Biological Explanations

Question 1

What do most modern health practitioners accept?

Answer 1

That Sz is biological in nature

Question 2

Why is stating Sz runs in families weak evidence?

Answer 2

They tend to share the same environment

Question 3

What have studies focused on?

Answer 3

Genetic similarity - 100% identical twins, 50% with a parent etc - there is a strong risk between genetic similarity and risk of Sz

Question 4

What was Gottesman’s study?

Answer 4

He did a large scale family study and found that 1% general population. 5% grandchildren, 9% siblings, 17% fraternal twins and 48% identical twins

Question 5

As individual genes are associated with the risk of inheritance what does this mean?

Answer 5

A small number of genes appear to confer a small increased risk of Sz - it appears Sz is polygenic as it requires a number of factors to work in combination
Sz is possibly aetiologically heterogenous i.e. a number of factors can lead to the condition

Question 6

What was the research conducted by Ripke et al?

Answer 6

Carried out a large study combining all previous data from genome wide studies of Sz
37,000 patients were compared with 113,000 controls - 108 separate genetic variations were associated with the risk of Sz
Genes associated include a number of neurotransmitters including dopamine

Question 7

What is the dopamine hypothesis?

Answer 7

Neurotransmitters work differently in the brains of patients with Sz - dopamine is widely thought to be involved as D is important in the functioning of several brain systems that may be implicated in Sz
Hyperdopaminergia in the sub cortex was initially studies

Question 8

What is an example of dopamines possible involvement?

Answer 8

An excess of dopamine receptors in Broca’s area may be associated with speech poverty and auditory hallucinations

Question 9

What was Goldman-Rakic et al’s research into the role of dopamine?

Answer 9

He identified a role for the low levels of dopamine (hypodopaminergia) in the prefrontal cortex which is responsible for thinking and decision making, in the negative symptoms of Sz
It may be that both hyper and hypo are correct explanations and that both high and low levels of dopamine in different regions of the brain are involved in Sz

Question 10

What are neural correlates of Sz?

Answer 10

These are the measurements of the structure or function of the brain that correlates with experience. Both positive and negative symptoms have neural correlates

Question 11

What are neural correlates of negative symptoms?

Answer 11

Avolition involves the loss of motivation, motivated involves anticipation of reward and areas of the brain are involved in this (ventral striatum) so this area may be involved in the symptom
Juckel et al measured neural activity in the VS in Sz and found lower levels of activity than those observed in controls. They observed a negative correlation between activity levels in the VS and the severity of overall negative symptoms

Question 12

What are the neural correlated of the positive symptoms?

Answer 12

Allen et al scanned the brains of patients experiencing auditory hallucinations and compared them to the control group whilst they identified pre-recorded speech as theirs or others
Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucinations group who also made more errors than the control group
A reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations

Question 13

What are the multiple sources of evidence for genetic susceptibility? (eval)

Answer 13

Gottesman shows how genetic similarity and share risk of Sz are related 
Adoption studies (Tienari) showed that children who are adopted from Sz families are still susceptible 
There is also evidence from studies at a molecular level showing genetic variation (Ripke) 
But these studies do not show Sz as purely genetic - there are also environmental forces but genetic susceptibility is very important

Question 14

What is the mixed evaluation for the dopamine hypothesis? (eval)

Answer 14

Dopamine antagonists like amphetamines that increase the level of dopamine make Sz worse and produce Sz type symptoms in non-sufferers
Antipsychotic drugs that reduce dopamine also show that dopamine plays an important role in Sz
Lindstroem looked at radioactive studies and found the chemicals needed to produce dopamine are taken up faster in the brains of Sz sufferers than controls suggesting that they produce more dopamine

Question 15

Why is the dopamine hypothesis not entirely valid?

Answer 15

Dopamine does not produce a full explanation as other neurotransmitters are involved (current research has focused on glutamate
Evidence for the dopamine theory is at best mixed

Question 16

Why is correlation-causation a problem?

Answer 16

There is a correlation between levels of activity in the ventral striatum and negative symptoms of Sz so it may be that there is something wrong in the striatum is causing the negative symptoms or it may be that the negative symptoms themselves mean less information passes through, leading to less activity
Another theory = another factor influences both the negative symptoms and V.S activity - the existence of neural correlates tells us little

Question 17

What is the role of mutation?

Answer 17

Sz can take place in families with no history. One explanation is a mutation, e.g. in the paternal sperm cell- this could be caused by a viral infection or radiation. A positive correlation between paternal age and risk of Sz increasing from 0.7% in fathers under 25 to 2% in fathers over 50yrs (Brown et al)

Question 18

What is the role of the psychological environment?

Answer 18

The role of this is important but unclear - although genetics play an important role, other factors = equally important. The possibility of developing Sz is below 50% for identical twins