Meta-analytic review of neurocognition in bipolar II disorder

Authors

  • E. Bora,

    1. Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Carlton
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  • M. Yücel,

    1. Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Carlton
    2. Orygen Research Centre, Melbourne
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  • C. Pantelis,

    1. Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Carlton
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  • M. Berk

    1. Orygen Research Centre, Melbourne
    2. Department of Clinical and Biomedical Sciences, Barwon Health, The University of Melbourne, Geelong
    3. Mental Health Research Institute, Melbourne and Deakin University, Geelong, Vic., Australia
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Emre Bora, Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Alan Gilbert Building NNF level 3, Carlton, Vic. 3053, Australia.
E-mail: emrebora@hotmail.com; boremre@gmail.com

Abstract

Bora E, Yücel M, Pantelis C, Berk M. Meta-analytic review of neurocognition in bipolar II disorder.

Objective:  The clinical distinction between bipolar II disorder (BD II) and bipolar I disorder (BD I) is not clear-cut. Cognitive functioning offers the potential to explore objective markers to help delineate this boundary. To examine this issue, we conducted a quantitative review of the cognitive profile of clinically stable patients with BD II in comparison with both patients with BD I and healthy controls.

Method:  Meta-analytical methods were used to compare cognitive functioning of BD II disorder with both BD I disorder and healthy controls.

Results:  Individuals with BD II were less impaired than those with BD I on verbal memory. There were also small but significant difference in visual memory and semantic fluency. There were no significant differences in global cognition or in other cognitive domains. Patients with BD II performed poorer than controls in all cognitive domains.

Conclusion:  Our findings suggest that with the exception of memory and semantic fluency, cognitive impairment in BD II is as severe as in BD I. Further studies are needed to investigate whether more severe deficits in BD I are related to neurotoxic effects of severe manic episodes on medial temporal structures or neurobiological differences from the onset of the illness.

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