OBSTETRIC COMPLICATIONS IN SCHIZOPHRENIC PARENTS

Some evidence indicates that OCs may be an etiological factor of importance in the development of schizophrenia. A currently important question not addressed by this review is whether OCs replace other etiological factors, or in some way interact with other factors such as genetic influence (Murray et al., 1988). The data relevant to question 3 are to considerable importance for testing possible interactions of OCs and implied genetic influence, particularly if one can show that increased obstetric complications in a low genetic risk control group does not increase the risk for schizophrenia. The findings from Mednick and Schulsinger's longitudinal study clearly suggest that OCs are related in a special manner to the characteristics of the offspring of schizophrenics, including the development of schizophrenia in the offspring. This would speak for an interaction between OCs and genetics. However, other high-risk have not (at least yet) contributed much evidence that OCs strongly interact with or add to the implied genetic vulnerability found in the offspring of schizophrenics. With time, some of the other longitudinal high- risk studies may be at least partially able to confirm or disconfirm the Mednick-Schulsinger results. Some of the recent uncertainty in this field concerns not so much the data but rather the concepts and terminology sorrounding 'OCs'. Surprisingly great interest has been focussed on offspring birthweight, possibly because of its ease and reliability of measurement and its relationship to early developmental retardation and adult ventricular enlargement. Obstetricians often view low birthweight as an obstetric 'OC' but researchers within psychopathology may tend to consider low birthweight among high-risk offspring as being due to genetic influence (Marcus et al., 1981) or to a prenatal virus hypothetically related to schizophrenia (Machon et al., 1983). Adequate tests of these interpretations (hypotheses) await the identification of the bearers of the schizophrenia gene(s) and of the relevant virus(es), to determine whether these persons have more 'OCs' as obstetricians know them. Until that time, the vast data indicating no substantial increases in OCs or low birthweight offspring in reproductions among schizophrenic parents will serve as the best possible available evidence that these OCs are not genetically determined (McNeil and Kaij, 1978; McNeil, 1987, 1988b). If this argument can be accepted, then the vast amount of empirical work concentrated on question 1 will have contributed not only to clinically applicable knowledge, but also to theoretical positions on the etiology of schizophrenia. © 1991.