Neural Correlates of Schizophrenia

Neural correlates

Neural correlates of schizophrenia refer to the specific brain regions/structures/functions that are implicated in the symptoms and behaviours associated with the disorder
There are neural correlates for both the positive and the negative symptoms of schizophrenia
The ventral striatum (VS), which is the largest structure in the basal ganglia, has been associated with the negative symptoms of schizophrenia e.g. avolition
The VS is part of the limbic system associated with anticipation of reward
Schizophrenic patients show less activity in the VS which is associated with apathy (Kirschener et al. 2016)
The superior temporal gyrus (STG), which is thought to control the processing of speech, has been associated with the positive symptoms of schizophrenia e.g. hallucinations
Schizophrenic patients show reduced volume of grey matter in the STG which is associated with hallucinations and thought disorder (Rajarethinam et al. 2000)

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The superior temporal gyrus is associated with the positive symptoms of schizophrenia.

Exam Tip

Make sure that you are able to use these specific, technical terms (e.g. ventral striatum) in an exam as this will help to add authority to your exam responses.

The dopamine hypothesis

Dopamine is one of the most researched neurotransmitters, associated with reward, motivation, reinforcement (and strongly implicated in the mechanisms of addiction)
The dopamine hypothesis (DH) is a theory which was first suggested by Van Rossum (1966) which, in essence, claims that an overstimulation of dopamine receptors may be a contributory factor to a person’s vulnerability to schizophrenia
This original version of the DH posits the idea that hyperdopaminergia (‘hyper’ = more) in the sub-cortex (sub = beneath) may be responsible for the onset of schizophrenia
The sub-cortex of the brain takes up 25% of total brain volume and includes the central areas such as the amygdala, the basal ganglia, the hippocampus and the nucleus accumbens
Hyperdopaminergia assumes that an excess of dopamine is active in these central areas, the effect being an altered perception of the world e.g. positive symptoms such as auditory hallucinations (link to Broca’s area which regulates speech production)
Van Rossum’s original DH was supported by research which showed that dopamine antagonists which blocked the dopamine pathways was linked to a reduction in positive symptoms
The newer version of the DH posits the idea that hypodopaminergia (‘hypo’ = less) in the prefrontal cortex (PFC) may be responsible for the onset of schizophrenia
The PFC of the brain is thought to control and regulate executive functions such as information-processing, rational thoughts, decision-making etc.
Hypodopaminergia assumes that low levels of dopamine in the PFC are linked to negative symptoms such as speech poverty: as the PFC plays a role in logical thinking, low levels of dopamine may lead to the inability to construct grammatical sentences
Current understanding of the role of dopamine in schizophrenia is that both hyperdopaminergia and hypodopaminergia may be at work in different brain areas to produce schizophrenia

Exam Tip

Be aware of which options topics (e.g. Schizophrenia) you have studied! This may sound like an obvious piece of advice but examiners report that despite clear instructions, some students answered questions on more than one optional topic per section - and this happens every year!

Research which investigates neural correlates of schizophrenia

Shenton et al. (1992) - Reduced grey matter volume was found in the left superior temporal gyrus which is related to thought disorder
Juckel et al. (2006) - low levels of activity in the ventral striatum may be associated with the negative symptom of avolition as this brain region is associated with evaluating rewards
Littrell & Schneiderhan (1996) - The antipsychotic drugs clozapine and risperidone act as dopamine antagonists (i.e. they reduce hyperdopaminergia) and are associated with a reduction in adverse schizophrenia symptoms
Davis et al. (1991) - Schizophrenia is linked to abnormally low PFC dopamine activity (hypodopaminergia) which leads to excessive dopamine activity (hyperdopaminergia) in the sub-cortex, therefore both high and low levels of dopamine activity are implicated in schizophrenia

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These PET scans show much lower activity in the frontal lobes of the schizophrenic brain which could be evidence of hypodopaminergia.

Evaluation of neural correlates of schizophrenia

Strengths

The use of brain-imaging techniques such as PET, MRI and fMRI provide objective evidence for neural correlates of schizophrenia as they pinpoint specific brain structures implicated in the symptoms of the disorder
Brain-imaging technologies are conducted under controlled clinical conditions which means that they are likely to show consistent results over time, hence they are likely to be reliable

Weaknesses

The research evidence for neural correlates takes (as the name suggests) a correlational approach to mapping brain regions to schizophrenia which means that it lacks a cause-effect explanation
There is no acknowledgement of the role of the environment to a neural correlates-based explanation of schizophrenia which means that it lacks external validity

Link to Issues & Debates:

A neural correlates explanation of schizophrenia is an example of biological determinism as it assumes that specific brain structures and/or dopaminergic activity in the brain play a key role in the onset of schizophrenia. A deterministic argument takes out the issue of free will i.e. it is not a foregone conclusion that someone with the brain structure/chemistry outlined above will develop schizophrenia at some point in their life: there may be protective factors which guard against it.

Worked example

Discuss neural correlates of schizophrenia.

[8]

AO1 = 3 marks, AO3 = 5 marks

For 6-8 marks the answer should provide a clear and coherent outline of the neural correlates explanation of schizophrenia, using a good level of detail. Effective use of examples should be given to support the points made. There should be confident use of terminology. Evaluation should be effective and should focus on biological explanations.

For 4-6 marks the answer should give a reasonably clear outline of the neural correlates explanation of schizophrenia, with some detail involved. There may be some lack of expansion or development of ideas. There should be some use of terminology. Evaluation will be present but may lack depth or range.

For 1-3 marks the answer will be only partially successful in providing a clear outline of the neural correlates explanation of schizophrenia, with possible inaccuracies present. Terminology will be sparse and there may be some vagueness or ambiguity to the response. Evaluation is likely to be sparse or absent altogether.

Possible answer content could include:

AO1: The dopamine hypothesis suggests that schizophrenia is due to dysfunctional dopamine neurotransmission either due to hyperdopaminergia in the subcortex (overly high levels of dopamine) linked to positive symptoms or hypodopaminergia in the cortex (low levels of dopamine) linked to negative symptoms. The ventral striatum has also been implicated in the development of avolition as this area is associated with reward and motivation. Research has found lower activity in the ventral striatum is associated with higher levels of avolition. A genetic explanation looks at the heritability of schizophrenia, with candidate genes being implicated in the onset of schizophrenia, particularly genes which have been linked to the action of dopamine.

AO3: Research suggests that dopamine may play a key role in schizophrenic symptomatology e.g. et al. (1999), Desbonnet (2016) with brain-imaging studies demonstrating high activity in dopamine-rich areas of the brains of schizophrenics. There may, however, also be other neurotransmitters involved in schizophrenia: Grunder & Cumming (2016) point out that the dopamine hypothesis should be modified to include the role of glutamate as a key contributory factor in promoting schizophrenic symptoms. There is also the issue of cause/correlation to consider as it is still unclear as to whether abnormal brain activity in specific regions such as the ventral striatum actually causes schizophrenia or is the relationship between the two the result of other factors as yet unknown? This is an issue with all biological explanations: they do not account for a range of other factors which may equally contribute to schizophrenia e.g. home life, socio-economic status, stress, education, environmental factors such as pollution, noise, overcrowding etc.

AQA A Level Psychology

Revision Notes