patients are more likely to continue to take them and so are more likely to see an improvement in their symptoms
85
Although second generation anti-psychotics seem to be better, what does evidence show?
A meta analysis by Crossley found there was no difference in the efficacy of the two types. Those taking typical had more extrapyramidal symptoms but those taking atypical gained more weight
86
What was other research for anti-psychotics generally?
Leucht et al carried out a meta analysis of 65 studies (1959-2011) involving nearly 6000 patients that had all been stabilised on either typical or atypical anti-psychotics. Some were taken off their medication and given a placebo while the remaining patients remained on their regular anti-psychotic. Within 12 months, 64% of those given the placebo had relapsed, compared to 27% of those who stayed on the anti-psychotic drug
87
What is another evaluation point for anti-psychotics?
Motivational deficits. Ross and Read argue that when people are prescribed anti-psychotic medication, it reinforces the view that there is 'something wrong with them'. This prevents the individual from thinking about possible stressors that might be possible for their condition. This reduces their motivation to look for possible solutions that might alleviate these stressors and reduce their suffering
88
What are the psychological treatments of schizophrenia?
Family therapy, token economy and CBTp
89
What is family therapy?
It is aimed at reducing expressed emotion (linked to relapse). The patient is at the centre of their own treatment but all family members are encouraged to listen to each other. Families are provided with information about schizophrenia, how to support a schizophrenic family member and resolving practical problems. There are a range of interventions aimed at different family members of the patient, and it is not a 'one size fits all' approach. Also there should be at least 10 sessions lasting between 3 and 12 months
90
What does NICE recommend about family therapy?
NICE recommended it should be offered to all patients in touch with family, and it should be a priority for those at high risk of relapse
91
What is the link between etiology and treatment for family therapy?
Poor relationships/high EE means more likely to relapse. Therefore the aim of family therapy is to improve relationships, by supporting carers in reducing stress in the home. The long term outcome of someone suffering from schizophrenia has been found to be profoundly influenced by their family
92
What are some of the strategies used in family therapy?
Psychoeducation (helping the person and their carers to understand and be better able to deal with the illness). Forming alliance with relatives who care for the patient with schizophrenia. Maintaining reasonable expectations. Reducing emotional climate and burden of care for family members
93
What is supporting research for family therapy?
Garety found that the relapse rate halved for those in family therapy compared to those who are not. Also Pharoah et al reviewed RCT studies from Asia, Europe and North America where patients had family therapy, or just antipsychotic drugs
94
What is an RCT study?
Randomised controlled trials
95
What things did Pharoah et al look at in the study?
Mental state, compliance with medication, social functioning and relapse and readmission
96
What were Pharoah et al's findings on mental state?
Overall impression was mixed. Some studies reported an improvement in the overall mental state of patients compared to those receiving standard care, whereas others did not
97
What were Pharoah et al's findings on compliance with medication?
The use of family intervention increased patients compliance with medication
98
What were Pharoah et al's findings on social functioning?
Although appearing to show some improvements on general functioning, family intervention did not appear to have much of an effect on more concrete outcomes
99
What were Pharoah et al's findings on relapse and readmission?
Reduction in risk of relapse and a reduction in hospital admission
100
What is a conclusion of Pharoah et al's study?
It could actually be evidence for the effect of biological treatments as it could be the medication that was affecting the results rather than the family therapy
101
However, what were the methodological issues with Pharoah et al's study?
There are problems with random allocation as a large number of studies in this review had been from the People's Republic of China, and evidence from many of these studies show that random allocation had not actually happened where they said that it had. Also there was a lack of 'blinding' where observer bias could have affected results. 10 studies did not use blinding, and a further 16 did not state whether they had or hadn't used blinding
102
What is a strength of family therapy for society as a whole?
It has economic benefits as it reduces relapse and readmission rates which saves costs (shown by the NICE review of family therapy studies)
103
Although Garety found support for family therapy, what is a limitation of the findings?
They failed to show any difference in relapse between those in family therapy and those with carers at home-the only difference was between those with and without family. This suggests that it isn't family therapy that is effective, it is just having a family. Garety et al suggest that for many people, family intervention may not improve outcomes further than a good standard of treatment as usual
104
Who does family therapy help?
It helps the whole family, which is a strength as drug therapy just helps the patient
105
How does family therapy and biological therapies (both using antipsychotic drugs) treat schizophrenia?
By focusing on, and reducing, positive symptoms
106
How does token economy treat schizophrenia?
By focusing on negative symptoms and is aimed at encouraging patients to lead 'normal' lives
107
What is token economy based on?
It is therapy based on the idea of operant conditioning, with elements of classical conditioning, and centres on the use of reinforcement to encourage desirable behaviour
108
What is a brief outline of operant conditioning?
Reinforcement (positive or negative) to encourage behaviour, and punishment (positive or negative) to discourage behaviour
109
What is a brief outline of classical conditioning?
Learning through association (UCS=UCR then UCS+NS=UCR then eventually CS=CR)
110
Token economy involves what type of reinforcers?
Primary reinforcers and secondary reinforcers. Primary reinforcers are rewards, and secondary reinforcers are things that are associated with the reward-they are the tokens, they have no value on their own until they are associated with a reward
111
Who introduced token economy to the treatment of schizophrenia?
Nathan Azrin used token economy therapy for managing female schizophrenic patients in a hospital based setting in America. Before the therapy patients would not get involved in day to day activities eg brushing hair or teeth, or engage in social interactions. During the therapy they could earn tokens for positive behaviour. The tokens were embossed with 'one gift' and could be exchanged for privileges such as watching a film, or getting nice food. The desirable behaviour increased as a result
112
What is the procedure for token economy?
Patients engage in desirable behaviour and reduces inappropriate behaviour. Then given tokens for engaging in these behaviours (should be immediate at first). The patient can then trade the token for a desirable item or privilege (too much time between the token and reward could negatively affect the efficiency, and there should be a variety of options offered for rewards to increase efficiency). Tokens are paired with rewarding stimuli and become secondary reinforcers. Then the cycle repeats
113
What are the evaluation points for token economy?
Research support, difficulties assessing the success of a token economy, less useful for patients living in the community, ethical concerns and does it actually work
114
How is research support an evaluation point for token economy?
Dickerson et al found token economy systems were effective in a psychiatric setting. 11/13 studies showed a positive result. This shows it is a good treatment to target negative symptoms and in increasing adaptive behaviours of patients. However he did point out there are methodological issues in assessing token economy
115
How is 'difficulties in assessing the success of a token economy' an evaluation point for token economy?
It would be too unethical to have a control group (because in a institution setting all patients should be included) and so there is no group to compare results with and so a major weakness is that many of the studies into the effectiveness are uncontrolled (Comer)
116
How is 'less useful for patients living in the community' an evaluation point for token economy?
Token economy has been showed to be less useful for those that are not in hospitals as patients in psychiatric ward setting receive 24 hour care so there is better control for staff to monitor and reward patients appropriately. Patients in the community only receive care for, at most, a couple hours a day and so the token method could only be used for part of the day and so even if it did work, the results may not continue outside that care setting. This means it is not an effective treatment for all patients with schizophrenia
117
How is 'ethical concerns' an evaluation point for token economy?
Token economy has been criticised based on ethical grounds. Critics have argued that it breaks basic human rights to things such as the right to food, and privacy, as these things are held back to be used as rewards (primary reinforces)
118
How is 'does it actually work?' an evaluation point for token economy?
A lack of randomised trials to support the use has led to a decline in the use of such approaches to treatment in today's society as we are very evidence driven when it comes to using treatments. However this doesn't mean that the therapy is not important or effective, but the lack of evidence leads to an inconclusive answer of wether they should be used or not. Therefore we need more research to answer whether it should or should not be used for schizophrenia
119
What is cognitive behavioural therapy?
A combination of cognitive therapy (a way of changing maladaptive thoughts and beliefs) and behavioural therapy (a way of changing behaviour in response to these thoughts and beliefs)
120
What is the basic assumption of CBTp?
That people often have distorted beliefs, which influence their feelings and behaviours in maladaptive ways. Eg someone with schizophrenia may believe their behaviour is being controlled by someone or something else. Delusions are though to result from faulty interpretations of events, and CBTp is used to help the patient identify and correct these faulty interpretations
121
How is CBTp delivered?
It can be delivered in groups, but it is more usual that it is delivered on a one to one basis. NICE recommended at least 16 sessions when used in the treatment of schizophrenia
122
What is the aim of CBTp when used in this context?
To help people establish links between their thoughts, feelings, or actions and their symptoms and general level of functioning. By monitoring their thoughts, feelings or behaviour with respect to their symptoms, patients are better able to consider alternative ways of explaining why they feel and behave in the way that they do. This reduces distress and so improves functioning
123
What is the nature of CBTp?
Patients encouraged to trace back origins of their symptoms to get better idea of how they may have developed. Also encouraged to evaluate content of delusions or any voices, and to consider ways they might test validity of their faulty beliefs. Patients may be set behavioural assignments so they might improve their general level of functioning. The learning of maladaptive responses to life problems is often result of distorted thinking by the schizophrenic or mistakes in assessing cause and effect. During CBTp the therapist lets patient develop own alternatives to previous maladaptive beliefs, ideally by looking for alternative explanations and coping strategies already present in patient's mind
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How does CBTo work?
It usually proceeds through the following stages: assessment, engagement, the ABC model, normalisation, critical collaborative analysis, and developing alternative explanations
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What is assessment in CBTp?
Patient expresses their thoughts about their experiences to the therapist. Realistic goals for therapy are discussed, using patient's current distress as motivation for change
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What is engagement in CBTp?
Therapist empathises with patient's perspective and their feelings of distress, and stresses that explanations for their distress can be developed together
127
What is the ABC model in CBTp?
Patient gives their explanation of the activating events that appear to cause their emotional and behaviour consequences. The patient's own beliefs, which are actually the cause of C can then be rationalised, disrupted and changed. Eg the belief that 'people won't like me if I tell them about my voices' might be changed to a more healthy belief eg 'some may, some may not, Friends may find it interesting'
128
What is normalisation in CBTp?
Information that many people have unusual experiences such as hallucinations and delusions under many different circumstances reduces anxiety and sense of isolation. By placing psychotic experiences on a continuum with normal experiences, the patient feels less alienated and stigmatised and the possibility of recovery seems more likely
129
What is critical collaborative analysis in CBTp?
Therapist uses gentle questioning to help patient understand illogical deductions and conclusions. Eg 'if your voices are real, why can't other people hear them?' Questioning can be carried out without causing distress, provided there is an atmosphere of trust between patient and therapist, who remains empathetic and non-judgemental
130
What is developing alternative explanations in CBTp?
Patient develops own alternative explanations for their previously unhealthy assumptions. These healthier explanations may have been temporarily weakened by their dysfunctional thinking patterns. If the patient is not forthcoming with alternative explanations, new ideas can be constructed in cooperation with the therapist
131
What are the evaluation points for cognitive behavioural therapy?
Advantages of CBTp over standard care, effectiveness of CBTp is dependent on stage of disorder, lack of availability of CBTp, problems with meta-analyses of CBTp as a treatment for schizophrenia, and the benefits of CBTp may have been overstated
132
How is 'advantages of CBTp over standard care' an evaluation point for cognitive behavioural therapy?
NICE review of treatments for schizophrenia found consistent evidence that, when compared with standard care (antipsychotic medication alone), CBTp was effective in reducing re-hospitalisation rates up to 18 months following end of treatment. It was also shown to be effective in reducing symptom severity, and when compared to standard care, there was evidence for improvements in social functioning. However most studies of effectiveness of CBTp have been conducted with patients treated at same time as antipsychotics so it's difficult to assess effectiveness of CBTp independently
133
How is 'effectiveness of CBTp is dependent on stage of disorder' an evaluation point for cognitive behavioural therapy?
CBTp appears more effective when made available at specific stages of disorder and when delivery is adjusted to the stage the individual is currently at. Eg Addington and Addington claim in the initial acute phase, self-reflection is not particularly appropriate. Following stabilisation of psychotic symptoms with antipsychotics, however, individuals can benefit more from group-based CBTp. This can help normalise their experience by meeting other individuals with similar issues. Research has consistently shown it is individuals with more experience of their schizophrenia and greater realisation of problems that benefit more from individual CBTp
134
How is 'lack of availability of CBTp' an evaluation point for cognitive behavioural therapy?
Despite being recommended by NICE as a treatment for people with schizophrenia, it is estimated that in UK only 1 in 10 of those who could benefit get access to it. This is even lower in some areas of the country. Haddock et al's survey of North West of England found that of 187 randomly selected schizophrenia patients, only 6.9% had been offered CBTp, and of those offered it as a treatment, a significant number either refuse of fail to attend these sessions, so limiting its effectiveness even more
135
How is 'problems with meta-analyses of CBTp as a treatment for schizophrenia' an evaluation point for cognitive behavioural therapy?
One reason why meta-analyses in this area can reach unreliable conclusions about CBTp effectiveness is failure to take into account study quality. Some studies fail to randomly allocate participants to CBTp or control condition, others fail to mask treatment condition for interviewers carrying out the assessments of symptoms and general functioning. Despite such differences and failing, all studies are grouped together for a meta analysis. Jüni et al concluded there was clear evidence that problems associated with methodologically weak trials translated to biased findings. Wykes et al found that the more rigorous the study, the weaker the effect of CBTp
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How is 'the benefits of CBTp may have been overstated' an evaluation point for cognitive behavioural therapy?
More recent and methodologically sound meta-analyses of effectiveness of CBTp as sole treatment for schizophrenia suggest its effectiveness may be lower than originally thought. A recent large scale meta analysis found only a 'small' therapeutic effect on key symptoms of schizophrenia, such as hallucinations/delusions. However, even these small effects disappeared when symptoms were assessed 'blind'. Many studies of effectiveness of CBTp appear to have similar design problems, and in their meta-analysis, this uncertainty over whether non-drug therapies such as CBTp really do offer superior outcomes to antipsychotic medication has led to conflicting recommendations even within UK. In England and Wales, NICE emphasise non-drug therapies, but Scotland emphasise antipsychotic medications
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What is the interactionist approach to schizophrenia?
The diathesis-stress model, which sees schizophrenia as the result of an interaction between biology and environmental influences. Family studies suggest people have varying levels of inherited genetic vulnerability to schizophrenia, from very low to very high. However, whether or not the person develops schizophrenia is partly determined by this vulnerability and also patly by among and level of stresses they experience over their lifetime
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What is the diathesis part of the diathesis stress model?
The genetic component in terms of vulnerability. Twin studies and adoption studies support the idea of a genetic role for schizophrenia. However in about 50% of identical twins in which one twin is diagnosed with schizophrenia, the other never meets the diagnostic criteria. This disconcordance among identical twins indicates the tole of environmental factors as well
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What is the stress part of the diathesis stress model?
Stressful life events can trigger schizophrenia and explain the concordance rates in twins. Varese et al found that if someone experiences a traumatic event before the age of 16, they are three times more likely to develop schizophrenia. Research has also suggested high level of urbanisation associated with increased risk of developing a range of different psychoses including schizophrenia. A meta-analysis by Vassoss et al found risk for schizophrenia in most urban areas was estimated 2.37 times higher than in most rural environments, but the reason for this is unclear, though possible it may be due to more adverse living conditions of densely populated areas may be a contributory factor. The relationship between urban stress and schizophrenia is conditional on some other factor eg biological vulnerability for schizophrenia
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What is the additive nature of diathesis of stress?
Several ways in which a combination of diathesis and stress can lead to onset of schizophrenia. Eg relatively minor stresses may lead to onset of disorder for individual who is highly vulnerable, or major stressful event may cause similar reaction in person with low vulnerability. Whatever the combination, this idea pre-supposes additivity (that diathesis and stress add together in some way to produce the disorder)
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What is the key study into the interactionist approach for schizophrenia?
Tienari et al which tested the hypothesis that genetic factors moderate susceptibility to environmental risks associated with adoptive family functioning
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What was Tienari et al's study into diathesis stress?
By reviewing hospital records, Tienari investigated the combination of genetic vulnerability and parenting style (the trigger). Children adopted from 19,000 Finnish mothers with schizophrenia were followed up. Their adoptive parents were assessed for child-rearing style, and the rates of schizophrenia were compared to a control group. Style which had high levels of criticism and conflict and low levels of empathy was found to cause schizophrenia but only in those with high genetic risk. This is strong support for the interactionist approach and diathesis-stress model.
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What are the evaluation points for the interaction approach for schizophrenia?
Diathesis may not be exclusively genetic, urban environments are not necessarily more stressful, difficulties in determining causal stress, limitations of the Tienari et al study, implications for treatment
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How is 'diathesis may not be exclusively genetic' an evaluation point for the interaction approach for schizophrenia?
Risk could also result from brain damage caused by environmental factors. Verdoux et al found that complications at birth means child is four times more likely to develop schizophrenia
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How is 'urban environments are not necessarily more stressful' an evaluation point for the interaction approach for schizophrenia?
Unlike Vassos et al, Romans-Clarkson et al found no urban-rural differences in mental health among women in New Zealand. Other studies that have found urban-rural differences notes that these differences disappeared after adjusting for the socioeconomic differences for the two groups, suggesting although social adversity may be significant trigger for onset of schizophrenia, claims that social adversity and urbanisation are synonymous is likely an over-simplification
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How is 'difficulties in determining causal stress' an evaluation point for the interaction approach for schizophrenia?
Stressors early in life influence response to later stressful events and increase susceptibility. Eg Hammen argues maladaptive methods of coping with stress in childhood and through development means the individual fails to develop effective coping skills, which in turn compromises resilience and increases vulnerability. Ineffective coping skills may, therefore, make life generally more stressful for the individual and so trigger mental illness
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How is 'limitations of the Tienari et al study' an evaluation point for the interaction approach for schizophrenia?
Assessment of family function is only at one point fails to reflect developmental changes over time (Tienari acknowledged this). Also acknowledged that observing reciprocal interactions between adoptive and the adoptees makes it impossible to determine how much of the stress observed is assigned to the family and how much is actually caused by the adoptee him or herself
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How is 'implications for treatment' an evaluation point for the interaction approach for schizophrenia?
Børglum et al found that women infect with cytomegalovirus during pregnancy were more likely to have a child who developed schizophrenia, but only if both mother and child carried a particular gene defect. This suggests that anti-viral medicine during pregnancy may prevent onset of schizophrenia in offspring of women known to have this gene defect
