Biological Explanations Flashcards
(24 cards)
What is the lifetime risk of development SZ if you have both parents with SZ?
46%
What is the lifetime risk of developing SZ if you have a spouse with SZ?
2%
What did Gottesman 1991 find in his twin study? (Genetics)
How does this support the genetic cause of SZ?
After summarising 40 studies he found that the concordance rate of MZ twins was 48% while DZ had a concordance rate of 17%/ MZ twins are more genetically similar to DZ twins so if they have a higher risk it shows that their genetics have influenced their risk
What did Rosenhan find in her quadruple study that suggests a limitation of genetics as a cause of SZ?
They had different symptoms and different times of onset, if it was biological they would be the same and they had a traumatic childhood so had similar environmental traumas so biology island isn’t everything
What did Tienari study find in his adoption study with SZ relatives?
155 schizophrenic mothers who had given their children up for adoption were compare to 155 children who hadn’t been given up for adoption/ 10% with schizorenc mothers/ 1.1% who weren’t adopted
What did Wahlberg find with adoption study that suggested a limitation in the genetic cause of SZ?
Those with High genetic link did well when adoptive family was supportive/ this considers environmental factors are important / would be100% for identical twins if it wasn’t enviro,entail/ sample see
What is the percentage of lifetime risk of developing SZ if you have a monozygotic twin with SZ?
48%
What is the original dopamine hypothesis?
It states that SZ is caused by too much of the neurotransmitter dopamine in the brain
What is the revised dopamine hypothesis?
It states that SZ is caused by too many dopamine receptors in the brain and is found in autopsies
What is the dopamine hypothesis?
It is a biological explanation for the cause of SZ with a focus of dopamine in its hypothesis
What is dopamine?
A neurotransmitter that is located in thee brain in the part that controls motor actions
How does the drug chlorpromazine give evidence to support the dopamine hypothesis?
It is useful to treat SZ, it blocks dopamine receptors which suggests that too much dopamine causes SZ and therefore the dopamine hypothesis is correct
How does the drug L-dopa give evidence to support the dopamine hypothesis?
It is a drugged used to increase dopamine levels in order to treat conditions like Parkinson’s disease, it can however produce many of the symptoms of SZ which suggests that an increase or too much dopamine can cause SZ, suggests the hypothesis is correct
How does the drug amphetamine give evidence to support the dopamine hypothesis?
It activates dopamine/ when small doses were given to patients with SZ it worsened their symptoms
Why is it difficult to assess brain levels of dopamine patients?
Cannot be done indirectly apart from a dangerous procedure which involved putting a needle into the spine/ or through post mortals/
What did Moncrief (2009) argue about the conclusiveness of the dopamine hypothesis?
Stimulants such as amphetamine effect other neurotransmitters such as serotonin/ dopamine concentrations in post-mortem brain tissue had been inconclusive
What are neural correlates?
Measurements of the structure of the brain that correlate with an expiedmcd/ brain structures
What can brain scans show?
The fMRI scans gives pictures of
What did Li et al (2010) find when performing a meta analysis of fMRI scans to investigate the difficulties SZ often have in processing facial emotions
The activation of the bilateral amygdala when facial processing was limited in SZ sufferers/ abnormal functioning in the brain in those with S may explain their difficulties in processing facial emotions
What did the MRI scans on 155 SZs, 186 of their non schizophrenics and 122 non related SZS, show in Boos et al (2012) study?
SZ patients have decreased grey matter density and cortical thinning compared with other ppts/ brain tissue differences in SZ are an effect of having the disorder rather than being due to genetic factors
What did Johnstone et al (1976) find with SZ patients?
However what did Weyandt find that might contradict this?
They had enlarged ventricles/ non sufferers did not- SZ is related to loss of tissue/ Weyandt found that enlarged ventricles are associated with negative symptoms only- cannot explain all SZ symptoms
What is a good thing about the Li et al study?
It uses scientific evidence/ brain scans are objective measurements- not subjective so we can know there is a psychical difference and this info is accurate
What is a weakness of neural correlates?
We do not know whether large verticles cause SZ of whether SZ causes large verticles, we do not know the cause and effect
What is another weakness of the biological explanation?
It takes the nature approach- neglects the Nuture- simplistic/ interactionist approach offers an alternative explanation and had nature and Nuture
