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Neurocognitive impairment in the deficit subtype of schizophrenia

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Abstract

Schizophrenia is a heterogeneous disorder characterized by numerous diverse signs and symptoms. Individuals with prominent, persistent, and idiopathic negative symptoms are thought to encompass a distinct subtype of schizophrenia. Previous work, including studies involving neuropsychological evaluations, has supported this position. The present study sought to further examine whether deficit patients are cognitively distinct from non-deficit patients with schizophrenia. A comprehensive neurocognitive battery including tests of verbal memory, vigilance, processing speed, reasoning, and working memory was administered to 657 patients with schizophrenia. Of these, 144 (22 %) patients were classified as deficit patients using a proxy identification method based on severity, persistence over time, and possible secondary sources (e.g., depression) of negative symptoms. Deficit patients with schizophrenia performed worse on all tests of cognition relative to non-deficit patients. These patients were characterized by a generalized cognitive impairment on the order of about 0.4 standard deviations below that of non-deficit patients. However, when comparing deficit patients to non-deficit patients who also present with negative symptoms, albeit not enduring or primary, no group differences in cognitive performance were found. Furthermore, a discriminant function analysis classifying patients into deficit/non-deficit groups based on cognitive scores demonstrated only 62.3 % accuracy, meaning over one-third of individuals were misclassified. The deficit subtype of schizophrenia is not markedly distinct from non-deficit schizophrenia in terms of neurocognitive performance. While deficit patients tend to have poorer performance on cognitive tests, the magnitude of this effect is relatively modest, translating to over 70 % overlap in scores between groups.

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Acknowledgments

This work was supported, in part, by a Vanier Canada Graduate Scholarship (to G. Fervaha). This funding source had no further role in study design, statistical analysis, or interpretation of findings; in writing of the manuscript; or in the decision to submit for publication. Data used in the preparation of this article were obtained from the limited access datasets (version 1) distributed from the NIH-supported “Clinical Antipsychotic Trials of Intervention Effectiveness in Schizophrenia” (CATIE-Sz). This is a multisite, clinical trial of persons with schizophrenia comparing the effectiveness of randomly assigned medication treatment. The study was supported by NIMH Contract #N01MH90001 to the University of North Carolina at Chapel Hill. The ClinicalTrials.gov identifier is NCT00014001. This manuscript reflects the views of the authors and may not reflect the opinions or views of the CATIE-Sz study investigators or the NIH.

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Authors and Affiliations

  1. Schizophrenia Division and Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, 250 College Street, Room 320, Toronto, ON, M5T 1R8, Canada

    Gagan Fervaha, Ofer Agid, George Foussias, Ishraq Siddiqui, Hiroyoshi Takeuchi & Gary Remington

  2. Institute of Medical Science, University of Toronto, Toronto, ON, Canada

    Gagan Fervaha, Ofer Agid, George Foussias, Ishraq Siddiqui & Gary Remington

  3. Department of Psychiatry, University of Toronto, Toronto, ON, Canada

    Ofer Agid, George Foussias, Hiroyoshi Takeuchi & Gary Remington

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  1. Gagan Fervaha
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  2. Ofer Agid
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  5. Hiroyoshi Takeuchi
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Correspondence to Gagan Fervaha.

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Conflict of interest

Dr. Agid has received research support from Pfizer Inc. and Janssen-Ortho, consultant fees from Janssen-Ortho, Eli Lilly Inc. US, Eli Lilly Canada, Sepreacor, Sunovion and Lundbeck, and speaker’s fees from Janssen-Ortho, Eli Lilly Inc. US, Eli Lilly Canada, Novartis, Sepracor and Sunovion. Dr. Foussias has been involved in research sponsored by Medicure Inc. and Neurocrine Bioscience, has received consultant fees from Roche, and has received speaker fees from Roche, Lundbeck, and Novartis. Dr. Takeuchi has received fellowship grants from the Japanese Society of Clinical Neuropsychopharmacology and Astellas Foundation for Research on Metabolic Disorders and manuscript fees from Dainippon Sumitomo Pharma. Dr. Remington has received research support from Novartis, Medicure, and Neurocrine Bioscience, consultant fees from Laboratorios Farmacéuticos ROVI, Synchroneuron, and Novartis, and speaker’s fees from Novartis. The other authors have no conflicts to disclose.

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Fervaha, G., Agid, O., Foussias, G. et al. Neurocognitive impairment in the deficit subtype of schizophrenia. Eur Arch Psychiatry Clin Neurosci 266, 397–407 (2016). https://doi.org/10.1007/s00406-015-0629-6

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