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Schizophrenia Bulletin Advance Access originally published online on September 29, 2007
Schizophrenia Bulletin 2008 34(1):30-36; doi:10.1093/schbul/sbm103
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Published by Oxford University Press 2007.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Cortical Brain Development in Schizophrenia: Insights From Neuroimaging Studies in Childhood-Onset Schizophrenia

Nitin Gogtay1,2
2 Child Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Building 10, Room 3N202, 10 Center Drive, MSC-1600 Bethesda, MD 20892

1 To whom correspondence should be addressed; tel: 301-435-4494, fax: 301-402-0296, e-mail: gogtayn{at}mail.nih.gov.

Childhood-onset schizophrenia (COS; defined as onset by age 12 years) is rare, difficult to diagnose, and represents a severe and chronic phenotype of the adult-onset illness. A study of childhood-onset psychoses has been ongoing at the National Institute of Mental Health (NIMH) since 1990, where children with COS and severe atypical psychoses (provisionally labeled "multidimensionally impaired" or MDI by the NIMH team) are studied prospectively along with all first-degree relatives. COS subjects have robust cortical gray matter (GM) loss during adolescence, which appears to be an exaggeration of the normal cortical GM developmental pattern and eventually mimics the pattern seen in adult-onset cases as the children become young adults. These cortical GM changes in COS are diagnostically specific and seemingly unrelated to the effects of medications. Furthermore, the cortical GM loss is also shared by healthy full siblings of COS probands suggesting a genetic influence on the abnormal brain development.

Keywords: childhood-onset schizophrenia / structural brain imaging


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[Abstract] [Full Text] [PDF]


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