Childhood neuromotor dysfunction in schizophrenia patients and their unaffected siblings: A prospective cohort study

Citation
Im. Rosso et al., Childhood neuromotor dysfunction in schizophrenia patients and their unaffected siblings: A prospective cohort study, SCHIZO BULL, 26(2), 2000, pp. 367-378
Citations number
51
Categorie Soggetti
Psychiatry,"Neurosciences & Behavoir
Journal title
SCHIZOPHRENIA BULLETIN
ISSN journal
05867614 → ACNP
Volume
26
Issue
2
Year of publication
2000
Pages
367 - 378
Database
ISI
SICI code
0586-7614(2000)26:2<367:CNDISP>2.0.ZU;2-S
Abstract
Neuromotor dysfunction is a consistent finding in high-risk and archival st udies of schizophrenia, but the sources of this dysfunction and its role in the developmental course of the disorder remain poorly understood. This st udy examined childhood motor predictors of adult psychiatric outcome in a b irth cohort sample (72 patients with schizophrenia or schizoaffective disor der, 63 unaffected siblings, and 7,941 nonpsychiatric controls), evaluated prospectively with neurologic examinations at 8 months, 4 years, and 7 year s of age. Deviance on motor coordination measures at 7 years was associated with both adult schizophrenia and unaffected sibling status, suggesting th at a co-familial (and perhaps genetic) factor underlies motor coordination deficits in schizophrenia. Unusual movements at ages 4 and 7 predicted adul t schizophrenia but not unaffected sibling status, indicating that these de ficits may be specific to those who will develop the clinical phenotype. No ne of the motor precursors were confined to patients with an early age at f irst treatment contact. Fetal hypoxia predicted unusual movements at 4 but not 7 years among the preschizophrenia subjects, suggesting neurodevelopmen tal dependence of its functional effects. Neither prenatal complications no r birth weight were associated with motor dysfunction in preschizophrenia s ubjects or their unaffected siblings at any age. Finally, preschizophrenia children did not show the expected developmental decline in unusual movemen ts, perhaps reflecting aberrant functional maturation of cortical-subcortic al pathways.