Paper 3: Schizophrenia Flashcards

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1
Q

What are the positive symptoms of schizophrenia?

A

Hallucinations.
Delusions, beliefs not based in reality.

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2
Q

What are the negative symptoms of schizophrenia?

A

Avolition, lack of desire or motivation for anything.
Speech poverty reduction in the quality or amount of speech.

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3
Q

What are the two ways of diagnosing schizophrenia and whats the difference?

A

DSM-5 (the American guide to diagnose schizophrenia) and the ICD-10 (the World health Organisation’s guide). DSM-5 requires at least 1 positive symptom to be present while the ICD-10 requires only negative symptoms.

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4
Q

How reliable are schizophrenia diagnosis?

A

Beck et al found a 54% concordance rate with diagnosis between doctors.
Soderberg found an 81% concordance rate with the DSM-5 compared to Jakobsen with a 98% concordance rate with the ICD-10.

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5
Q

Strengths of the reliability Diagnosis of Schizophrenia?

A

Improvements in reliability over time, greater concordance rate in newer studies.

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6
Q

Weaknesses of the reliability diagnosis of schizophrenia?

A

Low reliability between the DSM-5 and the ICD-10, in general the DSM-5 is seen as more reliable due to its specific criteria.
Co-morbidity, people often suffer from depression alongside schizophrenia, often confusing the diagnosis.

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7
Q

Who studied the validity of the schizophrenia diagnosis?

A

Rosenhan, used 8 healthy volunteers and all were falsely admitted to hospital and diagnosed with schizophrenia. Took between 7-52 days to release them.

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8
Q

Strengths of the validity of schizophrenia diagnosis?

A

Although Rosenhan appears to make the diagnosis invalid, more recent studies suggest it has improved eg Mason et al.
Realistic gender difference in schizophrenia, Kulkarni et al found women’s estrogen can be responsible for the gender disparity in schizophrenia diagnosis.
Cultural differences, there is a valid disparity in schizophrenia diagnosis due to the higher rates of schizophrenia in Afro-Caribbean people.

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9
Q

Weaknesses of the validity of schizophrenia diagnosis?

A

Shares symptom overlap with other disorders eg speech poverty found in both schizophrenia and autism.
Gender differences, Cotton et al suggests the better interpersonal functioning of women may cause doctors to miss the symptoms of schizophrenia.
Cultural differences, there is an invalid disparity in diagnosis of Afro-Caribbean people due to over-diagnosis in Britain or under-diagnosis in the Caribbean.

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10
Q

What are the 3 factors in the biological explanations for schizophrenia?

A

These include genetics, neural (brain) abnormalities, and abnormalities in dopamine.

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11
Q

Who conducted schizophrenia twin studies and what were the results?

A

Gottesman found 48% concordance rate for schizophrenia in identical twins compared to non-identical.
Other studies include Tienari et al who found adopted children of a schizophrenic biological mother were more likely to have schizophrenia than a control group of adoptees.

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12
Q

Strengths of the genetic explanations for schizophrenia?

A

Supporting evidence: The familial and twin studies of schizophrenia above support the genetic explanation of schizophrenia because they show that being closely related (and thus having similar genes) to someone with schizophrenia increases the likelihood of suffering from schizophrenia.
Multiple genes: It is unlikely that there is a single gene responsible for schizophrenia. Instead, multiple genes likely combine to increase a person’s risk of developing schizophrenia. In a study of more than 36,000 schizophrenic patients, Ripke et al (2014) found 108 different genetic variations that were correlated with schizophrenia, supporting the existence of a genetic component to the disorder. Further, many of these genetic variations were related to dopamine transmission, so genetic explanations can be combined with the dopamine hypothesis to provide a holistic explanation of schizophrenia.

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13
Q

Weaknesses of the genetic explanation for schizophrenia?

A

Other factors: Although most studies suggest genetics play a part in the development of schizophrenia, it is clear that other factors are important too. If schizophrenia was 100% genetic, you would expect concordance rates between identical twins to be 100%. However, most studies find concordance rates among identical twins to be less than 50%, which suggests there is more to schizophrenia than just genetics. This suggests an interactionist approach is best for explaining schizophrenia.
Methodological issues surrounding twin studies: Twin studies typically assume that twins have identical upbringings and so any differences in concordance rates between identical and non-identical twins must be explained by genetics. However, environmental factors likely play a role too. For example, looking identical probably makes parents treat identical twins more similarly than they would non-identical twins. As such, greater similarities in environment could contribute to higher concordance rates for schizophrenia among identical twins, with the influence of genetics being exaggerated.

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14
Q

What are neural correlates?

A

Examinations of the brain comparing a normal brain to a schizophrenic brain.

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15
Q

What were 2 neural correlate studies conducted?

A

Johnson et al found enlarged ventricles in correlation to schizophrenia.
Li et al took a meta-analysis and found reduced activity during facial processing tasks.

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16
Q

Weaknesses of the neural correlate explanation?

A

Conflicting evidence: Although several studies have found correlations between enlarged ventricles and schizophrenia, there are many exceptions. There are many people with enlarged ventricles who do not have schizophrenia, and there are many people with schizophrenia who do not have enlarged ventricles.
Correlation vs. causation: Although there are correlations between schizophrenia and certain neural patterns, it can be difficult to determine whether abnormal brain functioning causes schizophrenia symptoms or whether it is an effect of schizophrenia. For example, does reduced activity in the bilateral amygdala of schizophrenic patients cause difficulties in emotional processing, or do schizophrenics’ reduced emotional processing (caused by some other factor) result in reduced blood flow and activity in the bilateral amygdala?

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17
Q

What is the neurotransmitter explanation for schizophrenia?

A

The Dopamine Hypothesis. Seeman et al and other studies reported a reduction in schizophrenic symptoms when on dopamine inhibitors.

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18
Q

What further evidence supports the Dopamine Hypothesis?

A

Curran et al found that drug that cause an increase in dopamine can be responsible for causing schizophrenia in non-schizophrenic people.
Post-mortum, Bird et al found greater dopamine concentration in schizophrenic brains than normal brains.

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19
Q

What is the extension of the dopamine hypothesis?

A

That it isn’t just about dopamine increase but instead the increase in specific parts of the brain and a reduction in others.

20
Q

Weaknesses of the Dopamine Hypothesis?

A

Farde et al found no difference in dopamine levels between a schizophrenic and normal brain.
Suggestion that there are other neurotransmitters involved eg Marsman found a decrease in glutamate activity.
Allegations of bias, pharmaceutical companies have a reason to sell more dopamine inhibitors.

21
Q

What is the main biological treatment to schizophrenia and what forms does it take?

A

Drug therapy.
Typical Antipsychotics which are older and target dopamine.
Atypical Antipsychotics which are newer and target dopamine, serotonin and glutamate.

22
Q

What are the side effects of the biological treatments of schizophrenia?

A

Typical antipsychotics, movement problems similar to Parkinsons
Atypical antipsychotics, weight gain, increased risk of heart attack, increased risk of diabetes, and extrapyramidal symptoms.

23
Q

Strengths of drug therapies to treat schizophrenia?

A

Evidence supporting drug therapy: Several studies have found both typical and atypical antipsychotics to be more effective than placebo in reducing schizophrenia symptoms.
Atypical antipsychotics more effective than typical antipsychotics: A systematic review by Bagnall et al (2003) looked at data from over 200 trials of antipsychotic drugs. In general, atypical antipsychotics were more effective than typical antipsychotics. However, data supporting the most recent atypical antipsychotics was of poor quality.

24
Q

Weaknesses of schizophrenia drug therapy?

A

Criticism of the distinction between typical and atypical: While atypical antipsychotics were designed to be more effective with less side effects than typical antipsychotics, some studies question whether this is actually the case. Further, while typical antipsychotic drugs were thought to target the dopamine neurotransmitter only, more recent evidence suggests both generations of antipsychotics target other neurotransmitters such as serotonin. For these reasons, some commentators (e.g. Leucht et al (2013) and Tyrer and Kendall (2008)) have questioned whether the distinction between typical and atypical antipsychotics is a meaningful one.
Side effects: All antipsychotics carry a risk of side effects to varying degrees. These side effects can range from mild (e.g. weight gain, dizziness) to potentially fatal (e.g. heart attack, stroke, neuroleptic malignant syndrome). Lieberman et al (2005) found that 74% of 1,342 schizophrenic patients discontinued antipsychotic drug treatment within 18 months due to side effects.

25
Q

What are the 2 psychological explanations of schizophrenia?

A

Family dysfunction and cognitive explanations.

26
Q

Who studied family dysfunction as an explanation for schizophrenia and what was their explanation?

A

Batesman, believed schizophrenia came from the double bind. Contradictory behaviour expressed by the parent eg hugging but being critical with words. Creates illogical perception of reality.
Another explanation is expressed emotion, particularly criticism and stress that leads to increased risk of schizophrenia.

27
Q

Strengths of family dysfunction?

A

Evidence supporting the family dysfunction explanation: Adoption studies suggest that dysfunctional family environments increase the risk of schizophrenia. For example, in a follow-up to their longitudinal study described above, Tienari et al (2004) rated familial dysfunctionality among the adoptive environments of adoptees whose biological mothers had schizophrenia. They found that adoptees raised in families rated as dysfunctional had much higher rates of schizophrenia (36.8%) compared to adoptees raised in families rated as healthy (5.8%).
Evidence supporting the role of expressed emotion: A meta-analysis of 26 studies by Butzlaff and Hooley (1998) found relapse rates are higher among schizophrenic patients who return to live with families with a high degree of expressed emotion. The role of expressed emotion in schizophrenia is further supported by the success of family therapies that aim to reduce expressed emotion. However, this research doesn’t support expressed emotion as a cause of schizophrenia, but it does suggest it contributes to maintaining schizophrenia.

28
Q

Weakness of family dysfunction?

A

Exceptions: Not everyone raised in a dysfunctional family goes on to develop schizophrenia, and not everyone with schizophrenia was raised in a dysfunctional family. This suggests that other factors are important in explaining schizophrenia, such as biology.
Correlation vs. causation: Even if schizophrenia is correlated with family dysfunction, this doesn’t prove that family dysfunction causes schizophrenia – it could be the other way round. For example, it seems possible that having a schizophrenic family member could itself cause stress and dysfunction within the family, rather than that family dysfunction causes schizophrenia. It’s a chicken or egg scenario: Which comes first?
Methodological concerns: Bateson et al’s double bind explanation of schizophrenia is based on a handful of case studies and interviews. Some critics have suggested researchers focus on examples that support the explanation while ignoring examples that conflict with it (selection bias).

29
Q

What are the 3 cognitive explanations of schizophrenia?

A

Dysfunctional thought processing- Schizophrenic patients have an inability to metacognate. May be hearing their own voices.
Cognitive biases may be the explanation to delusions eg interpreting people’s actions as sinister.
Cognitive deficits, Bowie and Harvey describe various cognitive deficits such as attention, speech and memory.

30
Q

Strengths of cognitive explanations of schizophrenia?

A

Evidence supporting cognitive explanations: Several studies have found evidence of cognitive impairment in schizophrenic patients. Bowie and Harvey’s (2006) review above cites many examples. Cognitive impairments are often present before the patient’s first schizophrenic episode and persist throughout the disorder, but therapies that reduce cognitive impairment (e.g. CBT) often improve schizophrenia symptoms. This all supports a role for cognitive explanations of schizophrenia.
Practical applications: Cognitive explanations have been used to develop effective therapies for treating schizophrenia, such as CBT.
Complements other explanations: Cognitive explanations can be combined with other explanations (e.g. biological) to give a more holistic account of schizophrenia.

31
Q

Weaknesses of cognitive explanations of schizophrenia?

A

Evidence against cognitive explanations: Many people have the cognitive biases and cognitive deficits associated with schizophrenia (for example, as a result of brain damage) and yet do not develop schizophrenia. This suggests that cognitive explanations alone are too reductionist: There is more to explaining schizophrenia than just cognitive explanations.
Does not explain the cause of schizophrenia: Cognitive theories simply describe the thought processes of schizophrenia but do not explain why people with schizophrenia have these thought processes in the first place.

32
Q

What is the psychological treatment of schizophrenia and how does it work?

A

CBT, the therapist helps identify and challenge irrational thoughts
May also teach behavioural coping skills and relaxation techniques.
Used to treat the symptoms of OCD and is used alongside drug therapies.

33
Q

Strengths of OCD?

A

Zimmerman found it significantly reduced the symptoms of 1,500 patients.
Complements other treatments to become more effective.
No side effects as comparison to antipsychotic drugs.

34
Q

Weaknesses of OCD?

A

A meta-analysis by Jauhar showed it had little effect on the symptoms.
In blind studies, there were even less effects present.
Not suitable for the hyper paranoid /anxious patients.

35
Q

What is another theraputic treatment of schizophrenia and how does it work?

A

Family therapy, the cognitive belief is that it originates in the family and therefore should be solved through family related CBT. It aims to:
Improve communication patterns: Increase positive communication and decrease negative communication among the family (i.e. reduce levels of expressed emotion)
Increase tolerance and understanding: Educate family members about schizophrenia and how to deal with it (e.g. how to support each other)
Reduce feelings of guilt and anger: Family members may feel guilty (e.g. that they are responsible for causing schizophrenia) or angry towards the schizophrenic patient

36
Q

What are the strengths of family therapy?

A

Evidence supporting efficacy of family therapy: Several studies have demonstrated lower rates of schizophrenia relapse among patients receiving family therapy. For example, a meta-analysis by Pilling et al (2002) looked at 18 studies of family therapy for schizophrenia and found that it had a clear effect on reducing relapse rates.
Complements other treatments: Evidence suggests that family therapy plus antipsychotic drug therapy is more effective at reducing relapse than antipsychotic drug therapy alone. For example, Xiong et al (1994) randomly allocated 63 subjects to either a drug therapy group or a drug therapy plus family therapy group. After one year, relapse rates were lower in the drug therapy plus family therapy group (33%) compared to the drug therapy only group (61%).
Less side effects: Family therapy has very few (if any) side effects relative to antipsychotic drugs.
Cost effective: The Schizophrenia Commission (2012) estimate that family therapy results in cost savings of around £1000 per patient over a 3 year period.

37
Q

Weaknesses of family therapy for schizophrenia:

A

Could be counterproductive: Family therapy for schizophrenia emphasises being open and honest. However, in some families, open communication may reveal difficult truths or reignite old arguments. This could increase, rather than decrease, negative communication and potentially make the problem worse.
Not suitable for all patients: Some schizophrenic patients do not have dysfunctional families and so family therapy is unlikely to be an effective treatment for them.

38
Q

What’s a behaviourist approach to treating schizophrenia?

A

The Token Economy, used to treat negative symptoms of schizophrenia such as avolition.

39
Q

Strengths of token economies as a treatment of schizophrenia?

A

Evidence supporting efficacy of token economies: Several studies suggest token economies can improve symptoms of schizophrenia. For example, a review of studies by McMonagle and Sultana (2000) found token economies reduced the negative symptoms of schizophrenia. However, the researchers note that the evidence is not conclusive, with questions about the replicability of the findings and uncertainty about whether behavioural changes can be maintained after the treatment ends.
Complements other treatments: Token economies can be used in conjunction with other treatments, such as antipsychotic drugs.

40
Q

Weaknesses of token economies as a treatment for schizophrenia?

A

Ethical concerns: Use of token economies could be seen as unethical for several reasons. Firstly, some argue that token economies are dehumanising as they take away the patient’s rights to make their own choices. Secondly, some argue that token economies are discriminatory: Severely ill patients will have greater difficulty complying with behavioural demands and thus get fewer privileges than patients who are less severely ill. Token economies may thus discriminate against the most severely ill patients.
Relapse: If improvements in behaviour are dependent on receiving tokens, the schizophrenic patient may relapse once token economy therapy is withdrawn.

41
Q

What is the interactionist approach to explaining phobias and who proposed it?

A

Meelh, the diathesis-stress model in which there is a dormant schizophrenic gene that becomes active under stress.

42
Q

What are the strengths of the diathesis-stress model?

A

Evidence supporting diathesis-stress model: There is strong evidence for both the genetic and environmental components of schizophrenia. For example, Gottesman’s family studies described above support a role for genetics but schizophrenia concordance rates among identical twins are much less than 100%, demonstrating environmental plays a role too. With regards to the diathesis-stress model specifically, several studies suggest that stress is a key environmental component. For example, a review by Walker et al (2008) found schizophrenia is associated with elevated baseline stress hormones (e.g. cortisol) and that drugs that increase stress hormones worsen schizophrenia symptoms. Further, a meta-analysis by Varese et al (2012) found that stressful events in childhood increase the risk of schizophrenia, further supporting the hypothesis that stress is a key trigger of schizophrenia in those genetically prone.
Holistic: Rather than reducing schizophrenia to one single cause, the diathesis-stress model accounts for the multitude of factors that contribute to the disorder. This can be seen as a more complete picture of schizophrenia.

43
Q

Weaknesses of the diathesis-stress model?

A

Incomplete: Although there is strong evidence supporting the role of both biological diathesis and stress in the development of schizophrenia, the mechanisms through which they cause schizophrenia are not clear.

44
Q

What is the interactionist approach to treating schizophrenia?

A

Using both cognitive, behavioural and biological treatments simultaneously to have a more effective treatment.

45
Q

Strengths of the interationist treatment to schizophrenia

A

Evidence supporting interactionist treatment approaches: Several studies suggest combination therapy is more effective than monotherapy. For example, Xiong et al (1994) randomly allocated 63 schizophrenic patients to either a drug therapy group or a drug therapy plus family therapy group. After one year, relapse rates were lower in the drug therapy plus family therapy group (33%) compared to the drug therapy only group (61%). These findings are supported by a study of 103 schizophrenic patients conducted by Hogarty et al (1986), who reported relapse rates of 19% among patients treated with drug therapy plus family therapy compared to 41% for patients treated with drug therapy alone. Further, Sudak (2011) describes how cognitive behavioural therapy makes patients more likely to adhere to drug therapy because it helps the patient rationally understand the benefits of doing so. This suggests antipsychotic drug therapy plus cognitive behavioural therapy will be more effective than drug therapy alone.
Holistic: There are both biological and psychological components to schizophrenia, but interactionist approaches treat both. This is a more complete approach to treatment, which might explain why interactionist approaches are more effective. For example, antipsychotic drugs may address the chemical imbalances of schizophrenia while cognitive behavioural therapy addresses the irrational thought processes.

46
Q

Weaknesses of the interactionist approach to treating schizophrenia?

A

Increased costs: Interactionist treatment approaches will be more expensive than monotherapy because you have to pay for multiple treatments (e.g. CBT, family therapy, and antipsychotic drugs) rather than just one. However, if interactionist treatment approaches lead to lower relapse rates than monotherapy, this may save money in the long run because it prevents further costs to the health service down the line.
Conflicting evidence: Some studies raise questions as to whether some interactionist approaches to therapy really are more effective than monotherapy. For example, Jauhur’s meta analysis described in the AO3 points for CBT above questions whether CBT really is an effective treatment for schizophrenia. If CBT is not an effective treatment for schizophrenia, then CBT+antipsychotic drug therapy is unlikely to be any more effective than antipsychotic drug therapy alone.