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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 (FAS) is a major known cause of fetal malformations and mental retardation. Prevention/intervention of FAS can only be achieved with identification of the mechanisms by which alcohol induces birth defects. The purpose of this paper is to discuss the data on possible mechanisms of FAS, and to give a number of suggestions for future research areas.
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PMID:Perspectives on the pathophysiology of fetal alcohol syndrome. 208 15

A large number of congenital disorders are due to alcohol consumption during pregnancy. These anomalies are also known as the "fetal alcohol syndrome". Data available on this subject is very important and leaves no doubt in the disastrous effects of prenatal alcohol intake. Babies born with fetal alcohol syndrome present constant characteristics such as pre and post natal growth retardation, cranio-facial dysmorphism and central nervous system abnormalities. The mechanism by which alcohol produces these defects are linked to: 1. The alteration of essential aminoacid transfer. 2. Fetal hypoxia. 3. Central nervous system cellular proliferation and differentiation inhibition (mainly in the cerebellum and hippocampus). 4. Auto-immune reaction to S-100 protein. 5. Hormonal dysfunction. 6. Postnatal inhibition of response to growth hormones. The major risk is undoubtfully the excessive daily alcohol intake (2-6 consumptions/day). Social type of alcohol consumption brings more discrete effects and often these happen much later. Low birth weight and mental retardation may be seen with the absorption of 15 ml of alcohol per day (1 beer or 1 glass of wine or 40 ml of liquor) 52 mg/100 ml of blood alcohol has been identified as the fetal threshold activity concentration, while 140 mg/100 ml is associated with evident teratogenicity. Other factors such as maternal age and genetic predisposition also add to the risks of prenatal alcohol exposure.
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PMID:[alcohol and pregnancy: what is the level of risk?]. 220 63

An ophthalmological study was conducted on a series of 28 Swedish children suffering from mild mental retardation without an obvious aetiological diagnosis. The eye examination supported a diagnosis of foetal alcohol syndrome in five out of six suspected cases and revealed two additional not previously suspected (25%). Eye anomalies were observed in 16 patients (57%) with fundus abnormalities (optic nerve hypoplasia, retinal dystrophy) being most frequent, occurring in 11 cases (39%). Four patients had substantially reduced visual acuity in both eyes. Eight children had abnormal features of the face and outer eye region. Ocular motility disturbances (strabismus or nystagmus) were seen in five patients. The ophthalmological study disclosed that at least 10% of this group of children with mild mental retardation suffered from the foetal alcohol syndrome. It is concluded that, in children with mental retardation, an ocular examination is a valuable diagnostic tool for revealing prenatal origin.
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PMID:Contribution of ocular examination to the diagnosis of foetal alcohol syndrome in mentally retarded children. 226 51

Within 3 years 48 caretakers and parents of children with fetal alcohol syndrome were asked about the childrens experience and contact with alcohol. The children were mainly raised in foster and adoptive families (40/48 cases), where usually moderate or restricted consumption of alcohol was common. The children were between 4-18 years (means = 7; 5) of age. In 5 children alcohol consumption was observed once or several times. Some children showed signs of increased desire for drinking alcohol. A substance related addiction was never observed until now. Nevertheless the risk of addiction development has to be considered as dangerous in any case of fetal alcohol syndrome. All conditions and risk factors for addiction development are present: a) Hereditary factors in the family of origin. b) Early use and adaption in the prenatal period by maternal drinking. c) The social surroundings and family. d) The particular structure of personality in these children, characterised by uncritical behavior, mental retardation, emotional instability and easy seduction. The risk of addiction development can be estimated to 30%. In a society of lacking alcohol prohibition it will be impossible to keep alcohol away from the children. As in dry alcoholics the children have to learn "to live in association with alcohol without drinking it". Besides it is important for the parents, that they learn to help their child to cope with the danger of alcohol. This ist possible by means of information, strengthening of a positive self-image and faith in the child's capacity for insight.
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PMID:[Are children with alcohol embryopathy latent alcoholics? A study of the risk for developing dependence]. 237 81

Fetal alcohol syndrome (FAS) is noted for poor growth, developmental delays, and mental retardation. In animals, prenatal alcohol exposure alters anatomical, physiological, and neurochemical maturation and produces behavioral changes similar to those in children. Since thyroid hormones are critical trophic factors for normal somatic and neural maturation, and since fetal thyroid hormones are profoundly affected by acute maternal ethanol administration, we hypothesized that postnatal effects of prenatal alcohol exposure may be related to abnormal thyroid hormone development. We report here that young rats exposed to alcohol in utero have significantly lower serum total thyroxine (T4) concentrations than normal and pair-fed control rats. The results suggest prenatal ethanol exposure may compromise thyroid development in ways not attributable to undernutrition or developmental delays alone. Lowered total T4 levels may be a teratogenic outcome of prenatal alcohol exposure, which could contribute to impaired growth, altered neural organization, and behavioral dysfunction.
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PMID:Lower serum thyroxine levels in rats following prenatal exposure to ethanol. 237 31

Recent data have shown that the structure and function of layer V pyramidal neurons, e.g. corticospinal neurons, is altered by prenatal exposure to ethanol. We examined the effect of ethanol on the ultrastructure of layer V in somatosensory cortex. Timed pregnant rats were fed a diet containing 6.7% (v/v) ethanol (E) or pair-fed a nutritionally matched control diet (C). Thirty-day-old offspring of these mothers were prepared by standard electron microscopic techniques. The somata of pyramidal and local circuit neurons and the neuropil were analysed. Prenatal exposure to ethanol induced alterations in the somata of both populations of neurons. The parallel stacking of cisternae characteristic of C-treated rats was disorganized in E-treated rats. Moreover, the Golgi complex and lysosomes occupied a larger fraction of the somata of E-treated rats. The number and frequency of symmetric axosomatic synapses, but not asymmetric axosomatic synapses, formed by both types of neurons were significantly greater in E-treated rats. Gestational exposure to ethanol produced a variety of changes in the neuropil. Dendrites, particularly dendritic shafts, occupied less space in E-treated rats. In contrast, axons accounted for significantly more of the neuropil in E-treated rats than in controls. This increase in axonal space was due to a significantly greater coverage by non-myelinated axons and a significantly smaller coverage by myelinated axons in E-treated rats than in C-treated rats. Although the overall frequency of synapses was similar in both treatment groups, there were significantly more asymmetric synapses in E-treated rats, and most of these were axospinous synapses. These differences may contribute to documented physiological changes such as the lower rate of glucose utilization in layer V of somatosensory cortex of E-treated rats and they may underlie the mental retardation which is characteristic of children with foetal alcohol syndrome.
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PMID:Effect of prenatal exposure to ethanol on the ultrastructure of layer V of mature rat somatosensory cortex. 262 73

We investigated the effects of ethanol exposure on the shape of the cell and the morphology of intermediate filaments (IF) of cortical astrocytes in primary culture. The content and distribution of glial fibrillary acidic protein (GFAP), the major component of glial IF, was assessed using an anti-GFAP monoclonal antibody and fluorescence scanning densitometry together with quantitative pre- and post-embedding immunogold electron microscopy. The astrocytes were from 21-day-old fetuses obtained from both control and chronic alcoholic rats and were cultured for 28 days in the absence or presence of ethanol (25 mM). The main findings were: (a) ethanol-exposed astrocytes failed to develop processes or to acquire a filamentous IF distribution pattern; (b) these cells showed less GFAP than astrocytes without alcohol; (c) ethanol interfered with the reorganization of the anti-GFAP binding sites from clustered to random; and (d) astrocytes from alcohol-exposed fetuses cultured in the absence of ethanol also showed these alterations, suggesting initial damage to astrocyte precursor cells. Since the glial filaments play a crucial role in creating a scaffolding that guides neuronal migration, the effect of ethanol on astrocyte IF may possibly be correlated with the mechanisms underlying mental retardation and motor dysfunction which are characteristics of fetal alcohol syndrome.
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PMID:Effects of prolonged ethanol exposure on the glial fibrillary acidic protein-containing intermediate filaments of astrocytes in primary culture: a quantitative immunofluorescence and immunogold electron microscopic study. 264 42

A review is provided of the impact of fetal alcohol syndrome (FAS) and the realities of the consumption of alcohol by women. The worldwide incidence of FAS is 1.9 per 1,000 live births. FAS is recognized as the leading cause of mental retardation in the West, in addition to producing a constellation of birth defects. One in six women of childbearing age drinks enough alcohol to jeopardize a developing fetus. Warning labels on alcohol should be considered to publicize the dangers to the fetus.
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PMID:Fetal alcohol syndrome and the realities of our time. 268 2

The first discovered exogenous teratogen causing mental retardation was rubella embryopathy described in 1940. Later, cytomegalic virus infection and toxoplasmosis during pregnancy and ionogenic radiation has been shown to cause embryofetopathies with concomitant mental retardation. Methyl mercury in high doses cause severe central nervous system pathology in both mothers and their fetuses. The fetal alcohol syndrome is now generally accepted as causing mostly mild mental retardation. Of therapeutic drugs, antiepileptics have been shown to carry a risk for the fetal antiepileptic syndrome complex. We have recently been able to describe fetal pathology following high intake of benzodiazepines during pregnancy.
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PMID:Prenatal factors including fetal alcohol syndrome. 289 25

Recently numerous reports show deleterious effects of alcohol abuse on pregnant women giving their children a high risk of stillbirth and/or several developmental abnormalities and mental retardation, i.e. the Fetal alcohol syndrome (FAS). In the present study, the effects of maternal alcohol consumption on lipid metabolism in the litter liver were investigated in rats. These rats showed not only quite less lipid deposition in spite of large amount of alcohol consumption up to adulthood, but also showed increased FFA oxidation in the livers. In addition, increased level of very low density lipoprotein and hypoglucagonemia were found. 40 micrograms/kg of glucagon which is known as an inhibitory factor of apoprotein production in the liver, was injected for 2 weeks into the rat tail vein and resulted in apparent fatty liver and hypolipoproteinemia. Norepinephrine injection (1 mg/kg) caused plasma glucagon to be depressed in the rat as compared with adult alcohol rats. Plasma cyclic AMP response to glucagon was also depressed in these rats. From these results, it is suggested that the deranged glucagon secretion from the pancreas and lowered glucagon-induced cyclic AMP response would relate to the abnormal lipoprotein metabolism in the rat.
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PMID:[Experimental studies on lipoprotein metabolism in rats reared with liquid alcohol diet from the fetal life]. 298 81


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