PSYA4- biological explanations for schizophrenia

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  • biological explanations for schizophrenia
    • genetic hypothesis
      • schizophrenia runs In families
        • some studies have shown that the risk of developing schizophrenia is directly proportional to the amount of genes an individual shares
        • however even in twin studies the rick is not even 100% so there must be some environmental factor
    • Twin studies
      • MZ twins are genetically identical
      • DZ twins share 50% of genes
      • Gottesman- summarised 40 studies and found 48% concordance rate for schizophrenia in mz twins and 17% in dz twins
      • Rosenthal- case study of quadruplets- all 4 developed schizophrenia but differed in age of onset and symptoms- strong evidence for genetic component
        • however the girls had a bad upbringing so we cannot separate the eniromental from genetic
      • cardono et al- based on the maudsley twin register- found concordance rate of 26.5% in mz twins and 0% for dz twins
      • there are some issues with twin studies
        • mz twins are rare especially with sciz (1%) so sample size is often small
          • Mcguffin et al- found different diagnostic criteria was used so comparisons cant be made between studies
            • different criteria was used to distinguish mz from dz twins
              • concordance rates can be calculated in different ways
                • marshall-  the better controlled the study the lower the concordance rate
    • Adoption studies
      • looks at children with schizophrenic mothers and reared apart
      • kety- found high rates of schizophrenia in children in individuals whose biological parents suffered from it- but were adopted by healthy parents
      • tienari- finnish adoption study- 155 children whose bio mothers had sciz compared to matched group of adopted children with no family history of schiz- 10% of sciz mothers group also developed it compared to 1% of control group
        • strong evidence for biological cause but has some methodological issue so lacks validity
    • biochemical factors
      • neurotransmitters are chemical messengers
        • dopamine hypothesis
          • schizophrenia results from an excess of dopamine activity at certain synaptic sites; support for this is found in
            • phenothiazine's- drugs that block dopamine at the synapse can alleviate symptoms of sciz
              • clozapine- one of the most effective treatments for schiz- Farde et al- good for blocking dopamine receptors
                • L-dopa- drug to treat Parkinson's- increases dopamine but produces symptoms of schiz
                  • post mortems- found increased dopamine in parts of the brain- Seeman- found an increase in dopamine receptor density of 60-110%
                    • pet scans- wong et al- found increase in dopamine receptor density in non-drug treated sciz patients compared to treated patients
          • however
            • phenothiazine's don't work for everyone with sciz and only alleviates positive symptoms
              • L-dopa doesn't worsen symptoms in all people with schiz
                • post mortem findings are found in patients who have been on neuroleptic drugs for years so brain changes may be a result of this
                  • later pet scan studies by fare et al- have not replicated wongs findings
            • it is likely that dopamine is involved however this is and oversimplified explanation- reductionist
    • Gottesman- 63% of all people diagnosed with schiz have no family history
  • children with two affected parents; risk is 46%
    • for dizygotic twins or children of one affected parent; risk is 17%
      • grandchildren the risk is 5%
        • the general population; risk is 1%
  • the two syndrome hypothesis explains contradictions in some studies  but its oversimplified as most patients show a mixture of symptoms
    • type 2- neurodevelopmental disorder/ arising from prenatal or perinatal insults/ negative symptoms/ develops over period of time/ chronic/ doesn't respond well to drugs


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