Autism is unlikely to be caused by a single obstetric factor. The increased prevalence of obstetric complications among autism cases is most likely due to the underlying genetic factors or an interaction of these factors with the environment.
ObjectivesTo estimate the prevalence of fetal alcohol spectrum disorder (FASD) among young people in youth detention in Australia. Neurodevelopmental impairments due to FASD can predispose young people to engagement with the law. Canadian studies identified FASD in 11%–23% of young people in corrective services, but there are no data for Australia.DesignMultidisciplinary assessment of all young people aged 10–17 years 11 months and sentenced to detention in the only youth detention centre in Western Australia, from May 2015 to December 2016. FASD was diagnosed according to the Australian Guide to the Diagnosis of FASD.Participants99 young people completed a full assessment (88% of those consented; 60% of the 166 approached to participate); 93% were male and 74% were Aboriginal.Findings88 young people (89%) had at least one domain of severe neurodevelopmental impairment, and 36 were diagnosed with FASD, a prevalence of 36% (95% CI 27% to 46%).ConclusionsThis study, in a representative sample of young people in detention in Western Australia, has documented a high prevalence of FASD and severe neurodevelopmental impairment, the majority of which had not been previously identified. These findings highlight the vulnerability of young people, particularly Aboriginal youth, within the justice system and their significant need for improved diagnosis to identify their strengths and difficulties, and to guide and improve their rehabilitation.
Objective To investigate the relationship between prenatal alcohol exposure and fetal growth and preterm birth and to estimate the effect of dose and timing of alcohol exposure in pregnancy.Design A population-based cohort study linked to birth information on the Western Australian Midwives Notification System. Setting Western Australia.Population A 10% random sample of births restricted to nonindigenous women who had delivered a singleton infant (n = 4719) in 1995-1997. MethodsThe impact of alcohol consumption in pregnancy on fetal growth (small-for-gestational-age [SGA] and large-forgestational-age infants [LGA]) and preterm birth (<37 weeks of gestation) was assessed using multivariate logistic regression analysis and adjusting for confounding factors.Main outcome measures Odds ratios and 95% CI, attributable risk, and population attributable risk were calculated.Results The percentage of SGA infants and preterm birth increased with higher levels of prenatal alcohol exposure; however, the association between alcohol intake and SGA infants was attenuated after adjustment for maternal smoking. Low levels of prenatal alcohol were not associated with preterm birth; however, binge drinking resulted in a nonsignificant increase in odds. Preterm birth was associated with moderate and higher levels of prenatal alcohol consumption for the group of women who ceased drinking before the second trimester. This group of women was significantly more likely to deliver a preterm infant than women who abstained from alcohol (adjusted OR 1.73 [95% CI 1.01-3.14]).Conclusions Alcohol intake at higher levels, particularly heavy and binge drinking patterns, is associated with increased risk of preterm birth even when drinking is ceased before the second trimester. This finding, however, is based on small numbers and needs further investigation. Dose and timing of prenatal alcohol exposure appears to affect preterm delivery and should be considered in future research and health education.
Our data are the only prospective national data available on FAS throughout the world. These findings highlight the severity, complexity and impact of FAS, the need for effective strategies for prevention, and the necessity for education to facilitate earlier diagnosis, referral and reporting of cases.
A craniomaxillofacial unit was established recently in Western Australia, and a study was carried out to provide some baseline characteristics of primary craniosynostosis in Western Australia and to investigate whether there has been any significant temporal change in birth prevalence. A case control study was conducted, using cases identified from a population-based register of birth defects, and a random sample of all births without a birth defect formed the control group. All subjects were born in Western Australia over the period 1980-1994 inclusive. The prevalence of craniosynostosis over the period 1980-1994 in Western Australia was 5.06 per 10,000 births. There was a significant linear increase in lambdoid synostosis over this period of 15.7% per year. Craniosynostosis was significantly more common among male infants, infants born preterm (<37 weeks gestation), breech presentation or presentations other than vertex, and infants born to fathers 40 years of age or older, even after accounting for known autosomal dominant syndromes. Other major birth defects were found in 11.2% of children with nonsyndromic craniosynostosis. Only 43 children (25.3%) with craniosynostosis were reported to have been seen by a geneticist. Thus, the prevalence of craniosynostosis in Western Australia is among the lowest reported. There is no current explanation for the increase in lambdoid synostosis. The increased risk of so-called nonsyndromic craniosynostosis with paternal age raises the possibility of undiagnosed new dominant mutations. This, along with the excess of other birth defects in children with craniosynostosis emphasises the need to ensure that these families are offered genetic counseling.
The objective of the study was to identify the origin (s) of the association between cerebral palsy (CP) and birth defects in the absence of cerebral birth defects. Data from the 1980 to 1994 Western Australian birth cohorts (355 659 neonatal survivors) were linked to the Cerebral Palsy Register (941 links) and the Birth Defects Registry (17070 links). Associations between CP (congenital or acquired) and birth defects (cerebral or exclusively non-cerebral) were estimated. The origin of the association between non-cerebral defects and acquired CP was investigated with an observational study, and the origin of the association between non-cerebral defects and congenital CP was investigated with a blinded case-control study of births with non-cerebral defects with or without CP. With non-cerebral defects, the odds ratio for CP was 4.8 (95% CI 3.1-7.4) if acquired and 4.7 (3.9-5.7) if congenital. For acquired CP, the association arose primarily as a result of cardiac defects. For congenital CP, the association arose partly from ascertainment bias and partly from defects known to be associated with cerebral defects (but not identified in these data). However, a significant portion remained unexplained. The presence of non-cerebral defects should heighten clinical alertness to the possibility of CP and of cerebral birth defects.
Paediatricians identified the need for educational materials about FAS and alcohol use in pregnancy for themselves and their clients. Lack of knowledge about FAS diagnosis and management will limit opportunities for diagnosis, prevention and early intervention.
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