CUC serves as a consultant, advisor and/or lecturer for AstraZeneca, Bristol-Myers Squibb, Eli Lilly & Co., Intra-Cellular Therapeutics, Janssen Pharmaceutica, Otsuka and Solvay. JMK serves as a consultant, advisor and/or lecturer for Abbott, AstraZeneca, Bristol-Myers Squibb, Eli Lilly & Co., Janssen Pharmaceutica, Lundbeck, Otsuka and Wyeth. BAC serves as a consultant for Bristol-Myers Squibb and Janssen Pharmaceutica. JBP, TL, AA, CWS and AKM do not have any reported conflicts of interest.
Early identification and high-risk strategies for bipolar disorder
Article first published online: 1 JUN 2007
Volume 9, Issue 4, pages 324–338, June 2007
How to Cite
Correll, C. U., Penzner, J. B., Lencz, T., Auther, A., Smith, C. W., Malhotra, A. K., Kane, J. M. and Cornblatt, B. A. (2007), Early identification and high-risk strategies for bipolar disorder. Bipolar Disorders, 9: 324–338. doi: 10.1111/j.1399-5618.2007.00487.x
- Issue published online: 1 JUN 2007
- Article first published online: 1 JUN 2007
- Received 14 April 2006, revised and accepted for publication 18 January 2007
- bipolar disorder;
- early identification;
Objectives: To describe and compare the relative merits of different identification strategies for individuals at risk for bipolar disorder (BPD).
Methods: Selective review of data that support early identification in BPD, with a particular focus on emerging clinical high-risk strategies.
Results: Early detection of individuals at risk for BPD can utilize genetic, endophenotypic and clinical methods. Most published work focuses on genetic familial endophenotypic risk markers for BPD. However, despite encouraging results, problems with specificity and sensitivity limit the application of these data to early prevention programs. In addition, offspring studies of BPD patients systematically exclude the majority of subjects without a first-degree bipolar relative. On the other hand, emerging work in the clinical-high-risk arena has already produced encouraging results. Although still preliminary, the identification of individuals in subsyndromal or attenuated symptom ‘prodromal’ stages of BPD seems to be an under-researched area that holds considerable promise deserving increased attention. Required next steps include the development of rating tools for attenuated and subsyndromal manic and depressive symptoms and of prodromal criteria that will allow prodromal symptomatology to be systematically studied in patients with recent-onset bipolar, as well as in prospective population-based phenomenology trials and attenuated symptom-based high-risk studies.
Conclusions: Given the current limitations of each early identification method, combining clinical, endophenotypic and genetic strategies will increase prediction accuracy. Since reliable biological markers for BPD have not been established and since most patients with BPD lack a first-degree relative with this disorder, clinical high-risk approaches have great potential to inform early identification and intervention programs.