carlsson

Question 1

aims

Answer 1

• present a review of the evidence for and against the dopamine hypothesis.
• to consider the role of other neurotransmitters such as glutamate and serotonin.
• to explore new antipsychotics, especially for people who are treatment resistant or who experience extreme side effects.

Question 2

procedure

Answer 2

• literature review of 32 studies of research findings, including:
• neurochemicals in patients
• animal studies
• use of recreational drugs eg. pcp
• brain scanning evidence
  used meta analysis - gathering lots of evidence and analysing - secondary data.

Question 3

findings

Answer 3

1) hyperdopamanergic model - the traditional view that sz is the result of increased level of dopamine.
evidence=
PET scan studies show that amphetamines and PCP which increase levels of dopamine enhance sz like symptoms in people with sz more than controls.
this is not challenged by the second model, only extended as dopamine is not the only neurotransmitter linked.

2) hypoglutamergic model - the idea that low levels of glutamate play a part in the development.
it can increase or decrease dopamine levels eg. when glutamate decreases, dopamine increases.
- Glutamte also affects the production of GABA which decreases dopamine.
- therefore, low levels of glutamate can cause an increase or decrease in dopamine activity because of GABA.
evidence=
PCP blocks glutamate receptors and induces symptoms.
also clozapine reduces both dopamine and serotonin and may be more effective in treating hypoglutamatergic type.

Question 4

conclusions

Answer 4

• provides a useful update to the dopamine hypothesis which includes the role of glutamate. - original theory was more reductionist
• shows that further research is necessary in understanding the role of other neurotransmitters and pathways in brain.
• overall; there could be different causes for different types of sz which has implications for treatment; diff people might need diff drugs.

Question 5

generalisability

Answer 5

:) review which is based on 32 peer reviewed journal articles. therefore evidence has scientific credibility.
CA= however, of the 32 articles reviewed, 16 had been written by carlsson which may have affected their objectivity.

Question 6

reliability

Answer 6

:) carlsson could assess the findings across a range of literature. therefore, he could assess the consistency of data across different bodies of research.
some of the research used within literature was highly standardised, such as the use of PET scans.
CA= however, the reliability of the review could be compromised by the fact that studies within a meta analysis are very different. one study he includes was not actually published and therefore not peer reviewed.

Question 7

validity

Answer 7

:( as the data was secondary there may well be bias in the selection.
CA= that said, the use of secondary data meant a wide body of literature could be used to support carlssons research.
however, the use of animal studies might compromise the literature review as animals may respond differently to glutamate and dopamine and cannot be diagnosed with sz.

:( another weakness of the review is that it ignores the role of culture.
this is because of its focus on the role of neurotransmitters only which means that it takes only a biological approach.
- this is a problem because of the clear cultural differences highlighted in other research eg. lurhmann 2015 which shows different experiences of hallucinations in US participants compared to Indian.
- this implies that such research fails to capture the holistic experience of people suffering.

Question 8

ethics

Answer 8

:) the use of secondary data meant that no further harm could come to animals in research.