Schizophrenia - Paper 3 Flashcards

1
Q

What is schizophrenia?

A

A psychological disorder characterised by loss of contact with reality - it is classified as a psychosis.

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2
Q

Where does schizophrenia occur?

A

. In around 1% of the population (0.7%)
. More commonly diagnosed in men than women
. More common in urban environments
. More common in working class populations
. Average age of onset is between 25-30 years

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3
Q

What is meant by diagnosis and classification?

A

To be able to diagnosed with a disorder, psychiatrists must first classify it. This is done by consulting a diagnostic manual to classify the disorder, and then they are diagnosed by identifying their symptoms.

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4
Q

What are the two main classification systems?

A

DSM-5 and ICD-10

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5
Q

What is the difference between ICD-10 and DSM-5?

A

ICD-10 - Only negative symptoms need to be present
DSM-5 - Only positive symptoms need to be present

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6
Q

What are the two types of symptoms of schizophrenia?

A

Positive and Negative symptoms

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7
Q

What are positive symptoms?

A

Symptoms that aren’t typically present in a normal person. They reflect an excess or distortion of normal thinking

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8
Q

What are negative symptoms?

A

Symptoms which cause a decline in functioning - where the sufferer looses something they previously had. They reflect a loss of normal functioning

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9
Q

What are the positive symptoms of schizophrenia?

A

. Delusions - False beliefs which are firmly held despite being illogical or having no supporting evidence. Irrational beliefs
. Hallucinations - Disturbances in perception, where someone senses something this isn’t there or is unusual
. Psychomotor disturbances - Repetitive behaviours, such as twitches or rocking back and forth
. Catatonia

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10
Q

What are the common types of delusions?

A

. Delusions of persecution
. Delusions of grandeur
. Delusions of control

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11
Q

What are the common types of hallucinations?

A

Auditory, Visual

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12
Q

What are the negative symptoms of schizophrenia?

A

. Speech poverty/alogia - Reduction in the quality or quantity of a persons speech HOWEVER speech disorganisation, where speech is incoherent or the speaker changes topic midsentence, is classified as a positive symptom
. Avolition - ‘Apathy’ - where individuals struggle to become motivated or keep up with goal oriented activity. Andreasen (1982) identified three signs of avolition: poor hygiene and grooming, lack of persistence in education/work, lack of energy

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13
Q

What are some strengths of the classification and diagnosis of schizophrenia?

A

+ High reliability - In terms of psychiatric diagnosis, reliability is achieved when different diagnosing clinicians reach the same diagnosis for an individual (inter-rater reliability) and when the same clinician reaches the same diagnosis for an individual on two occasions (test-retest reliability) - when diagnoses are consistent. Osorio et.al (2019) reported high reliability in the diagnosis of 180 individuals using the DSM-5, where pairs of interviewers achieved inter-rater reliability of +.97 and test-retest reliability +.92. This gives psychologists faith in the diagnosis of schizophrenia, as they can be reasonably sure that it is consistently applied

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14
Q

What are some limitations of the classification and diagnosis of schizophrenia?

A
  • Low validity - Cheniaux et.al (2009) had 2 psychologists independently assess the same 100 clients using ICD-10 and DSM-5. 68 were diagnosed with schizophrenia under the ICD system, and 39 under DSM. This suggests that schizophrenia can be over or under diagnosed according to the diagnostic system, and shows that the criterion validity of diagnostic tools is low. Also demonstrated by Rosenhan (1973) in which 8 psuedopatients were kept in hospital after being falsely diagnosed, despite then behaving normally while in hospital. In a follow up study, doctors rejected genuine patients who they assumed were part of the deception, suggesting that the validity of diagnosis’ might be poor.
    —- COUNTER —- The Osorio et.al (2019) study reported excellent agreement between clinicians when the methods used to diagnose schizophrenia both derived from the DSM system. So criterion validity can be high, provided the diagnostic tools come from one system.
  • Co-morbidity - Conditions often occur at the same time, which challenges the validity of diagnosis and classification, as two conditions may be identified when the patient is actually only suffering from one. Schizophrenia is frequently diagnosed with other conditions, such as depression, substance abuse or OCD (Buckley et.al). Schizophrenia may not exist as a distinct condition, but be a name given to the symptoms of other disorders. This challenges the validity and accuracy of schizophrenia diagnoses.
  • Gender Bias - Since the 1980’s men have been diagnosed with schizophrenia more commonly than women (a ratio of 1.4:1, according to Fischer and Buchanan 2017). One possible explanation of this is that women are less vulnerable than men. However it also seems likely that women are underdiagnosed because they have closer relationships, and therefore receive greater support (Cotton et.al 2009) and function better. The methods of diagnosing schizophrenia do not take this into account, meaning that women with schizophrenia may not receive the support they need.
  • Culture Bias - Some symptoms of schizophrenia have different meanings within different cultures. For example, hearing voices may be considered abnormal in British culture, but is believed in Haiti to be a communication from ancestors. British people of Afro-Caribbean heritage are up to 9x more likely to receive a schizophrenia diagnosis than their white British counterparts (Pinto and Jones 2008). These rates of diagnosis are not reflected in African-Caribbean countries, ruling out a genetic explanation. This difference could be explained by culture bias in diagnosis, where psychologists from a different cultural background overinterpret symptoms of schizophrenia in black British people (Escobar 2012). As such, the diagnosis system for schizophrenia may be culturally biased, leading to inaccurate diagnosis.
  • Symptom overlap - There is considerable overlap between the symptoms of schizophrenia and other mental health disorders. Slater and Roth (1969) say that hallucinations are the least important of all symptoms, as they are not exclusive to schizophrenia. For example, both schizophrenia and bipolar involve both positive symptoms, such as delusion, and negative symptoms such as avolition. This could suggest that it is incorrect to classify them as two separate conditions - they may be variations of the same condition. Symptom overlap means that schizophrenia may not exist as a distinct condition, and that even if it does diagnosis is difficult as it does not have any unique and distinct symptoms, which could lead to inaccurate diagnosis.
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15
Q

What are the biological explanations of schizophrenia?

A

. Genetic basis of schizophrenia
. Neural correlates

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16
Q

What do family studies show?

A

Family studies have confirmed that the risk of developing schizophrenia increases in line with genetic similarity to someone with the disorder, as demonstrated by Gottesmann (1991)

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17
Q

What were the findings of Gottesmann (1991)?

A

As genetic similarity to someone with schizophrenia increases, so does the probability of developing the disorder
. General population - 1%
. Uncles/Aunts - 2%
. Grandchildren - 5%
. Parents - 6%
. Siblings - 9%
. Identical twins - 48%

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18
Q

What are candidate genes?

A

Genes that are believed to code for a particular disorder. Early research looked into the role of one single faulty gene. However recent research suggests schizophrenia is polygenic, likely involving genes that code for neurotransmitters such as dopamine. The identification of different candidate genes in research into schizophrenia also suggests that it is aetiologically heterogenous ( different combinations of factors, including genetic variations, can lead to the disorder in different people)

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19
Q

What was Ripke et.al (2014)

A

. Combined all previous data from genome-wide studies of schizophrenia
. The genetic makeups of 37,000 people with a diagnosis of schizophrenia were compared to those of 113,000 controls
. 108 separate genetic variations were found to be associated with increased risk of schizophrenia

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20
Q

What is the role of mutation?

A

Schizophrenia can have a genetic origin in the absence of family history. One explanation of this is a mutation in the parental DNA, which may be caused by radiation, poison or viral infection. Evidence for mutation comes from positive correlations between paternal age (which is associated with increased risk of sperm mutation) and risk of schizophrenia - from 0.7% with fathers under 25 to over 2% with fathers over 50 (Brown et.al 2002)

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21
Q

What are some strengths of the genetic basis of schizophrenia?

A

+ Strong evidence base - Family studies such as Gottesman (1991) show that risk of developing schizophrenia increases with genetic similarity to a family member with schizophrenia. This was supported by Tienari et.al (2004) which demonstrated that biological children of parents with schizophrenia have an increased risk of developing the disorder, even when raised in adoptive families. Hilker et.al (2018) also showed a concordance rate of 33% for identical twins, compared to 7% for non-identical twins, supporting the genetic explanation. As such, the theory can be seen as having high reliability, as findings consistently support the theory.

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22
Q

What are some limitations of the genetic basis of schizophrenia?

A
  • There is clear evidence to suggest that environmental factors increase the risk of developing schizophrenia - not just genetic. These environmental factors can include biological influences, such as birth complications (Morgan et.al 2017) and smoking THC rich cannabis in the teenage years (Di Forti et.al 2015), and psychological influences such as childhood trauma. Morkved et.al (2017) found that 67% of people with schizophrenia and related psychotic disorders reported at least 1 childhood trauma, vs 38% of a matched group with non-psychotic mental health issues. Furthermore, the fact that concordance rates for schizophrenia are not 100% means that it cannot be wholly explained by genes. This means that the genetic explanation is an incomplete one, and one that over emphasises nature and ignores nature.
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23
Q

What are neural correlates?

A

Patterns of structure or activity in the brain that occur in conjunction with an experience. The best known neural correlate of schizophrenia is the neurotransmitter dopamine, which is key in the function of several of the brain systems involved in the symptoms of schizophrenia

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24
Q

What is the original dopamine hypothesis?

A

. Subcortical Hyperdopaminergia
. Based on the discovery that drugs used to treat schizophrenia - such as antipsychotics which reduce dopamine - cause symptoms similar to those of Parkinson’s disease, which is associated with low dopamine levels (Seeman 1987)
Parkinson’s involves a reduction in dopamine levels, so the drugs used to treat it increase dopamine production - but these drugs worsen symptoms of schizophrenia
. Therefore schizophrenia may be the result of high dopamine levels in the subcortical areas of the brain eg. an excess of dopamine receptors in pathways from the subcortex to Broca’s area - Broca’s area is associated with speech production, so abnormal functioning here could explain symptoms such as speech poverty or auditory hallucinations

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25
Q

What is the updated dopamine hypothesis?

A

. Cortical Hypodopaminergia
. Proposed by Davis et.al (1991)
. Suggests schizophrenia is the result of abnormally low dopamine levels in the cortex
. Used to explain symptoms of schizophrenia eg. low dopamine in the prefrontal cortex, which is responsible for thinking, could explain some negative symptoms of schizophrenia
. It has been suggested that cortical hypodopaminergia can lead to subcortical hyperdopaminergia - so the updated hypothesis involves both high and low levels of dopamine
. It argues that genetic variations and early experiences of stress make people more sensitive to cortical hypodopaminergia, and by extension subcortical hyperopaminergia ( Howes et.al 2017)

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26
Q

What are some strengths of the dopamine hypothesis?

A

+ Research support for the role of dopamine in schizophrenia - Curran et.al (2004) found that amphetamines, which increase dopamine levels, worsen symptoms in people with schizophrenia and induce symptoms in people not diagnosed with the disorder. Tauscher et.al (2014) also found that antipsychotic drugs reduce dopamine activity and reduce the intensity of symptoms. Furthermore, several of the candidate genes linked to schizophrenia act on the production of dopamine, or on dopamine receptors. Finally, Tenn et.al (2003) induced schizophrenia like symptoms in rats using amphetamines, and reduced them using drugs that reduce dopamine action. This supports the link between dopamine and schizophrenia, strengthening the dopamine hypothesis.

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27
Q

What are some limitations of the dopamine hypothesis?

A
  • There is also evidence for the importance of other neurotransmitters in causing schizophrenia, notably glutamate - Post-mortem and live brain scan studies have consistently found higher levels of glutamate in several brain regions of people with schizophrenia (McCutcheon et.al 2020). Additionally, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing. The dopamine hypothesis arguably overemphasises the role of dopamine, at the expense of other neurotransmitters, and as a result can be seen as an incomplete explanation.
  • Other drugs which increase dopamine levels, such as apomorphine, do not cause schizophrenia-like symptoms (Depatie and Lai 2001). Also, Noll (2009) argued that around 1/3 of patients do not respond to drugs which block dopamine, so other neurotransmitters are causes must be involved.
  • Biologically deterministic
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28
Q

What is meant by family dysfunction?

A

Processes within a family, such as poor family communication, cold parenting, and high levels of expressed emotion, which can be risk factors for the development and maintenance of schizophrenia

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29
Q

What are the 3 types of Family Dysfunction explanation?

A

. Schizophrenogenic mother
. Double - bind theory
. Expressed Emotion

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30
Q

What is the Schizophrenogenic mother?

A

. Psychodynamic explanation proposed by Fromm-Reichmann (1948) based on accounts from her patients about their childhoods
. Said that patients described a particular type of parent called the schizophrenogenic mother
. The schizophrenogenic mother is cold, rejecting and domineering, and creates a family environment based on tension and secrecy. This environment leads to distrust, which develops into paranoid delusions and then schizophrenia

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31
Q

What is the Double - bind theory?

A

. Bateson et.al (1972) agreed that the family climate played a role, but emphasised the importance of the families communication style
. The developing child regularly finds themselves in situations where they fear doing the wrong thing but receives mixed messages about what the wrong thing is. They feel unable to speak up and clarify this
. When they do the ‘wrong’ thing, they are punished by withdrawal of love, leaving them to see the world as confusing and dangerous
. This leads to the development of symptoms such as paranoid delusions and disorganised thinking

32
Q

What is Expressed Emotion?

A

. The level of emotion, particularly negative emotion, expressed towards a person by carers/family members
. It includes verbal criticism of the individual, occasionally accompanied by violence…hostility towards the person, including anger and rejection…and emotional overinvolvement in the life of the person, including needless self-sacrifice
. High levels of expressed emotion cause high levels of stress
. This explanation is typically used to explain relapses in people who already have schizophrenia
. However it has also been suggested the stress can trigger the onset of schizophrenia in someone already vulnerable to schizophrenia

33
Q

What are some strengths of family dysfunction explanations of schizophrenia?

A

+ Research support for the link between family dysfunction and schizophrenia - Indicators of family dysfunction include insecure attachment and exposure to childhood trauma, especially abuse. Read et.al (2005) suggested that adults with schizophrenia are disproportionately likely to have an insecure attachment. The research also reported that 69% of women and 59% of men with schizophrenia have a history or physical/sexual abuse. This strongly suggests that family dysfunction makes people more vulnerable to schizophrenia.

34
Q

What are some limitations of family dysfunction explanations of schizophrenia?

A
  • Poor evidence base - There is strong evidence to suggest a link between family-based stress and adult schizophrenia, but a lack of evidence to link schizophrenia and traditional family-based theories, such as the schizophrenogenic mother and double bind explanation. Both of these theories are based on clinical observations of patients and informal assessments of mothers’ personalities. but not on systematic evidence. This means that family explanations cannot account for the link between childhood trauma and schizophrenia.
  • Socially sensitive topic - can be seen to blame parents for schizophrenia, especially mothers (which could also link to gender bias).
  • Schizophrenogenic mothers - Problems with cause and effect. Mishchler and Waxler (1968) found significant differences between the ways that mothers spoke to their schizophrenic daughters and their normal daughters. This suggests that the dysfunctional communication associated with the schizophrenogenic mother explanation may be a result of having schizophrenia, rather than a cause.
35
Q

What is meant by cognitive explanations for schizophrenia?

A

Explanations which focus on mental processes such as thinking, language and attention. Schizophrenia is associated with several forms of dysfunctional thought processing

36
Q

What are the 3 cognitive explanations for schizophrenia?

A

. Dysfunctional thinking
. Metarepresentation dysfunction
. Central Control dysfunction

37
Q

What is dysfunctional thinking?

A

Schizophrenia is characterised by a disruption to normal thought processing.
Reduced thought processing in the ventral striatum is associated with negative symptoms
Reduced processing of information in the temporal and cingulate gyri is associated with hallucinations (Simon et.al 2015)
This abnormal level information processing suggests cognition is likely to be impaired

38
Q

What is metarepresentation dysfunction?

A

Frith et.al (2002) identified two types of dysfunctional thought processes - the first is metarepresentation
Metarepresentation is the cognitive ability to reflect on your own thoughts and behaviours , and to interpret the actions of others
Dysfunction in metarepresentation can cause a person to not recognise their thoughts and behaviours as their own - they see them as been carried out by someone else
This explains hallucinations and delusions such as thought insertion

39
Q

What is central control dysfunction?

A

Frith et.al (2002) also identified issues with the cognitive ability to supress automatic responses when performing deliberate actions
Speech poverty and thought disorder could result from the inability to supress automatic thoughts and speech - this can explain derailment of thoughts, because each word triggers associations and the individual cant supress automatic responses to these

40
Q

What are some strengths of cognitive explanations of schizophrenia?

A

+ Research support for dysfunctional thought processing - Stirling et.al (2006) compared the performance of 30 people with schizophrenia and 30 people without on various cognitive tasks. This included the Stroop test, where participants are required to say the font colour of a word, rather than the word itself, which would be a colour (eg. the word red written in orange - pps would have to say orange). People with schizophrenia took 2x as long to name the font colour than the control group, suggesting a difficulty suppressing automatic thoughts. This supports the idea of the cognitive processes of people with schizophrenia being impaired.
+ Practical benefits - Yellowless et.al (2002) developed a machine which produces virtual hallucinations, with the intention of showing schizophrenics that their hallucinations aren’t real. The existence of this suggests that understanding the effects of cognitive dysfunctions can allow for new methods of treating or managing schizophrenia.

41
Q

What are some limitations of cognitive explanations of schizophrenia?

A
  • Cognitive explanations only address the proximal origins of symptoms - They address what is happening currently to produce symptoms, but do not explain what initially caused schizophrenia (a distal explanation). Cognitive theories alone only provide partial explanations for schizophrenia, which could lead to the acceptance of genetic and family dysfunction explanations over cognitive, as they are more complete (both are distal explanations)
  • Reductionist approach - doesn’t consider other factors such as genes
42
Q

What is Biological therapy for schizophrenia?

A

The biological approach to treating schizophrenia involves the use of drugs, in particular antipsychotics. They aim to reduce the severity of the symptoms of psychotic disorders (psychosis=losing some contact with reality)

43
Q

Describe the use of antipsychotic medication

A

Antipsychotics may be used in the short or long term - some people may use a short course and stop without the return of symptoms, other people may require them for life to prevent a relapse of schizophrenia. There are two types of antipsychotic - typical and atypical

44
Q

When were typical antipsychotics introduced?

A

1950’s - however typical prescribed doses have declined over the last 50 years (Liu and de Haan 2009)

45
Q

What are some examples of typical antipsychotics?

A

Chlorpromazine and Haloperidol

46
Q

What are typical antipsychotics?

A

. Dopamine antagonists - There is a strong association between the use of typical antipsychotics and the dopamine hypothesis. They work by acting as dopamine antagonists - by blocking dopamine receptors (eg. D2 receptors in the mesolimbic pathway) in the synapses of the brain, in turn reducing dopamine levels. This aims to normalise neurotransmission in key areas of the brain, reducing symptoms such as hallucinations. It reduces the intensity of positive symptoms
. Sedation effects - chlorpromazine has a powerful sedative effect, and is often used to calm individuals with schizophrenia, especially when hospitalised
. Includes drugs such as chlorpromazine - can be taken as tablets, syrup or by injection. For most people the dosage is increased gradually throughout treatment from 400mg to 800mg

47
Q

When were atypical antipsychotics introduced?

A

1970’s

48
Q

What are atypical antipsychotics?

A

. Developed with the aim of maintain/improve the effectiveness of typical antipsychotics while also minimising side effects
Common types of atypical antipsychotics are Clozapine and Risperidone

49
Q

What is Clozapine?

A

. Developed in the 1960’s - however it was initially recalled as it was linked to deaths from a blood condition called agranulocytosis
. It was reintroduced, but requiring regular blood tests to ensure the patient is not developing agranulocytosis
. Daily dosage is 300 to 450mg a day, and it is not available as an injection
. Clozapine is similar to chloropromazine in that it binds to dopamine receptors, but it also acts on seratonin and glutamate receptors
. This is believed to help improve mood and reduce depression and anxiety in patients. This in turn improves cognitive functioning
. The mood enhancing effects of clozapine means it is sometimes prescribed for individuals at risk of suicide - 30-50% of people with schizophrenia

50
Q

What is Risperidone?

A

. Developed in the 1990’s
. Designed to be as effective as Clozapine but without its serious side effects
. It can be taken as tablets, syrup or an injection. Typical dosage increases from 4-8mg with a maximum of 12mg
. It is believed to bind to dopamine and serotonin receptors, but binds more closely to dopamine receptors than clozapine, so is effective in smaller doses

51
Q

What are some strengths of drug therapy?

A

+ Evidence to support the effectiveness of antipsychotics - Thornley et.al (2003) reviewed studies comparing the effects of chlorpromazine and control conditions. Data from 13 trials with 1121 participants showed that chlorpromazine was associated with better overall functioning and reduced symptom severity than with a placebo. In terms of atypical antipsychotics, Meltzer (2012) concluded that clozapine is more effective than typical antipsychotics and other atypical antipsychotics, effective in 30-50% of treatment-resistant case where typical antipsychotics failed. This demonstrates a strong evidence base in support of drug therapy
—- COUNTER —- Healy (2012) suggested serious flaws within this evidence. Most studies only assess short term effects, so limited examples are available of whether antipsychotics are effective in reducing symptom severity in the long term. Also, some successful trials have had their findings republished multiple times, exaggerating the evidence base for the benefits of antipsychotics beyond the reality of how positive they actually are

52
Q

What are some limitations of drug therapy?

A
  • The likelihood of side effects - Typical antipsychotics are associated with a range of side effects, including dizziness, agitation, sleepiness, stiff jaw, and weight gain. Long-term use can also result in tardive dyskinesia, caused by dopamine supersensitivity. This involves involuntary face movements, such as grimacing and blinking. The most serious side effect, which is more common in typical antipsychotics, is Neuroleptic Malignant Syndrome (NMS), which is believed to occur when the drug blocks dopamine action in the hypothalamus. It results in high temperatures, delirium, comas, and even death. This may mean that the risks of antipsychotics outweigh its benefits, making it an ineffective treatment, as it may do little to improve quality of life, or be avoided entirely.
  • Ethical concerns - Moncrieff (2013) suggested than antipsychotics have been used in hospital situations to calm people with schizophrenia in order to make them easier to deal with - to the benefit of staff, rather than to the patient. This is a serious ethical concern, and abuse of human rights, with some critics even comparing antipsychotics to straightjackets.
  • Problems with the efficacy of atypical antipsychotics - Kahn et.al (2008) found that antipsychotics are generally effective for at least one year, but that second generation drugs were no more effective than first-generation ones.
53
Q

What are the two types of psychological treatment for schizophrenia?

A

. Cognitive Behavioural Therapy
. Family Therapy

54
Q

What is Cognitive Behavioural Therapy?

A

. Aims to deal with both thoughts and behaviour, by challenging negative cognitions and creating behavioural techniques
. CBT can help individuals with schizophrenia to understand their irrational cognitions, such as hallucinations and delusions, and how these impact their behaviour
. It doesn’t get rid of the symptoms of schizophrenia, but helps people cope with them, reducing their distress and improving their ability to function adequately
. Reality testing - process of challenging delusions by the therapist and patient jointly examining the likelihood that their delusions are true. Even when delusions are resistant to reality testing, CBT can be used to deal with the anxiety and depression part of living with schizophrenia
. Normalisation - Helps auditory hallucinations by convincing the patient that hearing voices is an extension of the ordinary experience of thinking in words.
.

55
Q

What are some strengths of CBT?

A

+ Evidence of the effectiveness of CBT as a treatment for schizophrenia - Jauhar et.al (2014) reviewed 34 studies in which CBT was used to treat schizophrenia. Evidence was found for small but significant effects on both positive and negative symptoms. Pontillo et.al (2016) found reductions in the frequency and severity of auditory hallucinations. Clinical evidence from NICE (2019) recommends CBT for schizophrenia. This supports the use of CBT, with both research and clinical experience demonstrating its benefits.

56
Q

What are some limitations of CBT?

A
  • Concerns over the quality of evidence - A wide range of techniques and symptoms have been included in research into CBT, with studies varying widely from one another. Thomas (2015) pointed out that different studies involve different methods of approaching the therapy, and patients with differing combinations of positive and negative symptoms. The overall benefits of CBT are modest, and likely conceal a variety of different methods on different symptoms. This uncertainty makes it difficult to assume how effective CBT will be as a treatment for a particular person, limiting its generalisability and applicability as a treatment method.
  • May be ineffective as a treatment - CBT requires self-awareness and willingness to engage, both of which may be limited by the nature of schizophrenia eg. symptoms such as avolition and delusions
57
Q

What is Family Therapy?

A

. Involves the identified patients and their families
. The therapy aims to improve the quality of communication and interaction between family members, in line with psychological explanations such as the schizophrenogenic mother
. Pharoah et.al (2010) Identified a range of strategies used by therapists to improve family functioning:
- Reduces negative emotions - Family therapy aims to reduce levels of expressed emotion - reducing general levels of emotions, but in particular negative levels of emotion, such as anger and guilt which create stress (reducing stress helps reduce the likelihood of relapse)
- Improve the family’s ability to help - The therapist encourages the family to form a therapeutic alliance. In this, they all agree on the aims of therapy, the therapist attempts to improve the families beliefs about schizophrenia, and they aim to ensure a balance between the family members caring for the individual and maintaining their own lives

58
Q

What is meant by a ‘model of practice’?

A

Burbach (2018) proposed a model for working with families dealing with schizophrenia.
Phase 1 - sharing basic information and providing emotional and practical support. It then develops progressively through deeper levels.
Phase 2 - involves identifying recourses, including what family members can and cannot 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 skills training eg. learning stress management techniques.
Phase 6 - looks at relapse prevention planning.
Phase 7 - maintenance for the future.

59
Q

What are some strengths of Family Therapy?

A

+ Evidence for the effectiveness of family therapy as a treatment for schizophrenia - In a review of studies, McFarlane (2016) concluded that family therapy was one of the most consistently effective treatments for schizophrenia. Relapse rates were found to be reduced by 50-60% in most cases. McFarlane also concluded that using family therapy as mental health initially starts to decline is especially effective. Anderson et.al (1991) found a relapse rate of almost 40% when patients used drugs only, compared to 20$ when family therapy or social skills training were used. NICE recommends family therapy for everyone with a diagnosis of schizophrenia. Family therapy appears to be an effective treatment, with practical benefits to people with both early and ‘full-blown’ or long term schizophrenia
+ Has benefits for all family members, not just the sufferer - Lobban and Barrowclough (2016) concluded that the effects of family therapy on the family of the identified patient are vital as they provide the bulk of care. By strengthening the functioning of the family, the negative impacts of schizophrenia are lessened, and their ability to support the patient is strengthened. This can also help reduce the likelihood of a relapse.
Not only is family therapy a beneficial treatment for the immediate sufferer, but it also has wider benefits for the family.
+ Economic benefits - Strengthening family functioning enables the family to provide the bulk of care for the patient. This means the state does not have to contribute as much to treatment as in CBT or drug therapy.

60
Q

What are some limitations of Family Therapy

A
61
Q

What are Token economies?

A

A form of behavioural modification, where desirable behaviours are encouraged by the use of selective reinforcement.
In terms of schizophrenia, it is commonly used in the case of institutionalised patients (especially those who have developed patterns of maladaptive behaviours from spending long periods in psychiatric hospitals), in order to manage their behaviours.
Token economies were used extensively in the 1960’s and 1970’s when the norm for treating schizophrenia was long-term hospitalisation. In the UK, use has now declined, partially because of a growth in community-based care, and partially because of complex ethical issues raised by restricting pleasures and rights for patients.

62
Q

What did Ayllon and Azrin (1968) find about token economies?

A

Ayllon and Azrin trialled a token economy system in a ward of female schizophrenia patients. Every time patients carried out a task, such as making their beds or cleaning up, they were given a plastic token. These tokens could then be swapped for ward privileges eg. being able to watch a film. The number of desirable tasks being carried out increased significantly.

63
Q

What is Institutionalisation?

A

Develops following periods of prolonged hospitalisation. It can lead to the development of bad habits, such as poor hygiene and inability to socialise.
Matson et.al (2016) identified 3 categories of institutional behaviour commonly tackled by token economies: personal care, condition-related behaviours eg. apathy, and social behaviour

64
Q

What is the rationale behind token economies?

A

Modifying institutional behaviour does not cure schizophrenia, but has two major benefits:
. Improves the individuals quality of life within the hospital setting eg. makeup for someone who normally takes pride in their appearance
. ‘Normalises’ behaviour, making it easier for patients to adapt back into everyday life and their communities

65
Q

How do token economies work?

A

The idea is that tokens are given immediately to individuals who have carried out a desirable behaviour. They can then be swapped out for a real, tangible reward. Having an immediate reward is important as delayed rewards are less effective.
Target/desirable behaviours are decided on an individual basis, and it is important to know the patient personally to decide on the most appropriate behaviours for them (Cooper et.al 2007)
Token economies are an example of behaviour modification (behavioural therapy based on operant conditioning). Tokens act as secondary reinforcers because they only have value once the individual exchanges them for rewards, which are primary reinforcers.
Tokens can also be exchanged for a range of different primary reinforcers. These are particularly powerful secondary reinforces, known as generalised reinforcers.
In order for the tokens to become secondary reinforcers, they are paired with primary reinforcers - at the start of a token economy programme, they are administered together.

66
Q

What are some strengths of token economies?

A

+ Research support for the effectiveness of token economies - 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. All studies showed a reduction in negative symptoms, and a decline in the frequency of unwanted behaviours. This supports the value of token economies.
—- COUNTER —- Limited evidence base due to the small size of the sample, so problems with generalisability. Also, the small sample size could reflect the file drawer problem (where studies with undesirable findings are ‘filed away’), which leads to a bias towards positive published findings.

67
Q

What are some limitations of token economies?

A
  • Ethical issues - The use of token economies gives professionals considerable power to control the behaviour of patients. It involves imposing one individuals or one institutions norms onto others, which can result personal freedoms being restricted unnecessarily. Also, restricting the availability of pleasures, so that they are only used as a form of reward, worsens the quality of life of patients who are already experiencing a distressing situation. This has even resulted in legal action by family members of institutionalised patients, showing the severity of this concern. Additionally, the use of token economies could result in discrimination, as severely ill patients may be less able to engage in desirable behaviours, so do not receive rewards, while more moderately ill patients can perform desirable behaviours so are rewarded. The benefits of token economies may be outweighed by their impact on personal freedoms and quality of life.
  • Other, more ethical alternatives - Chiang et.al (2019) concluded that art therapy may be a good alternative to token economies, as it appears to be a high-gain, low-risk substitute. It is a pleasant experience, without the major risks of ethical abuses. NICE guidelines recommend art therapy for schizophrenia. As such, token economies may not be the best treatment for schizophrenia.
68
Q

What is the interactionist approach to explaining schizophrenia?

A

An approach which acknowledges that there a biological, psychological and social factors involved in the development of schizophrenia. Biological factors can include genetic vulnerability and neurochemical and neurological abnormalities. Psychological factors include stress eg. from life events and social factors eg. poor quality interactions within the family.
A key aspect of the approach is the diathesis-stress model

69
Q

What is the diathesis-stress model?

A

. Diathesis - vulnerability
. Stress - negative experience
. The diathesis-stress model suggests that both an existing vulnerability to schizophrenia and a stress-trigger are necessary to develop the disorder.
. Underlying factors make the individual vulnerable to developing schizophrenia, but the onset of the condition is triggered by stress

70
Q

What was Meehl’s (1962) original diathesis-stress model?

A

Meehl’s original diathesis-stress model (1962) - suggests that the diathesis aspect is entirely genetic, the result of a particular ‘schizogene’.
This led to the idea of a biologically based schizotypic personality - one characteristic of which is sensitivity to stress. According to Meehl, if someone doesn’t have the schizogene then no amount of stress will result in schizophrenia.
However in carriers of the gene, chronic childhood/adolescent stress, such as having a schizophrenogenic mother, can result in the development of the disorder

71
Q

What is the modern understanding of diathesis?

A

. Diathesis:
. Many genes each appear to increase genetic vulnerability slightly, rather than one single ‘schizogene’ (Ripke et.al 2014)
. The modern view also considers a range of factors as the diathesis (vulnerability) beyond genetic, including psychological trauma (Ingram and Luxton 2005).
. Read et.al (2001) proposed a neurodevelopmental model, in which early trauma affects the developing brain. Severe, early trauma (such as child abuse) can affect several areas of brain development, such as hypothalamic-pituitary-adrenal (HPA) system (which controls how the body responds to a chronic stressor). This can become overactive, making a person more vulnerable to later stress

72
Q

What is the modern understanding of stress?

A

. Psychological stress is still considered important, as in the Meehl’s original model, but it is not the only stressor
. The modern definition of stress includes anything that risks triggering schizophrenia (Houston et.al 2008)
. For example, the use of cannabis has been suggested as a stressor, as research suggests that increases the risk of schizophrenia by up to 7x according to dose. This may be because cannabis interferes with the dopamine system

73
Q

How does the interactionist model suggest schizophrenia can be treated?

A

. The interactionist model acknowledges both biological and psychological factors, so is compatible with both biological and psychological treatments
. The model is associated with combining antipsychotic medication and psychological therapies, such as CBT
. Turkington et.al (2006) - said that it was possible to accept biological explanations for schizophrenia and use CBT to relieve symptoms, provided an interactionist model is adopted.

74
Q

What are some strengths of the interactionist approach to explaining schizophrenia?

A

+ Evidence for the role of both vulnerability and stressors/triggers - Tienari et.al (2004) investigated the impact of genetic vulnerabilities and psychological triggers (in the form of dysfunctional parenting). The study followed 19,000 Finnish children whose biological mothers had been diagnosed with schizophrenia. In adulthood, this high genetic risk group were compared with a low risk control group, without a family history of schizophrenia. Adoptive parents were assessed for child rearing style, and it was found that high levels of criticism and hostility, and low levels of empathy, were strongly associated with the development of schizophrenia, but only in the high risk group. This supports the idea that a combination of genetic vulnerability and family stress can lead to increased risk of developing the disorder, strengthening the validity of the approach.

75
Q

What are some limitations of the interactionist approach to explaining schizophrenia?

A
  • The original explanation is too simplistic - diathesis and stress are complex - Meehl’s original model portrayed diathesis as a single schizogene, and stress as schizophrenogenic parenting. However later research has suggested that multiple genes in combination are responsible for genetic vulnerability. Also, diathesis can be influenced by psychological factors, and stress by biological. This was shown in a study by Houston et.al (2008).
76
Q

What are some strengths of the interactionist approach to treating schizophrenia?

A

+ The interactionist approach allows for a combination of biological and psychological treatments, which has real world benefits - Studies suggest that combining treatments enhances their effectiveness. Tarrier et.al (2004) randomly allocated 315 participants to one of three conditions. (1) medication and CBT, (2) medication and counselling, and (3) medication only. Participants in the two combination groups showed reduced symptoms after the trial than the medication only group. This shows that there is a clear practical advantage to adopting an interactionist approach to treating schizophrenia, as it provides superior treatment outcomes
—- COUNTER —- Jarvis and Okami (2019) point out that saying a successful treatment outcome justifies an explanation is equivalent to saying alcohol reduces shyness, so shyness causes alcohol (treatment-causation fallacy). The success of combined treatments does not prove that an interactionist approach is correct.
+ Holistic approach - It identifies that schizophrenia has several roots and triggers eg. genes providing a wider explanation. It also means that different treatment options can be considered.
+ Research support for the ‘stress’ aspect of the model - Vasos (2012) found that the risk of developing schizophrenia was 2.37 times greater in cities than in the countryside, which has been linked to stress levels. Pederson and Mortensen (2001) found Scandinavian villages had low levels of psychosis, but there was an increased risk after 15 years of living in a city. Also, Fox (1990) suggested that factors associated with living in poorer conditions, such as stress, can trigger the onset of schizophrenia. Finally, Bentall (2012) conducted a meta-analysis and found that stress arising from abuse in childhood increases the risk of developing schizophrenia.