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Prevention of bipolar disorder in at-risk children: Theoretical assumptions and empirical foundations

Published online by Cambridge University Press:  07 July 2008

David J. Miklowitz  and
Kiki D. Chang
David J. Miklowitz*
Affiliation:
University of Colorado, Boulder
Kiki D. Chang
Affiliation:
Stanford University School of Medicine
*
Address correspondence and reprint requests to: David J. Miklowitz, Department of Psychology, University of Colorado at Boulder, 345 UCB, Boulder, CO 80309; E-mail: david.miklowitz@colorado.edu.
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Abstract

This article examines how bipolar symptoms emerge during development, and the potential role of psychosocial and pharmacological interventions in the prevention of the onset of the disorder. Early signs of bipolarity can be observed among children of bipolar parents and often take the form of subsyndromal presentations (e.g., mood lability, episodic elation or irritability, depression, inattention, and psychosocial impairment). However, many of these early presentations are diagnostically nonspecific. The few studies that have followed at-risk youth into adulthood find developmental discontinuities from childhood to adulthood. Biological markers (e.g., amygdalar volume) may ultimately increase our accuracy in identifying children who later develop bipolar I disorder, but few such markers have been identified. Stress, in the form of childhood adversity or highly conflictual families, is not a diagnostically specific causal agent but does place genetically and biologically vulnerable individuals at risk for a more pernicious course of illness. A preventative family-focused treatment for children with (a) at least one first-degree relative with bipolar disorder and (b) subsyndromal signs of bipolar disorder is described. This model attempts to address the multiple interactions of psychosocial and biological risk factors in the onset and course of bipolar disorder.

Type
Research Article
Information
Development and Psychopathology , Volume 20 , Issue 3 , Summer 2008 , pp. 881 - 897
Copyright
Copyright © Cambridge University Press 2008

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Footnotes

Preparation of this manuscript was supported by Grants MH62555, MH073871, and MH077856 (to D.J.M.), a Faculty Fellowship from the University of Colorado, a Distinguished Investigator Award from the National Alliance for Research on Schizophrenia and Depression (to D.J.M.), and an NIMH K-Award (to K.D.C.).

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