Biological explanations of schizophrenia Flashcards
What are the 3 biological explanations for schizophrenia?
- Genetic explanations for schizophrenia
- The dopamine hypothesis for schizophrenia
- Neural correlates of schizophrenia
Genetic explanations
Gottesman and Shields (1976)
* reviewed 5 twin studies
* reported a concordance rate of 75% and 91% for Mz twins with severe schizophrenia
* there was an increased incidence of schizophrenia in adopted children with a biological parent with schizophrenia and an increased incidence of schizophrenia in siblings with schizophrenia
* this suggests that genetics plays a larger role with chronic forms of the disorder
* they conclude that as genetic similarity increases, so does the probability of sharing schizophrenia. For example, twins have a higher chance of sharing schizophrenia than cousins
Dopamine hypothesis
A neurochemical approach
1. Hyperdopaminergia in the sub cortex
* high levels of dopamine in the sub cortex
* for example, high levels of dopamine in Broca’s area may explain speech poverty
2. Hypodopaminergia in the cortex
* low levels of dopamine in the prefrontal cortex
* this may account for negative symptoms as the prefrontal cortex is responsible for thinking and decision making
Neural correlates
- neuroanatomical approach - relating to differences in brain structure
1. Ventral striatum - abnormalities here may explain avolition. Low levels of activity found here in the brains of a schizophrenic person
2. Temporal gyrus- low levels of activity here may explain auditory explanations
3. Cingulate gyrus - low levels of activity here may explain auditory hallucinations
4. Enlarged ventricles - people with schizophrenia have enlarged ventricles which are assoicated with damage to central brain areas and the prefrontal cortex. Such damage has often associated with negeative symptoms.
Evaluation
+ Support for genetic explantaions (Tienari et al)
+ Support for genetic explanations (Joseph)
+ Support for neural correlates (Weinberger)
- Neural correlates cannot establish cause and effect
+ Support fot the dopamine hypothesis (Randrup and Munkvad)
- Dopamine hypothesis is too simple
Tineari et al (2004)
Found that children of schizophrenic sufferers are still at heightened risk of schizophrenia if adopted into families with no history of schizophrenia. This shows that the genetic explanation is high in validity as it suggests nature is more important in explaining schizophrenia than nurture.
Joseph (2000)
Compared the concordance rates of Mz twins to Dz twins. Found a concordance rate of 40.4% for Mz twins and 17% for Dz twins in relation to schizophrenia.
- However, the evidnece isnt strong enough as the figures are low so genetics arent the only cause.
Weinberger
Carried out MRI scans on 2 28 year old Mz twins. The brain scans showed that like the twin who suffered from schizophrenia enlarged ventricles compared to the twin who did not have the disorder. This supports the neural correlates of schizophrenia.
- However, this is a case study so it has a small sample size meaning its low in population validity.
Neural correlates cannot establish cause and effect
Research into the neural correlates of schizophrenia is correlational. Jukel et al (2006) found lower levels of activity in the ventral striatum in patients with schizophrenia. It follows that abnormality in the areas like the ventral striatum may be involved in the development of avolition. There are problems with correlational research as we cannot establish cause and effect.
Randrup and Munkvad (1966)
Created schizophrenic like behaviour in rats by giving them amphetamines which activate dopamine production and then reversed the effects by giving them neuroleptic drugs, which inhibits the release of dopamine.
Dopamine hypothesis is too simple
Dopamine hypothesis is accused of being over-simplistic. It suggets too much or too little levels of dopamine can cause schizophrenia, however there may be other neurotransmitters involved in the development of schizophrenia.
