Neural correlates

• Explain what is meant

  by ‘neural correlates’ of schizophrenia.

  There is a correlation between abnormalities in brain structure/function and symptoms of schizophrenia.
• Outline the dopamine hypothesis as a neural correlate for schizophrenia.

  Proposes that schizophrenia can result from hyperdopaminergia (too much dopamine activity) in the subcortex of the brain.

  This is because there are too many D2 receptors for dopamine to bind to.

  As dopamine is an excitatory neurotransmitter, its increased activity makes neurons more likely to fire. This results in positive symptoms e.g. hallucinations and delusions.
• Outline the dopamine hypothesis as a neural correlate for schizophrenia.

  The dopamine hypothesis also proposes that schizophrenia can result from hypodopaminergia (too little dopamine activity) in the cortex.

  This is because there is reduced binding of dopamine to D1 receptors in the prefrontal cortex.

  As this area is responsible for decision making and is near Broca’s area, reduced activity is linked to the negative symptoms of schizophrenia e.g. avolition and speech poverty.
• Outline one other neural correlate for schizophrenia.

  Another neural correlate for schizophrenia is enlarged ventricles (fluid-filled gaps in the brain).

  These are proposed to be enlarged because there is a loss of brain tissue, particularly in the prefrontal cortex.

  The prefrontal cortex plays a role in motivation, planning and decision making so reduced tissue/activity here can be linked to the symptom of avolition.
• Evaluate the neural correlates for schizophrenia: supporting evidence. 


  E.g. research has found that drugs that increase dopamine activity worsen schizophrenic symptoms and can produce schizophrenic-like symptoms. Brain scanning studies have found that when the brains of individuals with schizophrenia are compared to neurotypical controls, there are structural differences in the brains. These include enlarged ventricles and decreased brain activity in the pre-frontal cortex. This is a strength as it supports the idea that schizophrenia may be caused by atypical brain function/structure.
• Evaluate the neural correlates for schizophrenia: practical applications when treating schizophrenia. 


  E.g. the dopamine hypothesis led to the use of antipsychotic drugs that work by decreasing dopamine activity in the brain. Such drug therapies are found to be more effective than placebos. This is a strength because if the treatment is effective, then the explanation itself must have merit. |
• Evaluate the neural correlates for schizophrenia: contradictory evidence.


  E.g. atypical antipsychotics (that affect various neurotransmitters including serotonin and dopamine) are found to be more effective than typical antipsychotics (that only affect dopamine), especially when treating negative symptoms. This is a limitation of the dopamine hypothesis as it suggests that additional neurotransmitters may play a role in schizophrenia.
• Evaluate the neural correlates for schizophrenia: biologically deterministic.


  This is because it proposes that schizophrenia is determined by brain abnormalities which are out of the individual’s control, so can result in feelings of hopelessness. This is a limitation as it can worsen their symptoms and lead to additional mental health difficulties such as depression.
• Evaluate the neural correlates for schizophrenia: biologically reductionist.

  This is because they are attempting to explain the complex disorder of schizophrenia by reducing it down to neurotransmitter/brain structure abnormalities. This is a limitation because it fails to consider the impact of additional factors in the development of schizophrenia e.g. a dysfunctional family environment. Indeed, many psychologists now use the diathesis-stress model which proposes that schizophrenia can only develop if you have a combination of factors.