ABSTRACT
Introduction Why does schizophrenia happen when it does? The neurodevelopmental hypothesis championed by Robin Murray provides a powerful explanatory framework for addressing this question (Murray, Lappin, & Di Forti, 2008). The hypothesis is that psychosis arises from the interaction of a very early brain lesion (which could be genetic, environmental or a combination of the two) with adolescent neurodevelopment. The perturbation of neurodevelopment during the critical period of adolescence then gives rise to the syndrome that we call psychosis. This compelling model contains two “Black Holes”, which are not straightforward to investigate. First, what is the nature of the early lesion(s)? Second, what is going wrong with brain development during the transition from adolescence to adulthood? In this chapter we will explore the second Black Hole in a group of people who were at high risk of early brain injury by virtue of being born prematurely. By considering how their brains grow and develop between adolescence and adulthood we hope to give some insights into adolescent neurodevelopment. But first, some more background information is in order.
