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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fetal Alcohol Syndrome, a permanent birth defect caused by maternal alcohol use during pregnancy, is a leading preventable cause of mental retardation. Neuropsychological deficits have been well documented, however interventions developed have not been evaluated. We describe a successful 12-month community pilot intervention with 19 young women with Fetal Alcohol Spectrum Disorders (FASD). Improved outcomes (including decreased alcohol and drug use, increased use of contraceptives and medical and mental health care services, and stable housing) were obtained by implementing a community intervention model of targeted education and collaboration with key service providers, and by using paraprofessional advocate case managers as facilitators.
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PMID:A pilot community intervention for young women with fetal alcohol spectrum disorders. 1567 89

Fetal exposure to alcohol is the major known cause of mental retardation in the Western world. For more than half of the 20th century, the placenta was widely believed to be an effective barrier against environmental agents. The discovery that offspring of pregnant women who were exposed to German measles or administered thalidomide were often malformed raised awareness that teratogens could be any environmental agent, including viruses and drugs, that caused abnormal development. Alcohol was not identified as a teratogen until the 1970s. Fetal exposure to alcohol can cause fetal alcohol syndrome (FAS), which is characterized by specific physical traits and central nervous system dysfunctions. The development of animal model systems has facilitated our study of the effects of fetal alcohol exposure and the elucidation of the mechanisms involved in alcohol-induced abnormal development. Despite our current understanding of the effects of fetal alcohol exposure, the occurrence of FAS and associated fetal alcohol spectrum disorders is still widespread and the associated health-care costs are staggering. This symposium provides an up-to-date analysis of fetal exposure to alcohol and FAS. It is directed not only to investigators working in the field but to a diverse group of scientists working in the biological and biomedical fields to stimulate cross-disciplinary awareness, interest, and collaboration.
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PMID:Fetal alcohol syndrome: an assessment of the field. 1595 70

The fetal alcohol syndrome (FAS) is a known cause of mental retardation in humans. Studies based on experimental models of FAS have demonstrated deep alterations of the cerebral cortex. Here, the anatomical organization of cortical interneurons immunoreactive for different calcium binding proteins has been studied in adult rats exposed to alcohol inhalation during the first week of postnatal life. The main finding is represented by an increase of calretinin neurons in ethanol-treated animals compared to controls and by a corresponding decrease of calbindin neurons. The radial distribution of these neurons was also modified in ethanol-treated cases. These changes were evident both in the primary motor and somatosensory area. No significant differences were found in the number and distribution of parvalbumin interneurons. The functional implications of these data and their significance for FAS are discussed.
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PMID:Altered organization of cortical interneurons in rats exposed to ethanol during neonatal life. 1638 14

Fetal alcohol syndrome (FAS) continues to be the leading preventable cause of mental retardation in the United States. Because abstaining from alcohol prior to and throughout pregnancy is the only way to prevent FAS, some prevention programs try to target women before they become pregnant. The Fetal Alcohol Spectrum Teaching and Research Awareness Campaign (FASTRAC) is a multimedia, peer-delivered educational presentation designed to reduce the incidence of FAS. Results from an ethnically diverse sample of high school students indicate that the program increased participants' knowledge regarding FAS but had no significant effect on participants' attitudes, beliefs about the dangers of FAS or intention to use alcohol during pregnancy. The FASTRAC program failed partly because of its didactic approach and the lack of health education principles that have been shown to be effective in changing other substance use behaviors. Suggestions for improving FAS prevention education programs are offered.
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PMID:The effectiveness of a multimedia program to prevent fetal alcohol syndrome. 1680 34

Fetal Alcohol Spectrum Disorders (FASD) represent a leading cause of mental retardation and learning disabilities in children seen in pediatric offices today. This article provides an overview of FASD and describes a model program, the Family Empowerment Network (FEN). FEN is an information, referral, and support network for children and families affected by Fetal Alcohol Spectrum Disorders (FASD) and the professionals who serve them. FEN's mission includes: (a) increasing awareness about FASD by providing education, training and resources to families, providers, and the general public; (b) providing support and referrals to families affected; and (c) increasing opportunities for diagnosis and intervention. We hope to increase awareness of the resources available to nurses and their patients and provide a template that can be replicated in other service delivery systems. Pediatric nurses are in a unique position not only to assist in the recognition of children at risk of FASD, to link families to appropriate diagnostic and intervention services, but also to work to develop additional local and regional resources with other providers.
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PMID:The Family Empowerment Network: a service model to address the needs of children and families affected by Fetal Alcohol Spectrum Disorders. 1692 22

Alcohol consumption during pregnancy is a significant public health problem and is an established cause of serious birth defects and developmental delay collectively described as fetal alcohol syndrome (FAS). FAS is caused by congenital alcohol-induced damages and is a cause of mental retardation. It is characterised by facial abnormalities and growth deficiency. Infants affected by the syndrome show intellectual impairment, and difficulties in learning, memory, problem-solving, and attention as well as experiencing additional problems with mental health and social interactions. However, an absence of the characteristic facial defects and growth deficiency may result in a failure to identify children with prenatal alcohol exposure, which can further present as alcohol-related neurodevelopment disorder (ARND) or alcohol-related birth defects (ARBD). Estimates of prevalence of FAS in U.S.A. range between 0.3 to 2.2 per 1,000 live births, but much higher rates occurring in some communities. Harmonisation of the methodology used for epidemiological studies, with research activities that establishes real baseline prevalence of FAS and identification of women who are at highest risk of bearing a FAS-affected child, are an essential prerequisite to prevention. In addition, it is essential to assess different FAS preventive approaches through carefully controlled studies. Universal, selected, and indicated preventive strategies have been identified, targeting different kind of populations. Since FAS and other adverse effects of drinking during pregnancy are theoretically completely preventable, it is vital to make more efforts to improve the application of the most appropriate interventions. Although in Italy alcohol consumption has constantly increased, mainly amongst the young (including women of childbearing age), knowledge on FAS and alcohol-related effects is completely lacking. Because of the high cost for care of individuals with this syndrome, it is essential to apply appropriate interventions to prevent this problem.
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PMID:[Alcohol consumption, pregnancy and fetal alcohol syndrome: implications in public health and preventive strategies]. 1708 55

Alcohol is detrimental to the developing brain and remains the leading cause of mental retardation in developed countries. The mechanism of alcohol brain damage remains elusive. Studies of neurological problems in adults have focused on alcohol's cerebrovascular effects, because alcoholism is a major risk factor for stroke and cerebrovascular injuries. However, few studies have examined similar cerebrovascular effects of fetal alcohol exposure. We examined the effect of chronic binge alcohol exposure during the second trimester on fetal cerebrovascular and metabolic responses to hypoxia in near-term sheep and tested the hypothesis that fetal alcohol exposure would attenuate cerebrovascular dilation to hypoxia. Pregnant ewes were infused with alcohol (1.5 g/kg) or saline intravenously at 60-90 days of gestation (full term = 150 days). At 125 days of gestation, we measured fetal cerebral blood flow (CBF) and oxygen metabolism at baseline and during hypoxia. Maternal blood alcohol averaged 214 +/- 5.9 mg/dl immediately after the 1.5-h infusion, with similar values throughout the month of infusion. Hypoxia resulted in a robust increase in CBF in saline-infused fetuses. However, the CBF response to hypoxia in fetuses chronically exposed to alcohol was significantly attenuated. Cerebral oxygen delivery decreased in both groups of fetuses during hypoxia but to a greater degree in the alcohol-exposed fetuses. Prenatal alcohol exposure during the second trimester attenuates cerebrovascular responses to hypoxia in the third trimester. Altered cerebrovascular reactivity might be one mechanism for alcohol-related brain damage and might set the stage for further brain injury if a hypoxic insult occurs.
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PMID:Binge alcohol exposure in the second trimester attenuates fetal cerebral blood flow response to hypoxia. 1734 36

Fetal alcohol syndrome (FAS), a condition occurring in some children of mothers who have consumed alcohol during pregnancy, is characterized by craniofacial malformations, and physical and mental retardation. It is significant that even children with history of gestational ethanol exposure but relatively unaffected overall IQ performance, often exhibit learning difficulties and behavioral problems, suggestive of impaired memory formation. Hence, the specific aim of this study was to examine memory formation in chicks exposed to ethanol during early gestation toward the understanding of neurobehavioral disturbances in FAS. Chicks were exposed to alcohol on gestational days 1-3 by injection of ethanol into the airspace of freshly fertilized eggs. The effects of prenatal ethanol on physical growth and development, and memory formation were studied. The one-trial passive avoidance learning paradigm in 1-day-old chicks was used to study memory formation in these chicks. It was observed that chick embryos exposed to 10% ethanol on gestational days 1-3 had significant reduction in all body parameters when compared with appropriate controls. Further, ethanol-exposed chick embryos had significantly impaired (P<.05) long-term memory (LTM) formation after training, though short-term or intermediate-term memory formation was unimpaired. Thus, the findings of the current study demonstrate the detrimental effects of ethanol exposure during early pregnancy on developing chick embryos in general and on memory formation in particular. Hence, it is suggested that impairment in LTM could be a fundamental mechanism for learning disorders and neurobehavioral abnormalities observed in FAS.
Alcohol 2007 Sep
PMID:Effect of gestational ethanol exposure on long-term memory formation in newborn chicks. 1762 12

Exposure to ethanol during development induces severe brain damage, resulting in a number of CNS dysfunctions including microencephaly and mental retardation. Potential targets of ethanol-induced neurotoxicity include neurotrophic factors and their signal transduction pathways. In the present study, rat pups were given ethanol at the dose of 5 g kg(-1) via gavage from postnatal day (PND) 5 to 8, and mRNA expression of nerve growth-factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophic factor-3 (NT-3) in the cerebral cortex was examined, with attention to signal transduction, on PND 8. The mRNA level of BDNF was decreased by ethanol while those of NGF or NT-3 were not changed. Brain weights were decreased and the levels of phospho-MAPK, phospho-p70S6K and phospho Akt were decreased while phosphor-PKCzeta and phospho-CREB remained unchanged. These results suggest that BDNF and its related signal pathways involving Akt, MAPK and p70S6K are potential targets of ethanol-induced developmental neurotoxicity.
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PMID:Effects of postnatal ethanol exposure on neurotrophic factors and signal transduction pathways in rat brain. 1768

BACKGROUND There is a need to educate health professionals in regard to Fetal Alcohol Syndrome and Fetal Alcohol Spectrum Disorders across many health and allied health fields. OBJECTIVE Conduct evaluations of educational programs designed to assess knowledge, attitudes and beliefs in relation to Fetal Alcohol Spectrum Disorders (FASD) among health and allied health professionals in the northeastern United States. METHODS FASD related educational efforts were carried out and evaluated in New Jersey for various health-related professional groups over a four-month period using a common set of materials. Pre and post-test evaluation comprised 20 questions on FASD recognition, diagnosis, treatment, and prevention. Groups surveyed included nurses, social workers, counselors, therapists, clinicians and allied health professionals comprising physician assistants, dieticians, physical therapists, occupational therapists. RESULTS Results showed that a majority of health care professionals in New Jersey possess basic knowledge related to FASD and the effects of alcohol on a child in utero. They also had significant awareness of the importance of early diagnosis and the importance of reducing secondary disabilities. The study did however reveal areas for improvement in some professional groups. CONCLUSIONS FASD is the most important preventable cause of mental retardation. Health professionals attending workshops typically had a good basic understanding of FASD, though with some weaknesses specific to their discipline. Educational efforts in regard to FASD should be sensitive to the various health professionals engaged in preventing, diagnosing and treating FASD.
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PMID:Fetal alcohol syndrome related knowledge assessment and comparison in New Jersey health professional groups. 1819 6


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