ABSTRACT
The neurodevelopmental model of schizophrenia pathogenesis proposes that the observed patterns of early abnormal brain development are related to and induced by genetic risk factors and/or exogenous environmental causes. I In accordance with the excess of schizophrenic birthrates in the winter and spring months, one attractive hypothesis suggests that viral infections during crucial periods of brain maturation are of etiological importance.2,3 The influenzaschizophrenia theory emerged from findings on midgestational exposure to the 1957 influenza epidemic,2 followed by numerous studies on schizophrenia risk among those exposed to annual peaks of infectious disease.4 Subsequently, individual maternal viral infection was reported in schizophrenic offspring,S-7 and altered fetal brain development was found in animal models after prenatal viral infection.8 Based on epidemiological findings, however, the relative risk of maternal viral infection in schizophrenia seems to be low at -1.5, indicating that prenatal infections could account only for a small proportion of schizophrenia cases.9 Another attractive hypothesis is that the infection theory is of key importance in distinct schizophrenic phenotypes only.s,lo Here, we present a summary of our studies on birthrate patterns and individual exposure to prenatal infections across the spectrum of schizophrenic psychoses.
