Over 150 post-mortem, computed tomography, and magnetic resonance imaging (MRI) studies have documented the presence of structural brain pathology in schizophrenic patients. Several empirical studies suggest that many of the structural deviations observed in schizophrenics reflect genetic and/or teratogenic disruptions of brain development during gestation and birth, and that these neurodevelopmental abnormalities may play a role in the etiology and pathophysiology of some forms of schizophrenia. Studies which have examined the role of prenatal and perinatal factors in schizophrenia have used two sources for the obstetric information: 1) retrospective maternal recall, and 2) hospital or midwife records produced at the time of the delivery. The hospital and midwife records have the advantage of being unbiased and prospective. However, these records are incomplete; there is rarely any information concerning complications during pregnancy. This study will make use of a total birth cohort on which we have previously collected detailed information concerning pregnancy and delivery complications. The cohort consists of all children born in the city of Helsinki, Finland in 1955 (N=6,789). The existing data bank on this cohort includes complete, standard records of pregnancy and delivery complications produced during the pregnancies and at the time of deliveries by Finnish obstetricians and midwives. We have also previously collected information on neurological and behavioral disorders during infancy and childhood in the cohort offspring. We now wish to search the Finnish psychiatric hospitalization register and hospital archives to obtain the adult psychiatric diagnoses of all of the cohort members and all of their parents. Cohort members with schizophrenic parents and matched controls whose parents are free of mental illness will be interviewed and given an MRI scan. This information will be used to test the following primary hypotheses: 1) cohort offspring who became schizophrenic will have suffered a higher rate of severe obstetric complications (OCs) than those with other disorders and no mental illness; 2) high-risk (HR) subjects will evidence increased signs of cortical dysgenesis on MRI scan compared to low-risk (LR) subjects; 3) genetic risk for schizophrenia and OCs will interact in the prediction of subcortical pathology (i.e., ventriculomegaly, reduced hippocampal and thalamic volumes) and adult schizophrenia; and 4) genetic risk for schizophrenia, OCs, and developmental brain changes will be related to neurological and behavioral abnormalities during infancy and childhood and the type of schizophrenic symptom pattern displayed in adulthood.
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