Huiru Cui1, Anthony J Giuliano2, Tianhong Zhang3, Lihua Xu3, Yanyan Wei3, Yingying Tang3, Zhenying Qian3, Lena M Stone4, Huijun Li5, Susan Whitfield-Gabrieli6, Margaret Niznikiewicz7, Matcheri S Keshavan8, Martha E Shenton9, Jijun Wang10, William S Stone11. 1. Shanghai Key Laboratory of Psychotic Disorders, SHARP Program, Shanghai Mental Health Center, Shanghai Jiaotong University School of Medicine, Shanghai, China; Psychiatry Neuroimaging Laboratory, Department of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. 2. Worcester Recovery Center & Hospital, Massachusetts Department of Mental Health, MA, USA. 3. Shanghai Key Laboratory of Psychotic Disorders, SHARP Program, Shanghai Mental Health Center, Shanghai Jiaotong University School of Medicine, Shanghai, China. 4. McLean Hospital, Schizophrenia and Bipolar Disorder Research Program, Belmont, MA, USA. 5. Florida A&M University, Department of Psychology, Tallahassee, FL, USA. 6. Department of Psychology, Northeastern University, Boston, MA, USA. 7. Department of Psychology, Northeastern University, Boston, MA, USA; Department of Psychiatry, VA Boston Healthcare System, Brockton Division, Brockton, MA, USA. 8. Department of Psychiatry, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. 9. Department of Psychiatry, VA Boston Healthcare System, Brockton Division, Brockton, MA, USA; Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Research and Development, VA Boston Healthcare System, Brockton Division, Brockton, MA, USA. 10. Shanghai Key Laboratory of Psychotic Disorders, SHARP Program, Shanghai Mental Health Center, Shanghai Jiaotong University School of Medicine, Shanghai, China. Electronic address: jijunwang27@163.com. 11. Department of Psychiatry, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: wstone@bidmc.harvard.edu.
Abstract
OBJECTIVES: 1) to assess generalizability of neurocognitive deficits reported in previous Western clinical high-risk (CHR) for psychosis studies in a prodromal program in Shanghai, China; and 2) to investigate neurocognition in CHR subjects in relation to a broader range of clinical outcomes (e.g. remission) than presence or absence of psychosis. METHOD: Baseline neurocognitive assessments of CHR (n = 217) and healthy control (HC; n = 133) subjects were compared based on 1-year follow-up clinical status using MANOVA. CHR subjects were first divided into 'converter' (CHR-C; n = 41) and 'non-converter' (CHR-NC; n = 155) to psychosis groups and compared to HC and to each other. CHR subjects were then divided into 'remission' (i.e. achieved remission; n = 102), 'symptomatic' (persistent positive symptoms in the absence of conversion; n = 37) and 'poor-outcome' (converted and symptomatic subjects who did not respond to treatment; n = 57) groups. RESULTS: CHR neurocognitive performance was broadly impaired compared to HC; CHR-C subjects showed lower performance in processing speed and visual learning than CHR-NC. CHRs with poor clinical outcomes showed lower performance on most MCCB tasks compared to HC, particularly in learning and processing speed, as clinical outcome worsened from remission to symptomatic to poor outcome groups. CONCLUSIONS: Level and pattern of baseline neurocognitive weaknesses in SHARP CHR subjects were similar to those in NAPLS-2. Outcome stratification into remission, symptomatic and poor groups was associated with increasing cognitive deficits in learning and processing speed. These findings support cross-cultural generalizability and advance understanding of CHR neurocognitive heterogeneity associated with 1-year clinical outcomes.
OBJECTIVES: 1) to assess generalizability of neurocognitive deficits reported in previous Western clinical high-risk (CHR) for psychosis studies in a prodromal program in Shanghai, China; and 2) to investigate neurocognition in CHR subjects in relation to a broader range of clinical outcomes (e.g. remission) than presence or absence of psychosis. METHOD: Baseline neurocognitive assessments of CHR (n = 217) and healthy control (HC; n = 133) subjects were compared based on 1-year follow-up clinical status using MANOVA. CHR subjects were first divided into 'converter' (CHR-C; n = 41) and 'non-converter' (CHR-NC; n = 155) to psychosis groups and compared to HC and to each other. CHR subjects were then divided into 'remission' (i.e. achieved remission; n = 102), 'symptomatic' (persistent positive symptoms in the absence of conversion; n = 37) and 'poor-outcome' (converted and symptomatic subjects who did not respond to treatment; n = 57) groups. RESULTS: CHR neurocognitive performance was broadly impaired compared to HC; CHR-C subjects showed lower performance in processing speed and visual learning than CHR-NC. CHRs with poor clinical outcomes showed lower performance on most MCCB tasks compared to HC, particularly in learning and processing speed, as clinical outcome worsened from remission to symptomatic to poor outcome groups. CONCLUSIONS: Level and pattern of baseline neurocognitive weaknesses in SHARP CHR subjects were similar to those in NAPLS-2. Outcome stratification into remission, symptomatic and poor groups was associated with increasing cognitive deficits in learning and processing speed. These findings support cross-cultural generalizability and advance understanding of CHR neurocognitive heterogeneity associated with 1-year clinical outcomes.