Developmental Medicine & Child Neurology
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AIM The aim of this study was to investigate the association between heavy maternal alcohol consumption and pre- peri- and postneonatally acquired cerebral palsy (CP). METHOD The records of all mothers with an International Classification of Diseases, revision 9 or 10 (ICD-9 ⁄ -10) alcohol-related diagnostic code, indicating heavy alcohol consumption, recorded on population-based health, mental health, and drug and alcohol data sets from 1983 to 2007, and their children were identified through the Western Australian Data-linkage System. This ‘exposed’ cohort was frequency matched with mothers without an alcohol-related diagnosis and their offspring (comparison group). Cases of CP were identified through linkage with the Western Australia CP Register. Analyses were undertaken using multivariate logistic regression.
RESULTS There were 23 573 live births in the exposed group (58.6% non-Aboriginal; 41.4% Aboriginal) and 292 cases of CP. The odds of pre ⁄ perinatally acquired CP were elevated for children of non-Aboriginal mothers with an alcohol-related diagnosis recorded during pregnancy (adjusted odds ratio 3.32; 95% confidence interval [CI] 1.30–8.48) and for Aboriginal children when an alcohol-related diagnosis was recorded up to 12 months before the mother’s pregnancy (adjusted odds ratio 2.49; 95% CI 0.99–6.25). Increased odds of postneonatally acquired CP following any alcohol-related diagnosis were found for non-Aboriginal children (adjusted odds ratio 7.92; 95% CI 2.23–28.14).
INTERPRETATION These results suggest that heavy maternal alcohol consumption is a direct cause of pre ⁄ perinatally acquired CP, and an indirect cause of postneonatally acquired CP, in non-Aboriginal children. The lack of an association for Aboriginal children requires further investigation but may be due to under ascertainment of alcohol use disorders during pregnancy and other aetiological pathways.