Schizophrenia Flashcards

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1
Q

Outline schizophrenia

A
  • severe mental disorder characterised by profound disruption of cognition and emotion
  • This affects a person’s language, thought, perception, emotions and even their sense of self
  • The schizophrenic believes things that cannot possibly be true (delusions) or hears voices or sees visions when there are no sensory stimuli to create them (hallucinations)
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2
Q

Describe the occurrence of schizophrenia

A
  • experienced by around 1% of the population
  • moat commonly diagnosed in men, people who love in cities, and people in lower socio-economic groups
  • symptoms often interfere so severely with every day life that many end up homeless or hospitalised
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3
Q

Briefly outline the mechanisms of diagnosis and classification

A
  • interlinked
  • in order to diagnose specific medical disorder, we need to distinguish one from another
  • we do this by identifying clusters of symptoms that occur together, and classifying this as one disorder
  • diagnosis is then possible by identifying symptoms and deciding what disorder a person has
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4
Q

Name the two locations of criteria used for the diagnosis of schizophrenia

A

1) The WHO’s International Classification of Disease (ICD 10/11)
2) The American Psychiatric Associations Diagnostic and statistical manual edition 5 (DSM V)

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5
Q

Describe the differences between the DSM and the ICD in the diagnosis of schizophrenia

A
  • In the DSM it is essential that the patient is experiencing at least one positive symptom to be diagnosed with schizophrenia- this is not the case in the ICD (where two or more negative symptoms would be enough)
  • The ICD also has subtypes of schizophrenia such as catatonic and paranoid- These were removed from the DSM V
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6
Q

Outline positive symptoms of schizophrenia, name 2

A

Positive symptoms are those that appear to reflect an excess or distortion of normal functions- additional experiences beyond ordinary existence
- hallucinations and delusions

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7
Q

Outline negative symptoms of schizophrenia, name 2

A
  • those that appear to reflect a reduction or loss of normal functions, which often persist even during periods of low (or absent) positive symptoms
  • About 1 in 3 schizophrenia patients suffer from significant negative symptoms
  • speed poverty and avolition
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8
Q

Describe hallucinations

A
  • unusual sensory experiences
  • some related to events in the environment whereas others are not connected sensory stimuli
  • e.g. voices heard talking to or commenting on person, often criticising them
  • can be experienced in relation to any sense
  • e.g. may see distorted facial expressions or people/animals that aren’t really there
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9
Q

Describe delusions

A
  • also known as paranoia
  • irrational beliefs
    -e.g. being important historical/religious figure
  • also commonly involve being persecuted, perhaps by government
  • also may involve body e.g. perceiving they are under external control
  • can make one behave in way that makes sense to them but seems bizarre to others
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10
Q

Describe speech poverty

A
  • changes in patterns of speech- emphasis on reduction in amount and quality of speech in schizophrenia
  • sometimes accompanied by delay in persons verbal responses during conversation
  • modernly, more emphasis placed on speech disorganisation- speech becomes incoherent or speaker changes topic mid-sentence- this is classified in DSM as positive symptom but speech poverty is negative symptom
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11
Q

Describe avolition

A
  • AKA apathy- finding it hard to begin or keep with goal-directed activity
  • often have sharply reduced motivation to carry out range of activities
  • Andreasen (1982)- 3 signs of avolition- poor hygiene/grooming, each of persistence in work/education, lack of energy
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12
Q

Describe specific elements of the DSM V diagnosis of schizophrenia

A
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13
Q

Outline what is meant by reliability in diagnosis of schizophrenia

A
  • Diagnostic reliability means that a diagnosis of schizophrenia must be repeatable i.e. clinicians must be able to reach the same conclusions at 2 different points in time (test-retest reliability) or different clinicians must reach the same conclusions (inter-rater reliability)
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14
Q

Describe how schizophrenia diagnostic reliability can be assessed

A
  • Inter-rater reliability is measured by a statistic called a kappa score
  • A score of 1 indicates perfect inter-rater agreement; a score of 0 indicates zero agreement
  • A kappa score of 0.7 or above is generally considered good
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15
Q

Describe the kappa score of schizophrenia that suggests poor reliability

A

Regier et al (2013)- In the DSM-V field trials
the diagnosis of schizophrenia had a kappa score of only 0.46- suggests low reliability

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16
Q

Describe a study of the diagnostic reliability of schizophrenia that suggests good reliability

A

Osorio et al (2019):
- 180 individuals using DSM V
- Pairs of interviewers achieved inter-rater reliability of +0.97 and test-retest reliability of +0.92

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17
Q

Name a challenge to the reliability of schizophrenia diagnosis

A

Cultural differences in diagnosis

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18
Q

Describe cultural differences in the diagnosis of schizophrenia

A
  • Research suggests there is a significant variation between countries when it comes to diagnosing schizophrenia i.e. culture has an influence on the diagnostic process
  • One of the main characteristics of schizophrenia, ‘hearing voices,’ also appears to be influenced by cultural environment- e.g. in Haiti some believe that voices are communications from ancestors
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19
Q

name studies surrounding cultural differences in the diagnosis of schizophrenia

A
  • Different cultures of psychiatrist- Copeland (1971)
  • Differences in symptoms- Luhrman et al (2015)
  • Misrepresentation of symptoms in people with different heritages- Pinto and Jones (2008), Escobar (2012)
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20
Q

Describe Copeland’s study into cultural differences in the diagnosis of schizophrenia

A
  • gave 134 US and 194 British psychiatrists a description of a patient
  • 69% of the US psychiatrists diagnosed schizophrenia, but only 2% of the British ones gave the same diagnosis
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21
Q

Describe Luhrman’s study into cultural differences in the diagnosis of schizophrenia

A
  • interviewed 60 adults diagnosed with schizophrenia, 20 each in Ghana, India and the US
  • Each was asked about the voices they heard
  • while many of the African and Indian subjects reported positive experiences with their voices, describing them as playful or offering advice, not one American did
  • Rather the US subjects were more likely to report the voices they heard as violent and hateful – and indicative of being ‘sick
  • Luhrman suggests that the ‘harsh, violent voices so common in the West may not be an inevitable feature of schizophrenia’
  • This suggests that schizophrenia has a lack of consistent characteristics.
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22
Q

Describe Pinto and Jones’ /Escobar’s study into cultural differences in the diagnosis of schizophrenia

A
  • British people of African-caribean origin are up to 9 times more likely to receive diagnosis as white British people, but people living in African-Caribean countries are not (ruling out genetic vulnerability
  • suggests cultural bias in psychiatrists from different cultural background that leads to an overinterpreatation of symptoms in black Brostish people (Escobar, 2012)
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23
Q

Describe expectations vs reality of schizophrenia diagnosis

A

It was originally hoped that the use of diagnostic tools (DMS and ICD) could provide a standardised method of recognising mental disorders. However, the behaviour of an individual is always open to some interpretation. The process is actually more subjective than we hoped. The most famous study testing the subjectivity, reliability and validity of diagnostic tools was Rosenhan et al (1972).

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24
Q

Weaknesses of reliability in schizophrenia diagnosis

A

Lack of inter-rater reliability:
- Whaley (2001)- found inter-rater reliability correlations in the diagnosis of schizophrenia as low as 0.11
- Further problems with the inter-rater reliability of the diagnosis of schizophrenia are illustrated in the Rosenhan study

Unreliable symptoms:
- For a diagnosis of schizophrenia only one of the characteristic symptoms is required ‘if delusions are bizarre.
- However, this creates problems for reliability of diagnosis
- Mojtabi and Nicholson- When 50 senior psychiatrists in the US were asked to differentiate ‘bizarre’ and ‘non bizarre’ delusions, they produced inter-rater reliability correlations of only around .40
- even this central diagnostic requirement lacks sufficient reliability for it to be a reliable method of distinguishing between schizophrenia and non-schizophrenic patients

Cultural differences in prognoses:
- The prognosis for members of ethnic minority groups may actually be more positive than the majority group members
- The ethnic culture hypothesis predicts that ethnic minority groups experience less distress associated with mental disorders because of the protective characteristics and social structures that exist in most ethnic minority cultures
- Brekke and Barrio (1997)- found evidence to support this hypothesis in a study of 184 individuals with schizophrenia or a schizophrenia-spectrum disorder
- The sample was drawn from two non-white minority groups (African-Americans and Latinos) and a majority group (white Americans)
- They found that the white Americans were more symptomatic than members of the other 2 groups, findings which support the ethnic culture hypothesis

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25
Q

Outline what is meant by validity in diagnosis of schizophrenia

A
  • the extent to which something is measuring what it sets out to measure
  • The extent to which he diagnosis an accurate reflection of the disorder and is the diagnosis distinct from other disorders
  • Criterion validity- whether different assessment tools arrive at the same diagnosis for the same patient
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26
Q

Outline gender bias In diagnosis of schizophrenia

A
  • said to occur when accuracy of diagnosis is dependent on the gender of an individual
  • The accuracy of diagnostic judgements can vary for a number of reasons, including gender biased diagnostic criteria or clinicians basing their judgements on stereotypical beliefs held about gender
  • e.g. critics of the DSM diagnostic criteria
    argue that some diagnostic categories are biased toward pathologising one gender rather than the other
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27
Q

Name studies into gender bias in schizophrenia diagnosis

A
  • Longnecker et al- meta analysis
  • Cotton et al- predisposing factors
  • Fisher and Buchanan- ratio of diagnosis
  • Loring and Powell-
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28
Q

Describe Longnecker’s study into gender differences in the diagnosis of schizophrenia

A
  • reviewed studies of the prevalence of schizophrenia
  • found that, since the 1980s, men have been diagnosed with schizophrenia more often than women (prior to this there seems to be no differences)
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29
Q

Describe Cotton’s conclusions about gender bias in the diagnosis of schizophrenia

A
  • Argued female patients typically function better than men, and are more likely too have good family relationships- could explain why some women have not been diagnosed with schizophrenia whereas men with similar symptoms may have been; their better interpersonal functioning may bias practitioners to under-diagnose schizophrenia, either because symptoms are masked by good interpersonal functioning, or because the quality of interpersonal functioning makes the case seem too mild to warrant a diagnosis
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30
Q

Describe Fisher and Buchanans study into validity of schizophrenia diagnosis

A
  • found that since the 19880s, men have been diagnosed with schizophrenia more commonly than women (ratio of 1:4.1)
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31
Q

Describe Loring and Powell’s study into validity of schizophrenia diagnosis

A
  • selected 290 male and female psychiatrists to read cases studies of patients’ behaviour and make a judgement on these people using standardised diagnostic criteria (e.g. DSM)
  • When the patients were described as ‘male’ or no info about gender was given, 56% of psychiatrists have a schizophrenia diagnosis
  • When patients were described as ‘female’, only 20% were given a diagnosis of schizophrenia
  • the gender bias was not as evident among the female psychiatrists, suggesting that diagnosis is influenced not only by gender of the patient but also the gender of the clinician
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32
Q

Describe co-morbidity in relation to diagnosis of schizophrenia

A
  • refers to the extent that 2 or more conditions can occur at the same time
  • Psychiatric co-morbidities are common among patients with schizophrenia
  • These include substance abuse, anxiety and symptoms of depression
  • questions validity as if conditions occur together a lot of the time, it may actually be a single condition
  • It poses a challenge for the diagnosis of schizophrenia
  • If half the schizophrenia patients are also diagnosed with depression then maybe we are just quite bad at telling the difference between the 2 conditions. In terms of classification, it may be that, if very severe depression looks a lot like schizophrenia
    and vice versa, then they might be seen as a single condition
  • This confusing picture is a weakness of diagnosis and classification
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33
Q

Name studies Ito co-morbidity in schizophrenia diagnosis

A
  • Buckley et al (2009)
  • Swets et al (2014)
  • Weber et al (2009)
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34
Q

Describe Buckley et al’s research into co-morbidity

A
  • estimated that co-morbid depression occurs in 50% of patients, and 47% of patients also have a lifetime diagnosis of co-morbid substance abuse
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35
Q

name a condition with which schizophrenia is commonly co-morbid with

A

OCD

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36
Q

Describe the link between OCD and schizophrenia

A
  • 2 distinct psychiatric conditions
    Roughly 1% of the population develop schizophrenia, and roughly 2-3% develop OCD
  • Since both are fairly uncommon, we would expect that only a few people with schizophrenia would develop OCD and vice versa, however, evidence suggests that the 2 conditions appear together more often than chance would suggest
  • A meta-analysis by Swets et al (2014) found that at least 12% of patients with schizophrenia also fulfilled the diagnostic criteria for OCD and about 25% displayed significant obsessive-compulsive symptoms.
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37
Q

Describe the consequences of co-morbidity for patients with schizophrenia

A
  • A number of studies have examined single co- morbidities with schizophrenia, but these studies have usually involved very small sample sizes
  • By contrast, a US study (Weber et al 2009) looked at nearly 6 million hospital discharge records to calculate co-morbidity rates
  • Not only did they find co-morbidity of other psychiatric disorders with schizophrenia (45%), they also found evidence of co-morbid non-psychiatric disorders such as asthma, hypertension and type 2 diabetes
  • concluded that the very nature of a diagnosis of a psychiatric disorder is that they tend to receive a lower standard of medical care, which in turn adversely affects the prognosis of patients with schizophrenia
    HOWEVER, may also be that schizophrenia prevents from working, meaning they may not have medical insurance
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38
Q

Describe symptom overlap in schizophrenia diagnosis

A
  • Despite the claim that the classification of positive and negative symptoms would make for more valid diagnoses of schizophrenia, many of these symptoms are also found in other disorders, such as depression and bipolar disorder
  • e.g. bipolar- may share positive symptoms (delusions) and negative symptoms (avolition)
  • For example, Ellason & Ross (1995) point out that people with dissociative identity disorder (DID) actually have more schizophrenic symptoms than people diagnosed as being schizophrenic
  • Most people diagnosed with schizophrenia have sufficient symptoms of other disorders that they could also receive at least one other diagnosis (Read, 2004)
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39
Q

Describe a further issue with validity of diagnosis of schizophrenia

A

Differences in prognosis:
- In the same way that people diagnosed as schizophrenic rarely share the same symptoms, likewise there’s no evidence that they share the same outcomes
- The prognosis for schizophrenia varies with about 20% recovering their previous level of functioning, 30% showing some improvement with intermittent relapses and 10% achieving significant and lasting improvement
- A diagnosis of schizophrenia has little predictive validity – some people never recover from the disorder
- If each person has such different outcomes after treatment, how can we be sure schizophrenia is actually what they have?

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40
Q

Name the 3 main sources of evidence for the genetic basis of schizophrenia

A
  • family studies
  • twin studies
  • adoption studies
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41
Q

Outline family studies as evidence for the genetic basis of schizophrenia

A
  • These show that there is a tendency for schizophrenia to run in families, therefore it may be being passed from one generation to the next through the action of genetics
  • First-degree relatives share an average of 50% of their genes, and second-degree relatives share approximately 25% of their genes
  • If schizophrenia is genetically inherited, we would expect that people who share genes, share the disorder
  • ## There is now a considerable body of evidence that suggests the closer the genetic relationship to someone with schizophrenia, the greater the risk of developing schizophrenia
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42
Q

Describe a family study of schizophrenia

A

GOTTESMAN (1991):
- found someone with aunt with schizophrenia has 2% chance of developing
- 9% if sibling
- family members also share aspects of environment, so correlation represents both genes and environment

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43
Q

Outline twin studies as evidence for the genetic basis of schizophrenia

A
  • If monozygotic (MZ – genetically identical) twins are more concordant than dizygotic (DZ – who share only 50% of their genes), then this suggests that the greater similarity is due to genetic factors
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44
Q

Describe 2 twin studies into the genetic basis of Schizophrenia

A

Joseph (2004):
- calculated that the pooled data for all schizophrenia twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4%, and 7.4% for DZ twins
- More recent, methodologically sound studies (e.g. those using ‘blind’ diagnoses where the researchers assessing don’t know whether the twins are MZ or DZ) have tended to report a lower concordance rate for MZ twins than earlier studies
- Despite this, however, such studies still support the genetic position because they show a concordance rate for MZ twins that is many times higher than for DZ twins

Gottesman (1991):
- summarised 40 studies that included considerable differences in the severity of the symptoms of schizophrenia
- The concordance rate was 48% when a monozygotic twin had schizophrenia, but only 17% when a dyzygotic twin had schizophrenia
- These findings strongly suggest that genetic factors are important – the reason why mz’s have a much higher concordance rate than dz’s is because they are much more similar genetically
- also reported that the concordance rate for mz twins brought up apart was similar to those brought up together
- This suggests that the high concordance rate for identical twins is not due to them being treated in a very similar way within the family

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45
Q

Describe adoption studies as evidence for the genetic basis of schizophrenia

A
  • Adoption studies provide the most unequivocal test of genetic influence, because they allow the clearest separation of genetic and environmental factors
  • These look at the incidence of schizophrenia when a child is born to parents of whom one or both are schizophrenic, and are adopted early in life into a ‘normal’ family
  • If schizophrenia is biological, we would expect a higher rate of the disorder compared to those who are adopted where their biological parents do not have schizophrenia
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46
Q

Describe an adoption study into the genetic basis of schizophrenia

A

Tienari et al (2000):
- in Finland
- Of the 164 adoptees whose biological mothers had been diagnosed with schizophrenia, 11 (6.7%) also received a diagnosis of schizophrenia, compared to just four (2%) of the 197 control adoptees (born to non- schizophrenic mothers
- The investigators concluded that these findings showed that the genetic liability to schizophrenia had been ‘decisively confirmed’

47
Q

Describe candidate genes involved with schizophrenia

A
  • schizophrenia is polygenic
  • Most likely genes would be those coding for neurotransmitters including dopamine
  • Ripke et al (2014)- combined data from all previous genome-wide studies
  • genetic make up of 37000 people with a diagnosis of schizophrenia was compared to 113000 controls
  • 108 separate genetic variations were associated with slightly increased risk of schizophrenia
  • as different studies have identified different candidate genes, it appears that schizophrenia is etiologically heterogenous (meaning differed combinations of factors, including genetic variation, can lead to the condition
48
Q

Describe the role of mutation in the genetic basis of schizophrenia

A
  • schizophrenia can also have genetic origin in the absence of a family history
  • one explanation is mutation in parental DNA which can be caused by radiation, poison, or viral infection
  • evidence for mutation comes from positive correlations between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia
  • Broen et al (2002)- increases from 0.7% with fathers under 25, to over 2% in fathers over 50
49
Q

Strengths of the genetic basis of schizophrenia

A

Research evidence:
- support from family and twin studies (Gottesman, Joseph)
- support from adoption studies (Tienari)

Specific genes:
- Genetic research may be useful in trying to identify a specific gene or genes that might be responsible for schizophrenia
- e.g. Sherrington (1988) has linked schizophrenia to an abnormality on chromosome 5, although these findings have not been replicated by others
- However, a recent study by Hong et al (2001) found that a variation in the TPH gene was significantly more common in Chinese patients with schizophrenia than in Chinese controls

Genetic counselling:
- if one or more potential parents have a relative with schizophrenia, they risk having a child that would go on to develop the condition
- HOWEVER only estimate- not actual probability as environmental factors involved

50
Q

Weaknesses of the genetic basis of schizophrenia

A

Issues with family studies:
- family members also share same environment
- therefore, any patterns could be environment not genetics

Issues with twin studies:
- MZ twins may be treated more similarly than DZ twins
- also more similar conditions in the womb as share same placenta

Issues with adoption studies:
- issues with this evidence such as of adopted children in relation to the population
- Clearly, not all mothers with schizophrenia have their children adopted
- It is thus possible that there was something different about these particular mothers or their babies that led to the adoptions and also contributed to the development of schizophrenia

  • aslo, a central assumption of adoption studies is that adoptees are not ‘selectively placed’ i.e. adoptive parents who adopt children with a schizophrenic biological parent are no different to adoptive parents who adopt children whose background is normal
  • Joseph (2004) claims that this is unlikely to have been the case, particularly in early studies
  • In countries like Denmark and the US, potential adoptive parents would have been informed of the genetic background of children prior to selection for adoption
  • As Kringlen (1987; cited in Jospeh 2004) points out, ‘Because the adoptive parents evidently received information about the child’s biological parents, one might wonder who would adopt such a child.’

Reductionism:
- By focusing on genetics, one can be criticised for adopting a reductionist approach
- This is when we try and explain an aspect of human behaviour by only looking at one single factor, in this case genes
- Perhaps it is better to utilize the diathesis-stress model which states that when considering why certain people develop schizophrenia, it is important that we not only consider their biological vulnerability to a disorder (diathesis) but we must also consider environmental factors or stressors
- Therefore, if a person is biologically predisposed to develop schizophrenia because of genetic factors, they may well not develop the disorder if they have a ‘good’ environment
- may also be biological risk factors e.g. birth complications (Morgan et al, 2017) and smoking THC-ric cannabis in teenage years (Di Forte et al, 2015), psychological risk factors e.g. childhood trauma (Morkved et al, 2017- found that 67% of people with schizophrenia and related psychotic disorders reported at least 1 childhood trauma, as opposed to 38% of a matched group with non-psychoticmental health issues )

51
Q

Describe the dopamine hypothesis

A
  • The dopamine hypothesis suggests that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of schizophrenia
  • Messages from neutrons that transmit dopamine fire too easily or too often, leading to hallucinations and delusions that are the characteristic positive symptoms of schizophrenia
  • Schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing
52
Q

Name two sources of evidence for the dopaminee hypothesis

A
  • Drugs that increase dopaminergic activity
  • Drugs that decrease dopaminergic activity
53
Q

Describe drugs that increase dopaminergic activity as evidence for the dopamine hypothesis

A
  • Amphetamine is a dopamine agonist i.e. it stimulates nerve cells containing dopamine, causing the synapse to be flooded with this neurotransmitter
  • ‘Normal’ individuals who are exposed to large doses of dopamine-releasing drugs such as amphetamines can develop the characteristic hallucinations and delusions of a schizophrenic episode
  • Done by Curran et al (2004)
  • This generally disappears with abstinence from the
    drug
  • Likewise, some people who suffer Parkinson’s disease, a neurodegenerative disease categorised by low levels of dopamine, who take the drug L-Dopa top raise their dopamine levels have been found to develop schizophrenia type symptoms (Grilly, 2002).
54
Q

Describe drugs that decrease dopaminergic activity as evidence for the dopamine hypothesis

A
  • Antipsychotics- by reducing the activity in neural pathways of the brain that use dopamine as the neurotransmitter, these drugs eliminate symptoms such as hallucinations and delusions
  • The fact that these drugs (known as dopamine antagonists because they block its action) alleviated many of the symptoms of schizophrenia strengthened the case for the important role of dopamine in this disorder
  • Done by Tauscher et al (2014)
55
Q

Describe the revised dopamine hypothesis

A
  • Davis and Kahn (1991) proposed that the positive symptoms of schizophrenia are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway
  • The negative and cognitive symptoms of schizophrenia are thought to arise from a deficit of dopamine in areas of the prefrontal cortex (the mesocortical pathway)
56
Q

Describe evidence for the revised dopamine hypothesis

A

Neural imaging:
- Patel et al (2010), using PET scans to assess dopamine levels in schizophrenic and normal individuals, found lower levels of dopamine in the dorsolateral prefrontal cortex of schizophrenic patients compared to their normal controls

57
Q

Strengths of the dopamine hypothesis

A

Drug evidence:
- Tenn et al (2003- induced schizophrenia-like symptoms in rats using amphetamines and then relieved symptoms using drugs that reduce DA action
BUT- other drugs that also increase DA levels (e.g. apomorphine) do not cause schizophrenia-like symptoms (DePatie and Lal, 2001). Garson (2017) challenged idea that amphetamine psychosis closes mimics schizophrenia

Post mortem and PET scans:
- These have revealed a specific increase of dopamine in the left amygdala (Falkai et al. 1988) and Increased dopamine receptor density in the caudate nucleus putamen (Owen et al 1978)
BUT- cause and effect- not clear whether these increases are a cause or a result of Sz- since anti-psychotic drugs act on dopamine levels in the brain, it is not surprising that dopamine is abnormal in schizophenics.

58
Q

Weaknesses of the dopamine hypothesis

A

Positive vs negative symptoms:
- drugs alleviate the positive symptoms, but are less effective with the negative symptoms
- also, 1/3 with Sz don’t respond to drugs at all- suggests there may be other causes for symptoms

Clozapine:
- One of the most effective drugs in treating Sz is clozapine
- This drug has a major effect on the serotonin system rather than the dopamine system, suggesting that other neurotransmitters could also play a role in Sz

Glutamate:
- evidence for central role of glutamate
- post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia (McCutheon et al, 2020)
- further, several candidate genes for schizophrenia are believed too be involved with glutamate production or processing
- means equally strong case can be made for importance of other neurotransmitters

Inconclusive evidence:
- Moncrieff (2009) claims that evidence for the dopamine hypothesis of schizophrenia is far from conclusive
- E.g. although stimulant drugs such as cocaine and amphetamine have been shown to induce schizophrenic episodes, such stimulants are known to affect many neurotransmitters other than dopamine
- Likewise, evidence for dopamine concentrations in post-mortem brain tissue has either been negative or inconclusive
- also points out that other confounding sources of dopamine release, such as stress or smoking, have rarely been considered
- Therefore, she suggests, the idea that the symptoms of Sz are caused by the over-activity of the dopaminergic system is not supported by current evidence

Noll (2009):
- claims there is strong evidence against both the original dopamine hypothesis and the revised dopamine hypothesis
- argues that antipsychotic drugs do not alleviate hallucinations and delusions in about one-third of people experiencing these problems
- also points out that, in some people, hallucinations and delusions are present even though dopamine levels are normal - Blocking the D2 receptors of these people has little or no effect on their symptoms
- This suggests that, rather than dopamine being the sole cause of positive symptoms, other neurotransmitter systems may also produce the positive symptoms associated with sz

59
Q

Outline neural correlates

A
  • This is when we assess the areas of the brain that are active whenever something is happening
  • Both positive and negative symptoms of SZ have neural correlates
  • This means that there is unusual levels of activity (either higher or lower than average) in certain areas of the brain when a person experiences each symptom of schizophrenia
  • Neural correlates are identified using brain scans such as fMRI scans e.g. if we had a group of patients who all experienced auditory hallucinations we could look at which areas of the brain were/ were not active compared to the brain of people who don’t experience any auditory hallucinations- if an area was different, we could reasonable conclude that this area of the brain plays a role in that symptom.
60
Q

name examples of neural correlates of schizophrenia

A
  • The ventral Striatum is a neural correlate for the negative symptoms of schizophrenia
  • The superior temporal gyrus and the anterior cingulate gyrus are neural correlates of schizophrenia- specifically for auditory hallucinations
61
Q

Strengths of neural correlates of schizophrenia

A

Research support 1:
- Juckel et al (2006)
- compared the activity levels in this brain area for SZ patients and controls
- SZ patients had significantly lower activity in this area of the brain
- There was also a negative correlation between activity in the ventral striatum and severity of negative symptoms such as avolition
- Therefore activity in the ventral striatum is a neural correlate of negative symptoms of Sz

research support 2:
- Allen et al (2007) compared the brain scans of schizophrenic patients suffering from auditory hallucination and a control group
- In the schizophrenic group there was lower activity in both the superior temporal gyrus and the anterior cingulate gyrus
- Therefore reduced activity in the superior temporal gyrus and the anterior cingulate gyrus is a neural correlate of auditory hallucination

62
Q

Weakness of neural correlates of schizophrenia

A

Correlational:
- Much of the research is correlational- this is problematic
- cannot say that lower activity in one area of the brain causes a symptom, it could be that the symptom causes lower activity
- could be a third factor that causes the relationship between activity in the ventral striatum and severity of negative symptoms- e.g. what if dopamine levels were causing lower activity in certain areas of the brain and this in turn lead to the symptoms?

63
Q

Name psychological explanations of schizophrenia

A

Family dysfunction- schizophrenogenic mother, double-bind, expressed emotion

Cognitive- dysfunctional thinking, meta-representation, central control

64
Q

Describe the The schizophrenogenic mother theory

A
  • Fromm-Reichmann
  • theory that the schizophrenogenic mother (literally meaning ‘schizophrenia-causing) caused an individual to develop schizophrenia
  • cold, dominant, moralistic, controlling and rejecting
  • This theory was an addition to the psychodynamic explanation of schizophrenia which suggested that schizophrenia is a result of internal conflict between the different parts of the Psyche
  • This type of mother leads to a family climate characterised by secrecy and tension
  • This leads to distrust and later paranoid delusions and ultimately schizophrenia
65
Q

Describe the double-bind theory

A
  • Bateson et al (1956)
  • suggests that children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia
  • e.g. if a mother tells her son that she loves him, yet at the same time turns her head away in disgust, the child receives two conflicting messages about their relationship on different communicative levels, one of affection on the verbal level and one of animosity on the non-verbal level
  • The developing child regularly finds themselves trapped in situations where they fear doing the wrong thing, but receive mixed messages about what this is, and also feel unable to comment on the unfairness of the situation or seek clarification
  • When they ‘get it wrong’ (which is often) the child is punished by withdrawal of love
  • This leaves them with an understanding of the world that is confusing and dangerous, and this is reflected in their symptoms like disorganised thinking and paranoid delusions
  • Bateson was clear that this was neither the main type of communication in the family of schizophrenia-sufferers nor the only factor in developing it, just a risk factor
66
Q

Outline the expressed emotion theory

A
  • primarily an explanation for relapse in patients with schizophrenia, although it’s been suggested that it may be a source of stress that can trigger the onset of schizophrenia who is already vulnerable
  • This family variable associated with schizophrenia is a negative emotional
    climate, or more generally, a high degree of expressed emotion (EE)
  • EE is a family communication style in which members of a family of a psychiatric patient talk about the patient in a critical or hostile manner or in a way that indicates emotional over-involvement or over-concern with the patient or their behaviour
  • research by Kuipers et al (1983) found that high EE relatives talk more and listen less
  • A patient returning to a family with high EE is about 4 times more likely to relapse that a patient whose family is low in EE (Linszen et al 1997)
  • This suggests that people with schizophrenia have a lower tolerance for intense environmental stimuli, particularly intense emotional comments and interactions with family members- appears that the negative emotional climate in these families arouses the patient and leads to stress beyond his or her already impaired coping mechanisms, thus triggering a schizophrenic episode
  • In contrast, a family environment that is relatively supportive and emotionally undemanding may help the person with schizophrenia to reduce their dependence on antipsychotic drugs and help reduce the likelihood of relapse (Noll, 2009)
67
Q

name elements of expressed emotion

A
  • Verbal criticism of the patient, occasionally accompanied by violence
  • Hostility towards the patient, including anger and rejection
  • Emotional over-involvement in the life of the patient
68
Q

Strengths of family dysfunction explanations

A

Support for family relationships:
- importance of family relationships in the development of schizophrenia can be seen in an adoption study by Tienari et al (1994)
- those adopted children who had schizophrenic biological parents were more likely to become ill themselves than those children with non-biological parents
- However, the difference only emerged in situations where the adopted family was rated as disturbed
- In other words, the illness only manifested itself under appropriate environmental conditions- genetic vulnerability alone was not sufficient

Support for family dysfunction:
- other evidence to suggest that difficult family relationships in childhood are associated with increased risk of schizophrenia in adulthood
- Read et al (2005) reviewed 46 studies of child abuse and schizophrenia and found concluded that 69% of adult women in-patients with a diagnosis of schizophrenia had a history of physical abuse, sexual abuse or both in childhood
- 59% for men
- Morkved et al (2017)- most adults with schizophrenia had at least 1 childhood trauma, mostly abuse
- Adults with insecure attachments to their primary carer are also more likely to have schizophrenia (Berry et al, 2008)

Support for double bind:
- Berger (1965) found that schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics. BUT- this evidence may not be reliable as patients’ recall may be affected by their schizophrenia. Other studies are not so supportive- Liem (1974) measured patterns of parental communication in families with a schizophrenic child and found no difference when compared to normal families

69
Q

Weaknesses of family dysfunction explanations

A

Weak evidence for family based explanations:
- Although there’s plenty of evidence supporting the broad principle that poor childhood experiences in the family are associated with adult schizophrenia, there is almost none to support the importance of double bind
- Double bind is based on clinical observation of the patients, and early evidence involved assessing the personality of the mothers for ‘crazy-making characteristics’ - an approach that makes modern psychiatrists wince
- schizophrenogenic mother and double bid based ion informal assessment of mothers personalities, rather than systematic evidence

Social sensitivity:
- this theory is that it’s led to parent-blaming
- Parents who have already suffered at seeing their child’s descent into schizophrenia and who are likely to bear life-long responsibility for their care underwent further trauma by receiving blame for the condition

70
Q

Describe dysfunctional thinking as an explanation of schizophrenia

A
  • schizophrenia characterised by dysfunction to normal thought processing
  • specific neural correlates suggest that cognition is involved
    Frith et al (1992) identified 2 kinds of dysfunctional thought processing that could underlie some symptoms: metarepresentation, central control
71
Q

Describe meta-representation

A
  • the cognitive ability to reflect on thoughts and behaviour
  • This allows us insight into our own intentions and goals
  • also allows us to interpret the actions of others
  • Dysfunction in metarepresentation would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else
    -This would explain hallucinations of voices and delusions like thought insertion (the experience of having thoughts projected into the mind by others)
72
Q

Describe central control

A
  • the cognitive ability to suppress automatic responses while we perform deliberate actions instead
  • Disorganised speech and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts
  • e.g. sufferers with schizophrenia tend to experience derailment of thoughts and spoken sentences because each word triggers associations and the patient cannot suppress automatic responses to these
73
Q

Strengths of cognitive explanations of schizophrenia

A

Supporting evidence:
- Sarin and Wallin (2014) reviewed recent research evidence relating to the cognitive model of schizophrenia
- found supporting evidence for the claim that the positive symptoms have their origins in faulty cognition
- e.g. delusional patients were found to show various biases in their information processing, such as jumping to conclusions and lack of reality testing
- Likewise, schizophrenic individuals with hallucinations were found to have impaired self-monitoring and also tended to experience their own thoughts as voices
- In addition, they found that patients with negative symptoms also displayed dysfunctional thought processes such as having low expectations regarding pleasure and success

Other research evidence:
- Stirling et al (2006) compared performance on a range of cognitive tasks in 30 people with schizophrenia and 30 people without
- included the troop test
- people with schizophrenia took longer- double on average- central control theory

Success of cognitive therapies:
- The claim that the symptoms of schizophrenia have their origin in faulty cognition is reinforced by the success of cognitive-based therapies
- In cognitive- behavioural therapy for psychosis (CBTp), patients are encouraged to evaluate the content of their delusions or of any voices, and to consider ways they might test the validity of their faulty beliefs
- The effectiveness of this approach was demonstrated in the NICE review of treatments for schizophrenia (NICE, 2014). This review found consistent evidence that, when compared with antipsychotic drugs, CBT was more effective in reducing symptom severity and improving levels of social functioning

74
Q

Weaknesses of cognitive explanations of schizophrenia

A

Integrated model:
- A problem with any psychological model of schizophrenia is that it deals adequately with one aspect of the disorder (e.g. cognitive impairment) but fails to explain, or ignores, another aspect (e.g. neurochemical changes).
- Howes and Murray (2014) addressed this problem with an integrated model of schizophrenia- argue that early vulnerability factors (e.g. genes/birth complications etc) together with exposure to significant social stressors, sensitises the dopamine system, causing it to increase the release of dopamine
- Increased dopamine activity results in paranoia and hallucinations, and eventually the development of psychosis- this contributes to the stress experienced by the individual, leading to more dopamine release, more symptoms and so on

Proximal explanation:
- only explain proximal origins of symptoms
- only explain what is happening now to produce symptoms- not a distal explanation (focus on initial cause)- possible distal are family dysfunction and genetics
- currently unclear how genetic variation or childhood trauma may lead to problems with meta-representation or central control

74
Q

Weaknesses of cognitive explanations of schizophrenia

A

Integrated model:
- A problem with any psychological model of schizophrenia is that it deals adequately with one aspect of the disorder (e.g. cognitive impairment) but fails to explain, or ignores, another aspect (e.g. neurochemical changes).
- Howes and Murray (2014) addressed this problem with an integrated model of schizophrenia- argue that early vulnerability factors (e.g. genes/birth complications etc) together with exposure to significant social stressors, sensitises the dopamine system, causing it to increase the release of dopamine
- Increased dopamine activity results in paranoia and hallucinations, and eventually the development of psychosis- this contributes to the stress experienced by the individual, leading to more dopamine release, more symptoms and so on

Proximal explanation:
- only explain proximal origins of symptoms
- only explain what is happening now to produce symptoms- not a distal explanation (focus on initial cause)- possible distal are family dysfunction and genetics
- currently unclear how genetic variation or childhood trauma may lead to problems with meta-representation or central control

74
Q

Weaknesses of cognitive explanations of schizophrenia

A

Integrated model:
- A problem with any psychological model of schizophrenia is that it deals adequately with one aspect of the disorder (e.g. cognitive impairment) but fails to explain, or ignores, another aspect (e.g. neurochemical changes).
- Howes and Murray (2014) addressed this problem with an integrated model of schizophrenia- argue that early vulnerability factors (e.g. genes/birth complications etc) together with exposure to significant social stressors, sensitises the dopamine system, causing it to increase the release of dopamine
- Increased dopamine activity results in paranoia and hallucinations, and eventually the development of psychosis- this contributes to the stress experienced by the individual, leading to more dopamine release, more symptoms and so on

Proximal explanation:
- only explain proximal origins of symptoms
- only explain what is happening now to produce symptoms- not a distal explanation (focus on initial cause)- possible distal are family dysfunction and genetics
- currently unclear how genetic variation or childhood trauma may lead to problems with meta-representation or central control

74
Q

Weaknesses of cognitive explanations of schizophrenia

A

Integrated model:
- A problem with any psychological model of schizophrenia is that it deals adequately with one aspect of the disorder (e.g. cognitive impairment) but fails to explain, or ignores, another aspect (e.g. neurochemical changes).
- Howes and Murray (2014) addressed this problem with an integrated model of schizophrenia- argue that early vulnerability factors (e.g. genes/birth complications etc) together with exposure to significant social stressors, sensitises the dopamine system, causing it to increase the release of dopamine
- Increased dopamine activity results in paranoia and hallucinations, and eventually the development of psychosis- this contributes to the stress experienced by the individual, leading to more dopamine release, more symptoms and so on

Proximal explanation:
- only explain proximal origins of symptoms
- only explain what is happening now to produce symptoms- not a distal explanation (focus on initial cause)- possible distal are family dysfunction and genetics
- currently unclear how genetic variation or childhood trauma may lead to problems with meta-representation or central control

75
Q

briefly outline drug treatments for schizophrenia including types

A
  • treated with antipsychotics
  • usually administered orally (as a tablet or syrup) or intravenously (using an injection the drug is put directly into the bloodstream)
    TYPES:
  • typical- been around since the 1950s- chlorpromazine, haloperidol
  • atypical- used since the 1970s to treat psychosis but reduce side effects- clozapine, risperidone
76
Q

Describe chlorpromazine

A
  • Typical antipsychotic
  • works as a dopamine antagonist- reduces the action of the neurotransmitter dopamine
  • blocks the dopamine receptors in the synapse so that dopamine cannot be absorbed by the adjoining neurone
  • According to the dopamine hypothesis, increased levels of dopamine in the sub cortex is responsible for some of the symptoms of schizophrenia, such as hallucinations- therefore by blocking the action of dopamine, we should be able to reduce the symptoms of schizophrenia
  • also has sedative effect- effect on histamine receptors- used to calm individuals with schizophrenia and other conditions (usually administered in syrup for this purpose as faster effect)
77
Q

Describe haloperidol

A
  • typical antipsychotic
  • Blocks dopamine receptor sites and thus decreases dopamine activity
78
Q

Describe clozapine

A
  • atypical antipsychotic
  • works in a similar way to Chlorpromazine in that it binds to dopamine receptors
  • However, also blocks the action of serotonin and glutamate
  • This helps to not only improve schizophrenic symptoms but to enhance mood and improve cognitive functioning in those who take it
  • This can be very beneficial given that many individuals with schizophrenia have suicidal thoughts and 30 to 50% of them make an attempt to take their own lives
  • Typical daily dose 300-450mg.
79
Q

Describe risperidone

A
  • works by binding to dopamine and serotonin receptors. It binds more strongly to dopamine receptors than the drug Clozapine allowing smaller doses to be given that are just as effective, typical dose 4-8mg daily with maximum 12mg
  • There is some evidence to suggest that this leads to fewer side effects than is common for antipsychotics
80
Q

Strength of drug therapies for schizophrenia

A

Research evidence for chlorpromazine:
- Barlow & Durand (1995)- chlorpromazine is effective in reducing schizophrenic symptoms in about 60% of cases
- most impact on positive symptoms; treated patients may still suffer from severe negative symptoms
- Thornley et al (2003)- compared a control group who received a placebo to a group who received Chlorpromazine
- the group given the antipsychotic drug had better overall functioning and reduced symptom severity than those given the placebo
- This study also has high population validity as it contained over 1000 participants- means that the sample is likely to contain a wide variety of people making results generalizable

Research evidence for Haloperidol:
- Schooler et al (2005) randomly allocated 555 patients in first episode of schizophrenia, to either treatment with haloperidol or risperidone. In both groups 75% showed a reduction in symptoms.

Research evidence for Clozapine:
- Pickar et al (1992) compared clozapine with other neuroleptics and a placebo and found clozapine to be the most effective in reducing symptoms, even in patients who had previously been treatment resistant
- Meltzer (2012)- reported that the atypical antipsychotic clozapine was more effective than typical and other atypical drugs and that it had been used effectively for those who had not responded well to typical antipsychotics

Research evidence for Risperidone:
- Emsley (2008) found that patients who were injected with risperidone early in course of disorder had low relapse rates and high remission rates; 84% of patients showed at least a 50% reduction in both +ve and -ve symptoms and 64% went into remission

Instant effect:
- One strength of using antipsychotics to treat schizophrenia is that they work instantly
- This can therefore allow the patient to become more functional in a shorter space of time than with other therapies
- CBT, for example, takes many sessions to complete

Atypical have less side effects:
- Risperidone lower relapse rate than haloperidol, 45% compared with 55%, (Schooler et al 2005); Also fewer side effects than haloperidol

81
Q

Weaknesses of drug therapies

A

Continuous use:
- continuous use is needed to remain free from psychotic symptoms
- If the patient stops taking the antipsychotic drugs then symptoms will return
- HaloperidoL- 55% relapse rate in Schooler et al (2005) study
- This is a problem because it means that drugs do not provide a long term, permanent solution in eliminating schizophrenia

Issues with research:
- Healy (2012) has suggested serious flaws with evidence for effectiveness.
– for example, most studies are of short term effects.
- also, because antipsychotics have powerful calming effects, it is easy to demonstrate that they have some positive effect on people experiencing the symptoms of schizophrenia – this is not the same as saying they really reduce the severity of psychosis
– means that the evidence pays for antipsychotic effectiveness is less impressive than it first appears.

Mechanisms unclear:
We do not know why they work.
– our understanding of the mechanism by which antipsychotic drugs work is strongly tied up with the original dopamine hypothesis – the idea that symptoms of schizophrenia are linked to high levels of dopamine activity in the subcortex of the brain.
– however, we now know that this original dopamine hypothesis is not a complete explanation for schizophrenia, and that, in fact, dopamine levels in other parts of the brain are too low, rather than too high.
– if this is true, then most antipsychotic should
-given that there are questions over the effectiveness of antipsychotics- this adds to the argument that they are, in fact ineffective
– means that at least some of the antipsychotics may not be the best treatment to opt for-perhaps some other factors involved in their apparent success.

Side effects:
- often have a lot of side effects. For example, patients who take Clozapine have to have regular blood tests to ensure that they do not develop a condition known as agranulocytosis (reduced granulocytes in the blood leave the individual vulnerable to infection)- when first introduced, people taking Clozapine died from this condition
- The fact that there is the potential for an individual to experience fatal side effects from antipsychotics means that we may question whether or not quality of life and functioning does actually improve with the use of drugs
- Many side effects of typical antipsychotics including tardive dyskinesia following prolonged usage. Characterized by involuntary facial movements such as grimacing, blinking and lip smacking
- Typical antipsychotics can cause a fatal condition called neuroleptic malignant syndrome (NMS)- hy reducing the amount of dopamine action in the hypothalamus NMS can occur
- Chlorpromazine- Muscle tightening in neck and jaw, tardive dyskinesia, decrease of spontaneous movement,, decrease in emotional spontaneity and motivation, motor restlessness and fidgeting, sedation, dry mouth, constipation, weight gain
BUT Meltzer (2012) argued that an attempt to reduce the side effects in the newer atypical antipsychotics has been successful, cost-benefit analysis

82
Q

Name psychological therapies for schizophrenia

A
  • CBT
  • Family therapy
83
Q

Briefly outline the use of CBT for treating schizophrenia

A
  • takes between 5 and 20 sessions
  • can be delivered in group for 1-to-1
  • aims to deal with both cognitions and behaviour
  • allows the patient to make adjustments two their thinking that help them to cope- doesn’t get rid of their symptoms
  • assumes that thoughts, feelings and behaviour are all linked- means that if you change a person’s thoughts then their feelings and behaviour will also change
84
Q

Describe how CBT can be used to help someone with schizophrenia

A
  • uses both cognitive and behavioural principles to alter a patient’s thought processes and behaviour
  • Can be used to challenge maladaptive thoughts
  • Schizophrenic people are often unaware that they are subject to cognitive errors, or that there are problems with their thinking- the therapist will try to make these maladaptive thoughts conscious, and then by challenging them, the patient will see that there is no basis for these thoughts
  • for auditory hallucinations, the therapist may explain that the voice actually comes from the malfunctioning speech centre in their brain and that it cannot hurt them if they ignore it- becomes less frightening and less debilitating- doesn’t eliminate symptom, but reduces distress and improves ability to function adequately
  • may also use normalisation- explaining that voice hearing is an extension of the ordinary experience of thinking in words
  • delusions may challenged by reality testing- patient and therapist jointly examining likelihood that beliefs are true- patient is made to consider the evidence in the hope that they will realise that there are alternative explanations
  • The therapist will also set behavioural assignments to the patient to challenge dysfunctional thoughts, and to encourage levels of functioning e.g. a patient who believes that they can predict the future may be asked to predict what happens next during a paused TV show- by testing out their beliefs, the patient can acknowledge their faulty thinking, and then change it
  • CBT offers psychological explanations for the symptoms the patient is experiencing- in understanding why they are happening the patient will hopefully see that they are not part of reality.
  • in some cases where delusions are resistant to reality testing, CBT can still be used to tackle the anxiety and depression yet result from living with schizophrenia
85
Q

Describe a case example of using CBT for treating schizophrenia

A

Turkington et al (2004)- example of using CNY to challenge where a paranoid clients delusions come from:
Patient: the Mafia are observing me to decide how to kill me
Therapist: you are obviously very frightened… there must be a good reason for this
Patient: do you think it’s the Mafia
Therapist: It’s a possibility but there could be other explanations. How do you know that it’s the Mafia?

86
Q

Strengths of CBT as a treatment for schizophrenia

A

Research evidence:
- Jauhar et al (2014)- analysed the findings from 34 studies- found that CBT has a small but significant effects on both positive and negative symptoms
- other studies focused on symptoms- Pontillo et al (2016)- found reductions in frequency and severity of auditory hallucinations
- clinical evidence from NICE (national institute for health and care excellence) recommends CBT for schizophrenia
- means that both research and clinical experience support the benefits of CBT for schizophrenia

Research evidence 2:
- Bateman et al (2007)
- looked at the effects of CBT with a specific focus on the benefits to reducing suicidal thoughts- given that 30-50% attempt it at some point this is important
- 99 patients split into 2 groups- CBT/ no CBT
- All had been resistant to antipsychotics
- CBT was found to reduce suicidal ideation both immediately after therapy and in a follow up 9 months later

Effectiveness for first episode:
- Bentall et al (1994)
- suggests that cognitive therapy may be most effective for patients experiencing their first episode of schizophrenia
- may possibly be because it is easier for the patient to recognise their disordered thinking at this stage rather than years into the illness where the pattern of maladaptive thinking has been long established

87
Q

Weaknesses of CBT as a treatment for schizophrenia

A

Quality of evidence:
- methodological problems with research
- Most of the research that reports a positive effect of CBT on schizophrenia includes patients who also receive antipsychotics- difficult to distinguish between the effects of the drug and the effects of CBT
- Thomas (2015)- different studies have involved use of different CBT techniques and people with different combinations of positive and negative symptoms
- means the overall modest benefits of CBT for schizophrenia probably conceal a wide variety of effects of different CBT techniques on different symptoms
- makes it hard to say how effective CBT will be for a particular person with schizophrenia

Effect on symptoms:
- While CBT improves the quality of life, allowing the schizophrenic patient to acknowledge their irrational thoughts and change their behaviour, it does not actually get rid of the symptoms
- schizophrenia appears to be a largely biological condition- would expect that a psychological therapy like CBT only improves ability to live with the disorder rather than curing it
BUT- still significant effect on positive and negative symptoms- suggests CNT does more than just enhancing coping

Ethics:
- may be unethical to tell someone the thoughts they have are irrational
- may be interfering with freedom of thought

time consuming:
- CBT usually has to take place weekly, and can last for months
- Therefore it can be costly and time consuming when compared to other therapies

Focus just on symptoms:
- CBT only focuses on treating the symptoms of schizophrenia; it ignores the role of society and the family in maintaining the illnes

88
Q

Briefly outline family therapy as a treatment of schizophrenia

A
  • Families are believed to play a role in the onset of schizophrenia- psychological explanations- the schizophrenogenic mother and double bind theory
  • takes places with families as well as the identified patient (one member of a dysfunctional family who expresses the family’s conflicts)
  • aims to improve the quality of communication and interaction between family members
  • aims to reduce the level of expressed emotion within families
89
Q

Describe how family therapy can help with schizophrenia

A

Pharoah et al (2010) identified the following strategies that reduce the level of expressed emotion:
- aims to reduce levels of expressed emotion (reduce elves of emotion generally but especially negative emotions e.g. anger and guilt yay vitiate stress)- reducing stress is important in reducing likelihood of relapse
- improves the families ability top help- therapist encourages family members to form a therapeutic alliance whereby they all agree on the aims of the therapy- also tries to improve families beliefs about and behaviour towards schizophrenia, ensures family members achieve a balance between caring for the individual and maintaining their own lives

90
Q

describe a model of practice of using family therapy for schizophrenia

A

Burbach (2018):
- proposed a model for working with families dealing with schizophrenia
- begins with sharing basic information and providing emotional and practical support
- then develops through progressively deeper levels
- phase 2 involves identifying resources including what different family members can/can’t offer
- phase 3 aims to encourage mutual understanding, creating a safe space for all family members to express their feelings
- phase 4 involves identifying unhelpful patterns of interaction
- phase 5 is about learning skills training such as learning stress management techniques
- phase 6 looks at relapse prevention planning
- phase 7 is about maintenance for the future

91
Q

Strength of family therapy as a treatment of schizophrenia

A

Evidence for effectiveness 1:
- Pharoah
- reviewed several studies and concluded that there was a lower rate of relapse within a year amongst those who received family therapy

Evidence for effectiveness 2:
- McFarlane (2016)
- review of studies- concluded that family therapy was one of the most consistently effective treatments available for schizophrenia
- In particular release rates found to be reduced by around 50-60%
- Also concluded that using family therapy as metal health initially starts to decline is particularly promising
- Clinical evidence from NICE recommends family therapy for everyone with a diagnosis of schizophrenia
- Means that family therapy is likely to be of benefit of pope with both early and developed schizophrenia

Benefits whole family:
- Lobban and Barrowclough (2016)
- concluded positive effects on family are important as they provide bulk of care
- by strengthening the functioning of the functioning of the family as a whole, lessens the impact of schizophrenia on other family members and strengthens the ability of the family to support the person with schizophrenia
- means daily therapy has wider benefits beyond the obvious positive impact on the identified patient

Long term effects:
- the patient is supported whilst outside of the institution and the skills gained by family members should support the patient even after the therapy is complete

Economic benefit:
-reduces relapse Aries and makes families better able to provide the bulk of care
- economic benefits as state doesn’t need today as much

92
Q

Weaknesses of family therapy as a treatment of schizophrenia

A

Not cure:
- Like other psychological therapies it is not providing a cure for symptoms

Requirements for family:
- Requires the family members to be willing to engage with therapists
- Therefore it may not be available to all if their family members are not around or are simply not willing to get involved

Social desirability:
- how accurate will the accounts that family members give about the progress their SZ relative is making actually be?
- Family members may want to relieve themselves of this burden and suggest that the individual with schizophrenia is not doing well
- They may really want them to get better and so report that they are even if they’re not

93
Q

briefly outline token economies

A
  • used in psychiatric hospitals
  • do not cure the positive symptoms of schizophrenia but can help with the negative symptoms
94
Q

Describe the rationale for token economies

A
  • institutionalisation develops under circumstances of prolonged hospitalisation
  • Often causes people to develop bad habits e.g. may stop maintaining personal hygiene or socialising with others- understandable response to living without usual routine and small pleasures
  • Matson et al (2016)- identified 3 categories of institutional behaviour commonly tackled with token economies- personal care, condition related behaviour (e.g. apathy) and social behaviour
  • modifying these behaviours doesn’t cure schizophrenia but has 2 major benefits
    1) improves persons quality of life within the hospital setting e.g. makeup for someone who usually takes pride in their appearance or socialising for someone who’s usually sociable
    2) Normalises behaviour- makes it easier for people who have spent a long time in hospital to adapt back into life in the community e.g. by getting dressed in morning and making their bed
95
Q

Describe the theory behind token economies

A
  • example of behaviour modification- a behavioural therapy based on operant conditioning
  • tokens are secondary reinforcers as they only have value once the person using them has learnt that the can be used to obtain primary reinforcers-meaningful rewards e.g. walk outside or sweets
  • those token that can be used to obtain a range of different primary reinforcers are generalised reinforcers- particularly powerful
  • in order for the tokens to become secondary reinforces they ate paired with primary reinforcers, so at the start of a token economy programme tokens and primary reinforcers are administered together
96
Q

Describe what is involved in a token economy

A
  • tokens e.g. coloured disks are given immediately to individuals when they have carried out a desirable behaviour
  • target behaviours are decided on an individual basis- important to know the person in order to identify the most appropriate target behaviours for them (Cooper, 2007)
  • Although the tokens have no value themselves they are later tapped for more tangible rewards
  • having some sort of immediate rewards for target behaviour is important because delayed rewards are less effective- tokens therefore administered as soon as possible after target behaviour
  • rewards in a hospital may include objects like sweets or magazines, or activities e.g. walk outside/film, or appointment with social worker to plan for life after hospitalisation
97
Q

Describe an example of where a token economy was used for managing schizophrenia

A

Ayllon and Azrin:
- trialled a token economy for women with schizophrenia
- every time PPs carried out a task e.g. making their bed or cleaning up they were given a plastic token embossed with the words ‘one gift’
- these tokens could then be swapped for ward privileges e.g. being able to watch a film
- the number of tasks carried out increased significantly
- token economies were extensively used in the 1960s and 70s when the norm for treating schizophrenia was long-term hospitalisation- use has now declined in then UK due to growth of community-based care and the closure of many psychiatric hospitals, and also due to ethical issues raised by restricting rewards to people with mental disorders But still remain standard approach in many parts of world

98
Q

Strengths of using token economies to manage schizophrenia

A

Evidence of effectiveness:
- Glowacki et al (2016)
- identified 7 high quality studies published between 1999 and 2013 that examined the effectiveness of token economies for people with chronic mental health issues such as schizophrenia and involved patients living in a hospital setting
- all the studies showed a reduction in negative symptoms and a decline in the frequency of unwanted behaviours
BUt- 7 studies is small evidence base- ‘file drawer problem’- leads to bias towards positive published findings as undesirable results have been ‘filed away’- particular problem in reviews that only include a small number If studies

Improving relationships:
- effective in producing better relationships between patients and psychiatrists
- can help with the smooth daily functioning of a psychiatric hospital
- Furthermore, building up a trusting relationship between the psychiatrist and patient is essential for effective treatment- patient will be more likely to listen to the advice of the psychiatrist

99
Q

Weaknesses of using token economies to manage schizophrenia

A

Re-entering society:
- If the patient did eventually re-enter society they would no longer be rewarded for behaviours such a making the bed and getting dressed
- tokens could to be administered immediately and target behaviours can’t be monitored closely
- It is therefore possible that they will stop with the desired behaviour and will not be able to function properly in society
BUT some with schizophrenia may only get the chance to live outside the hospital if their personal care and social interaction can be improved- perhaps best way to improve this is using token economy during patient care

Ethical issues:
- gives professionals considerable power to control the behaviour of the people in the role of the patient
- This inevetably involves imposing a persons or institutions norms onto others- especially problematic if the target behaviours aren’t identified sensitively e.g. someone who likes to look scruffy and get up late may have these personal freedoms restricted
- restricting availability of pleases e.g. having sweets or seeing films for people who don’t behave was desired means that seriously ill people, who are already experiencing distressing symptoms, have an even worse tiem
- legal action fly families who see their relative in these position has now been a major factor in the decline in the use of token economies
- means that the benefits of token economies may be outweighed by their impact on personal freedom and short-term reduction in quality of life

Alternative approaches:
- may be more pleasant and ethical alternatives
- even if token economies can be helpful for managing schizophrenia, there are other approaches with a comparable evidence base that don’t rase the same ethical issues
- e.g. review by Chiang et al (2019)- concluded art therapy might be a good alternative- evidence base is relatively mall and gas some methodological limitations, but appears to show that art therapy is a. high-gain low-risk approach
- event if the benefits of art therapy are modest, this is generally true for all approaches to treatment and management of schizophrenia, and unlike alternatives, art therapy is a pleasant experience without major risks of side effects or ethical absuses- NICE guidelines reccomend art therapy

Issues with research:
- McMonagle and Sultana (2009)
- criticised much of the research into token economies because they had used an independent measures design without randomly allocating patients to conditions
- Of the 3 studies that had used random allocation, only one reported an improvement in symptoms

100
Q

Briefly outline the interactionist Approach

A
  • acknowledges there are biological, psychological and social factors in the development of schizophrenia- holistic
  • biological factors include genetic vulnerability and neurochemical and neurological abnormally
  • psychological factors include stress e.g. from life events and daily hassles
  • social factors e.g. poor quality interactions in family
  • includes the diathesis stress model
101
Q

Outline the diathesis stress model

A
  • idea that someone may be vulnerable to schizophrenia (the diathesis part) but they will only develop the disorder is something triggers it (the stressor).
102
Q

Who proposed the original diathesis stress model

A

Meehl

103
Q

Outline Meehl’s diathesis stress model

A
  • diathesis entirely genetic- result of a single ‘schizogeny
  • Without the gene it is not possible to develop schizophrenia (no matter how much stress) but having the gene doesn’t mean you always get the disorder
  • The gene may leave someone with a personality that is particularly sensitive to criticism, perhaps from parents- biology based ‘schizotypic personality’
  • So if they don’t have overly critical parents they will not develop schizophrenia, but if they do then this will trigger the disorder
  • The diathesis part is the ‘schizogene’ while the stressor is said to be the schizophrenogenic mother.
104
Q

Describe the modern understanding of diathesis (diathesis tress model of schizophrenia)

A
  • no single ‘schizogeny’- many genes increase genetic vulnerability (Ripke et al, 2014)
  • also may be psychological trauma (Ingram and Luton, 2005)- trauma becomes diathesis rather than stressor
  • Read et al- neurodevelopment model- childhood trauma alters the developing brain leaving a person vulnerable to schizophrenia- this can then be triggered by some kind of environmental factor- e.g. the hypothalamic-pituitary-adrenal (HRA) system can become overactive, making a person much more vulnerable to later stress
105
Q

Describe the modern understanding of stress (diathesis tress model of schizophrenia)

A
  • may not necessarily be a psychological factors- while it can be parents, Houston et al (2008) suggests it includes anything that risks triggering schizophrenia
  • High doses of THC-rich cannabis- increases risk up to 7 times according to dose- may be as interfered with dopamine system- most people doesn’t develop schizophrenia after using cannabis as may not have the vulnerability
106
Q

Describe treatment of schizophrenia according to the diathesis stress model

A
  • acknowledges with biological and psychological factors- therefore compatible with both biological and psychological treatments
  • Model associated with combining antipsychotic medication and psychological therapies (CBT most commonly)
  • Turkington et al (2006)- can believe in biological causes of schizophrenia and still practice CBT to relieve psychological symptoms- BUT needs interactionist approach to believe
  • Britain- increasingly standard practice to treat people with combination of antipsychotic drugs and CBT
  • US- kore of a history of conflicts between psychological and biological models- slower adoption of interactions approach- medication without accompanying psychological treatment more common in US then UK- US more drug focused- privitised health care system need employment ‘ for healthcare but hard for schizophrenics to keep employment
107
Q

Name a key study into the interactionist model of schizophrenia

A

Tienari et al (2004)

108
Q

Describe Tienari et al’s procedure (interactionist model of schizophrenia)

A
  • Hospital records were reviewed for nearly 20,000 women admitted to Finish psychiatric hospitals between 1960 and 1979, identifying those that had been diagnosed at least once with schizophrenia
  • list was checked to find those mothers who had one or more of their offspring adopted away
  • The resulting sample of 145 adopted-away offspring (the high-risk group) was then matched with a sample of 158 adoptees without this genetic risk (low risk group)
  • Both groups of adoptees were independently assessed after an interval of 12 yrs, with a follow up after 21 yrs
  • Psychiatrists also assessed family functioning in the adoptive families using a scale – the Oulu Family Rating Scale- measures families on various aspects of functioning such as parent-offspring conflict, lack of empathy and insecurity
  • The interviewing psychiatrists were kept blind as to whether the biological mother was schizophrenic or not
109
Q

Describe Tienari et al’s findings (interactionist model of schizophrenia)

A
  • of the 303 adoptees, 14 developed schizophrenia over the course of the study
  • 11 of these were from the high risk group and 3 from the low risk group
  • However, being reared in a ‘healthy’ adoptive family appeared to have a protective effect even for those that had a high genetic risk
  • In adoptees at high risk of schizophrenia, but not in those at low genetic risk adoptive-family stress was a significant predictor of the development of schizophrenia
  • summary- high levels of criticism, hostility, and low levels of empathy were strongly associated with the development of schizophrenia, but online the high risk genetic group- combination of genetic vulnerability and family stress can lead to greatly increased risks of schizophrenia
110
Q

Strengths of the interactionist approach too schizophrenia

A

Supporting research:
- Tienrai- see previous cards

Holistic:
- interactions approach to treating is hollistic
- Treating the patient using more than one type of treatment means that every aspect of schizophrenia is targeted
- For example, using antipsychotics will target the positive symptoms such as hallucinations but it will not get rid of maladaptive behaviours that might prevent the individual from leading a normal life
- Combining antipsychotics with a token economy will not only get rid of symptoms but allow the patient to cope better with life

Research for treatment/practical application:
- Tarrier et al (2004) provides support for adopting an interactionist approach in the treatment of schizophrenia
- They used random allocation to assign 315 schizophrenic patients to one of three conditions: medication + CBT/ medication + counselling/ control group (medication only)
- found that the groups given a combination of treatments displayed less symptoms than the control group
- However, there was no difference in the rate of relapse between the two groups suggesting that combination treatment does not
- One strength of the study conducted by Tarrier is that they have used random allocation- means that researcher bias could not possible have had an effect on the results as the researcher had no control over who was in which condition- e.g. couldn’t choose all of the patients they expected to do well in CBT to go in to the group given CBT- increases the validity of the study.necessarily produce longer lasting changes
BUT- Jarvis and Okami- saying that a successful for treatment for mental disorders justifies a particular explanation is the logical equivalent of saying that alcohol reduces shyness, shyness is caused by lack of alcohol- ‘treatment-causation fallacy’- cannot automatically assume that the success of combined therapies means interactionist explanations are correct

Urbanisation:
- schizophrenia is more commonly diagnosed in urban than rural areas
- statistic is sometimes sue dot justify the interactionist approach as assumes that urban living is more stressful than rural living and therefore acts as trigger
BUT- may be that schizophrenia sis more likely to be diagnosed in cities, or that people with a diathesis for schizophrenia (e.g. teenagers abused as children) tend to migrate to cities

111
Q

Weaknesses of the interactionist approach too schizophrenia

A

Diathesis and stress are complex:
- original modle- over simplicity
- now clear that original model with shcizogene is simplistic- multiple genes in multiple combinations influence diathesis
- stress also comes in many forms- included but not limited to dysfunctional parenting
- diathesis may be psychological and stress may be biological
- Houston (2008)- childhood sexual abuse may be vulnerability
- cannabis may be trigger
- means there are multiple factors, both biological and psychological, affecting both diathesis and stress- supports modern understanding of both diathesis and stress