Schizophrenia Flashcards
1
Q
Classification of mental disorder:
A
The process of organising symptoms into categories based on which symptoms into categories based on which symptoms frequently cluster together.
2
Q
Schizophrenia:
A
A severe mental disorder where contact with reality and insight are impaired, an example of psychosis.
3
Q
Hallucinations:
A
A positive symptom of schizophrenia. They are sensory experiences that have either no basis in reality or are distorted perceptions of things that are there.
4
Q
Delusions:
A
A positive symptom of schizophrenia. They involve beliefs that have no basis in reality, for example, a person believes that they are someone else or that they are the victim of a conspiracy.
5
Q
Negative symptoms of schizophrenia:
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Atypical experiences that represent the loss of a usual experience such as a loss of clear thinking or a loss of ‘normal’ levels of motivation.
6
Q
Examples of negative symptoms:
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Avolition
Apathy
Slow movement
Change in sleep patterns
Poor grooming or hygiene
Difficulty in planning and setting goals
Speech poverty
Changes in body language
Lack of eye contact
Reduced range of emotions
A tendency not to interact with other people
Little interest in having hobbies
Little interest in sex.
7
Q
Speech poverty:
A
A negative symptom of schizophrenia. It involves reduced frequency and quality of speech.
8
Q
Avolition:
A
Negative symptom. Involves loss of motivation to carry out tasks and results in lowered activity levels.
9
Q
Co-morbidity:
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The occurrence of 2 disorders or conditions together, for example a person who has both schizophrenia and a personality disorder. Where 2 conditions are frequently diagnosed together it calls into question the validity of classifying the 2 disorders.
10
Q
Symptom overlap:
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Occurs when two or more conditions share symptoms. Where conditions share many symptoms this calls into question the validity of classifying the two disorders seperately.
11
Q
Positive symptoms of schizophrenia:
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Atypical symptoms experienced in addition to normal experiences. They include hallucinations and delusions.
12
Q
Positive symptoms examples:
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Hallucinations
Delusions
Disorganised thinking
13
Q
How to distinguish one disorder from another:
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Identify clusters of symptoms that occur together and classifying this as one disorder.
14
Q
Difference between ICD-10 (WHO) and DSM-5 (American psychiatric association’s diagnostic an statistical manual):
A
In DSM-5 one of the positive symptoms must be present for diagnosis whereas 2 or more negative symptoms or sufficient under ICD-10.
15
Q
ICD and DSM on subtypes:
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Both recognised subtypes (e.g paranoid schizophrenia), because they tended to be inconsistent.
16
Q
Diagnosis and Classification
+Good reliability:
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A psychiatric diagnosis is said to be reliable when different diagnosing clinicians reach the same diagnosis for an individual (inter-rater reliability) and when the same clinician reaches the same conclusion on two occasions (test-retest reliability). Flavia Osoria et al (2019) report excellent reliability for the diagnosis of schizo in 180 individuals using DSM-5
17
Q
Diagnosis and Classification
-Low validity:
A
One way to assess the validity of a psychiatric diagnosis is criterion validity. Elie Cheniaux et al (2009) had two psychiatrists independently asses the same 100 clients using ICD-10 and DSM-5 criteria and found that 68 were diagnosed with schizo under ICD and 39 under DSM.
18
Q
Diagnosis and Classification
-Co-morbidity:
A
Limitation- If conditions occur together a lot of the time then this calls into question the validity of their diagnosis and classification because they might actually be a single condition. Schizo may not exist as a distinct condition, and is a problem for diagnosis.
19
Q
Diagnosis and Classification
-Gender bias:
A
Men have been diagnosed more than women. One explanation is women are less vulnerable than men, perhaps due to genetics. It seems more likely that women are under diagnosed because they have closer relationships and get support. Women with schizo function better than men.
20
Q
Diagnosis and Classification
-Culture bias:
A
Some symptoms (hearing voices) have different meanings in different cultures. Afro-Caribbean say voices may be attributed to communication from ancestors.
21
Q
Genetic basis of schizo-
Family Studies:
A
Family studies have confirmed that risk of schizo increases with genetic similarity to a relative with the condition. The correlation represents nature AND nurture as they often tend to share a similar environment.
22
Q
Genetic basis of schizo-
Candidate genes:
A
Number of different genes are involved. Most likely genes would be those coding for neurotransmitters including dopamine.
23
Q
Genetic basis of schizo-
Candidate genes, Stephen Ripke et al (2014):
A
Combined all previous data from genome-wide studies of schizophrenia. The genetic make up of 37,000 people with a diagnosis of schizophrenia was compared to that of 113,000 controls, 108 separate genetic variations were associated with slightly increased risk of schizo.
24
Q
Neural correlates-
A
Patterns of structure or activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience.
25
Dopamine-
A neurotransmitter that generally has an excitatory effect and is linked to the sensation of pleasure. Unusually high levels are associated with schizophrenia and unusually low levels are associated with Parkinson's disease.
26
Genetic basis of schizo-
Role of mutation:
Genetic origin in the absence of a family history of the disorder. One explanation for this is mutation in paternal DNA which can be caused by radiation, poison or viral infection. Evidence comes from positive correlations between paternal age and risk of schizo.
27
Neural correlates of schizo-
Original dopamine hypothesis:
Based on a discovery that drugs used to treat schizo caused symptoms similar to those in people with Parkinson's disease, a condition associated with low DA levels, therefore schizo might be the result of high levels of DA in subcortical areas of the brain.
28
Neural correlates of schizo-
Kenneth Davis et al (1991)'s upated dopamine hypothesis:
Proposed the addition of the cortical hypodopaminergia (very low DA in brain's coretx). Low DA in the prefrontal cortex could explain cognitive problems. It has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia.
29
Neural correlates of schizo-
Howes at al (2017)'s upated dopamine hypothesis:
Both genetic variations and early experiences of stress, both psychological and physical, make some people more sensitive to cortical hypodopaminergia and hence subcortical hyperdopaminergia.
30
Biological explanation evaluation (genetic basis)-
Research Support:
Family studies such as Gottesman show that risk increases with genetic similarity to a family member with schizo. Adoption studies such as Pekka Tienari et al (2004) show that biological children of parents with schizo are at heightened risk even if they have been adopted. A twin study by Rikke Hilker et al (2018) showed a concordance rate of 33% for identical and 7% for non-identical twins.
31
Biological explanation evaluation (genetic basis)-
Environmental factors:
Include both biological and psychological influences. Biological risk factors include birth complications (Morgan et al 2017) and smoking THC-rich cannabis in teenage years (Di Forti et al 2015). Psychological risk factors include childhood trauma which leaves people more bulnerable mentally as adults. Nina Morkved at al (2017) 67% of people with schizo and related conditions had at least one childhood trauma as opposed to 38% of a matched group with no mental problems.
32
Biological explanation evaluation (genetic basis)-
Genetic Counselling:
Genetic counselling. If one of more potential parents have a relative with schizo, they risk having a child who will develop the condition. The risk estimate provided by genetic counselling is just an average figure. It will not really reflect the probability of a child going on to develop schizo becuase they wil experinece an environment which also has risk factors.
33
Biological explanation evaluation (neural correlates)-
Evidence for dopamine:
Amphetamines increase DA and worsen symptoms in people with schizo and induce symptoms in people without (Curran et al 2004). Also, antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms (Tauscher et al 2014). Thirdly, some candidate genes act on the production of DA or DA receptors.
34
Biological explanation evaluation (neural correlates)-
Glutamate, limitation:
Evidence for a central role of glutamate.
Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizo (McCutcheon et al 2020). Several candidate genes for schizo are believed to be involved in glutamate production/ processing.
35
Psychological explanation- Family dysfunction:
Abnormal processes within a family such as poor family communication, cold parenting and high levels of expressed emotion. These may be risk factors for both the development and maintenance of schizo.
36
Schizophrenogenic mother: Frieda Fromm-Reichmann (1948):
Proposed a psychodynamic explanation for schizophrenia based on the accounts she heard from patients. Fromm-Reichmann noted many patients had a 'schizophrenogenic mother', meaning schizo-causing. The Schizophrenogenic mother is cold, rejecting and controlling and tends to create a family environment of tension and secrecy.
37
Double-bind theory:
Bateson et al (1972) emphasised the role of communication style within a family. Developing children often find themselves in places where they fear doing the wrong thing but receive mixed msgs about what this is and cannot speak on the unfairness of it. When they 'get it wrong' the child is punished by withdrawal of love. This leaves them understanding the world as confusing/ dangerous which is reflected in symptoms like disorganised thinking and paranoid delusions. Not the only factor in schizo, just a risk factor.
38
What is expressed emotion and what is the elements?
Expressed emotion (EE) is the level of emotion, in particular negative emotion, expressed towards a patient by their carers who are often family members. Contains several elements:
-Verbal criticism of patient, maybe with violence.
-Hostility to patient, with anger and rejection.
-Emotional over-involvement in their life
39
How does expressed emotion effect chances of schizo?
High levels of EE directed towards the patient are a source of stress. This explains relapse in patients with schizo. It has been suggested that it may be a source of stress that can trigger the onset of schizo in a person who is already vulnerable (e.g genetic make-up).
40
Cognitive explanations-
Dysfunctional thinking:
Schizo is characterised by disruption to normal thought processing. Reduced thought processing in the ventral striatum is associated with negative symptoms, whilst reduced processing of info in the temporal and cingulate gyri are associated with hallucinations (Simon et al 2015).
41
Cognitive explanations-
Meta-representation dysfunction:
Frith et al (1992) identified two kinds of dysfunctional thought processes. 1st- meta-representation, cognitive ability to reflect on thoughts and behaviour. Dysfunction here would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves. Explains hallucinations, etc.
42
Cognitive explanations-
Central control dysfunction:
Frith et al also saw issues with the cognitive ability to suppress automatic responses while we perform deliberate actions. Speech poverty/ thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts.
43
Family dysfunction evaluation-
Research support:
Indicators of family dysfunction include insecure attachment and exposure to childhood trauma/abuse. According to Read et al (2005) adults with schizo are likely to have insecure attachment (type c or d). Read et al reported 69% of women, 59% of men with schizo have a history of physical/sexual abuse.
44
Family dysfunction evaluation-
Explanations lack support:
Almost no support for the importance of traditional family based theories such as the schizophrenogenic mother and double bind. Both theories are based on clinical observation of patients and informal assessment of the personality of mothers of patients but no systematic evidence.
45
Cognitive explanations evaluation-
Research support:
Stirling et al (2006) compared performance on a rage of cognitive tasks in 30 people with schizo and a control group of 30 people without. Tasks included the Stroop task where p/pants had to name font-colours of colour-words. As predicted by Frith's central control theory people with schizo took on average twice as long.
46
Cognitive explanations evaluation-
A proximal explanation:
They are proximal explanations because they explain what is happening now to produce symptoms not what initially caused it. What is unclear is how genetic variation or childhood trauma might lead to problems with meta-representation or central control.
47
Antipsychotics:
Dugs used to reduce the intensity of symptoms, in particular the positive symptoms, of psychotic conditions like schizophrenia.
48
Typical antipsychotics:
The first generation of drugs for schizo and other psychotic conditions, having been used since the 1950s. They work as dopamine antagonists and include chlorpromazine.
49
Typical antipsychotics dosage:
Can be taken as tablets, syrup or by injection. If taken orally it is administered daily up to a max of 1000mg, initially doses are much smaller and for most people the dosage is gradually increased to 400-800mg. Typical prescribed doses have declined over the last 50 years.
50
Dopamine antagonists:
Typical antipsychotics work by acting as antagnists in the dopamine system. Antagonists are chemicals which reduce the action of a neurotransmitter. Block dopamine receptors in the synapses of the brain, reducing the action of dopamine. Normalises neurotransmission in key areas of the brain reducing symptoms like hallucinations.
51
Sedation effect:
Chlorpromazine is also am effective sedative. Related to its effect on histamine receptors but it is not fully understood how this leads to sedation.
52
Atypical antipsychotics:
Drugs for schizo developed after typical antipsyschotics. They typically target a range of neurotransmitters such as sopmaine and serotonin. E.g clozpine and risperidone.
53
Clozapine:
Developed 1960s, trialed 1970s. It binds to dopamine receptors in the same way that chlorpromazine does, but in addition it acts on serotonin and glutamate receptors. This improves mood and reduces anxiety/depression and may improve cognitive functioning. Sometimes prescribed if patient is high suicide risk. 30-50% of people with schizo attempt suicide.
54
Why was Clozapine a problem?
It was withdrawn for a while in the 1970s following the deaths of some patients from a blood codition called agranulocytosis.
55
Risperidone:
1990S.
Developed in an attempt to produce a drug as effective as clozapine but without serious side effects. Lasts about two weeks. Believed to bind to dopamine and serotonin receptors. Binds more strongly to dopamine receptors than clozapine and is therefore effective in smaller doses.
56
Drug therapy evaluation-
Evidence for effectiveness:
Thornley et al (2003) reviewed studies comparing the effects of chlorpromazine to control conditions. Data from 13 trials with 1121 p/pants showed that chlorpromazine was associated with better oeverall functioning and reduced symproms compared to placebo. Meltzer (2012) concluded that clorapine is more effective than typical antipsychotics and other atypicals. It is effective in 30-50% of treatment-resisant cases where typical antipsychotics failed.
57
Drug therapy evaluation-
Limitation of evidence for effectiveness:
Healy (2012) suggested serious flaws w/ evidence for effectiveness. Most studies are short-term effects only and some successful trial published their data many times to exaggerate the evidenmce of positive effects. Their calming effects have positive effects on people experiencing schizo not reducing the severity of psychosis.
58
Drug therapy evaluation-
Serious side effects:
AP (antipsychotics)
Typical AP have side effects of dizziness, agitation, sleepiness, stiff jaw, weight gain, and itchy skin. Long-term use can result in tardive dyskinesia, causes involuntary facial movements. Most serious side effect is neuroleptic malignant syndorme, cuased when the drug blocvks dopamine action in the hypothalamus. NMS results in high temperature, delirium and coma and can be fatal.
59
Drug therapy evaluation-
Mechanism unclear:
Understanding of AP drugs is linked with the dopamine hypothesis, however we know that the original dopamine hypothesis is incomplete and that dopamine levels in other parts of the brain are too low rather than too high. If this is true then most APs should not work. Given that there are questions over the effectiveness of APs this adds to the argument.
60
Cognitive behaviour therapy (CBT):
A method for treating mental disorders based on both cognitive and behavioural techniques. From the cognitive viewpoint the therapy aims to deal with thinking, such as challenging negative thoughts. Includes behavioural techniques.
61
How does CBT help?
Helps clients make sense of how their irrational cognitions impact their feelings/behaviour. Explaining where symptoms come from, e.g voices in their head can't hurt them, it's just the malfunctioning speech centre. It will not eliminate symptoms, but make it easier to cope with- improves ability to function adequately. Normalisation- helping them understand understand it is only an extension of a noraml experience. Can tackle the anxiety/depression.
62
Family therapy:
A psychological therapy carried out with all or some members of a family with the aim of improving the communications within the family and reducing the stress of living as a family.
63
How family therapy helps:
Pharoah et al (2010) identified strategies that family therapists use to improve the functioning of the family:
-Reduces negative emotions: Reduce the level of emotion generally but especially bad emotions such as anger and guilt that create stress.
-Improves the family's ability to help: Encouraged family members to form a therapeutic alliance. Tries to improve families' beliefs and behaviour towards schizo. Ensure balance between craing for the schizo and having their own lives.
64
Burbach's (2018) model for working with families dealing with schizophrenia:
Begins with sharing basic info and providing emotional/practical support.
Phase 2 involves identifying resources including what family members can and can't offer.
Phase 3 encourages mutual understanding, creating a safe space for all family members to express feelings.
Phase 4 identifies unhelpful patterns of interaction.
Phase 5 is skill training such as learning stress management techniques.
Phase 6 looks at relapse prevention and phase 7 is maintenance for future.
65
CBT evaluation-
Evidence of effectiveness:
Jauhar et al (2014) reviewed 34 stuydeis of using CBT with schizo, concluding there is small but significant effects on both positive and negative symptoms. Pontillo et al (2016) found reductions in frequency and severity of audio hallucinations. NICE (2019) recommends CBT for schizo.
66
CBT evaluation-
Quality of evidence:
CBT techniques and schizo symptoms vary widely from one case to another. Thomas (2015) points out that different studies have involved the use of different CBT techniques and people with different combos of positive and negative symptoms. The overall modest benefits of CBT for schizo probably conceal a wide variety of effects of different CBT techniques on different symptoms.
67
Family therapy evaluation-
Evidence of effectivenes:
McFarlane (2016) concluded that family therapy was one of the most consistently effective treatments avaliable for schizo. In particuar relapse rates were found to be reduced by 50-60%. McFarlane also concluded that using family therapy as mental health declines is promising. Clinical advice from NICE recommends family therapy for everyone with a diagnosis of schizo.
68
Family therapy evaluation-
Benefits to the whole family:
Lobban and Barrowclough (2016) concluded that these effects are important because families provide the bulk of care for people with schizo. By strengthening the functioning of a whole family, family therapy lessens the negative impact of schizo on other family members and strengthens the family support.
69
Token economies:
A form of behavioural modification, where desirable behaviours are encouraged by the use of selective reinforcement. The tokens are secondary reinforcers and can then be exchanged for primary reinforcers- food/privileges.
70
Token economy in schizo-
Ayllon and Azrin (1968):
Trialled a token economy system in a ward of women with schizo. Every time p/pants carried out a task such as maing their bed or cleaning up they wre given a token with the words 'one gift'. These tokens could be swapped for ward privileges.
71
When were token economies primarily used?
In the 1960s and 70s when the norm for treating schizo was long-term hospitalisation.
72
Institutionalisation in schizo:
Develops under circumstances of prolonged hospitalisation. One outcome is that poeple often develop bad habits.
73
Insitutional behaviour Matson et al (2016):
Identified three categories of instituional behaviour commonly tackled by means of token economies: personal care, condition-related behaviours and social behavioiurs.
74
The 2 major benefits to Matson's categories of institutionalised behaviour:
-Improves the person's quality of life within the hospital setting, e.g makeup for someone who takes pride in their appearance.
-Normalises behaviour which makes it easier for peopple who have spent a time in hospital to adapt back into life in the community, e.g getting dressed in the morning or making their bed.
75
Theoretical understanding of token economies:
Token economies are an example of behaviour modification- a behavioural therapy based on operant conditioning. Tokens are secondary reinforcers because they only have value once the person recieving them has learned that they can be used to obtain meaningful rewards. Meaningful rewards are primary reinforcers.
76
Token economy evaluation-
Evidence of effectiveness:
Glowaki et al (2016) identified seven high quality studies published between 1999 and 2013 that examined the effectiveness of token economies for people with chronic mental illnesses and involved patients living in a hospital setting. All showed evidence of reduced negative symptoms.
77
Token economy evaluation-
Evidence of effectiveness, counterpoint:
Seven studies is rather small. One issue with a smaller number of studies is the file drawer problem. This phenomenon leads to bias towards positive published findings because undesirable results have been filed away.
78
Token economy evaluation-
Ethical issues:
It gives professionals considerable power to control the behaviour of people in the role of the patient. This inevitably involves imposing ones norms on another person which is problematic if target behaviours are not identified sensitively. Restricting the availability of pleasures means that seriously ill people have an even worse time.
79
Token economy evaluation-
Alternative approaches:
There are other approaches with a comparable evidence base that do not raise the same ethical issue. Chiang et al (2019) concluded that art therapy might be a good alternative. The evidence base is regularly small and has some methodological limitations, but it appears to show that art therapy is a high-gain low-risk approach to managing schizo. NICE guidelines recommend art therapy for schizo.
80
Interactionist approach:
A way to explain the development of behaviour in terms of a range of factors, including both biological and psychological ones. Most importantly such factors don't simply add together but combine in a way that can't be predicted by each one separately.
81
Diathesis-stress model:
Diathesis means vulnerability. The diathesis-stress model says that both a vulnerability to schizo and stress-trigger are necessary in order to develop the condition.
82
Meehl's diathesis model:
Meehl's model: the original diathesis-stress model diathesis was genetic, the result of a single 'schizogene'. Led to a biologically based schizotype personality, one characteristic is sensitivity to stress. Meehl says a person does not have the schizogene then no amount of stress would lead to schizo. Chronic stress through childhood especially in the presence of a schizophrenogenic mother, could result in the development of the condition.
83
Modern understanding of diathesis:
It is now clear that many genes each appear to increase genetic vulnerability only slightly. Also includes a range of factors beyond the genetic, including psychological trauma. Read et al (2001) proposed a neurodevelopmental model where the early trauma alters the developing brain.
84
Treatment according to the interactiontist appraoch Turkington et al (2006):
Point out that it is perfectly possible to believe in biological causes of schizo and still practice CBT to relieve psychological symptoms. This requires adopting an interactionist model- it is not possible to have a purely biological approach.
85
Interactionist approach evaluation-
Support for vulnerability and triggers:
Tienari et al (2004) investigated the impact of both genetic vulnerability and a psychological trigger. The study followed 19,000 Finnish children whose biological mothers had been diagnosed with schizo. In adulthood this high genetic risk group were compared to a control group of adoptees without a family of schizo. Found high levels of criticism, hostility and low levels of empathy were strongly associated with developing schizo but only in the high risk group.
86
Interactionist approach evaluation-
Diathesis and stress are complex:
Oversimplified.
Original model portrayed one schizogene and portrayed stress as schizophrenogenic parenting too simply. Multiple genes in multiple combinations. Stress also comes in many forms, including but not limited to dysfunctional parenting. Diathesis can be influenced by biological factors and stress can be biological. Houston et al (2008) showed in childhood sexual abuse emerged as the major influence on vulnerability to schizo and cannabis use.
87
Interactionist approach evaluation-
Real-world application:
Combning treatments enhance effectiveness. Tarrier et al (2004) randomly allocated 315 participants to 1) medication+CBT 2) medication+counselling or 3) control group, meds only. P/pants in combo groups showed lower symptoms following the trial than the medication-only group. No difference in hospital readmission.
88
Interactionist approach evaluation-
Real-world application, counterpoint:
Jarvis and Okami (2019) point out that saying that a successful treatment for mental disorder justifies a particular explanation is the logical equivalent of saying that because alcohol reduces shyness, shyness is caused by lack of alcohol. Treatment causation fallacy.
