Schizophrenia Flashcards

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1
Q

Define schizophrenia

A

A severe mental illness where people cannot distinguish between what is real and what is not
- an example of psychosis

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2
Q

Which 2 major systems are used for the classification of mental disorders?

A
  1. IDC-10 (In Europe)

2. DSM - 5 (In America)

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3
Q

Outline 2 differences between the ICD-10 and the DSM-5?

A
  1. In DSM-5. 1 positive symptom (hallucinations, delusions or speech disorganisation) is needed to classify schizophrenia whilst ICD needs 2 or more.
  2. IDC-10 recognises subtypes of schizophrenia, e.g. paranoid schizophrenia (focus on delusions and hallucinations) and catatonic schizophrenia (disturbance to movement, leaving sufferer immobile), whilst DSM-5 doesn’t recognise them.
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4
Q

Define:

  • positive symptom

- negative symptom

A

Positive symptom: A symptom that sufferers have, that normal people do not have

Negative symptom: A symptom that sufferers do not have, that normal people do have

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5
Q

Outline 2 positive symptoms of schizophrenia

A
  1. Hallucinations: sensory experiences of stimuli that have no basis in reality/are distorted perceptions of things that are there
  2. Delusions: beliefs that have no basis in reality e.g. someone is out to kill them.
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6
Q

Outline 2 negative symptoms of schizophrenia

A
  1. Avolition: Loss of motivation to carry out usual tasks, which leads to lower activity levels
  2. Speech Poverty: Reduced frequency and quality of speech
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7
Q

Evaluate the diagnosis and classification of schizophrenia

A

Strengths
1. Diagnosis has led to treatments being made available for patients with schizophrenia.

Weaknesses

  1. Cheniaux et al results showed poor inter-rater reliability and criterion validity: Out of 100 patients, One psychiatrist diagnosed 26 with schizophrenia according to DSM, and 44 according to ICD. Whilst other diagnosed 13 with DSM, and 24 with ICD.
    - Criterion validity focuses on whether different assessment systems arrive at same diagnosis for same patient. Not supported by Cheniaux results
  2. Symptom overlap: Different conditions may show same symptoms as schizophrenia e.g. Bipolar disorder also includes delusions and avolition. This makes it hard to distinguish between 2 conditions.
  3. Gender Bias: Women may be underdiagnosed as female patients tend to have better interpersonal skills, and this quality makes the case seem too mild to warrant a diagnosis
  4. Cultural bias: Researchers found that black people are more likely to be diagnosed as they may over-interpret symptoms and distrust the honesty of black people.
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8
Q

What 3 ideas make up the biological explanation for schizophrenia?

A
  1. Schizophrenia has genetic basis
  2. Dopamine hypothesis
  3. Neural correlates
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9
Q

Outline the findings of a study that suggests schizophrenia has genetic basis

A

Gottesman (1991)

- found that MZ twins have greatest shared risk of schizophrenia (48%), compared to DZ twins (17%) and siblings (9%)

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10
Q

Is schizophrenia:

  • monogenetic or polygenetic?
  • aetiologically heterogenous or non-aetiologically heterogenous?
A

Schizophrenia is polygenetic - Each individual gene confers a small increased risk of schizophrenia
2. Schizophrenia is aetiologically heterogenous - Different combinations of genes can lead to schizophrenia

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11
Q

What provides evidence for schizophrenia being polygenetic and aeterologically heterogenous?

A

The existence of different candidate genes and Ripke et al’s study (Ripke et al studied 37,000 patients and found 108 separate genetic variations associated with increased risk; many coded for dopamine neurotransmitter)

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12
Q

What is dopamine?

A

Dopamine is a neurotransmitter that generally has an excitatory effect and is associated with the feeling of pleasure.

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13
Q

In what ways can dopamine be linked to schizophrenia?

A
  1. Hyperdopaminergia (subcortex): High dopamine activity in subcortex (central areas of the brain). e..g an excess of dopamine receptors in the Broca’s area is associated with hallucinations and speech poverty.
  2. Hypodopaminergia (prefrontal cortex): New version of dopamine hypothesis shows patients can show low levels of dopamine in prefrontal cortex (responsible for negative symptoms - thinking and decision-making)
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14
Q

What are neural correlates?

A

Patterns of structure/activity in brain that occur in conjunction with an experience (positive and negative symptoms) and may be implicated in the origins of that experience

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15
Q

Outline a neural correlate for avolition (example)

A

The ventral striatum

Ventral striatum is involved in motivation. Loss of motivation in schizophrenics may be explained by low activity levels here.
- Juck et al found a negative correlation between ventral striatum activity and overall negative symptoms

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16
Q

Outline a neural correlate for hallucinations (example)

A

The superior temporal gyrus

Allen et al found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus

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17
Q

Evaluate the biological explanation for schizophrenia.

A

Strengths

  1. Gottesman’s evidence
  2. Role of mutation supports genetic explanation. Schizophrenia can take place in absence of family history of disorder through mutations. Brown et al found a link between paternal age (associated with increased risks of mutation) and the risk of schizophrenia, increasing from 0.7% in fathers under 25 to 2% in fathers over 50.

Limitations

  1. Correlation does not equal causation: Negative correlation in ventral striatum doesn’e necessarily indicate it as a cause of schizophrenia. Hence, neural correlates relatively little about the causes of schizophrenia
  2. Interactionist approach: Gottesman’s results didn’t show 100% concordance rate for MZ twins, so environment must be involved.
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18
Q

Name 2 psychological explanations for schizophrenia

A
  1. Family dysfunction

2. Cognitive explanations

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19
Q

Outline the 3 main ideas that make up the ‘family dysfunction’ explanation.

A
  1. Schizophrenic mothers
  2. Double-bind theory
  3. Expressed emotion
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20
Q

How can schizophrenogenic mothers cause schizophrenia?

A

studies found that schizophrenics had similar types of mothers known as ‘schizophrenogenic mothers’ (mothers who cause schizophrenia). They were ‘cold, rejecting, controlling, and create family of tension/ secrecy. This leads to distrust, paranoid delusions (schizophrenia).

21
Q

How can the double-bind theory cause schizophrenia?

A

Children may feel trapped in situations where they fear doing the wrong thing, and receive conflicting messages about what counts as wrong. They cant express feelings about unfairness of situation
- When they ‘get it wrong’ (often), child is punished by withdrawal of love, and as a result, they start to see world as dangerous (disorganised thinking and delusions)

22
Q

How can expressed emotion cause schizophrenia?

A

Expressed emotion: the level of emotion expressed towards schizophrenic patient and includes:

  1. Verbal criticism of patient
  2. Hostility towards them
  3. Emotional over-involvement in their life

High levels of EE can lead to stress in a patient, a primary explanation for relapse in patients with schizophrenia.

23
Q

Outline the main idea that makes up the cognitive explanation for schizophrenia

A

Dysfunctional thought processing: lower levels of info processing in some areas of the brain suggest cognition is impaired e.g. ventral striatum linked to negative symptoms
- includes idea of metarepresentation and dysfunction of central control

24
Q

What is metarepresentation?

A

Metarepresentation: The cognitive ability to reflect our own thoughts and behaviour.
- Disrupts ability to recognise thoughts as our own - could lead to sensation of hearing voices and having thoughts placed in mind by others (hallucinations).

25
Q

What do we mean by ‘dysfunction of central control’?

A

Central control: the cognitive ability to suppress automatic responses while performing deliberate tasks.
- schizophrenics suffer from speech poverty as each word triggers automatic associations that they cannot suppress.

26
Q

Evaluate psychological explanations for schizophrenia?

A

Strengths
1. Support for dysfunction of central control: Stirling et al (2006) compared schizoprenics and non-patients on a task (read colour of the word, not word itself). Found that patients took a lot longer to suppress impulse to read the word and read ink colour instead.

Limitations

  1. Subjective: family experiences may be interpreted differently by different psychologists so can’t make general principles.
  2. Ignores role of biological factors
  3. lack of internal validity in stirlings study: Low sample size as Stirling only used 30 patients and 18 non-patients so hard to generalise.
27
Q

Name 2 categories of drugs used to treat schizophrenia

A
  1. Typical antipsychotics

2. Atypical antipsychotics

28
Q

Give an example of 1 typical antipsychotic drug?

A

Chlorpromazine

29
Q

What does chlorpromazine do?

A
  1. Acts as dopamine antagonists = blocks dopamine receptors in synapses in brain, reducing action of dopamine. Initially, dopamine levels build up after taking chlorpromazine, but then production is reduced.
    - this reduces symptoms such as hallucinations
  2. Chlorpromazine also has an effect on histamine receptors, which appears to lead to sedation effect. Therefore, it’s used to calm anxious patients when they are first admitted to hospital.
30
Q

Give examples of 2 atypical antipsychotic drugs

A
  1. Clozapine

2. Risperidone

31
Q

What does clozapine do?

A
  1. It binds to dopamine receptors like chlorpromazine does but also acts on serotonin and glutamate receptors.
  2. It reduces depression and anxiety in patients as well as improving cognitive functioning. It also improves mood, which is important as up to 50% of schizophrenics attempt suicide.
32
Q

Why was risperidone develped and what does it do?

A

Why it was developed: As clozapine was involved in deaths from a blood condition called agranulocytosis.

What it does: Rizperidone like clozapine binds to dopamine and serotonin receptors but risperidone binds more strongly to dopamine receptors and is therefore more effective in smaller doses than most antipsychotics, and has fewer side effects.

33
Q

Since when has clozapine been used?

A

Since the 1970s, until the development of risperidone.

34
Q

Evaluate the use of antipsychotic drugs

A

Strengths

  1. Moderately effective: Thornley et al reviewed data from 13 trials (1121 ppts) and found that chlorpromazine was associated with better functioning and reduced symptom severity
  2. Benefits of clozapine: more effective than typical antipsychotics in reducing depression and anxiety in patients as well as improving cognitive functioning. It also improves mood.
  3. Benefits of risperidone: risperidone binds more strongly to dopamine receptors, than clozapine and other antipsychotics, and is therefore more effective in smaller doses, and has fewer side effects.

Limitations

  1. Side effects: Typical antipsychotics are associated with dizziness, agitation, sleepiness, weight gain, repeated actions e.g. lip smacking, and neuroleptic malignant syndrome (syndrome that can be fatal as it disrupts regulation of body systems). Even though atypical psychotics were developed to reduce side effects, some still exist e.g. clozapine.
  2. hypodopaminergia: antipsychotics follows logic of hyperdopaminergia but could be hypodopaminergia. Any positive effects of drugs could be due to pharmacological effects rather than blocking dopamine.
  3. Exaggerated results: findings supporting use of drugs may have been exaggerated to promote sales. studies only report short term effects/
  4. Chemical Cosh: Suggested that antipsychotic drugs only used to calm patients down so that they’re easier to work with. Some see this as a breach of human rights.
35
Q

Name 3 examples of psychological therapies for schizophrenia

A
  1. CBT
  2. Family therapy
  3. Token economies
36
Q

How does CBT treat schizophrenia?

A

Patients irrational thoughts are tested by helping them make sense of how their delusions and hallucinations impact on their feelings and behaviour.
- Helping patient understand their symptoms reduces anxiety and helps them realise that their beliefs are not based on reality.

37
Q

What are the aims of family therapy?

A

To improve communication and interaction in the family and to reduce stress of caring for a relative with schizophrenia (reduce expressed emotion).

38
Q

According to Pharoah et al, what are the main strategies family therapists use to reduce the likelihood of relapse?

A
  1. Reduce stress of caring for relative with schizophrenia.
  2. Reduce guilt and anger in family members
  3. Improve families ability to anticipate/solve problems.
  4. Improve perception of schizophrenia.
39
Q

How can token economies be used to treat schizophrenia?

A

THROUGH OPERANT CONDITIONING

Tokens may be given to patients who carry out desirable behaviours (e.g. eating their breakfast), and these tokens are swapped for a tangible reward (e.g. sweets). the tokens are given immediately after the good action, as results are not as effective with delayed rewards (delay discounting).
- This reward reinforces the desirable behaviour

40
Q

Why are tokens secondary reinforcers?

A

They are secondary reinforcers as they only have value due to the learned association with innate primary reinforcers (e.g. sweets)

41
Q

Evaluate psychological therapies for schizophrenia

A

Strengths

  1. Support: McGonagle and Sultana found 1 of 3 studies of token economies that used random allocation showed improvement. (and random allocation eliminates researcher bias)
  2. CBT provides more comprehensive understanding of schizophrenia: Takes into account sufferers thoughts/feelings.

Limitations

  1. They don’t cure schizophrenia, only reduce it’s symptoms.
  2. Overemphasis on cognition in CBT: Patients may need to change the situation their in e.g suffering abuse, in order to be treated, but focus on cognitive aspect may disrupt that. (so family therapy may be better)
  3. Ethical issues in Token economy systems: Not fair that severely ill patients would be less likely to receive privileges than moderately ill patients as they would naturally find it harder to comply.
  4. Mcgonagle and Sultana study found no improvement in other 3 studies so support is limited.
42
Q

How does the interactionist approach explain schizophrenia?

A

Via the diathesis stress model

  • we may have a genetic vulnerability to schizophrenia, but stressors in the environment trigger it
43
Q

What did the OLD diathesis-stress model argue?

A

MEEHL’S MODEL

Meehl argued that diathesis/vulnerability was entirely the result of a schizogene and that someone without this gene can never get schizophrenia, no matter how many chronic stressors they were exposed to.

44
Q

What is our modern understanding of ‘diathesis’?

give an example

A

DIATHESIS:

  • vulnerability not due to a single ‘schizogene’, but many genes interacting.
  • vulnerability doesnt have to be genetic. Can be early psychological trauma that affects brain development. e.g. child abuse affects the hypothalamic-pituitary adrenal system (HPA) system, making a child vulnerable to stress.
45
Q

What is our modern understanding of ‘stress’?

give an example

A

STRESS
- Anything that risks triggering schizophrenia (including psychological stress). e.g. Cannabis is a stressor as it can increase the risk of schizophrenia up to 7 times depending on dose - probably because it interferes with the dopamine system.

46
Q

What treatments would interactionists use?

and what would psychologists need to consider when prescribing one of these treatments

A

A mixture of antipsychotic drugs & CBT
- They would have to adopt an interactionists approach whilst carrying out CBT. They would tell patients that their condition is purhisely biological and then would treat their symptoms by challenging their irrational beliefs.

47
Q

Between the UK and the US, which one adopts the interactionist approach more?

A

The UK

48
Q

Evaluate the interactionist approach to schizophrenia

A

Strengths

  1. Research support for diathesis-stress model: Tienari et al studied children adopted from 19000 Finnish schizophrenic mothers. Adoptive parents parenting styles were assessed and rates of schizophrenia in children were compared with control group of adoptees with no genetic risk. A child-rearing style with high levels of criticism and conflict and low levels of empathy was related to development of schizophrenia but only for children with high genetic risk.
  2. Large sample size in Tienari study: 19000 schizophrenic mothers, so more representative.

Limitations

  1. Vulnerability not always inherited: Houston et al found childhood trauma was a diathesis and cannabis was a trigger.
  2. We dont exactly understand how diathesis and stress produce symptoms.
  3. Sample in Tienari’s study was from finnish mothers: Culture bias.