Fetal Hypoxia and Structural Brain Abnormalities in Schizophrenic Patients, Their Siblings, and Controls

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Abstract
STRUCTURAL BRAIN abnormalities are robust correlates of schizophrenia, but their causes have not been conclusively established.1-3 Neuromotor and cognitive deficits in preschizophrenic children4-6 and cortical laminar neuron displacement in schizophrenic patients at autopsy7-10 suggest that at least some of the anatomical changes associated with schizophrenia are neurodevelopmental in origin.11 Genetic influences in schizophrenia are substantial,12 but the mode of inheritance is complex. It involves at least several genes13 and certain neurally disruptive environmental exposures, such as obstetric complications (OCs).14-27 Of the many types of OCs found to predict schizophrenia, fetal hypoxia has shown the strongest association, accounting for a greater proportion of liability than exposure to infections during gestation, fetal growth retardation, and other obstetric factors.27 Because no study using objective birth records has found that hypoxic OCs are more frequent in the first-degree relatives of schizophrenic patients than in the general population,17-24 these complications do not appear to be consequences of genetic liability to schizophrenia. It is also unlikely that these early influences cause schizophrenia on their own because more than 90% of individuals who experience fetal hypoxia, even in its severe form, do not develop schizophrenia.17,18,25,26 Hypoxic OCs must thus act additively or interactively with genetic factors in influencing disease liability.27