Schizophrenia Flashcards

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1
Q

What is schizophrenia?

A

Schizophrenia is a mental disorder characterised by profound disruption of cognition and emotion
It is a type of psychosis in which thoughts and emotions are severely impaired
Schizophrenia affects an individuals perceptions, emotions, language and sense of self

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2
Q

What are positive symptoms of schizophrenia?

A

Positive symptoms…

  • Add to everyday experience e.g. having a hallucination
  • May be an excess or distortion of normal functions
  • E.g. hearing. voices or feeling like someone is spying on them
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3
Q

What are negative symptoms?

A

Negative symptoms…

  • Take away from everyday experience
  • Make it difficult to carry on with day to day activities
  • May be present without positive symptoms
  • E.g. speech poverty, avolition
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4
Q

What are the positive symptoms of schizophrenia?

A
  • Hallucinations
  • Disorganised speech
  • Delusions
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5
Q

What are the negative symptoms of schizophrenia?

A
  • Speech poverty/ alogia

- Avoliotion

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6
Q

What are the two main classification systems used to diagnose Sz?
Who published them and where are they used?

A
  • DSM-5: Diagnostic and Statistical Manual Edition 5, American publishers, used in USA
  • ICD-10: International Classification of Disease Edition 10, used in Europe
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7
Q

What is the DSM-5 criteria for diagnosis of schizophrenia?

A

Patient has experienced one or more of the positive symptoms that has caused problems with work, relationships or personal care. Disturbances need to have lasted approx. 6 months, with at least one month of symptoms.

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8
Q

What are classification systems used for?

A

Psychiatrists used classification systems to specify symptoms that should be shown if a diagnosis of schizophrenia is to be given

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9
Q

Do all classification systems have the same criteria that needs to be met for diagnosis?

A

No, they vary in criteria

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10
Q

What is the ICD-10 criteria for diagnosis of schizophrenia?

A

Two or more negative symptoms is sufficient under the ICD-10. ICD-10 recognises subtypes of Sz e.g. catatonic Sz

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11
Q

EVALUATION: What is a problem with reliability then classifying schizophrenia? (DSM and ICD)

A

An indicator of problems with reliability comes from differences. between DSM and ICD. They use different criteria to diagnose Schizophrenia so they can be inconsistent with each other.
(Lowers reliability)

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12
Q

EVALUATION: What is a problem with reliability when classifying schizophrenia? (Cheniaux et al)

A

2 psychiatrists diagnosed 100 patients
Psychiatrist 1: diagnosed 26% with Sz using DSM and 44% using ICD
Psychiatrist 2: diagnosed 13% with Sz using DSM and 24% using ICD
This suggests you are more likely to get a diagnosis with ICD which shows that the two classification systems are not comparable/ consistent with eachother
Decreases inter-rater reliability

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13
Q

EVALUATION: What is a problem with reliability when classifying schizophrenia? (Copeland 1971)

A

There are cultural differences
Study involved 194 British psychiatrists and 134 USA psychiatrists
They were given a description of a patient to diagnose
2% of British psychiatrists diagnosed Sz
69% of USA psychiatrists diagnosed Sz
This suggests that culture may influence diagnosis which decreases the internal validity of DSM and ICD as classification systems

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14
Q

EVALUATION: What is a strength of reliability when classifying schizophrenia?

A

The classification systems (DSM and ICD) are updated overtime
This means that the information is increasingly reliable due to new research and updated findings/ theories forming the basis of the classification systems
Whilst reliability is not at it’s best, it is improving and this leads to patients receiving better diagnosis and treatment

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15
Q

Validity definition?

A

Validity is whether it measures what it claims to measure
e.g. If DSM and ICD are valid systems to classify and diagnose Schizophrenia they will measure what they claim to measure (schizophrenia)

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16
Q

Inter-rater reliability definition?

A

Consistency between different clinicians e.g. if different clinicians look at the same set of symptoms, they should give the same diagnosis

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17
Q

Test-retest reliability definition?

A

Consistency over time e.g. a person presenting the same set of symptoms should receive the same diagnosis on different occasions

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18
Q

EVALUATION: What is a problem with validity when classifying schizophrenia? (gender bias - Broverman et al and Longnecker et al)

A

Research has shown that gender bias is a problem in the diagnosis of Sz

Broverman et al argued that DSM was based on what is classified as “normal” male behaviour, therefore women may be classed as unwell because they aren’t behaving in a “male” way rather than because they are ill

Further evidence to support the existence of gender bias in diagnosis of Sz comes from Longnecker et al: found that since 1980s, more men have been diagnosed than women. They argue that this may be because women tend to show better interpersonal functioning which may mask the need for a diagnosis of Sz

Gender bias influences diagnosis in more than one way -> problem because people may not receive appropriate diagnosis and care to manage symptoms

Validity is therefore questioned

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19
Q

EVALUATION: What is a problem with validity when classifying schizophrenia? (symptom overlap)

A

Some symptoms of Sz overlap with other disorders
E.g. both Sz and bipolar disorder have positive symptoms like delusions and negative symptoms like a-volition
This means under ICD a patient may be diagnosed a schizophrenic; however, many of same patients may receive a diagnosis of bipolar disorder according to DSM criteria
This suggests the two disorders may not be two different conditions, but one
Decreases validity of the classification and diagnosis of Sz, as it fails to measure what it claims to be measuring

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20
Q

EVALUATION: What is a problem with validity when classifying schizophrenia? (co-morbidity - Buckley et al)

A

Limitation:
Research shows that there are high co-morbidity rates when diagnosing patients with Sz
Buckley et al (2009) suggested 50% of patients diagnosed with Sz also had a diagnosis of depression or 47% substance abuse. PTSD also occurred in 29% of patients, and OCD in 23%
If conditions occur, they tend to occur together a lot of the time. This then calls into question the validity of their diagnosis and classification as they might be a single condition
The diagnosis of 50% having depression and schizophrenia suggests poor understanding of the difference between the two conditions. In terms of classification, it may be that if severe depression looks like Sz, they may be better as being seen as one single condition

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21
Q

What is co-morbidity?

A

Co-morbidity refers to more than one disorders or diseases that exist alongside a primary diagnosis, which is the reason a patient gets referred and/or treated

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22
Q

EVALUATION: What is a problem with validity when classifying schizophrenia? (cultural bias)

A

Research has shown that there is cultural bias in diagnosis
African American and English people of Afro-Caribbean origin are more likely to be diagnosed with Sz than white people, even though rates of Sz are not particularly high in Africa and the West-Indies
This suggests that diagnosis is almost certainly not due to genetic vulnerability, and more to do with culture bias issues. This could be due to the African culture being more accepting of hearing voices (example of a positive symptom) due to cultural beliefs of communication with ancestors. However when reported to a psychiatrist in Western culture, this is seen as irrational

EXTRA: Javier Escobar (2012) pointed out that overwhelmingly white psychiatrists may tend to over-interpret symptoms and distrust the honesty of black people during diagnosis.
Lowers generalisability (across cultures) and validity
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23
Q

Evidence that supports genetics (biological) explanations of Sz (Family studies - Gottesman)

A

Family study
Systematic investigation
As genetic similarity increases so does the probability of sharing Sz
e.g. % risk of developing Sz for different family members such as Mz twins is 48%, Dz twins is 17% , children is 13% and parents is 6%
Shows how genetic similarity and shared risk of Sz are closely related

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24
Q

Evidence that supports genetics (biological) explanations of Sz (Adoption Studies - Tienari et al 2000 - Finland)

A
Looked at 164 adoptees with biological mothers who were diagnosed with Sz, and 197 controls born to mothers without diagnosis of Sz
11 adoptees (6.7%) developed Sz compared to 4 (2%) of control adoptees
Shows that children of Sz patients are still at a heightened risk of Sz if adopted into families with no Sz
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25
Q

Evidence that supports genetics (biological) explanations of Sz (Sz is polygenic - Ripke et al 2014)

A

This study was carried out at molecular level

Showed that particular genetic variations significantly increase the risk of Sz

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26
Q

Strengths of evidence that supports genetic explanation of Sz (biological explanation)

A
  • drug treatment is used to help patients with Sz therefore Sz must have some link to genes APPLICATION
  • multiple sources of evidence for genetic vulnerability RELIABILITY
  • current genetic research gives a positive contribution into the nature/ nurture debate (how much contributes of each) which links to the interactionist explanation
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27
Q

Limitations of evidence that supports genetic explanation of Sz (biological explanation)

A
  • there are a no. of factors in the environment associated with risk of Sz e.g. family dysfunction (expressed emotion - refers to level of emotion shown to a patient by carers…high levels of neg EE act as a serious source of stress for patient)
  • if diagnosis isn’t correct (e.g. don’t have Sz or have a different disorder such as bipolar, which has similar positive symptoms), making a genetic link will also be false
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28
Q

What is the dopamine hypothesis?

A

Dopamine is a neurotransmitter (chemical messenger) involved in several brain systems, it appears to be involved in Sz. It has been suggested that both too little or too much dopamine might be associated with symptoms of Sz and that this may depend on the area of the brain involved

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29
Q

Original version of the hypothesis: definition of hypeERdopaminergia?

A

Concerns high levels of dopamine activity

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30
Q

Original version of the hypothesis: area of the brain involved?

A

Subcortex/ central areas e.g. Broca’s area

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31
Q

Original version of the hypothesis: functions of that area of the brain?

A

E.g. Broca’s area: speech production

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32
Q

Original version of the hypothesis: symptoms of Sz that may be involved?

A

Poverty of speech or auditory hallucinations

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33
Q

More recent versions of the hypothesis: definition of hypOdoperminergia?

A

Concerns low levels of dopamine activity

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34
Q

More recent versions of the hypothesis: area of the brain involved?

A

Prefrontal cortex

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35
Q

More recent versions of the hypothesis: functions of that area of the brain?

A

Thinking and decision making

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36
Q

More recent versions of the hypothesis: symptoms of Sz that may be involved?

A

Negative symptoms

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37
Q

Dopamine pathways

  • mesolimbic pathway
  • mesocortical pathway
A

Researchers have also looked at levels of dopamine in relation to pathways in the brain.
Mesolimbic: over activity and dopamine excess: associated with positive symptoms e.g. hallucinations (and some negative symptoms according to original hypothesis)
Mesocortical: dopamine deficit: associated with negative symptoms such as a-volition and apologia

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38
Q

Evaluation of the dopamine hypothesis: STRENGTH (drugs)

A

Research has shown that drugs that increase your levels of dopamine (e.g. amphetamines) produce psychotic (schizophrenic) symptoms
This is a strength because it shows there is a link between dopamine levels and psychotic symptoms
TMT drugs can control symptoms, which lends to increased RELIABILITY as there is supportive evidence

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39
Q

Evaluation of the dopamine hypothesis: WEAKNESS (drugs)

A

Clozapine is the most effective drug at reducing schizophrenic symptoms. It acts on serotonin as well as dopamine
This is negative because if drug effects both neurotransmitters, how do you know which one is the important one
Don’t know if level of serotonin or dopamine effects Sz symptoms
Questions VALIDITY as it is unfalsifiable

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40
Q

Evaluation of the dopamine hypothesis: WEAKNESS (high levels of dopamine could be symptom)

A

High levels of dopamine could be a symptom of Sz
This is a drawback because there is a problem with not knowing if it’s a cause or effect
Can’t manipulate Sz or dopamine so can’t find out
Decreases VALIDITY

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41
Q

Evaluation of the dopamine hypothesis: STRENGTH (anti-psychotic drugs)

A

Anti-psychotic drugs that reduce Sz do so by blocking this neurotransmitter to reduce the amount of it
This is a strength because it suggests dopamine levels play an important role in managing the symptoms of Sz
This increases the RELIABILITY of the dopamine hypothesis as a biological explanation of Sz

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42
Q

What is the neural correlates of schizophrenia?

A

Measurements of the brain that link/ correlate with symptoms of Sz. There are correlates for positive and negative symptoms and we can study them using brain imaging techniques such as fMRI and EEG scans

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43
Q

Neural correlates of negative symptoms:

  • part of the brain
  • symptoms linked to this area
  • summary of research
A
  • the ventral striatum
  • a-volition and loss of motivation
  • Juckel et al (2006) negative correlation between activity levels and severity of overall symptoms. Lower levels of activity in this area compared to controls
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44
Q

Neural correlates of positive symptoms:

  • part of the brain
  • symptoms linked to this area
  • summary of research
A
  • superior temporal gyrus and anterior cingulate gyrus
  • auditory hallucinations
  • Allen et al (2007) patients had to identify whether speech was theirs of someone else’s. Lower levels of activity in these areas compared to controls
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45
Q

However, other than the ventral striatum and the superior temporal gyrus & anterior cingulate gyrus, what is another neural mechanism linked to Sz?
What is the function of it and it’s role in Sz?
SHOWS COMPLEXITY OF SZ AND THEREFORE HARD TO EXPLAIN WITH JUST NEURAL EXPL. (ENVIRONMENTAL TOO?)

A
  • Prefrontal cortex
  • Helps logical thinking and organisation of thoughts
  • Many people with Sz have lower activity in this area which could be linked to delusions and disorganised thoughts
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46
Q

Drug treatments (biological treatments of Sz)

A

The dopamine hypothesis has linked levels of dopamine (neurotransmitter) with symptoms of Sz. Therefore drug treatment aims to alter dopamine levels in order to reduce symptoms

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47
Q

What is the broad term for the type of drug used to treat Sz symptoms?

A

Anti-psychotic

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48
Q

How do anti-psychotic drugs work?

A

By affecting D2 receptors in the brain

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49
Q

What are the two types of anti-psychotics?

A

Typical anti-psychotics and a-typical anti-psychotics

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50
Q
Typical anti-psychotics:
Chlorpromazine:
Date use began
Forms available
Dosage
How the drug affects dopamine levels
Symptoms treated and beneficial effects
Side effects (short and long term)
A
  • 1950s
  • Tablets, syrup (effective quicker), injection
  • Orally administrated daily: 400-800mg, maximum is 1000mg
  • Dopamine levels build up, but then it’s reduced. Block dopamine receptors in the synapses of the brain reducing the action of dopamine.
  • Reduces positive symptoms e.g. hallucinations. Given to anxious &/ agitated patients
  • Short term: shaking muscle spasm, stiffness
  • Long term: tardive dyskinesia or neural malignant syndrome
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51
Q
A-typical anti-psychotics:
Clozapine:
Date use began
Forms available
Dosage
How the drug affects dopamine levels
Symptoms treated and beneficial effects
Side effects (short and long term)
A
  • Early 1970s
  • Syrups and tablets
  • 300-450mg
  • Block D2 receptors, but this is temporary. Also works of serotonin and glutamate receptors
  • Helps cognitive symptoms e.g. depression and suicide
  • Have to get regular blood tests as risk of agranulocytosis (which can be fatal)
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52
Q
A-typical anti-psychotics: (most recent)
Risperidone:
Date use began
Forms available
Dosage
How the drug affects dopamine levels
Symptoms treated and beneficial effects
Side effects (short and long term)
A
  • 1990s
  • Tablets, syrups or injection that lasts about two weeks
  • Small dose is given initially & this is built up to a typical daily dose of 4-8mg & a maximum of 12mg
  • It binds to dopamine and serotonin receptors.
  • Effective in smaller doses, without serious side effects such as that of clozapine
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53
Q

Why can the a-typcial anti-psychotic drug risperidone be taken in smaller doses than the a-typical anti-psychotic clozapine?

A

This is because it binds more strongly to dopamine receptors than clozapine does and is therefore effective in smaller doses than most anti-psychotics

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54
Q

What are the three key features of the psychological explanation of Sz (family dysfunction)?

A
  • The schizophrenogenic mother
  • Double binds
  • Expressed emotion (EE)
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55
Q

Explain the schizophrenogenic mother (Fromm-Reichmann 1948)

A

Shcizophrenogenic means: sz causing
The characteristics of this type of mother are: cold, rejecting and controlling
The family climate tends to be tense with secrecy, this leads to distrust, which develops into paranoid delusions, which leads to Sz

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56
Q

Explain Double-Binds (Bateson 1956)

A

This is the theory that confusing communication is a risk factor for Sz (double bind communication was outlined as risk factor however, he was aware this wasn’t the only type of communication in families where someone experiences symptoms of Sz

57
Q

Double binds:

  • type of communication child receives
  • child’s feelings
  • effects of child “getting it wrong”
  • associated symptoms of Sz
A
  • mixed messages
  • fear of doing wrong thing and feel unable to comment on the situation or ask for classification
  • child is punished by withdrawal of love
  • feel the world is confusing and dangerous, may show some disorganised thinking and paranoid delusions
58
Q

What were the two key types of double bind communication between parents which could influence a child developing Sz that Lidz (1973) came up with?

A

Martial schism:
Parents emotionally distant, neither mother or father compromise, may be competition for children’ attention

Martial skew:
One parent dominant, the other submissive and yielding to over-bearing dominance of the other

59
Q

Explain expressed emotion (EE)

A

EE refers to the level of emotion shown to a patient by carers.
This explanation suggests that high levels of negative emotion act as a serious source of stress for patients

60
Q

What are the key aspects of negative EE?

A
  • verbal criticism sometimes with violence
  • hostility toward patient including anger and rejection
  • emotional over involvement including needless self-sacrifice
61
Q

What is the EE explanation mainly used to explain?

A

Relapse of Sz

62
Q

How can EE be used to explain onset of symptoms of Sz?

A

It might explain onset because the source of stress can act as a trigger to someone who has a genetic vulnerability

63
Q

Cognitive explanations of Sz:

Firth et al - Dysfunctional Thought Processing

A

Metarepresentation: ability to reflect on thoughts and behaviour. Dysfunction affects ability to recognise who is carrying out actions. Could explain thought insertion, hallucinations and delusions
Central control: ability to suppress automatic responses so we can carry out deliberate actions. Dysfunction could lead to disorganised speech and thought disorder because cannot suppress other thoughts interrupting and triggering others

64
Q

Evaluation of neural correlates of Sz WEAKNESS

A

The correlation-causation problem
Neural correlates of Sz are just correlates; we do not know whether they cause Sz or they are an effect of Sz
Evidence of activity levels in different parts of the brain doesn’t tell us whether activity levels are cause or effect or if it just happens alongside Sz. E.g. negative symptoms may be caused by low activity in the ventral striatum or low activity observed here is the result of reduced info processing due to some other factor
Therefore DECREASES INT. VALDITY

65
Q

Evaluation of neural correlates of Sz STRENGTHS (points)

A
  • insight into a range of factors
  • brain structure and neurotransmitter dopamine are involved
  • use of scanning and drug research adds to objectivity and measurability of research
66
Q

Evaluation of neural correlates of Sz WEAKNESSES (points)

A
  • range of evidence from many sources can make it difficult to assess evidence
  • evidence doesn’t tell us how environmental factors could play a role
  • difficult to resolve the correlation-causation problem
  • still need an explanation that incorporates all biological aspects
67
Q

Biological treatment of Sz EVALUATION: STRENGTH (atypical anti-psychotics)

A

Meltzer concluded that Clozapine was:
- more effective than both typical antipsychotics and other atypical antipsychotics
- effective in 30-50% of treatment resistant cases where typical antipsychotics have been ineffective
Drug therapy allows people to be treated as outpatients - not only effective, also appropriate way to reduce symptoms of Sz

68
Q

Biological treatment of Sz EVALUATION: STRENGTH (typical anti-psychotics)

A

Thornley et al: review of Chlorprozamine research
- examined effects of chlorpromazine by making comparisons to controls who received a placebo
Total of 13 trials with 1121 patients showed the drug was associated with reduced severity of symptoms and better overall functioning
Chlorprozamine was also associated with a lower relapse rate

69
Q

Biological treatment of Sz EVALUATION: WEAKNESS

A

Side effects
Typical anti-psychotics can lead to a wide range of side effects including sleepiness, stiff jaw, weight gain and itchy skin. Long term use can result in tardive dyskinesia - caused by dopamine super-sensitivity
Further, even though a-typical antipsychotics are meant to reduce side effects, some serious ones remain e.g. neuroleptic malignant syndrome (NMS)
Therefore, additional medication may be needed for the individual taking the anti-psychotics to manage the side effects
This shows effective treatment isn’t always appropriate
ETHICAL issues

70
Q

EVALUATION: family dysfunction STRENGTH (Read et al)

A
  • Reviewed 46 studies of child abuse and Sz

- 69% of women and 59% of men with schizophrenia had physical or emotional trauma or abuse in childhood

71
Q

EVALUATION: family dysfunction WEAKNESS (parent blaming)

A
  • Parent blaming: added trauma to the experience of caring for a child with a mental illness. No longer seen as appropriate as parents are key part of the team for community care.
    ETHICS
72
Q

EVALUATION: family dysfunction WEAKNESS (lack of evidence)

A

Lack of evidence for schizophrenogenic mothers and double binds (Lidz marital skew findings are not backed up)

73
Q

EVALUATION: family dysfunction WEAKNESS (retrospective research)

A

May record distorted memories

VALIDITY DECREASES

74
Q

EVALUATION: cognitive explanations STRENGTH: troop test

A

Stirling et al (2006) found that info processing is different in sz patients
Used stroop test on sz patients (30) and controls (18) and sz patients took over double the length of time to process the activity
SUPPORTS THE IDEA OF FAULTY PROCESSING…RELIABILITY

75
Q

EVALUATION: cognitive explanations STRENGTH: (CBT)

A

Success old cognitive therapies such as CBT was found by NICE (2014).
They found consistent evidence suggesting that by evaluating content of delusions CBT was more effective at treating and reducing symptoms than drugs
Because psychogical therapy was more effective than biological, lends support to psychological explanation of Sz as faulty information processing

76
Q

EVALUATION: cognitive explanations WEAKNESS: incomplete

A

Explains proximal causes of symptoms and doesn’t explain the origin of the condition and how it arises
Incomplete explanation doesn’t explain origins of Sz
VALIDITY

77
Q

EVALUATION: cognitive explanations WEAKNESS:

A

Explains one aspect of the disorder (cognitive impairment) but not neurochemical changes
Incomplete explanation as doesn’t explain biological aspects associated with Sz

78
Q

Psychological treatments of Sz

What is family therapy?

A

Based on family dysfunction explanations of Sz, this therapy works on the basis that certain factors lead to symptoms of Sz e.g: double bind communication and negative EE

79
Q

Psychological treatments of Sz

What are the aims of family therapy?

A

Broad Aims:
To involve families
To improve quality of communication and interaction between family members
To reduce stress that might add to risk of relapse and reduce levels of negative EE

80
Q

Psychological treatments of Sz

Duration of family therapy?

A

3-12 months (minimum 10 sessions)

81
Q

Strategies used by family therapists (6): Pharaoh et al (2010)

A
  1. Forming a therapeutic alliance with all family members
  2. Reducing the stress of caring for a relative with Sz
  3. Improving the ability of the family to anticipate and solve problems
  4. Reduction of anger and guilt in family members
  5. Helping family members achieve a balance between caring for the individual with schizophrenia and maintaining their own lives
  6. Improving families’ beliefs about and behaviour towards Sz
82
Q

What does Pharaoh et al suggest? (family therapy)

A

They suggest that the reduction of stress and expressed emotion helps to increase compliance wot medication. In turn, this helps to reduce relapse and hospital readmission.

83
Q

What is family therapy used in conjunction with?

A

Family therapy forms part of an overall treatment package used in conjunction with medication and outpatient care.

84
Q

KEY RESEARCH: Pharaoh et al (2010) Meta-Analysis of 53 studies of family therapy:

Countries involved and date of studies examined?

A

Countries involved: Europe, Asia and North America

Date of studies examined: Published 2002-2010

85
Q

KEY RESEARCH: Pharaoh et al (2010) Meta-Analysis of 53 studies of family therapy:

Measure of effectiveness (positives) and the effect of family therapy compared to standard therapy?

A

Compliance with medication: The use of family intervention increased patients compliance with medication

Relapse and readmission is reduced: There was a reduction in the risk of relapse and a reduction in hospital admission during treatment and in the 24 months after

86
Q

KEY RESEARCH: Pharaoh et al (2010) Meta-Analysis of 53 studies of family therapy:

Measure of effectiveness (negatives) and the effect of family therapy compared to standard therapy?

A

Mental state: the 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
Social functioning: Some general improvement but not much evidence of increased independent living or employment

87
Q

Outline evidence assessing the effectiveness of family therapy (methodological issues

A

Lack of random allocation in China: Wu et al suggest random allocation was not used

Possible observer bias: Because there were studies where no ‘blinding’ was used to prevent observers knowing which condition the participants were in (ie family therapy or standard care), it is possible that the results were biased

88
Q

Assess whether family therapy is effective or appropriate in the treatment of Sz:
EVAULATION: STRENGTH (NICE - cost savings)

A

Increased compliance and reduced relapse
Economic benefits NICE review 2009 showed cost savings when people received family therapy in addition to standard care eg lower hospital costs
Reduced stress also benefits other family members
Ethical problems are reduced as families work together rather than therapist controlling situation

89
Q

Assess whether family therapy is effective or appropriate in the treatment of Sz:
EVAULATION: WEAKNESS

A

Methodological problems make it difficult to assess effectiveness of family therapy eg how do you separate effects of other therapies? How long do the benefits last? Further follow up research is needed.
Family therapy cannot claim to ‘cure’ symptoms of Sz

90
Q

Assess whether family therapy is effective or appropriate in the treatment of Sz:
EVAULATION: STRENGTH (relapse rates)

A

Garety et al (2008) suggest that relapse rates of schizophrenics sit at approximately sit at approximately 25% when engaging in family therapy to reduce EE. This is compared to 50% relapse in those receiving standard care alone.

91
Q

Psychological treatments of Sz - Cognitive behavioural therapy

Assumptions of CBT

A
  • CBT stands for cognitive behavioural therapy
  • CBT was created by Beck, who suggested that psychopathological conditions were a result of faulty thinking and irrational beliefs
  • The aim of CBT is to identify the negative/ irrational thoughts and then discuss them
  • This often involves argument or discussion, and then the therapist helps the patient to consider realistic alternatives to their faulty beliefs
92
Q

Psychological treatments of Sz - Cognitive behavioural therapy

Examples of challenging faulty beliefs in CBT

A

“If your voices come from the radiator, why can’t anyone else hear them?”

93
Q

Psychological treatments of Sz - Cognitive behavioural therapy

Symptoms of Sz addressed by CBT

A

Irrational thoughts e.g. delusions and hallucinations

94
Q

Psychological treatments of Sz - Cognitive behavioural therapy

Role of therapist in CBT for Sz

A
  • Help patient identify and challenge irrational thoughts through argument and discussion
  • Talk about where symptoms come from -> can reduce fear of hallucinations and learn that delusions are not based on reality
  • They help patient develop alternative beliefs and coping strategies
95
Q

What does CBT lead to for Sz patients

A

Reduced anxiety and distress

96
Q

Psychological treatments of Sz - Cognitive behavioural therapy

STRENGTH of CBT: KEY RESEARCH - TURKINGTON ET AL (2004)

A

CBT has good effect on positive and negative symptoms of Sz

Some aspects can be delivered by nurses in brief intervention programmes

97
Q

Psychological treatments of Sz - Cognitive behavioural therapy

STRENGTH of CBT: KEY RESEARCH - JAUHAR (2014)

A

Meta-analysis of 34 studies

CBT had a small but significant effect on positive and negative symptoms

98
Q

Psychological treatments of Sz - Cognitive behavioural therapy

STRENGTH of CBT: KEY RESEARCH - NICE (2014)

A

CBT was more effective than just medication
CBT helped improve social functioning compared to people receiving standard care
CBT reduced rehospitalisation for up to 18 months after ending treatment
CBT can be effective when combined with medication
APPLICATION

99
Q

What do NICE do? (national institute for clinical excellence)

A

They make recommendations to government about what treatments are effective, their cost, etc.

100
Q

Psychological treatments of Sz - Cognitive behavioural therapy

WEAKNESS of CBT: effectiveness

A

Effectiveness of CBT is dependant on the stage of the disorder: more effective when made available at specific stages of the disorder, and when the delivery of the treatment is adjusted to the stage the individual is currently at
APPLICATION

101
Q

Psychological treatments of Sz - Cognitive behavioural therapy

WEAKNESS of CBT: availability

A

Availability varies: Haddock et al (2013) - in North West England only 13 of 187 randomly selected patients had been offered CBT for Sz
If availability is limited -> ethical implications -> if not available for everyone it also limits it’s effectiveness

102
Q

Psychological treatments of Sz - What are token economies? (manage Sz, not treat)

A

TE are systems that are used to MANG=AGE rather than treat some symptoms of Sz.
They are based on behaviourist principles of operant conditioning.

103
Q

What setting uses token economies?

A

Psychiatric hospitals, where patients have become institutionalised.

104
Q

What maladaptive behaviours may have developed, which has led to the need for TE systems in the psychiatric hospitals?

A
  • not getting dressed
  • poor hygiene
  • social withdrawal
105
Q

What is the intended outcome/ benefit of the token economy?

A
  • improved quality of life

- increased likelihood of living outside hospital setting

106
Q

What is the process of token economies?

A

Desirable behaviour for an individual patient is identified e.g. talking to other patients, showering or doing allocated house keeping tasks
Desirable behaviour is then targeted for reinforcement
Immediate reward is given to the patient when a desirable behaviour has been carried out
Immediacy of reward is important to prevent: “delay discounting”

107
Q

What is delay discounting (in token economy systems)?

A

A reduced effect of reinforcement because of a time delay

108
Q

What is the nature of the rewards?

  • immediate rewards
  • tangible rewards
  • secondary reinforcers
A

The immediate reward given takes the form of coloured tokens
Tokens have no monetary value, but can be swapped or exchanged later for more tangible rewards e.g. a walk outside, more pleasant accommodation
According to operant conditioning, tokens are seen as secondary reinforcers because they only have value after the patient has learned they can use them to obtain rewards

109
Q

Psychological treatments of Sz - Token Economy

Evaluation: STRENGTH - effectiveness -> application

A

Dickerson et al (2005) reviewed 13 studies - 11 reported beneficial effects (but methodical drawbacks were noted)
APPLICATION

110
Q

Psychological treatments of Sz - Token Economy

Evaluation: STRENGTH - appropriatness -> ethics and application

A

Patients behaviour becomes more socially acceptable promoting reintegration into society.
Suitable for use in institutions.

111
Q

Psychological treatments of Sz - Token Economy

Evaluation: WEAKNESS - effectiveness -> application

A

McMonagle and Sultana (2009) could only find 3 studies with random allocation of Ps to treatment and control gps. Only 1 study showed any improvement, and none gave any useful info re behaviour change.
Improvements seen may be due to increased staff attention not the token economy.

112
Q

Psychological treatments of Sz - Token Economy

Evaluation: WEAKNESS - appropriateness -> ethics and application

A

Doesn’t cure schizophrenia.
Patients with more severe symptoms find it most difficult to comply with token economy, so may experience discrimination in addition to symptoms. In USA legality has been challenged and use of token economies has reduced.
Issues of control re desirable behaviour and rewards given.
Not suitable for use in community.

113
Q

The interactionist (bio-social) approach to explaining Sz

What is the interactionist approach?

A

The interactionist approach is sometimes called the Bio-social approach because it includes biological, psychological and societal factors

114
Q

The interactionist (bio-social) approach to explaining Sz

What are the three factors in the development of Sz?

A

Biological factors
Psychological factors
Societal factors

115
Q

The interactionist (bio-social) approach to explaining Sz

Explain the biological factors in the development of Sz

A

Genetic vulnerability, neurochemical and neurological abnormality

116
Q

The interactionist (bio-social) approach to explaining Sz

Explain the psychological factors in the development of Sz

A

Stress e.g. resulting from life events and daily hassles including poor quality interactions in the family

117
Q

The interactionist (bio-social) approach to explaining Sz

Explain the societal factors in the development of Sz

A

e.g. Urbanisation

118
Q

The interactionist (bio-social) approach to explaining Sz

Explain how the diathesis-stress model attempts to explain how factors might interact to develop Sz

A
Diathesis = underlying vulnerability
Stress = acts as a trigger (a negative psychological experience

This leads to schizophrenia

119
Q

The interactionist (bio-social) approach to explaining Sz

In the original diathesis-stress model by Paul Meel (1962), what is the role of genetics?

A

Entirely genetic vulnerability.
Result of single schizogene.
Argued schizotypal personality had biologically based sensitivity to stress.
Without the gene, Sz could not develop.

120
Q

The interactionist (bio-social) approach to explaining Sz

In the original diathesis-stress model by Paul Meel (1962), what are the important stressors?

A
  1. Chronic stress through childhood and adolescence.

2. Presence of schizophrenogenic mother.

121
Q

The interactionist (bio-social) approach to explaining Sz

There is a modern understanding of the diathesis-stress explanation of Sz:

What does Ripke et al (2014) say about the role of genetics?

A

No single schizogene

Polygenic

122
Q

The interactionist (bio-social) approach to explaining Sz

There is a modern understanding of the diathesis-stress explanation of Sz:

What does Ingram and Luxton (2005) say about other vulnerabilities (not just genetics)?

A

Psychological trauma can be diathesis rather than stressor

123
Q

The interactionist (bio-social) approach to explaining Sz

There is a modern understanding of the diathesis-stress explanation of Sz:

What does Read et al (2001) say about other vulnerabilities (not just genetics)?

A

Proposed a neurodevelopmental model in which early trauma eg child abuse affects aspects of brain development. Hypothalamic-pituitary adrenal (HPA) system can become over active making person much more vulnerable to later stress

124
Q

The interactionist (bio-social) approach to explaining Sz

There is a modern understanding of the diathesis-stress explanation of Sz:

What is said about the role of cannabis being a psychological stressor?

A

Cannabis increases risk of Sz by 7x
Interferes with dopamine.
Not everyone develops Sz after smoking so this suggests also that there must be several vulnerability factors.

125
Q

The interactionist (bio-social) approach to explaining Sz

There is a modern understanding of the diathesis-stress explanation of Sz:

What does Houston et al (2008) suggest about other stressors?

A

Modern definition includes anything that risks triggering Sz

126
Q

The interactionist (bio-social) approach to explaining Sz

There is a modern understanding of the diathesis-stress explanation of Sz:

What could be a psychological stressor?

A

Eg stress resulting from parenting

127
Q

The interactionist (bio-social) approach to explaining Sz

Evidence to support the diathesis-stress explanation of Sz: Tienari et al (2004)

Aim and sample?

A

Aim: Investigated the combination of genetic vulnerability and parenting style (the trigger)
Sample: Children adopted from 19,000 Finnish mothers with Sz between 1960 and 1979

128
Q

The interactionist (bio-social) approach to explaining Sz

Evidence to support the diathesis-stress explanation of Sz: Tienari et al (2004)

Method?

A

Assessed adoptive parents’ child rearing style

Looked at children’s rates of Sz and compared this to a control group of adoptees who had no genetic risk of Sz

129
Q

The interactionist (bio-social) approach to explaining Sz

Evidence to support the diathesis-stress explanation of Sz: Tienari et al (2004)

Findings?

A

In the group of adoptees with high genetic risk of Sz, parenting style was implicated in development of Sz
The parenting style implicated was characterised by high levels of criticism and conflict, and low levels of empathy
This was not the case for the control group with no genetic risk of developing Sz

130
Q

The interactionist (bio-social) approach to explaining Sz

Evidence to support the diathesis-stress explanation of Sz: Tienari et al (2004)

Conclusions? How do these findings support the interactionist approach in explaining Sz?

A

Evidence suggests that genetic vulnerability and family related stress (triggers) are involved in the development of Sz
Genetically vulnerable children appear more sensitive to parenting behaviour

131
Q

The interactionist approach to treatment of Sz

What type of therapies do they use?

A

An interactionist approach incorporates both biological and psychological factors in Sz, therefore it is appropriate to use both biological (medication) and psychological therapies

132
Q

The interactionist approach to treatment of Sz

In the UK, what does a typical treatment combination include?

A

Anti-psychotic drugs and CBT

133
Q

The interactionist approach to treatment of Sz

What type of therapies are generally used with patients who are also receiving anti-psychotics?

A

Psychological therapies e.g. family, CBT and token economies

134
Q

The interactionist approach to treatment of Sz

How does the approach to treatment in the USA differ to the UK?

A

Medication without psychological therapy is more common in the USA
This is because there has been greater conflict between biological and psychological approaches to treatment for Sz in America.
As a result, the system in the USA has been slower to adopt an interactionist approach

135
Q

Interactionist approach to Sz

Evaluation: Tienari et al - supportive

A

Tienari et al is good supportive evidence for the interactionist approach to Sz
Shows genetic evidence for genetic vulnerability
Possible trigger (parenting style)
Suggests good validity?

136
Q

Interactionist approach to Sz

Evaluation: Strength - fuller explanation

A

Genetic explanation of Sz = gives an incomplete understanding of why someone might develop symptoms of schizophrenia.
Genetic approach does not explain elements that are not inherited eg Gottesman showed concordance rates of 46% when both parents had symptoms of schizophrenia, showing that greater genetic relatedness to someone with Sz is linked with increased likelihood of developing symptoms. This concordance rate is not 100%, so other factors must be involved.
A fuller explanation = taking an interactive approach to account for other factors eg early trauma and family dysfunction.
Diathesis-stress explanation gives greater insight into how they might interact together. Interactionist explanations using a diathesis-stress approach suggest that genetic factors are one type of vulnerability that can be triggered by stressors eg family dysfunction and cannabis use to contribute to the development of symptoms of Sz.

137
Q

Interactionist approach to Sz

Evaluation: Weakness - Original model = over simplified

A

We used toes vulnerability as purely biological and stress as psychological
However, recent evidence suggests that early trauma causes vulnerability and that biological events like cannabis smoking can be environmental stressors

138
Q

Interactionist approach to Sz

Evaluation: Weakness - we don’t know exactly how diathesis or stress work

A

May be that both particular genetics and early trauma make the developing brain less resilient to later stress but the precise mechanisms by which this might take place are unclear

139
Q

Interactionist approach to Sz

Evaluation: support for the effectiveness of combination therapies

A

Tarrier et al (2004)
315 patients randomly allocated to different treatment groups
- A. medication and CBT
- B. Medication and supportive counselling
- C. Control group (medication only)
Patients in the combination treatment groups showed lower symptom levels than those in the control group (no difference in rates of hospital readmission)