AQA A-level psychology schizophrenia year 13
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| Example of candidate genes for schizophrenia | COMT and DRD4
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| Genetic factors of schizophrenia | Is polygenic (caused by a number of genes which each impart a small risk) and aetiologically heterogeneous (different combinations of genes causes SZ in different people)
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| Concordance study Gottesman (1991) | Concordance rates of schizophrenia with different familial relations. Identical twins had 48% concordance rate which shows that SZ isn’t purely genetic
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| Concordance twin study Joseph (2004) | 40.4% concordance for MZ and 7.4% for DZ
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| Adoption study Tienari et al. (2004) | 19,000 adopted Finnish children with SZ biological mothers. Control group of adoptees without genetic predisposition. 6.7% of experimental group had SZ compared to 2% of the control group
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| Genetic meta-analysis Ripke et al. (2014) | Combined all previous data of genome sequencing and sequenced 37,000 participants and found 108 genes to be implicated
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| “On Being Sane in Insane Places” Rosenhan et al. (1973): outline | Rosenhan and 7 other psychologically healthy “pseudopatients” feigned auditory hallucinations to be admitted to various psychiatric hospitals. They claimed to hear the words “empty, hollow, thud” but ceased this behaviour after admission
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| “On Being Sane in Insane Places” Rosenhan et al. (1973): results | Pseudopatients remained in hospitals for an average of 19 days with a range from 7-52 before being discharged with “schizophrenia in remission” and a course of antipsychotics
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| Neural correlates for schizophrenia: definition | Abnormalities in certain areas of the brain that have an association with schizophrenia
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| Neural correlates for schizophrenia: examples | Enlarged ventricles (holes) in the brain, hyperdopaminergia (too many DA receptors) in the subcortex, hypodopaminergia (too few DA receptors) in the prefrontal cortex
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| Tilo et al. (2001) | Gave fMRI scans to 6 SZ patients looking at Rorschach ink-blots. Severity of disorder correlated negatively with activity in the WERNICK’S and BROCA’s regions of the brain
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| Curren et al. (2004) | Tested dopamine agonists such as cocaine and amphetamines on schizophrenic patients and found that they worsen symptoms
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| Dopamine hypothesis | An excess of dopamine or an oversensitivity in certain areas of the brain may be a contributing factor to the onset of SZ
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| Typical antipsychotics: Evaluation | Only inhibit dopamine, older, prevents only positive symptoms, many harsh side effects, cheap. E.g., chlorpromazine
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| Atypical antipsychotics: Evaluation | Inhibits a range of neurotransmitters, newer, prevents most symptoms, fewer side effects but worse (agranulocytosis: suppressed immune response), expensive. E.g., clozapine
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| Dopamine antagonists | Chemicals which decrease dopamine activity in the brain by binding to receptors and preventing binding of dopamine
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| Placebo | Pretend drug with no active ingredients intended purely for psychological benefits
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| Evidence for biological treatments: Thornlet et al. (2003) | Meta analysis of over 55 studies comparing chlorpromazine with a placebo and found that it reduces symptoms
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| Evidence for biological treatments: Meltzer (2012) | Study to compare clozapine to typical antipsychotics and found it worked in 40% of cases that typical drugs didn’t work
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| Evidence against biological treatments: David Healy (2012) | Suggested drug companies publish successful trials multiple times to create the illusion of universal credibility and success
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| Evidence against biological treatments: Sedative effects | Since antipsychotic drugs are sedatives, they can calm patients down which makes it seem like the patient’s positive symptoms have been reduced
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| Evidence against biological treatments: Goldacre (2013) | Believed that research funded for by drug companies may be biased and should therefore be treated with caution
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| Evidence against biological treatments: Moncrief (2013) | Sees the sedative effects of antipsychotics as a human rights abuse
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