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Schizophrenia Flashcards

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1
Q

What is SZ

A
  • serious mental psychotic disorder
  • characterised by profound disruption of cognition and emotion
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2
Q

What can SZ affect

A
  • language
  • thought and perception
  • emotion
  • sense of self
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3
Q

How many people suffer from SZ

A
  • 1% of the population
  • affects about 4 in 1000 people (Saha et al., 2005)
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4
Q

What is the onset for SZ

A
  • between 15 and 35 years
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5
Q

Who does SZ affect more

A
  • men than women
  • cities than countryside
  • working class than middle class
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6
Q

SZ is psychotic and not neurotic, what does psychotic mean

A
  • mental illness causing abnormal thinking and perceptions
  • people lose touch with reality and even sense of self
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7
Q

What happens to people suffering from SZ

A
  • end up homeless or hospitalised
  • not uncommon to commit or attempt suicide
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8
Q

What can be used to diagnose SZ

A
  • DSM 5 (the Diagnostic and Statistical Manual of Psychiatric Disorders)
  • ICD 11 (the International Classification of Diseases)
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9
Q

Where are the DSM and ICD used

A
  • DSM is used in America
  • ICD used in Europe and other parts of the world
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10
Q

How does diagnoses between the DSM and ICD differ

A
  • DSM states you need at least 2 positive symptoms or 1 positive and 1 negative for a period of 1 month as well as extreme social withdrawal for 6 months
  • ICD states you need to show 1 positive and 1 negative or 2 negative symptoms for at least 1 month
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11
Q

What are the types of SZ

A
  • Type 1
  • Type 2
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12
Q

Who made a distinction between the types of SZ

A
  • Crow (1980)
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13
Q

What is Type 1 SZ

A
  • characterised more by positive symptoms
  • better prospects for recovery
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14
Q

What is Type 2 SZ

A
  • characterised more by negative symptoms
  • poorer prospects for recovery
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15
Q

What’s the difference between positive and negative symptoms

A
  • positive add to an individual’s behaviour
  • negative takes from an individual’s behaviour
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16
Q

What are examples of positive symptoms

A
  • hallucinations
  • delusions
  • disorganised speech
  • grossly disorganised or catatonic behaviour
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17
Q

What are hallucinations

A
  • sensory experiences of stimuli that have no basis in reality or are distorted perceptions of things
  • different types
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18
Q

What are the different types of hallucinations

A
  • auditory; person experiences hearing voices making comments or talking to them in their head, normally criticising then
  • visual; seeing things that are not real
  • olfactory; smelling things that are not real
  • tactile; touching things that are not there
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19
Q

What are delusions

A
  • irrational, bizarre beliefs that seem real to the person with SZ
  • can involve being an important historical, religious or political figure
  • may also involve being persecuted by the government, aliens or superpowers
  • involve body, may believe body is under external control
  • can lead to aggression
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20
Q

What is disorganised speech

A
  • result of abnormal thought processes
  • may slip from one topic to another (derailment)
  • speech may be very incoherent (word salad)
  • diagnosed by DSM but not ICD
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21
Q

What is grossly disorganised or catatonic behaviour

A
  • inability or lack of motivation to initiate or even complete a task
  • can lead to problems of personal hygiene or be overactive
  • catatonic refers to adopting rigid postures or aimless repetition of same behaviour
  • diagnosed by DSM but not ICD
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22
Q

What are examples of negative symptoms

A
  • speech poverty (alogia)
  • avolition
  • affective flattening
  • anhedonia
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23
Q

What is speech poverty

A
  • SZ characterised by changes in patterns of speech
  • emphasis is on reduction in amount and quality of speech
  • sometimes accompanied by delay in sufferer’s verbal responses during conversation
  • may be reflected in less complex syntax
  • appears associated with long illness and earlier onset of illness
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24
Q

What is avolition

A
  • finding it difficult to begin or keep up goal directed activity
  • SZ sufferers often have reduced motivation to carry out a range of activities
  • Andreason (1982) identifies signs; poor hygiene and grooming, lack of persistence in work or education and lack of energy
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25
Q

What is affective flattening

A
  • reduction in range and intensity of emotional expression
  • SZ sufferers have fewer body and facial movements and smiles, and less co-verbal behaviour
  • patients may show deficit in prosody (intonation, tempo, loudness and pausing) when speaking, giving cues to emotional content of conversation
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26
Q

What is anhedonia

A
  • loss of interest or pleasure in all or most activity
  • lack of reactivity to normally pleasurable stimuli
  • physical anhedonia is inability to experience physical pleasures such as pleasure from food or bodily contact
  • social anhedonia is inability to experience pleasure from interpersonal situations such as interacting with other people
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27
Q

What are issues associated with the classification and diagnosis of SZ

A
  • reliability
  • validity
  • co-morbidity
  • symptom overlap
  • gender bias
  • cultural bias
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28
Q

How is reliability an issue for the classification and diagnosis of SZ

A
  • Whaley (2001) found interrater reliability between diagnosticians was as low as 0.11 using the DSM
  • Cheniaux et al. (2009) also found low inter rater reliability
  • had 2 psychiatrists independently diagnose 100 patients using ICD and DSM
  • inter rater reliability was poor with one diagnosing 26 with DSM and 44 with ICD but other psychiatrist diagnosed 13 with DSM and 24 with ICD
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29
Q

How is validity an issue for the classification and diagnosis of SZ

A
  • can be assessed using criterion validity (using different assessment systems to arrive at same diagnosis, e.g. DSM and ICD)
  • SZ diagnosis more likely using ICD than DSM according to Cheniaux’s study, showing over diagnosis in ICD and under diagnosis in DSM
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30
Q

What studies have been carried out to test validity of SZ diagnosis and classification

A
  • Rosenhan (1973)
  • Birchwood and Jackson (2001)
  • Osario (2019)
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31
Q

What studies have been carried out to test reliability of SZ diagnosis and classification

A
  • Osario et al. (2019)
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32
Q

How did Osario et al. (2019) test reliability in SZ

A
  • reported interrater reliability between pairs of psychiatrists was 0.97
  • test-retest reliability was 0.92
  • suggests most recent diagnosis of SZ using DSM is good and reliable
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33
Q

How did Rosenhan (1973) test validity in SZ

A
  • 8 pseudo patients able to get admitted in psychiatric hospital using symptoms of hearing voices
  • during stay, all patients behaved normally and showed no signs of mental illness
  • found all 8 patients stayed for 7-52 days
  • all but one patient discharged with SZ in remission
  • shows diagnosis was poor
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34
Q

How did Birchwood and Jackson (2001) test validity in SZ

A
  • found 20% of patients of SZ show complete recovery and never have another SZ episode
  • 10% show significant improvement
  • 30% show some improvement
  • 40% never recover
  • 10% affected and commit suicide
  • great variation in prognosis suggests poor predictive validity
  • however, Mason (1997) found use of newer classification has improve the predictive validity of diagnosis, particularly when the 6 month criteria for diagnosis was used rather than 1 month
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35
Q

How did Osario (2019) test validity in SZ

A
  • suggests that because reliability is so high using DSM, validity would also be high using this single diagnostic system, suggested ICD needs more revision
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36
Q

How is co-morbidity an issue for the classification and diagnosis of SZ

A
  • idea that 2+ mental disorders occur together
  • if this is the case, we can question validity of diagnosis for SZ
  • Buckley et al. (2009) concluded around half patients with SZ also have depression (50%), or substance abuse (47%)
  • PTSD (29%) and OCD (23%) also occurred
  • poses challenge as it shows we are unable to distinguish between disorders
  • might mean severe depression looks like SZ, or vice versa
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37
Q

How is symptom overlap an issue for the classification and diagnosis of SZ

A
  • means there is considerable overlap between symptoms of SZ and other conditions, such as depression and bipolar disorder
  • Ellason and Ross (1995) point out people with DID having more SZ symptoms than people diagnosed with SZ
  • most people diagnosed with SZ have sufficient symptoms of other disorders that they could also receive at least one other diagnosis (Read, 2004)
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38
Q

How is gender bias an issue for the classification and diagnosis of SZ

A
  • Longenecker et al. (2010) reviewed SZ studies since 1980s, finding men more likely to be diagnosed
  • may happen to be a gender bias in diagnosis as women seem to function better than men, having good family relationships and more likely to work (Cotton, 2009)
  • therefore less likely to be diagnosed with SZ as women show better interpersonal function
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39
Q

How is cultural bias an issue for the classification and diagnosis of SZ

A
  • African American and English people of Afro Caribbean origin are 9 times more likely to be diagnosed with SZ (Pinto and Jones, 2008)
  • positive symptoms (auditory hallucinations) are acceptable in Africa because of cultural beliefs in communication with ancestor which are acceptable and not warranted to a diagnosis in Africa
  • may be because Western cultures doubt honesty of black people (Escobar, 2012)
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40
Q

What are the advantage of classification and diagnosis of SZ

A
  • communication shorthand; patient with mental disorder often has numerous symptoms. Simpler to incorporate these symptoms into a single diagnosis, making communication between mental health professionals easier
  • treatment; often specific to certain disorders so a reliable diagnosis can point to a therapy that will alleviate symptoms
  • although variation, there are many underlying biological abnormalities seen in people with SZ. It is hoped that a greater understanding will lead to more effective treatment
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41
Q

What are the two biological explanation factors of SZ

A
  • genetic basis
  • neural correlates
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42
Q

How can the genetic basis be tested

A
  • family studies
  • twin studies
  • adoption studies
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43
Q

How are family studies used to investigate biological explanations of SZ

A
  • find individuals who have SZ and determine whether biological relatives are similarly affected more often than non-biological relatives
  • family studies show that the closer the genetic relatedness, the greater the risk to get SZ
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44
Q

Who has done research into family studies as a biological explanation of SZ

A
  • Gottesman (1991)
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45
Q

What did Gottesman (1991) find when investigating family studies as a biological explanation of SZ

A
  • 46% chance of SZ if both parents have it
  • 13% chance of SZ if one parent has it
  • 9% chance of SZ if a sibling has it
  • shows the closer you are genetically related, the more likely you are to get SZ
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46
Q

How are twin studies used to investigate biological explanations of schizophrenia

A
  • an opportunity for researchers to investigate nature/nurture debate in terms of contribution of heredity and environmental influences of SZ
  • MZ twins share 100% of genes but DZ twins share 50% of genes
  • concordance rate should be higher for MZ than DZ if SZ is genetic
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47
Q

Who has done research into twin studies as a biological explanation of SZ

A
  • Gottesman (1991)
  • Jospeh (2004)
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48
Q

What did Gottesman (1991) find when investigating twin studies as a biological explanation of SZ

A
  • found 48% concordance rate for MZ twins
  • 17% concordance rate for DZ twins
  • shows the more genetically similar you are, the more likely you are to get SZ
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49
Q

What did Joseph (2004) find when investigating twin studies as a biological explanation of SZ

A
  • did a review of twin studies that were carried out up to 2001
  • found an overall concordance rate for MZ twins as 40% but 7.4% for DZ twins
  • as concordance rate is still relatively high for MZ twins, his study supports idea of genes playing a big part in SZ
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50
Q

How are adoption studies used to investigate biological explanations of schizophrenia

A
  • difficult to separate genetic from environmental influences in twin and family studies
  • carried out to understand influence of nature/nurture
  • adopts studies are researched to see nature/nurture influences when MZ twins may be reared apart of offspring from SZ parents are adopted
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51
Q

Who has done research into adoption studies as a biological explanation of SZ

A
  • Tienari et al. (2001)
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52
Q

What did Tienari et al. (2001) find when investigating adoption studies as a biological explanation of SZ

A
  • carried out study in Finland
  • 164 adoptees who’s mothers had SZ, 11 (6.7%) also diagnosed with SZ compared to control group of 197 adoptees where only 4 (2%) were diagnosed with SZ
  • shows although percentage of children adopted by non schizophrenic parents having SZ was low, there was a small link between genes and SZ with children whose biological mothers were schizophrenic
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53
Q

What are candidate genes in relation to SZ

A
  • specific genes seemed to be associated with SZ
  • now agreed SZ is polygenic => combination of different genes that have been implicated in SZ
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54
Q

Who has done research into candidate genes as a biological explanation of SZ

A
  • Ripke et al (2014)
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55
Q

What did Ripke et al. (2014) find when investigating candidate genes as a biological explanation of SZ

A
  • compared genetic makeup of 37k SZ patients worldwide with 113k controls
  • found 108 separate genetic variations associated with increasing SZ
  • the genes that were particularly vulnerable were the ones with connections to functioning of certain neurotransmitters, such as dopamine
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56
Q

What are examples of evaluation points for the genetic basis of SZ

A
  • research supported
  • nature nurture
  • family history
  • diathesis stress model
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57
Q

How does the genetic basis of SZ being research supported act as an evaluation point

A
  • positive evaluation point
  • lots of research evidence supporting genetic basis for SZ; Gottesman, Joseph and Tienari
  • shows link between genes and SZ
  • strength as it shows if a child grows up in a family where both biological parents have SZ, chances is heightened than if one or no parents have it
  • shows genetics is an important factor
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58
Q

How is the nature nurture debate an example of an evaluation point for the genetic basis of SZ

A
  • problem with twin and family studies is separating nature from nurture
  • e.g. MZ twins are normally reared together making it difficult to separate upbringing frmo genes
  • even when looking at adoption studies, children tend to be adopted by relatives who may still have similar rearing as biological parents
  • adoption studies thus may not always be a good comparison for the effects of nature or nurture
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59
Q

How does family history act as an example of an evaluation point for the genetic basis of SZ

A
  • SZ can take place in absence of a family history
  • one explanation is a mutation in parental DNA, such as in paternal sperm cells
  • can be caused by radiation, poison or infection
  • evidence for role of mutation comes from Brown et al’s. 2002 study showing positive correlation between paternal age and increased risk of SZ increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50
  • suggests although genes are not directly involved, person can still get SZ if father was old at time of fertilisation
  • suggests role of nature and nurture both play a part rather than just genes
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60
Q

How is the diathesis stress model an example of an evaluation point for the genetic basis of SZ

A
  • states there is a genetic vulnerability in SZ
  • vulnerability only likely to be triggered if there is a stress-trigger in the individual’s life
  • an individual may be born with a gene which makes them particularly vulnerable to SZ but if life is stress free then they may not end up with disorder
  • thus we need to be cautious when looking at genetic factors since they alone may not trigger SZ
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61
Q

What is neural correlates as a biological explanation for SZ

A
  • measurements of the structure or function of the brain that have a relationship with SZ, especially different regions of the brain
  • refers to how different neurotransmitters, such as dopamine and serotonin, in different parts of the brain can also play a part in SZ
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62
Q

What type of SZ symptoms have neural correlates

A
  • both positive and negative symptoms
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63
Q

Who has done research into neural correlates of SZ

A
  • Torrey (2002)
  • Weinberger and Gallhofer (1997)
  • Conrad et al. (1991)
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64
Q

How has Torrey (2002) researched into neural correlates of SZ

A
  • using brain imaging techniques, researchers have discovered many SZs have enlarged ventricles, cavities in the brain that supply nutrients and remove waste
  • ventricles of a person with SZ are 15% bigger than normal (Torrey, 2002)
  • people with SZ with enlarged ventricles display more negative than positive symptoms
  • these people also respond poorly to typical antipsychotics
  • enlarged ventricles may be result of poor brain development or tissue damage, leading to development of SZ
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65
Q

How have Weinberger and Gallhofer (1997) researched into neural correlates of SZ

A
  • prefrontal cortex (PFC) is main area of brain involved in executive control
  • research shows this is impaired in SZ patients
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66
Q

How has Conrad et al. (1991) researched into neural correlates of SZ

A
  • hippocampus is an area of brain in temporal lobe
  • several studies have reported anatomical changes in hippocampus in SZ patients
  • deficits in nerve connections between the hippocampus and prefrontal cortex have found to correlate with the degree of memory impairments in SZs
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67
Q

What are the strengths of neural correlates as a biological explanation of SZ

A
  1. evidence to support structural changes in brain between SZ and non SZ
    - e.g. Torrey’s research with reference to enlarged brain ventricles and Conrad’s study with regards to the hippocampus
  2. research evidence can be validated through brain scanning => objective
    - shows face validity to the neural correlates explanation
    - because one can observe structural brain changes occurring with SZ patients
    - can help to tailor make treatments to reduce symptoms of SZ
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68
Q

What are the weaknesses of neural correlates as a biological explanation of SZ

A
  1. problem with looking at different brain regions is the fact that there are individual differences in sufferers of SZ
    - not all patients have deficits in functioning of different brain regions
  2. there are different brain regions involved in SZ
    - may be difficult to pinpoint which brain region is causing symptoms
  3. may be difficult to establish cause and effect in terms of neuroatomy
    - evidence is correlational
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69
Q

What is an important aspect of the neural correlates aspect as a biological explanation for SZ

A
  • dopamine hypothesis
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70
Q

What is the dopamine hypothesis

A
  • claims an excess of the neurotransmitter dopamine in certain regions of the brain is associated with positive symptoms of SZ
  • thus messages from neurons that transmit dopamine often lead to hallucinations and delusions
  • SZs are thought to have high levels of D2 receptors on receiving neurons resulting in more dopamine binding and therefore more neurons firing
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71
Q

What are the two consequences of the dopamine hypothesis

A
  • hyperdopaminergia
  • hypodopaminergia
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72
Q

What is hyperdopaminergia

A
  • based on original version of dopamine hypothesis in explanation SZ
  • states there are high levels of dopamine in the subcortex
  • e.g. excess of dopamine receptors in the Broca’s area may be associated with problems in speech and/or experience of auditory hallucinations
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73
Q

What is hypodopaminergia

A
  • recent versions of the dopamine hypothesis have focused on lower levels of dopamine in the cortex
  • Goldman-Rakic et al (2004) have focused on the role of low levels of dopamine in the prefrontal cortex on negative symptoms of SZ
  • been suggested hypodopaminergia leads to subcortial hyperdopamingeria
74
Q

What is dopamine

A
  • brain neurotransmitter
  • helps regulate movement, attention, learning, and emotional responses
  • enables us to see rewards and take action to move towards them
  • contributors to feelings of pleasures and satisfaction as part of the reward system, so also plays a part in addiction
75
Q

What does dopamine do and use an example

A
  • involved in motor system
  • when brain fails to produce enough dopamine, can result in Parkinson’s disease
  • primary treatment is L-dopa, spurring production of dopamine
  • dopamine also implicated in SZ and ADHD, but role is not fully understood
  • people with low dopamine may be more prone to addiction
  • presence of a certain kind of dopamine receptor is associated with sensation-seeking (risk-taking)
76
Q

What are the strengths for the dopamine hypothesis

A
  1. supported through drug research
    - dopamine antagonists tend to increase dopamine levels and make SZ symptoms worse in sufferers
    - can produce SZ like symptoms in non-sufferers thus supporting hyperdopaminergia
  2. antipsychotics act like antagonists
    - act to reduce levels of dopamine in SZ patients
    - supports idea that dopamine levels are high in SZ and can be reduced through drugs (Tauscher et al, 2014)
  3. Lindstroem et al. (1999), found chemicals needed to procure dopamine are taken up faster in brains of SZs compares to controls
    - suggests SZs produce more dopamine
77
Q

What are the weaknesses for the dopamine hypothesis

A
  1. dopamine hypothesis cannot be seen as sole cause of SZ
    - other biological and psychological factors contributing which focus on impaired thinking which could explain hallucinations and delusions
    - recent research has focused on attention of glutamate => another neurotransmitter implicated in SZ (Moghadamm and Javitt, 2012)
    - suggests dopamine is not only neurotransmitter responsible for SZ
  2. correlation-causation problem
    - number of neural correlates with many important unanswered questions
    - does high/low levels of dopamine cause SZ or other way?
78
Q

What are the psychological explanations for SZ

A
  • family dysfunction
  • cognitive explanations
79
Q

What is family dysfunction as a psychological explanation for SZ

A
  • attempt to link SZ to childhood and adult experiences of living in a dysfunctional family
80
Q

How can family dysfunction be explained as a psychological explanation for SZ

A
  • the schizophrenic mother
  • double-blind theory
  • expressed emotion
81
Q

Who done research into the schizophrenic mother

A
  • Fromm Reichmann (1948)
82
Q

What did Reichmaan (1948) propose in terms of the schizophrenic mother

A
  • proposed psychodynamic explanation for SZ based on accounts from patients about childhood
  • noted man spoke about particular parents (she called them the schizophrenic mother)
  • characteristics include cold, rejection and controlling as well as creating a family climate full of secrecy and tension
  • leads to lack of trust in relationships later developing into paranoid delusions, leading to SZ
  • father is often passive and not involved in child upbringing
83
Q

Who done research into the double blind theory

A
  • Bateson et al. (1972)
84
Q

What did Bateson et al. (1972) find in terms of the double blind theory

A
  • agreed family climate is important in development of SZ => more focused on actual family communication style
  • suggested this affects children receiving contradictory messages => mixed message
  • child is unable to comment about the unfairness of the situation or seek clarification
  • child would be punished by withdrawal of love when wrong
  • child then feels confused about world and sees it as a dangerous place => reflected in SZ symptoms such as paranoid delusions
  • Bateson classified this was a risk factor of SZ and not a sole cause
85
Q

What does expressed emotion (EE) in relation to family dysfunction suggest

A
  • level of emotion, in particular negative emotion, towards a patient by their carers
  • has several parts
  • high levels of EE by carer creates serious source of stress
  • may be a reason for the SZ patient to relapse
  • EE can be a trigger for onset of SZ especially if person has a genetic vulnerability to the disorder (diathesis-stress model)
86
Q

What are examples of strengths of family dysfunction as a psychological explanation for SZ

A
  • Tienari et al. (1994)
  • Read et al. (2005)
  • insecure attachment
  • Berger (1965)
87
Q

How is Tienari et al. (1994) an example of a strength for family dysfunction as a psychological explanation for SZ

A
  • research supporting
  • adopted children who had SZ biological parents more likely to have SZ than children with non SZ biological parents
  • difference only emerged in situations where adopted family rated as disturbed or dysfunctional
  • illness only shown under appropriate environmental conditions
  • shows family dysfunction is a contributing factor to SZ
88
Q

How is Read et al. (2005) an example of a strength for family dysfunction as a psychological explanation for SZ

A
  • reviewed 46 studies of child abuse and SZ
  • concluded that 69% of adult women in-patients with a diagnosis of SZ had history of physical abuse, sexual abuse or both in childhood
  • for men, figure was 59%
  • shows family dysfunction contributes to an individual developing SZ
89
Q

How is insecure attachment an example of a strength for family dysfunction as a psychological explanation for SZ

A
  • adults with insecure attachments to their primary carer are more likely to develop SZ
  • strengthens family dysfunction explanation
90
Q

How is Berger (1965) an example of a strength for family dysfunction as a psychological explanation for SZ

A
  • supports double-blind theory in SZ
  • found SZs reported higher recall of double-blind statements by mothers than non SZs
  • however, this evidence may not be reliable as patient’s recall might be affected by SZ => hallucinations and delusions
  • may be assuming that their mothers used more double blind statements and we don’t know if their memory was affected by symptoms
91
Q

What are examples of weaknesses of family dysfunction as a psychological explanation for SZ

A
  • Liem (1974)
  • Altorfer et al. (1998)
  • parent blaming
92
Q

How is Liam (1974) an example of a weakness for family dysfunction as a psychological explanation for SZ

A
  • in regards to double blind theory
  • measured patterns of parental communication in families with a SZ child
  • found no difference when compared to normal families
  • shows this theory may not be specifically related to SZ
93
Q

How is Altorfer et al. (1998) an example of a weakness for family dysfunction as a psychological explanation for SZ

A
  • not all patients who live in high EE families relapse
  • not all patients who live in low EE homes avoid relapse
  • found one quarter of patients they studied showed no physiological responses to stressful comments from their relatives
  • shows the evidence for EE as a contributing factor towards relapse and EE is mixed
94
Q

How is parents blaming an example of a weakness for family dysfunction as a psychological explanation for SZ

A
  • dysfunctional family explanations for SZ leads to parent blaming
  • parents who already suffer seeing child develop SZ and have to bare responsibly for their care also suffer further trauma by being blamed for their child’s condition
  • means family dysfunctional may not be entirely ethical
  • may cause more harm than help both sufferer and parents
95
Q

What are cognitive explanations for SZ

A
  • focus on role of mental processes
  • SZ is associated with several types of dysfunctional thought processing thus provide explanations for SZ as a whole
  • Frisch et al. (1992) identified two types of dysfunctional thought processing that could underlie some symptoms
96
Q

What were the two kinds of dysfunctional thought processing identified by Frith et al. (1992) as cognitive explanations for SZ

A
  • meta representation
  • central control
97
Q

What did Frith et al. (1992) identify about metarepresentation

A
  • cognitive ability to reflect on thoughts and behaviour
  • enables us an insight into our own intentions and goals as well as allowing us to interpret actions of others
  • dysfunction in metarepresentation would disrupt ability to recognise own actions and thoughts as being our own rather than someone else
  • could explain auditory hallucinations and delusions
98
Q

What did Frith et al. (1992) identify about central control

A
  • cognitive ability to suppress automatic responses while we perform other actions instead
  • speech poverty and thought disorder could result from inability to ignore own automatic thoughts as well as what others could be saying
  • sufferers of SZ tend to experience derailment of their thoughts and what they say
  • too much going on in their thought processes thus lose control of their own thoughts
99
Q

What are the strengths of cognitive explanations of SZ

A
    1. Stirling et al. (2006)
  • compared 30 patients with diagnosis of SZ with 18 controls on cognitive tasks such as strop effect
  • found patients with SZ took twice as long to say colour of word than controls
  • shows dysfunctional thought processing as they struggled separating colour word from actual colour
    1. success of CBT used alongside drugs to treat SZ
  • SZ is a thought disorder so drugs cannot completely treat
  • CBT aims to question and challenge hallucinations and delusions
  • proven to be effective thus supporting cognitive explanations
100
Q

What are the weaknesses of cognitive explanations of SZ

A
    1. difficult to establish whether dysfunctional thoughts processing is a cause or consequence of SZ
  • challenges research support
    1. problematic as it fails to take into account biological factor
  • does not acknowledge fact that dysfunctional thought processing could be due to abnormal dopamine levels in brain
  • reductionist as it simplifies SZ to very basic elements instead of considering other factors which all been shown to contribute to SZ
101
Q

What are biological forms of treatment for SZ

A
  • drugs (antipsychotic drugs)
  • can be given as tablets, syrup or injections
  • injections given to those at risk of not taking their medication or not taking it properly
  • injections given every 2-4 weeks
102
Q

How can antipsychotic drugs be divided

A
  • typical
  • atypical
103
Q

How do typical antipsychotics works

A
  • act as dopamine antagonists and reduce effects of dopamine, this reducing symptoms of SZ
  • drugs bind to dopamine receptors, particularly D2 receptors in the mesolimbic dopamine pathway
  • do not stimulate receptors and thus block actions
  • reduces positive symptoms of SZ
104
Q

What is an example of a typical antipsychotic

A
  • chlopromazine
  • can be taken as a tablet, syrup or injection
  • been around since 1950s
105
Q

Apart from reducing SZ symptoms, what else can chlopromazine do

A
  • act as a sedative
  • calms patients not only with SZ but other conditions
  • faster absorbed in syrup form rather than tablet hence it being an effective sedative
106
Q

What is the dosage for chlorpromazine

A
  • maximum dosage is 1000mg
  • when first given, dosage would be smaller then gradually increased
  • 400mg to 800mg
107
Q

Explain the link between typical antipsychotics and the dopamine hypothesis

A
  • hypothesis suggests that schizophrenic symptoms are due to high levels of dopamine
  • typical antipsychotics are dopamine antagonists so block the dopamine receptors in the synapses of the brain, reducing actions of dopamine
  • when patient first takes chlorpromazine, dopamine levels build up but then production of dopamine reduces
  • therefore, this antagonist normalises dopamine production and transmission, reducing symptoms of SZ such as hallucinations
108
Q

What are atypical antipsychotics

A
  • emerged in 1970s
  • used to improve effectiveness of typical antipsychotics and minimise side effects that occurred
  • beneficial effect for negative symptoms and cognitive impairment are suitable for treatment-resistant patients
109
Q

How do atypical antipsychotics work

A
  • similar to typical antipsychotics
  • block D2 receptors
  • only temporarily occupy D2 receptors then rapidly dissociate to allow normal dopamine transmission
  • it is the rapid disassociation that is thought to be responsible for lower levels of side effects
110
Q

What are examples of atypical antipsychotics

A
  • clozapine
  • risperidone
111
Q

When was clozapine developed

A
  • developed in 1960s but trialed in 1970s
  • withdrawn after side effects
  • came back in 1980s as it was more effective than typical antipsychotics
112
Q

What is the side effect of clozapine

A
  • agranulocytosis
  • low number of white blood cells to fight infection in the immune system
  • patients given regular blood tests to make sure they do not have agranulocytosis
  • not used as an injection to prevent it from entering the blood stream
113
Q

What is the dosage of clozapine

A
  • 300-450mg a day
114
Q

How does clozapine work

A
  • binds to dopamine receptors
  • also acts on serotonin and glutamate receptors
  • by working on other neurotransmitters, this helps reduce depression and anxiety and improve cognitive functioning
  • improves mood so is given to patients at high risk of suicide
  • important as research shows 30-50% of patients with SZ are likely to attempt suicide
115
Q

When was risperidone developed

A
  • emerged in 1990s
  • attempt to reduce serious side effects of clozapine
  • still as effective as clozapine
116
Q

What is the dosage of risperidone

A
  • 4-8mg a day
  • maximum of 12mg
  • taken as syrup, tablet or injection
117
Q

How does risperidone work

A
  • binds to dopamine receptors but works better in binding to dopamine receptors than clozapine, leading to less side effects
  • much smaller doses required
  • evidence suggests this leads to fewer side effects than most antipsychotics
118
Q

What are examples of strengths for drug therapy for SZ

A
  • Thornley et al. (2003)
  • Meltzer (2012)
  • Leucht et al. (2012)
119
Q

How is Thorney et al. (2003) an example of a strength for drug therapy for SZ

A
  • compared uses of chlorpromazine with a placebo
  • data from 13 trials with total of 1121 participants showed chlorpromazine was associated with reduced symptoms and better overall functioning
  • data from three trials with 512 participants showed relapse rate was lower when chlorpromazine was taken
  • study shows typical antipsychotics were effective in reducing symptoms of SZ compared to placebo showing that drug therapy is appropriate in treating SZ
120
Q

How is Meltzer (2012) an example of a strength for drug therapy for SZ

A
  • concluded clozapine is more effective than typical antipsychotics and other atypical antipsychotics in treating SZ
  • clozapine seen as effective in 30-50% of cases where typical antipsychotics had failed
  • study shows use of clozapine as treatment is an appropriate drug as Meltzer showed especially when other drugs failed
121
Q

How is Leucht et al. (2012) an example of a strength for drug therapy for SZ

A
  • carried out meta analysis of 65 studies, published between 1959 and 2012, involving nearly 6000 patients
  • some patients taken off antipsychotics and given placebos instead
  • within 12 months, 64% of those patients on placebo relapsed whereas only 27% on antipsychotic relapsed
  • results clearly show antipsychotic medication is effective and appropriate in preventing SZ patient from relapsing
122
Q

What are examples of weaknesses of drug therapy for SZ

A
  • side effects
  • Healy (2012)
  • ethical issues
  • dopamine hypothesis
123
Q

How are side effects an example of a weakness for drug therapy for SZ

A
  • biggest weakness of drug therapy is side effects
  • typical antipsychotic side effects include dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin
  • more profound side effect can result in tardive dyskinesia, caused by dopamine supersensitivity and manifests as involuntary facial movements
  • most serious typical side effect is NMS, which could lead to high temperature, delirium and coma and even death => occurs in 0.1-2% of SZ patients
  • atypical developed to overcome side effects but they still exist, such as agranulocytosis
124
Q

How is Healy (2012) an example of a weakness for drug therapy for SZ

A
  • effectiveness of drugs challenged by Healy
  • suggested some successful drug trials had data published on multiple occasions thus exaggerating effectiveness
  • also because antipsychotics have powerful calming effects, it seems as though drugs are successful
  • however this does not show how much the drugs actually reduce symptoms
  • most published studies only assess short term benefits rather than long term, especially for patients who stopped taking drugs
125
Q

How are ethical issues an example of a weakness for drug therapy for SZ

A
  • ethical issues related to using drug therapy for SZ
  • most profound would be consent
  • SZ is a psychotic disorder, so patients may not be in right frame of mind to give fully informed consent in taking drugs
  • drugs have severe side effects so one would question extent of harm (physical and mental) and whether facts do drugs were reversible, especially with NMS and tardive dyskinesia
126
Q

How is the dopamine hypothesis an example of a weakness for drug therapy for SZ

A
  • understating of antipsychotic drugs is tied with dopamine hypothesis
  • relates to abnormally higher levels of dopamine in subcortex of brain
  • although it is now known that dopamine levels can be abnormally low
  • if this is true, it is not clear how antipsychotics (dopamine antagonists) help treat symptoms of SZ
  • in fact, modern understanding of relationship between dopamine and psychosis suggests antipsychotics shouldn’t work
  • undermined faith of some people that antipsychotics do work
127
Q

What are the three psychological therapies for SZ

A
  • cognitive behavioural therapy (CBT)
  • family therapy
  • token economies
128
Q

How does CBT help SZ patients

A
  • NICE recommended all people should be offered CBT
  • this form of therapy is known as CBTp for SZ
  • originally developed to provide treatment for residual symptoms that persist despite the use of antipsychotic medication
  • treatment with antipsychotic drugs still leaves many patients with persistent positive and negative symptoms hence introduction of CBTp to deal with symptoms and improve patients’ functioning
129
Q

What are the different phases of CBTp

A
  • assessment
  • engagement
  • ABC model
  • normalisation
  • critical collaborative analysis
  • developing alternative explanations
130
Q

What does assessment in CBTp consist of

A
  • patient expresses their thoughts to therapist
  • realistic goals for therapy are discussed using patients current distress as motivation for change
131
Q

What does engagement in CBTp consist of

A
  • therapies emphasis with patient’s perspective and feelings of distress
  • stresses that explanations for their distress can be developed together
132
Q

What does the ABC model in CBTp consist of

A
  • patient gives explanation of activity event that appear to cause emotional and behaviour consequences
  • patient’s one beliefs can be rationalised, disputed and changed
133
Q

What does normalisation in CBTp consist of

A
  • conveying to patients that many people have unusual experiences such as hallucinations and delusions under many circumstances
  • reduces anxiety and sense of isolation
  • by doing this, patient feels less alienated and stigmatised
  • possibility of recovery seems more likely
134
Q

What does critical collaborative analysis in CBTp consist of

A
  • therapist uses gentle questioning to help patient understand illogical deductions and conclusions
  • questioning can be carried out without causing distress, provided there is atmosphere of trust
  • therapist needs to remain emphatic and non judgemental
135
Q

What does developing alternative explanations in CBTp consist of

A
  • patient develops own alternative explanations for previously unhealthy assumptions
  • if patient is not forthcoming with healthy alternative explanations, new ideas can be constructed in cooperation with therapist where therapist encourages positive self talk
136
Q

How is CBTp carried out

A
  • can be delivered in groups
  • more usual that it is delivered on a one to one basis
  • NICE recommend at least 16 sessions in treating SZ
  • aim of CBTp is to help people establish links between their thoughts, feelings or actions and their symptoms and general level of functioning
137
Q

What are patients encouraged to do during CBTp

A
  • trace back origins of their symptoms in order to get a better idea of how they might have developed
  • encouraged to evaluate content of delusions and considers watts to test validity of faulty beliefs
  • during CBTp, therapist lets patient develop own alternatives to those previously maladaptive beliefs, ideally looking for alternative explanations and coping strategies that are already present in the patients mind
138
Q

What are positive evaluation points for CBT

A
  • effectiveness
  • stage of disorder
139
Q

How is effectiveness a positive evaluation for CBT

A
  • CBTp seems to be more effective in treating SZ compared to antipsychotic medication alone
  • NICE (2014) review of treatments for SZ found consistent evidence when compared with drugs, CBTp was effective in reducing rehospitalisation rates up to 18 months following end of treatment
  • also shown to be effective in reducing severity of symptoms as well as improvements in social functioning
  • however, difficult to assess effectiveness of CBTp alone as patients were being treated with both medication and CBTp
140
Q

How is stage of disorder a positive evaluation for CBT

A
  • effectiveness of CBTp is dependent on stage of disorder
  • appears to be more effective when available at certain stages and when delivery is adjusted to current stage
  • Addington and Addington (2005) claim initial acute phase of SZ, self reflection is not appropriate
  • however following stabilisation of psychotic symptoms with medication, patients can benefit from group CBTp
  • research shows more experienced SZ patients with greater realisation are most likely to benefit from CBTp
141
Q

What are examples of negative evaluation points for CBT

A
  • availability
  • meta analysis
142
Q

How is availability a negative evaluation for CBT

A
  • despite being recommended by NICE as treatment for SZ, it is estimated only 1 in 10 people in UK with SZ have access to CBTp
  • figure is even lower in some areas of the UK
  • survey by Haddock et al. (2013) found those in north west of England out of 187 patients, only 13% had been offered CBTp (7%)
  • however some offered weather refuse or fail to attend sessions (Freeman et al., 2013) limiting its effectiveness
143
Q

How is meta analysis a negative evaluation for CBT

A
  • problems with meta analysis is failure to take into account quality of studies
  • e.g. some studies fail to randomly allocate patients to CBTp or a control conditions
  • other studies fail to assess patients subsequently assessment of symptoms and general functioning after they have been treated with CBTp
  • Juni et al. (2011) concluded there was lack of evidence that problems associated with methodologically weak trials translated into biased findings about effectiveness of CBTp
  • Wykes et al. (2008) found the more rigorous the study, the weaker the effects of CBTp
144
Q

How can families help SZ patients

A
  • families can play an important role in helping a person with SZ to recover and stay well
  • main aim of family therapy is to provide support for carers in an attempt to make family life less stressful and so reduce rehospitalisation
145
Q

What is family therapy

A
  • name given to range of interventions aimed at family of someone with SZ
  • in their guide ace on treatment and management of SZ, NICE recommend family therapy be offered to all individuals diagnosed with SZ who are in contact or live with family members
  • also stress such interventions should be considered priority where there are persistent symptoms of a high risk of relapse
  • research shows SZs in familiarise that expressed high levels of criticism, hostility or over involvement had more frequent relapses than people with same problems who lived in families that were less expressive in their emotions
146
Q

How is family therapy offered

A
  • offered for a period of 3-12 months and at least 10 sessions
  • family based interventions are aimed at reducing level of expressed emotion within the family, as expressed emotion has been demonstrated to increase likelihood of relapse
  • Garety et al. (2008) estimates relapse rate for individuals who receive family therapy as 25% compared to 50% of those who received standard care alone
  • involves providing family members with information about SZ, finding ways of supporting an individual with SZ and resolving practical problems
147
Q

How does family therapy work

A
  • reduces levels of expressed emotion and stress
  • increases capacity of relatives to solve related problems
  • attempts to reduce incidence of relapse for person with SZ
  • uses a number of strategies
148
Q

What are the strategies used by family therapy

A
  • psychoeducation; helping person and carers to understand and be better able to deal with illness
  • forming an alliance with relatives with care for the person with SZ
  • reducing emotional climate within the family and the burden of care for family members
  • enhancing relatives’ ability to anticipate and solve problems
  • reducing expressions of anger and guilt by family members
  • maintaining reasonable expectations among family members for patients performance
  • encouraging relatives to set appropriate limits whilst maintaining some degree of separation when needed
149
Q

Is family therapy used by itself in treating SZ

A
  • forms part of an overall treatment package
  • commonly used in conjunction with routine drug treatment and outpatient clinical care
  • during family therapy sessions, individual with SZ is encouraged to talk to their family and explain what sort of support they find helpful
150
Q

Who carried out research into family therapy

A
  • Pharoah et al. (2010)
151
Q

What was the procedure by Pharoah et al. (2010) for research into family therapy

A
  • reviewed 53 studies published between 2002 and 2010 to investigate effectiveness of family intervention
  • studies chosen conducted in Europe, Asia and North America
  • studies compared outcomes from family therapy to drugs
  • researchers concentrated on studies that were randomised controlled trials
152
Q

What were the findings by Pharoah et al. (2010) into family therapy

A
  • mental state; overall impression was mixed, some studies reported improvement in overall mental state of patients compared to those receiving drugs, whereas others did not
  • compliance with medication; use of family therapy increased patients compliance with medication
  • social functioning; although appearing to show some improvement on general functioning, family intervention did not appear to have much of an effect on more concrete outcomes such as living independently or employment
  • reduction in relapse and readmission; reduction in risk of relapse and reduction in hospital admission during treatment and in the 24 months after
153
Q

What are positive evaluation points for family therapy as a treatment for schizophrenia

A
  • Pharoah et al. (2010)
  • economy
  • family
154
Q

How is Pharoah et al. (2010) a positive evaluation for family therapy

A
  • shows family therapy increases patient compliance with medication which can lead to improvements in their mental state and social functioning
  • suggests family therapy is effective as it teaches family members important of taking medication rather than other factors
  • does this mean that it is the medication or the family therapy that improves patient symptoms? Overall the evidence according to Pharoh’s study is mixed
155
Q

How is economy a positive evaluation for family therapy

A
  • economic benefits to family therapy
  • NICE receive of family therapy studies (NCCMH, 2009) demonstrated family therapy is associated with significant cost savings when offered to people with SZ than drugs
  • extra cost of family therapy offset by reduction in costs of hospitalisation because of lower relapse rates
  • also evidence family therapy reduces relapse rates for significant period after completion of intervention
  • means cost savings associated would be even higher
156
Q

How is family a positive evaluation for family therapy

A
  • impact of family therapy on family members is also advantageous
  • e.g. Lobban et al. (2013) analysed results of 50 family therapy studies that had included an intervention to support relatives
  • 60% of these studies reported a significant positive impact of the intervention on at least one outcome category for relatives
  • although the methodological quality of most of these 50 studies was poor, making it difficult to distinguish effective from ineffective interventions
157
Q

What is a negative evaluation point for family therapy

A
  • overall problem with lack of blinding in family therapy studies
  • e.g. in Pharoah’s study, 10 of 53 studies reported in meta analysis did not use any form of blinding
  • means raters were not blinded to the condition to which participant has been allocated
  • meant they knew whether participants were attached to experiment or control conditions
  • may create rater bias as raters know which conditions participants are in so may rate participants allocated to family therapy as showing improvements
  • problems as it does not show whether family therapy is really effective
158
Q

What are token economies

A
  • reward systems used to manage behaviour of patients with SZ in hospital settings
  • particularly those who developed maladaptive behaviours through spending too long in hospital with other patients who may show catatonia
  • under these circumstances, it is common for patients who are institutionalised to develop bad habits
  • changing bad habits does not cure SZ but improves patient’s quality of life and makes it more likely they can live outside a hospital setting
159
Q

How do token economies work

A
  • based on principles of operant conditioning
  • patient is given a token (reward) for carrying out a behaviour (positive reinforcement)
  • this should encourage them to repeat behaviour in hope for another token
  • tokens then accumulated and swapped for tangible reward
160
Q

How do tokens in a token economy work

A
  • tokens are given immediately to patients when they carry out a desirable behaviour that has been targeted for reinforcement
  • each individual patient will be assessed and given token for them showing certain behaviours
  • given immediately to allow for association to be built between positive behaviour and reward
161
Q

How do rewards in a token economy work

A
  • although tokens have no value in themselves, they can be swapped for more tangible rewards
  • tokens are secondary reinforcers as they only have value once patients has learned they can be used to obtain rewards
162
Q

What are positive evaluation points for token economies as treatment for SZ

A
  • research support, e.g. Dickerson et al. (2005)
  • reviewed 13 studies in use of token economies in treating SZ
  • 11 studies had reported beneficial effects, directly attributable to use of token economies
  • concluded that these studies provide evidence of the token economy’s effectiveness in increasing the adaptive behaviours of patients with SZ
  • however, Dickerson cautioned many studies had methodological issues which could affected impact of token economies
163
Q

What are negative evaluation points for token economies as treatment for SZ

A
  • ethics
  • ecological validity
  • effectiveness
164
Q

How is ethics a negative evaluation for token economies

A
  • ethical concerns for use of token economy programmes in psychiatric settings
  • e.g. in order to make reinforcement effective, clinicians may exercise control over important primary reinforcers such as food, privacy, or access to activities that stop patients being bored
  • patients may then exchange tokens if they display the target behaviour
  • however it is generally accepted all humans have certain basic rights that should not be violated, regardless of the positive consequences that could be achieved
165
Q

How is ecological validity a negative evaluation for token economies

A
  • although token economy programme has shown to be effective in reducing negative symptoms, it only has worked in a hospital setting
  • Corrigan (1991) argues there are problems administrating token economy with outpatients
  • in a hospital, patients receive 24h care and can be given tokens straight away
  • in the real world, who will give SZ patients tokens straight away and how will these be exchanged for a tangible item?
  • token economies thus lack ecological validity
166
Q

How is effectiveness a negative evaluation for token economies

A
  • there is no real conclusive evidence to whether token economies really work
  • e.g. there are very few randomised trials that have been carried out in token economy research
  • in an era where everything requires research support, token economy programmes are not used in the developed world but would be very prominent if randomised trials were used so there may be hope for this programme in treating SZ in the future especially in a hospital setting
  • critics argue token economies are only used in hospitals to manage and control symptoms rather than treat
167
Q

What is the interactive approach for SZ

A
  • interactionist approach (biosocial approach) is an approach acknowledging there are biological, psychological and societal factors in development of SZ
  • biological factors induce genetic vulnerability and neurochemical and neurological abnormality
  • psychological factors include stress resulting from life events and daily hassles, including poor quality interactions in the family
168
Q

What is the Diathesis Stress Model

A
  • model explaining the onset of SZ
  • diathesis means vulnerability; SZ has genetic component in terms of vulnerability
  • stress means a negative psychological experience
  • model states both a vulnerability to SZ and a stress trigger are necessary in order to develop the condition
  • one or more underlying factors make a person particularly vulnerable to developing SZ but the onset of the condition is triggered by stress
169
Q

What are the different models for the Diathesis Stress Model

A
  • Meehl’s (1962) Model
  • Read et al.’s (2001) Model
170
Q

What is Meehl’s (1962) Diathesis Stress Model

A
  • original diathesis stress model
  • diathesis was entirely genetic ad there was one specific gene ‘schizogene’
171
Q

Why was Meehl’s (1962) model changed

A
  • modern understanding of diathesis is clear that many genes increase genetic vulnerability and there is no single gene
  • modern views of diathesis include genes but also psychological trauma (Ingram and Luton, 2005) so traume becomes diathesis rather than the stressor
172
Q

What is Reed et al.’s (2001) Diathesis Stress Model

A
  • proposed a neurodevelopmental model in which early trauma affects brain development
  • in fact, early and severe enough trauma can seriously affect brain development
  • e.g. HPA systems can become overactive making the person more vulnerable to stress
173
Q

Why was Reed et al.’s (2001) model changed

A
  • modern understanding of stress as opposed to original understating is that it is anything that risks triggering SZ
  • e.g. cannabis use makes it 7x more likely got a person to develop SZ symptoms
  • this is because cannabis interferes with dopamine system, although most people do not develop SZ through cannabis use as most people do not take cannabis but will develop SZ, suggests there are other stressors which contribute to development of SZ
174
Q

What treatments would be used for SZ according to the interactionist model

A
  • acknowledges both biological and psychological factors in SZ
  • compatible with both biological and psychological treatments, in particular model is associated with combining antipsychotics and psychological therapies
  • in Britain, it is increasingly standard practise to treat patients with combination of drugs and CBT
  • it is unusual to treat SZ using psychological therapies alone
175
Q

What are positive evaluation points for the interactionist approach

A
  • Tienari et al. (2004)
  • Tarrier et al. (2004)
176
Q

How is Tienari et al. (2004) a positive evaluation for the interactionist approach

A
  • research support for dual role for genetic vulnerability to SZ and stress triggers
  • e.g. Tienari studies children adopted away from SZ mothers
  • adoptive patents’ parenting styles were assessed and compared with a control group of adoptees with no genetic risk
  • a child rearing style with high levels of criticism and conflict and low levels of empathy was implicated in the development of SZ but only for children with high genetic risk
  • shows strong direct support for interactionist approach; genetic vulnerability and family related stress combine in the development of SZ
177
Q

How is Tarrier et al. (2004) a positive evaluation for the interactionist approach

A
  • randomly allocated 315 patients to (1) medication and CBT group, (2) medication and supportive counselling group, or (3) control group
  • patients in two combination groups showed lower symptom levels than those in control (medication only)
  • no difference in hospital readmission
  • studies like this show clear practical advantage to adopting an interactionist approach in form of superior treatment outcomes
178
Q

What are negative evaluation points for the interactionist approach

A
  • Houston et al. (2008)
  • function
  • Turkington et al. (2006)
179
Q

How is Houston et al. (2004) a negative evaluation for the interactionist approach

A
  • original diathesis stress model is too simplistic
  • multiple genes increase vulnerability, each with small effect of its own
  • stress comes in many forms, including dysfunctional parenting
  • researchers now believe stress can also include biological factors
  • e.g. Houston found childhood sexual trauma was a diathesis and cannabis use a trigger
  • shows old idea of diathesis as biological and stress as psychological turned out to be overly simple
180
Q

How is function a negative evaluation for the interactionist approach

A
  • it is unknown exactly how diathesis stress works
  • strong evidence to suggest that some sort of underlying vulnerability coupled with stress can lead to SZ
  • but we don’t understand mechanisms by which symptoms of SZ appear and how both vulnerability and stress produce them
  • this does not undermine support for the approach but means we have an incomplete understanding of the actual medication
181
Q

How is Turkington et al. (2006) a negative evaluation for the interactionist approach

A
  • argue the fact that combined biological and psychological therapies are more effective than either on their own does not mean necessarily that the interactionist approach is correct
  • similarly, the fact that drugs help does not mean that SZ is biological in origin
  • this error of logic is called the treatment causation fallacy
  • means that the superior outcomes of combined therapies should not be over interpreted in terms of evidence in support of the interactionist approach
182
Q

Compare biological and psychological explanations for SZ

A
  • both have led to treatment
  • both are deterministic; biological and environmental determinism
  • both are reductionist; biological and environmental reductionism
  • role of family differs; biological implicate family passively through heritability whereas psychosocial see family as more actively responsible through their behaviour
  • societal attitudes; psychological blames family as cause whereas biological does not
  • neither establishes causality; in both cases the presumed cause might actually be a consequence, family might become dysfunctional as a result or altered neurochemistry/neuroanatomy might be effect

A Level Psychology (12 decks)

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