scientists to develop predictive models by concluding that the larger the size of the ventricles, the higher the risk of schizophrenia (Castle et al., 1998). Nevertheless, what does not add up is that if the cerebral ventricles of the brain are enlarged, it does not account for the reason that immigrants and certain BME groups have a higher incidence of schizophrenia. Do they have larger cerebral ventricles? There has not been any evidence to suggest that the size of the ventricle changes by ethnicity or country of origin. What neuro-imaging experiments also found is that there is a negligible difference between a normal and psychotic patient under an MRI scan. If a child falls and harms itself while playing, the repercussion of the fall is the cut he receives, but it does not tell us how or why the fall happened. The same is true for the aetiology of schizophrenia: one can witness through the brain scan the changes that occurred as a result of an onset of schizophrenia, but it does not explain its nosological pattern. Although the neurological model is an observable and highly valid scientific model, it fails to address or explain why certain minorities experience schizophrenia at higher rates than indigenous populations. Littlewood (1992) also suggested that there has been no substantiation thus far for anyone to believe that African-Caribbeans share a common vulnerability to schizophrenia. Unless novel research is able to prove that African-Caribbeans, for instance, have larger cerebral ventricles than White British patients then this model is not seen as worth to be tested further.
Thesis from Brunnel University, United Kingdom, London