Neural Correlates

Neural Correlates: Schizophrenia

Neural correlates are instances where brain structure differences correlate with certain psychological disorders or symptoms. Neural correlates in schizophrenia suggest that structures in the brain are associated with the positive and negative symptoms of schizophrenia, such as in the enlarged ventricles found in schizophrenic patients.

Biological Explanations of Schizophrenia: Neural Correlates

Neural correlates are a biological explanation of schizophrenia, but how do neural correlates apply to schizophrenia? Well, research into the topic has highlighted various aspects of brain abnormalities associated with schizophrenia, namely in certain brain structures such as the basal ganglia and thalamus and brain ventricles. Let's explore neural correlates in schizophrenia further.

Neural Correlates in Schizophrenia: Brain Structure Abnormalities

A study by Torrey (2002) examined neurological differences in schizophrenic patients (who were not prescribed antipsychotic medications) and healthy controls. For this purpose, he reviewed 65 studies on the topic.

Torrey (2002) found significant abnormalities in the brains of people with schizophrenia compared to people without schizophrenia in these studies. He concluded that many interconnected neurophysical differences in the brains of schizophrenic patients increased the likelihood of developing the disorder.

These interconnected neurophysical differences in the brain include:

• The basal ganglia
• The medial temporal lobe
• The prefrontal cortex
• The thalamus

Because the studies were conducted on participants who had never received antipsychotic medication, Torrey (2002) also concluded that the neurophysical abnormalities in these participants were inherently part of the disorder and not a side effect of treatment.

Neural Correlates in Schizophrenia: Ventricles

Torrey (2002) also found that in schizophrenia patients, the ventricles in the brain (fluid-filled cavities in the brain that help supply the brain with vital nutrients and eliminate toxins) are 15% larger, meaning that their brains weigh less than those of neurotypical people.

A link has been found between enlarged ventricles in schizophrenia and loss of grey matter in some brain areas. Grey matter is involved in the control of movements, memories, and emotions. It plays a vital role in normal daily functioning.

Fig. 2 - Torrey (2002) found schizophrenic patients had enlarged ventricles¹.

Supporting Evidence For Neural Correlates in Schizophrenia

There is substantial evidence that brain structure or functioning abnormalities cause schizophrenia. Torrey (2002) as we discussed above, highlights particular areas of the brain associated with schizophrenia. Further research corroborates these claims.

Suddath et al. (1990)

Suddath et al. (1990) found that in 15 pairs of twins, one of whom was schizophrenic and the other non-schizophrenic, 12 had significant ventricular size differences on MRI scans. These differences were not present in the seven control twin pairs studied.

Suddath et al. (1990) suggest that there are neural correlates for schizophrenia. Since this is a twin study, it is reasonable to assume that these neurophysical differences cause schizophrenia or that schizophrenia causes them. It is unlikely to be due to individual biological differences or external factors since twins are genetically identical and usually grow up in a similar environment.

Reliability is another strength of this study. The method used was MRI brain imaging, which is highly scientific due to its objective and controlled study method. This makes it more likely to obtain similar results if the study were repeated.

Reliability of Testing Methods in Neural Correlates

Testing methods often employ neuroimaging techniques, such as magnetic resonance imaging (MRI) machines and positron emission tomography (PET) scans to identify abnormal areas of the brain.

Both imaging techniques are reliable because they are highly detailed and provide consistent results when patients are scanned.

Limitations of Neural Correlates

Is our biology to blame for our actions? Shouldn't we also consider environmental factors? After all, do neurological differences cause schizophrenia or vice versa? Let us add the opposite stance to our evaluation and find the answers ourselves.

Biological Determinism and Reductionism

Neural correlates as an explanation for schizophrenia is a biologically deterministic theory, i.e., it supports the notion that our thoughts and behaviours are dictated purely by biological factors rather than our own free will.

Biological determinism can negatively impact attempts to treat harmful behaviours and mental disorders.

Moreover, biological determinism has negative implications for our justice system. Suppose we conclude that behaviour is biologically determined and does not require human decision-making. In that case, it will become increasingly difficult to justify punishment for severe crimes because the offender might cite biologically deterministic ideas as an excuse.

Biological reductionism highlights how neural correlates tend to reduce a complex disorder, such as schizophrenia, to its simple biological components. As we will discuss below, it ignores other factors which may affect the development of schizophrenia, namely upbringing, family dysfunction and cognitive explanations, and environmental factors such as cannabis use and obstetrical complications.

Correlation and Causation

As mentioned earlier, we cannot yet determine whether schizophrenia causes these neurological differences or the other way around. Causation issues make it challenging to apply this theory to treating schizophrenic symptoms. If we cannot identify the cause, we cannot treat the cause.

Although ample scientific evidence suggests that these neurological differences likely contribute to schizophrenia, this theory is limited because it cannot explain why these differences exist or if they are just a product of schizophrenia rather than the cause.

Environmental Factors

Another limitation is that this theory does not consider environmental factors that may contribute to the development of schizophrenia. The treatment developed based on biological theories may not work because environmental factors are not considered and could become a confounding variable (an external factor that affects an outcome).

Vilain et al. (2013) reviewed the scientific literature surrounding the environmental risk factors of schizophrenia. In the review, Vilain et al. (2013) highlighted how environmental factors such as cannabis use, migration and obstetrical complications are associated with the risk of developing schizophrenia.

However, Vilain et al. (2013) were quick to highlight how the association was relatively weak. They noted that a limitation of environmental factor investigation in their research review was found in their populations' geographic limitations.

Patel et al. (2020) reviewed the association between cannabis use and increased risk of developing schizophrenia and psychosis symptoms. Of the 12 studies they examined, they concluded that a component of cannabis, tetrahydrocannabinol (THC), is one of the main contributors to psychosis and schizophrenia development when people use cannabis.

They highlighted, however, how more research is needed into the topic, specifically with the recent legalisation patterns coming into force.

Patel et al. (2020) show how environmental factors influence the development of schizophrenia. The biological argument used by biological explanations, such as the one for neural correlates, tends to ignore environmental factors.

Fig. 3 - Environmental factors influence schizophrenia development, a factor often ignored by biological explanations.

Applications of neural correlates

Since neural correlates do not prove causality, it is challenging to perform treatments based on this theory. All this theory does at this point is help us understand the neural differences between schizophrenic and neurotypical people. We can then begin to understand that brain abnormality is correlated with schizophrenia, but we cannot establish a causal link.

The information does not provide much practical application beyond a potential association.

Suppose further research were to be done to investigate whether there are causal links between brain structure and schizophrenia. In that case, it could help us develop more medical treatments for the disease, but this is not currently possible.