Eric C Meyer1, Ricardo E Carrión2, Barbara A Cornblatt2, Jean Addington3, Kristin S Cadenhead4, Tyrone D Cannon5, Thomas H McGlashan6, Diana O Perkins7, Ming T Tsuang8, Elaine F Walker9, Scott W Woods6, Robert Heinssen10, Larry J Seidman11. 1. VA VISN 17 Center of Excellence for Research on Returning War Veterans, Waco, TX; Department of Psychiatry and Behavioral Science, Texas A&M Health Science Center, College of Medicine, College Station, TX; 2. Division of Psychiatry Research, The Zucker Hillside Hospital, North Shore - Long Island Jewish Health System (NS-LIJHS), Glen Oaks, NY; 3. Department of Psychiatry, University of Calgary, Calgary, Alberta, Canada; 4. Department of Psychiatry, UCSD, San Diego, CA; 5. Departments of Psychology and Psychiatry and Biobehavioral Sciences, UCLA, Los Angeles, CA; Department of Psychiatry, Yale University, New Haven, CT; 6. Department of Psychiatry, Yale University, New Haven, CT; 7. Department of Psychiatry, University of North Carolina, Chapel Hill, NC; 8. Department of Psychiatry, UCSD, San Diego, CA; Center for Behavior Genomics and Institute of Genomic Medicine, UCSD, La Jolla, CA; 9. Departments of Psychology and Psychiatry, Emory University, Atlanta, GA; 10. Schizophrenia Spectrum Research Program, Division of Adult Translational Research, National Institute of Mental Health, Bethesda, MD; 11. Department of Psychiatry, Harvard Medical School at Beth Israel Deaconess Medical Center, Boston MA; Department of Psychiatry, Harvard Medical School at Massachusetts General Hospital, Boston MA lseidman@bidmc.harvard.edu.
Abstract
OBJECTIVES: Impaired social, role, and neurocognitive functioning are preillness characteristics of people who later develop psychosis. In people with schizophrenia, neurocognition and negative symptoms are associated with functional impairment. We examined the relative contributions of neurocognition and symptoms to social and role functioning over time in clinically high-risk (CHR) individuals and determined if negative symptoms mediated the influence of cognition on functioning. METHODS: Social, role, and neurocognitive functioning and positive, negative, and disorganized symptoms were assessed in 167 individuals at CHR for psychosis in the North American Prodrome Longitudinal Study Phase 1 (NAPLS-1), of whom 96 were reassessed at 12 months. RESULTS: Regression analyses indicated that negative symptoms accounted for unique variance in social and role functioning at baseline and follow-up. Composite neurocognition accounted for unique, but modest, variance in social and role functioning at baseline and in role functioning at follow-up. Negative symptoms mediated the relationship between composite neurocognition and social and role functioning across time points. In exploratory analyses, individual tests (IQ estimate, Digit Symbol/Coding, verbal memory) selectively accounted for social and role functioning at baseline and follow-up after accounting for symptoms. When negative symptom items with content overlapping with social and role functioning measures were removed, the relationship between neurocognition and social and role functioning was strengthened. CONCLUSION: The modest overlap among neurocognition, negative symptoms, and social and role functioning indicates that these domains make substantially separate contributions to CHR individuals.
OBJECTIVES: Impaired social, role, and neurocognitive functioning are preillness characteristics of people who later develop psychosis. In people with schizophrenia, neurocognition and negative symptoms are associated with functional impairment. We examined the relative contributions of neurocognition and symptoms to social and role functioning over time in clinically high-risk (CHR) individuals and determined if negative symptoms mediated the influence of cognition on functioning. METHODS: Social, role, and neurocognitive functioning and positive, negative, and disorganized symptoms were assessed in 167 individuals at CHR for psychosis in the North American Prodrome Longitudinal Study Phase 1 (NAPLS-1), of whom 96 were reassessed at 12 months. RESULTS: Regression analyses indicated that negative symptoms accounted for unique variance in social and role functioning at baseline and follow-up. Composite neurocognition accounted for unique, but modest, variance in social and role functioning at baseline and in role functioning at follow-up. Negative symptoms mediated the relationship between composite neurocognition and social and role functioning across time points. In exploratory analyses, individual tests (IQ estimate, Digit Symbol/Coding, verbal memory) selectively accounted for social and role functioning at baseline and follow-up after accounting for symptoms. When negative symptom items with content overlapping with social and role functioning measures were removed, the relationship between neurocognition and social and role functioning was strengthened. CONCLUSION: The modest overlap among neurocognition, negative symptoms, and social and role functioning indicates that these domains make substantially separate contributions to CHR individuals.
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