期刊
CEREBRAL CORTEX
卷 19, 期 5, 页码 1107-1123出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/cercor/bhn152
关键词
cortex; development; imaging; neurotoxicity; schizophrenia
资金
- National Institute for Biomedical Imaging and Bioengineering,
- National Center for Research Resources
- National Institute on Aging
- National Library of Medicine
- National Institute for Child Health and Development [EB01651, RR019771, AG016570, LM05639, HD050735]
- National Center for Research Resources [RR13642]
- National Institute of Mental Health [MH00537, MH33127, MH52376]
- University of North Carolina Mental Health and Neuroscience Clinical Research Center
- Chapel Hill, NC
- National Alliance for Research on Schizophrenia and Depression Foundation, Great Neck, NY
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD050735] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [P41RR013642, R21RR019771] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH052376, P30MH033127, P50MH033127] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P50AG016570] Funding Source: NIH RePORTER
- NATIONAL LIBRARY OF MEDICINE [R01LM005639] Funding Source: NIH RePORTER
Using time-lapse maps, we visualized the dynamics of schizophrenia progression, revealing spreading cortical changes that depend on the type of antipsychotic treatment. Dynamic, 4-dimensional models of disease progression were created from 4 repeated high-resolution brain magnetic resonance imaging scans of 36 first-episode schizophrenia patients (30 men/6 women; mean age: 24.2 +/- 5.1 SD years) randomized to haloperidol (HAL) (n = 15) or olanzapine (OLZ) treatment (n = 21), imaged at baseline, 3, 6, and 12 months (144 scans). Based on surface-based cortical models and point-by-point measures of gray matter volume, we generated time-lapse maps for each treatment. Disease trajectories differed for atypical versus typical neuroleptic drugs. A rapidly advancing parietal-to-frontal deficit trajectory, in HAL-treated patients, mirrored normal cortical maturation but greatly intensified. The disease trajectory advanced even after symptom normalization, involving the frontal cortex within 12 months with typical drug treatment. Areas with fastest tissue loss shifted anteriorly in the first year of psychosis. This trajectory was not seen with OLZ. Whether this association reflects either reduced neurotoxicity or neuroprotection cannot be addressed with neuroimaging; changes may relate to glial rather than neural components. These maps revise current models of schizophrenia progression; due to power limitations, the findings require confirmation in a sample large enough to model group x time interactions.
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