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

The development of the fetal central nervous system can be effected by drugs. In this paper we review the neurological consequences of intrauterine exposure to alcohol, cocaine, opiates and marijuana. Ethanol causes the fetal alcohol syndrome: mental retardation, intrauterine and postnatal growth retardation, and peculiar dysmorphic features. Is pathogenesis has been explained on the basis of maternal nutritional deficiencies or due to abnormalities in the conversion of ethanol to aldehyde, or abnormalities in the metabolism of prostaglandins or retinoic acid, the neurotransmitter systems, the neuronal excitotoxic activity, the development of the white matter, the production of gangliosides, and/or genetic regulation cell-cell adhesion. Cocaine has been related to congenital malformations, neurologic abnormalities during the neonatal period and psychomotor and cognitive development deficits. Characteristic dysmorphic features and a higher incidence of the sudden infant death syndrome (SIDS) have also been described. The following mechanisms have been implicated in the pathogenesis: vascular effects, superoxide formation, chelation of calcium ion channels, and abnormalities in the production of glycosphingolipids, the synthesis of DNA, the functioning of neurotransmitter systems, the neuronal growth and differentiation, the neuronal excitotoxic activity and/or the expression of early immediate genes. Opiates produce intrauterine and postnatal growth retardation, neonatal abstinence syndrome, and deficits of the psychomotor and cognitive development. They also increase the incidence of SIDS. The pathogenesis has been related to abnormalities in the sensitivity of the locus ceruleus, the functioning of the neurotransmitter systems, and/or the expression of early immediate genes. Marijuana has been associated with intrauterine growth retardation, dysmorphic features, and abnormalities of the behavior during the neonatal period, the psychomotor and cognitive development, and the sleep. The pathogenesis is thought to be due to an action upon specific receptors, or upon the neurotransmitter systems, and/or to an increase in the production of carbon monoxide. The best treatment of the syndrome of intrauterine exposure to drugs in the prophylaxis. The identification of emotional and drug addiction problems in the mother can avoid disastrous consequences. The care of these children is complex and requires a good pediatric follow-up and an early intervention program while the mother on the parents continue with the drug addiction therapy. The coordinations of all the necessary services with the active participation of social workers, physicians, educators and teachers is crucial for a successful treatment.
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PMID:[Intrauterine exposure to drugs]. 920 93

Fetal alcohol syndrome is one of the leading causes of mental retardation in the United States, but the pathogenesis of the associated brain damage is unknown. We tested the hypothesis that neonatal cerebrovascular responses to CO2 and/or hypoxia may be altered by moderate chronic maternal ethanol exposure early in gestation. We studied 26 newborn lambs (1-4 d old). Their mothers had received daily i.v. infusions of either ethanol (1 g/kg; ethanol concentration = 167 +/- 3 mg/dL; mean +/- SEM) or a similar volume of saline for 3 wk during the first trimester. In nine lambs, we studied cerebral responses to CO2 (saline, n = 4; ethanol, n = 5) and in 17 lambs, cerebral responses to hypoxia (saline, n = 7; ethanol, n = 10). Cerebrovascular responses to CO2 were not different between the groups. However, the cerebral vasodilatory response to hypoxemia was significantly attenuated in the ethanol lambs, such that cerebral O2 delivery was not maintained. During severe hypoxia (arterial PO2 = 30 mm Hg), cerebral blood flow increased 106 +/- 23% (mean +/- SEM) above baseline in the saline-treated group, but increased only 32 +/- 15% above baseline in the ethanol-treated group (p < 0.02). Similarly, cerebrovascular resistance in the saline group decreased 52 +/- 6% from baseline, but decreased only 16 +/- 11% in the ethanol group (p < 0.02). We conclude that moderate maternal ethanol infusion early in pregnancy attenuates neonatal hypoxic, but not CO2, cerebrovascular responsivity.
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PMID:Newborn cerebrovascular responses after first trimester moderate maternal ethanol exposure in sheep. 921 35

Six new cases of alcoholic embryopathy on newborn children are described. We found out that the mother suffers from chronicle alcoholism. The diagnosis fetal alcohol syndrome is made because there are the minimal diagnostically syndromes: prenatalis hypotrophia, microcephalia, mental retardation, face dysmorphism, cardinal anomalies. We have observed an unfolded clinical picture with added hypertrophia on the clitoris and anomalies of the kidneys on one of the children. With the description of the cases we direct obstetrician's and neonatologist's attention to this current in this moment medical problem.
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PMID:[The clinical picture of the fetal alcohol syndrome]. 925 61

In the USA, fetal alcohol syndrome (FAS) is the leading known cause of mental retardation. FAS is estimated to affect 4000 infants yearly in the USA with an additional 7000 children suffering various forms of fetal alcohol effects in the absence of the full syndrome. A comparable incidence would be expected in other industrialized countries, but essentially no data are available from either developing or third world countries. An understanding of the biochemical causes of FAS has been slow to develop, but progress has been made toward a molecular causation theory of FAS. This paper summarizes much of the current work as to the effects of fetal ethanol exposure on mitotic and metabolic parameters as well as ethanol's effect on the cellular signalling pathways thought to regulate these processes. Based upon these studies, it is apparent that exposure of embryonic tissue to ethanol results in decreased growth and that alcohol adversely affects a multitude of cellular functions critical for the growth of the developing organism, including inhibition of protein and DNA synthesis. In addition, ethanol alters the uptake of critical nutrients such as glucose and amino acids and causes changes in several kinase-mediated signal transduction pathways that regulate these biochemical processes.
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PMID:Metabolic and mitotic changes associated with the fetal alcohol syndrome. 926 50

Fetal alcohol syndrome is the leading cause of mental retardation in the United States. The tragedy is that while FAS is irreversible, it is 100% preventable. FAS is caused by maternal consumption of alcohol during pregnancy. Alcohol is a teratogen and acts in different ways to produce physical and central nervous system malformations and defects in the developing embryo and fetus. FAS is characterized by a history of maternal alcohol ingestion, central nervous system dysfunction, growth deficiencies, and specific physical anomalies. Adolescents and adults with FAS have behavioral problems that differentiate them from other mentally disabled individuals. Nurse practitioners can have an impact on the prevalence of FAS by educating clients about FAS and its relationship to alcohol consumption. NPs need to carefully identify high-risk women and their partners before a pregnancy occurs and assist with interventions to stop active alcoholism or alcohol use during pregnancy. NPs have the capability to decrease the severity of alcohol's effects during pregnancy through education, counseling, and intervention. NPs have the skills to work with case-finding and early identification of infants and children who display signs and symptoms of FAS. With such case-finding, early identification, and prompt referral to the appropriate diagnostic and/or supportive community agencies, individuals with FAS can receive timely intervention to minimize the effects of FAS. Adults with behavioral problems can be assessed for FAS and referred for appropriate assistance as well. Finally, NPs can facilitate public awareness of FAS through educational efforts with individuals, families, and communities.
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PMID:Fetal alcohol syndrome: the nurse practitioner perspective. 928 78

Exposure to ethanol during pregnancy is detrimental to brain development. Individuals affected by the Fetal Alcohol Syndrome present a number of central nervous system dysfunctions including microencephaly and mental retardation. Studies on the mechanisms of ethanol's developmental neurotoxicity have focused on its interaction with neurons; however, emerging evidence is suggesting that ethanol can significantly affect glial cells as well. A number of in vitro studies have shown that ethanol can inhibit the proliferation of various glial cells (mostly primary astrocytes or astrocytoma cells) at relatively high concentrations (100-200 mM). On the other hand, proliferation induced by some, but not all mitogens, is inhibited by low concentrations (10-50 mM) of ethanol. These inhibitory effects of ethanol may contribute to its developmental neurotoxicity observed following in vivo exposure. Animal models have indeed shown that ethanol causes microencephaly when given during the brain growth spurt, a period of brain development characterized by astroglial proliferation and maturation.
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PMID:The effects of ethanol on glial cell proliferation: relevance to the fetal alcohol syndrome. 932 12

This critical review examines mental retardation (MR) from a neuropsychological perspective. Competing definitions of MR are discussed and the prevalence is estimated. Descriptions are given of idiopathic MR and the five major identifiable prenatal causes of MR: fetal alcohol syndrome, Down's syndrome, fragile X syndrome, Prader-Willi syndrome, and Angelman syndrome. Similarities and differences among syndromes are examined. Cognitive deficits common to all disorders were in attention, short-term memory, and sequential information processing, whereas language and visuospatial abilities were varied. Neuroanatomical abnormalities common to all disorders were in the hippocampus and cerebellum; individual disorders typically showed a unique pattern of other neurological abnormalities. Both knowledge of individual MR-related disorders and comparative research between disorders are important for researchers and clinicians. Further research is called for in both areas.
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PMID:The neuropsychology of mental retardation. 937 1

Fetal alcohol syndrome (FAS) is caused by heavy alcohol consumption during pregnancy and is characterized by specific anomalies of the face; prenatal and postnatal growth deficits; and a variety of central nervous system (CNS) abnormalities, including mental retardation. Children with either full or partial FAS often incur severe and costly secondary disabilities. Despite the importance of surveillance for establishing the magnitude of FAS and in monitoring trends in the occurrence of this disease, population-based surveillance for FAS has been difficult because the syndrome can be diagnosed only by clinical observation and often is not recognized until after the child reaches school age. Although most FAS surveillance has been based on diagnoses among newborns, most (89%) cases (full FAS and partial FAS) are diagnosed after the age of 6 years. To develop a more accurate estimate of the prevalence of FAS in a defined population, in 1997 CDC linked data from the Metropolitan Atlanta Congenital Defects Program (MACDP) and the Metropolitan Atlanta Developmental Disabilities Surveillance Program (MADDSP) for children born in Atlanta during 1981-1989 (the most recent birth year for which data were available for 3-10-year-olds). This report presents a multiple-source method for FAS surveillance that is more complete than previous methods and that enables comparison of rates between states.
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PMID:Surveillance for fetal alcohol syndrome using multiple sources -- Atlanta, Georgia, 1981-1989. 939 58

Ethanol exposure during development is teratogenic. The central nervous system (CNS) is particularly susceptible to ethanol toxicity. In fact, heavy gestational ethanol consumption is one of the leading known causes of mental retardation in the Western world. Ethanol exposure disrupts the proliferation of glia and neuronal precursors in the developing CNS. Depending upon cell population and blood ethanol concentration, ethanol can either inhibit or stimulate cell proliferation. Two features of cell proliferation that are affected by ethanol exposure are the growth fraction (the proportion of cells that is actively cycling) and the cell cycle kinetics, particularly in the length of the G1 phase of the cell cycle. Cell proliferation in the developing CNS reflects the action of positive (mitogenic growth factors) and negative (anti-proliferative factors) regulators. Increasing evidence shows that ethanol interferes with the action of growth factors. In vitro systems are a good model to investigate ethanol neurotoxicity, since the effects of ethanol on cultured cells parallel the effects of ethanol in the developing CNS. The inhibitory effects of ethanol on cell proliferation may result from interference with mitogenic growth factors (e.g., bFGF, EGF, PDGF, IGF-I). Conversely, the stimulatory effects of ethanol may result from the interference with growth inhibiting factors (e.g., TGFbeta1). Interestingly, both in vivo and in vitro studies show that proliferating neural cells display differential sensitivity to ethanol. This differential sensitivity correlates with their response to mitogenic growth factors; that is, cells that are actively regulated by mitogenic growth factors are much more susceptible to ethanol than cells that are less or unresponsive to such factors. Ethanol interference with growth factor action could occur at three levels: ligand production, receptor expression, and/or signal transduction. Thus, ethanol-induced alterations in the developing CNS that characterize fetal alcohol syndrome apparently result from alterations in the regulatory action of growth factors.
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PMID:Growth factor-mediated neural proliferation: target of ethanol toxicity. 962 17

Fetal alcohol syndrome (FAS) is commonly believed to be the leading known cause of mental retardation in the United States, although surveillance at state and national levels is problematic. The most serious consequence of fetal alcohol exposure is central nervous system (CNS) dysfunction. While the facial features of FAS become more subtle with age, growth deficits and, particularly, the CNS impairment appear to be permanent. Among factors that affect the risk and severity of fetal alcohol damage are the timing of the alcohol exposure, binge drinking that produces high blood alcohol concentrations, polydrug use, and genetic variations. From various studies, the incidence of FAS ranges from 0.2 to 3.0 affected birth per 1000 live births. The methods of measuring FAS occurrence are fraught with difficulties and inaccuracies, as are surveys of alcohol use by women during pregnancy. Still, indirect studies both in Texas and the United States suggest that the occurrence of FAS is increasing. A first, important step to reducing the incidence of FAS and related problems is to increase the awareness of physicians and other health care providers about the issues of FAS diagnosis, prevention, and treatment. Referral and information resources about FAS are provided.
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PMID:Fetal alcohol syndrome: a review for Texas physicians. 966 21


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