Over the past decade our research efforts have focused on the identification of prenatal risk factors for schizophrenia. In this chapter, we summarize our study designs and methods, describe our findings, discuss the implications of these findings for the field, and present our plans for future investigations. In order to provide a conceptual framework for these findings, we shall first discuss the neurodevelopmental hypothesis of schizophrenia, and briefly review previous studies by other investigators in this research domain.

NEURODEVELOPMENTAL HYPOTHESIS OF SCHIZOPHRENIA

The neurodevelopmental model of schizophrenia posits that adverse in utero events influence critical processes in the genesis of brain structures, which predispose to the emergence of schizophrenia in adulthood (Brown et al., 1999; Susser, 1999). The evidence that led to this hypothesis derives from many diverse areas of investigation; however, there appear to be three pivotal supportive findings. First, patients destined to develop schizophrenia have a tendency for diminished neurocognitive (David et al., 1997; Jones et al., 1994), neuromotor (Walker et al., 1994), and behavioral (Done et al., 1994) function. Second, patients with schizophrenia, as compared with healthy controls, have an increased frequency and severity of minor physical anomalies, particularly of the craniofacial area, which are suggestive of an in utero developmental disruption (Green et al., 1989; Waddington, 1993). Third, neuroimaging studies indicate that several of the brain abnormalities in schizophrenia, such as ventriculomegaly and diminished hippocampal volume, occur among patients in their first episode of psychosis (Bogerts et al., 1990; DeGreef et al., 1992; Nopoulos et al., 1995).