Biological explanations of schizophrenia Flashcards
evidence of genetic explanation of schizophrenia
Gottesman & Shields(1960s):
-conducted twin studies on schizophrenia
-found that the concordance rate for MZ twins was 74% whilst 24% for DZ twins
-this therefore shows genetics contribute to the diagnosis of schizophrenia
-however, as the concordance rate of MZ twins was not 100%, concluded that environmental factors also play a role in the diagnosis of schizophrenia
limitation of Gottesman and shields twin study
-one limitation of twin studies are that they assume MZ and DZ twins have a similar shared environment
-which might be false as identical twins might be treated the same rather than DZ twins who look different
- this therefore means the high concordance rate in MZ twins could be down to a shared environment rather than genetics
adoption studies
Tienari et al:
-compared adopted children who’s biological mothers suffered from schizophrenia (experimental group) to a control group who were also adopted but their biological mothers didn’t suffer from schizophrenia
-found that children of biological mothers who who had schizophrenia were more likely to develop schizophrenia themselves
-therefore concluded that similarities between the child and the biological mother were due to genetics and also, genetics had more of an influence on the development of schizophrenia then the environment
limitation of adoption studies(Tienari et al)
-they assume that any similarity between adopted child and biological parent is due to genetics
-they also ignore the similarities in environments shared between the adopted child and biological parent as adopted children are often matched with adults that are similar to their biological parents
-this therefore means similarities in behaviour could be down to shared environment between the adopted child and the biological parent
-this therefore means adoption studies may overexaggerate the role of genetics
brain abnormalities that cause schizophrenia: Neural correlates hypothesis
-neural correlates states that schizophrenia is caused by abnormal brain structure like:
-larger ventricles in the brain
-smaller frontal cortex
evidence of neural correlates
Torrey(2002)
-conducted MRI scans to look at the brains of people with schizophrenia
-then compared their brain with a healthy control group who didn’t have schizophrenia
-found that participants with schizophrenia had 15% larger ventricles than the people in the control group
-this therefore supports the idea that people with schizophrenia have larger ventricles in the brain
limitations of neural correlates theory
-the correlation between schizophrenia and brain abnormalities such as enlarged ventricles doesn’t mean that brain abnormality is causing schizophrenia
-for instance, the enlarged ventricles might be a side effect of taking anti-psychotic drugs
-another limitation of the neural correlates hypothesis is that individual differences in brain abnormality:
-studies reporting enlarged ventricles haven’t always been replicated, and some research found no difference in the brain structure of a schizophrenic patient to a healthy person
the dopamine hypothesis
-suggest that schizophrenia is caused by abnormal brain function:
states that people with schizophrenia have higher levels of dopamine in some parts of their brain than healthy
-so the neurons generate more electrical activity which causes overactivity in the mesolimbic pathway
-neuron activity causes delusions and hallucinations
-this therefore supports the theory that abnormal brain function causes schizophrenia
the revised dopamine hypothesis
-suggests that there is too much dopamine in the mesolimbic system
-these increased levels of dopamine lead to neurons becoming overactive, this then leads to the positive symptoms of schizophrenia like hallucinations and delusions
-the revised dopamine hypothesis also suggests that in some parts of the brain like the frontal cortex, dopamine is too low
-therefore, low levels of dopamine cause underactivity of neurons in the frontal cortex, and as the frontal cortex ply\as as role in making us feel motivated to achieve our goals
-underactivity in the frontal cortex will therefore cause negative symptoms of schizophrenia like avolition
evidence of dopamine hypothesis
drug studies:
-drug studies show when normal people take amphetamines, they can experience hallucinations or delusions
-drug studies also show that drugs that reduce dopamine decrease the likelihood of people with schizophrenia having hallucinations and delusions
imitations of dopamine hypothesis
-drugs that decrease dopamine levels don’t always prevent hallucinations and delusions
-can cause other parts of the brain to have even lower dopamine(frontal cortex)
-which could therefore lead to negative symptoms like avolition
Noll(2009)
-Noll reviewed all of the drug studies in which doctors gave drugs to people with schizophrenia in order to decrease their dopamine levels
-Noll found that for many patients, decreasing the levels of dopamine did stop hallucinations and delusions
-this suggests that for these patients, their positive symptoms were caused by abnormally high levels of dopamine
-but for 1/3rd of patients, the drugs didn’t stop them experiencing hallucinations and delusions
-this therefore suggests that for these patients, their positive symptoms weren’t caused by high levels of dopamine in the mesolimbic system
limitation of drugs studies
Montcreiff
-one limitation of drug studies is that evidence is inconclusive
-this is because there is little evidence that people with schizophrenia have an imbalance of dopamine activity
-he concluded that drugs that increase dopamine(amphetamine) also increase other neurotransmitters, so we don’t know that its the increased dopamine that is causing these symptoms
-some post-mortem studies reported increased dopamine in the mesolimbic pathway, but other studies reported no difference compared to the brains of the control group
biological treatment for schizophrenia:
how do Antipsychotic drugs work:
-antipsychotic medication works by reducing dopamine activity in the brain
-it does this by preventing dopamine from biding to post-synaptic receptors
-therefore, reducing the overactivity of neurons in the mesolimbic pathway
-thus therefore preventing the positive symptoms of schizophrenia to occur
limitation of anti-psychotic drugs:
-one limitation of anti0psychotic drugs is that they cause side effects such as extra-pyramidal symptoms which are loss of control of movement and also other physical side effects like heart problems, obesity and diabetes
-another limitation of anti0psychotic drugs is that they do not treat the negative symptoms of schizophrenia such as avolition and speech poverty
