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Potentially important periods of change in the development of social and role functioning in youth at clinical high risk for psychosis

  • Eva Velthorst (a1) (a2), Jamie Zinberg (a3), Jean Addington (a4), Kristin S. Cadenhead (a5), Tyrone D. Cannon (a6), Ricardo E. Carrión (a7), Andrea Auther (a7), Barbara A. Cornblatt (a7), Thomas H. McGlashan (a6), Daniel H. Mathalon (a8) (a9), Diana O. Perkins (a10), Larry J. Seidman (a11) (a12), Ming T. Tsuang (a5), Elaine F. Walker (a13), Scott W. Woods (a6), Abraham Reichenberg (a1) and Carrie E. Bearden (a3)...

Abstract

The developmental course of daily functioning prior to first psychosis-onset remains poorly understood. This study explored age-related periods of change in social and role functioning. The longitudinal study included youth (aged 12–23, mean follow-up years = 1.19) at clinical high risk (CHR) for psychosis (converters [CHR-C], n = 83; nonconverters [CHR-NC], n = 275) and a healthy control group (n = 164). Mixed-model analyses were performed to determine age-related differences in social and role functioning. We limited our analyses to functioning before psychosis conversion; thus, data of CHR-C participants gathered after psychosis onset were excluded. In controls, social and role functioning improved over time. From at least age 12, functioning in CHR was poorer than in controls, and this lag persisted over time. Between ages 15 and 18, social functioning in CHR-C stagnated and diverged from that of CHR-NC, who continued to improve (p = .001). Subsequently, CHR-C lagged behind in improvement between ages 21 and 23, further distinguishing them from CHR-NC (p < .001). A similar period of stagnation was apparent for role functioning, but to a lesser extent (p = .007). The results remained consistent when we accounted for the time to conversion. Our findings suggest that CHR-C start lagging behind CHR-NC in social and role functioning in adolescence, followed by a period of further stagnation in adulthood.

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Corresponding author

Address correspondence and reprint requests to: Eva Velthorst, Department of Psychiatry and Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai, 1425 Madison Avenue, New York, NY 10029; E-mail: eva.velthorst@mssm.edu.

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This study was supported by grants from the National Institute of Mental Health of the National Institutes of Health (U01 MH081928 to L.J.S., U01 MH066134 to J.A., R01 MH60720 to K.S.C., R01 MH065079 to T.D.C., R01 MH061523 to B.A.C., U01 MH066069 and K23 MH001905 to D.O.P., RO1MH062066 to E.F.W., U01 MH066160 to S.W.W., and K05MH01654 to T.H.M.), the Commonwealth of Massachusetts (SCDMH82101008006 to L.J.S), and the Netherlands Organization for Scientific Research (VENI 916-15-005 to E.V.). The content of this article is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. The authors have no conflicts of interest in relation to the subject of this study.

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Development and Psychopathology
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