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Bio. explanation SZ

AQA A-level psychology schizophrenia year 13

TermDefinition
Example of candidate genes for schizophrenia COMT and DRD4
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)
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
Concordance twin study Joseph (2004) 40.4% concordance for MZ and 7.4% for DZ
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
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
“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
“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
Neural correlates for schizophrenia: definition Abnormalities in certain areas of the brain that have an association with schizophrenia
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
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
Curren et al. (2004) Tested dopamine agonists such as cocaine and amphetamines on schizophrenic patients and found that they worsen symptoms
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
Typical antipsychotics: Evaluation Only inhibit dopamine, older, prevents only positive symptoms, many harsh side effects, cheap. E.g., chlorpromazine
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
Dopamine antagonists Chemicals which decrease dopamine activity in the brain by binding to receptors and preventing binding of dopamine
Placebo Pretend drug with no active ingredients intended purely for psychological benefits
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
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
Evidence against biological treatments: David Healy (2012) Suggested drug companies publish successful trials multiple times to create the illusion of universal credibility and success
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
Evidence against biological treatments: Goldacre (2013) Believed that research funded for by drug companies may be biased and should therefore be treated with caution
Evidence against biological treatments: Moncrief (2013) Sees the sedative effects of antipsychotics as a human rights abuse
Created by: Study_B
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