3 - Schizophrenia Flashcards

1
Q

Define schizophrenia

A

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. It affects an individual’s perceptions, emotions, language and sense of self.

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2
Q

What is a psychosis?

A

A severe mental disorder in which thought and emotions are so impaired that contact is lost with external reality

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3
Q

What is a positive symptom?

A

A symptom that adds to everyday experiences. This may be an excess or distortion of normal functions eg: hearing voices, hallucinations, feeling like someone is spying on them.
They can be present without negative symptoms.

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4
Q

What is a negative symptom?

A

A symptom that takes away from everyday experiences. This makes it difficult to carry on with day to day activities.

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5
Q

What is a hallucination?
Is it a positive or negative symptom?
Give some examples

A

An unusual sensory experience that can relate to all senses. This can be linked to what is happening in the environment or completely unrelated. They may distort what is actually there.
Positive symptom.
Eg: warping faces, poster turning to obscenities, jeering voices, smelling gas.

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6
Q

What is disorganised speech?
Is it a positive or negative symptom?
Give some examples

A

Disorganised speech reflects problems in organising thoughts. Derailment is one aspect of this - where a person may shift from topic to topic so that what they are saying doesn’t follow a coherent story.
Positive symptom.
Eg: “red change dog well”

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7
Q

What are delusions?
Is it a positive or negative symptom?
Give some examples

A

Firm but false beliefs that can take many forms.
Positive symptom.
Eg: delusions of grandeur, paranoid delusions, a person may feel chosen to complete a secret mission, government sending messages in the paper, martians are trying to poison water.

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8
Q

What is speech poverty?
What is it also known as?
Is it a positive or negative symptom?

A

Deficits in fluency of spoken language. Fewer words are spoken with less complex grammar. They also reflect blocked thoughts.
Alogia.
Negative symptom.

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9
Q

Define avolition
Is it a positive or negative symptom?
Give some examples

A

Lack of motivation for self-goals/self-directed purposeful activities. Apathy is also a part of this, and can lead to doing nothing for ages.
Negative symptom.
Eg: poor hygiene and grooming, unable to maintain a job or education, constant lack of energy.

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10
Q

State the 2 types of classification systems for schizophrenia.
Who published them?
What are their full names?
Where are they used?

A

DSMV (Diagnostic and Statistical Manual Edition 5).
Published by the American Psychiatric Association.
Used in the USA.

ICDX (International Classification of Disease Edition 10).
Published by the World Health Organisation.
Used in Europe.

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11
Q

What are the requirements of the DSM-5 needed to diagnose someone with schizophrenia?

A

The following 3 categories:
A: symptoms - 2 or more from:
Delusions, disorganised speech, grossly disorganised or catatonic behaviour, hallucinations, negative symptoms eg: avolition, alogia etc.
B: social/occupational dysfunction - problems affecting work, personal relationships or self-care.
C: duration - approx. 6 months of disturbances with at least 1 month of symptoms from category A.

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12
Q

How much of the global population are affected by schizophrenia?

A

Approximately 1%

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13
Q

What gender is more commonly diagnosed with schizophrenia?

A

Men

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14
Q

At what age are people commonly diagnosed with schizophrenia?

A

Late adolescence/early adulthood

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15
Q

A good classification system…

A

Should help professionals to diagnose Sz and suggest treatment to alleviate symptoms

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16
Q

If a diagnosis is not reliable…

A

It can’t be valid

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17
Q

Define inter-rather reliability

A

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

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18
Q

Define test-retest reliability

A

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

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19
Q

State 2 differences between DSM 5 and ICD 10

A

DSM 5: only 1 symptom needed for diagnosis.
ICD 10: 2 or more symptoms needed for diagnosis.
DSM 5: dropped subtypes of Sz when DSM 5 was published.
ICD 10: recognises subtypes of Sz. Eg: catatonic Sz.

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20
Q

List the 3 studies that are evidence for poor reliability in diagnosis of schizophrenia

A

Rosenhan (‘73): on being sane in insane places
Copeland (‘71): cultural differences - USA and UK
Cheniaux (‘09): diagnosis of 100 patients by 2 psychiatrists

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21
Q

Explain the procedure and findings of Rosenhan’s study on being sane in insane places. How did this show poor reliability in diagnosis?

A

He tested reliability of mental health diagnosis and the effect of labelling diagnoses.
Patients were interviewed and reported symptoms - they were admitted into an asylum but once they were in their symptoms ended.
Findings:
Initial study - no pseudo-patients were suspected by staff. 12 diagnosed with Sz and 1 for manic depression.
Follow up study - all were genuine patients - 193 arrived - 41 rated as pseudo-patients by 2 members of staff. 23 by psychiatrists and 19 by both.

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22
Q

Explain the procedure and findings of Copeland’s study on cultural differences. How does this show poor reliability in diagnosis?

A

It has cultural bias as he only looked at 2 Western societies and ignored all the other non-western societies.
USA and U.K. psychiatrists diagnosed Sz differently to each other.

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23
Q

Explain the procedure and findings of Cheniaux et al’s study on diagnosis of 100 patients by 2 psychiatrists. How does this show poor reliability in diagnosis?

A

2 psychiatrists independently diagnosed 100 patients using DSM and ICD. The inter-roster reliability was poor - 1 psych diagnosed 26 people with Sz (DSM) but another (ICD) diagnosed 22. Then the 2nd DSM psychiatrist diagnosed 13 and the second ICD diagnosed 24.
There is no consistency between classification systems.

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24
Q

Evaluate reliability in diagnosis and classification of schizophrenia

A
  • Rosenhan’s study highlighted reliability problems in diagnosis. The study showed there was a lack of consistency in diagnosis. This is because most of the patient who got sent to hospitals didn’t actually have Sz but they still got admitted to the ward. This suggests that there is a lack of reliability in diagnoses. Demonstrates hows people’s expectations alter their diagnosis.
  • cultural differences impact reliability (shown by Copeland). C.D also lower reliability of a diagnosis. This questions validity of the concept of Sz as it suggests that the understanding of it is not consistent across different cultures.
  • reliability problems in DSM and ICD. Inter-rather reliability. Different psychologists come to different conclusions using the same diagnosis method. Both DSM and ICD have problems diagnosing Sz reliably. But Cheniaux only based this on 2 psychologists.
    + reliability of diagnosis has improved. Critics say we shouldn’t generalise. Research findings may not reflect day to day diagnoses. Inter-rather reliability can be strengthen by using standardised assessment that improves diagnosis reliability. Moore recent studies have shown that the overall concordance rate between diagnosis is improved to 98% according to Jakobsen et al (‘05). The issues may be reducing over time.
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25
Q

Reliability is…

A

Consistency

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26
Q

If diagnosis is not reliable, it affects patients because…

A

They may be diagnosed and ‘labelled’ inaccurately and receive the wrong treatment or none at all.

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27
Q

Define validity

A

A test’s ability to measure what it is supposed to measure.

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28
Q

If DSM and ICD are valid systems to classify and diagnose schizophrenia they will… (3 things)

A

Define symptoms in a way that allows clear and objective diagnosis,
Define schizophrenia in a way that practitioners can use consistently,
Define schizophrenia in a way that makes it distinct from other disorders.

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29
Q

If the classification system lacks reliability, how will validity be affected?

A

A classification system cannot be valid if it is unreliable (a reliable system could still lack validity)

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30
Q

State the 4 main issues that affect the validity of DSM and ICD for diagnosis of schizophrenia

A

Symptom overlap
Co-morbidity
Gender bias
Cultural bias

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31
Q

Evaluate the validity of diagnosis and classification of schizophrenia

A
  • symptom overlap - the idea of + and - symptoms was created to make it easier to diagnose Sz. Bipolar and Sz both involved delusions and avolition.
  • co-morbidity - the concept that a single person can have more than one disorder at one time. Buckley (‘09) prompted that approx. Half of patients with Sz had depression or substance abuse. This is evidence for either the idea of co-morbidity of that one disorder instigates another. This decreases validity as it creates obscurities in diagnosis.
  • cultural bias - people of African origin are more diagnosed - in tribes it’s praised to hear voices (symptom of Sz). When they come to the West these “blessings” are diagnosed.
  • gender bias - Since 1980, more men have been diagnosed. Could be because we’re genetically vulnerable, or Cotton et al (‘09) found that female patients typically function better, more likely to work, have family relationships. Could explain why less have been diagnosed.
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32
Q

State the 3 studies that act as evidence that support a genetic influence on schizophrenia

A

Gottesman (1991) - family studies
Tiernari et al (200) - adoption studies in Finland
Ripke et al (2014) - Sz is polygenic

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33
Q

Explain Gottesman’s study about genetic influence on schizophrenia

A

Family study: He found that as genetic similarity increases, so does the probability of sharing schizophrenia. This shows how genetic similarity and shared risk of schizophrenia are closely related.

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34
Q

Explain Tienari et al’s study about genetic influence on schizophrenia

A

Adoption study in Finland: Children of schizophrenia sufferers still at heightened risk of schizophrenia if adopted into families with no history of schizophrenia. 164 adoptees who’s biological mothers had schizophrenia, and 197 without (control group). 11 adoptees (6.7%) developed schizophrenia compared to 4 (2%) from control group.

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35
Q

Explain Ripke et al’s study about genetic influence on schizophrenia

A

Schizophrenia is polygenic: huge study combing all previous data from genome wide studies.
Genetic makeup of 37,000 patients compared to 113,000 countries.
108 separate genetic variations associated with increased risk of schizophrenia.

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36
Q

Evaluate the genetic approach to explaining schizophrenia

A

+ multiple sources of evidence for genetic vulnerability (Gottesman, Tierani et al, Ripke et al).
+ positive correlation between paternal age and schizophrenia. Brown supports existence of genetics.
- psychological environment eg: stressful upbringing suggests biological explanations isn’t complete.
- Joseph (2014) said they stick schizophrenia orphans in selective places. This is contrary to popular beliefs that they aren’t selectively placed. But if foster families knew this, they wouldn’t want an Sz child.

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37
Q

What is dopamine?

A

A neurotransmitter involved in several brain systems. It appears to be involved in schizophrenia. It has been suggested that both too little or too much dopamine might be associated with symptoms of schizophrenia and that this may depend on the area or the brain involved.

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38
Q

Define hyperdopaminergia and hypodoperminergia.

Which is the original hypothesis and which is the more recent?

A

Hyperdopaminergia - concerns high levels of dopamine activity - original
Hypodoperminergia - concerns low levels of dopamine activity - more recent

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39
Q

What area of the brain is involved, and what is the function in:
The original version of the dopamine hypothesis,
The more recent version of the dopamine hypothesis.

A

Original - subcortex/central areas. Eg: Broca’s area - brain function.
Recent - prefrontal cortex - thinking and decision making.

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40
Q

What symptoms of schizophrenia may be involved in:
The original version of the dopamine hypothesis,
The more recent version of the dopamine hypothesis.

A

Original - poverty of speech or auditory hallucinations.

Recent - negative symptoms.

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41
Q

State and explain the 2 dopamine pathways in the brain

A

Mesolimbic pathway - over activity and dopamine excess is associated with positive symptoms.
Mesocortical pathway - dopamine deficit is associated with negative symptoms.

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42
Q

Evaluate the dopamine hypothesis and neural correlates of schizophrenia

A

+ research has shown that drugs increase levels of dopamine. Eg: amphetamines produce psychotic (schizophrenic symptoms). It shows dopamine charges lead to schizophrenia.
+ clozapine is the most effective drug at reducing schizophrenic symptoms. It acts on serotonin as well as dopamine. It shows that a drug can help lower the levels of dopamine in a person and this can help lower the levels of dopamine and this can help lower the strength of the symptoms a sufferer is going through.
- high levels of dopamine could actually be a symptom of schizophrenia. We don’t know if it’s cause or effect.
- an excess number of dopamine receptors have been found in Broca’s area which is linked to speech production and auditory hallucinations. This contradicts ideas that it aids brain function, acting as mixed evidence.

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43
Q

What are neural correlates of schizophrenia?

A

Measurements of the brain that link/correlate with symptoms of schizophrenia. 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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44
Q

Neural correlates of negative symptoms of schizophrenia;
What part(s) of the brain is involved?
What symptoms are associated with this?
Explain the research involved in this - is the higher or lower levels of activity in the area(s) compared to controls?

A

The ventral system
Avolition and loss of motivation
Juckel et al (2006) - negative correlation between activity levels and severity of overall symptoms. Lower levels of activity were found in this area compared to controls.

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45
Q

Neural correlates of positive symptoms of schizophrenia;
What part(s) of the brain is involved?
What symptoms are associated with this?
Explain the research involved in this - is the higher or lower levels of activity in the area(s) compared to controls?

A

Superior temporal gyrus and the anterior cingulate gyrus
Auditory hallucinations
Allen et al (2007) participants had to identify whether speech was there own or someone else’s. Lower levels of activity were found in these areas compared to controls.

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46
Q

What is the prefrontal cortex’s function and role in schizophrenia?

A

Helps logical thinking and organisation thoughts.
Many people with schizophrenia have lower activity in this area which could be linked to delusions and disorganised thoughts.

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47
Q

What are the visual cortex and auditory cortex’s functions and roles in schizophrenia?

A

Processes information received from the eyes and ears.
Schizophrenics have the same activity in these areas when they hallucinate as sane people do when they have genuine visual and auditory experiences.

48
Q

What is the basal ganglia’s function and role in schizophrenia?

A

Located deep inside the brain and affects movement and thinking skills.
Research has shown that this structure is larger in schizophrenics which could cause motor damage.

49
Q

What is the amygdala’s function and role in schizophrenia?

A

Responsible for basic feelings such as fear, lust and hunger.
This area is smaller in schizophrenics so can link to loss of emotion (affective flattening).

50
Q

Define affective flattening

A

Loss of emotion

51
Q

What is dopamine’s function and role in schizophrenia?

A

Responsible for feelings of pleasure and also affects thinking and movement.
Low levels in certain brain areas are linked to negative symptoms and a loss of pressure. High levels have also been linked to positive symptoms.

52
Q

1 positive evaluation point and 1 negative evaluation point for neural correlates of schizophrenia

A

+ there’s a range of supportive evidence. Goldman-Rakilc et al. found a role for low levels of dopamine in the prefrontal cortex. This shows supporting evidence that increases validity.
- the correlation-causation problem. We have no way of knowing neural correlates are correlation or causation. Eg: the correlation between levels of activity in the ventral striatum and negative symptoms of schizophrenia. Or there’s a 3rd factor involved. This reduces external validity.

53
Q

What is the biological treatment for schizophrenia?

A

Drug treatment

54
Q

The broad name for the type of drug used to treat symptoms of schizophrenia is…

A

Anti-psychotic

55
Q

What receptors in the brain do drugs affect?

A

Dopamine receptors

56
Q

What are the 2 types of anti-psychotics?

A

Typical anti-psychotics

Atypical anti-psychotics

57
Q

What are the example of a typical anti-psychotics and 2 examples of atypical anti-psychotics?

A

Chlorpromazine

Clozapine, risperidone

58
Q
Chlorpromazine:
Date use began
Form available
Dosage
Mode of action, are other neurotransmitters affected?
Symptoms treated and beneficial effects
Side effects
A

1950s
Tablets, syrup and injection. Syrup is quicker than tablets for sedative effects
400-800mg
Reduces dopamine levels, binds to dopamine receptors, no other neurotransmitters affected
Schizophrenia and bipolar symptoms, also acts as a sedative
Dry mouth, constipation, weight gain

59
Q
Clozapine:
Date use began
Form available
Dosage
Mode of action, are other neurotransmitters affected?
Symptoms treated and beneficial effects
Side effects
A

1970s
Tablet
450mg
Binds to dopamine, serotonin and glutamate receptors
Schizophrenic symptoms, improves mood, reduces depression. 30-50% of schizophrenics attempt suicide. This helps.
Constipation, muscle shrinkage, weight gain

60
Q
Risperidone:
Date use began
Form available
Dosage
Mode of action, are other neurotransmitters affected?
Symptoms treated and beneficial effects
Side effects
A

1990s
All 3
4-8mg
Binds to dopamine and serotonin receptors. More effective in smaller doses.
Schizophrenic, bipolar and autism symptoms.
Struggle to move, dizziness, other symptoms typical for anti-psychotic side effects.

61
Q

Explain evidence for effectiveness of typical antipsychotics in drug therapy for schizophrenia

A

Thornley et al (2003) reviewed chlorpromazine research. He examined effect of chlorpromazine by making comparisons to controls who received a placebo. 13 trials - 1121 participants showed the drug was associated with reduced severity of symptoms and better overall functioning. Chlorpromazine was also associated with a lower relapse rate.

62
Q

Explain evidence for effectiveness of atypical antipsychotics in drug therapy for schizophrenia

A

Meltzer (2012) concluded that clozapine was:
More effective than both typical antipsychotics and other artpical antipsychotics.
Effective in 30-50% of treatment resistant cases where typical antipsychotics have been ineffective.

63
Q

Evaluate drug therapy for schizophrenia

A

+ effective in reducing symptoms of Sz. Thornley’s research in typical anti-psychotics showed that the drug leads to better overall functions compared to a placebo. Meltzer’s research showed that chlorpromazine is 30-50% more effective than other drugs. People can be treated as outpatients not in hospitals, app.

  • methodological problems with research into effectiveness. Healy showed that positive effects may be been exaggerated coz the data was published multiple times he also said studies that show neg symptoms weren’t always published. He also highlighted design flaws in research, meaning doctors don’t get a full picture of the drugs they prescribe, app.
  • side effects (name some). Neuroplatic malignant syndrome can be fatal, ethics.
  • ethics. Moritz et al (2013) used patient self-report to conclude that drugs dampened emotions, not treating symptoms. Chemical cosh. Human rights abuse.
64
Q

What is the chemical cosh argument?

A

Where the drugs are frequently used to make life easier to work with patients and not to ease symptoms

65
Q

State the 3 key features of family dysfunction as a psychological explanation of schizophrenia

A

Schizophrenogenic mother
Double-binds
Expressed emotion

66
Q

Explain what Fromm-Reichmann did (1948)

A

Looked at the backgrounds and childhood of her patients using a psychodynamic perspective. She found that patients experiencing symptoms of schizophrenia often had what she called ‘schizophrenogenic’ mothers.

67
Q

Define schizophrenogenic

A

Causes schizophrenia

68
Q

State 3 characteristics of a schizophrenogenic mother

A

Cold, rejecting and controlling

69
Q

Explain how schizophrenogenia can cause schizophrenia

A

Typical family climate characteristics include tension and secrecy.
This leads to distrust which develops into paranoid delusions, causing schizophrenia.

70
Q

What did Bateson do in 1956?

A

Emphasised the role of communication style within the family. He outlined the double-bind communication as a risk factor in schizophrenia - he was clear this wasn’t the only communication style in families where someone experiences symptoms of schizophrenia.

71
Q

Explain how the double-bind works

A

The type of communication the child receives mixed messages - this is a risk factor. The child’s feels fear of doing the wrong thing and feel unable to comment on the situation or ask for clarification. If the child gets it wrong, the child is punished by withdrawal of love. Associated symptoms of schizophrenia include feeling the world is confusing and dangerous, they may show disorganised thinking and paranoid delusions.

72
Q

Who came up with 2 key types of double bind communication between parents which could influence a child developing schizophrenia?
What are they?

A

Lidz (1973)
Marital schism
Marital skew

73
Q

What is a marital schism?

A

Where parents are emotionally distant, neither mother or father compromise, may be for children’s attention

74
Q

What is a marital skew?

A

Where one apprentice is dominant and the other is submissive and yielding to over-bearing dominance of the other.

75
Q

Define expressed emotion

A

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

76
Q

Summarise the key aspects of negative expressed emotion

A

Verbal criticism, sometimes with verbal hostility towards the patient, including anger and rejection.
Emotional over-involvement including needless self sacrifice.

77
Q

What is the expressed emotion explanation mainly used to explain in regard to schizophrenia?

A

Relapse of schizophrenia

78
Q

Explain how expressed emotion can be used to explain onset of symptoms of schizophrenia

A

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

79
Q

Evaluate family dysfunction as a psychological explanation of schizophrenia

A

+ research support - Read et al (2005) reviewed 46 studies of child abuse and schizophrenia. 69% of women and 59% of men with schizophrenia has physical or emotional trauma/abuse in childhood. Berry et al (2008) found that adults with insecure attachments to primary carers are mor likely to have schizophrenia. Reliability.

  • lack of evidence. There’s lots of evidence to support broad principle, but not double bind or Szg mother. Both theories are based on clinical observation of patients and assessing personalities of mothers of patients for ‘crazy-making characteristics.’ Not approved by modern psychologists. Also, it naturally blames parents who are already suffering schizophrenic children. Ethics.
  • independent differences in EE vulnerability - not all patients in high EE families relapse and visa versa. Altorfer et al (1998) found that 25% patients studied showed no psychological responses to stressful comments from relatives. Vulnerability to EE influences could be psychological. Lebell et al (1993) suggests that how patients appraise relative behaviour is important where it’s not perceived as negative/stressful, they can prosper. Reliability.
  • no consideration for biology - bio and psych factors can separately produce the same symptoms. Are both outcomes really Sz? Although they can be viewed in terms of diathesis stress model - diathesis may be biological or psychological. Internal validity.
80
Q

What does the cognitive explanation of schizophrenia focus on?

A

The role of mental processes

81
Q

What is the ventral striatum’s role in the cognitive explanation of schizophrenia?

A

Reduced processing of this is associated with negative symptoms

82
Q

What are the temporal gyrus and cingulate gyrus’ roles in the cognitive explanation of schizophrenia?

A

Reduced processing of information in these areas are associated with hallucinations. This suggests cognition is impaired.

83
Q

What is the cognitive explanation of schizophrenia characterised by?

A

Disruption to normal processing and abnormal information processing

84
Q

State the 2 kinds of dysfunctional thought processing that could underlie some symptoms
Who theorised this?

A

Central control
Metarepresentation
Frith et al (1992)

85
Q

What is central control?

How is a kind of dysfunctional thought processing that could underlie some symptoms?

A

The cognitive ability to suppress automatic responses while we perform deliberate actions instead.
Disorganised speech and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts.

86
Q

What is metarepresentation?

How is it a kind of dysfunctional thought processing that could underlie some symptoms?

A

The cognitive ability to reflect on thoughts and behaviour.
This allows us insight into our own intentions and goals. Dysfunction in this would disrupt ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else. This would explain voice hallucinations and thought insertion (a type of delusion).

87
Q

Evaluate cognitive explanations of schizophrenia

A

+ Stirling et al (2006) found that info processing is different in Szs. He used the stroop test on 30 Szs and 18 controls. Szs took over twice as long. Reliability.
- biological and cofnivite explanation have been able to explain the same symptoms. Reliability
- only explains one aspect of the disorder (cognitive impairment) but no neurochemical changes. External validity
+ Sz symptoms include +ve symptoms associated with the mind (delusions and hallucinations). Reliability

88
Q

Define family therapy

A

Based on the family dysfunction of schizophrenia, this therapy works on the basis that certain factors lead to symptoms of schizophrenia eg: double bind communication and negative expressed emotion.

89
Q

What are the broad aims of family therapy?

How long does it last?

A

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 expressed emotion.
Duration: 3-12 months (minimum 10 sessions).

90
Q

State the 6 strategies used by family therapists.

Who developed these?

A

Pharaoh et al (2010).
1 - psychoeducation - helping the person and their careers to understand and be better able to deal with the illness.
2 - forming an alliance with relatives who care for the person with Sz.
3 - enhancing relatives’ ability to anticipate and solve problems.
4 - reducing expressions of anger and guilt by family members.
5 - maintains reasonable expectations among family members for patient performance.
6 - encouraging relatives to set appropriate limits whilst maintaining some degree of separation when needed.

91
Q
Explain Pharoah et Al’s meta-analysis:
How many studies?
Date?
From where?
What did it include?
A

53 studies of family therapy from 2002-2010 from Europe, Asia and North America.
He had measures of effectiveness and found the effect of family therapy on it compared to standard therapy.
Mental state - overall impression was mixed. Some reported improvement in overall mental state compared to those receiving standard care.
Compliance with medication - family interventions increased patients’ compliance.
Social functioning - general improvement, not much evidence of increased independent living or employment.
Relapse and re-admission - reduction in this in hospital during treatment and in the first 24 months after.

92
Q

What are the methodological problems with Pharoah et al’s study?

A

Lack of random allocation in China.
Wu et al suggest random allocation was not used.
Possible observer bias.
There were studies where no “blinding” was used to prevent observers knowing which condition participants were in.

93
Q

What did Gareth et al (2008) suggest?

A

That relapse rates of schizophrenics sit at approximately 25% when engaging in family therapy to reduce expressed emotion. This is compared to 50% relapse in those receiving standard care alone.

94
Q

What did the NICE review of family intervention studied (2009) show?

A

That use of therapies is associated with significant cost savings when offered to people in addition to standard care

95
Q

Evaluate family therapy; is this point related to effectiveness or appropriateness?

A

+ increased compliance and reduced relapse - E
+ economic benefits NICE review 2009 showed cost savings when people received family therapy in addiction to standard care eg: lower hospital costs - A
+ Reduced stress also benefits other family members - A
+ ethical problems are reduced as families work together rather than therapist controlling situations - 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 - E
- family therapy cannot claim to ‘cure’ Sz symptoms - E

96
Q

CBT stands for…
It was created by… who suggest…
The aim of it is…
This often involves…

A

Cognitive Behavioural Therapy
It was created by Beck who suggested that psychopathological conditions were a result of faulty thinking and irrational beliefs.
The aim of it 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.

97
Q

How does CBT work for schizophrenia?

A

Symptoms of schizophrenia addressed by CBT - irrational thoughts eg: delusions and hallucinations.
Role of therapist - help identify and change irrational thoughts through argument and discussion. Helps patient develop alternative beliefs and coping strategies. Helps reduce hallucinations and delusions. This reduces anxiety and distress.

98
Q

Explain the 3 key research studies of CBT

A

Tarkington et al (2004) - CBT has good effect on positive and negative symptoms of schizophrenia. Some aspects can be delivered by nurses in brief intervention programmes.
Jauhar (2014) - meta-analysis of 34 studies. CBT had a small but significant effect on positive and negative symptoms.
NICE (2014) (National Institute for Clinical Excellence) - CBT:
Was more effective than just medication,
Helped improve social functioning compared to people receiving standard care,
Reduces rehospitalisation for up to 18 months after ending treatment,
Can be effective when combined with medication.

99
Q

Evaluate CBT for schizophrenia

A

+ Jauhar et al reviewed 34 CBT studies and concluded that CBT has a significant but fairly small effect on both positive and negative symptoms - effectiveness.
- Only 1 in 10 in the UK benefit. Haddock et al (2013) in N.W. England - 187 randomly selected Szs, only 131 (6.9%) had been offered it. Freeman et al (2013) of those offered CBT, significant refuse/fail to attend therapy sessions.
+ comparison with drug treatment - CBT aims to make Sz more manageable and improve quality of life. However, there are problems separating effect of CBT and medication.
+ improving quality of life - patient has more active role in recovery. a CBT helps patients to manage and make more sense of their symptoms. Doesn’t cure Sz. This shows that CBT is appropriate, particularly when compared to side effect of drugs.
- challenging a person’s paranoia interferes with someone’s freedom of thought. Eg: challenging a patients’ belief in a highly controlling government, they can easily stray into modifying their politics.
- problems with meta-analyses - don’t account for study quality. Some studies don’t have random allocation or a control group. Juni et al (2001) said it leads to biased findings. Wykes et al (2008) found that more rigorous the study, the weaker CBT effect.

100
Q

What are token economies?

A

Systems used to manager rather than treat some symptoms of schizophrenia. They are based on behaviourist principles or operant conditioning.

101
Q

Give an overview of token economies. Include:
Setting,
Maladaptive behaviour developed,
Intended outcome/benefit.

A

Psychiatric hospitals, where patients have become institutionalised.
Not getting dressed, poor hygiene, social withdrawal, independence.
Improved quality of life, increased likelihood of living outside hospital setting.

102
Q

Evaluate token economies for schizophrenia

A

+ effectiveness - Dickerson et al (2005) reviewed 13 studies - 11 reported beneficial effects (but methodological drawbacks were noted) - application
+ appropriateness - patients’ behaviour becomes more socially acceptable promoting reintegration into society. Suitable for use in institutions - ethics, application
- effectiveness - McMonagle and Sultana (2009) could only find 3 studies with random allocation of patients to treatment and control GP’s. Only 1 study showed any improvement, and none gave any useful information about re-behaviour
- appropriateness - ethics. Clinicians may exercise control over Szs. However they stick to basic human rights that can’t be violated.

103
Q

What is the interactionist approach?

What is it also known as?

A

The bio-social approach
A broad approach to explaining schizophrenia which acknowledges a range of factors including biological and psychological factors that are involved in the illness.

104
Q

Give examples of biological factors in the interactionist approach

A

Genetic vulnerability, neurochemical and neurological abnormality

105
Q

Give examples of psychological factors in the interactionist approach

A

Stress from life events and daily hassles

106
Q

Give examples of societal factors in the interactionist approach

A

Eg: urbanisation

107
Q

Define diathesis

A

Vulnerability

108
Q

What does the diathesis-stress model attempt to explain?

A

How factors might interact to develop schizophrenia

109
Q

Define stress

A

Significant stressors

110
Q

Explain the original diathesis-stress explanation of schizophrenia.
When was it made?
Who made it?
Include the role of genetics and examples of important stressors.

A
Paul Meehl (1962) said that schizophrenia is entirely genetic - there is one schizogene. This led to the schizotypic personality. One of the characteristics is sensitivity to stress. Meehl: “if they don’t have the schizogene, no amount of stress can cause schizophrenia.”
Examples of important stressors: schizophrenogenic mother, chronic stress through childhood and adolescence.
111
Q
Explain the modern understanding of the diathesis-stress explanation of schizophrenia. Include:
The role of genetics,
Other vulnerabilities,
Psychological stressors,
Other stressors,
The role of cannabis.
A

Ripke et al (2014): there is no single schizogene. Schizophrenia is polygenic.
Ingram and Luxton (2005): range of factors include psychological trauma. Trauma becomes the diathesis, not the stressor.
Read et al (2001): proposed a neurodevelopmental model - early trauma alters brain development eg: child abuse can make the hypothalamic-pituitary-adrenal (HPA) system become over-active, which makes them more vulnerable to stress in later life.
Psychological stressors: anything that risks triggering schizophrenia.
Other stressors: Houston et al (2008): modern stress is anything that risks triggering schizophrenia.
Role of cannabis: it’s a stressor that increases Sz risk X7. It interferes with the dopamine system but people don’t develop it straight from cannabis so other vulnerability factors must be involved.

112
Q
Explain Tienari et al’s study as evidence to support the diathesis-stress explanation of schizophrenia. Include:
Date,
Aim,
Sample,
Method,
Findings,
Conclusions.
A

2004 - to investigate the role of genetic vulnerability and parenting style (as a trigger)
Sample: children adopted from 19,000 Finnish mothers with schizophrenia between 1960 and 1979.
Method: they assessed adoptive parents’ child rearing style then looked at children’s rates of schizophrenia and compared this to a control group of adoptees who had no genetic risk of schizophrenia.
Findings: 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.
Conclusion: evidence suggests that genetic vulnerability and family related stress (triggers) are involved in development of Sz. Genetically vulnerable children appear more sensitive to parenting behaviour.

113
Q

State the 2 typical types of treatment used in the U.K. and the typical types of treatment used in the U.S.A. when using the interactionist approach to explaining schizophrenia

A

U.K: Anti-psychotic drugs, CBT

U.S.A: Anti-psychotic drugs and a psychological therapy eg: family therapy, CBT, token economies

114
Q

The interactionist approach to treatment in the U.S.A. differs to the U.K. in that…

A

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

115
Q

Evaluate the interactionist approach to schizophrenia

A

+ supporting evidence - Tienari et al study - reliability
+ evidence through treatment - Turkington et al (2006): it is not really possible to use a combo of treatments without adopting an interactionist approach. Studies show an advantage of using a combo. Tarrier et al study - reliability.
- difficulties in determining casual stress - debate over whether stress is close to Sz onset or early life. Hammen (1992): maladaptive methods of coping with childhood stress causes impaired development - they fail to develop effective coping skills. This compromises resilience and increase vulnerability - validity.
- the original diathesis-stress model is oversimplified - multiple genes increase vulnerability to Sz. There’s no schizogene. Stress can come in many forms, therefore vulnerability and stress don’t have 1 single source.

116
Q

Explain Terrier et al’s study

A

2004
315 patients were randomly allocated to a group:
Meds and CBT, meds and supportive counselling, just meds (control). Patients in combo groups showed lower symptom levels than those in control. Although, there was no difference found in hospital readmission rates.