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Schizophrenia Flashcards

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1
Q

What does it mean by “classification of a mental disorder”?

A

The process of organising symptoms into categories based on which symptoms frequently cluster together.

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2
Q

What is schizophrenia?

A

A severe mental disorder where contact with reality and insight are impaired, an example of psychosis.

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3
Q

What are the two main systems used for diagnosing schizophrenia?

A

ICD-10. DSM-5.

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4
Q

What is a positive symptom of schizophrenia?

A

Additional experiences beyond those of ordinary existence.

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5
Q

What is a negative symptom of schizophrenia?

A

Loss of usual abilities and experiences.

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6
Q

Name the positive symptoms we have looked at:

A

Hallucinations/delusions and disorganised speech.

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7
Q

Name the negative symptoms we have looked at:

A

Avolition, speech poverty and diminished emotional expression.

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8
Q

What are hallucinations?

A

Hallucinations are an unusual sensory experience. Some are related to the events in the environment whereas others bear no relationship to what the senses are picking up.

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9
Q

What are delusions?

A

Also known as paranoia, they are irrational beliefs.
e.g Being an important historical, political or religious figure.

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10
Q

What is speech poverty?

A

A reduction in the amount and quality of speech. May also involve a delay in the person’s verbal responses.

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11
Q

What is avolition?

A

Often called apathy- it means finding it difficult to keep up with goal-directed activity.
Lack of motivation to carry out activities.

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12
Q

What is comorbitiy?

A

Two disorders or conditions are diagnosed together, E.G a person may have schizophrenia and personality disorder.
If two conditions are diagnosed commonly together the validity of the classification may be questioned.

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13
Q

What is symptom overlap?

A

Two or more conditions share symptoms.
If symptoms overlap into other disorders it may call into question the validity of classification.

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14
Q

What is the DSM-5 criteria for diagnosis of schizophrenia?

A

Two or more symptoms present for a significant portion during a one month period- one must be a positive symptom.
Continuous sign of disturbance for 6 months.
Schizoaffective disorder/bipolar ruled out
Not due to substance abuse
If a history of autism, diagnosis only made if hallucinations or delusions present.

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15
Q

Why is there gender bias in diagnosis of schizophrenia?

A

Men have been diagnosed more with schizophrenia since 1980s. (1.4:1)
Arguments around the idea women have more close relationships and get more support.

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16
Q

Why might there be culture bias in the diagnosis of schizophrenia?

A

Some symptoms have different meaning in different cultures e.g may be a good thing to “hear voices” in certain cultures attributed to spiritualism etc.

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17
Q

What are genetics?

A

DNA strands.

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18
Q

What is the genetic assumptions of schizophrenia?

A

That genes cause schizophrenia. You can inherit these from family members. The closer the relative (1st degree/2nd degree etc) the higher the likelihood of development of SZ.

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19
Q

What did Gottesman (1991) do in order to investigate the concordance rates of SZ?

A

A longitudinal family study with both DZ and MZ twins (62 people diagnosied with SZ) and compared likelihood of SZ.

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20
Q

What are some of the findings of Gottesman (1991)?

A

If the following have SZ:
Aunt- 2% chance of developing
Sibling- 9% chance of developing
48% identical twin.

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21
Q

What might be an issue with the twin studies in Gottesman (1991)?

A

Can’t separate out environment, purely correlational.

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22
Q

Sz is polygenic- what does this mean?

A

That it appears there are several genes that may be involved in the development of Sz- not just one.

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23
Q

How many separate genetic variations did Ripke (2014) find in his genome wide study?

A

108.

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24
Q

What is a candidate gene and an example of one?

A

a gene that is believed to be related to a particular trait, such as a disease or a physical attribute (SZ in this case).
E.G PCM1

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25
Q

What is aetioloogically hetereogenous?

A

Different studies have identified that different candidate genes which means that schizophrenia is aetiologically heterogeneous – i.e. a number of different combinations of genes can lead to the illness.

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26
Q

What is the role of mutation in genetics?

A

SZ can also have a genetic component even without a family member having it- due to mutation.
E.G Parental DNA (fathers under 25 0.7% passing it on vs over 50 2%).
(BROWN 2005)

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27
Q

A strength of the genetic explanation is research support from….

A

Gottesman

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28
Q

However, a weakness of Gottesmans research is….

A

The concordance rates are not 100% so suggestive of other factors involved.
Environment/diathesis stress model etc.

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29
Q

Practical application with the genetic explanation?

A

Genetic counselling- but the risk factor is an average figure and not usually accurate due to things like environment.

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30
Q

A weakness of the genetic explanation is that it is reductionist… why?

A

It ignores other components such as hormones/trauma etc.

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31
Q

What is the main neurotransmitter suggested as a neural correlate of SZ?

A

Dopamine.

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32
Q

What led to the understanding of how dopamine might lead to SZ symptoms?

A

Antipsychotics, known to reduce DA, caused symptoms similar to those with Parkinson’s disease (associated with low levels of DA)

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33
Q

What was the original hypothesis?

A

SZ might be the result of high levels of DA in the subcortical areas of the brain.

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34
Q

Why did they believe in the original hypothesis that SZ patients had high levels of dopamine?

A

Due to an excess of D2 receptors in pathways from the subcortical area e.g Broca’s area (responsible for speech production).

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35
Q

What is hyperdopaminergia?

A

High levels of DA.

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36
Q

How did the updates version of the dopamine hypothesis change?

A

Proposed the idea also of cortical hypodopaminergia.

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37
Q

What is cortical hypodopaminergia?

A

Abnormally low DA in the brain’s cortex.

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38
Q

What did cortical hypodopaminergia cause?

A

Negative symptoms, due to lack of DA effect on the cognitive system (in the pre-frontal cortex).

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39
Q

Which pathway is associated with the subcortical area of the brain?

A

Mesolimbic pathway

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40
Q

Which pathway is associated with the cortical area of the brain?

A

Mesocortical pathway

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41
Q

Strength of the dopamine hypothesis?

A

Research support from the use of amphetamines and antipsychotics.

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42
Q

Limitation of dopamine hypothesis?

A

Free will/determinism debate
Holism/reductionism debate.

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43
Q

What are antipsychotics?

A

Drugs used to reduce the intensity of symptoms e.g positive symptoms of schizophrenia.

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44
Q

What are the two types of antipsychotics?

A

Typical and a-typical.W

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45
Q

Which came first (Typical/A-Typical)?

A

Typical.

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46
Q

What is an example of a typical antipsychotic?

A

Originated in 1950- e.g Chlorpromazine.

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47
Q

What is Chlorpromazine?

A

Typical antipsychotic.
Taken by tablet, syrup, injection.
Dosage recommended max of 1000mg.

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48
Q

What did Chlorpromazine do on the dopamine system?

A

Acted as a dopamine antagonist (blocked the D2 receptors) reduced the positive symptoms of SZ.

49
Q

What other effects did Chlorpromazine have?

A

Sedative- had an effect on the histamine receptors.
Often used to calm down patients when first admitted to hospital.

50
Q

What was an issue with Chlorpromazine/typical antipsychotics?

A

Side effects - tardive dyskinesia)
Worsened negative symptoms in someone with already low levels of DA in cortical area.

51
Q

Why were a-typical antipsychotics created?

A

Used since 1970s - created to maintain/improve effectiveness of drugs in regards to symptoms and also reduce side effects.

52
Q

What was the initial issue with Clozapine (a-typical drug).

A

Caused a rare blood condition called agranulocytosis. (Loss of white blood cells).
Was taken of the shelves and re-distributed much later).

53
Q

What is the dosage of Clozamine?

A

300-400MG.

54
Q

What makes clozapine different to chlorpromazine?

A

It binds to DA receptors in the same way but in addition to this it acts on serotonin and glutamate receptors. Believed to help improve mood and reduce depression and anxiety in patients.

55
Q

What is another example of an atypical drug?

A

Risperidone.

56
Q

What is risperidone?

A

More recently developed.
Another attempt to reduce side effects.
Binds more strongly to receptors so MG is less (4-8mg daily)

57
Q

Weakness of drug therapy?

A

Serious side effects.
Revolving door syndrome.
To care for patient or to subdue?
Informed consent?

58
Q

Strength of drug therapy?

A

Economic impact- cheaper than therapy.
Help people to live without the need for hospital admission
Research evidence (Thornly- effective reduction of symptoms using typical drugs).

59
Q

What is family dysfunction?

A

Abnormal processes within a family such as poor communication, cold parenting and high levels of expressed emotion.
These may be risk factors for both the development and maintenance of SZ.

60
Q

What is the Schizophrenogenic mother?

A

Basically means “schizophrenia causing”.
A psychodynamic explanation for SZ based on accounts from patients in childhood.
A mother who is cold, rejecting and controlling. Creates an environment of tension/secrecy.

61
Q

What is the double-bind theory?

A

The child finds themselves trapped in situations where they fear doing the wrong thing, but receive mixed messages about what this is- they feel unable to comment on the unfairness or seek clarification.
Child is punished by withdrawal of love when they get it wrong.
Confusion.

62
Q

What is expressed emotion?

A

Level of emotion expressed towards a patient by their carers.

Verbal criticism, accompanied by violence at times.
Hostility towards patients, including anger and rejection.
Emotional over-involvement, including needless self-sacrifice.

63
Q

What is expressed emotion primarily an explanation for?

A

Relapse in patients with SZ
Also been suggested it may be a source of stress that can trigger onset of SZ in someone already vulnerable (diathesis-stress model).

64
Q

Strengths of family dysfunction?

A

Possible practical application e.g family therapy

Insecure attachments (Type C or D) are seen more in Schizophrenic patients (Berry, 2008) and history of physical or sexual abuse (69% F and 59% M) (Read et al., 2005)

High predictive validity for relapse rates in high EE families (Kavanagh, 1992; Butzlaff and Hooley, 1998)

65
Q

Weakness of family dysfunction?

A

Socially sensitive- blames mother
Cause an effective, is it the dysfunction causing SZ or SZ causing dysfunction?
May ignore components of biology, may be more of a trigger (fd) not a cause.

66
Q

What is the purpose of family therapy?

A

Carried out with all or some of the family members with the aim of improving the communications within the family and reducing the stress of living as a family.

67
Q

What types of dysfunction does family therapy try to improve?

A

Double-bind, schizophrenic mother and also reduce levels of expressed emotion.

68
Q

What is the focus of FT to reduce?

A

Reduce anger, guilt which is what creates stress.
Stress is the key thing that may lead to relapse.

69
Q

How does the family therapist involve other family members?

A

Encourages family members to form a therapeutic alliance whereby they all agree on the aims of therapy.

70
Q

Who create the a model of practice for family therapy?

A

Burbach: phase model.
Begins with sharing basic information and providing emotional/practical support.
Involves identifying unhelpful patterns of interaction, looks at skills training etc.

71
Q

What are some strengths of family therapy?

A

Free will- no reliance on medication.

Takes an idiographic approach and more holistic.

No side effects.

72
Q

What are some limitations of family therapy?

A

Relies on informed consent- ethical boundaries may be crossed.

Requires active involvement from family members.

Long process- people may drop out.

Focus on treating symptoms/home life not a cure.

73
Q

How did William McFarlane (2016) support family therapy?

A

Concluded that FT was one of the most consistently effective treatments available for schizophrenia.
Relapse rates found to be reduced typically by 50-60%.

74
Q

What is the idea behind the cognitive explanation?

A

It focusses on mental processes such as thinking, language and attention.

75
Q

What do the cognitive explanations suggest SZ symptoms come from?

A

SZ is associated with several types of dysfunctional thought processing.
Characterised by disruption to normal processing.

76
Q

Where does the cognitive approach suggest reduced cognitive functioning comes from?

A

Reduced thought processing in the ventral striatum is associated with negative symptoms.
Reduced processing of information in the temporal and cigulate gyri are associated with hallucinations.

Lower level of information processing suggest cognition likely to be impaired.

77
Q

What is metarepresentation dysfunction?

A

The cognitive ability to reflect on thoughts and behaviour.
Allows insight into our own intentions and goals, and to interpret the actions of others.
Dysfunction here- would disrupt our ability to recognise our own actions and thought as being carried out by ourselves (rather than others).

78
Q

What type of symptoms would a dysfunction in metarepresentation lead to?

A

Hallucinations of hearing voices or delusions like thought insertion (the experience of having thought projected into the mind by others).

79
Q

What is central control dysfunction?

A

Issues with the cognitive ability to suppress automatic responses whilst performing deliberate actions.
People with SZ tend to experience derailment of thoughts because each word triggers associations, and the person cannot suppress automatic responses to them.

80
Q

How did John Stirling (2006) provide support for the cognitive explanation?

A

Compared performance on a range of cognitive tasks in 30 people with SZ and control group of 30 without.

Tasks included stroop task and others.

In support of the central control theory, people with SZ took longer, over twice as long on average.

81
Q

What is a limitation of the cognitive explanation?

A

Reductionist - some symptoms such as delusions are incredibly common so to reduce them down to being due to metarepresentation dysfunction only is quite over simplistic

Social sensitivity - placing blame on the individual for their symptoms.

Cause and effect problems.

82
Q

Over how long of a period does CBT usually last when treating SZ?

A

5-20 sessions.

83
Q

What does CBT aim to deal with?

A

Thoughts, feelings and behaviour.

84
Q

What does the CBTp aim to do with the patient?

A

Identify and change faulty cognitions/irrational thoughts.

85
Q

How may a therapist help to reduce/change faulty cognitions?

A

Normalisation
Reality testing
Using logic

86
Q

What other model is adopted when using CBT for SZ patients?

A

ABCDE model.
Focus on cognitively restructuring the irrational beliefs e.g dispute and effect.

87
Q

What is reality testing?

A

Person with SZ and their therapist jointly examine the likelihood that the beliefs are true.

88
Q

What is normalisation?

A

E.G People hearing voices can be helped by teaching them that voice-hearing is an extension of the normal experience of thinking in words.

89
Q

What other things might CBT aim to reduce in someone with sz?

A

Anxiety/depression

90
Q

How did Jauhar support the idea of CBT for sz?

A

He reviewed 34 studies of CBT finding small but significant effects on both positive and negative symptoms (P<0.001)

91
Q

How did Tarrier (2000) support the idea of CBT for SZ?

A

Found people with schizophrenia receiving 20 sessions of CBT in 10 weeks, coupled with drug therapy, followed by four booster sessions during the next year, had a better reduction in symptoms than sufferers receiving drug therapy alone.

92
Q

What are some general strengths of CBT?

A

FREE WILL
IDIOGRAPHIC
LACK OF SIDE EFFECTS

93
Q

What are some general limitations of CBT?

A

Lengthy & time consuming (drop out rates/economic cost)

Issues with availability - NICE said 1/10 other research suggested less than 7% of people and fewer take it up.

Not a cure/symptoms might still also be present.

94
Q

What is an interactionist approach?

A

A way to explain the development of behaviour in terms of a range of factors, include both biological and psychological ones.

95
Q

What is the “diathesis” component

A

The vulnerability

96
Q

What is the “stress” component

A

The trigger.

97
Q

What was Meehl’s original model of diathesis stress?

A

That the vulnerability was entirely genetic (schizogene)
Chronic stress through childhood/adolescence e.g SZ mother may trigger SZ.

98
Q

Why did Meehl’s original model change?

A

SZ is not just the result of a “schizogene”. SZ is polygenic, with 100s of genetic variations.

99
Q

What is the modern understanding of the diathesis (vulnerability)?

A

Many genes may increase genetic vulnerability.
Psychological trauma (becomes the diathesis rather than the stressor).
Early trauma alters the brain (causes the vulnerability).

100
Q

How does early trauma alter the brain and cause the “diathesis”?

A

HPA System: Hypothalamic-pituitary adrenal- becomes overactive making a person vulnerable to later stress.

101
Q

What is the modern understanding of the stress (trigger)?

A

Originally the “stress” seen as psychological e.g parenting. But, although still important other things also may trigger e.g cannabis use.

102
Q

How might cannabis trigger SZ?

A

It increases the risk of SZ by up to 7X due to interfering with the dopamine system.

103
Q

What treatment would the interactionist approach use?

A

Drugs and talking therapies.

104
Q

What did Turkington et al. (2006) say?

A

It is perfectly possible to believe in a biological cause of Sz and still engage in CBT - but this requires an interactionist approach.

105
Q

Why might a combination of talking therapies and drugs be better?

A

In severe cases of Sz it is expected that patients struggle to engage with a talking therapy, if a drug treatment can reduce symptoms it can enhance their ability to engage with psychological therapies, giving sufferers the skills needed to change their faulty cognitions or unhealthy family environments.

106
Q

General strengths of the interactionist approach?

A

Was a limited model but the modern model has evolved and is more holistic and thorough, this may be more valid that other explanations.

Houston et al. (2008) childhood sexual abuse is a major influence, with cannabis use being the major trigger.

Supporting research in Tarrier and Gottesman.

Practical applications in the form of effective combined treatment models.

107
Q

General limitations of the interactionist approach?

A

The fundamental mechanisms about how stress can trigger biological responses is still unclear. Many complex factors are involved in this response which can be hard to gauge empirically.

Jarvis and Okami (2019) suggest a treatment fallacy in that a successful treatment doesn’t identify the cause - alcohol reduces shyness by we cannot conclude the cause of shyness is a lack of alcohol.

108
Q

In Allyon and Azrins study why were the women on the wards rewarded?

A

For self care related activities

109
Q

What principle is a token economy based on?

A

operant conditioning but immediate associations are based on classical conditioning

110
Q

What 3 categories of behaviours are usually targeted through token economies?

A

personal care, condition related behaviours, social behaviours

111
Q

Why are token administered ASAP once a behaviour is performed?

A

So patients know it is in relation to the behaviour just done rather than ones done later if there is a delay

112
Q

What is an example of a secondary reinforcer?

A

The token

113
Q

What is an example of a primary reinforcer?

A

Anything the patient sees as a reward eg. 15 mins extra video gaming time.

114
Q

A strength in relation to the effectiveness of token economies is?

A

Glowacki reviewed 7 studies and found token economies helped reduce negative symptoms and undesirable behaviours

115
Q

What percentage of people do not respond to token economies?

A

10-20% very low number.

116
Q

Instead of token economies what type of therapy is seen as a good alternative?

A

Art therapy: Chiang said it has low risk and high gain.

117
Q

A weakness of token economies includes?

A

Ethical issues, potentially restricting pleasurable activities to create a reward based system can be considered unethical.

118
Q

What do token economies do to behaviour?

A

Help encourage positive behaviours in the management of schizophrenia

119
Q

People that do not respond to token economies usually have what type of schizophrenia symptoms?

A

Severe negative symptoms.

A2 Psychology (10 decks)

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