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Schizophrenia Flashcards

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1
Q

What is Schizophrenia?

A

A psychotic disorder, meaning that the patient has lost touch with reality and may/may not know that they are ill.

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2
Q

Who identified Schizophrenia?

A

First identified by Kraeplin (1886) who referred to it as ‘Dementia Praecox’
Bleuler (1911) coined the term ‘Schizophrenia’

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3
Q

How much of the population is affected by Schizophrenia?

A

1%

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4
Q

What is the prevalence of Schizophrenia in males and females?

A

It’s equally common but the age of onset is different
Males diagnosed in mid-20s
Females diagnosed in their early 30s

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5
Q

What percentage of people fully recover?

A

20%

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6
Q

What percentage of people recover from positive symptoms?

A

40%

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7
Q

What percentage of people show no improvement?

A

40%

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8
Q

What percentage of people show ‘some improvement’?

A

60%

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9
Q

When are symptoms most sever according to Bleuler?

A

Symptoms are most sever in early adulthood during the first 5 years of onset

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10
Q

What are positive symptoms?

A

The presence of abnormal functions

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11
Q

What are negative symptoms?

A

The absence of normal funstions

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12
Q

What are the positive symptoms of Schizophrenia?

A

Hallucinations, Delusions and Disorganised thinking & speech

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13
Q

What are the negative symptoms of Schizophrenia?

A

Speech poverty (alogia), Lack of emotion (flat affects), Avolition (social withdrawal) and Apathy

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14
Q

Definition and examples of Hallucinations

A

False sensation that have no identifiable source
Most common types are auditory (e.g. hearing voices) and Visual (e.g. seeing people who aren’t there)
Less common types are Olfactory (phantom odours) and tactile (sensations of being touched on/within the body)

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15
Q

Definition and examples of Delusions

A

False beliefs not based on facts or evidence
Many types including those of Persecution (belief that you are being victimised/spied on), Grandeur (belief that you have great power/status) and Control (the belief that your thoughts/actions are being controlled by others

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16
Q

Definition and examples of Disorganised thinking & speech

A

This makes it hard to concentrate on anything, thoughts drift from one thing to another although there is no connections between them.
Thoughts are described as being misty or hazy
e.g. They will have trouble finishing reading an article or watching a programme and may struggle with college/work
Words may become jumbled/confused making it hard to understand what is said - ‘word salad’

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17
Q

Definition and examples of Speech Poverty (alogia)

A

Reduction in communication, thought to be a result from the slowing/blocking of thoughts.
Manifested in short, empty replies to questions, patients may have difficulty starting and maintaining conversations

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18
Q

Definition and examples of Flat affects (lack of emotion)

A

A reduction or flattening of emotions.

The range/intensity of facial expressions, tone of voice and eye contact are reduced. Body language is hard to interpret

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19
Q

Definition and examples of Avolition (social withdrawal)

A

Difficulty in planning and setting goals, no interest in socialising or hobbies.
They may not want to do anything and will sit in the house for hours or days

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20
Q

Definition and examples of Apathy

A

Lack of motivation, neglecting household chores leading to poor grooming and hygiene, also likely to have a low sex drive

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21
Q

What ‘other’ symptoms of Schizophrenia are there? Definition

A

Inappropriate effect - where emotional expressions are unsuitable for the situation e.g. laughing at serious things

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22
Q

What is ‘classification’?

A

It involves identifying groups or patterns of behavioural, emotional, physical and/or motivational symptoms that occur together to form a type of mental disorder.

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23
Q

Why is classification important?

A

Once someone has been classified as suffering from a disorder they can access treatment, identify the cause of their disorder, and prognosis

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24
Q

What is the DSM classification system?

A
  • First published in 1952, gone through many revisions the most recent being DSM V may 2013
  • Contains over 300 mental disorders arranged intro main categories
  • Each disorder has a specific diagnosis require to be met
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25
Q

What are the positive implications of being diagnosed with a disorder?

A

They can access therapy and can benefit by the removal of symptoms

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26
Q

What are the negative implications of being diagnosed with a disorder?

A

There is a stigma with a label like ‘schizophrenia’ e.g. violence, socially dysfunctional, inconsistent which can place restrictions on the patients life

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27
Q

What is inter-rater reliability?

A

This occurs when clinicians make identical but independent diagnosis’ of the same patient - this should be high considering they are highly trained and use the DSM diagnosis model

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28
Q

Becks research and what it shows about inter rater reliability

A

Beck et al (1961) found that when 153 patients were assessed by two different psychiatrists the agreement rate was only 54% - implying low inter rater reliability

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29
Q

What factors could influence a low rate of diagnosis agreement between clinicians?

A
  • Different training at different uni’s
  • Different levels of experience
  • different ethnicities
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30
Q

Copeland’s research and what it shows about inter rater reliability

A
  • Copeland (1970) gave a description of a patient to 134 US and 194 British psychiatrists
  • Found that 69% of the US psychiatrists diagnoses the patient with Schizophrenia but only 2% of British psychiatrists did
  • Illustrates how the culture of the clinician can damage inter rater reliability as US clinicians are more likely to diagnose
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31
Q

What is test-retest reliability?

A

This occurs when clinicians makes the same diagnosis of the patient on separate occasions from the same information.
Clinicians have detailed manuals to use but patients and their symptoms change with time.

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32
Q

Read’s research and what it shows about test-retest reliability.

A
  • Read (2004) reported that test-retest analysis is as low as 37% for schozophrenia
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33
Q

Why is having low test-retest reliability concerning?

A

It can create false positive and false negatives - if people are no diagnosed when they have the condition they cannot access treatment

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34
Q

What does Farmers research show about improving the reliability of diagnosing Schizophrenia?

A
  • Farmer (1988) found that a standardised interview technique known as the Present State Examination increased the reliability of diagnosis
  • The PSE focuses on the frequency and severity of symptoms, meaning all patients are asked the same things
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35
Q

What are unreliable symptoms? (reliability)

A

Some symptoms are problematic and can lower the reliability of diagnosis e.g. recognising the difference between bizarre and non-bizarre delusions can be difficult

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36
Q

Mojtabi and Nicholson’s research and what it shows about unreliable symptoms

A
  • Mojtabi and Nicholson (1995) asked 50 senior US psychiatrists to differentiate between ‘bizarre’ and ‘non-bizarre’ delusions
  • This produced inter-rater reliability correlations of only 0.40
  • This shows that the central diagnostic requirement lacks sufficient reliability to be distinguishing between symptoms
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37
Q

What is co morbidity? (validity)

A

When a patient actually has 2 or more health conditions that co-exist and can be accurately, validly diagnosed in two ways - this can make diagnosing schizophrenia difficult e.g. social withdrawal is shown in depression and schizophrenia

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38
Q

Buckley’s research and what it shows about co morbidity

A
  • Buckley (2009) identified co morbid conditions with schizophrenia and argued that they could be sub-types of schizophrenia
    15% had panic disorder
    29% had PTSD
    23% had OCD
    50% had depression
    47% had substance abuse
  • Shows we need to re consider co morbid conditions
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39
Q

What are overlapping symptoms? (validity)

A

None of the symptoms of schizophrenia are exclusive to the disorder (they are not pathognomic) making it difficulty to achieve a valid diagnosis - Bipolar, OCD and autism are some disorders that have overlapping symptoms

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40
Q

What did Read find about overlapping symptoms?

A

Read et al (2011) estimated that about 13% of the population hear voices, but only 1% are diagnosed

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41
Q

Konstantaneas and Hewitt’s research and what it shows about overlapping symptoms (validity)

A
  • Konstantaneas and Hewitt (2001) compared 14 male autistic patients with 14 male schizophrenic patients
  • Found that none of the schizophrenic patients had symptoms of Autism but 50% of autistic patients had symptoms of schizophrenia
  • This shows some support for symptoms overlap
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42
Q

What is predictive validity?

A

The extent to which the diagnosis of schizophrenia can accurately predict the development, treatment and prognosis of the disorder - if this is accurate and informative we can say it has good predictive validity

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43
Q

Bleuler’s research and what it shows about predictive validity

A
  • According to Bleuler’s (1978) longitudinal study of 2000 schizophrenic patients, symptoms are most sever in early adulthood, during the first 5 years after onset
  • There is too much variety in the outcomes from schizophrenia and predictive validity remains low
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44
Q

How can cultural bias affect diagnosis of Schizophrenia?

A
  • It can affect it in many ways
  • Some suggest that the American DSM and other manuals are culturally biased and do not take into account diverse cultural values and the impact on diagnosis
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45
Q

How can cultural interpretations of schizophrenia affect the diagnosis of the disorder?

A

Religious and Cultural groups can have a marked effect on perceptions of schizophrenia, what can be seen as ‘insane’ in one culture may be highly desirable in another. which can complicate a valid diagnosis

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46
Q

Malagdy’s research and what it shows about cultural interpretations affecting a diagnosis

A
  • Malagdy’s (1987) research demonstrated how different cultures interpret symptoms of mental disorders in a very unique way
  • In traditional Costa Rican culture, hearing voices is interpreted as spirits talking to the individual (abnormal but prized)
  • Whereas in the USA the same symptoms is a core sign of schizophrenia
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47
Q

How can negative cultural attitudes to schizophrenia affect the diagnosis?

A

Psychological distress and mental health issues attract different levels of stigma in different cultures

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48
Q

Kim and Berrigon’s research and what it shows about how negative cultural attitudes affect a diagnosis

A
  • Kim and Berrigon (2001) outlined how different cultures attribute different meaning to different disorders
  • In some Asian languages schizophrenia = ‘the disease of a disorganised mind’
  • In japan this idea is so stigmatised that psychiatrists are reluctant to diagnose patients with schizophrenia
  • As a result 20% of people in Japan receive a formal diagnosis
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49
Q

How can the culture/nationality of the clinician affect a diagnosis?

A

Some nationalities diagnose schizophrenia in very different ways, which can create reliability and validity issues. US clinicians seem far more likely to diagnose schizophrenia that UK clinicians.

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50
Q

Copeland’s research and what it shows about how the culture/nationality of the clinician affects diagnosis

A
  • Copeland (1971) gave a description of a patient to 134 US and 194 UK psychiatrists
  • He found that 69% of US diagnoses the patient with schizophrenia but only 2% of UK psychiatrists did
  • This shows how american clinicians are far more likely to diagnose schizophrenia than UK psychiatrists.
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51
Q

How can race discrimination affect the diagnosis of schizophrenia?

A

Research has implied that some nationalities have considerably more/less cases of schizophrenia, suggesting that mental health professional perceive diverse ethnic and cultural groups very differently

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52
Q

Blake’s research and what it shows about race discrimination affecting a diagnosis

A
  • Blake’s (1973) research found that clinicians are 6 times more likely to diagnose a patient with schizophrenia if the case summary referred to them as African American, than if they were referred to as white
  • This shows how the race and culture of the patient can affect the reliability of the diagnosis
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53
Q

What are some of the unreported facts when diagnosing schizophrenia in men and women?

A

Men are seen to suffer more severe negative symptoms than women, as well as suffering from more substance disorders.
Men are also more likely to be involuntarily committed to psychiatric wards (Goldstein 1993)

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54
Q

Cotton’s research and what it shows about unreported facts when diagnosing men and women

A
  • Cotton’s (2009) research has implied that women seem to recover more and suffer less relapse than males
  • Ignoring these facts implies a beta bias in clinicians not considering these important factors in the diagnosis and recovery from schizophrenia
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55
Q

How does biased research affect the diagnosis of schizophrenia in men and women?

A

Some psychologists have claimed that research into schizophrenia has neglected to use female patients, which questions it’s usefulness and representativness

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56
Q

Nasser et al’s research and what it shows about biased research affecting diagnosis in men and women

A
  • Nasser et al’s (2002) research found that much of the early research into schizophrenia was conducted on men only
  • This means lots of research into treatments and explanations of the disorder may be inappropriate for women
  • This research can be accused of androcentrism
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57
Q

What are the implications of under diagnosing female patients suffering from schizophrenia?

A

Research has suggested that women go under diagnosed in comparison to men, this implies that many women could be denied access to treatment and have to continue suffering from symptoms of schizophrenia

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58
Q

Loring and Powell’s research and what is shows about the under diagnosis of female patients

A
  • Loring and Powell (1985) randomly selected 290 male and female psychiatrists to read two cases, and were asked to offer their judgements using standard diagnostic criteria
  • When the patient was described as ‘male’ or no info was given then 56% gave a diagnosis of schizophrenia
  • When the patient was described as ‘female’ then only 20% gave a diagnosis of schizophrenia
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59
Q

How many genes and what chromosomes were identified that mediate a vulnerability to schizophrenia and by who?

A

Crespi et al (2007) reported 76 genes could mediate a vulnerability, including variations of chromosomes 8 and 11

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60
Q

What specific gene variation was identified in Chinese patients with schizophrenia and by who?

A

Hong et al (2000) found that a variation of the TPH gene was more common in Chinese patients with Schizophrenia

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61
Q

How do genetic variations contribute to schizophrenia?

A

They can cause a person to inherit biochemical imbalances, or brain structure abnormalities

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62
Q

How does a close genetic relationship affect the risk of developing schizophrenia?

A

The closer the genetic relationship to a person who has schizophrenia, the higher the risk of developing the disorder.

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63
Q

What is the chance of a child of two schizophrenic patients also developing schizophrenia according to Gottensman (1991)

A

46%

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64
Q

What is the chance of developing the disorder if a degree relative has schizophrenia? (Gottensman)

A

They have a 13% chance of developing the disorder if the relative (e.g. parent) has been diagnoses

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65
Q

How much genetic similarity do first degree relatives share?

A

50%

66
Q

How much genetic similarity do second degree relatives share?

A

25%

67
Q

What is the chance of developing the disorder if a second degree relative has schizophrenia? (Gottensman)

A

They have a 5% of developing the disorder if the relative (e.g. grandparent) has been diagnosed

68
Q

Joseph’s twin study and what it shows about genetic similarity

A
  • Joseph’s (2004) research showed how genetic similarity increases risks of developing the condition
  • He pooled data carried out before 2001 and found a 40% concordance rate in schizophrenia for MZ twins and 7% concordance for DZ twins
  • Environmental influences for both groups assumed to be similar
  • Suggests genes do have some influence
69
Q

What was the concordance rate for MZ twins and schizophrenia according to Joseph?

A

40%

70
Q

What was the concordance rate for DZ twins and schizophrenia according to Joseph?

A

7%

71
Q

What have MacDonald and Schultz suggested about twins and schizophrenia?

A

They suggested that in MZ twins, if one twin is diagnosed with schizophrenia, then the other twin is 99 times more likely to suffer from the condition

72
Q

What is the main advantage of adoption studies over twin/family studies?

A

They help to isolate nurture as a factor as it removes the possible influence of a dysfunctional family

73
Q

What was Tienari et al’s adoption study? What did it find?

A
  • Tienari et al (2001) completed an adoption study in Finland with over 164 adopted kids whose biological mother had schizophrenia
  • He matched these kids with others whose mother did not have schizophrenia
  • Study found that 7% (11) of the kids with schizophrenic mothers were also diagnosed with schizophrenia, in comparison to 2% (4) from the control group
  • This validates the idea that schizophrenia has genetic components
74
Q

How many children with biological mother who had schizophrenia took part in Tienari et al’s study?

A

164

75
Q

What percentage of the control group developed schizophrenia in Tienari et al’s study?

A

2% (4 kids)

76
Q

What percentage of the experimental group developed schizophrenia in Tienari et al’s study?

A

7% (11)

77
Q

Strengths of genetic inheritance as an explanation for schizophrenia? (3)

  • evidence to support
  • practical applications
  • scientific
A

1) Evidence to support from Heston (1966) - 50 kids of schizophrenic mother were adopted by non-s mothers at 1 month old - 10% went on to develop schizophrenia -this has concurrent validity with Gottensmans study - making the explanation compelling
2) Has had useful practical applications - vulnerable groups in society who have relatives with schizophrenia can be advised on their risks, can also have an impact on family planning - has benefited society and schizophrenia sufferers
3) Explanation promotes psychology as a scientific discipline - based off of statistics and facts and does not take into account less scientific explanations - pushed psychology to scientific rounds

78
Q

Weaknesses of genetic inheritance as an explanation for schizophrenia? (3)

  • incomplete
  • methodological issues
  • deterministic
A

1) The explanation is incomplete as genetics cannot be the sole cause of schiz - if this were true then MZ twins (with 100% genetic similarity) would have a concordance rate of 100% - this nurturing influences must play a role
2) Family studies have methodological problems - if you are in the same household as someone suffering from schiz, or they are your role model, then you readily adopt ways of behaving, including symptoms - this explanation is questionable
3) Biologically deterministic - this explanation overlooks personal responsibility and free will - the condition needs triggering from environmental influences

79
Q

What do biochemical explanations argue about schizophrenia?

A

That it is caused by elevated levels of dopamine at key synaptic sites

80
Q

What does an excess of dopamine cause?

A

It can cause a ‘system overload’ were too many impulses are being transmitted, which arguably produces positive symptoms

81
Q

What happens at a post-synaptic level to account for elevated levels of dopamine?

A
  • The enzymes are not destroying any left over dopamine
  • The re-uptake channel is blocked
  • Too many receptmores
82
Q

What have postmortem’s shown that support the dopamine hypothesis?

A

Higher than normal concentrations of dopamine have been found in the postmortems of patients that suffered from schizophrenia

83
Q

How does the use of drugs support the dopamine hypothesis?

A

Drugs that increase dopamine production make symptoms worse - Amphetamines based drugs (dopamine antagonists) increase dopamine activity and produced symptoms of schizophrenia

84
Q

How does the use of anti-psychotics support the dopamine hypothesis?

A

Anti-psychotics that relieve symptoms of schiz work by blocking the activity of dopamine - these have been shown to be effective in up to 85% of patients

85
Q

What is the revised dopamine hypothesis?

A

Davis et al (1991) pointed out that in the prefrontal cortex there are no D2 receptors and there actually appears to be a deficiency of dopamine in this region.
Davis et al suggested that low levels of dopamine in this region is more responsible for negative symptoms of schiz

86
Q

What is the role of glutamate in the dopamine hypothesis?

A

Researchers have suggested other NT’s are involved in schizophrenia, and have noticed that many schiz patients suffer from low levels of glutamate, which plays a key part in learning, attention and memory.
This NT has an excitatory role in the brain and also acts to reduce dopamine, so low levels of glutamate encourage the increased firing and release of dopamine

87
Q

What are the strengths of the dopamine hypothesis in explaining schizophrenia? (3)

  • evidence to support
  • practical applications
  • scientific
A

1) Evidence to support from Randrup and Munkvad (1966) - rats were given amphetamines 3 times a day for 6 days - the rats then showed long lasting abnormalities e.g. being unable to filter out irrelevant sounds - this was reversed using anti-psychotics - proves the role of dopamine
2) The dopamine hypothesis has had practical applications - anti-psychotics that aim to decrease dopamine have been seen to be 85% effective in patients with schiz - thus the DA hypothesis has identified issues and helped solve them
3) It is scientific - there are many ways to measure dopamine e.g. brain scanning devices (PET scans) - making the explanation objective

88
Q

What are the weakness of the dopamine hypothesis in explaining schizophrenia? (2)

  • incomplete
  • no cause and effect
A

1) The explanation is incomplete as it does not consider how anti-psychotics do not work for patients - they lower dopamine in 100% of patients who take them, but 15% still experience symptoms - meaning something other than dopamine causes schizophrenia
2) We cannot infer cause and effect - high levels of dopamine can be seen in all patients, however this could be a result of external factors such as urban living or a traumatic childhood - which would contribute both to schiz and high dopamine levels - the explanation is correlational

89
Q

How can the dopamine hypothesis be used as part of the diathesis stress account of schizophrenia?

A

The biological vulnerability of having high dopamine levels already pre-exist in many individuals, however environmental stimuli may trigger this to create schizophrenia e.g. trauma in childhood

90
Q

What are some further neural correlates of schizophrenia?

A

Enlarged ventricles and reduced blood flow in the prefrontal cortex (hypofrontality)

91
Q

How can enlarged ventricles explain schizophrenia?

A
  • Neuroimaging has revealed that some schizophrenia patients have enlarged ventricles
  • The differences (15%) has also been found in un medicated patients and so is not a result of drugs
  • The enlargements appear at the onset of illness rather than as a result of detertioration
  • Some studies have linked enlarged ventricles and negative symptoms such as apathy and flat affect
92
Q

How can hypofrontality explain schizophrenia?

A
  • This is reduced blood flow in the prefrontal cortex

- This is often seen those suffering negative symptoms - specifically the emotional and cognitive kind

93
Q

What are the strengths of the neural correlates explanation of schizophrenia? (2)

  • scientific
  • comprehensive
A

1) A scientific and falsifiable concept - enlarged ventricles can be objectively identified by methods such as MRI scans - these also require less sophisticated interpretation
2) It’s a comprehensive account - each abnormality links to specific aspects of schiz e.g. enlarged ventricles can explain negative symptoms of schizophrenia whereas high dopamine levels can explain positive symptoms - making the account holistic

94
Q

What are the weaknesses of the neural correlates explanation of schizophrenia? (3)

  • no cause and effect
  • not exclusive
  • unsure of the cause
A

1) Cannot establish cause and effect - We have no before measurements of people with schiz and so we are unsure if life experiences have caused enlarged ventricles leading to schiz, or if schiz creates enlarged ventricles - the explanation has theoretical flaws
2) Are they exclusive to schiz? - they are not, they’re also found in brains of those with Parkinson disease, as well as other ‘normal’ individuals - means there is more to the explanation
3) Unsure of what causes these abnormalities - McEwan (2007) argued nurturing influences could instigate these structural changes, adolescent and child brains are sensitive to chronic stressors which can reshape the structure of the cortical regions, leading to schiz - the explanation is partial

95
Q

What do family dysfunction explanations of schizophrenia emphasise?

A

They emphasise the family orientated theories of the disorder, that highlight the important of nurture
They stress how maladaptive family relationships and poor household communication can contribute to the development of schiz

96
Q

How can Freudian ideas help explain how family dysfunction can contribute to schizophrenia?

A

Freudian ideas suggests if a child experiences trauma in childhood then this could be repressed using defence mechanisms, creating an unconscious issue which will reappear/manifest in adult hood in the form of schizophrenia symptoms

97
Q

What is poor communication within a household?

A

Receiving contradictory messages, such as angry/aggressive verbal messages, but warm/emotional non verbal messages - leading to a confusion/uncertainty on how to react

98
Q

How can poor communication within a household contribute to the onset of schizophrenia?

A

Contradictory messages to do with emotions and expressing them can create an issue where the child represses and does not deal with a problem
This becomes an unresolved unconscious issue that can create turmoil in the growing child’s mind and manifest in adult hood as symptoms of schizophrenia e.g. flat effect

99
Q

What is a Schizophrenogenic mother? Who suggested this idea?

A

Fromn-Reichman (1948) used this term to describe a domineering and insensitive mother, who can be controlling, overprotective and rejecting.
This mother micro-manages her children and does not acknowledge their independence.
In 1970’s this was broadened to fathers and whole families

100
Q

How can having a Schizophrenogenic mother lead to schizophrenia?

A

The behaviour sets up lines of faulty communication between her and her child, creating excessive stress that could possibly trigger psychotic thinking and develop into schiz in adulthood

101
Q

What is the double-blind hypothesis? Who suggested it?

A

Bateson et al (1958) suggested this as ideas about contradictory communication, families that communicate like this may make their kids more susceptible to schiz e.g. a mother telling her child she loves him but also turns away

102
Q

How can the double-blind hypothesis lead to schizophrenia?

A

The child receives conflicting messages and is placed in a no win situation, resulting in the child feeling confused and suspicious. They may also be unable to develop an internally coherent construction of reality. This can lead to the development of schiz due to paranoia and disorganised thinking

103
Q

What is high expressed emotion in the family dysfunction explanation? Who suggested this?

A

This revolves around family interactions after the development of schizophrenia rather than the onset.
High expressed emotion families often express a lot of emotion as well as higher levels of concern of hostility to the patient.
Kuipers et al (1983) found high EE relatives talk more and listen less
Linzen et al (1997) found patient returning to high EE households are more likely to relapse

104
Q

What are the strengths of the dysfunctional family explanation of schizophrenia? (3)

  • evidence to support
  • evidence to support
  • practical applications
A

1) Evidence to support - Lidz et al (1965) - Investigated family backgrounds of 50 schizophrenic patients - 90% had seriously disturbed families, 60% had one or both parents with a serious personality disorder, parental marriages had 1 dominant and 1 submissive parents (skewed families) - explanation is credible
2) Evidence on how returning to high EE households effects relapse - Butzlaff and Hooley (1998) - meta-analysis of 26 studies found twice the rate of relapse in symptoms when returning
3) Practical applications - family therapy identifies issues in the family that may explain the onset of schizophrenia - thus has helped to identify how family issues effect the sufferer

105
Q

What are the weaknesses of the dysfunctional family explanation of schizophrenia? (3)

  • no cause and effect
  • alternate explanations
  • creates problems
A

1) Cause and effect argument - behaviour may be a result of the child being diagnosed in an attempt to protect them or shelter them - the child may have developed schizophrenia as a result of other factors i.e. urban living
2) Alternate explanations are more scientific and more credible - this explanation is based off factors/concepts that are subjective - the dopamine hypothesis is less socially sensitive and is also easier to objectively study levels of dopamine e.g. MRI scans
3) Can be criticised for creating problems - suggests family behaviour has a direct impact on the development of schiz - a socially sensitive topic and violates protection from harm as it may cause high levels of distress - may cause more harm and confusion

106
Q

What does the cognitive explanation emphasise about schizophrenia?

A

It emphasise the role of faulty information processing - it claims many patients suffering have dysfunctional thought processing, and that the symptoms are due to cognitive deficits

107
Q

What is meta representation?

A

Also known as meta-cognition, it’s the ability to reflect upon thoughts, behaviours and feelings ad gives us the sense of self-awareness

108
Q

What does cognitive psychology claim about schizophrenia sufferers?

A

They have problems with meta-representation and may experience several dysfunctional aspects of thought processing, contributing to different symptoms

109
Q

What are the three cognitive dysfunctions identified in the cognitive explanation of schizophrenia? What symptoms are identified with each?

A

1) Dysfunction in the ‘central monitoring system’ - hallucinations
2) Dysfunction within the ‘supervisory attention system’ - negative symptoms e.g. speech poverty
3) Dysfunction within insight/egocentric bias - delusions

110
Q

What does the ‘central monitoring system’ do?

A

The CMS labels and recognises actions and thoughts as being done by ‘me’ or ‘mine’

111
Q

How can dysfunctions in the ‘central monitoring system’ explain aspects of schiz?

A
  • Dysfunctions in the CMS can explain positive symptoms e.g. hallucinations and delusions
  • Faults with misattributions of our inner speech/articulatory control process (WMM) to external sources such as others voices
112
Q

What does the ‘supervisory attention system’ do?

A

The SAS is responsible for generating self initiated actions

113
Q

How can dysfunctions in the ‘supervisory attention system’ explain aspects in schiz?

A
  • Dysfunctions in the SAS can contribute to negative symptoms e.g. speech poverty, flat affect or avolition
  • Not responding to environmental stimuli with appropriate/any emotions because of faulty SAS
114
Q

What is an egocentric bias?

A

Individuals believe that everything relates to them specifically and jump to false conclusions - the inability to see they are not the central component to all events - usually we grow out of this

115
Q

How can a dysfunction with insight and egocentric bias explain aspects in schiz?

A
  • Individuals may jump to false conclusions and may be resistant to consider other alternatives
    e.g. muffled voices = peoples criticism
    flashes of light = signals from god
  • delusions of control
116
Q

What are the strengths of the cognitive explanation of schizophrenia? (3)

  • evidence to support
  • practical applications
  • links aspects
A

1) Evidence to support - Bentall et al (1991) - asked pt’s to generate category items (e.g. animals beginning with B) or read out generated ones - one week later pt’s were asked whether they had generated the words, read them out or if the list was new - found that schiz patients with hallucinations performed worse than those without - highlights how positive symptoms of schiz are linked to a faulty CMS
2) Has practical applications - CBT aims to challenge irrational thinking e.g. dysfunctions with our SAS - Gabrret (2009) described using CBT to successfully change a patients mind about taking anti-psychotics prescribed - has benefited people
3) Links physiological and psychological aspects together - cognitive neuroscience links areas of the brain together to explain behaviour - by looking at damage to the hippocampus and WMM we can see how they contribute to cognitive deficits

117
Q

What are the weaknesses of the cognitive explanation of schizophrenia?

  • cause and effect issue
  • other explanations
A

1) Cause and effect issue - cognitive deficits may be a result of biological issues such as high dopamine levels, rather than the cognitive deficits being a result of schizophrenia - the explanation is oncomplete
2) Other explanations are more scientific - faulty information processing is hard to study objectively, whereas the dopamine hypothesis considers factors that are easier to measure - means the cognitive explanation is not as objective

118
Q

What are four treatments for schizophrenia?

A

1) Typical and Atypical anti-psychotics
2) Cognitive behavioural therapy
3) Family therapy
4) Token economies

119
Q

What is the aim of anti-psychotics?

A

To reduce, modulate or stabilise the balance of dopamine in four key dopamine pathways and alleviate some on the symptoms of schizophrenia

120
Q

What are the basic principles of all anti-psychotics?

A
  • The drugs must be taken on a regular basis to keep symptoms under control
  • It will take about 7 days before the drug starts to show and effect and symptoms reduce
  • Initially positive symptoms are dramatically reduced and slowly some negative symptoms subside
121
Q

What is the aim of typical anti-psychotics?

A

To antagonise (reduce) levels of dopamine in the brain

122
Q

How do typical anti-psychotics work? How effective are they?

A

They bind to D2 receptor sites, lowering dopamine transmission and reducing positive symptoms
Kapur (2000) said that approximately 60-75% of D2 receptor sites are blocked in the mesolimbic pathway

123
Q

What are some of the potential problems with typical anti-psychotics?

A

As 60-75% of D2 receptor sites were permanently blocked dopamine levels may become too low, aggravating negative motor symptoms e.g. catatonic rigidity

124
Q

What is an example of a typical anti-psychotic?

A

Chlorpromazine Haleporidol

125
Q

What is the aim of atypical anti-psychotics?

A

To modulate (change) levels of dopamine and serotonin in key dopamine pathways in the brain

126
Q

How do atypical anti-psychotics work?

A

They regulate the functioning of dopamine and serotonin in several areas

127
Q

What are some examples of atypical anti-psychotics?

A

Clozapine, Olanzapine and Serquel

128
Q

What does the mesolimbic dopamine pathway do?

A

It’s a sensory pathway involved with emotions and sensations of pleasure

129
Q

What does the nigrostriatal dopamine pathway do?

A

It’s a sensory pathways that has a role in controlling movement and involves dopamine and seratonin

130
Q

How do atypical anti-psychotics work in the mesolimbic dopamine pathway using ‘the hit and run’ technique?

A
  • The pathway is concerned with emotions and sensations of pleasure to reducing the hyperactivity of dopamine should reduce positive symptoms
  • AP’s use a hit and run technique (rapid dissociation) by having their effect on dopamine receptors and then leaving the receptor sites
  • This allows AP’s to have their effect but then allows the receptors to become available for naturally occurring dopamine before the next dose
131
Q

How do atypical anti-psychotics work in the nigrostriatal dopamine pathway?

A
  • The pathway is involved with movements, so the blocking/reducing of dopamine receptor sites can lead to motor side effects
  • Serotonin here inhibits dopamine so the AP’s action is to block serotonin receptors to increase levels of natural dopamine
  • Natural dopamine fills receptor sites and prevents a blockade from AP’s in this area
  • Helps to tackle negative symptoms and reduces motor side effects
132
Q

What are the strengths of using anti-psychotics to treat schizophrenia? (2)

  • evidence to support
  • effective as part of wider treatment
A

1) Evidence to support their effectiveness - Davis et al (1980) analysed results of 29 studies (3519 patients) looking into the effectiveness of anti-psychotics - relapse occurred in 55% where AP’s were replaced with a placebo, compared to 19% of those still taking AP’s - implies their effectiveness in preventing relapse
2) Effective as part of a wider treatment - effectiveness increased when combined with psychological therapies, medications can suspend delusional thoughts and allow the patient to address cognitive and family issues through CBT

133
Q

What are the weaknesses of using anti-psychotics to treat schizophrenia? (3)

  • methodological issues
  • not effective in all indivduals
  • ethical issues
A

1) Methodological issues with Davis’ research - Ross and Read (2004) pointed out that D’s research could be misleading - 45% of those taking the placebo did benefit, so of the 81% who benefited from the drug, 45% could of benefited from the placebo - not 100% effective
2) Not effective in all - Elesser’s longitudinal study discovered that AP’s are not a cure, they can eliminate symptoms and make experiences less distressing, but don’t help everyone and don’t remove all - Typical AP’s help 65% while Atypical help 85% - not for everyone
3) Unethical - as there are many side effects (not protected from harm) e.g. Tardive dyskinesia which affects 60% of patients, characterised by jerky bodily and facial movements

134
Q

What are some of the side effects of anti-psychotics? What percentage of patients do they effect?

A

Tardive dyskinesia = jerkily bodily and facial movements and affects 60% of patients
Muscles tremors and rigidy = 20-40% experience
Dystonia = muscle contractions producing uncontrollable movements in the face, neck and back
Akatisia = psychological, restlessness, agitation, discomfort of limbs
Agranulorsosis = life threatening drop in white blood cells and affects 1% of patients

135
Q

What are the weaknesses of using anti-psychotics to treat schizophrenia? (2)

  • Appropriateness
  • Don’t treat actual cause
A

1) Appropriateness as they require adherence - some patients stop taking AP’s due to side-effects - around 50% stop after year and 75% after 2 years - not suitable in the long term
2) Don’t treat the actual cause - if DA levels are a result of schizophrenia then targeting DA levels is not actually curing schizophrenia, only the symptoms - not a full cure

136
Q

According to the cognitive approach what causes schizophrenia?

A

Faulty information processing, such as cognitive deficits e.g. problems in the CMS and SAS

137
Q

What is the aim of cognitive behavioural therapy in treating Schizophrenia?

A

The aim is to help patients to identify their faulty, delusional beliefs and to help them develop more rational constructive ways of thinking, coping and behaving

138
Q

What are the two techniques used in CBT to treat schizophrenia?

A

Integrated Psychological Therapy (IPT)

Coping Strategy Enhancement (CSE)

139
Q

What is Integrated psychological therapy (CBT) used for?

A

It’s used to try and identify specific cognitive deficits and remedy them, and is most useful for improving attention and refining concept formation (best for the SAS)

140
Q

How does Integrated psychological therapy (CBT) work?

A
  • Clients are taught to recognise and respond appropriately to social cues - combating avolition and appropriate effect - and to understand and evaluate verbal statements accurately - combating alogia and disorganised thinking.
  • Also tries to identify and remove false beliefs using reality tests
141
Q

How did Chadwick et al (1996) use integrated psychological therapy?

A
  • He reported the case of an individual who believed he could make things happen by thinking of them
  • Chadwick showed him 50 video clips and asked him to say what would happen next
  • He did not get a single prediction right and so could understand he did not have the power to influence events
142
Q

What is Coping strategy enhancement (CBT) used for? Who came up with it?

A

Tarrier 19987 - It’s used to teach the individual better ways to manage the severity and frequency of their psychotic symptoms

143
Q

How does Coping strategy enhancement (CBT) work?

A

Through a process of education the patient is taught a range of coping strategies to help manage specific symptoms e.g. distinctive thoughts and positive self-talk (cognitive) and relaxation techniques and drowning out hallucinatory voices (behavioural) - practised in session and then given to apply in the real world

144
Q

What are the strengths of using cognitive behavioural therapy? (4)

  • evidence to support
  • evidence to support
  • successful with other treatments
  • ethical
A

1) Evidence to support - Startup et al (2004) investigated CBT on 90 patients, 43 used standard care (AP’s + nursing) and 47 had standard care + 25x90 min CBT - 60% of CBT showed reliable and clinical improvements and fewer symptoms compared to 40% of control group
2) Tarrier (1987) found CSE successful - used distraction, positive self talk, relaxation etc. and found 73% of sample reported they were successful in managing symptoms
3) CBT is useful in encouraging patients to take anti-psychotics - Garret (2008) managed to successfully persuade a patient to take her anti-psychotics
4) CBT is ethical, patients are protected from harm as they are not experiencing side effects of anti-psychotics - also promotes free will as the patients are taking control of their symptoms

145
Q

What are the weaknesses of using cognitive behavioural therapy? (2)

  • Not suitable all patients
  • Not suitable for all symptoms
A

1) Not suitable for all patients - many clinicians have criticised the use of CBT as schizophrenic patients often do not have coherent thinking and insight into their condition e.g. delusionary patients may not accept that they are ill
2) Not suitable for all symptoms - Zimmermann et al (2005) found CBT useful in auditory and visual hallucinations as it reduces distress - but it is less helpful in treating some negative symptoms

146
Q

What is family therapy based off of?

A

It’s based on social and psycho-dynamic issues surrounding the dysfunctional backgrounds that patients may originate from

147
Q

What is the process of family interventions? (6 steps)

A

1 - Therapy is aimed at helping the patient and their family develop constructive practical coping skills - can take 20 sessions
2 - The focus is developing co-operative and trusting relationships with the family (they meet in a supportive environment)
3 - The therapist educates the group about symptoms, causes and prognosis of schizophrenia, while the family brings together their experiences (psycho-education)
4 - The goal is to provide the patient and family with a set of practical coping skills so they can manage everyday difficulties (behavioural and cognitive techniques)
5 - Family is taught how to express concerns without resorting to high EE
6 - The family and patient are taught to recognise the early signs of potential relapse

148
Q

What are the strengths of using family therapy to treat schizophrenia? (3)

  • evidence to support
  • reduces ‘revolving door syndrome’
  • evidence to support
A

1) Evidence to support - Leff et al (1982) used 24 pt’s following a programme that educated symptoms, nature, methods and coping strategies (pt’s also on AP’s) they were evaluated in follow up sessions two years later, 78% of control group readmitted compared to 19% of experimental
2) Reduces revolving door syndrome - prevents possibility of relapse and the need to re enter therapy - the comprehensive account significantly reduces patients coming back for more treatment so it’s cheaper in the long term
3) Evidence that it works in diverse cultural settings - Xiong et al randomly selected 63 Chinese to enter drug care or drug care + family therapy - 61% of drug patients relapsed compared to 36% of drug care + family therapy

149
Q

What are the weaknesses of using family therapy to treat schizophrenia? (3)

  • methodological flaws with research
  • effective when with other therapies
  • not cost effective?
A

1) Leff’s research only used patients on anti-psychotics - means that there is no evidence for the effectiveness of family therapy on its own
2) Most effective when in conjunction with other anti-psychotics - Vaughn and Leff (1976) found that returning to high EE families saw an increase in relapse, with no medication this was 92% - suggesting that family therapy is only effective when it is used with medication
3) Family therapy may be more expensive than anti-psychotics, especially as most families require up to or over 20 sessions, which may make over treatments such as drug therapy more attractive

150
Q

What is the aim of token economies?

A

It aims to unlearn abnormal behaviours and learn normal behaviours using operant conditioning - in schizophrenia behaviours such as social withdrawal and mutism are attempted to be unlearnt, as well as reducing the expression of psychotic symptoms

151
Q

How do token economies work?

A
  • They are based on operant conditioning techniques i.e. positive reinforcement
  • “Normal” behaviours that are desired are positively rewarded and so are likely to be repeated e.g. self care behaviours and responding to social cues
  • The desirable behaviours are reinforced by the use of plastic tokens - secondary reinforcers
  • The tokens can be exchanged for primary reinforcer (basic needs) e.g. TV time, cigarettes, time out, chocolate or 100 tokens = a social worker
  • The primary reinforces must be highly desirable to the patient
  • In hospitals this may also use negative reinforcement - tokens are removed until the patient behaves normally or punishment where they may be put in time out for abnormal behaviour
152
Q

What are the strengths of using token economies to treat schizophrenia? (2)

  • humane treatment
  • evidence to support
A

1) Regarded as one of the first humane treatments - in the past patients would be isolated and confined, use of token economies allowed patients to be treated more humanely and with more freedom/independence - more ethical
2) Evidence to support the effectiveness - Allyon and Azrin (1968) set aside a ward in a psychiatric hospital with 45 female patients avg. 16 y/o - initially screamed, were mute, assultive, ate without cutlery etc. following TE they were rewarded for hard work and self care, token could be exchanged for music, private room or social worker, which led to improvements in self care - but when removed this stopped - implies effectiveness

153
Q

What are the weaknesses of using token economies to treat schizophrenia? (3)

  • ethical issues
  • not a cure
  • not useful for all symtoms
A

1) Questionable ethics as it infringes some basic human rights - some individuals may not be given a choice in the programme, so TE may be imposed against their wishes, civil rights infringed when privileges are withheld
2) Don’t cure the disorder - TE only targets the undesirable behaviour shown and temporarily rectifies them, it does not fix the root cause of the problem and so it only a coping mechanism also they cannot be imposed in the outside world - benefits are institutionally bound
3) Don’t help all symptoms - may only be appropriate for negative symptoms as patients don’t have control over positive symptoms such as hallucinations - implies they are only a partial treatment

154
Q

What does the ‘diathesis-stress’ approach mean?

A

Diathesis = inheriting a predisposition to develop schizophrenia
This is combined with stress from the environment that can trigger this vulnerability

155
Q

What are ‘uncontrollable stressors’ and how are they implicated in the diathesis stress model?

A

Uncontrollable stressors are events that occur that are attributed to external sources and out of the persons control e.g. early family or geographical locations - thought to be bigger triggers in the diathesis stress model than controllable stressors

156
Q

How is the diathesis stress model implicated in schizophrenia?

A

It implies that these factors could combine together and lead to schiz - e.g. relatively minor stressors may lead to the onset of schiz for those with high vulnerabilites

157
Q

How was an interactionist approach used in Startup’s (2004) study?

A

He investigated the use of CBT, 47 patients received standard care and 25x90 min sessions of CBT, which proved to be the most effective - shows him combining biological and cognitive aspects

158
Q

How was an interactionist approach used in Garret’s study (2008)

A

He used CBT to get a patient to change her mind about taking anti-psychotics which reduced her symptoms as a result - combining cognitive aspects to influence biological aspects

159
Q

How was an interactionist approach used in Leff’s (1982) study?

A

All patients were on anti-psychotics while being treated using family therapy, showing him combining a biological treatment on AP’s with an environmental approach??

160
Q

How was an interactionist approach used in Vaughn and Leff’s (1976) study?

A

They researched how high EE families may clash in conjunction with AP’s, with no medication relapse was 92% - shows them suggesting how biological and other approaches work best in conjunction with each other

161
Q

What are the strengths of using the interactionist approach to explain and treat schizophrenia? (3)

  • a realistic perspective
  • effective for clinicians providing treatment
  • explains different cases
A

1) A realistic perspective including nature and nurture - Gottensman found MZ twins have a 46% concordance rate in development of schizophrenia - showing that there is more to the the development of schizophrenia than biology
2) Allows clinicians to address biological and psychological factors - Startup (2004) used CBT and standard care in 47 patients, which was the most effective option, shows how effective a biological and cognitive approach it
3) Can explain different cases of schizophrenia - by addressing bio vulnerabilities and environmental factors the model can explain diverse prognosis’ as patients may come from different environments

162
Q

What are the weaknesses of using the interactionist approach to explain and treat schizophrenia? (2)

  • doesn’t explain all the effects of stress
  • treatments based on the approach are more expensive
A

1) The approach does not explain how stress impacts the nervous system, triggering the condition - e.g. does not illustrate how urban living could inflate dopamine levels or create hypofrontality in patients - more research is needed
2) Treatments are more expensive than singular based treatments - the approach combines treatments e.g. AP’s and CBT meaning the patient must pay for two therapies - do it may not benefit all patients

psychology (11 decks)

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