Schizophrenia for exam Flashcards

1
Q

will not be an exam question but

What are the biological explanations for schizophrenia?

A

Biological explanations emphasise the role of inherited factors and dysfunction of brain activity in the development of a behaviour/mental disorder.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are 2 results Gottesman found of family studies showing genetic factors contribute to schizophrenia.

A

If a parents has schizophrenia, child is more likely to have schizophrenia.
Gottesman found:
2 parents with it = 46% chance of child developing schizo
1 parent with it = 13% chance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What did Joeseph (2004) find in twin studies (genetic factors)

A
  • Monozygotic (genetically identical) more similar than dizygotic (sharing 50% of genes)
  • concordance rate showed MZ twins with schizo = 40% compared to 7%.
  • Tf, MZ much more likely to both have it if one has it.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a limitation of working on twin studies with schizophrenia.
eval point.

A

Twins are extremely hard to find both with schizophrenia, so there is a very limited sample size. Also, it is very time consuming, because you have to search far and wide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What did Tienari (2000) find in adoption studies.

eval point

A

Of 160 adoptees whose biological mother had been diagnosed with schizo - 11 adoptees also received diagnosis for schizo.
Compared to 4/197 control adoptees those born with non schizo mothers.
Tf, investigators could confirm the genetic liability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a limitation of Tienari’s (2000) adoption study?

eval point

A

Dependent on how long they were with their biological mother could affect results. The older, the less likely they are to be influenced by their environment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does neural correlates(correlations) mean in the biological explanations for schizo.

A

Focuses on the important role of the neurotransmitter dopamine AND on areas of the brain influential in the onset and development of this disorder.

Changes in neuronal events and mechanisms that result in the characteristic symptoms of a behaviour or mental disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Does more dopamine in the brain trigger negative or positive symptoms of schizo?

A

POSITIVE. think more causes an excess.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the dopamine hypothesis?

A

Claims an excess of dopamine in certain regions of the brain often associated with positive symptoms of schizo.
People with schizo are believed to have abnormally high numbers of D2 receptors on receiving neurons - resulting in more dopamine binding and Tf firing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give an example of 1 drug that increases dopamine activity in the brain - how does this happen.

A

Amphetamine = dopamine agonist

Stimulates nerve cells containing dopamine, causing synapse to be flooded with this neurotransmitter - more is uptaken

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a limitation (AO3) of increasing dopamine activity.

A

Dopamine enters the whole brain, not just the area where it is needed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Davis + Kahn’s (1991) revised version of the dopamine hypothesis?

A

Positive symptoms of schizo are caused by an excess of dopamine in subcortial areas of the brain - particularly mesolimbic pathway.
Negative symptoms arise from deficit of dopamine in areas of the prefrontal cortex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name 2 areas of the brain involved in schizo.

A
  • Prefrontal cortex

- Hippocampus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is the prefrontal cortex involved in schizo?

A

Main area involved in executive control.

Research shows that this area is impaired in schizophrenics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is the hippocampus involved in schizo?

A

Deficits nerve connection between hippocampus and prefrontal cortex.
Central cognitive impairment in schizo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give 2 weaknesses for genetic factors for schizo.

eval point.

A

-May be a limitation of research into MZ twins because they are more likely to encounter similar environments than DZ twins.
Joseph (2004) highlights potential ‘identity confusion’ as they are treated more as ‘twins’ than 2 distinct individuals.

-Adoptees may be selectively placed
Central assumption of adoption studies is that adoptees do not have schizophrenic tendencies is the child does.
But not always the case.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give one strength of the dopamine hypothesis.

eval point

A

-Evidence from success of treatment.
Antipsychotic drugs are used to reduce effects of dopamine in the brain - reduce schizo.
Leucht (2013) all antipsychotics, more effective than placebo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Give a weakness of the dopamine hypothesis.

eval point

A

-Noll (2009) Challenges hypothesis, argues antipsychotics do not alleviate hallucinations + hallucinations still occur despite dopamine levels being normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 2 psychological explanations for schizophrenia?

A
  • Family dysfunction

- Cognitive explanations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What 2 things to family dysfunction include?

A
  • Double bind theory

- Expressed emotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is family dysfunction in psychological explanations for schizophrenia?

A

Linking schizophrenia with childhood and adult experiences living in a dysfunctional family. Claims schizophrenia is caused by abnormal patterns of communication within family.

schizophrenia is due to family experiences of conflict, communication problems, criticism and control.

22
Q

What is the double bind theory in psychological explanations for schizophrenia?

A

Bateson et al (1956) says when a child is developing and regularly finding themselves in situations where they fear doing the wrong thing - but receive contradictory messages about what to do. They feel unable to seek clarification, they are more likely to develop schizophrenia.

23
Q

What is an example of double bind theory?

A

Mother tells son that she loves him but at the same time turns her head away in disgust - child receives 2 conflicting feelings.

24
Q

What is expressed emotion?

A

Members of family of a psychiatric patient show exaggerated involvement, control and critical/hostile which increases the likelihood of relapse (Kavanagh).

25
Q

What are the three types to express negative emotion

A
  • Verbal criticism of patient
  • Hostility towards patient, anger
  • Emotional over-involvement, including self-sacrifice.
26
Q

How much more likely are patients liable to relapse returning to a family in a high EE environment.

A

4 times

27
Q

What did Kuipers et al (1983) find about expressed emotion?

A

Found high EE relatives talk more and less listen less. High levels of EE most likely to affect relapse rates.

28
Q

What does cognitive explanations involve in psychological explanations for schizophrenia?

A

Dysfunctional thought processing - process info differently concerned with internal mental processes.

29
Q

What are cognitive explanations of delusions in psychological explanations of schizo?

A
  • Patients interpretations of experiences are controlled by inadequate information processing.
  • Perceives themselves as central component in events (egocentric)
30
Q

What are cognitive explanations of hallucinations in psychological explanations of schizo?

A
  • Auditory hallucinations common for people diagnosed with schiz. 73% reporting experiences of them.
  • Aleman (2001) suggests hallucination - prone to find it difficult to distinguish between imagery and sensory perception.
31
Q

Eval for family dysfunction.

Family relationships?

A

Tienari (1994) found that adopted children who had schizophrenic biological parents were more likely to develop schizophrenic symptoms than those whose parents were not schizophrenic. However, this
difference emerged only in situations where the adopted families were rated as disturbed.

Suggests that the illness only manifests itself under
appropriate environmental conditions, and therefore genetic vulnerability on its own is not a sufficient trigger.

unreliability of recall leading to data that may lack validity – patients report childhood
experiences retrospectively. Recall may be inaccurate and distorted by the need to explain.

32
Q

Eval for family dysfunction.

Double bind theory?

A

Berger (1965) found schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics.

33
Q

Eval for family dysfunction.

Individual differences in vulnerability to expressed emotion.

A

Not all individuals who live in high EE environments relapse + not all those living in low EE home avoid relapse.
Altofer (1998) found 25% of patients studied showed no psychological responses.

34
Q

Eval for family dysfunction.
Cognitive explanations
RWA.

A

Sarin + Wallin (2014) found supporting evidence for the claim that positive symptoms of schizo have origins in faulty cognition.
REAL WORLD APPLICATION
Delusional patients showed various biases in info processing, eg: jumping to conclusion + lack of reality.
Tf, therapist can use info to design techniques for treatment of patients.

35
Q

What are the two types of antipsychotic? and their generation

A
  • Typical - conventional / first-generation

- Atypical - 2nd generation / generally fewer side effects.

36
Q

What do typical antipsychotics do?

A
  • Combat positive symptoms (hallucinations)
  • Work in reducing amount of dopamine.
  • Dopamine antagonists bind but do not stimulate dopamine receptors (mainly D2 receptors) thus blocking their action - not stimulating them.
37
Q

What is an example of a typical antipsychotic.

A

Chlorpromazine.

38
Q

What do atypical antipsychotics do?

A
  • Used to treat positive symptoms + claimed effect on negative symptoms.
  • Work on dopamine system + block serotonin receptors.
  • Also block d2 receptors for a short duration prevent some uptake of dopamine then rapidly dissociate to allow normal dopamine transmission.
  • Thought to carry lower levels of extrapyramidal side effects.
39
Q

What is an example of an atypical antipsychotic.

A

Clozapine.

Olanzapine

40
Q

Kapur (2000) did research into typical antipsychotics, what did Kapur find?

A

Approx. 60-75% pf D2 receptors need to be blocked in mesolimbic pathway for drugs to be effective
But as a result, D2 receptors are also blocked from the rest of the brain.

41
Q

Give 2 strengths of drug therapy.

A

-Allows patient to live in society rather than hospitalisation which is cheaper and allows the patient to still live their live relatively normally.

-Leucht (2012) meta anaysis. 65 studies nearly 6000 patients between 1959 - 2011
Large sample size + temporal validity.
Found 64% of placebo group relapsed compared to 27% who stayed on antipsychotic drug.

42
Q

Give 3 limitations of drug therapy.

A
  • Reduces whole brain activity
  • Extrapyramidal side effects, typical antipsychotics can sometimes produce movement problems for patient as the drugs interfere with extrapyramidal parts of the brain which helps to control motor activity.
  • Antipsychotics purely deal with the symptoms, cannot kill/change the cause of schizophrenia.
  • Motivational deficits, Ross and Read (2004) argue people prescribed antipsychotic medication reinforces the view ‘something is wrong with them’. Could contribute to condition.
43
Q

What is token economy?

A

Token economy is a form of behavioural therapy where clinicians set target behaviours they believe will improve patient’s engagement in daily activities.

44
Q

When are token are awarded in the token economy?
Give an example.
and what does this allow?

A
  • Rewards are given when desirable behaviour is demonstrated.
    eg: maintaining personal hygiene.
  • Rewards usually tokens/points - can then be exchanged.
45
Q

What is the primary and secondary reinforcer in the token economy?

A

Tokens have no intrinsic value - secondary reinforcers.

What can be exchanged with your tokens are the primary reinforcer.

46
Q

What are the 4 stages to the token economy cycle?

A

1 - Tokens paired with rewarding stimuli, so become secondary reinforcers
2 - Patient engages in target behaviours or reduces inappropriate ones.
3 - Patient given tokens for engaging in these target behaviours, like dressing themselves.
4 - Patient trades these tokens for access to desirable items.

47
Q

What is reinforcing the target behaviours about?

A

Generalisation - learning theory principles is important because once behaviours are reinforced and established in an institution, they then need to be generalised to the outside world.

48
Q

Give 2 limitations of the token economy.

NOT TO DO WITH STAFF

A
  • Dependency; patients may only produce the desired behaviour in order to receive a token, not because they have learned.
  • Transference; desired behaviours in real life can lead to rewards but often not, (eg: getting dressed). Tf there can be great difficulty in transferring this from an institution to real life.

-Less useful for patients living in community. Shown to reduce negative symptoms, only in hospital settings.
Corrigan (1991) argues outpatients struggle - only receive care a few hours a day. Tf, t.e. limited time, results may not be maintained beyond environment.

49
Q

Give 2 reasons why token economy may not work. Another evaluation point for the limitation of the token economy.

A
  • Staff not committed to programme, do not focus sufficiently.
  • Inconsistent rewards given for same behaviour - could confuse patient.
  • Failure to plan for transferring to environment outside the institution.
50
Q

Give 2 strengths of token economies. (FIGURES)

A
  • Cheap methods of rehabilitating
  • Anyone can reward with tokens.

-Found to be successful by many studies, approx 10-20% people do not respond well.

-Research support, Dickerson et al. (2005) reviewed 13 studies, use of token economy systems.
Overall 11/13 studies reported beneficial effects , studies provide evidence of t.e. effectiveness.