Introduction

There is now compelling evidence that many neurological disorders which become apparent after birth have their origins during fetal life. For example, epidemiological studies have shown that cerebral palsy, a heterogeneous group of non-progressive motor impairment disorders, most frequently results from prenatal rather than perinatal or postnatal causes (Nelson and Ellenberg 1986). Minimal cerebral brain dysfunction, typified by children having general reading, writing and cognitive problems, is often associated with intrauterine growth restriction (IUGR), suggesting that the neurological problems have their origins in utero. Schizophrenia, one of the most debilitating of mental disorders, affecting about 1% of the population, cannot be accounted for entirely by genetic inheritance. On the basis of histological and neurochemical observations it has been proposed that prenatal insults result in a vulnerability of the developing brain, predisposing an individual with risk factors (seen as genetic inheritance) to develop the symptoms of schizophrenia in the teenage or young adult years (Akil and Weinberger 2000). Other disorders such as epilepsy and autism are also thought to result in part from neurodevelopmental deficits. Thus there is growing evidence that abnormal development of the brain during gestation contributes to many neurological disorders which manifest in later life.

Over the last few decades there have been major advances in our understanding of the intricate sequence of events that results in the formation of the entire nervous system from a specialised sheet of cells on the dorsal surface of the embryo.