Evidence for disruption in prefrontal cortical functions in juvenile bipolar disorder

Authors

  • Carrie E Bearden,

    1. Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California at Los Angeles, Los Angeles, CA
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  • David C Glahn,

    1. Division of Mood and Anxiety Disorders, Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
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  • Sheila Caetano,

    1. Division of Mood and Anxiety Disorders, Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
    2. Institute of Psychiatry, University of São Paolo School of Medicine, São Paulo, Brazil
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  • Rene L Olvera,

    1. Division of Child and Adolescent Psychiatry, Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
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  • Manoela Fonseca,

    1. Division of Mood and Anxiety Disorders, Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
    2. Psychiatry Research Unit, School of Medicine, Federal University of Rio Grande do Sul, Pôrto Alegre, Brazil
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  • Pablo Najt,

    1. Division of Mood and Anxiety Disorders, Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
    2. South Texas Veterans Health Care System, Audie L Murphy Division, San Antonio, TX, USA
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  • Kristina Hunter,

    1. Division of Mood and Anxiety Disorders, Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
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  • Steve R Pliszka,

    1. Division of Child and Adolescent Psychiatry, Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
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  • Jair C Soares

    1. Division of Mood and Anxiety Disorders, Department of Psychiatry, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
    2. South Texas Veterans Health Care System, Audie L Murphy Division, San Antonio, TX, USA
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  • The authors of this paper do not have any commercial associations that might pose a conflict of interest in connection with this manuscript.

Carrie E. Bearden, PhD, Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, 300 Building Medical Plaza, Suite 2265, Los Angeles, CA 90095, USA. Fax: +1 310 794 9517; e-mail: cbearden@mednet.ucla.edu

Abstract

Objectives:  Systematic parsing of executive function processes is critical for the development of more specific models of neurobiological processes mediating disturbed cognition in youth with bipolar disorder (BPD).

Methods:  A sample of 33 children and adolescents with bipolar I disorder (BPD I) (mean age 12.1 ± 3.0 years, 39% female) and 44 demographically matched healthy participants (mean age 12.9 ± 2.8 years, 50% female) completed a neurocognitive battery including measures aimed at detection of disruption in prefrontal cortical circuitry (i.e., working memory, set shifting, and rule attainment).

Results:  Compared to healthy controls, BPD I children exhibited significant deficits in spatial working memory, visual sequencing and scanning, verbal fluency and abstract problem solving, particularly when a memory component was involved. In our spatial delayed response task, memory set size was parametrically varied; the performance pattern in BPD I children suggested deficits in short-term memory encoding and/or storage, rather than capacity limitations in spatial working memory. Earlier age at onset of illness and antipsychotic medication usage were associated with poorer performance on speeded information-processing tasks; however, severity of mood symptomatology and comorbidity with disruptive behavior disorders were not associated with task performance.

Conclusions:  These results suggest impairment in measures of prefrontal cortical function in juvenile BPD I that are similar to those seen in the adult form of the illness, and implicate both the ventral and dorsolateral prefrontal cortex as loci of pathology in juvenile BPD. As these deficits were not associated with clinical state or comorbidity with other disorders, they may reflect trait-related impairments, a hypothesis that will be pursued further in longitudinal studies.

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