Discuss Biological Explanations of SZ (8+16) (45 Mins)

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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.
      • 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
                        • 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
                      • 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
                  • Firstly, there is the issue of cause&effect
                • However, there are issues with this research which undermine support for the theory
              • These findings clearly show support for the NP theory that SZ is caused by brain wastage
            • Lambert & Kinsey showed that people with SZ have enlarged ventricles, along with smaller frontal &temporal lobes
          • A strength of this theory is that it has recieved a great deal of  support from research
    • 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
              • 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
            • These findings clearly support the biochemical theory and the idea that SZ is caused by an excess of D at the synapse
          • Owen (1978) - Found that in post-mortems of SZ patients, there was a greater density of D receptors compared to individuals without SZ
  • 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
            • 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?
            • These findings clearly support the biochemical theory and the idea that SZ is caused by an excess of D at the synapse

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