Introduction

This chapter will begin with a review of developmental theories of schizophrenia to provide a foundation for a discussion of functional brain imaging studies of childhood-onset schizophrenia. Two examples of such studies conducted with the National Institute of Mental Health (NIMH) childhood-onset schizophrenia sample are provided, followed by a discussion of future directions. Schizophrenia with onset during late adolescence or early adulthood is referred to as “adult-onset schizophrenia” whereas childhood-onset schizophrenia is usually defined as onset by the age of 12 years.

Etiology of schizophrenia

Since the 1970s, etiologic hypotheses about schizophrenia have shifted away from a view of the disorder as arising from pathologic processes occurring shortly prior to the onset of symptoms leading to diagnosis toward a neurodevelopmental conceptualization of the disorder. The neurodevelopmental hypothesis of schizophrenia asserts that schizophrenia results from an interaction between normal brain maturational events and a congenital brain lesion(s) (Weinberger, 1987). This shift in thinking is the result of cumulative evidence supporting the existence of brain morphologic and functional abnormalities in schizophrenia, together with the observation that disease onset typically occurs during late adolescence or early adulthood. Neurodevelopmental hypotheses argue that some brain abnormalities in people destined to develop schizophrenia may exist from birth, although symptoms of schizophrenia do not appear until affected brain areas and related circuitry mature (Murray and Lewis, 1987; Weinberger, 1987, 1995; Done et al., 1994; Jones et al., 1994; Murray, 1994).

One line of compelling evidence in support of the neurodevelopmental hypothesis of schizophrenia has come from animal studies.