Neuropsychological and electrophysiological indices of neurocognitive dysfunction in bipolar II disorder

Authors

  • Stein Andersson,

    1. Department of Neuropsychiatry and Psychosomatic Medicine, Division of Clinical Neurosciences, Rikshospitalet University Hospital, Oslo
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  • Helene E Barder,

    1. Department of Neuropsychiatry and Psychosomatic Medicine, Division of Clinical Neurosciences, Rikshospitalet University Hospital, Oslo
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  • Tone Hellvin,

    1. Department of Neuropsychiatry and Psychosomatic Medicine, Division of Clinical Neurosciences, Rikshospitalet University Hospital, Oslo
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  • Hans Løvdahl,

    1. Department of Neuropsychiatry and Psychosomatic Medicine, Division of Clinical Neurosciences, Rikshospitalet University Hospital, Oslo
    2. Department of Psychiatry, Sørlandets sykehus HF – Arendal, Arendal
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  • Ulrik F Malt

    1. Department of Neuropsychiatry and Psychosomatic Medicine, Division of Clinical Neurosciences, Rikshospitalet University Hospital, Oslo
    2. Institute of Psychiatry, University of Oslo, Oslo, Norway
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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.

Stein Andersson, PhD, Department of Neuropsychiatry and Psychosomatic Medicine, Division of Clinical Neurosciences, Rikshospitalet, N-0027 Oslo, Norway.
Fax: +47 23 07 41 70; e-mail: stein.andersson@rikshospitalet.no

Abstract

Objectives:  There are conflicting findings regarding the nature and degree of neurocognitive dysfunction in bipolar II disorder (BD II). The aim of this study was to describe different levels of neurocognitive functioning in BD II by combining behavior-based methods (neuropsychological testing) and event-related potentials (ERP).

Methods:  Twenty-five consecutively referred outpatients fulfilling DSM-IV criteria for BD II and 28 matched controls performed a neuropsychological test battery targeting working memory/attention, executive functions, verbal and visual memory, and psychomotor speed. In addition, ERPs for measuring early and controlled stages of information processing were recorded using a duration mismatch negativity (MMN) paradigm and a three-tone auditory oddball paradigm.

Results:  Compared to controls, BD II patients’ performance was significantly impaired on all neuropsychological measures, except for phonemic verbal fluency, with moderate to strong effect sizes ranging from 0.62 to 1.34. The ERP results indicate dysfunctions in early stages of information processing, showing a significant MMN latency increase and attenuated frontal amplitudes in BD II patients. Female patients showed increased P3a latency compared to female controls, but no group differences were found for P3b latency or amplitude, the ERP component expressing controlled information processing.

Conclusions:  The functional significance of neuropsychological impairment is discussed. Differences regarding some aspects of executive function may be related to psychomotor speed, and not primarily to dysexecutive functioning. ERP results must be interpreted with caution, but the differences found in MMN latency and amplitudes may be related to fronto-temporal circuitry underlying pre-attentive stimulus change detection as measured by MMN, and are discussed in relation to previous research on MMN in other neuropsychiatric conditions.

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