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Schizophrenia Flashcards

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1
Q

What is schizophrenia?

A

A psychotic disorder
A severe mental disorder where contact with reality and impaired

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2
Q

What does schizophrenia affect?

A

Thought processes and ability to determine reality

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3
Q

Which groups are more likely to receive a diagnosis of schizophrenia?

A

Men
City dwellers
Lower class

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4
Q

How do you diagnose a specific disorder by distinguishing one from another? How is schizophrenia diagnosed?

A
  1. Identify clusters of symptoms that occur together, classify as one disorder
  2. Diagnose by identifying symptoms and deciding what disorder a person has

For schizophrenia…
ICD-11 says 2 negative symptoms sufficient for diagnosis
DSM-5 says must have at least 1 positive symptom

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5
Q

What are the 2 broad types of symptoms of schizophrenia?

A

Positive or negative

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6
Q

What are positive symptoms?

A

Additional experiences beyond those of ordinary experience

Hallucinations and delusions

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7
Q

What are negative symptoms?

A

Loss of usual abilities and experiences

Speech poverty and avolition

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8
Q

What are hallucinations?

A

Bizzare, unusual sensory experiences
They are
- either distorted/exaggerated perceptions
OR
- have no basis in reality

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9
Q

What are 4 types of hallucinations? Give an example for each

A

Auditory- eg: hearing voices others can’t
Visual- eg: distorted facial expressions
Olfactory- eg: smelling burning
Tactile- eg: bugs crawling on skin

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10
Q

What are delusions?

A

Firmly held (yet false) irrational belief held by the person that have no basis in reality

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11
Q

What are 4 types of delusions? Give an example for each

A

Delusions of grandeur- eg: believing you have superpowers
Paranoia- eg: paranoia that you are under executive control
Delusions of persecution- eg: claims people are hiding to find you
Delusions of reference- eg: personal message communicated through TV

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12
Q

What is speech poverty?

A

Reduction in the frequency and quality of speech, may also be a delay in verbal responses

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13
Q

Do people with schizophrenia know the same words as people without schizophrenia?

A

Yes, but they have difficulty producing information → slowed or blocked thoughts

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14
Q

What is speech disorganisation?

A

A positive symptom in DSM-5
Speaker changes topic mid-sentence or speech is jumbled/incoherent

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15
Q

What is avolition?

A

Sometimes called apathy
Difficult to begin/keep up with goal-directed and self-initiated activity

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16
Q

Who named the 3 signs of avolition? What are they?

A

Andreasen

  1. Poor hygiene and grooming
  2. Lack of motivation and persistence in work/education
  3. Lack of energy
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17
Q

Comment on reliability and validity for the diagnosis of schizophrenia

A

Good reliability for diagnosis
- high diagnostic reliability (test-retest), the diagnosis of schizophrenia is consistent/repeatable at 2 different points in time
- high inter-rater reliability, different clinicians reach the same conclusions about the same patient
- reliability has improved with DSM-5
- Osório et al found excellent reliability for diagnosis of sz- IR +0.97 and TRT +0.92
Certain that the diagnosis is consistently applied

Low criterion validity for diagnosis
- whether different assessment systems arrive at the same diagnosis for the same patient
- Cheniaux et al found that out of same 100 patients, 68 diagnosed with sz under ICD, only 39 under DSM
Either over or under diagnosed in the diagnostic system, so criterion validity is low

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18
Q

What is the issue with comorbidity in the diagnosis/classification of schizophrenia?

A

Sz has comorbidity with other conditions
- if occurs frequently, validity is questioned as it may be a single condition
- sz commonly diagnosed with other conditions, Buckley found that about half also had depression/substance abuse
Problem for classification, may not be a distinct/precise condition, some people may just have unusual cases of eg: depression

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19
Q

What is the issue with gender bias in the diagnosis/classification of schizophrenia?

A

Gender bias in diagnosis
- 1.4:1 ratio of men diagnosed to women
- women may be just less vulnerable to women bcos of genetics
- but Cotton et al found that women are underdiagnosed as they have closer r/ships, and hence get support, so escape diagnosis
The underdiagnosis means that men and women with similar symptoms may experience differing diagnosis, and women may not receive services/treatment to benefit them

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20
Q

What is the issue with culture bias in the diagnosis/classification of schizophrenia?

A

Culture bias in diagnosis
- some symptoms have different meanings in different cultures (eg: hearing voices)
- Pinto and Jones found that African-Caribbean Brits are up to 9x as likely to receive a diagnosis than white Brits
- through Western lens, overinterpretation of symptoms, thus over-diagnosis
Maybe discriminated against by a culturally biased diagnostic system, more/less likely to be diagnosed just because of ethnicity- questions reliability

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21
Q

What is the issue with symptom overlap in the diagnosis/classification of schizophrenia?

A

Symptom overlap with other conditions
- symptoms may not be unique, may be found in other disorders
- sz and bipolar both have positive symptoms (eg: delusions) and negative symptoms (eg: avolition)
- in terms of classification, sz and bipolar may just be variations of a single conditions
Classification and diagnosis flawed as hard to diagnose/distinguish, and may not even be its own condition

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22
Q

What are the 2 biological explanations to schizophrenia?

A

Genes
Neural correlates

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23
Q

What do family studies show about the likelihood of developing schizophrenia?

A

Risk of schizophrenia increases in line with genetic similarity to a relative with it

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24
Q

Who did large-scale family studies for schizophrenia?

A

Gottesman

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25
Q

According to Gottesman, what is the risk of developing schizophrenia for the general population?

A

1%

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26
Q

According to Gottesman, what is the risk of developing schizophrenia if your aunt/uncle has it?

A

2%

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27
Q

According to Gottesman, what is the risk of developing schizophrenia if your sibling has it?

A

9%

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28
Q

According to Gottesman (and Sheild), what is the risk of developing schizophrenia if you have a dizygotic twin who has it?

A

17%

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29
Q

According to Gottesman (and Sheild), what is the risk of developing schizophrenia if you have a monozygotic twin who has it?

A

48%

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30
Q

What does the correlation/high concordance rate in Gottesman’s family study represent?

A

How families share genes (and environment)

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31
Q

Who did an adoption study for schizophrenia?

A

Tienari et al
164 adoptees whose biological mothers had diagnosed schizophrenia

Strong evidence for a genetic basis to schizophrenia as the adoptees cannot be influenced by their biological parents’ environment

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32
Q

What are candidate genes?

A

Number of different genes involved in schizophrenia, so the condition is polygenetic

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33
Q

What type of candidate genes are involved in sz?

A

Ones coding for dopamine (links to dopamine hypothesis)

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34
Q

What is the study into the candidate genes for schizophrenia?

A

Ripke et al combined all previous data from genome-wide studies of schizophrenia
Very large sample size

108 separate genetic variations associated with increased risk of schizophrenia

Because so many candidate genes identified, schizophrenia is aetiologically heterogenous, so causes vary

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35
Q

How can mutations play a role in the development of schizophrenia?

A

Can have a genetic origin in the absence of family history
May be due to mutation in parental DNA from things like radiation/poison/viral infection

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36
Q

What is the study into how mutation plays a role in the development of schizophrenia?

A

Brown et al

Positive correlation between parental age (associated with increased risk of sperm mutation) and risk of schizophrenia
Fathers over 50 = 2% risk
Fathers under 25 = 0.7% risk

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36
Q

What are neural correlates?

A

Measurements/patterns of the structure and function of the brain that corresponds with an experience and may be implicated in the origins of the experience

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36
Q

What is a strength and weakness of the genetic (biological) explanation for schizophrenia?

A

Research support
- family studies (Gottesman) show risk increases with genetic similarity
- Tienari et al, genes heighten risk
People more vulnerable to schizophrenia because of genetic makeup

Clear that environmental factors also increase risk
- birth complications, smoking TNC-rich cannabis in teens
- Mørkved et al 67% with schizophrenia had childhood trauma
Genetic factors alone not a complete explanation for schizophrenia, interactionist approach better

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37
Q

What is the best-known neural correlate of schizophrenia?

A

Dopamine

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38
Q

What type of neurotransmitter is dopamine?

A

An excitatory neurotransmitter, so increases rate of firing between neurons

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39
Q

What does the original dopamine hypothesis suggest?

A

Antipsychotics reduce dopamine caused similar symptoms to Parkinson’s disease, associated with low dopamine levels

Thus, schizophrenia may result from high levels of dopamine (hyperdopaminergia) in subcortical areas of the brain

Excess dopamine receptors in pathways from subcortex to Broca’s area (responsible for speech production) explains symptoms such as auditory hallucinations
–> As more dopamine binds, so more neurons fire

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40
Q

Who devised the updated dopamine hypothesis?

A

Davis et al

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41
Q

What does the updated dopamine hypothesis suggest?

A

Added the concept of hypodopaminergia (abnormally low levels of dopamine) in the cortex
–> Low dopamine in the prefrontal cortex (responsible for thinking) could explain cognitive problems (negative symptoms)

Cortical hypodopaminergia leads to subcortical hyperdopaminergia
–> So both high and low levels of dopamine in different brain regions can explain schizophrenia

42
Q

Why would people be more sensitive to cortical hypodopaminergia (hence subcortical hyperdopaminergia)?

A
  1. Genetic variations
  2. Early experiences of stress (physical and psychological)
43
Q

What is a strength and weakness of neural correlates (biological) explaining schizophrenia?

A

Research support for the involvement of dopamine
- amphetamines increase dopamine
- worsens symptoms/can induce symptoms
- also antipsychotic drugs that lower dopamine effective in reducing symptom
- candidate genes for sz act on production of dopamine/ dopamine receptors
Strongly suggests dopamine is involved in symptoms of sz

Evidence for central role of glutamate
- McCutcheon et al, post-mortem + live scans consistently found raised levels of NT glutamate in several brain regions of schizophrenics
- also several candidate genes for schizophrenia involved in glutamate production/processing
Equally strong case made for role of other NTs

44
Q

What are the 2 types of biological therapy treatment for schizophrenia?

A

Antipsychotic drugs
Typical (traditional 1950s)
Atypical (newer/second generation 1970s)

45
Q

What is the concept of antipsychotics based on?

A

Dopamine hypothesis- blocks receptors so less dopamine binds

46
Q

How long are antipsychotics used for?

A

May be needed for a short course without the return of symptoms, or for life

47
Q

What do typical antipsychotics do, and how are they taken?

A

Block the receptors for dopamine (dopamine antagonists- reduces dopamine activity)

Taken as tablet/syrup/injection

48
Q

What are 2 examples of typical antipsychotics?

A

Chlorpromazine
Haloperidol

49
Q

How does chlorpromazine work? What is the daily dosage?

A

Initially, dopamine increases, then normalises and dopamine production reduced
Also has a sedation effect, as have been shown to affect histamine receptors –> can be used to calm patients with sz and other disorders, often when first admitted to hospital

Max dosage 1000mg/day

50
Q

How does haloperidol work?

A

Rebalances dopamine to improve thinking/mood/behaviour (cognitive functioning)

51
Q

Why were atypical antipsychotics developed?

A

To improve effectiveness of treating symptoms and minimise side effects

52
Q

What are 2 examples of atypical antipsychotics?

A

Clozapine
Risperidone

53
Q

How does clozapine work? Who is it prescribed for? What is the daily dosage?

A

Binds to dopamine receptors and acts on serotonin + glutamate receptors (increases mood and reduce depression/anxiety)

Prescribed for patients at high suicide risk as 30-50% of people with schizophrenia attempt suicide

Dose 300-450mg/day

54
Q

What is a risk of clozapine? How is this risk managed?

A

A blood condition called agranulocytosis, so patients have to manage this with regular blood tests

55
Q

How does risperidone work? What is the daily dosage?

A

Binds to dopamine and serotonin receptors. More strongly to dopamine receptors than clozapine so is effective in much smaller doses

Max dose 12mg/day

56
Q

What is a strength of biological therapy for schizophrenia?

A

Evidence for effectiveness
- Thorley et al review of studies found chlorpromazine associated with ↑ overall functioning and ↓ symptom severity
- Meltzer found clozapine effective in 30-50% treatment-resistant cases where typical antipsychotics failed
Evidence they work

57
Q

What are 3 weaknesses of biological therapy for schizophrenia?

A

But flaw in evidence for effectiveness
- most only assess short-term benefit, may not be as effective in LT
- same data published multiple times exaggerates +effects
Not that effective, more research needed

Serious side effects
- typical egs: dizziness, weight gain, itchy skin
- LT use…
tardive dyskinesia from dopamine supersensitivity involuntary muscle movements eg: grimacing
neuroleptic malignant syndrome blocks dopamine activity in hypothalamus eg: high temp, coma- can be fatal
- frequency 0.1-2%
Harm means meds not taken, can relapse so ineffective

Mechanism of why they work unclear
- use of antipsychotics depends on original dopamine hypothesis
- now, not a complete explanation as low levels in cortex in sz, if this is true, antipsychotics should not work
- drugs that lower dopamine activity only effective to cure some symptoms
Not the most effective treatment for sz

58
Q

What are the 2 psychological explanations to schizophrenia?

A

Family dysfunction
Cognitive explanations

59
Q

What is family dysfunction?

A

Maladaptive relationships and patterns of communication within families as a source of stress

60
Q

What are 3 examples of family dysfunction contributing to schizophrenia?

A

The schizophrenogenic mother
Double-bind theory
High levels of expressed emotion (EE)

61
Q

Who devised the schizophrenogenic mother explanation for schizophrenia? What approach does it follow? What does it literally mean?

A

Psychodynamic explanation from Fromm-Reichmann
Means schizophrenia-causing

62
Q

How can a schizophrenogenic mother explain schizophrenia?

A

Mother is cold + rejecting + controlling
Creates family environment characterised by tension and secrecy
Leads to distrust that develops into paranoid delusions, and ultimately sz

63
Q

Who devised the double-bind theory?

A

Bateson et al
He felt family climate + communication style important risk factor in development of sz

64
Q

How does the double bind theory explain schizophrenia?

A

Child receives contradictory messages -> fear doing wrong thing, but don’t know what is right
Feels unable to comment on unfairness/seek clarification
When gets it wrong, punished by withdrawal of love
Understand world as confusing and dangerous -> paranoid delusions/disorganised thinking

65
Q

What is expressed emotion (EE)?

A

Level of negative emotion expressed towards person with sz by carers

66
Q

What 3 elements does expressed emotion (EE) contain? How does this explain schizophrenia?

A
  1. Verbal criticism, often with violence
  2. Hostility, including anger + rejection
  3. Emotional overinvolvement, including needless self-sacrifice

Serious source of stress -> can explain relapse or can trigger onset in vulnerable person

67
Q

What is a strength of family dysfunction explaining schizophrenia?

A

Research support linking family dysfunction to sz
- Read et al adults with sz disproportionally likely to have insecure attachment C/D
- Mørkved et al 67% with schizophrenia had childhood trauma
Family dysfunction makes people more vulnerable to sz

68
Q

What are 2 weaknesses of family dysfunction explaining schizophrenia?

A

Poor evidence base for explans
- none to support traditional family-based theories (sz mother/double bind)
- just based on clinical observation of schizophrenic patients & informal assessment of mothers’ personalities
- not systematic evidence
Family explanations not able to account for link between childhood trauma + sz

Socially sensitive as leads to parent blaming
- is difficult to watch children struggle and take high responsibility for care
- if was the case, more would have the disorder
Not constructive and doesn’t consider other factors influencing sz

69
Q

What are the 3 cognitive (psychological) explanations for schizophrenia?

A

Dysfunctional thinking
Metarespresentation dysfunction
Central control dysfunction

70
Q

What is dysfunctional thinking?

A

Disruption to normal thought processing

71
Q

How can dysfunctional thinking explain the symptoms of sz?

A

Reduced thought processing in ventral striatum associated with negative symptoms
Reduced information processing in temporal and cingulate gyri associated with hallucinations

72
Q

What does metarepresentation dysfunction do?

A

Disrupts ability to recognise own actions and thoughts as being carried out by ourself, not someone else

73
Q

How can metarepresentation dysfunction explain the symptoms of sz?

A

Explains auditory hallucinations and delusions like thought insertion (experience of having thoughts projected into mind by others)

74
Q

What is central control dysfunction?

A

Issue with the cognitive ability to suppress automatic responses whilst performing deliberate actions

75
Q

How can central control dysfunction explain the symptoms of sz?

A

Disorganised speech and thought disorder- inability to stop automatic thought/speech
Derailment of thoughts because each word triggers associations and cannot suppress automatic responses

76
Q

What is a strength and weakness of cognitive (psychological) explanations for schizophrenia?

A

Research support for dysfunctional thinking
- Stirling et al cognitive tasks eg: Stroop test in 30 schizophrenics / 30 non-schizophrenics
- Have to name font-colours of colour-words, so have to suppress tendency to say word aloud
- Schizophrenics took over twice as long to name font-colours, predicted by lack central control
Shows cognitive processes are impaired

Only explains proximal origins of symptoms
- explains what is happening now to produce symptoms
- Not distal explanation which focuses on what initially caused condition
- Unclear how genetic variation/childhood trauma may lead to meta-representation or central control
Cognitive theories only provide partial explanations for sz

77
Q

What are the 2 psychological therapies for schizophrenia?

A

Cognitive behavioural therapy
Family therapy

78
Q

How long does CBT for schizophrenia take place for?

A

5-20 sessions individually or in a group

79
Q

What are the 3 principles of CBT for schizophrenia?

A

Helps client make sense of how their irrational cognitions impact on their
feelings/behaviour by explaining where the symptoms come from -> reduces
fear/distress/debilitation associated with dysfunction (eg: voice from
malfunctioning speech centre of the brain)
2. Normalisation: those hearing voices can be taught that this is an extension of the
ordinary experience of thinking in words -> will feel less stress/ashamed
3. Delusions can be jointly explored + logically examined with therapist to determine if they are likely to be true; if delusions are resistant to RT, it can be used to tackle accompanying anxiety and depression

80
Q

What is CSE?

A

Coping strategy enhancement: CBT specifically for schizophrenia
Tarrier

81
Q

How does coping strategy enhancement work?

A

Building upon the existing coping strategies of people with schizophrenia (as
individuals could identify triggers for schizophrenic episodes) to reduce
symptoms and accompanying stress
- Cognitive coping strategies: eg positive self-talk
- Behavioural coping strategies: eg loud music to drown out voices
- Overall, aims to have two effective strategies for each specific distressing
symptom

82
Q

What is one strength of CBT as a psychological therapy for schizophrenia?

A

Research and clinical evidence for effectiveness
- Jauhar et al meta-analysis, significant yet small effect of CBT on both +/- symptoms
- clinical advice from NICE (national institute for health and care excellence) recommends + feels CBT is appropriate for sz
Both research & clinical experience support benefits of CBT for sz

83
Q

What are 2 weaknesses of CBT as a psychological therapy for schizophrenia?

A

Quality of evidence poor
- range of techniques and people with varying combinations of +/- symptoms
in studies
- unclear which techniques affected which symptoms
Hard to say how effective it will be for a
particular person

Not a cure
- cannot eradicate symptoms of sz as not a cure
- sz is mainly biological, so CBT only helps patients live with symptoms
- but does improve general QOL
Still open to debate whether CBT can do more than help coping with symptoms

84
Q

Who does family therapy involve?

A

Family and identified patient for 3-12 months

85
Q

What is the aim of family therapy?

A

To improve the quality of communication + interaction to improve family function

86
Q

What are the 5 strategies of family therapy?

A
  1. Forming therapeutic alliance with all family members with trust
  2. Lower EE as learn constructive ways of interaction and communication,
    encouraging focus on good things -> reduces negative emotions (eg: anger/guilt)
    which causes stress
  3. Reasonable expectations for patient’s performance
  4. Set boundaries for balance b/w caring for patient and maintaining own life
  5. Education: to help understand + support + manage, patients encourage stop
    explain what support is useful and what is worse
87
Q

What are the 7 stages of Burbach’s model for family therapy

A
  1. Emotional + practical support
  2. Identify family members’ resources
  3. Understanding + safe space
  4. Identify unhelpful interaction
  5. Skills training eg: stress management
  6. Prevent relapse
  7. Maintenance for future
88
Q

What are 2 strengths of family therapy for schizophrenia?

A

Research for effectiveness
- McFarlane
- Fam Therapy 50-60% reduction in relapse rates
- consistently effective, particularly at onset of MH decline
Likely to benefit those with early or advanced sz

Appropriate on number of levels
- very apt to focus on reducing EE as high EE increases chance of relapse
- schizophrenics do lack social skills (eg: disorganised speech), therapy reduces isolation and emphasises the importance of social functioning
- cost savings -> offset by reduction in hospitalisation costs (lower relapse)
Beneficial from range of perspectives

89
Q

What are token economies?

A

Reward systems to modify maladaptive behaviours where desired behaviours are encouraged using selective reinforcement (tokens) on basis of operant conditioning

90
Q

Although token economies don’t cure schizophrenia, what does it do?

A

Improves quality of life + normalisation

91
Q

What are tokens?

A
  • Objects given to patients when they carry out correct/desirable behaviour to
    prevent ‘delay discounting’ (reduces effect)
  • Secondary reinforcer as have value because can obtain more tangible rewards (primary reinforcer)
92
Q

According to who, what are the 3 categories of institutional behaviour dealt with by using token economies?

A
  1. Personal care
  2. Condition related behaviours eg: apathy
  3. Social behaviour
93
Q

How has the use of token economies changed overtime?

A

Extensive use of token economies in 60s/70s where normal treatment for sz was LT
hospitalisation -> but now: growth in community-based care / ethical issues with
restricting rewards to those with mental disorders
- but still standard treatment to manage sz elsewhere in world

94
Q

Who did research into the effectiveness of token economies?

A

Ayllon + Azrin: women in psychiatric ward with sz
- Every time they carried out a task (eg: making bed) receive plastic token which can be exchanged for privileges (eg: watch film)
- Number of tasks carried out increased significantly

95
Q

What is a strength of token economies in managing schizophrenia?

A

Effective in management
- Glowacki et al 7 high quality studies where sz treated (partly) using token economies in hospital
- all showed reduction in negative symptoms + decline in frequency of unwanted behaviours
Value for managing schizophrenic patients

96
Q

What are 3 weaknesses of token economies in managing schizophrenia?

A

However, small evidence base
- file drawer phenomenon
- bias towards + findings as undesirable results filed away
Questions validity of evidence

Maybe only effective in institutional setting
- institutions 24h care but outpatients in community only a few hours/day
- beneficial effects of reinforcement reduced if reinforcement not continuous as tokens not administered immediately
Not appropriate for most patients treated within community

Alternative approaches that are more pleasant + ethical
- art therapy high-gain low-risk approach where patients have more personal freedom over their recovery
- lacks any major side effects
- recommended by NICE as an apt therapy
May be better alternatives with less negative aspects

97
Q

What is the interactionist approach for explaining and treating schizophrenia?

A

Broad approach acknowledging that a range of factors (biological + psychological + social) are involved in the development of schizophrenia

98
Q

How does the diathesis-stress model explain schizophrenia?

A

Diathesis (vulnerability) + Stress (negative experience trigger) = Schizophrenia

99
Q

What was Meehl’s interactionist model to explain schizophrenia? (outdated)

A

Diathesis was entirely genetic- the result of a single ‘schizogene’

If one does not have the gene… no amount of stress can result in sz
If one does have the gene… chronic stress (particularly the schizophrenogenic mother) results in development of disorder

100
Q

What is the modern understanding of diathesis?

A

Many genes appear to increase vulnerability slightly (Ripke et al)

Also, can be a psychological trauma
Read et al: neurodevelopmental model in which early trauma alters the brain development
Eg: hypothalamic-pituitary-adrenal system can become overactive

101
Q

What is the modern understanding of stress?

A

Anything that risks triggering schizophrenia
Can still be psychological eg: poor parenting
Cannabis use is a stressor, increasing risk of sz by up to 7x due to interfering with dopamine system (although most don’t develop as lack vulnerability)

102
Q

What is the interactionist approach for the treatment of schizophrenia in the UK and US?

A

In UK, it is standard practice to treat with antipsychotics + CBT
In USA meds without psychological therapy is more normal as less acceptance of the interactionist approach

103
Q

What are 2 strengths of the interactionist approach in explaining and treating schizophrenia?

A

Research supporting the role of both vulnerability + triggers
- Tienari et al adoption study
- biological mothers had sz, and control group without
- child rearing style of adoptive parents assessed
- high criticism + hostility + low empathy associated w/ sz but only in high genetic risk group
Combination of genes + environment leads to greatly increased risk of sz

Real world application in combination of drug + psychological therapies
- Tarrier et al
- 1. Meds + CBT 2. Meds + counselling 3. Meds only
- Patients in 2 combination groups lower symptoms BUT no difference in hospital readmission
Clear practical advantage in interactionist approach for most effective treatment

104
Q

What are 2 weaknesses of the interactionist approach in explaining and treating schizophrenia?

A

Original model oversimplified
- diathesis/stress can no longer trace back to a single schizogene.
- modern understanding: polygenetic + psychological as diathesis
- drug abuse as stress
- Houston et al childhood sexual abuse main vulnerability to schizophrenia & cannabis usage the main trigger
Multiple factors affecting diathesis and stress, more complicated- supports modern understanding

Logical error: treatment-causation fallacy
- combination of treatments more effective than just one
- so if excess dopamine is not the cause of schizophrenia, but using drug treatment: not treating the root cause, just suppressing symptoms
- likewise, if sz roots not in the mind/ family but we are treating those aspects, underlying cause not dealt with
Cannot assume that success of therapies means interactionist explanation is correct

A-level Psychology (11 decks)

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