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Residual Negative Symptoms Differentiate Cognitive Performance in Clinically Stable Patients with Schizophrenia and Bipolar Disorder
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 diso...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4082914/ https://www.ncbi.nlm.nih.gov/pubmed/25024847 http://dx.doi.org/10.1155/2014/785310 |
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author | Krishnadas, Rajeev Ramanathan, Seethalakshmi Wong, Eugene Nayak, Ajita Moore, Brian |
author_facet | Krishnadas, Rajeev Ramanathan, Seethalakshmi Wong, Eugene Nayak, Ajita Moore, Brian |
author_sort | Krishnadas, Rajeev |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4082914 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-40829142014-07-14 Residual Negative Symptoms Differentiate Cognitive Performance in Clinically Stable Patients with Schizophrenia and Bipolar Disorder Krishnadas, Rajeev Ramanathan, Seethalakshmi Wong, Eugene Nayak, Ajita Moore, Brian Schizophr Res Treatment Research Article 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. Hindawi Publishing Corporation 2014 2014-06-12 /pmc/articles/PMC4082914/ /pubmed/25024847 http://dx.doi.org/10.1155/2014/785310 Text en Copyright © 2014 Rajeev Krishnadas et al. https://creativecommons.org/licenses/by/3.0/ 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. |
spellingShingle | Research Article Krishnadas, Rajeev Ramanathan, Seethalakshmi Wong, Eugene Nayak, Ajita Moore, Brian Residual Negative Symptoms Differentiate Cognitive Performance in Clinically Stable Patients with Schizophrenia and Bipolar Disorder |
title | Residual Negative Symptoms Differentiate Cognitive Performance in Clinically Stable Patients with Schizophrenia and Bipolar Disorder |
title_full | Residual Negative Symptoms Differentiate Cognitive Performance in Clinically Stable Patients with Schizophrenia and Bipolar Disorder |
title_fullStr | Residual Negative Symptoms Differentiate Cognitive Performance in Clinically Stable Patients with Schizophrenia and Bipolar Disorder |
title_full_unstemmed | Residual Negative Symptoms Differentiate Cognitive Performance in Clinically Stable Patients with Schizophrenia and Bipolar Disorder |
title_short | Residual Negative Symptoms Differentiate Cognitive Performance in Clinically Stable Patients with Schizophrenia and Bipolar Disorder |
title_sort | residual negative symptoms differentiate cognitive performance in clinically stable patients with schizophrenia and bipolar disorder |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4082914/ https://www.ncbi.nlm.nih.gov/pubmed/25024847 http://dx.doi.org/10.1155/2014/785310 |
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