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Schizophrenia Research and Treatment
Volume 2014 (2014), Article ID 785310, 6 pages
Research Article

Residual Negative Symptoms Differentiate Cognitive Performance in Clinically Stable Patients with Schizophrenia and Bipolar Disorder

1Sackler Institute of Psychobiological Research, Southern General Hospital, Room 25, University Corridor, Ground Floor, Neurology Building, Glasgow G51 4TF, UK
2Hutchings Psychiatric Center, NYS Office of Mental Health, Syracuse, NY 13210, USA
3Gartnavel Royal Hospital, Glasgow G12 0XH, UK
4Department of Psychiatry, KEM Hospital, Mumbai 400012, India
5Newcastle General Hospital, 1st Floor, Building 15, Westgate Road, Newcastle upon Tyne NE4 6BE, UK

Received 21 February 2014; Accepted 23 May 2014; Published 12 June 2014

Academic Editor: Luis San

Copyright © 2014 Rajeev Krishnadas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cognitive deficits in various domains have been shown in patients with bipolar disorder and schizophrenia. The purpose of the present study was to examine if residual psychopathology explained the difference in cognitive function between clinically stable patients with schizophrenia and bipolar disorder. We compared the performance on tests of attention, visual and verbal memory, and executive function of 25 patients with schizophrenia in remission and 25 euthymic bipolar disorder patients with that of 25 healthy controls. Mediation analysis was used to see if residual psychopathology could explain the difference in cognitive function between the patient groups. Both patient groups performed significantly worse than healthy controls on most cognitive tests. Patients with bipolar disorder displayed cognitive deficits that were milder but qualitatively similar to those of patients with schizophrenia. Residual negative symptoms mediated the difference in performance on cognitive tests between the two groups. Neither residual general psychotic symptoms nor greater antipsychotic doses explained this relationship. The shared variance explained by the residual negative and cognitive deficits that the difference between patient groups may be explained by greater frontal cortical neurophysiological deficits in patients with schizophrenia, compared to bipolar disorder. Further longitudinal work may provide insight into pathophysiological mechanisms that underlie these deficits.