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6 - Maternal Influences on Prenatal Neural Development Contributing to Schizophrenia

Published online by Cambridge University Press:  10 August 2009

Jason Schiffman
Affiliation:
Social Science Research Institute, University of Southern California
Sarnoff A. Mednick
Affiliation:
Social Science Research Institute, University of Southern California
Ricardo Machón
Affiliation:
Social Science Research Institute, University of Southern California
Matti Huttunen
Affiliation:
Social Science Research Institute, University of Southern California
Kay Thomas
Affiliation:
Social Science Research Institute, University of Southern California
Seymour Levine
Affiliation:
Department of Psychology, University of California-Davis
Dante Cicchetti
Affiliation:
University of Rochester, New York
Elaine F. Walker
Affiliation:
Emory University, Atlanta
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Summary

Research has identified disturbances in the nervous system as underlying schizophrenia since Kraepelin (1919) first proposed the term dementia praecox. Ample evidence now supports this earlier speculation. More recent evidence has established a neurodevelopmental basis for schizophrenia and other major mental disorders (Akbarian et al., 1993; Mednick, Cannon, Barr, & Lyon, 1991; Mednick & Hollister, 1995; Machón, Mednick, & Huttunen, 1997). In this chapter we will examine some of this evidence establishing a neurodevelopmental basis for major mental disorders, including schizophrenia, as well as propose two related mechanisms involving maternal stress and immune response processes that may mediate the maternal infection and subsequent, adult mental disorder outcome.

FETAL NEURAL DEVELOPMENT

The development of fetal neural structures is a delicate process. Neurons creating the human neocortex proliferate by the fifth month of gestation. Rapid migration and differentiation occur in the central nervous system during the second trimester (CNS; Nowakowski, 1991). The cortical subplate, essential for the formation of the cerebral cortex, also develops during the second trimester. Disruption during a critical period of proliferation may dramatically disorganize neural development leading to observable physical anomalies. Jones and Akbarian (1995) conclude, however, that the existing data suggest as “unlikely that the proliferative phase of forebrain ontogenesis is compromised in any major way in schizophrenia” (p. 29).

Kovelman and Scheibel (1984) suggest that disrupted neural migration may result in the excess of ectopic neurons found in the hippocampi of schizophrenia patients.

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Publisher: Cambridge University Press
Print publication year: 2003

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