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Schizophrenia

Schizophrenia

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Schizophrenia

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  1. Schizophrenia

  2. Clinical Characteristics (Symptoms)

  3. Explanations – Biologicalvs Psychological Nature vs Nurture

  4. Diathesis Stress Model • No-one believes Schizophrenia is completely caused by either genes or the environment. • There must be an INTERACTION between the two. • Diathesis = Genetic tendency to develop schizophrenia. • Stress = Environmental “trigger” that starts it off.

  5. Diathesis Stress Model • Interesting Questions: • What is More important – nature or nurture? • How do we separate the effects of nature and nurture? (People who share genes tend to share the same environment)

  6. Biological Explanations Genetics Bio chemicals Brain Structure

  7. Genetics – Twin Studies(AO1) • Gottesman 1991 suggests that schizophrenia is inherited through genes. • QUESTIONS: • Why study identical twins? • What would you expect to find?

  8. Genetics – Family Studies(AO1) • Gottesman also concluded that if both your parents suffer from Schizophrenia, you have a 46% chance of developing it yourself (compared to a 1% chance of someone selected at random will suffer) • The more genetically similar relatives are, the more concordance is found.

  9. Schizophrenia: genetics www.psychlotron.org.uk Source: Gottesman (1991)

  10. Genetics – Adoption Studies(AO1) QUESTION: Why did Kety et al (1988) study adopted people with schizophrenia? He found: 14% biological relatives developed schizophrenia 2.7% adopted relatives developed schizophrenia QUESTION: what does this suggest?

  11. Miyakawa et al (2003) switched off an immune system gene in a mouse: What happened? How can this lead to new drug developments? Molecular Biology(AO1)

  12. Evaluating Genetic Explanations(AO2) • Make two evaluation points about: • Family Studies • Adoption Studies • Molecular Biology

  13. Biochemical Factors – The Dopamine Hypothesis This theory claims that excessive amounts of dopamine or an oversensitivity of the brain to dopamine is the cause of schizophrenia There are 3 pieces of evidence to support this: 1. Drugs which block dopamine (Phenothaiazines) reduce the symptoms of schizophrenia.

  14. The Dopamine Hypothesis - • 2. L-Dopa – a drug for Parkinson’s disease actually increases dopamine – this in turn can produce symptoms of schizophrenia. • 3. Post mortems of schizophrenics, show an increase of dopamine in parts of the brain. (Seeman 1987)

  15. Schizophrenia & dopamine • The dopamine hypothesis: • Schizophrenia is caused by excessive DA activity. • This causes abnormal functioning of DA-dependent brain systems, resulting in schizophrenic symptoms • DA can increase or decrease brain activity depending on the system you’re looking at psychlotron.org.uk

  16. The dopamine hypothesis • Wise & Stein (1973) report abnormally low levels of DBH in post-mortem studies of S patients • Would suggest abnormally high DA activity as DBH needed to break DA down • Can’t rule out cause of death or post-mortem changes as a source or error psychlotron.org.uk

  17. The dopamine hypothesis • Overdose of amphetamine (DA agonist) can produce S-like symptoms. S patients have abnormally large responses to low amphetamine doses • Suggests a role for DA in S symptoms • Suggests that the issue is over-sensitivity to DA rather than excessive DA levels psychlotron.org.uk

  18. The dopamine hypothesis • S symptoms can be treated with DA antagonists (e.g. chlorpromazine). These are effective in 60% of cases with more impact on positive symptoms. • Supports role of DA again, but what about 40% who don’t respond? • Lack of impact on negative symptoms hints at two separate syndromes psychlotron.org.uk

  19. Evaluating the Dopamine Hypothesis(AO2) • Write six evaluation points, examining the evidence on your handout.

  20. Brain Structure People with schizophrenia have abnormally large ventricles in the brain. Ventricles are fluid filled cavities. This means that the brains of schizophrenics are lighter than normal.

  21. Brain Structure Evidence • Andreasen et 1990 – conducted a controlled CAT scan study and found significant enlargement of the ventricles in schizophrenics compared to controls.

  22. Biological explanations • No one is sure if there are a range of different biological problems which together cause schizophrenia or if there are actually different types of schizophrenia which may have different causes.

  23. Two Syndrome Hypothesis - Crow 1985 – there maybe two different types! • Type one - genetically inherited associated with dopamine – characterised by positive symptoms. • Type Two – Neurodevelopmental disorder – to do with Brain structure – characterised by negative symptoms.

  24. Positive and Negative Symptoms • Positive - hallucinations, delusions, racing thoughts (high) • Negative - apathy, lack of emotion, poor social functioning, and cognitive disorganized etc. (low).

  25. Advantages of the biological model • 1. It is scientific • 2. It offers drug therapy • 3. It may offer a cure

  26. Problems with biological model 1. There is conflicting biological evidence 2. We cannot be sure that schizophrenia is one disorder 3. We cannot prove cause and effect 4. There are alternative explanations 5. It is difficult to separate out genes from social situations. 6. Genetic inheritance it is only a predictor of a ‘predisposition’ and is not a predictor of actually getting the disorder. 7. Biological explanations are therefore incomplete

  27. Psychological Explanations for schizophrenia - Behaviourism • Behaviourists would look not only at how patients ‘learn’ to develop faultybehaviour patterns but also at how they learnfaulty thinking!

  28. Operant Conditioning & schizophrenia • Children who do not receive reinforcement for ‘normal’ behaviour may put inappropriate attention into irrelevant environmental cues. • For example: paying attention to the sound of a word rather than meaning.

  29. This behaviour will eventually appear ‘weird’ to others. • These strange behaviours may be rewarded by attention and sympathy and so are reinforced. • This can continue until the behaviour becomes labelled as schizophrenic. (Rosenhan)

  30. Punishment and schizophrenia • Another suggestion is that early experience of punishment may lead the child to retreat into a rewarding inner world. Others then label them as ‘odd’ or ‘strange’. (Think MPD and Eve White)

  31. Social learning & schizophrenia • Families affect social learning. • Bizarre behaviour by parents is copied by children. • Parents then reinforce this behaviour, until eventually the child acquires the label of being ‘schizophrenic’.

  32. Evidence to support operant conditioning & reinforcement in schizophrenia • Ullman (1969) observed mental health nurses in their interactions with patients and concluded that staff actually reinforce schizophrenic behaviour by giving more attention to these patients – thus increasing the likelihood of the behaviour reoccurring.

  33. Evidence for Social learning and schizophrenia • Roder et al. (2002) used social skills training techniques to help schizophrenics. The success of training programmes in teaching new skills and reintegrating schizophrenics back into the community suggests that these are social skills that schizophrenics failed to learn in the first place.

  34. The Cognitive Model of Schizophrenia • Beck explains the disorder is due to genetic, environmental, psychosocial and cognitive factors which all interact. • The cognitive model of schizophrenia can, therefore, be considered a holistic approach to the disorder.

  35. The Stress diathesis ModelCognitive • Genetic abnormalities create a predisposition for the development of the disorder, but the disorder only develops in response to stress. The more stressors accumulate, the greater the risk a susceptible person has of developing schizophrenia. • Stress affects the development of the hippocampus which in turn affects cognitive skills.

  36. The Diathesis-Stress Model • A person with a predisposition to develop schizophrenia has limited cognitive resources due to biological factors such as high dopamine, larger ventricles and poor hippocampus development. However, as long as life is relatively stress-free they are able to compensate for this and their behaviour appears normal.

  37. Cognitive treatments for schizophrenia • Bradshaw 1998 (Case Study) • Bradshaw used CBT in the long-term outpatient care of a young woman with schizophrenia. Measures of psychosocial functioning, severity of symptoms, compliance with treatment and reductions in hospital visits were used to assess change over the 3- year treatment period and at 1-year follow-up. Results indicate considerable improvement in all outcomes.

  38. Evaluation for psychological explanations for schizophrenia • Behavioural explanations lack conviction. It is highly unlikely we can ‘learn’ schizophrenia! • Behaviourist explanations may explain maintenance, or differences in ability to deal with the disorder, rather than being a cause of the disorder • The cognitive explanation is however more holistic and complete (and therefore less reductionist) than either the biological or behaviourist model

  39. Evaluation • Psychological models are very useful in treatment programmes. Giving patients the cognitive skills to deal with their disorder can reduce the symptoms. • Behavioural techniques can help patients fit into the community by improving social skills. • Cognitive / behavioural therapies are less unethical, and have no side effects compared to drug therapy. They are however expensive.

  40. Evaluation • On the other hand, some patients are just too sick to responds to psychological therapy and are also too sick to self report about their experiences, making this area very difficult to investigate with any reliability or validity. • Psychological explanations are unlikely to lead to a cure!