User:LBird BASc/sandbox/ATK/Seminar6/Evidence/Evidence in Schizophrenia

Schizophrenia as a brain disease

Evidence that Schizophrenia is a brain disease stems from research (Nemade and Dombeck, n.d)¹ utilising brain imaging techniques (MRI and CT) documenting structural differences in brains between those with and without schizophrenia. Other studies (Juckel et al. 2006)² have also correlated negative symptoms (avolition) with lower levels of brain activity in certain areas (eg, the ventral striatum). Such evidence justifies the hypothesis that schizophrenia is a disease of the brain and this method of theory formation is a function of Bayesian thinking.

Despite this evidence being highly replicable and representative due to controlled procedures in brain scanning procedures, it might only be able to constitute as suitable evidence for a relationship between neural deficits and symptoms of schizophenia and, against other theories suggesting alternative origins of the illness. It is, however, unable to prove that schizophrenia is biological in origin.

According to Karl Popper, theories can be falsified though testing them against empirical evidence or known facts. Evidence can disprove theories through presenting inconsistent facts or evidence against them but cannot prove theories to be correct due to other inconsistent evidence that might exist.³ The approach used by researchers in this area seeks to complement the existing hypothesis - that Schizophrenia is a disease of the brain. Using the approach suggested by Popper, observations derived from controlled studies initially used as supporting evidence might therefore be only useful in the falsification of alternative explanations discussed below (ie psychodynamic explanations), rather than supporting the initial hypothesis itself.

It is difficult ascertaining whether schizophrenia is truly a brain disease with cherry-picked observations as sources of evidence. Multiple lines of evidence exist suggesting alternative explanations such as the role of social factors. When considering the whole pool of evidence, one might not agree with the statement that schizophrenia is a brain disease due to differing explanations.

Where two rational observers hold divergent beliefs, different conclusions form the same scientific evidence might be drawn. This is also consistent with the Bayesian scheme where conclusions are drawn based on previous knowledge held by observers and can be seen in the example of comparing explanations for schizophrenia where they differ based on whether schizophrenia itself is explained by a social psychologist or a cognitive neuroscientist.

For instance, the psychodynamic explanation by Fromm-Reichman (1948)⁴ suggests that family climates of secrecy and tension are created as a result of cold, controlling and rejecting mothers that create distrust and symptoms of paranoid delusions in the illness. Such explanations would thus suggest that neural effects are a result of symptoms caused by social factors. For example, avolition in schizophrenia might be caused by less information processing through the ventral striatum, resulting reduced activity observed in studies. The direction of causality therefore cannot be assumed where a cognitive neuroscientist might suggest the reverse where the reduced activity results in the negative symptoms observed, pointing to biological origins of the illness.

References

1. Nemade, R. and Dombeck, M. (n.d.). Gulf Bend MHMR Center. [online] Gulfbend.org. Available at: https://www.gulfbend.org/poc/view_doc.php?type=doc&id=8812&cn=7 [Accessed 24 Oct. 2019].

2. Juckel, G., Schlagenhauf, F., Koslowski, M., Wüstenberg, T., Villringer, A., Knutson, B., Wrase, J. and Heinz, A. (2006). Dysfunction of ventral striatal reward prediction in schizophrenia. NeuroImage, 29(2), pp.409-416.

3. Plato.stanford.edu. (2019). Karl Popper (Stanford Encyclopedia of Philosophy). [online] Available at: https://plato.stanford.edu/entries/popper/ [Accessed 24 Oct. 2019].

4. HIGGINS, J. (1968). The Schizophrenogenic Mother Revisited. British Journal of Psychiatric Social Work, 9(4), 205-208. Retrieved from http://www.jstor.org/stable/23702292