biological: neural correlates of schizophrenia

neural correlates

• Neural correlates of schizophrenia are the particular brain areas, structures, or functions that are linked to symptoms and behaviours characteristic of the disorder

• Neural correlates of negative symptoms:

  • The ventral striatum (part of the limbic system, associated with the anticipation of reward) has been associated with the negative symptoms of schizophrenia e.g. abolition (lack of motivation to initiate and persist in goal-directed behaviour)

  • Kirschener et al. (2016) found that schizophrenic patients show less activity in the ventral striatum, which is associated with apathy

• Neural correlates of positive symptoms:

  • The superior temporal gyrus (STG), which is thought to control the processing of speech, has been associated with positive symptoms of schizophrenia e.g. hallucinations

  • Rajarethinam et al. (2000) found that schizophrenic patients show reduced volumes of grey matter in the STG, which is associated with hallucinations and though disorder

van rossen’s dopamine hypothesis

• The dopamine hypothesis is a theory, first suggested by Van Rossum (1966), which claims that an overstimulation of dopamine receptors may be a contributory factor to a person’s vulnerability to schizophrenia

• The original version of the DH suggests the idea that hyperdopaminergia (abnormally high levels of dopamine) in the sub-cortex may be responsible for the onset of schizophrenia

• Hyperdopaminergia assumes that an excess of dopamine is active in areas such as the amygdala, basal ganglia, hippocampus, and nucleus accumbens, which creates an altered perception of the world

  • E.g. positive symptoms such as auditory hallucinations could be caused by hyperdopaminergia in Broca’s area, which regulates speech production

• Van Rossen’s DH was supported by research which showed that dopamine antagonists, which blocked the dopamine pathways, were linked to a reduction in positive schizophrenic symptoms

newer version of the dopamine hypothesis

• The newer version of the DH posits the idea that hypodopaminergia (abnormally low levels of dopamine) in the prefrontal cortex may be responsible for the onset of schizophrenia

  • The PFC is thought to control and regulate executive functions such as information processing, rational thought, and decision-making

• 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, and 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 hypodominergia may be at work in different brain areas to produce schizophrenia

research which investigates neural correlates of schizophrenia

• Shenton et al. (1992)

  • Found reduced grey matter volume in the left superior temporal gyrus (STG)

  • The structural abnormality observed serves as a neural correlate of the positive symptom thought disorder, suggesting that the brain region’s dysfunction contributes to the expression of that symptom

• Juckel et al. (2006)

  • Found that 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)

  • Found that the antipsychotic drugs clozapine and risperidone act as dopamine antagonists and are associated with a reduction of adverse schizophrenia symptoms

• Davis et al. (1991)

  • Found that schizophrenia is linked to hypodopaminergia in the PFC, which leads to hyperdopaminergia in the sub-cortex - meaning both hypodopaminergia and hyperdopaminergia are implicated in schizophrenia

strengths of neural correlates of schizophrenia

• The use of brain-imaging techniques such as PET, MRI and fMRI provides 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 result over time, supporting their reliability

weaknesses of neural correlates of schizophrenia

• The research evidence for neural correlates takes a correlational approach to mapping brain regions in schizophrenia, which means that it lacks a cause-and-effect explanation

• There is no acknowledgment of the role of the environment in this explanation of schizophrenia, meaning it lacks external validity

links of neural correlates explanation of schizophrenia to issues & debates

• The neural correlates explanation is reductionist, as it reduces schizophrenia to brain structures and neurochemical activity, which 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 can be ethically problematic, particularly in legal or clinical contexts where responsibility and personal agency are considered