Biological: Neural Correlates of Schizophrenia (AQA A Level Psychology): Revision Note

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)

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

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

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

Limitations

• 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

Issues & Debates

• The neural correlates explanation is reductionist, as it reduces schizophrenia to brain structures and neurochemical activity

  • This ignores psychological, cognitive, and environmental factors, such as trauma or stress, making the explanation overly simplistic for a complex mental disorder

  • Therefore, it may limit the development of holistic treatment approaches

• The neural correlates explanation supports a biological determinist view, suggesting that abnormal brain structures and imbalanced dopamine levels determine the onset of schizophrenia

  • This challenges the concept of free will, as it implies individuals have little control over their thoughts or behaviours if they stem from fixed brain activity

  • Such a deterministic stance can be ethically problematic, particularly in legal or clinical contexts where responsibility and personal agency are considered