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Psychology set 1 > Schizophrenia > Flashcards

Schizophrenia Flashcards

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1
Q

How do DSM-5 and ICD-10 differ in the diagnosis of schizophrenia?

A

DSM-5 = one positive symptom must be present.

ICD-10 = two or more negative symptoms are sufficient.

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2
Q

What does positive symptoms of schizophrenia mean?

A

Additional experiences beyond those of ordinary existence.

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3
Q

Give 2 positive symptoms of schizophrenia

A

1) Hallucinations - sensory experiences with no basis in reality or distorted perceptions of real things e.g. hearing voices.
2) Delusions - beliefs that have no basis in reality; changing behaviour that may make sense to schizophrenic but isn’t in reality e.g. believing one’s the victim of a conspiracy.

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4
Q

What does negative symptoms of schizophrenia mean?

A

Loss of usual abilities and experiences.

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5
Q

Give 2 negative symptoms of schizophrenia

A

1) Avolition - severe loss of motivation to carry out everyday tasks e.g. work = lower activity and unwillingness to carry out goal-directed behaviours.
2) Speech poverty (Alogia) - a reduction in the amount and quality in speech

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6
Q

Give 4 issues in the diagnosis of schizophrenia

A

1) Reliability - consistency of diagnosis.
2) Validity - extent to which diagnosis and classification measure what they are designed to measure.
3) Co-morbidity - occurrence of two illnesses together confusing diagnosis and treatment.
4) Symptom overlap - two or more conditions sharing symptoms questions validity of classification.

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7
Q

What did Cheniaux et al. (2009) find with the diagnosis of schizophrenia?

A
  • It had low reliability.
  • Two psychiatrists independently diagnosed 100 patients using both ICD and DSM criteria.
  • Low inter-reliability.
  • (1) 26 diagnosed with DSM and 44 with ICD.
  • (2) 13 diagnosed with DSM and 24 with ICD.
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8
Q

How is the diagnosis of schizophrenia questioned validity wise?

A
  • Cheniaux showed that Sz is much more likely to be diagnosed with ICD than DSM.
  • Over-diagnosed in ICD or under-diagnosed in DSM?
    = poor criterion validity.
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9
Q

A part from low validity and reliability, give a further limitation of the diagnosis of schizophrenia

A

1) Co-morbidity:
- two conditions = a single condition?
- Buckley et al. (2009) concluded half patients with Sz also have a diagnosis of depression (50%) or substance abuse (47%)

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10
Q

How is there gender bias in the diagnosis of schizophrenia

A

(i) Longenecker et al. (201) found that since the 1980s men have been diagnosed more often than women.
(ii) Cotton et al. (2009) - female patients typically function better than men = may escape diagnosis due to better interpersonal functioning.

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11
Q

What did Gottesman (1991) find the concordance rate of both schizophrenia was in MZ and DZ twins?

A 
MZ = 48%
DZ = 17%
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12
Q

How is schizophrenia polygenetic and aetiologically heterogeneous?

A 
P = each gene confers a small increased risk of schizophrenia.
AH = different combinations lead to schizophrenia
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13
Q

What did Ripke et al. (2014) find?

A
  • 108 separate genetic variations associated with increased risk
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14
Q

How is dopamine (DA) involved with schizophrenia?

A

Featured in the functioning of brain systems related to the symptoms of schizophrenia

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15
Q

Hyperdopaminergia is linked with what areas of the brain which may lead to what symptoms?

A
  • Subcortex.

- Hallucinations and speech poverty.

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16
Q

What is hyperdopaminergia?

A

High DA activity in the subcortex

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17
Q

What is hypodopaminergia?

A

Low levels of dopamine in the prefrontal cortex.

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18
Q

What can low levels of DA in the prefrontal cortex lead to?

A

Avolition.

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19
Q

Define neural correlates.

A

Measurements of the structure or function of the brain that correlate with the positive or negative symptoms of schizophrenia

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20
Q

How is avolition linked to the ventral striatum?

A
  • VS involved in anticipation of reward (motivation)
    = avolition explained by low levels here?
  • Juckel et al. (2006) found a negative correlation beween VS activity and overall negative symptoms.
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21
Q

In terms of neural correlates, what would a negative correlation mean?

A
  • There is a correlation between an area of the brain and the negative symptoms of schizophrenia
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22
Q

What part of the brain are hallucinations believed to be linked with?

A
  • Superior temporal gyrus.
  • Allen et al. (2007) - patients experiencing auditory hallucinations recorded lower activation levels in this area and anterior cingulate gyrus.
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23
Q

What strong evidence is there for genetic vulnerability of schizophrenia?

A
  • Gottesman with his family study of schizophrenia.
  • Tienari et al. (2004) did an adoption study.
  • Showed children of people with Sz are still at heightened risk of Sz if adopted into families without history of Sz.
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24
Q

How is there mixed support for the dopamine hypothesis?

A
  • Dopamine agonists, e.g. amphetamoines, that increase increase DA can induced schizophrenic-like symptoms in people without Sz.
  • Anti-psychotics that lower DA can be effective in reducing symptoms
  • Some candidate genes responsible for production of other genes
    = DA inadequate.
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25
Q

A part from mixed support for the DA hypothesis, give 2 further limitations of the biological explanation of schizophrenia

A

1) Correlation-causation problem:
- is it unusual activity in the brain causing the symptoms?
e.g. it is assumed that low activity in VS caused avolition
= could be that less info passes through the VS resulting in low activity?
= cause???

2) Clear that the environment is also involved:
- probability of developing Sz even if MZ twins is less than 50%
- suggests other factors like dysfunctional family
= interactionist approach more appropriate?

26
Q

What 2 types of drug treatments are there for schizophrenia?

A
  • Typical antipsychotics

- Atypical antipsychotics.

27
Q

Describe typical antipsychotic drugs.

A
  • E.g. Chlorpromazine, first introduced in the 1950s.
  • Aim to reduce the action of dopamine; acting as antagonists.
  • Work by blocking dopamine receptors in the synapses in the brain.
  • C’mazine normalises neurotranismission.
  • C’mazine also has effect on histamine receptors, leading to sedation effect.
28
Q

How do typical and atypical antipsychotics differ in what they target?

A

Typical = dopamine

Atypical = dopamine and serotonin.

29
Q

Describe atypical antipsychotic drugs

A
  • E.g. Clozapine, first introduced in the 1970s.
  • Aimed to improve effectiveness and suppress psychoses and also minimising side effects.
  • Bind to serotonin and dopamine receptor sites.
  • Also reduces depression and anxiety, improving cognitive functioning.
30
Q

Why is clozapine lowering mood significant?

A
  • Up to 50% of people suffering from schizophrenia attempt suicide.
31
Q

Why was risperidone developed after clozapine?

A
  • Clozapine involved in deaths because of a blood condition.

- It binds more strongly to DA receptors so is more effective in smaller doses and has fewer side effects.

32
Q

What evidence is there for the effectiveness of drug therapy for schizophrenia?

A
  • Thornley et al. (2003) - data from 13 trials found that chlopromazine was associated with better functioning and reduced symptom severity compared with placebo.
  • Meltzer et al. (2012) - clozapine more effective than typical drugs, 30-50% more effective in treatment-resistant cases
33
Q

Give 3 evaluative limitations of drug therapy as a treatment for schizophrenia

A

1) Side effects:
- typical drugs associated with dizziness, agitation - long term may lead to lip smacking due to DA super-sensitivity.
- Most serious is neuroleptic malignant syndrome (NMS)
= Rate of attrition? Mistrust?

2) Doubts about true effectiveness of antipsychotics:
- Healy (2002) - data from successful trials have been published multiple times, exaggerating positive effects.
- Also mostly short-term effects.
- As they calming effect = easy to demonstrate they have a positive effect.

3) Antipsychotics drugs may be a ‘chemical cosh’:
- may be used in hospital to calm patients and make them easier for staff to work with, not benefit patients directly.
- Human rights’ abuse? Ethics?

34
Q

In terms of psychological explanations for schizophrenia, how many family dysfunction explanations are there? Name them.

A
  • 3.
    1) Schizophrenogenic mothers.
    2) Double-bind theory.
    3) Expressed emotion.
35
Q

Describe schizophrenogenic mothers

A
  • Fromm-Reichmann (1948) psychodynamic explanation based on early experiences.
  • Cold, rejecting, creating a family climate of tension and secrecy.
  • Leading to distrust, paranoid delusions and Sz.
36
Q

Describe the double-bind theory.

A
  • Bateson et al. (1972) - child regularly trapped in situations where they fear doing the wrong thing; receiving conflicting messages about what counts as wrong.
  • Cannot express feelings about unfairness of situation.
  • When they ‘get it wrong’ - child is punished by withdrawal of love.
    = World is confusing and dangerous –> disorganised thinking and delusions.
37
Q

How’s expressed emotion different from schizophrenogenic mother and double-bind theory?

A
  • It’s to do with what can cause relapse, not the cause.
38
Q

Describe expressed emotion

A
  • EE is the level of emotion, mainly negative, expressed towards the Sz patient.
  • Verbal criticism of them, hostility, over-involvement in their life.
  • High levels of EE cause stress in the Sz patient = relapse.
39
Q

In terms of the psychological explanation for schizophrenia, what is the cognitive explanation?

A
  • Dysfunctional thought processing, low levels of it suggest impairment
    e. g. VS with negative symptoms
  • Metarepresentation.
  • Dysfunction of metarepresentation disrupts our ability to recognise our thoughts as our own, leading to sensation of hearing voices (hallucinations) and having thoughts placed in minds by others (delusions).
40
Q

What is metarepresentation?

A
  • The cognitive ability to reflect on thoughts and behaviour (Frith et al. 1992)
41
Q

How did Frith et al. (1992) say dysfunction of central control can lead to speech poverty?

A
  • Central control = cognitive ability to suppress automatic responses while performing deliberate actions.
  • People with Sz experience derailment of thoughts and spoke sentences because each word triggers automatic assocations they can’t suppress.
42
Q

What support is there for different information processing?

A
  • Stirling et al. (2006) compared 30 Sz patients with 18 patients on cognitive tests, e.g. Stroop Test.
  • Patients 2x longer than control group = had to suppress impulse to read word, supports Frith’s theory.
    = cause of symptoms or cause of disorder?
43
Q

How is evidence for family relationships a weakness?

A
  • Often retrospective.
  • Read et al. (2005) - 42 studies, 69% of all adult female patients with Sz had a history of abuse (as well as 59% of men).
  • Most info gathered after diagnosis.
  • Symptoms distorting patients’ recall?
44
Q

A part from family relationship evidence being retrospective, give 2 more evaluative limitations of psychological explanations of schizophrenia

A

1) Evidence for family-based explanations is weak:
- poor childhood experiences may be associated with Sz, but little evidence for family dysfunction.
- theories based on clinical observation.
- blame game on parents too.

2) Biological factors sometimes overlooked:
- can’t explain it psychologically with biological explanation too.
- can both separately produce same symptoms?
- diathesis-stress model instead?

45
Q

Give the 3 psychological therapies for schizophrenia

A

1) CBT
2) Family therapy
3) Token economies.

46
Q

In terms of psychological therapy for schizophrenia, describe CBT.

A
  • Aims to help patients identity irrational thoughts and try to change them,
  • Discussion of how true they are, considering less threatening possibilities.
  • Helps patients understand their symptoms, and how they impact on their feelings and behaviour
    = realise their beliefs are not based on reality-> reduced anxiety.
47
Q

In terms of psychological therapy for schizophrenia, describe family therapy

A
  • Improve communication and interaction in the family.

- Reduce stress in the family that may contribute to relapse; reduced EE.

48
Q

What do Pharoah et al. (2010) propose to improve family functioning?

A
  • To reduce likelihood of relapse and readmission.
    1) Reduce stress of caring for a relative with Sz.
    2) Improve ability to anticipate and solve problems.
    3) Reduce guilt and anger in family members.
    4) Improve beliefs about and behaviour towards Sz.
49
Q

In terms of psychological therapy for schizophrenia, describe token economies

A
  • Reward systems (tokens) for desirable behaviours, by operant conditioning e.g. getting dressed.
  • The reward reinforces desirable behaviour, reward given immediately preventing delay discounting.
  • Tokens have no value in themselves, but are swapped for rewards e.g. cigarettes
  • Tokens = secondary reinforcers as value is learned by association (classical conditioning) with innate primary reinforcers.
50
Q

How does evidence for psychological therapies show limited evidence?

A
  • Jauhar et al. (2014) CBT significant but small effect on positive and negative symptoms.
  • McMonagle + Sultana (2009) - 1 of 3 studies of token economies that used random allocation showed improvement.
  • Pharoah et al. reviewed his proposal and found moderate evidence for reduction in relapse over one year = evidence inconsistent.
51
Q

How might the therapies help but not be a cure?

A
  • CBT = make sense of symptoms.
  • Family therapy = reduce stress.
  • TE = behaviour socially acceptable.
    = do not cure.
52
Q

A part from limited benefits of psychological therapies and therapies helping but not being a cure, give 2 limitations of psychological therapies for schizophrenia.

A

1) Ethical usses:
- severely ill patients cannot get privileges b/c they are less able to comply with desirable behaviours than moderately ill patients.
- Also, CBT challenges paranoia but what about freedom of thought? Some may believe in a controlling Gov?
= challenging this may be modifying people’s political beliefs.

2) Quality of evidence:
- positive results found for therapies
- but these studies may lack a control group or random allocation
- overestimation of evidence?

53
Q

What does diathesis and stress also mean?

What is the diathesis-stress model?

A
  • Vulnerability and trigger.
  • Vulnerability (to Sz), stress in this context refers to negative psychological experiences.
    ; vulnerability and stress both needed to develop Sz.
54
Q

Describe Meehl’s model of schizophrenia?

A
  • Gene + stess = schizophrenia.
  • Someone without a ‘schizogene’ should never develop schizophrenia, no matter the exposed stress.
  • Those with the gene are vulnerable to the effects of chronic stress.
  • Gene not sufficient, just necessary for development of schizophrenia.
55
Q

What is the modern understanding of diathesis?

A
  • Diathesis not due to one schizogene, instead its many genes increasing vulnerability.
  • Diathesis not necessarily genetic, may be early psyhological trauma affecting brain development e.g. child abuse affects HPA, making vulnerability to stress.
56
Q

What is the modern understanding of stress?

A
  • Anything that risks triggering Sz, including psychological stress.
  • E.g. cannabis use can increase the risk of Sz 7x as it interferes with DA system.
57
Q

What is the treatment for schizophrenia according to the interactionist approach?

A
  • Combine antipsychotic medication and CBT.
  • Turkington et al. (2006) - possible to believe in biological causes and still practice CBT to relieve psychological syptoms.
  • One should not adopt solely one approach.
58
Q

How is the interactionist approach useful in treatment of schizophrenia?

A

(i) Tarrier et al. (2004)
- randomly allocated 315 patients to;
(1) medication + CBT
(2) medication + supportive counselling.
(3) control group
= patients in combo groups showed lower symptom levels than medication only.
= no difference in readmission though.

59
Q

How is the original diathesis-stress model too simplistic?

A
  • No sole ‘schizogene’
  • Stress also comes in ma forms.
  • Stress can also include biological factors.
  • Houston et al. (2008) - childhood sexual trauma was a diathesis and cannabis was the trigger.
60
Q

A part from simplicity of the diathesis-stress model, give 2 further limitations of the interactionsist approach to schizophrenia.

A

1) Don’t know exactly diathesis and stress work;
- evidence to suggest underlying vulnerability coupled with stress can lead to Sz.
- do not understand mechanisms by which Sz symptoms work, and how vulnerability and stress produce them.
= incomplete understanding.

2) Treatment-causation fallacy:
- Turkington et al. (2006) arguing that an interactionist approach is more effective does not mean it is simply correct.
- Drugs helping does not mean its biological in origin = treatment-causation fallacy.
- Superior outcomes of combined therapies should not be over-intererpreted in terms of evidence in support.

Psychology set 1 (9 decks)

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