Velocardiofacial syndrome in childhood-onset schizophrenia

Citation
Si. Usiskin et al., Velocardiofacial syndrome in childhood-onset schizophrenia, J AM A CHIL, 38(12), 1999, pp. 1536-1543
Citations number
49
Categorie Soggetti
Psychiatry
Journal title
JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
ISSN journal
08908567 → ACNP
Volume
38
Issue
12
Year of publication
1999
Pages
1536 - 1543
Database
ISI
SICI code
0890-8567(199912)38:12<1536:VSICS>2.0.ZU;2-T
Abstract
Objectives: Deletion of chromosome 22q11 (velocardiofacial syndrome) is ass ociated with early neurodevelopmental abnormalities and with schizophrenia in adults. The rate of 22q11 deletions was examined in a series of patients with childhood-onset schizophrenia (COS), in whom early premorbid developm ental and cognitive impairments are more pronounced than in adult-onset cas es. Method: Through extensive recruiting and screening, a cohort of 47 pati ents was enrolled in a comprehensive study of very-early-onset schizophreni a. All were tested with fluorescence in situ hybridization for deletions on chromosome 22q11. Results: Three (6.4%) of 47 patients were found to have a 22q11 deletion. All 3 COS patients with 22q11 deletions had premorbid imp airments of language, motor, and social development, although their physica l characteristics varied. Brain magnetic resonance imaging revealed increas ed midbody corpus callosum area and ventricular volume in relation both to healthy controls and to other COS patients. Conclusions: The rate of 22q11 deletions in COS is higher than in the general population (0.025%, p < .001 ) and may be higher than reported for adult-onset schizophrenia (2.0%, p = .09). These results suggest that 22q11 deletions may be associated with an earlier age of onset of schizophrenia, possibly mediated by a more salient neurodevelopmental disruption.