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The British Journal of Psychiatry (2005) 186: 32-40
© 2005 The Royal College of Psychiatrists

Neurocognitive impairment in euthymic patients with bipolar affective disorder

Jill M. Thompson, BSc, Peter Gallagher, BSc, MPhil, John H. Hughes, MBBS, MRCPsych, Stuart Watson, MBBS, MRCPsych, John M. Gray, MA, MPhil, PhD, AFBPS, I. Nicol Ferrier, FRCP, MD, FRCPsych and Allan H. Young, MB ChB, MPhil, PhD, FRCPsych

Stanley Research Centre, School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, UK

Correspondence: Professor A. H. Young, Stanley Research Centre, School of Neurology, Neurobiology and Psychiatry (Psychiatry), University of Newcastle upon Tyne, Leazes Wing, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, UK. Tel: +44 (0)191 2824473; fax +44 (0)191 2275108; e-mail: a.h.young{at}ncl.ac.uk

Declaration of interest None.

Funding detailed in Acknowledgements.

Background Persistent impairments in neurocognitive function have been described in patients with bipolar disorder whose disease is in remission. However, methodological issues such as the effect of residual mood symptoms and hypercortisolaemia may confound such studies.

Aims To assess neurocognitive functioning in prospectively verified euthymic patients with bipolar disorder.

Method Sixty-three patients with bipolar disorder and a matched control group completed a comprehensive neurocognitive test battery. Euthymia was confirmed in the patient group by prospective clinical ratings over 1 month prior to testing. Saliva samples were collected to profile basal cortisol secretion.

Results Patients were significantly impaired across a broad range of cognitive domains. Across the domains tested, clinically significant impairment was observed in 3% to 42% of patients. Deficits were not causally associated with residual mood symptoms or hypercortisolaemia.

Conclusions Neurocognitive impairment persists in patients whose bipolar disorder is in remission. This may represent a trait abnormality and be a marker of underlying neurobiological dysfunction.




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