The neurodevelopmental ‘hypothesis’ has been an influential model of the etiology of schizophrenia. It proposes that schizophrenia results from a subtle deviance in early brain development, the full adverse consequences of which are not manifest until early adulthood. Thus the existence of pre-and perinatal risk factors is central to the model.
The original neurodevelopmental model regarded schizophrenia as a distal consequence of disturbed brain development during the prenatal period, but did not specify the nature of the early brain disruption, define the mechanism of pathogenesis or propose potential risk factors.
Contemporary revisions regard neurodevelopmental deviance as one component of a more complex etiology. For example, the “developmental risk factor” model talks in terms of an interaction between early and late risk factors, and of a cascade of increasing deviance finally culminating in psychosis. Thus distal risk modifying factors operate pre- or perinatally, which may be modified by later experience (during childhood or adolescence). These factors may operate directly or indirectly. Risk modifying factors can be fixed (eg sex) or variable (eg alcohol intake), endogenous (eg genetic factors) or exogeneous (eg obstetric complications), protective or adverse.
We will outline the risk indicators and putative risk factors and proxies which have been found to support this developmental approach to the etiology of schizophrenia.