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Schizophrenia - Coggle Diagram

- - - - Improve communication and interaction between family members.
- - - - family studies = looking at people with sz to see if their biological relatives are similarly affected more than non-biological relatives
      - Gottesman (1991) found that MZ twins have a 48% risk of getting schizophrenia whereas DZ twins have a 17% risk rate = higher genetic similarity, higher chance of developing sz.
      - Kendler (1985) has shown that first-degree relatives of those with schizophrenia are 18 times more at risk than the general population.
      - The closer you are genetically to someone with sz, the higher risk you have of developing it yourself.
    - - Genetics are only partly responsible, otherwise concordance rates amongst MZ twins would be 100%.
      - Hard to separate out the influence of nature-v-nurture. Concordance rates are not 100% meaning sz cannot wholly be explained by genes and it could be that the individual has a predisposition to schizophrenia and simply makes the individual more at risk of developing the disorder. This suggests that the biological account cannot give a full explanation of the disorder.
      - Biologically reductionist. The Genome Project has increased understanding of the complexity of the gene. Sz is a multifactorial trait as it is the result of multiple genes and environmental factors. This suggests that the research into gene mapping is over-simplistic as sz is not due to a single gene.
  - - - The original dopamine hypothesis stated that schizophrenia suffered from an excessive amount of dopamine. Dopamine is a neurotransmitter which causes neurons to fire. With sz, neurons are firing too often and sending too many messages.
      - High dopamine activity leads to acute episodes, and positive symptoms.
      - A second explanation developed, suggests that it is not excessive dopamine but that there are more dopamine receptors. More receptors lead to more firing and an overproduction of messages.
      - Evidence for this comes from that fact that amphetamines increase the amounts of dopamine. Non sz people can experience positive symptoms when using them, and those with sz already can get worse.
      - A second explanation developed, suggests that it's not excessive dopamine but that there are more dopamine receptors. More receptors lead to more firing and an over production of messages.
    - - 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) argues around 1/3 of patients don't respond to drugs which block dopamine, so other neurotransmitters may be involved.
      - Cause and effect; 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.
      - Biological determinism; if the individual does have excessive amounts of dopamine then does it really mean that thy ey will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.
  - - - Neural correlates are patterns of structure or activity in the brain that occur in conjunction with schizophrenia.
      - People with schizophrenia have abnormally large ventricles in the brain. Ventricles are fluid filled cavities (i.e. holes) in the brain that supply nutrients and remove waste. This means that the brains of schizophrenics are lighter than normal. The ventricles of a person with schizophrenia are on average about 15% bigger than normal Torrey, 2002.
    - - Supporting evidence; Suddath et al. (1990) used MRI to obtain pictures of the brain structure of MZ twins where one twin had sz. The sz twin generally had more enlarged ventricles and a reduced anterior hypothalamus. The differences were so large the sz twins could be easily identified from the brain images in 12 out of 15 pairs.
      - Biologically deterministic; The reason for this is because if the individual does have large ventricles then does it really mean that they will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.
      - Specialist, high tech equipment such as MRI and PET scans means research has high reliability.
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- - - - Bateson et al (1956) - Double bind theory suggests that children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia.
      - Prolonged exposure to such interactions prevents the development of an internally coherent construction of reality; in the long run, this manifests itself as typically sz symptoms.
      - Laing - sz is not a disease, it's a result of social pressures in life. Sz was the result of social interactions of people, particularly family.
      - Expressed emotion = a family communication style that involves criticism, hostility and emotional over-involvement. Schizophrenics returning to such a family were more likely to relapse into the disorder than those returning to a family low in EE.
    - - Double bind strength comes from further empirical support provided by Berger (1965). They found that sz sufferers reported a higher recall of double bind statements by their mothers than non-sz. However, evidence may not be reliable as patient’s recall may be affected by their schizophrenia.
      - EE practical application; Hogarty (1991) produced a type of therapy session, which reduced social conflicts between parents and their children which reduced EE and thus relapse rates.
      - Individual differences; EE is associated with relapse but not all patients who live in high EE families relapse and not all patients in low EE families avoid relapse. Family dysfunction is an incomplete explanation for schizophrenia.
      - Problem of cause and effect. Mischler & Waxler (1968) found significant differences in the way mothers spoke to their schizophrenic daughters compared to their normal daughters, which suggests that dysfunctional communication may be a result of living with the schizophrenic rather than the cause of the disorder.
      - Ethical issues around blaming hte family for causing the mental illness, as well as gender bias as the mother tends to be the one who is blamed the most.
  - - - evidence that people diagnosed as schizophrenic have difficulties in processing various types of information, for example visual and auditory information, as well as attention deficits.
      - Researchers have suggested that difficulties in understanding other people’s behavior might explain some of the experiences of those diagnosed as sz. People with sz may struggle reading social cues.
- - - - Around since the 1950s. Works as an antagonists in the dopamine system meaning it reduces the actions of neurotransmitters (dopamine). Chlorpromazine is also used as a sedative
        
        Most commonly used is Chlorprozamine
    - - Data from 13 trials with 1121 participants showed chlorpromazine resulted in better overall functioning and reduced symptoms severity.
      - Supporting evidence may be published by drug companies with a bias
  - - - Developed later than typical antipsychotics around the 1970s
      - Clozapine was first introduced in the 60s and 70s. Has problems with blood clots. Binds to dopamine receptors as well as serotonin and glutamate receptors which reduces anxiety and depression. Often considered for patients who are suicidal
      - Risperidone - more recently developed (1990s). Less side affects than clozapine
    - - Serious side effects make it very difficult for some to live on antipsychotics
      - Does not cure schizophrenia and people may have to remain on drugs for their entire life
      - cheaper than therapy