ArticleSchizophrenia research and treatment2014
Residual negative symptoms differentiate cognitive performance in clinically stable patients with schizophrenia and bipolar disorder.
Article in Schizophrenia research and treatment, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Deconstructing Cognitive Impairment in Psychosis With a Machine Learning Approach.JAMA psychiatry · 2025Article
- Exploring current smartphone-based cognitive assessments in schizophrenia and bipolar disorder.Schizophrenia research. Cognition · 2024Review
- Article
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Authors and funding
5 authors.
Funding
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Abstract
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.
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Registered trials
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