Hypothesis states that overproduction of dopamine (DA) causes symptoms of Sz
Theory created when overdoses of drugs LSD and amphetamines which both enhance DA production, exhibited schizophrenic-like symptoms
Dopamine neurons found in frontal cortex and basal ganglia which deal with inital and control of movements
If DA system declines leads to Parkinsons development which is treated with dopamine replacement 'L-Dopa'.
If too much L-Dopa is taken it can also result in schizophrenic like symptoms
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AO2 - Dopamine Hypothesis
Research has only been carried out post-mortem so cannot establish cause and effect
Further research is being carried out on living Sz patients using PET scans which maps brain activity at particular times
Gelder et al 1989 stated evidence to support the overproductions of dopamine as the sole cause of Sz is inconclusive
PET scans only show how dopamine works
Drugs which reduce the levels of dopamine may effectively reduces the positive symptoms of type 1 Sz and not affect type 2 Sz
Dopamine hypothesis is seen as over-simplifying as anti-schizophrenic drugs work by affecting other neurotransmitters like serotonin and not just dopamine
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AO1 - Genetics
Risk of developing Sz is greater than the natural prevalence in the general population (1%)
Gottesman and Shields (1972 and 1991) found concordance rate for developing Sz amongst MZ twins was 48% and amongst DZ twins was 17% supporting the genetic contribution for developing Sz
To try and separate nature and nurture adoption study by Kety et al (1998) studied 5483 danish adopted Danish children, found 32% who had biological parent with Sz had developed it compared to control group where only 18% developed it
Children with no genetic history of Sz but were raised by Sz parents did not show rates of Sz above the predicted national rate - Kendler (1994)
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AO2 - Genetics
Likelihood of developing Sz amongst identical twins could be down to environment due to similar childhood experiences and reacted to in similar ways and have similar friends.
Concordance rate should have been 100% in MZ twins if purely down to genetics and 50% in DZ twins.
Concordance rate was 9% amongst siblings and 17% amongst non-identical twins even though both genetically dissimilar, supporting the theory that shared upbringing increases the risk of developing Sz.
Kamin (1997) explained children are often adopted by members of the same family which means identical twins which grow up apart may still experience similar environments
Small sample size as twins with schizophrenia is rare so lacks reliability
Cannot be purely genetic as it would be passed on to offspring
People probably inherit genetic predisposititions for Sz which may be triggered by environmental factors (diathesis-stress model)
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AO1 - Neuroanatomical
Brain scans have shown there to be structural abnormalities in Sz sufferers i.e. enlarged cerebral ventricles
Torrey (2002) stated that on average ventricles are 15% larger in people with schizophrenia, and especially those with type 2 Sz
Kinsey (2005) discovered the reason for the large ventricles is that Sz sufferers have smaller frontal and temporal lobes and also abonrmal blood flow to certain parts of the brain.
Support by Ho et al (2004) found those suffering from Sz had enlarged ventricles compared to those without the disorder.
Also found those with enlarged ventricales were less likely to have their symptoms eased or become more manageable.
Hata (2003) saw positive correlation between minor brain anomalies in lateral ventricles in young adolescents and the development of Sz. The larger the ventricles the greater the chance of developing Sz.
Molina et al (2005) carried out research into hypofrontality (where frontal lobes have less brain tissue than normal) and sz. Found those with hypofrontality later on had higher rate of developing sz.
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AO2 - Neuroanatomical
Difficult to determine whether differences in brain structure are cause or effect of Sz
Ventricles enlarge naturally with age and are usually larger in men so hard to determine what is 'large'
Measures are often averaged which leads to understatement of individual differences
Highley (1999) discovreed that different brain anomalies occur in diff. parts of the brain in men and women and anomalies have been found to be more developed in male sufferes
People suffering from manic depression also have enlarged ventricles
Differences in brain structure may also be caused by environmental factors such as birth complicationss, viruses or tixins.
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General AO2
Objective approach as based on empirical evidence
Nomothetic as classifies people into categories
Deterministic as it believes that behaviour is determined by internal and external factors that are out of our control
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