Paper 3 - Schizophrenia Flashcards

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1
Q

What is schizophrenia?

A

Schizophrenia is a mental disorder characterised by profound disruption of cognition and emotion. It is a type of psychosis in which thoughts and emotions are severely impaired.

Schizophrenia affects an individuals perceptions, emotions, language and sense of self.

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2
Q

How is sz diagnosed?

A

Schizophrenia affects approximately 1% of the population. It is most frequently diagnosed in individuals who are in late adolescence/early adulthood and is more commonly diagnosed in men.

Schizophrenia is diagnosed using the Diagnostic Statistical Manual of Mental Health, volume 5 (DSM-5) in the US. The DSM is a manual which is used to diagnose mental illnesses. It contains over 200 mental disorders and their common features group them together. In Europe, the International Classification of Diseases 10 (ICD- 10) is used.

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3
Q

What are the two types of symptoms?

A

Positive symptoms are symptoms which reflect an excess or distortion of normal functioning. These are symptoms which a patient ‘gains’ rather than something which is lost or damaged.
E.g. hallucinations (hearing voices) , delusions (irrational beliefs).

Negative symptoms reflect a reduction or loss of normal/ordinary functioning. These often persist even in absence of positive symptoms. E.g. speech poverty (reduction in amount and quality of speech), avolition (inability to begin or maintain goal orientated activity)

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4
Q

What is the difference between a hallucination and delusion?

A

Hallucinations are unusual sensory experiences that can relate to all senses. Can be linked to what is happening in the environment or completely unrelated. May distort what is actually there eg warping of faces, or the sound or visual hallucination may not be there at all.

Delusions are firm but false beliefs that can take many forms. Eg delusions of grandeur or paranoid delusions

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5
Q

Define the purpose of DSM and ICD

A
  • Diagnostic systems.
  • List symptoms needed for diagnosis of particular disorders.
  • Promote objectivity to allow clinicians to diagnose and ensure appropriate treatment.
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6
Q

DSM-5 criteria for diagnosis

A

Criteria A:
TWO or more of the following symptoms;
1. Delusions
2. Hallucinations
3. Disorganised speech
4. Grossly disorganised or catatonic behaviour
5. Negative symptoms e.g. avolition, alogia, affect flattening.

Criteria B :
Social/ occupational dysfunction.
Problems affecting work, personal relationships or even self-care.

Criteria C:
Duration needs to be approx. 6 months of disturbances with at least 1 month of symptoms from criteria A.

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7
Q

Differences between DSM-5 and ICD 11

A

ICD can make a diagnosis of Sz on 2 negative symptoms (DSM requires at least 1 positive).

ICD recognises different subtypes of Sz (DSM used to but dropped them in DSM-5).

These differences suggest lack of consistency and agreement on what schizophrenia is.

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8
Q

What is the purpose of classification systems?

A

A good classification system should help professionals to diagnose Sz and suggest treatment to alleviate symptoms.
It should be reliable: ► consistent
It should be valid: ► measure what it claims to
If a diagnosis is not reliable, it cannot be valid.

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9
Q

Define the two types of reliability: inter-rater & test re-test

A

Inter-rater reliability:
(Consistency between two different clinicians).
If two different psychologists were given the same set of symptoms they should give the same diagnosis.

Test re-test reliability:
(Consistency over time).
Person presenting the same set of symptoms would receive the same diagnosis on different occasions.

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10
Q

Evidence to show reliability in diagnosis of schizophrenia

3 studies

A

Rosenhan (1973):
Rosenhan sent 8 normal people to different hospitals all claiming that they had been hearing voices.
All people were admitted to hospital- 7 were diagnosed with sz and 1 with bipolar.
He then said he would be sending more ‘pseudo-patients’
The hospital discovered 41 fakes- Rosenhan revealed that he didn’t actually send any.

Copeland (1971):
Gave a description of a schizophrenic patient to 134 and 194 British psychiatrists. 69% of US diagnosed them with sz. However, only 2% of British diagnosed them with sz.

Cheniaux et al (2009):
2 psychiatrist independently diagnosed 100 patients using DSM & ICD. Inter-rater reliability was very poor. One psychologist diagnosed 26% with s according to DSM and 46% according to ICD. However, the other psychologist diagnosed 13% using DSM and 24% using ICD. this poor reliability is a weakness of diagnosis of sz.

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11
Q

Why is poor reliability in diagnosis a problem for patients?

A

Poor reliability is a problem because patients might be diagnosed with sz by one doctor but not by another. This means that they aren’t sure who is right and find it harder to seek help with their illness.

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12
Q

Reliability in diagnosis and classification of sz evaluation

A
  • Rosenhan
  • Copeland
  • Cheniaux
    + Reliability of diagnosis has improved. critics argue that we shouldn’t generalise from research findings because diagnosis in research scenarios may not reflect diagnoses made in day to day assessments. However, inter-rater reliability is strengthened using standardised assessments to help promote objectivity and consistent from one patient to another and one psychiatrist to another.
    Jakobsen et al (2005) used ICD 10 with 100 patients and found a concordance rte of 98% in diagnosing sz.
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13
Q

Define validity

A

Validity is the extent to which we are measuring what we are intending to measure.

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14
Q

Define 4 factors affecting validity

A

Co-morbidity - When two or more conditions occur together. If conditions occur together a lot we question the validity of their diagnosis because they might actually be a single condition.

Cultural bias - The tendency to judge all people in terms of your own cultural assumptions. For example, African Americans are several times more likely than white people to be diagnosed with sz. This is not due to genetics but due to cultural beliefs. E.g. hearing voices is acceptable in African cultures.

Gender bias - treating men and women the same. However, female patients tend to function better than men, they are more likely to work and have good relationships. This might be why some women haven’t been diagnosed but men with similar symptoms have been.

Symptom overlap - This occurs when two or more conditions share symptoms. When two conditions have many of the same symptoms this calls into question whether we should classify the two disorders separately.

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15
Q

Validity of diagnosis and classification of sz evaluation

A

1) Research has shown that symptom overlap is a problem in the diagnosis of sz. There is overlap between the symptoms of sz with other symptoms. Sz and bipolar have shared positive and negative symptoms. Under ICD a patient might be diagnosed with sz; however they could be diagnosed with bipolar according to DSM. This questions the validity of the disorders, it suggests that sz and bipolar are one condition not separate.
2) sz is commonly diagnosed with other conditions. Peter Buckley (2009) concluded that around half of patients with a diagnosis of sz also have a diagnosis of depression. This poses a challenge for the classification and diagnosis of sz.
3) Research has shown that cultural bias is a problem in the diagnosis of sz. One issue is that positive symptom such as hearing voices may be more acceptable in African cultures because of cultural beliefs, and thus people are more ready to acknowledge such experiences. When reported to a psychiatrist of a different culture these experiences are more likely to be seen as irrational.

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16
Q

Summarise Gottesman study

A

Gottesman found that the closer you are in relatedness to a schizophrenic person, the more likely you are to develop the illness.

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17
Q

Summarise genetics as a biological explanation of Sz

A

When examining genetics in sz we look at:

  • Family studies
  • Adoption studies
  • Twin studies

These studies allow us to examine the influence of genes and whether sz is inherited. The research indicates that the concordance rate of sz increases with closer genetic relatedness to someone with the illness. Gottesman looked at this between families and found a concordance rate 49% for both parents with sz, 13% for one parent with sz and 9% for siblings.

Tienari et al found that Children of parents with a diagnosis of Sz are still at higher risk of developing Sz when adopted into families with no history of the disorder.

Looked at 164 adoptees who biological mothers were diagnosed with Sz, and 197 controls born to mothers without diagnosis of Sz.
11 adoptees (6.7%) developed Sz compared to 4 (2%) of the control adoptees.

Ripke: Because several candidate genes offer a small increased risk of Sz, it is suggested that it is polygenic ie: that a number of genes work together in Sz.
Ripke looked at data from studies that looked at the whole human genetic make up (not just particular genes for Sz).
They compared 37,000 patients to 113,000 controls.
Ripke found that Sz is aetiologically heterogeneous -
108 different genetic variations are linked with increased risk of Sz.
These included genes linked with neurotransmitters eg dopamine.

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18
Q

Genetics as a biological explanation of sz

A

+ Research findings using a range of different methods support a genetic influence to Sz.
+ Ripke’s research uses a large sample of 37,000 to identify a polygenic role. This allows us to generalise with greater confidence.
- No research has found that genetics has a soley genetic basis, other factors are involved.
- Causes of Sz remain complex eg the polygenic basis makes it harder to identify causal factors in Sz,
Eg some people develop Sz when there is no family history of the disorder eg mutation of DNA in sperm through radiation, poison or viral infection.

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19
Q

What are neural correlates?

A

Neural correlates are measurements of the structure or function of the brain that correlate with a particular experience.
In schizophrenia both positive and negative symptoms have correlates.

The dopamine hypothesis can be used as a neural correlate of Sz.

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20
Q

Summarise key features of the dopamine hypothesis

A

Dopamine is a neurotransmitter (chemical messenger) involved in several brain systems, it appears to be involved in Sz.

It has been suggested that both too little or too much dopamine might be associated with symptoms of Sz and that this may depend on the area of the brain involved.

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21
Q

Differences between hyperdopaminergia and hypodoperminergia

A

Hyperdopaminergia concerns high levels of dopamine activity. Area of the brain involved: subcortex/central areas. Symptoms of Sz that may be involved: poverty of speech.

Hypodoperminergia concerns low levels of dopamine activity. Areas of the brain involved: prefrontal cortex. Symptoms of Sz that may be involved: negative symptoms.

22
Q

Describe neural correlates of negative and positive symptoms of Sz.

A

Neural correlates are measurements of the brain that link/ correlate with symptoms of Sz. These are correlates for positive and negative symptoms and we can study them using brain imaging techniques such as fMRI and EEG scans.

Neural correlates of negative symptoms:

  • The ventral striatum
  • Symptoms are avolition & loss of motivation
  • Juckel et al (2006)
  • Negative correlation between activity levels and severity of overall symptoms. Lower levels of activity in this area compared to controls.

Neural correlates of positive symptoms:

  • Superior Temporal Gyrus and Anterior Cingulate Gyrus
  • Symptoms are auditory hallucinations
  • Allen et al (2007)
  • Patients had to identify whether speech was theirs or someone else’s. Lower activity in these areas compared to controls.
23
Q

The dopamine hypothesis evaluation

A
  • One criticism of the dopamine hypothesis is there is a problem with the chicken and egg. Is the raised dopamine levels the cause of the schizophrenia, or is it the raised dopamine level the result of schizophrenia? It is not clear which comes first. This suggests that one needs to be careful when establishing cause and effect relationships in schizophrenic patients.
  • One of the biggest criticisms of the dopamine hypothesis came when Farde et al found no difference between schizophrenics’ levels of dopamine compared with ‘healthy’ individuals in 1990.
  • Noll (2009) also argues around one third of patients do not respond to drugs which block dopamine so other neurotransmitters may be involved.
  • A final weakness of the dopamine hypothesis is that it is biologically deterministic. The reason for this is because if the individual does have excessive amounts of dopamine then does it really mean that they will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.
24
Q

Neural correlates of Sz evaluation

A

+ A strength is that the research neurotransmitter levels have high reliability. The reason for this is because the research is carried out in highly controlled environments, which specialist, high tech equipment such as MRI and PET scans. These machines take accurate readings of brain regions such as the frontal and pre-frontal cortex, the basil ganglia. This suggests that if this research was tested and re-tested the same results would be achieved.

25
Q

Discuss drug treatments for Sz

A

The dopamine hypothesis has linked levels of dopamine with symptoms of Sz. Therefore, drug treatment aims to alter dopamine levels in order to reduce symptoms.

The broad name for the drug used to treat symptoms of Sz is anti-psychotic.
These drug work by affecting D2 receptors in the brain.
There are two types of anti-psychotics:
1) Typical anti-psychotics - e.g. chloropromazine
2) Atypical anti-psychotics - e.g. clozapine, risperidone

Typical;
symptoms: reduce hallucinations
side effects: muscle stiffness

Atypical;
Symptoms: reduces anxiety in patients
Side effects: may develop blood disease

26
Q

Benefits and drawbacks of drug therapy

A

+ Typical antipsychotics: Thornley et al - review of choropromazine- examined effects of chorpromazine by making comparisons to controls who received a placebo. Total of 13 trials with 1121 Ps showed the drug associated with reduced severity of symptoms and better overall functioning. Choropromazine was also associated with a lower relapse rate.
+ Atypical antipsychotics: Meltzer (2012) - concluded that clozapine was - more effective than both typical antipsychotics and other atypical antipsychotics, effective in 30-50% of treatment resistance cases where typical antipsychotics have been ineffective.
- Likelihood of side effects. Typical antipsychotic drugs have side effects such as sleepiness, dizziness. The most serious side effect is NMS. This is because typical antipsychotics block dopamine action in the hypothalamus. NMS results in high temperature, coma and can be fatal.
- Antipsychotics have been used in hospitals to calm patients and make it easier for workers, rather than for the benefits of the patients.This could be argued as a human rights abuse.

27
Q

Psychological explanation of Sz: Schizophrenogenic mothers

A

Fromm-Reichmann looked at the backgrounds and childhood of her patients using a psychodynamic perspective. She found that patients experiencing symptoms of Sz often had schizophrenogenic mothers.

Characteristics include: cold, rejecting and controlling, tension, secrecy

This leads to: distrust

Develops into: paranoid delusions –> schizophrenia

28
Q

What are the 3 key features of the psychological explanation of schizophrenia - family dysfunctions?

A

1) Schizophrenogenic mothers
2) Double-binds
3) Expressed emotion

29
Q

Psychological explanations of Sz: Double-Binds

A

Bateson outlined double bind communication as a risk factor in Sz (mixed messages). Children fear they’re doing the wrong thing, and feel unable to comment on the situation or ask for clarification. If the child gets something wrong they are punished by withdrawal of love. Associated Symptoms of SZ: Feel the world is confusing and dangerous, may show disorganised thinking and paranoid delusions.

Lidz - came up with two key types of double blind communication between parents which could influence a child to develop Sz:

Martial Schism - parents emotionally distant, neither parents compromise, may be in competition for children’s attention

Martial Skew - One parent is dominant, the other submissive

30
Q

Psychological explanations of Sz: Expressed Emotion (EE)

A

EE refers to the level of emotion shown to a patient by their carers.

This explanation suggests that high levels of negative expressed emotion act as a serious source of stress for patients.

Key aspects of Negative EE:
Verbal criticism sometimes with violence
Hostility toward patient including anger and rejection
Emotional over involvement including needless self sacrifice

The EE explanation is mainly used to explain relapse of Sz (high levels of EE cause serious levels of stress).
It might explain onset because the source of stress can act as a trigger to someone who has a genetic vulnerability.

31
Q

Family dysfunction evaluation

A

+ There is evidence to suggest that difficult family relationships in childhood are associated with increased risk of Sz in adulthood. Read et al reviewed 46 studies of child abuse and Sz and concluded that 69% of adult woman patients had a history of physical or sexual abuse in childhood. For men the figure was 59%. Thus, there is evidence to link family dysfunction with Sz.
+ A strength of research into expressed emotion (EE) is that it has practical applications. For example Hogarty (1991) produced therapy session, which reduced social conflicts between parents and their children which reduced EE and thus relapse rates. This suggests that gaining an insight into family relationships allows psychiatric professionals to help improve the quality of patient’s lives.
- Family explanations for Sz have led to parent-blaming. Parents, who have suffered enough, underwent further trauma by receiving the blame for their child’s condition. This is no longer seen as appropriate as parent’s are a key part of care.
- There is almost no evidence to support the importance of schizophrenogenic mother or double blind. Both these theories are based on clinical observations of patients, and assessing mothers of patients for ‘crazy-making characteristics’.

32
Q

Psychological explanations of Schizophrenia: Cognitive explanations of schizophrenia

A

The cognitive process focuses on mental processes. Sz is characterised by abnormal info processing.

Reduced processing in the ventral striatum is associated with negative symptoms of Sz. Whilst reduced processing in the Temporal and Cingulate Gyrus is associated with hallucinations.

Frith et al identified two kinds of dysfunctional thought processing:

1) Metarepresentation is the ability to reflect on thoughts and behaviour. Dysfunction affects ability to recognise who is carrying out our actions. This could explain thought insertion and hallucinations and delusions.
2) Central control is the ability to suppress automatic responses so we can carry out deliberate actions. Dysfunction could lead to disorganised speech and thought disorder because cannot suppress other thoughts interrupting.

Stirling et al (2006) - schizophrenics take twice as long on the Stroop test which highlights central control theory.
Shows that they process information in a different way to healthy controls.

33
Q

Cognitive explanations of Sz evaluation

A

+
+
-
-

34
Q

What is family therapy?

A

Family therapy is based on family dysfunction explanations of Sz, this therapy works on the basis that certain factors lead to symptoms of Sz, e.g. Double bind and negative EE.

It aims to involve families and improve quality of communication and interaction between family members in order to reduce stress that might lead to risk of relapse and reduce levels of negative EE.

35
Q

What strategies are used by family therapists?

A

1) Psychoeducation
2) Form an alliance with relatives and carers
3) Reduce emotional climate and burden of care
4) Enhance relatives ability to anticipate and solve problems.
5) Maintain reasonable expectations
6) Encourage relatives to set appropriate limits

36
Q

Family therapy study: Pharoah et al (2010)

A

Family therapy forms part of a treatment along with medication. Phoroah et al suggest that the reduction of stress and expressed emotion helps to increase compliance with medication. This helps to reduce relapse.

Phoarah et al conducted a meta-analysis of 53 studies of family therapy.

Findings:

  • Increased compliance with medication
  • Some improvement in social functioning but not much evidence of increased independent living
  • Reduction in relapse risk during treatment and up to 24 months after

Methodological problems:

  • Lack of random allocation in China - Wu et al suggested random allocation was not used
  • Observer bias - studies where no ‘blinding’ was used, observers know which group participants are in
37
Q

Family therapy evaluation

A

+ A study by Anderson et al. (1991) found a relapse rate of almost 40% when patients had drugs only, compared to only 20 % when Family Therapy or Social Skills training were used and the relapse rate was less than 5% when both were used together with the medication.
+ Economic Benefits: Family therapy is highly cost effective because it reduces relapse rates, so the patients are less likely to take up hospital beds and resources. Family therapy studies demonstrate that it was associated with significant cost savings when offered to patients alongside the standard care – Relapse rates are also lower which suggests the savings could be even higher.
+ Lobban (2013) reports that other family members felt they were able to cope better thanks to family therapy. In more extreme cases the patient might be unable to cope with the pressures of having to discuss their ideas and feelings and could become stressed by the therapy, or over-fixated with the details of their illness.
- Psychological treatments may improve quality of life, but don’t cure Sz. Biological treatments reduce the severity of symptoms. The failuire to cure Sz is a weakness of psychological treatments.

38
Q

What is CBT?

A
  • Cognitive Behavioural Therapy
  • CBT was created by Beck who suggested that psychopathological conditions are the result of faulty thinking and irrational beliefs
  • The aim of CBT is to identify the negative/ irrational thoughts and then discuss them
  • The therapist helps the patient consider realistic or alternatives to their faulty beliefs

Examples of challenging irrational beliefs:
- “If you hear voices coming from the radiator, why can’t anyone else hear them?”

39
Q

How does CBT work for Sz?

A

The therapist helps the person to identify and challenge irrational beliefs through arguments and discussion. Talking about where symptoms come from can be helpful and reduce fear of hallucinations and learn that delusions are not based on reality. This reduces anxiety and stress

40
Q

Describe differences between CBT and another treatment

A
  • Medication is easier to give out
  • Medication may have side effects
  • CBT can be very upsetting and requires commitment
41
Q

CBT evaluation

A

+ NICE review of treatments for Sz found consistent evidence that CBT was found to be more effective in reducing symptom severity, CBT helped improve social functioning compared to people recieving standard care, CBT helped reduce hospitalisation for up to 18 months after ending treatment.
+ Tarrier (2005) reviewed trials of CBT, finding evidence of reduced symptoms, especially positive ones, and lower relapse rates.
- In the Uk only 1 in 10 get access to this therapy. Haddock found of 187 randomly selected patients diagnosed with Sz, only 13 have been offered CBT. Of those who were offered CBT, a significant number refused the treatment. This limits the effectiveness of the treatment.
- Unethical - involves challenging someone’s paranoia and this can be very upsetting to hear

42
Q

What are token economies?

A

Token economies are often used in institutions to encourage desirable behaviours, e.g. good hygeine, socialising, being independent. In order to improve quality of life and increase likelihood of living outside hospital.

43
Q

How are token economies used to manage Sz?

A
  • Desirable behaviour is identified e.g. making bed.
  • Immediate reward is given to patient when desirable behaviour has been carried out - immediacy of reward is important to prevent delay discounting (a reduced effect of reinforcement due to time delay).
  • The reward is in the form of tokens.
  • These can be swapped for tangible rewards, e.g. sweets.
  • According to operant conditioning, tokens are seen as secondary reinforcers because they have no monetary value and they only have value when the patient has learned they can be swapped for rewards.
44
Q

Token economy evaluation

A

+ Dickerson et al reviewed 13 studies - 11 reported beneficial effects.
+ Patients Behaviour becomes more socially acceptable promoting reintegration into society.
-There have also been ethical concerns as it is seen as manipulative. Although patients make the decision to comply with the scheme, They can have privilages taken away for not complying, e.g exercise.
- Ethical issues – Severely ill patients can’t get privileges because they are less able to comply with desirable behaviours than moderately ill patients – They may suffer from discrimination

45
Q

What is the interactionist approach to explaining Sz?

A

The interactionist approach is sometimes called the Bio-Social approach because it includes biological, psychological and societal factors.

Examples:
Biological - genetic vulnerability, neurochemical and neurological abnormality.
Psychological - stress, poor quality interactions in the family.
Societal - urbanisation

The diathesis stress model explains how factors interact to develop Sz. Diathesis (vulnerability), Stess (childhood trauma).

46
Q

Describe the old diathesis-stress model by Paul Meel (1962)

A

The role of genetics:
- Entirely genetic, the result of the schizogene.

Stressors:
- Meel says that if a person doesn’t have the schizogene no amount of stress will lead to Sz.

47
Q

Describe the modern Diathesis-stres model to Sz

A

The role of genetics:

  • Ripke et al (2014)
  • Many genes appear to increase genetic vulnerability, ‘there is no single schizogene’
  • Read et al:
  • Child abuse effects the brain
  • Hypothalamic-pituitary adrenal system can become over active making a person more vulnerable to later stress

Stressors:

  • Anything that risks triggering Sz
  • Cannabis is a stressor increases risk of Sz by 7 times because it interferes with the dopamine system. However, not everyone that smokes cannabis develops Sz so there must be vulnerability factors.
48
Q

Evidence to support the Diathesis-Stress explanation of Sz- Tienari et al

A

Aims: To investigate what the role genetic vulnerability has and what role parenting style as as a trigger.

Sample: Children adopted from 19,000 Finnish mothers with Sz between 1960 and 1979.

Method: Assessed adopted parents style of parenting. Looked at children’s rates of Sz and compared this to a control group of adoptees who had no genetic risk of Sz.

Findings: Found adoptees with high genetic risk of Sz, the parenting style was characterised by high levels of criticism and conflict, and low levels of empathy. This was not the case for the control group with no genetic risk of developing Sz.

Conclusion: Evidence suggests that genetic vulnerability and family related stress are triggers. Genetically vulnerable children are more sensitive to parenting behaviour.

49
Q

How is the interactionist approach applied to the treatment of Sz?

A
  • In the UK Anti psychotic drugs and CBT are combined
  • Psychological therapies are used when patients are using antipsychotic drugs
  • The approach to treatment in the US differs. Medication no therapy. This is because there has been greater conflict between biological and psychological approaches to treatment for Sz. As a result, the system in the US has been slower to adopt an interactionist approach.
50
Q

The interactionist approach evaluation

A

+ Holistic – Identifies that patients have different triggers, genes etc. – Patients can receive different treatments for their SZ which will be more effective.
+ Tienari - found that genetic vulnerability and family related stress are triggers.
- We still don’t fully understand the mechanisms by which the symptoms of Sz appear and how vulnerability and stress produce them.
- The original diathesis-stress model is oversimplified. There is no singe schizogenes, there are multiple genes that increase the vulnerability of Sz.