Schizophrenia: biological explanations

Question 1

What does the biological approach state about schizophrenia?

Answer 1

• It has been proposed that there is a genetic component to schizophrenia which predisposes some individuals to the illness.
• Whether a person develops schizophrenia is at least partly due to their genes.
• This may explain why patients often have other family members with schizophrenia.

Question 2

Explain the evidence from family studies which shows that schizophrenia is genetic (Gottesman -> large-scale family)

Answer 2

• One very large-scale family study was carried out by Gottesman (1991).
• Findings have shown that the greater the degree of genetic relatedness, the greater the risk of developing schizophrenia.

Question 3

Explain the evidence from twin studies which shows that schizophrenia is genetic (Gottesman and Shields)
(Joseph)

Answer 3

• Gottesman and Shields (1962) found that the concordance rate for schizophrenia in MZ twins was 48% compared to 17% for DZ twins.
• Joseph (2004) - showed concordance of 40.4% MZ and 7.4% for DZ.
• Suggested that schizophrenia is inherited through shared genes.

Question 4

Explain the evidence from adoption studies which shows that schizophrenia is genetic (Heston) (Tienari)

Answer 4

• Heston (1966) compared 47 adopted children whose biological mother had schizophrenia with a control group of adopted children with no history of schizophrenia in their biological family.
• None of the control group was diagnosed with the illness, 16% of the offspring of mothers with schizophrenia were diagnosed.
• Tienari et al. (2000) - adoption study.
• 11% of 164 adoptees whose mothers have schizophrenia also had schizophrenia.

Question 5

what is the candidate gene? (Ripke)

Answer 5

• Schizophrenia is thought to be polygenic.
• Ripke et al. (2014) completed a study combining all data from a genome wide study of schizophrenia.
• 37,000 patients were compared to 113,000 controls; 108 separate genetic variations were associated with an increased risk of schizophrenia.

Question 6

What is the dopamine hypothesis?

Answer 6

• This theory claims that excessive amounts of dopamine is the cause of schizophrenia.
• The dopamine hypothesis states that messages from neurons that transmit dopamine fire too easily or too often, leading to the characteristic symptoms of schizophrenia.

Question 7

Explain how HYPERdopaminergia in the sub cortex can play a role in schizophrenia (dopamine hypothesis)

Answer 7

• higher levels of dopamine in the subcortex.
• excessive levels of dopamine receptors in Broca’s area.
  -> poverty of speech
  -> experience of auditory hallucinations

Question 8

Explain how HYPOdopaminergia in the sub cortex can play a role in schizophrenia (Goldman-Rakic)

Answer 8

• abnormal dopamine systems in the brain’s cortex.
• Goldman-Rakic identified a role for low levels of dopamine in the prefrontal cortex.
• This causes negative symptoms of schizophrenia as it effects thinking and decision making.

Question 9

list the evidence which support the dopamine hypothesis

Answer 9

• Amphetamines (dopamine agonist)
• Cocaine
• Antipsychotic drugs (dopamine antagonist)
• L-Dopa (a drug for Parkinson’s)
• post mortems

Question 10

Explain how amphetamines (agonist) are proof of the dopamine hypothesis

Answer 10

• a dopamine agonist -> this stimulates nerve cells containing dopamine causing the synapse to be ‘flooded’ – large doses of the drug can cause hallucinations and delusions of a schizophrenic episode.

Question 11

Explain how cocaine is proof of the dopamine hypothesis

Answer 11

• also increases the levels of dopamine in the brain (like amphetamines do) and can cause the positive symptoms of schizophrenia and exaggerate them in people who already have the disorder.

Question 12

Explain how antipsychotic drugs are evidence of the dopamine hypothesis

Answer 12

• dopamine antagonists which block the activity of dopamine in the brain, by reducing the stimulation of the dopamine system -> eliminates hallucinations and delusions.
• By alleviating many of the symptoms of schizophrenia, antipsychotic drugs strengthen the case for dopamine being a significant contributory factor.

Question 13

explain how L-dopa is evidence of the dopamine hypothesis

Answer 13

• L-Dopa – a drug for Parkinson’s * disease actually increases dopamine – this in turn can produce symptoms similar to that of schizophrenia.

Question 14

explain how post mortems are evidence of schizophrenia (Seeman)

Answer 14

• Post mortems of schizophrenics show an increase of dopamine in parts of the brains (Seeman 1987).

Question 15

What are Neural correlates (neural explanation of schizophrenia)?

Answer 15

• Neural correlates are measurements of the structure or function of the Brian that occur in conjunction. with an experience, in this case schizophrenia.
• Growing evidence that schizophrenia is down to structural abnormalities in the brain.
• Both positive and negative symptoms have neural correlates.

Question 16

what are the neural correlates of negative symptoms of schizophrenia (Juckel)

Answer 16

• Activity in ventral striatum has been linked to the development of avolition (loss of motivation).
• The ventral striatum is believed to be particularly involved in the anticipation of a reward for certain actions.
• Juckel et al. (2006)- lower levels of activity on the ventral striatum in people with schizophrenia compared to controls.
• Negative correlation between activity levels in the ventral striatum and the severity of overall negative systems.

Question 17

What are the neural correlates of positive symptoms of schizophrenia (Allen)

Answer 17

• Reduced activity in the superior temporal gyrus and anterior cingulate gyrus have been linked to the development of auditory hallucinations.
• Patients experiencing auditory hallucinations showed lower activation levels in these areas than controls.
• Therefore, reduced activity in these areas of the brain is a neural correlate of auditory hallucinations.
• (Allen et al., 2007).

Question 18

Evaluate twin studies as a way of explaining schizophrenia

Answer 18

(+)
- seem to indicate a strong genetic component to the disorder.
- there may be a predisposition to develop schizophrenia

(-) however, fact that both twins do not always develop schizophrenia means environmental factors must also play a part.
(-) concordance rate for twins is not 100% means schizophrenia cannot be accounted for by genetics alone.
(-) samples sizes are very small, very difficult to generalise findings.

Question 19

Evaluate adoption studies as a way of explaining schizophrenia

Answer 19

• results of studies only reveal small percentages, nonetheless support the idea that gens must play a role.
• Tienari -> 155 adoptees whose bio mothers had schizophrenia, 10% had also received a diagnosis of schizophrenia.
  -> compared to 1% of the 185 control adoptees -> this provides supporting evidence.
  -> however only conducted in Finland -> can’t generalise to other countries.

Question 20

Evaluate the dopamine hypothesis

Answer 20

(-) Mixed evidence:
- Curran found dopamine agonists actually increase dopamine and can make symptoms worse.
- Tauscher found antipsychotic drugs actually reduce levels of dopamine.
- Lindstoroem found that chemicals needed to produce dopamine are taken up faster in the people with schizophrenia -> suggests they produce more dopamine.

Question 21

Evaluate neural correlates as a way of explaining of schizophrenia

Answer 21

(-) correlation-causation problem
- neural correlations tell us little about the causes of schizophrenia.

• Findings are inconsistent and therefore inconclusive.
• issues of causality -> cause and effect can not be established with brain abnormalities -> uncertain whether structural abnormalities/reduced functioning predispose to schizophrenia, or whether the onset of the clinical symptoms causes these changes.