The Biological explanations for Schizophrenia (neural correlates)

Neural correlates (1)

• A brain based feature that is associated with schizophrenia

 

We do not know exactly what’s causes the symptoms of schizophrenia on a biological level, however research has identified some neural correlates (for example some brain structures or functions)

 

The best-known neural correlate of schizophrenia is the neurotransmitter dopamine (DA).

 

It is important in the functioning of several brain systems related to the symptoms of schizophrenia.

The original dopamine hypothesis (1)

The original dopamine hypothesis was based on the discovery that drugs used to treat schizophrenia (antipsychotics which reduce DA) caused symptoms similar to those in people with Parkinson’s disease, a condition associated with low DA levels.

 

Therefore, schizophrenia might be the result of high levels of DA in the subcortical areas of the brain.

• Too much dopamine, partiucalry in subrotical areas -> schizophrenia symptoms

• Underneath areas of the cerebral cortex

The original dopamine hypothesis (2)

For example, an excess of DA receptors in pathways from the subcortex to Broca’s area (responsible for speech production) may explain specific symptoms of schizophrenia such as poverty of speech and/or auditory hallucinations.

 

Schizophrenia -> Abnormal dopamine functioning -> symptoms

 

The original hypothesis particularly suggested excess dopamine in subcortical areas.

 

If there is abnormal dopamine activity/receptors affecting pathways involving Broca’s area, this could contribute to symptoms such as:

• Auditory hallucinations

• Poverty of speech

Updated versions of the dopamine hypothesis (1)

Davis (1991) proposed that cortical hypodopaminergia (low DA in the brains cortex) could explain symptoms of schizophrenia.

 

Low DA in the prefrontal cortex (responsible for thinking) could explain cognitive problems (negative symptoms)

 

Also cortical hypodopaminergia may lead to subcortical hypodopaminergia - so both high and low levels of DA in different brain regions are part of the updates hypothesis.

Updated versions of the dopamine hypothesis (2)

All well as explaining the links between atypical DA levels and symptoms, current versions of the dopamine hypothesis try to explain the orgina of atypical DA function.

 

So it seems that both genetic variations and early experiences of stress, both psychological and physical, make some people sensitive to cortical hypodopaminergia and hence subcortical hypodopaminergia.

 

Schizophrenia = abnormal dopamine functioning in different brain regions.

Updated versions of the dopamine hypothesis (3)

Brain area	Dopamine	Possible symptoms
Subcortical	↑ HIGH	Positive symptoms
Prefrontal cortex/cortical	↓ LOW	Negative/cognitive symptoms

 

The original dopamine hypothesis suggested excessive subcortical dopamine caused schizophrenia, whereas updated versions propose low cortical dopamine alongside abnormal/increased subcortical dopamine, potentially resulting from genetic vulnerability and early stress.

A03 - strength (evidence for dopamine)

One strength is research support for the link  between dopamine and schizophrenia.

 

First, emphetamines increase DA and worsen symptoms in people with schizophrenia and induce symptoms in people without symptoms.

 

Second, antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms.

 

Third, some candidate genes act on the production of DA or DA receptors.

 

This strongly suggests that DA is involved in the symptoms of schizophrenia

A03 - limitation (glutamate)

One limitation of the dopamine hypothesis is evidence for a central role of glutamate.

 

Post mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions or people with schizophrenia.

 

In addition, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing.

 

This means that an equally string case can be made for the role of other neurotransmitters.