biological explanations for SZ Flashcards

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1
Q

what is the biological explanation of sz?

A
  • genetic link
  • dopamine hypothesis
  • neural correlates
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2
Q

what is a genetic link in SZ?

A
  • the genetic explanation of schizophrenia looks at hereditary factors (genes) that contribute to the development of SZ
  • SZ tends to run in families through genes
  • SZ is polygenic (many genes contributing)
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3
Q

why are twin studies useful when looking at genetic factors?

A

twin studies are a useful way to determine whether or not a condition is inherited through genetics
- if it is more common for both identical twins to suffer from schizophrenia than it is for both non-identical twins, this would suggest a genetic component to schizophrenia

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4
Q

who conducted SZ twin studies?

A

Gottesman

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5
Q

what did Gottesman look at when conducting twin studies?

A

looked at how different family relationships to someone with schizophrenia are linked with risk of developing schizophrenia

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6
Q

what did Gottesman find?

A
  • Gottesman found that the closer the genetic relationship to the person with schizophrenia, the greater the risk of developing schizophrenia
  • for example, the concordance rate for schizophrenia among identical twins is 48%, whereas for non-identical twins it is 17%.
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7
Q

what do Gottesman’s findings suggest?

A
  • suggests there must be a genetic component in the development of SZ
  • however, it is unlikely that SZ is entirely genetic as the concordance rates for MZ twins (who share 100% DNA) was not 100%
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8
Q

what is the dopamine hypothesis?

A

it states that SZ results from an imbalance of the NT dopamine in the brain

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9
Q

what are the 2 dopamine genes that contribute to the development of SZ in the brain?

A
  • hypodopaminergia
  • hyperdopaminergia
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10
Q

where is hypodopaminergia found?

A

in the cortex

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11
Q

where is hyperdopaminergia found?

A

in the sub-cortex

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12
Q

what is hypodopaminergia in the cortex?

A
  • abnormally low dopamine levels
  • believed to be responsible for negative symptoms of SZ
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13
Q

what did Goldman-Rakic find about the hypodopaminergia?

A

identified a role for low levels of dopamine in the pre-frontal cortex, in the negative symptoms of SZ such as speech poverty and avolition
- this is because the prefrontal cortex is associated with logical thinking, so abnormally low dopamine levels
in this area may impair an individual’s ability to construct grammatical sentences (speech poverty) or the ability to make decisions about how to function in day to day
living (avolition)

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14
Q

what is hyperdopaminergia in the sub-cortex?

A
  • excess high levels of dopamine in sub-cortex
  • hyperdopaminergia in the frontal lobe, and specifically Broca’s area, which may have an excess of D2 receptors, may be responsible for the positive SZ symptom of auditory
    hallucinations, due to the overactivity of neurotransmission in the auditory areas of the brain
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15
Q

is the hypodopaminergia responsible for positive or negative symptoms of SZ? and examples

A

negative; speech poverty, avolition

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16
Q

is the hyperdopaminergia responsible for positive or negative symptoms of SZ?

A

positive; auditory hallucinations

17
Q

how has the dopamine hypothesis been refined (simplified summary)?

A

research suggests that schizophrenia is linked with high dopamine activity in some areas of the brain (the subcortex) but low dopamine activity in other areas (prefrontal cortex).

18
Q

what are neural correlates?

A

when a particular structural difference in the brain is associated with the development of SZ (difference in ventricle size)

19
Q

how do researchers use brain scanning to study neural correlates?

A
  • research uses non-invasive scanning techniques, such as fMRI, to compare the functioning of the brains of SZ patients and non-sufferers
  • to identify brain structures that may be linked to SZ
20
Q

what did Johnstone find when researching neural correlates?

A
  • focused on SZ patients having enlarged ventricles (which are associated to damage in central brain areas and the pre-frontal cortex)
  • such damage has often been associated with negative symptoms, as shown in studies such as Andreasen et al
21
Q

what did Allen find when researching neural correlates?

A
  • found that positive symptoms also have neural correlates
  • scanned the brains of patients experiencing auditory hallucinations and compared them to a control group
  • scanned brains whilst ppt’s asked to identify whether pre-recorded speech was theirs or others
  • SZ patients made more errors than control group
    -lower activation levels in 2 areas of the brain were found in the SZ patients, suggesting reduced brain activity is a neural correlate of Sz
22
Q

did Allen find that negative or positive symptoms have neural correlates?

A

positive symptoms (auditory hallucinations)

23
Q

evaluation genetics: supporting evidence

A

ID: there is now strong evidence for genetic vulnerability to SZ from a variety of research
Q: family and twin studies of schizophrenia support the genetic explanation of schizophrenia because they show that being closely related increases the likelihood of suffering from schizophrenia.
EV: for example, Gottesman found that MZ twins had a concordance rate of 48% and DZ twins had a concordance rate of 17%. additionally Tienari’s adoption study found that children of SZ sufferers are still at a wider risk of SZ if adopted into families with no history of SZ.
AN: these studies suggest there must be a genetic component in the development of SZ, however it may be unlikely that SZ is entirely genetic as MZ twins didn’t have 100% concordance rates. This suggests an interactionist approach is best for explaining schizophrenia.

24
Q

evaluation genetics: undermining evidence

A

ID: despite research supporting genetic vulnerability to SZ, there is also undermining evidence
- many researchers now accept that the fact that SZ appears to run in families may be more due to common rearing patterns or other factors that have nothing to do with heredity
EV: for example, a negative emotional climate in some families may lead to stress beyond an individual’s coping mechanisms, therefore triggering a SZ episode.
furthermore, the probability of developing SZ, even if your identical twin has it, is less than 50%
AN: this suggests that whilst a genetic vulnerability for SZ may be important, there are psychological factors that need to be taken into account. meaning it may be better to take an interactionist approach, combining biological and psychological factors.

25
Q

evaluation neural correlates: correlation vs causation

A

ID: a weakness of neural correlates as an explanation of SZ is that the evidence is correlational
Q: although studies are useful in flagging up particular brain systems that may not be working properly, this kind of evidence does not prove that the activity in the brain region causes the symptom
EV: for example, the link between lower levels of activation in the superior temporal gyrus and anterior cingulate gyrus, and the experience of auditory hallucinations. one explanation would be the lowered activation levels causing the hallucinations, or the hallucinations themselves causing the lowered activation levels
AN: Therefore, this demonstrates that correlational research cannot be used to reliably demonstrate a ‘cause and effect’ relationship between two variables.