ABSTRACT
The development of schizophrenia has, in a number of studies, been suggested to result from disturbances in the maturation of the nervous system.1 Although controversy still exists, there is a common belief that certain neuronal populations in the brains of patients suffering from schizophrenia have failed to develop normally due to disturbances in their migration and/ or synaptogenesis. The problem with this view is the lack of an explanation for the long delay between the time of insult and the onset of symptoms. Rarely do other human diseases or even animal models exhibit this kind of latency. Therefore, a progressive component has lately been put forward as an addendum to the purely neurodevelopmental hypothesis.2
