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Schizophrenia Bulletin Advance Access originally published online on January 29, 2008
Schizophrenia Bulletin 2008 34(2):341-353; doi:10.1093/schbul/sbm157
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© The Author 2008. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Longitudinal Brain Changes in Early-Onset Psychosis

Celso Arango1,2, Carmen Moreno2, Salvador Martínez3, Mara Parellada2, Manuel Desco4, Dolores Moreno, David Fraguas2, Nitin Gogtay5, Anthony James6 and Judith Rapoport5
2 Adolescent Unit, Department of Psychiatry, Hospital General Universitario Gregorio Marañón, Madrid, Spain
3 Instituto de Neurociencias, Universidad Miguel Hernandez, Alicante, Spain
4 Unidad de Medicina y Cirugía Experimental, Hospital General Universitario Gregorio Marañón, Madrid, Spain
5 Child Psychiatry Branch, National Institute of Mental Health, Room 3N202, Building 10, Center Drive, Bethesda, MD 20892
6 Highfield Adolescent Unit, Warneford Hospital, Oxford, UK

1 To whom correspondence should be addressed; Maryland Psychiatric Research Center, University of Maryland, College Park, MD; tel: 34-914265006, fax: 34-914265005, e-mail: Carango{at}mprc.umaryland.edu.

Progressive losses of cortical gray matter volumes and increases in ventricular volumes have been reported in patients with childhood-onset schizophrenia (COS) during adolescence. Longitudinal studies suggest that the rate of cortical loss seen in COS during adolescence plateaus during early adulthood. Patients with first-episode adolescent-onset schizophrenia show less marked progressive changes, although the number of studies in this population is small. Some studies show that, although less exaggerated, progressive changes are also present in nonschizophrenia early-onset psychosis. The greater loss of brain tissue seen in COS, even some years after the first episode, as compared to adolescent- or adult-onset schizophrenia may be due to variables such as sample bias (more severe, treatment refractory sample of childhood-onset patients studied), a process uniquely related to adolescent development in COS, differential brain effects of drug treatment in this population, clinical outcome, or interactions among these variables. Findings from both cross-sectional studies of first-episode patients and longitudinal studies in COS and adolescent onset support the concept of early-onset schizophrenia as a progressive neurodevelopmental disorder with both early and late developmental abnormalities. Future studies should look for correlates at a cellular level and for pathophysiological explanations of volume changes in these populations. The association of risk genes involved in circuitries associated with schizophrenia and their relationship to developmental trajectories is another promising area of future research.

Keywords: early-onset / MRI / children / adolescents / psychosis / neurodevelopment


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