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Significance of Adolescent Neurodevelopment for the Neural Circuitry of Bipolar Disorder

Authors

  • HILARY P. BLUMBERG,

    Corresponding author
    1. VA Depression Research Center (REAP), VA Connecticut Healthcare System (116-A), West Haven, Connecticut 06516, USA
    2. Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut 06511, USA
      Address for correspondence: Hilary P. Blumberg, M.D., Department of Psychiatry, Yale University School of Medicine, VA Depression Research Center (REAP), VA Connecticut Healthcare System (116-A), 950 Campbell Avenue, West Haven, CT 06516. Voice: 203-932-5711, Ext. 4376; fax: 203-937-3886 hilary.blumberg@yale.edu
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  • JOAN KAUFMAN,

    1. Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut 06511, USA
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  • ANDRÉS MARTIN,

    1. Yale Child Study Center, Yale University School of Medicine, New Haven, Connecticut 06520-7900, USA
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  • DENNIS S. CHARNEY,

    1. Mood and Anxiety Disorders Research Program, National Institute of Mental Health, Bethesda, Maryland 20892-1381, USA
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  • JOHN H. KRYSTAL,

    1. VA Depression Research Center (REAP), VA Connecticut Healthcare System (116-A), West Haven, Connecticut 06516, USA
    2. Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut 06511, USA
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  • BRADLEY S. PETERSON

    1. Department of Psychiatry, Columbia College of Physicians & Surgeons, New York, New York 10032, USA
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Address for correspondence: Hilary P. Blumberg, M.D., Department of Psychiatry, Yale University School of Medicine, VA Depression Research Center (REAP), VA Connecticut Healthcare System (116-A), 950 Campbell Avenue, West Haven, CT 06516. Voice: 203-932-5711, Ext. 4376; fax: 203-937-3886 hilary.blumberg@yale.edu

Abstract

Abstract: The deficits of executive control of emotions and impulses of adult BD implicate involvement of a ventral prefrontal cortex (VPFC) neural system that subserves these functions that include the VPFC, as well as its subcortical connection sites of amygdala, striatum, and thalamus. Differences in the timing of major developmental changes in the structures within this neural system suggest that abnormalities in particular components of this neural system may emerge during critical developmental epochs during the course of the illness. Our recent neuroimaging data suggest that abnormalities in the subcortical components of VPFC neural systems may be evident by early adolescence in BD, whereas VPFC deficits progress over the course of adolescence and may be difficult to detect prior to late adolescence or early adulthood. This potential neurodevelopmental model for BD could have important implications for the recognition of early signs of the disorder and for age-specific treatment strategies.

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