Biological Explanation

Question 1

What did Gottesman find?

Answer 1

• MZ twins have a 48% of getting sz whereas DZ twins have a 27% risk rate
• this shows the closer the genetic are the higher the risk of getting sz

Question 2

How is SZ polygenic?

Answer 2

it requires a number of factors to work

Question 3

How is SZ aetiologically heterogeneous?

Answer 3

different combinations can lead to the condition

Question 4

Nature v urture (weakness of Genetic basis of sz)

Answer 4

• it is difficult to separate out the influence of nature-v-nurture
• concordance rates are not 100% which means that genetic cannot be a single explanation
• could be that an individual has a pre-disposition to sz which makes the individual more at risk of developing SZ

Question 5

Methodological Problems (weakness of Genetic basis of sz)

Answer 5

• family, twin and adoption studies must be considered cautiously because they are retrospective, and diagnosis may be biased by knowledge of other family members with the disorder
• there may be problems of demand characteristics

Question 6

Hyperdopamonergia in the subcortex

Answer 6

• original dopamine hypothesis stated that sz suffered from an excessive amount of dopamine in the sub cortex
• this causes the neurons that use dopamine to fire too often and transmit too many messages
• an excess of dopamine receptors in broca’s area may result in poverty speech and/or auditory hallucinations

Question 7

High dopamine activity levels leads to

Answer 7

• positive symptoms: delusions, hallucinations,

Question 8

What does amphetamines do?

Answer 8

• increase the amount of dopamine

Question 9

What did large doses of amphetamines do to people who has no history of psychological disorders?

Answer 9

• produced behaviours which were similar to a paranoid sz

Question 10

What did small doses of amphetamines do to people who had sz?

Answer 10

worsened their condition

Question 11

Hypodopaminergia in the cortex

Answer 11

• recent explanation suggests that it is not an excessive dopamine but there are more dopamine receptors
• more receptors leads to more firing and an over production of messages

Question 12

What did Goldman-Rakic et al find?

Answer 12

a role for low levels of dopamine in the prefrontal cortex in the negative symptoms of sz

Question 13

Biologically deterministic (weakness of dopamine hypothesis)

Answer 13

• if the individual does have excessive amount of dopamine then does it mean they will develop sz?
• this does not account for free will

Question 14

What did Farde et al find?

Answer 14

no difference between sz levels of dopamine compared with ‘healthy’ individuals in 1990

Question 15

Neural Correlates

Answer 15

are patterns of structure or activity in the brain that occur in conjunction with sz

Question 16

What did Juckel et al do?

Answer 16

• measured activity levels in the ventral striatum in sz and found lower levels of activity than those observed in controls
• they observed a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms
• thus showing that activity in the ventral striatum is a neural correlate of negative symptom of sz

Question 17

What did Allen et al do?

Answer 17

• scanned the brains of patients experiencing auditory hallucinations and compared them to a control group
• lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group,
• therefore, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations

Question 18

High Reliability (strength neural correlates)

Answer 18

• research into enlarged ventricles and neurotransmitter levels have high reliability
• research is carried out in highly controlled environments
• high tech equipments is used such as MRI and PET scans which take accurate readings of brain regions
• suggest that if this research was tested and re-tested the same result would be achieved