lesson 5 - biological explanations for schizophrenia Flashcards
what is dopamine
neurotransmitter
in high amounts it increases motivation excitation and pleasure
assumptions about the dopamine hypothesis
schizo sufferers tend to have more dopamine receptors in the brain and this causes an increase in dopamine
winterer investigated dopamine receptors D1 and D2 and found that schizo sufferers had high ratios of dopamine
anti-psychotic drugs such as phenothiazines can block activity in dopamine receptors in the brain. These drugs minimise positive symptoms but not positive ones
drug L-dopa increases dopamine levels for those who have low levels of dopamine (Parkinson’s disease) side effect is that it can cause schizo symptoms
what is the dopamine hypothesis
by David and Neale
Schizophrenic patients’ tend to have excess levels of the neurotransmitter dopamine in subcortical areas of the brain which increases the firing of neurons (hyperdopaminergia).
When drugs such as phenothiazine’s (dopamine antagonist) are given to patients’ that block dopamine at synapses in the brain; the positive symptoms of schizophrenia seem to reduce (hallucinations and delusions). However, negative symptoms of schizophrenia seem to remain, and these symptoms are not decreased.
A drug called L-Dopa increases dopamine levels in the brain. This drug can induce symptoms of schizophrenia, and it has been tested on healthy non psychotic people. Drugs such as LSD and amphetamines (dopamine agonist) also increase dopamine levels in the brain and can induce schizophrenic symptoms. Davis and Neale based the dopamine hypothesis on the following facts:
* Post mortem studies have found that schizophrenic patients’ have an increased amount of dopamine receptors and dopamine in the left amygdala of the brain.
* Glutamate is another neurotransmitter in the brain and central nervous system that is excitatory. It helps to keep the brain functioning properly. Glutamate plays a major role in shaping learning and memory. Schizophrenia patients tend to have issues with making and using glutamate in the body.
how can you monitor dopamine metabolism
- Dopamine metabolism in schizophrenic patients’ seems to be abnormal, and this can be monitored by PET scanning (Positron Emission Tomography) which looks at brain activity and imaging.
strengths of the dopamine hypothesis
1) There is a great deal of research to support the hypothesis that schizophrenic patients have a high level of dopamine in their brain. For instance research by Davidson found that when schizophrenic patients were given the drug L-Dopa their schizophrenic symptoms got worse and intensified. (+)
5) An advantage of this theory is that there is a great deal of scientific evidence and support for the dopamine hypothesis as a cause of schizophrenia. Most of the research has used evidence that have come from brain scans (PET and fMRI) which is highly valid and reliable information. (+)
weaknesses of the dopamine hypothesis
2) A problem with this theory is that cause and effect is not clear. Could it be that an increase in dopamine causes schizophrenia to develop; or could it be that the illness develops first (due to another cause) and then this causes dopamine levels to increase? PET scanning might be able to answer some of these questions (-)
3) A problem with the neurotransmitter dopamine is that it is not only associated with the illness of schizophrenia. Dopamine has also been associated with mania (bipolar depression), and this illness is not alleviated by phenothiazine drugs. Therefore is seems that dopamine has a complex role in the brain and might be associated with many psychological illnesses and not schizophrenia alone. (-)
4) A disadvantage of this theory is that the dopamine hypothesis could be viewed as being reductionist. It looks at the complicated phenomenon of the causes of schizophrenia and reduces it down to the component of dopamine alone. There might be other factors or causes of schizophrenia that have been ignored e.g. neuroanatomy of the brain. (-)
factors that can affect drug dosage
age
weight
bmi
other illnesses
other medication
neural correlates - A01
Schizophrenia might develop due to structural and functional brain abnormalities. In the past, post mortems were used to investigate the structure of the brain in patients who had schizophrenia, but we now use fMRI (Functional Magnetic Resonance Imaging). Patients with schizophrenia are given cognitive and memory tasks to do, and this is compared with normal healthy patients whilst also conducting fMRI.
EXPLAIN neural correlates a study by Swayze
Swayze reviewed 50 studies of schizophrenic patients and examined their brain imaging using MRI (Magnetic Resonance Imaging). From these brain images, the structure of the brain could be examined and it was found that schizophrenic patients’ have structural abnormalities in their brain including:
* A decrease in brain weight
* Enlarged ventricles (that are filled with water)
* A smaller hypothalamus
* Less grey matter (this is where the intelligence is held and it seems to deteriorate)
* Structural abnormalities in the pre frontal cortex (where the personality is held)
strengths of neural correlates
5) There is a great deal of supporting evidence to suggest that neural correlates do seem to be an important factor when looking at the cause of schizophrenia e.g. research by Swayze and Juckel have all pointed out that there are problems in brain functioning/structure that could have contributed to causing the illness. (+)
3) There is a strong amount of supporting psychological evidence to state that schizophrenia is caused by neural correlates changing in the brain that occur during pre natal development in the womb. However, this does not explain why schizophrenia occurs in early adulthood (and not straight away during infancy). Weinberger (1987) has stated that the pre frontal cortex (an area effected by schizophrenia) develops during adolescence and therefore damage to this part of the brain would only be noticed during adolescence and adulthood (when the symptoms of schizophrenia become apparent) (+)/ (-)
weaknesses of neural correlates
1) Andreason (1982) has criticised the neural correlates explanation for schizophrenia. He found that the extent to which the ventricles in the brain are enlarged in schizophrenic patients is not significant; and therefore there is actually very little difference between the neural correlates of schizophrenic patients’ and normal people. (-)
2) A problem with this theory is that cause and effect needs to be established. Is it the fact that abnormal neural correlates actually causes schizophrenia to occur, or does schizophrenia occur first (due to other factors) and then cause the brain structure/neural correlates to alter? (-)
3) There is a strong amount of supporting psychological evidence to state that schizophrenia is caused by neural correlates changing in the brain that occur during pre natal development in the womb. However, this does not explain why schizophrenia occurs in early adulthood (and not straight away during infancy). Weinberger (1987) has stated that the pre frontal cortex (an area effected by schizophrenia) develops during adolescence and therefore damage to this part of the brain would only be noticed during adolescence and adulthood (when the symptoms of schizophrenia become apparent) (+)/ (-)
4) Davison and Neale (2001) have found contradictory evidence to suggest that enlarged brain ventricles are not only found in schizophrenia patients, but that sufferers of mania also have enlarged ventricles. Therefore enlarged ventricles alone cannot cause schizophrenia, but it could be a vulnerability factor that increases the risk of getting the illness (damage to the brain structure). Diathesis stress model? (-)
