Prodromal symptoms and atypical affectivity as predictors of major depression in juveniles: implications for...

Given the long-term morbidity of juvenile-onset major depressive disorder (MDD), it is timely to consider whether more effort should be dedicated to its primary and secondary prevention.

We reviewed studies of prodromal symptoms that may herald a first episode pediatric MDD and considered whether that literature has made an impact on secondary prevention (efforts to prevent progression from symptoms to full disorder). We also reviewed studies of children at familial risk for MDD that addressed atypical affectivity and the regulation of sad, dysphoric affect (mood repair) and related physiological systems, and considered whether research in those areas has made an impact on primary prevention of pediatric MDD (efforts to prevent the disorder).

A compelling body of literature indicates that depressive symptoms in youngsters predict subsequent MDD across the juvenile (and early adult) years and that any combination of several symptoms for at least one week is informative in that regard. These findings are echoed in the case selection criteria used by many secondary prevention programs. Convergent findings also indicate that (compared to typical peers) young offspring at familial risk for depression manifest low positive affectivity and compromised mood repair, along with signs of dysfunction in three intertwined physiological systems that contribute to affectivity and mood repair (the hypothalamic-pituitary-adrenal (HPA) axis, cerebral hemispheric asymmetry, and cardiac vagal control). While all these affect-related parameters are suitable for case selection and as intervention targets, they have not yet made an impact on primary prevention programs.

According to recent meta-analyses, attempts to prevent pediatric depression have not lived up to expectations. Based on our review, possible reasons for this include: (a) the use of case selection criteria that yield samples heterogeneous with regard to whether the symptoms are truly prodromal to an episode of MDD or are trait-like (which could affect response to the intervention), (b) failure to fully capitalize on the broad-ranging literature on vulnerability to pediatric MDD, as evidenced by the infrequent use of family history of depression (a robust index of vulnerability) or combined indices of vulnerability for case selection, and (c) lack of synchrony between dimensions of vulnerability and the content of the prevention program, as indicated by the overwhelming use of cognitive-behavioral interventions, irrespective of subjects' age, developmental readiness, and whether or not they evidenced the relevant cognitive vulnerability. Prevention trials of pediatric MDD could benefit from new approaches to case selection that combine various indices of vulnerability, more effective use of existing findings, and new or modified interventions that are developmentally sensitive.