Developmental risk factors: from infancy to onset

The Copenhagen High Risk Cohort (Schulsinger et al., 1987) reported that high-risk individuals (offspring of mothers with schizophrenia) who had had periods of institutionalization were more likely to develop schizophrenia than those high-risk individuals without episodes of institutional care. It is difficult to determine if the exposure of these high-risk children to institutional rearing is a true risk modifier (operating directly to increase the penetrance of the underlying genetic factor) or an epiphenomenon related to the temperament of the preschizophrenic child.

Tienari and colleagues (1994) examined carefully the families who had adopted high-risk children (i.e. offspring of mothers with schizophrenia). While members of the cohort are still to pass through much of their period of morbid risk, early results suggest that those high-risk children adopted into the highest functioning families appear to be 'protected'. These findings suggest that a modifying effect of the environment in high-risk children should be given added scrutiny. Further work is needed on how to identify susceptible children, and on how to identify the particular protective features of the environment.

There is now robust evidence that children who go on to develop schizophrenia display subtle neurodevelopmental deviations (Tarrant and Jones, 1999).

As a group, these children tend to have abnormalities of social functioning, delayed motor milestones, speech problems and impaired cognitive/educational abilities.

While it is not clear if these features operate within the causal chain (contribute to an increased risk of developing schizophrenia) or are passive risk indicators (markers of the underlying schizophrenia or the process that may modify risk), the findings suggest directions for primary prevention research. However, several key issues need consideration in order to develop this type of research.

{embed="ref/53"}

Are interventions available that could ameliorate features associated with increased risk of developing schizophrenia? Are these interventions safe, cheap and acceptable? Are the interventions associated with a broad range of positive outcomes other than reduced risk of schizophrenia, such as better school achievements, improved selfesteem, etc?

Research has found a significant excess of life events in the 6 months prior to the onset of psychosis, and that this association persisted when life events that may have been secondary to being psychotic were excluded (Bebbington et al., 1993; van Os et al., 1994). It is not clear how this finding could be translated to primary prevention. The effect may be mediated through individual vulnerability. This, then, would be a possible target for either primary or secondary intervention, with the aim of that intervention being reduction in vulnerability in some way or protection from life events insofar as that is possible.