Biological Explanations for Schizophrenia Flashcards
(24 cards)
AO3 (1) biological explanations for schizophrenia
A strength of the biological explanation of schizophrenia is that it has supporting evidence. For example, Gottesman found that the concordance rate for schizophrenia among identical twins is 48% whereas for non-identical twins it is 17%. This is a strength because it shows the genetic relationship to the person with schizophrenia, the greater the risk of developing schizophrenia which supports the idea that genetics plays a role in developing schizophrenia. However some psychologists may argue that there are methodological issues surrounding twin studies as greater similarities in environment could contribute to its higher concordance rates for schizophrenia among identical twins, with the influence of genetics being exaggerated. Despite this, genetics do contribute to the high concordance rates as there is data to show this.
AO3 (2) biological explanations for schizophrenia
- Biological explanation led to antipsychotic treatment
- E – block dopamine receptors
- E – alleviates symptoms = + quality of life
- CA: Reductionist – reduce the complexity of SZ to simply genetics Gottesman – identical twins only 48% concordance rate – if solely due to SZ this would be higher
- CA: crazy side effects
- Useful in treatments, practical approach
AO3 (3) biological explanations for schizophrenia
- A strength is that there is clear evidence of the role of dopamine
- General consensus that dopamine plays a key role in the development of SZ symptoms – hyperdopaminergia
- Hyperdopamingeria – high lvels of dopamine, access dopamine, receptors in Broca’s area – impairs speech production – results in speech poverty
- However, some of the candidate genes identified code for the production of other neurotransmitters such as glutamate, so dopamine may have limited role in the development of SZ symptoms. Recent research – hypodopmingeria – low levels of dopamine in the prefrontal cortex (Thinking and decision making) Goldman-Rakic
- One component of SZ – not the complete explanation for SZ – dopamine/gluatmate
Q: What did Gottesman (1991) find about schizophrenia in families?
A: A positive correlation between genetic similarity and risk of schizophrenia; monozygotic twins had 48% concordance, dizygotic 17%, siblings 9%, parents 6%.
Q: What does the less than 100% concordance rate in identical twins suggest?
A: Environmental factors also influence the development of schizophrenia.
Q: What does it mean that schizophrenia is polygenic?
A: Multiple genes contribute to the risk of developing schizophrenia.
Q: What did Ripke et al. (2013, 2014) discover about schizophrenia genes?
A: Identified 108 genetic variations associated with schizophrenia risk, including genes linked to dopamine function.
Q: How is paternal age linked to schizophrenia risk?
A: Older fathers (over 50) have a higher risk of passing mutations that increase schizophrenia risk
Q: How can schizophrenia arise without a family history?
A: Through mutations in parental DNA caused by factors like radiation, poisons, or viral infections.
Q: What does the original dopamine hypothesis suggest?
A: Schizophrenia is caused by excessive dopamine (hyperdopaminergia) in subcortical brain areas.
Q: What is the revised dopamine hypothesis?
A: Schizophrenia involves low dopamine (hypodopaminergia) in the cortex, especially the prefrontal cortex.
Q: What is the modern understanding of dopamine’s role in schizophrenia?
A: Both high dopamine activity in some brain areas and low dopamine activity in others contribute to schizophrenia symptoms.
Q: Which dopamine receptor is often increased in schizophrenia patients?
A: Dopamine D2 receptors, especially in Broca’s area.
Q: What symptoms might hyperdopaminergia in Broca’s area cause?
A: Positive symptoms like auditory hallucinations and speech poverty.
Q: What symptoms might hypodopaminergia in the prefrontal cortex cause?
A: Negative symptoms such as speech poverty and avolition.
What is meant by neural correlates in schizophrenia?
Brain structures or activity patterns that coincide with specific schizophrenia symptoms.
What did Juckel et al. (2006) find about the ventral striatum?
Reduced activity is linked to the negative symptom of avolition.
What did Allen et al. (2007) find about brain activity during auditory hallucinations?
Reduced activation in the anterior cingulate and left temporal cortex correlates with misidentification of self-generated speech.
Define neural correlates.
Brain patterns or structures that occur alongside certain psychological experiences or symptoms.
What is dopamine’s general function and role in schizophrenia?
Dopamine is a neurotransmitter involved in pleasure, movement, and thinking; abnormal levels are linked to schizophrenia symptoms.
What is the role of the prefrontal cortex and its link to schizophrenia?
It helps logical thinking; lower activity is linked to delusions and disorganized thoughts.
How do the visual and auditory cortex behave during hallucinations?
They show similar activity to that during real sensory experiences.
What is the basal ganglia’s involvement in schizophrenia?
It is larger in patients and linked to motor dysfunction.
How does the amygdala relate to schizophrenia symptoms?
Smaller size is linked to affective flattening (loss of emotional expression).
