The Wisconsin Fetal Alcohol Syndrome Screening Project.
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PROBLEM: Fetal Alcohol Syndrome (FAS) is preventable, under-diagnosed, and under-reported. Wisconsin rates for alcohol use and binge drinking in childbearing-age women exceed the national average. FAS prevalence in Wisconsin has not previously been systematically evaluated. METHODS: The Wisconsin Fetal Alcohol Syndrome Screening Project (WFASSP) used a multi-stage, multisource prospective population-based screening methodology to identify children born in 1998-1999 in Southeast Wisconsin who met a surveillance case definition for FAS. The 4-stage methodology used screening of electronic birth files, abstraction of neonatal medical records, and direct assessment of facial features, growth, and development at age 2 to 3 years. RESULTS: The FAS prevalence rate was 0.23 per 1000 births. Children directly evaluated had fewer demographic, pregnancy, and maternal substance use risk factors than lost-to-follow-up children. Thirty-two percent of children with weight and head circumference below the 10th percentile at birth were developmentally delayed and 47% had at least one physical growth delay. CONCLUSIONS: The WFASSP methodology identified children who had not previously been diagnosed with FAS. Using the combination of weight and head circumference below the 10th percentile at birth is a useful methodology for identifying children at substantial risk for growth and developmental delays from FAS or other unspecified etiologies. (+info)
A practical clinical approach to diagnosis of fetal alcohol spectrum disorders: clarification of the 1996 institute of medicine criteria.
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BACKGROUND: The adverse effects of alcohol on the developing human represent a spectrum of structural anomalies and behavioral and neurocognitive disabilities, most accurately termed fetal alcohol spectrum disorders (FASD). The first descriptions in the modern medical literature of a distinctly recognizable pattern of malformations associated with maternal alcohol abuse were reported in 1968 and 1973. Since that time, substantial progress has been made in developing specific criteria for defining and diagnosing this condition. Two sets of diagnostic criteria are now used most widely for evaluation of children with potential diagnoses in the FASD continuum, ie, the 1996 Institute of Medicine (IOM) criteria and the Washington criteria. Although both approaches have improved the clinical delineation of FASD, both suffer from significant drawbacks in their practical application in pediatric practice. OBJECTIVE: The purpose of this report is to present specific clarifications of the 1996 IOM criteria for the diagnosis of FASD, to facilitate their practical application in clinical pediatric practice. METHODS: A large cohort of children who were prenatally exposed to alcohol were identified, through active case-ascertainment methods, in 6 Native American communities in the United States and 1 community in the Western Cape Province of South Africa. The children and their families underwent standardized multidisciplinary evaluations, including a dysmorphology examination, developmental and neuropsychologic testing, and a structured maternal interview, which gathered data about prenatal drinking practices and other demographic and family information. Data for these subjects were analyzed, and revisions and clarifications of the existing IOM FASD diagnostic categories were formulated on the basis of the results. RESULTS: The revised IOM method defined accurately and completely the spectrum of disabilities among the children in our study. On the basis of this experience, we propose specific diagnostic criteria for fetal alcohol syndrome and partial fetal alcohol syndrome. We also define alcohol-related birth defects and alcohol-related neurodevelopmental disorder from a practical standpoint. CONCLUSIONS: The 1996 IOM criteria remain the most appropriate diagnostic approach for children prenatally exposed to alcohol. The proposed revisions presented here make these criteria applicable in clinical pediatric practice. (+info)
Ethanol exposure affects gene expression in the embryonic organizer and reduces retinoic acid levels.
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Fetal Alcohol Spectrum Disorder (FASD) is a set of developmental malformations caused by alcohol consumption during pregnancy. Fetal Alcohol Syndrome (FAS), the strongest manifestation of FASD, results in short stature, microcephally and facial dysmorphogenesis including microphthalmia. Using Xenopus embryos as a model developmental system, we show that ethanol exposure recapitulates many aspects of FAS, including a shortened rostro-caudal axis, microcephally and microphthalmia. Temporal analysis revealed that Xenopus embryos are most sensitive to ethanol exposure between late blastula and early/mid gastrula stages. This window of sensitivity overlaps with the formation and early function of the embryonic organizer, Spemann's organizer. Molecular analysis revealed that ethanol exposure of embryos induces changes in the domains and levels of organizer-specific gene expression, identifying Spemann's organizer as an early target of ethanol. Ethanol also induces a defect in convergent extension movements that delays gastrulation movements and may affect the overall length. We show that mechanistically, ethanol is antagonistic to retinol (Vitamin A) and retinal conversion to retinoic acid, and that the organizer is active in retinoic acid signaling during early gastrulation. The model suggests that FASD is induced in part by an ethanol-dependent reduction in retinoic acid levels that are necessary for the normal function of Spemann's organizer. (+info)
Screening for fetal alcohol spectrum disorder.
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QUESTION: I have several patients whom I suspect are drinking during pregnancy. How can I find out for sure if they are? ANSWER: You can use one of the validated tools to screen for problem drinking. Motherisk uses the TWEAK test, but others are just as good. Following birth, you can test infants' meconium for metabolites of ethanol to detect whether they were exposed in utero to excessive drinking. (+info)
Fetal alcohol spectrum disorder: Canadian guidelines for diagnosis.
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The diagnosis of fetal alcohol spectrum disorder (FASD) is complex and guidelines are warranted. A subcommittee of the Public Health Agency of Canada's National Advisory Committee on Fetal Alcohol Spectrum Disorder reviewed, analysed and integrated current approaches to diagnosis to reach agreement on a standard in Canada. The purpose of this paper is to review and clarify the use of current diagnostic systems and make recommendations on their application for diagnosis of FASD-related disabilities in people of all ages. The guidelines are based on widespread consultation of expert practitioners and partners in the field. The guidelines have been organized into 7 categories: screening and referral; the physical examination and differential diagnosis; the neurobehavioural assessment; and treatment and follow-up; maternal alcohol history in pregnancy; diagnostic criteria for fetal alcohol syndrome (FAS), partial FAS and alcohol-related neurodevelopmental disorder; and harmonization of Institute of Medicine and 4-Digit Diagnostic Code approaches. The diagnosis requires a comprehensive history and physical and neurobehavioural assessments; a multidisciplinary approach is necessary. These are the first Canadian guidelines for the diagnosis of FAS and its related disabilities, developed by broad-based consultation among experts in diagnosis. (+info)
Case study: using a virtual reality computer game to teach fire safety skills to children diagnosed with fetal alcohol syndrome.
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OBJECTIVE: To assess the effectiveness of a computer-based virtual reality (VR) game in teaching five children diagnosed with fetal alcohol syndrome (FAS) fire safety skills and to generalize these skills to a real world simulation. METHOD: Children participated in a study by using a multiple baseline, multiple probe design. Before the game, no child could correctly describe what actions to take during a home fire. A computerized game allowed them to learn the recommended safety steps in a virtual world. Skill learning and real-world generalization were tested immediately after the intervention and at 1-week post-test. RESULTS: All children reached 100% accuracy on the computer intervention, defined as successfully completing each of the safety steps. At the 1-week follow-up, all the children were able to perform the steps correctly in a real world simulation. CONCLUSIONS: The results suggest that this method of intervention warrants further study as an educational delivery system for children with FAS. (+info)
Brief intervention for prenatal alcohol use: a randomized trial.
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OBJECTIVE: To test the effectiveness of a brief intervention in the reduction of prenatal alcohol consumption by women when a partner is included. METHODS: Randomized trial of a single session brief intervention given by the study nurse or principal investigator for 304 pregnant women and their partners. The women had positive T-ACE (Tolerance, Annoyed, Cut down, Eye-opener, an alcohol screening test) results and were at risk for alcohol consumption while pregnant. All completed initial diagnostic and postpartum interviews. RESULTS: Fewer than 20% of participants (median 11.5 weeks of gestation) were abstinent at study enrollment, averaging more than 1.5 drinks per episode. Nearly 30% had 2 or more drinks at a time while pregnant. Prenatal alcohol use declined in both the treatment and control groups after study enrollment, based on a 95% follow-up rate. Factors associated with increased prenatal alcohol use after randomization included more years of education, extent of previous alcohol consumption, and temptation to drink in social situations. Brief interventions for prenatal alcohol reduced subsequent consumption most significantly for the women with the highest consumption initially (regression coefficient, b = -0.163, standard error (b) = 0.063, P < .01). Moreover, the effects of the brief intervention were significantly enhanced when a partner participated (b = -0.932, standard error (b) = 0.468), P < .05). CONCLUSION: Pregnant women with the highest levels of alcohol use reduced their drinking most after a brief intervention that included their partners. Recommendations include consistent screening for prenatal alcohol use followed by diagnostic assessment when indicated, and if confirmed by other studies, a patient-partner brief intervention for the heaviest drinkers. (+info)
A systems-based computational model for dose-response comparisons of two mode of action hypotheses for ethanol-induced neurodevelopmental toxicity.
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Investigations into the potential mechanisms for ethanol-induced developmental toxicity have been ongoing for over 30 years since Fetal Alcohol Syndrome (FAS) was first described. Neurodevelopmental endpoints are particularly sensitive to in utero exposure to alcohol as suggested by the more prevalent alcohol-related neurodevelopmental disorder (ARND). The inhibition of proliferation during neurogenesis and the induction of apoptosis during the period of synaptogenesis have been identified as potentially important mechanisms for ARND. However, it is unclear how these two mechanisms quantitatively relate to the dose and timing of exposure. We have extended our model of neocortical neurogenesis to evaluate apoptosis during synaptogenesis. This model construct allows quantitative evaluation of the relative impacts on neuronal proliferation versus apoptosis during neocortical development. Ethanol-induced lengthening of the cell cycle of neural progenitor cells during rat neocortical neurogenesis (G13-G19) is used to compute the number of neurons lost after exposure during neurogenesis. Ethanol-induced dose-dependent increases in cell death rates are applied to our apoptosis model during rat synaptogenesis (P0-P14), when programmed cell death plays a major role in shaping the future neocortex. At a human blood ethanol concentration that occurs after 3-5 drinks ( approximately 150 mg/dl), our model predicts a 20-30% neuronal deficit due to inhibition of proliferation during neurogenesis, while a similar exposure during synaptogenesis suggests a 7-9% neuronal loss through induction of cell death. Experimental in vitro and in vivo dose-response research and stereological research on long-term neuronal loss after developmental exposure to ethanol is compared to our model predictions. Our computational model allows for quantitative, systems-level comparisons of mechanistic hypotheses for perturbations during specific neurodevelopmental periods. (+info)