Biological Explanations Flashcards
Genetic Explanations: Family Studies: Gottesman (1991)
Risk of Sz:
-> Aunts, 2%
-> Grandchildren, 5%
-> Identical twins, 48%
Genetic Explanations: Twin studies: Joseph (2004)
If monozygotic twins are more concordant than dizygotic twins, this may suggest that the greater similarity is due to genes
- Calculations from pooled data showed a concordance rate of 40.4% for MZ twins, and 7.4% for DZ twins
Genetic Explanations: Adoption Studies: Tienari et al (2000)
- Of 164 adoptees in Finland whose bio mothers had Sz, 11 also were diagnosed
- Compared to 4 of the 197 of the control group
Genetic Explanations: Candidate Genes: Ripke
- 108 candidate genes associated with the increased risk of Sz
- Sz is aetiologically heterogenous
- Sz is polygenic
Genetic Explanations: Role of Mutation
- Mutation in parental DNA which can be caused by poison, radiation, or viral infection, epigenetics
- Positive correlation between parental age with increased risk of Sz
-> **Brown et al (2002): 0.7% with fathers under 25 to over 2% in fathers over 50
Genetic Explanation: :) Hilker et al (2018)
Concordance rate of 33% for MZ twins and 7% for DZ twins
Genetic Explanations: :) Genetic counselling
- Informing potential parents of probabilities prior
- :( it’s an average figure based on risk across the whole population, doesn’t account for the external risk factors
Genetic Explanations: :( Exclusionof environmental influences
- Morhved (2017): 67% of people with Sz and related psychotic disorder reported at least one childhood trauma
- Morgan et al (2017): birth complications
- Di Forti et al (2015): smoking THC-rich cannabis in teenage years
- Insufficient in providing a complete explanation for Sz
Neural Correlates: Original Dopamine Hypothesis
Hyperdopaminergia
- Sz is the result of high levels of dopamine in the subcortical regions of the brain
-> Dopamine is associated with positive symptoms
- Drugs that increase dopaminergic activity; develop Sz-like symptoms
- Drugs that decrease dopaminergic activity; eliminates Sz-like symptoms
- Broca’s Area: speech poverty and/or auditory hallucinations
Neural Correlates: Updated Dopamine Hypothesis
Hypodopaminergia
- Sz is the result of low levels of dopamine in cortical regions of the brain
- Davis & Kahn (1991): negative and cognitive symptoms are thought to arise from a deficit of dopamine
- Howes (2017): genetic variations + physical and environmental stressors = greater sensitivity
Neural Correlates: :) Leucht et al (2013)
- Meta-analysis of 212 studies
- All antipsychotic drugs were significantly more effective than placebo at treating positive and negative symptoms by reducing the effects of dopamine
Neural Correlates: :( Noll (2009)
- Antipsychotic drugs do nor alleviate hallucinations and delusions in about 1/3 of people
- In some people, hallucinations and delusions are still present despite levels of dopamine being normal
Neural Correlates: :) Patel (2010)
- PET scans to assess dopamine levels
- Lower levels of dopamine in the prefrontal cortex of schizophrenic patients compared to controls
Neural Correlates: Addington et al (2015)
- Early intervention may reduce the development of the later stages of this disorder
- “treatment as prevention”
- predicts who develops psychoses such as Sz
Typical Antipsychotics: AO1
- Attempts to reduce the action of dopamine (original dopamine hypothesis)
- Chlorprozamine is administered orally daily up to a max of 1000mg
- Dopamine antagonists by blocking dopamine receptors in synapses in the brain
Typical Antipsychotics: AO3
:( Impacts on the extrapyramidal areas of the brain
-> Parkinsonian symptoms: 50%+
:( Neuroleptic malignant syndrome
-> high temp, delirium, coma, can be fatal
:) Sedative effect
Atypical Antipsychotics: AO1
- aim to reduce even negative symptoms of Sz
- Clozapine: blocks dopamine receptors and serotonin and glutamate
- Resperidone: binds more strongly to dopamine receptors & serotonin
Atypical Antipsychotics: AO3
:( Clozapine: 30-50% of people with Sz attempted suicide
-> agranulocytosis
