Discuss Biological Explanations of SZ (8+16) (45 Mins)
- Created by: Emma Kwiecinska
- Created on: 08-10-13 20:12
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- Discuss Biological Explanations of SZ (8+16) (45 Mins)
- Neuro- pathological
- AO1- This theory states that SZ is caused by brain dysfunction and brain wastage, more specifically the left temporal lobe is seen as being most important
- ...the left temporal lobe processes auditory information, the wastage may be causing the auditory hallucinations that many SZ sufferers have
- This brain wastage also affects other areas such as the amygdala and hippocampus. The Amygdala regulates emotions and aggression, whilst the hippocampus plays a key role in memory function, symptoms such as word salad may come from this.
- ...the left temporal lobe processes auditory information, the wastage may be causing the auditory hallucinations that many SZ sufferers have
- AO2 - Evaluation of the theory
- Statement about support
- Findings of supporting research
- Link back to the neurological theory
- Explain that this evidence may be weak
- Why is this an issue here?
- Link back to how this affects the neurological theory
- We cannot say that it was the brain damage which led to SZ, it may have occurred as a result of having SZ
- Alternative explanation?
- Develop this point using further research
- Conclude and link back to the question/theory
- If this is the case, then we have to question whether brain damage causes SZ, or if SZ even has a biological cause
- To support this -Yates (1987)- found no difference in the ventricle size between SZ patients, mood disorder patients and the control group
- If this is the case, then we have to question whether brain damage causes SZ, or if SZ even has a biological cause
- GUR- monitored 20 first episode SZ patients and found that higher medication dosage led to greater brain wastage especially in the frontal&temporal lobes
- Madsen (1998) - compared brains of SZ patients as soon as they were diagnosed to after 5 years on neuroleptic drugs and found that brain wastage increased 6% for every additional 10mg
- Conclude and link back to the question/theory
- The antipsychotic medication may have led to the brain damage
- GUR- monitored 20 first episode SZ patients and found that higher medication dosage led to greater brain wastage especially in the frontal&temporal lobes
- Madsen (1998) - compared brains of SZ patients as soon as they were diagnosed to after 5 years on neuroleptic drugs and found that brain wastage increased 6% for every additional 10mg
- GUR- monitored 20 first episode SZ patients and found that higher medication dosage led to greater brain wastage especially in the frontal&temporal lobes
- Develop this point using further research
- Firstly, there is the issue of cause&effect
- Link back to how this affects the neurological theory
- However, there are issues with this research which undermine support for the theory
- Why is this an issue here?
- These findings clearly show support for the NP theory that SZ is caused by brain wastage
- Explain that this evidence may be weak
- Lambert & Kinsey showed that people with SZ have enlarged ventricles, along with smaller frontal &temporal lobes
- Link back to the neurological theory
- A strength of this theory is that it has recieved a great deal of support from research
- Findings of supporting research
- Statement about support
- AO1- This theory states that SZ is caused by brain dysfunction and brain wastage, more specifically the left temporal lobe is seen as being most important
- Biochemical
- AO1- The Dopamine Hypothesis - States that SZ is caused by a chemical imbalance in the brain, more specifically an excess of dopamine at the synapse which causes the symptoms of SZ
- ...In particular, there is an overstimulation of the D1 and D2 pathways, namely the mesolimbic (emotion and aggression) and mesocortical (thinking and reasoning) pathways.
- Statement about support
- A strength of this theory is that it has recieved a great deal of support from research
- Findings of supporting research
- Link back to the biochemical theory
- Explain that this evidence may be weak
- Why is this an issue here?
- Link back to how this affects the biochemical theory
- This oversimplified theory based on simple animal models ignores the complexity of SZ and so makes us question how much it can be applied to sufferers of SZ
- Develop this point using further research
- Conclude and link back to the question/theory
- Regarding this evidence, we must question how much we can link an excess of D receptors to a complete explanation of the causes of SZ.
- We have to consider the role of psychological factors in the causes of SZ
- Rappoport- divided 80 SZ patients into 2 groups, one recived anti-psychotic meds, the other was a placebo. After 3 years, 73% of the meds group had been readmitted compared to 8% of the placebo group
- This model also ignores the role of other chemicals in explaining SZ
- Andreason (2001) - states that other chemicals such as serotonin and glutamate are involved
- This undermines support for the BC theory and the idea that only a decrease in D levels affects SZ symptoms
- Rappoport- divided 80 SZ patients into 2 groups, one recived anti-psychotic meds, the other was a placebo. After 3 years, 73% of the meds group had been readmitted compared to 8% of the placebo group
- This undermines support for the BC theory and the idea that only a decrease in D levels affects SZ symptoms
- Andreason (2001) - states that other chemicals such as serotonin and glutamate are involved
- Conclude and link back to the question/theory
- Link back to how this affects the biochemical theory
- Although this evidence supports the theory, there are issues with the research which undermines support for the theory
- Contradictory evidence - Wong's preliminary study showed no increase in D receptors of SZ brains
- Could the medication have affected D levels in the brains, leading to changes?
- Owen (1978) - Found that in post-mortems of SZ patients, there was a greater density of D receptors compared to individuals without SZ
- Could the medication have affected D levels in the brains, leading to changes?
- Contradictory evidence - Wong's preliminary study showed no increase in D receptors of SZ brains
- Why is this an issue here?
- These findings clearly support the biochemical theory and the idea that SZ is caused by an excess of D at the synapse
- Explain that this evidence may be weak
- Owen (1978) - Found that in post-mortems of SZ patients, there was a greater density of D receptors compared to individuals without SZ
- Link back to the biochemical theory
- AO1- The Dopamine Hypothesis - States that SZ is caused by a chemical imbalance in the brain, more specifically an excess of dopamine at the synapse which causes the symptoms of SZ
- Neuro- pathological
- Findings of supporting research
- Link back to the biochemical theory
- Explain that this evidence may be weak
- Why is this an issue here?
- Link back to how this affects the biochemical theory
- This oversimplified theory based on simple animal models ignores the complexity of SZ and so makes us question how much it can be applied to sufferers of SZ
- Develop this point using further research
- Conclude and link back to the question/theory
- Regarding this evidence, we must question how much we can link an excess of D receptors to a complete explanation of the causes of SZ.
- We have to consider the role of psychological factors in the causes of SZ
- This model also ignores the role of other chemicals in explaining SZ
- Andreason (2001) - states that other chemicals such as serotonin and glutamate are involved
- This undermines support for the BC theory and the idea that only a decrease in D levels affects SZ symptoms
- This undermines support for the BC theory and the idea that only a decrease in D levels affects SZ symptoms
- Andreason (2001) - states that other chemicals such as serotonin and glutamate are involved
- Conclude and link back to the question/theory
- Link back to how this affects the biochemical theory
- Although this evidence supports the theory, there are issues with the research which undermines support for the theory
- Contradictory evidence - Wong's preliminary study showed no increase in D receptors of SZ brains
- Could the medication have affected D levels in the brains, leading to changes?
- Could the medication have affected D levels in the brains, leading to changes?
- Contradictory evidence - Wong's preliminary study showed no increase in D receptors of SZ brains
- Why is this an issue here?
- These findings clearly support the biochemical theory and the idea that SZ is caused by an excess of D at the synapse
- Explain that this evidence may be weak
- Link back to the biochemical theory
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