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Schizophrenia Flashcards

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1
Q

What are the positive symptoms of schizophrenia?

A
  • Hallucinations
  • Delusions/paranoia/grandeur
  • Disorganised speech
  • Disorganised/catatonic behaviours
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2
Q

What is meant by a positive symptom of schizophrenia?

A

They aren’t “positive” because they’re good

They’re thinsg that are ADDED & which “normal” people dont’ have

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3
Q

What are hallucinations?

A

Seeing/hearing things

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4
Q

What are Delusions/paranoia/grandeur?

A

Flase cognitions

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5
Q

What is disorganised speech

A

“word salad” - unable to form proper sentences

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6
Q

What is disorganized/catatonic behaviour?

A

Completion/motivation issues

Catatonic behaviour = freezing/ unable to move limbs or respond to speech

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7
Q

What is a negative symptom of schizophrenia?

A

Known as “defecits” if they’re present for at least a year

These are things that people have lost

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8
Q

What are the two types of drugs used to treat sz?

A
  • Typical

- Atypical

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9
Q

Give an example of a typical antipsychotic

A

Chloropromazine

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10
Q

Give an example of an atypical antipsychotic

A

Clozapine

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11
Q

What are sz symptoms also known as?

A

Psychosis

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12
Q

What is the general name for drugs that are used to treat sz?

A

Antipsychotics

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13
Q

What are typical antipsychotics like?

A
  • Developed in the 1950s

- Stop hallucinations/delusions

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14
Q

What are atypical antipsychotics like?

A
  • More modern than typical (popular since 1980s)
  • Treat +ive AND -ive symptoms
  • Work on “ hard-to-treat” patients
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15
Q

What are typical antipsychotics also known as?

A

Known as dopamine antagonists

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16
Q

Why are typical antipsychotics also known as dopamine antagonists?

(What is the action of typical antipsychotics?)

A

They bind to D2 receptors but they don’t stimulate them

Block the action of dopamine

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17
Q

What was the conclusion of Kapur et al.’s study on typical antipsychotics?

A

In order for them to work, 60-75% of mesolimbic pathway D2 receptors must be blocked

These drugs don’t only work on that pathway so there are some pretty horrible side effects

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18
Q

What is the action of atypical antipsychotics?

A

Act on D2 receptors - help with +ive symptoms

Side effects are less severe too, since blockage doesn’t last as long (rapid dossociation)

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19
Q

What is rapid dissociation?

A

In atypical antipsychotics?

Doesn’t block D2 recpetors for too long

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20
Q

How are atypical antipsychotics different to typical antipsychotics?

A

They act on serotonin as well as dopamine

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21
Q

Why are atypical antipsychotics better than typical antipsychotics?

A

They don’t only reduce SZ symptoms - also reduce depression & anxiety

Great as 30-50% of SZ patients attempt suicide at some point

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22
Q

Which studies led to the development of family therapy?

A

Batedon et al. (1956) - Double-Bind Theory

Kuipers et al. (1983) - Expressed Emotion

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23
Q

How long does family therapy (for SZ) usually last?

A

3-12 months

At least 10 sessions

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24
Q

What is family therapy (for SZ)?

A

Family members educated about SZ & how to help relatives cope

Learn to support the patient through treatment & spot/discuss problems positively

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25
Q

How successful is family therapy for treating SZ?

A
  • So successful that NICE recommends it for all SZ families

- It reduces the chance of relapse by up to 50% (Garety et al. 2008)

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26
Q

What sort of patient is family therapy used to treat?

A

A patient who suffers from SZ whose family is hostile/overly expressive

These sorts of families cause more relapses in SZ patients

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27
Q

What is used alongside family therapy to treat SZ?

A

It is commonly used in conjunction with drug therapy and outpatient clinical care

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28
Q

What happens in family therapy?

A

It is a range of interventions aimed at the family of someone with SZ

Should also involve the patient with SZ if practical

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29
Q

What is the aim of family therapy?

A

Aims to improve the quality of communication & intervention between family members & reduce the stress of living as a family & so reduce rehospitalsation

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30
Q

What happens during a family therapy session?

A

During sessions the individaul with SZ is encouraged to talk to their family & explain what sort of support they do & do not find helpful

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31
Q

How does family therapy improve family relationships for the patient with SZ?

A

It improves relationships within the household as the therapist encourages family members to listen to each other

Also to discuss problems & negotiate potential solutions together

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32
Q

What did Pharoah et al. (2010) suggest about the sucess of the strategies used in family therapy?

A

He suggested that the strategies reduce stress & expressed emotion

Also increasing the chances of patients complying with medication

It tends to result in a reduced liklihood of relapse & readmission to hospital

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33
Q

What are some strategies used in family therapy to treat SZ?

A
  • Helping patient & family understand & be better able to deal with SZ
  • Forming a theraputic alliance w family members
  • Reducing stress of caring for relative with SZ & emotional climate in family
  • Improving ability of family to anticipate & solve problems
  • Reduction of anger & guilt in family members
  • Helping family members achieve balance between caring for individual w SZ & maintaining own lives
  • Improving families knowledge & beliefs on SZ
  • Maintaining reasonable expectations among family members towards SZ
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34
Q

Give 3 evaluations of family therapy treating SZ?

A
  • Ethical benefit to quality of life for patients
  • Scientific & objective methodology in supporting research
  • Reduces the need to prescribe dangerous drugs with side effects
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35
Q

What are the two pychological explanations for SZ?

A
  • Dysfuncitonal families

- Cognitive explanations

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36
Q

Which pychological explanations for SZ does the Double bind theory come under?

A

Dysfuncitonal families

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37
Q

Who came up with the Double bind theory?

A

Bateson et al. (1956)

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38
Q

What is the double bind theory (give example too)?

A

A child receiving contradictory messages from parents is responsible for children becoming schizophrenic

e.g. mother tells he son she loves him while physically punishing you - child can get confused what reality is

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39
Q

What is the type of parenting called that leads to the Double bind theory?

Who came up with this?

A

“Schizophrenogenic mother”

Fromm-Reichmann - 1948

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40
Q

What did Fromm-Reichmann say about what a schizophrenogenic mother was like?

A

“A cold, rejecting and secretive mother creates a family environment that makes paranoia perfectly reasonable. The constant fear of persecution, if generalised, will be diagnosed with SZ”

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41
Q

Who came up with the Expressed Emotion theory for SZ?

A

Kuipers et al. (1983)

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42
Q

What was Kuipers et al.’s theory for SZ of Expressed Emotion?

A
  • Families w high “emotional expression” can trigger SZ
  • These families describe SZ relatives as hostile, critical terms
  • EE level in family/friends is strongly correlated with relapse rates
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43
Q

What did Noll (2003) suggest about the Expressed Emotion theory?

A

Negative emotions can trigger SZ episodes in vulnerable people

Supportive environments may be protective

This is a diathesis stress model

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44
Q

What is the cognitive explanation for SZ’s process for delusions?

A 
Inadequate info processing
-->
Egocentric bias
-->
Failure to contextualise events
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45
Q

What is the cognitive explanation for SZ’s process for hallucinations?

A

Hypervigilance
–>
Higher expectancy of voices
–>
Patients can’t distinguish between sensory info & internal images (Aleman 2001)
–>
Misattribute source of internal images to external sources (Baker & Morrison 1998)
–>
Don’t see disconfirming evidence as they don’t reality check
–>
Patients unable to perform “reality testing” (Beck & Rector, 2005)

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46
Q

What was Beck & Rector’s cognitive reason for why hallucinations occur overall?

A

Patients unable to perform “reality testing” (Beck & Rector, 2005)

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47
Q

Apply Beck and Rector’s stages for delusions occuring to the biological context that causes them

A

Cognitive processing biases = Hyperdopaminergia in/around mesolimbic pathway (MLP)

Misattribution of concequences to causes = Hyperdopaminergia in ACC and PFC

Failure to test reality with memory or logic = DLPFC - Hippocampus link atrophy or dysfunction

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48
Q

Link the cognitive process for delusions to the biological explanation for it:

  1. Cognitive processing biases = ?
A

Hyperdopaminergia in/around mesolimbic pathway (MLP)

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49
Q

Link the cognitive process for delusions to the biological explanation for it:

  1. Misattribution of concequences to causes = ?
A

Hyperdopaminergia in ACC and PFC

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50
Q

Link the cognitive process for delusions to the biological explanation for it:

  1. Failure to test reality with memory or logic = ?
A

DLPFC - Hippocampus link atrophy or dysfunction

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51
Q

What was Frith et al.’s study on?

A

A very influential cognitive study into SZ that described these deficits as the underlying cause of some symptoms

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52
Q

When can a token economy be used?

A

It is a system used for many psychological conditions

It’s been proven effective for SZ (Ayllon & Azrin, 1968)

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53
Q

What theory is the token economy based on and how is it used?

A

A behaviourist theory/learning theory

Patients learn to associate +ive behaviours with +ive outcomes

This, it is hoped, will lead to behavioural changes

54
Q

How is a token economy used to help SZ?

A

A form of behavioural therapy used int he management of SZ

It is used to shape & manage behaviour so that patients in long stay hospitals are easir to manage

55
Q

How does a token economy teach SZ patients desirable behaviours?

A

It involves these desirable behaviours being encourages through SELECTIVE REINFORCEMENT

56
Q

When are rewards given to a SZ patient in a token economy?

A

They are given immediately as secondary reinforcers when patients engage in desirable behaviours

e.g. getting dressed in the morning, making a bed, taking medication etc

57
Q

What is a secondary reinforcer in a token economy?

A

Reward tokens that are given immediately after the desirable behaviour

58
Q

What is a primary reinforcer in a token economy?

A

These are tangible rewards that can be redeemed later

e.g. sweets, magazines or other privileges

59
Q

How can tokens earned by SZ patients be used?

A

The tokens themselves have no actual value, they can however be swapped for more tangible rewardsw

(Primary reinforcers)

e.g. sweets, magazines and privileges etc

60
Q

How does a token economy encourange positive behaviours in SZ patients?

A

It encourages desirable behaviours to be repeated becuase they have become associated with rewards & privileges

61
Q

Is a token economy an effective way to deal with SZ?

A

Modifying these behaviours does not cure SZ, it does however improve patients’ quality of life

It makes it more likely that they can live outside a hospital setting

62
Q

What is the cycle for a token economy?

A
  1. Tokens paired with rewarding stimuli & become secondary reinforcers
  2. Patient engages in ‘target’ behaviours/reduces inappropriate ones
  3. Patient given tokens for engaging in these target behaviours
  4. Patient trades these tokens for access to desirable items/other privileges
63
Q

What did Kazdin (1977) find about the effectiveness of tokens in the token economy?

A

The quicker they’re exchanged, the more effective they are

64
Q

What did Sran & Borrero, (2010) say about rewards in a token economy?

A

The more variety of rewards available, the better the reinforcers work

65
Q

How is not knowing how/if the token economy works a limitation?

A

Researchers question its validity compared to evidence-based medical techniques like drugs or CBTp

However it is still used extensively in some developing countries - where successes are reported

66
Q

Why is a lack of potential in a token economy a limitation?

A

Corrigan (1991) highlights the difficulty in monitoring & administering this procedure with anyone outside of hospital

However, used in conjunction with family therapy it can be effective

67
Q

Why is CBTp used for conditions like SZ instead of regular CBT?

A

Normal CBT (e.g. for depression) is inappropriate for psychotic disorders (like SZ)

This is because SZ is largely biological & cannot yet be “cured”

68
Q

How do CBT and CBTp differ?

A

CBT (for depression) –> We try to change behaviours in order to SOLVE the probelm

CBTp (for SZ) –> We try to change behaviours in order to COPE with the problem

69
Q

What is the aim of CBTp?

A

Aims to help patients identify irrational thoughts & challange them (inc. origin of voices) & reality testing to reduce distress

70
Q

How long does NICE reccommend that CBTp should take place for?

A

5-20 minute sessions, NICE reccommends around 16 sessions

71
Q

What model does CBTp use?

A

The ABCDE model

72
Q

What does the ABCDE model stand for that is used in CBTp?

A

A - identifying the ACTIVATING events
B - & resulting BELIEFS that
C - cause emotional & behavioural CONCEQUENCES
D - these beliefs can then be rationalised, DISPUTED & changed through critical collaborative analysis
E - leading tothe EFFECT of restructured beliefs

73
Q

What is critical collaborative analysis?

A

The therapist uses gentle questioning to help the patient to understand & changeillogical deductions & conclusions

e.g. “if your voices are real, why can no one else hear them”

74
Q

How does CBTp help SZ patients?

A

Rather that “getting rid” of SZ, CBTp helps patients to COPE better with their symptoms as it reduces distress

75
Q

How do therapists use normalisation in CBTp?

A

The therapist shares with the patient that many people have unusual experiences such as hallucinations & delusions in many different circumstances

Reduces anxiety & sense of isolationby making patient feel less alienated & stigmatised

Makes posibility of recovery more likely

76
Q

What are behavioural assignments in CBTp?

A

Pateints are set these behavioural assignments to improve their general level of functioning

e.g. to shower everyday or to go out & socialise with friends once between now and the next session

77
Q

What are the stages in CBTp?

A
  • Assessment
  • Engagement
  • The ABC model
  • Normalisation
  • Critical collaborative analysis
  • Developing alternative explanations
78
Q

Give 3 evaluation points on CBTp

A

1 - Lack of availability - NICE found only 1/10 affected people in the UK get it

2 - Good research backing - NICE (2014) better outcomes after 18 months

3 - CBTp may have become over-hyped - Jauhar et al. (2014) found it only had a small effect on SZ symptoms

79
Q

What are the 4 types of negative symptoms?

A
  • Avolition
  • Speech poverty (Alogia)
  • Affective flattening
  • Anhedonia
80
Q

What is Avolition?

A

Reduced motivation/goal-directed behaviour where options are present

81
Q

What is speech poverty (alogia)?

A

Loss of fluency/productivity

They don’t know less - they just produce less in a given time

82
Q

What is affective flattening?

A

Reduced range/intensity of emotions, even body language

83
Q

What is anhedonia?

A

Loss of interest/pleasure, or reduced reaction to things that are pleasurable

Social aspect confused with depression - only physical anhedonia is reliable for SZ

84
Q

What is reliability (in terms of SZ)?

A

How consistently clinicians coem to the same conclusion using the criteria (test-retest reliability) & agree with each other (inter-rater reliability)

85
Q

What is validity (in terms of SZ)?

A

How far the DSM measures what it says it does & whether a diagnosis represents a clear, distinct “condition” (internal/external)

86
Q

What are the probelms that occur when diagnosing SZ?

A
  • Symptoms overlap wiht other disorders
  • Gender bias in diagnostic criteria (aimed at men)
  • Cultural differences (in some cultures you’d be revered if you saw things)
  • Comorbidity (which disorder came first and/oris the main cause of illness
87
Q

When and where did the “Being Sane in Insane Places” case study take place?

A

1973 - in 4 states

88
Q

What happened in the “Being Sane in Insane Places” study?

A
  • Covert ppt observation (1973)
  • Students reported only “dull thud” - not actual symptom (DSM-II)
  • All diagnosed with SZ & hospitalised
  • All given meds/treatment & not allowed to leave until the university intervened - in some cases after 2 months
89
Q

How reliable was the “Being Sane in Insane Places” study?

A

Inter-rater reliability good byt internal validity was poor

90
Q

Who conducted the “Being Sane in Insane Places” case study?

A

Rosenhan - 1973

91
Q

How did Rosenhan follow up his “Being Sane in Insane Places” study?

A
  • Later phoned the hospitals & said he was sending more fake patients over soon. Over next 2 weeks , 21% patients were labelled as “pseudopatients” & released
  • Rosenhan actually never sent any more people to the hospital
92
Q

How can comorbidity occur?

A
  • Depression, anxiety disorders, PTSD etc
  • The symptoms can overlap - disassociative personality disorder especially
  • Application issues, if treated with wrong drugs can make condition worse
93
Q

Is SZ completely biological?

A

Not completely - thought to be partly biological & partly psychological

This means genes, hormones, brain structure, cog. styles & emotional factors all had good research support

94
Q

How does SZ being partly biological & partly psychological affect the way we look at the condition?

A

We must consider all factors: biology & the environment interact to produce SZ

This is known as a diathesis-stress model

95
Q

What are biological explanations?

A

Emphasise the role of inherited factors & dysfunction of brain activity int he development of a behaviour or mental disorder

96
Q

What is the dopamine hypothesis?

A

Claims that an excess of the NT dopamine in certain regions of the brain is associated w +ive symptoms of SZ

97
Q

What is genetics?

A

Inherited factors make certain individuals more likely to devlop a behaviour or mental disorder

98
Q

Whatis neural correlates?

A

Changes in nueronal events & mechanisms that result in the characteristic symptoms of a behaviour or mental disorder

99
Q

What are cognitive explations?

A

Cognitive explations of mental disorders propose that abnormalities in cog. function are a key component of SZ

100
Q

What is dysfunctional though processing?

A

Cog. hobits pr beleifs that cause the individual to evaluate info inappropiately

101
Q

What is family dysfunction?

A

The presence of problems within a family that contribue to relapse rates in recovering SZs, including lack of warmth between parents & child, dysfunctional communication patterns & parental overprotection

102
Q

What are atypical antipsychotics?

A

Carry a lower risk of extrapyrimidal side effects, have a deneficial effect on -ive symptoms & cog. impairment & are suitable for treatment-resistan patients

103
Q

What is drug therapy?

A

Involves treatment of mental disorders such as SZ through the use of antipsychotics to reduce the symptoms of the disorder

104
Q

What are typical antipsychotics?

A

They’re dopamine antagonists in that they bind but do not stimulate sopamine receptors & so reduce the symptoms of SZ

105
Q

What is family therapy?

A

The name given to a range of interventions aimed at the fmaily of someone with a mental disorder

106
Q

What is a diathesis-stress model?

A

Explains mental disorders as the result of an interaction between biological (diathesis) & environmental (stress) influences

107
Q

What are the two genes implicated in SZ?

A
  • Dopamine receptor genes (D2, DRD2)
  • Glutamate receptor genes (AMPA)

They’re both excitatory NTs (learning, mem, motivation & arousal)

108
Q

What do dopamine receptor genes (D2) do?

A

Affect no. dopamine receptor sites & transpor proteins for dopamine

109
Q

What do glutamate receptor genes (AMPA) ?

A

Affects no. glutamate receptor sites

Especially important in the basal ganglia

110
Q

What were the 3 studies conducted on genetic factors contributing to SZ?

A
  • Family (Gottesman - 1991)
  • Twins (Joseph - 2004)
  • Adoption (Tienari et al. 2000)
111
Q

What happened in Gottesman’s (1991) study on genetic factors affecting SZ?

A

Study on families - studied concordance rates in children with SZ parent(s) or siblings

  • 2x SZ parents –> 46% concordance
  • 1x SZ parent –> 13%
  • 1x SZ sibling –> 9%
112
Q

What happened in Joseph’s (2004) study on genetic factors affecting SZ?

A

Twins - meta-analysis of data on MZ vs DZ twin concordance for SZ

  • MZ concordance –> 40.4%
  • DZ concordance - 7.4
113
Q

What happened in Tienari et al.’s (2000) study on genetic factors affecting SZ?

A

Adoption - compared siblings raised together vs. apart

  • 164 adoptees had SZ mothers. Of these, 6.7% also developed SZ
  • 197 adoptees were in control grp. 2% developed SZ

Conclusion - genetic liability for SZ is “decisively confirmed”

114
Q

How does the dopamine hypothesis cause SZ?

A
  • They have too many D2 receptors
  • Thier D2 receptors are too sensitive/fire too often
  • They produce too much dopamine
115
Q

What is dopaminergia?

A

What dopamine’s actions in the brain are known as

116
Q

What is hyperdopaminergia?

A

If you have too much dopamine

117
Q

What is hypodopaminergia?

A

If you have too little dopamine

118
Q

What sort of symptoms are hyperdopaminergia assocaited with?

A

Positive symptoms

119
Q

What sort of symptoms are hypordopaminergia assocaited with?

A

Negative symptoms

120
Q

Give an example of hyperdopaminergia causing +ive symptoms?

A

Broca’s area produces speech - too much dopamine here leads to the speech & hearing-related symptoms

121
Q

Give an example of hypordopaminergia causing -ive symptoms?

A

PFC is the sentral executive - too little dopamine here leads to avolition/catatonia

122
Q

How do we know that it’s dopamine that causes SZ?

A

Drugs that decrease dopamine levels reduce SZ symptoms

e.g. chloprozamine or clozapine

123
Q

What is the action of chloprozamine?

A

It acts on dopamine

124
Q

What is the action of clozapine?

A

Act on dopamine & serotonin

125
Q

What is the process of dopamine creating poitive symptoms?

A

Too much dopamine in MESOLIMBIC PATHWAY => positive symptoms

126
Q

What is the process of dopamine creating negative symptoms?

A

Too little dopamine in PREFRONTAL CORTEX -> negative symptoms

127
Q

What did Davis & Khan (1991) find about dopamine affecting SZ?

A
  • Too much dopamine in MESOLIMBIC PATHWAY = positive symptoms
  • Too little dopamine in PREFRONTAL CORTEX = negative symptoms
128
Q

What is the DLPFC?

A

Dorsilater Prefrontal Cortex

129
Q

What evidence is there for the dopamine hypothesis?

A

Patel et al. (2010) - PET scans

Wang & Deutch (2008) - rat study

130
Q

What did Patel et al.’s (2010) study using PET scans show?

A

The scans showed lower dopamine levels in the PFC of SZ patients compared to controls

Supports the dopamine hypothesis

131
Q

What did Wang & Deutch’s (2008) study on rats show?

A

They lowered rats’ levels of dopamine in their PFC - this impaired their cognition

They then gave them atypical antipsychotics (improve -ive symptoms) & this was reversed

Proved dopamine hypothesis

Psychology A-level (7 decks)

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