Family studies: family studies have shown that schziophernia is more common among biological relatives than non-biological. children with two schziophernic paretns have a concordance rate 46% one schizophernica parent 13% siblings 9%. it has been shown that schizophernia can be down to reearing patterns and not genetics
Twin studies: Joseph (2004) calculated that the pooled data for all schizophernia twin studies, carried out prior to 2001 showed that of a concordance for mz twins of 40.4% and dz 7.4% - however it has been argued that this concordance rates reflect nothing more than the environemtal differences of the types of twins due to more confusion in e.g identity and share the same environments
Adoption studies: Tiernari et all (2002) found that 164 adoptees whose biological mother had been schizophernic, 6.7% were diagnosed compared to 2% of the control group. there are many reasons for this however, such as a diagnosis may have only been given this when the children were adopted into environments were it was able to develop.
- dopamine hypothesis states that messages from neurons that transmit dopamine fire too often and too easily
- this then leads to characterisced schziphernic symptoms
- schizophernics are thought to have high no's of the d2 receptors on reciving neurons resulting in more dopamine binding and more dopamine firing.
- dopamine plays a key role in attention so disturbances in this may explain why schizophernics have problems in perception etc.
the key role played by dopamine was highlighted in these three sources:
1. amphetamines: it is a dopamine agonist stimulating nerve cells containing dopamine causing the synapse to be flooded. this leads to hallucinations
2. antipyschotic drugs: by reducing the stimulation of dopamine they cause positive symptoms to be elivated
3. parkinsos disease: people who have parkinsons take the drug l-dopa as they have low levels of dopamine, however this can cause them to have schizophernic symptoms
Dopamine hypothesis - weaknesses
- post mortem studies have showed that schizophernics who were taking antipsychotic drugs before death had raised levels of dopamine. showing that it may be the drugs that causes the high levels.
- evidence of neuroimaging such as PET scans has failed to show any increased in dopamine in schizophernics
- schziophernics ventricles are 15% bigger than those who don't suffer from the disorder
- they also tend to show negative symptoms rather than postive
- enlarged ventricles may be the result of poor brain development which then progresses into schizophernia
- however there was a meat-analysis which looked at over 90 CT scans and found that there was a substantial overlap in ventricle size when comparing schizophernics to people who don't suffer from it
- along with this, it was found that meciation dosage can effect the density of the brain thus resulting in enlarged ventricles