Evidence has accumulated during the past decade linking pregnancy and birth complications to later disorders of function. In 1956 Pasamanick et al. postulated that these complications might produce a “continuum of reproductive casualty…extending from fetal and neonatal death through cerebral palsy, epilepsy, mental deficiency, and behavior disorder.” Prenatal and perinatal complications have also been associated with childhood schizophrenia, although only two of the studies summarized used the patients' siblings as controls. Since siblings represent the best controls of environmental and hereditary variables (short of studying monozygotic twins discordant for childhood schizophrenia), they were used in the present study as controls. Accordingly, 33 childhood schizophrenics and their 83 siblings were analyzed with regard to prenatal and perinatal complications. Information was obtained from the patients' case records and from the hospital birth records and birth certificate records of both patients and their siblings. The childhood schizophrenics had a higher rate of prenatal complications than their siblings, but the difference was not significant. With regard to perinatal complications, however, the patients had a significantly higher rate than their siblings (p < .01). These findings confirm those of Vorster, Taft, and Goldfarb who also employed the siblings of the schizophrenic children as their controls. The schizophrenic children did not differ significantly in birth weight from their siblings. There was also a clear association between the schizophrenic child's ego status on admission to the hospital and his IQ and age of hospital admission. The schizophrenic children with poorer ego development compared to those with better ego development are admitted to the hospital earlier (p < .001) and also have significantly lower IQs (p < .01). While brain damage alone, resulting from birth complications, may not explain the unique symptoms of childhood schizophrenia, it is considered possible that in families already predisposed genetically for the development of this disorder, the addition of reproductive complications, especially perinatal factors (e.g., breech presentation, placenta previa, midforceps, induction of labor for complication, newborn distress, etc.) may be enough to tip the balance between health and disease, and profoundly disrupt the child's later development.