Psychological Medicine

Original Articles

Evolution of neuropsychological dysfunction during the course of schizophrenia and bipolar disorder

K. E. Lewandowskia1 c1, B. M. Cohena1 and D. Öngura1

a1 McLean Hospital and Harvard Medical School, Boston, MA, USA

Abstract

Background Neurocognitive dysfunction in schizophrenia (SZ), bipolar (BD) and related disorders represents a core feature of these illnesses, possibly a marker of underlying pathophysiology. Substantial overlap in domains of neuropsychological deficits has been reported among these disorders after illness onset. However, it is unclear whether deficits follow the same longitudinal pre- and post-morbid course across diagnoses. We examine evidence for neurocognitive dysfunction as a core feature of all idiopathic psychotic illnesses, and trace its evolution from pre-morbid and prodromal states through the emergence of overt psychosis and into chronic illness in patients with SZ, BD and related disorders.

Method Articles reporting on neuropsychological functioning in patients with SZ, BD and related disorders before and after illness onset were reviewed. Given the vast literature on these topics and the present focus on cross-diagnostic comparisons, priority was given to primary data papers that assessed cross-diagnostic samples and recent meta-analyses.

Results Patients with SZ exhibit dysfunction preceding the onset of illness, which becomes more pronounced in the prodrome and early years following diagnosis, then settles into a stable pattern. Patients with BD generally exhibit typical cognitive development pre-morbidly, but demonstrate deficits by first episode that are amplified with worsening symptoms and exacerbations.

Conclusions Neuropsychological deficits represent a core feature of SZ and BD; however, their onset and progression differ between diagnostic groups. A lifetime perspective on the evolution of neurocognitive deficits in SZ and BD reveals distinct patterns, and may provide a useful guide to the examination of the pathophysiological processes underpinning these functions across disorders.

(Received August 11 2009)

(Revised April 05 2010)

(Accepted April 10 2010)

(Online publication May 19 2010)

Correspondence

c1 Address for correspondence: Dr K. E. Lewandowski, AB347, McLean Hospital, 115 Mill Street, Belmont, MA 02478, USA. (Email: klewandowski@mclean.harvard.edu)

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