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

As part of the Health Promotion and Disease Prevention Questionnaire administered in the 1985 National Health Interview Survey, nearly 20,000 respondents ages 18-44 answered questions about their awareness of the risks of smoking and heavy drinking during pregnancy. In reference to smoking, interviewers asked about miscarriage, stillbirth, prematurity, and low birth weight; in reference to heavy drinking, they asked about miscarriage, mental retardation, low birth weight, and birth defects, as well as fetal alcohol syndrome. For each of these adverse outcomes, a majority of subjects acknowledged increased risk because of smoking or heavy drinking during pregnancy. The range was 66-80 percent of respondents for the four questions on smoking, with the perceived association to smoking strongest for low birth weight. Approximately 84 percent of respondents associated heavy drinking with increased risk for each of the suggested pregnancy outcomes. Smoking seemed to be perceived to pose a lesser risk to pregnancy than heavy drinking. This relative lack of awareness of the pregnancy risks of smoking was more apparent among respondents with less education and more pronounced among blacks than whites. Women were more likely than men to express some opinion on these pregnancy-related questions and were more cognizant than men of the risks. On this limited survey, Americans ages 18-44 were not very knowledgeable about fetal alcohol syndrome. Among the 55 percent who had heard of fetal alcohol syndrome, fewer than one in four correctly identified it as a set of birth defects when offered three possible definitions. It will be interesting to correlate responses to these "knowledge" questions with NHIS data still forthcoming on reported actual smoking and drinking behavior among women respondents who were recently pregnant.
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PMID:Perceptions of risks of smoking and heavy drinking during pregnancy: 1985 NHIS findings. 310 Nov 27

Historically, mankind has at least suspected that alcohol was somehow connected with undesirable effects on progeny. In the 18th century, physicians became aware that maternal alcohol consumption resulted in excess fetal and neonatal mortality, low birth weight, and many other deleterious effects. Perhaps as a response to the temperance and Prohibition periods, scientists lost sight of or interest in the effects of alcohol in pregnancy. In the late 1960s and early 1970s, the issue surfaced again, and scientists began systematic and in-depth studies of fetal alcohol syndrome (FAS) and alcohol-related birth defects (ARBD). Epidemiologic research now suggests that FAS has outranked Down's syndrome and spina bifida in prevalence and is now the leading known cause of mental retardation. Further, it is the only one of these three that is preventable. Because a safe limit of alcohol consumption in pregnancy is not defined, abstinence during pregnancy is the most prudent preventive measure. Factors such as race, beer drinking, maternal weight gain, and low socioeconomic status are associated with a statistical increase in the incidence of FAS. In families where one child has been diagnosed as having FAS, the incidence rate can be as much as 405-fold higher than the worldwide average. Neurobehavioral deficits can occur in the offspring of drinking mothers in the absence of a diagnosis of full FAS. The deficits differ with age and seem to persist into adulthood. Mental retardation or borderline mental retardation is a nearly ubiquitous neurological deficit in diagnosed FAS. In one study, it occurred in 75 percent of the non-FAS offspring of mothers who continued to drink heavily throughout their pregnancy.From the mid-1970s, having established that alcohol is a teratogen, scientists have been trying to uncover the mechanism by which alcohol exerts its embryotoxic effects. Recent promising neuroanatomical studies have demonstrated that alcohol has a deleterious effect on neuronal migration and hence on the development of the cerebral cortex. Other studies have shown that prenatal alcohol exposure,by adversely affecting hippocampal development,may be responsible for the learning deficits so frequently encountered in FAS children. Other research has implicated prostaglandins in the mechanism of alcohol-related dysmorphology.
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PMID:Alcohol-related birth defects: an update. 314 58

Seven hundred five cases of agenesis of the corpus callosum (ACC) are reviewed from the literature (n = 660) and from our own observations (n = 45). The diagnosis was made or confirmed using neuroradiological techniques (n = 519) and necropsy or surgery (n = 231). Association with abnormalities often of chromosomes 8, 11, 13-15 and 18 suggests their involvement in abnormal corpus callosum (CC) morphogenesis. Four syndromes (e.g. Aicardi, acrocallosal, Andermann and Shapiro) are characterized by ACC, while others are only sporadically associated (e.g. fetal alcohol syndrome, Dandy-Walker syndrome, Leigh disease, Arnold-Chiari II syndrome). In non-Aicardi patients, the male-to-female ratio was 3:2 and X-linked recessive inheritance is postulated to play a role in some cases. Common abnormalities in acallosal patients included: mental retardation (MR), 73% [corrected]; seizures, 42%; ocular anomalies, 42%; gyral abnormalities, 32%; hydrocephalus, 23%; other central nervous system (CNS) lesions, 29%; costovertebral defects, 24%. Developmental disabilities are not attributable to absence of the CC per se, but due to other CNS malformation or dysfunction, which may be genetic or non-genetic. Future research using recombinant DNA techniques will enable isolation and identification of specific chromosomal defects in those cases with a genetic abnormality.
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PMID:Clinicopathological findings associated with agenesis of the corpus callosum. 331 Jul 13

This study was designed to compare manifestations of FAS in the offspring of lower and upper middle class chronic alcoholic mothers, and to compare these offspring with those of nonalcoholic controls. There was highly significant difference in the incidence of FAS offspring between upper middle and lower class alcoholic mothers, 4.5% versus 70.9% respectively. Mean weight, length, and head circumference at birth in children of upper middle class alcoholic women was -ISD, those of lower class alcoholic women fell into -2SD. All other parameters, congenital malformation rate, failure to thrive, mental retardation were also significantly greater in children of lower class alcoholic women (p less than or equal to .01). Attention deficit disorder was found in 21% of upper middle class offspring of alcoholic women as compared to 71% in the children of the lower socioeconomic group (p less than or equal to .01).
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PMID:The influence of socioeconomic factors on the occurrence of fetal alcohol syndrome. 342 75

We report a case of Nager acrofacial dysostosis, whose clinical examination disclosed some undescribed features, as a contribution to a better delineation of this syndrome. Previously unreported features include lobulated tongue, cleft lip and mental retardation. Fetal alcohol syndrome is discussed. We propose to reunificate Richieri-Costa syndrome and Nager syndrome.
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PMID:Nager acrofacial dysostosis with cleft lip. 343 68

We examined the developing synaptic junctions in the rat frontal cortex in cases of fetal alcohol syndrome, the objective being to determine the synapse-mental retardation relationship. On day 21 of gestation, the ultrastructural synaptic junction revealed no obvious differences between the ethanol-exposed and control rats; however, the number of synapses in ethanol-exposed rats was one third that of the controls. The possible relationship between synaptic density in the frontal cortex and mental development has to be considered.
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PMID:Decreased density of synaptic formation in the frontal cortex of neonatal rats exposed to ethanol in utero. 350 16

The world-wide incidence of the fetal alcohol syndrome (FAS) is 1.9 per 1000 live births. Incidence rates vary considerably, however, depending on study site. Mental retardation is a cardinal feature of FAS and is now recognized as the leading known cause of mental retardation in the Western world. Conservatively estimated for the United States, the economic cost associated with FAS-related growth retardation, surgical repair of organic anomalies (e.g. cleft palate, Tetralogy of Fallot), treatment of sensorineural problems, and mental retardation, is +321 million per year. FAS-related mental retardation alone may account for as much as 11% of the annual cost for all mentally retarded institutionalized residents in the United States. Current treatment costs for FAS-related problems are about 100 times federal funding for FAS research necessary to develop cost-effective early identification and prevention strategies.
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PMID:Incidence of fetal alcohol syndrome and economic impact of FAS-related anomalies. 354 31

This article reviews the effects of alcohol on male and female gonads and hormonal levels; it further discusses the use of ethanol during pregnancy and its teratogenic effect on the fetus. Impotence is a common result of acute alcoholism, and testicular atrophy, infertility, and decreased libido are associated with alcoholism 70-80% of the time. In addition, alcohol consumption produces significant spermatozoal morphological changes involving breakage of the sperm head, distention of the midsection, and curling of its tail. Seminiferous tubules are filled mostly with spermatids that undergo degeneration and result in aspermia. Acute ethanol intoxication is accompanied by decreased plasma testosterone levels and a surge of luteinizing hormone. Ethanol appears to have a dual effect: locally on the gonads and centrally on the hypothalamus-pituitary axis, causing an adverse effect on spermatogenesis. Less is known about the effects of alcohol on the female reproductive function; however, inhibition of ovulation and a significant reduction of plasma estradiol and progesterone levels has been noted in rats following ethanol administration. Alcohol consumption during pregnancy is the most frequent known teratogenic cause of mental retardation. Infants most severely affected by maternal alcohol abuse during gestation possess a number of dysmorphic anomalies termed fetal alcohol syndrome. The abnormalities most typically associated with alcohol teratogenicity can be grouped into 4 categories: growth deficiencies, central nervous system dysfunctions, craniofacial abnormalities, and other major and minor malformations. The effects of maternal alcohol consumption on the fetus are independent of maternal nutritional status and smoking history. Alcohol abuse during pregnancy occurs in 2-13% of US women, and these women have a 50-70% chance of delivering an infant with a serious abnormality.
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PMID:Alcohol and reproductive function: a review. 354 7

Fetal Alcohol Syndrome (FAS) and Fetal Alcohol Effects (FAE) are preventable forms of mental retardation and developmental disability caused by heavy prenatal alcohol exposure. Our best evidence of the overall prevalence of FAS is around 1 in 750 live births, but this figure will vary according to the drinking habits of the community and the diagnostic skills and interests of local physicians. It is likely that many infants are born with FAS or FAE, are never recognized as such, and are never properly diagnosed or evaluated. Other diagnoses that are sometimes confused with FAS include Noonan syndrome and William syndrome. More often, children with milder FAS or FAE go unrecognized. Careful evaluation of possible maternal alcohol abuse during pregnancy can be an important factor in differential diagnosis and proper case management. Alcohol is a teratogenic drug that can produce a wide variety of deficits from prenatal exposure, depending on the dose, timing, and conditions of exposure, as well as on individual differences in sensitivity on the part of the mother and the child. Not all children who are exposed are affected. Perhaps 30-40% of the children of chronic alcoholic mothers who were drinking during pregnancy will have FAS. These children are at high risk for mental retardation or developmental disability. Even within this group, however, there can be large individual differences in eventual outcome. Prognosis involves an interaction between the extent of the damage and the stability and structure of the environment. Children whose mothers were abusing alcohol during pregnancy can be at risk for various learning and attentional problems even without FAS, but in the absence of morphologic effects, the diagnostic and prognostic picture is less clear. Systematic efforts toward both prevention and intervention can assure that each child develops to his or her own best potential.
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PMID:Fetal alcohol. Teratogenic causes of developmental disabilities. 361 65

Five children with fetal alcohol syndrome (FAS), ranging in age from 2 1/4 to 10 years, were noted to have abnormal neurological findings. These were mainly cerebellar. Others were attention deficit disorder in three, mental retardation in two, and epilepsy in one. The neuropathology seen in FAS provides a more than adequate basis for the clinical findings. Children with FAS, or a history of in utero alcohol exposure, and abnormal neurological signs, do not need investigation.
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PMID:Neurological findings in the fetal alcohol syndrome. 368 56


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