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

Prenatal exposure to alcohol produces many developmental defects of the central nervous system, such as microcephaly, mental retardation, motor dysfunction, and cognitive deficiencies. Therefore, the generation of neurons in the cerebral cortex was examined in the offspring of female rats fed a diet containing ethanol. Prenatal exposure to ethanol delayed and extended the period during which cortical neurons were generated, reduced the number of neurons in the nature cortex with the same time of origin, and altered the distribution of neurons generated on a particular day. Thus, the proliferation and migration of cortical neurons are profoundly affected by in utero exposure to ethanol.
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PMID:Effects of alcohol on the generation and migration of cerebral cortical neurons. 374 78

The study population consisted of 1010 in patients and 81 control subjects. Patients suffering from schizophrenia, cerebral atrophy of unknown origin, dementia, depression, mental retardation, and ethanol-induced brain deterioration (alcoholics) were skin tested with 25 micrograms of S-100 protein and neuron-specific enolase isolated from fresh human brain. Evaluation of delayed skin hypersensitivity reactions at 24 hr revealed a high incidence of positive responses to S-100 protein: heavy alcoholism, 96.8%; depression, 94.1%; cerebral atrophy, 92.6%; dementia, 91.2%; schizophrenia, 87.7%; and mental retardation, 69.4%. The incidence of positive reactions to neuron-specific enolase in schizophrenics was 91.6%. Of 58 control subjects tested with S-100 protein, 6.8% were positive, whereas of 23 normal individuals tested with neuron-specific enolase, 6.4% developed mild skin reactions. These data suggest a close relationship between delayed hypersensitivity to neural tissue antigens and immunopsychiatric diseases, and they imply that cell-mediated immune mechanisms are involved in the pathogenesis of certain mental disorders.
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PMID:Neural tissue hypersensitivity in psychiatric disorders with immunologic features. 400 35

Retarded fetal brain growth is associated with a high incidence of mental retardation among the offspring of chronic alcoholic mothers. Research using an embryonic chick model suggests that ethanol exposure suppresses fetal development including suppression of brain growth. Total brain cyclic AMP content and endogenous brain protein kinase specific activity are not altered by ethanol; however, ethanol exposure does significantly stimulate kinase catalytic activity measured in the presence of saturating amounts of exogenous cyclic AMP.
Alcohol Clin Exp Res
PMID:Ethanol-induced inhibition of chick brain growth. 609 89

Fetal alcohol syndrome (FAS) is the most prevalent known preventable health hazard to the human fetus by a noxious agent. It is associated with impairments of the central nervous system that are expressed in the forms of mental retardation of varying severity, learning disabilities, attentional deficits and an increased vulnerability to stress. Results of psychophysiological studies of the effects of ethanol on the central nervous system are reviewed, with the aim of exploring how conclusions derived from them can serve as testable hypotheses in FAS research. The experimental methods used in such studies are examined for their applicability to FAS research. It is concluded that FAS research effort will benefit from the inclusion of psychophysiological studies.
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PMID:The study of brain function impairment in fetal alcohol syndrome: some fruitful directions for research. 632 86

Suspicion of alcohol's teratogenic potential stretches back many centuries, but it is only recently that solid support for this possibility has been produced. There is now little doubt that alcohol can produce developmental defects, but there are many questions that still remain to be answered concerning the impact of alcohol on the conceptus. One major question that remains to be resolved is why only a small percentage of alcoholic women give birth to children with Fetal Alcohol Syndrome (FAS), whereas other alcoholic women who drink the same amount do not. Another important issue concerns the way in which alcohol produces its effects. Although one of the most likely ways in which alcohol's teratogenic actions are mediated appears to be via hypoxia, other mechanisms such as direct toxicity of alcohol or acetaldehyde may be involved. FAS refers to a pattern of defects in children born to alcoholic women. For a diagnosis of FAS to be made, the patient must have three main characteristics: (1) pre- and postnatal growth retardation (greater than or equal to 2 S.D. for length and weight), (2) facial anomalies, and (3) central nervous system dysfunction Pre- and postnatal growth retardation are the most reliable consequences of fetal alcohol exposure. In many cases, patients with the syndrome weigh less than 2500 g at birth and most do not exhibit postnatal 'catch-up growth' Among the distinctive facial anomalies seen in conjunction with the syndrome are absent-to-indistinct philtrum, epicanthic folds, thin upper lip and short upturned nose. Joint, limb and cardiac anomalies are also often present. Central nervous system dysfunction includes mental retardation, the most serious consequence of in utero alcohol exposure, hyperactivity, sleep disorders and miscellaneous behavioral difficulties. If only one or two of these broad characteristics are present and the mother is suspected of drinking during pregnancy, then a diagnosis of 'possible fetal alcohol syndrome,' or 'partial fetal alcohol syndrome,' or 'fetal alcohol effects,' or 'alcohol-related birth defects' may be made. However, without evidence of maternal drinking during pregnancy, this diagnosis is very tentative, since many of these effects are also observed in conjunction with many other congenital disorders.(ABSTRACT TRUNCATED AT 400 WORDS)
Drug Alcohol Depend 1984 Sep
PMID:Prenatal effects of alcohol. 638 8

Fourteen previously reported cases of the fetal alcohol syndrome (FAS) showed anomalies of brain structure varying in severity from microscopic disorganization of tissue structure, or abnormalities in neuronal or glial migration only visible microscopically, to complete or partial agenesis of regions such as the corpus callosum or cerebellum and large neuronal heteropias. The difficulty is illustrated of differentiating this type of damage, lacking in specificity and uniformity, from other syndromes of uncertain aetiology, such as De Lange, DiGeorge and Dubowitz, in at least one of which (DiGeorge syndrome) maternal alcoholism has been implicated. Similar brain damage is also seen in other conditions with known causes. In FAS and syndromes with this type of brain damage, most of the non-CNS features which make the conditions clinically recognizable may well be determined by timing or ancillary factors. Alcohol-related antenatal effects should not be identified to restrictively with FAS but should be considered in any condition of unknown aetiology with disorganization of brain structure and mental retardation.
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PMID:Range of alcohol-induced damage in the developing central nervous system. 656 85

Both cigarette smoking and alcohol consumption during pregnancy remain an important concern for the practicing obstetrician, who should provide current information on the potential detrimental effects of these habits. There appears to be a wide spectrum of fetal phenotypic response to the effects of alcohol. This phenotypic variability may be partially explained by the dose, timing, and pattern of gestational exposure, the metabolism of mother or fetus, or other environmental and genetic factors. At the most severe end of the spectrum are infants with the unique combination of anomalies termed the fetal alcohol syndrome (FAS). The abnormalities most typically associated with alcohol teratogenicity can be grouped into 4 categories: central nervous system (CNS) dysfunctions; growth deficiencies; a characteristic cluster of facial abnormalites, and variable major and minor malformations. To make a diagnosis of fullblown FAS, abnormalities in all 4 categories must be present. Along the continuum toward normal are infants with various combinations of FAS anomalies. One of the most common and serious defects associated with ethanol teratogenicity is mental retardation. Recent evidence supports the concept of a prenatal origin to the problem. At birth infants with FAS are deficient for both length and weight, usually at or below the 3rd percentile for both parameters. Growth and mental deficiency are seen in many conditions, but the rather striking facial appearance of children with FAS secures the diagnosis. The characteristic face in small children includes short palpebral fissures, short upturned nose, hypoplastic philtrum, hypoplastic maxilla, and thinned upper vermilion. A table lists the variety of malformations that may be found in other organ systems in patients with FAS. The likelihood of miscarriage increases directly with alcohol consumption. Risk of abortion is twice as high in women consuming 1 ounce of absolute alcohol (AA) as infrequently as twice a week. Alcohol has severe effects on a wide variety of animal species, and these effects are reviewed. FAS has been estimated to occur between 1 in 600 and 1 in 1000 live births in the US, France, and Sweden. Possible interference with placentation or implantation has been suggested by the observed increased frequency of spontaneous abortion of a chromosomally normal conceptus for women who smoke. On average, infants born to women who smoke during pregnancy are 200 gm lighter than babies born to comparable women who do not smoke. From a review of these studies, the relationship between smoking and reduced birth weight is independent of all other factors that influence birth weight. The finding of antepartum bleeding of unknown cause has consistently been found more often in smokers, compared with nonsmokers. In almost all studies, the incidence of preeclampsia has been found to be reduced in smokers. Sudden infant death syndrome has been found to be closely associated with both the frequency and level of maternal smoking during pregnancy.
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PMID:Alcohol consumption and cigarette smoking: effect on pregnancy. 685 Dec 92

When ethanol was administered intravenously to pregnant monkeys, a transient but marked collapse of umbilical vasculature was observed uniformly within about 15 minutes. The ethanol-induced impairment of umbilical circulation produced severe hypoxia and acidosis in the fetus; recovery occurred during the succeeding hour. This striking interruption of feto-placental circulation may explain one of the mechanisms of mental retardation, a frequent manifestation in children afflicted with fetal alcohol syndrome.
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PMID:Maternal ethanol exposure induces transient impairment of umbilical circulation and fetal hypoxia in monkeys. 689 Feb 35

From clinical and experimental studies it is evident that maternal alcohol intake produces deleterious effects on the development of offspring. In infants, these effects can range from lowered birth weight, general retardation of growth and development with functional deficits, to mental retardation with fetal alcohol syndrome. In animals, exposure to alcohol at a level not associated with classical teratological effects can still cause alterations in neural/synaptic development and hormonal secretion. Growth deficiencies and behavioral alterations have also been observed in pups exposed to ethanol in utero. The mechanisms underlying these actions of alcohol are not yet known because the factors that regulate normal growth and development of the central system are still poorly understood.
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PMID:Fetal alcohol syndrome: neurochemical and endocrinological abnormalities. 703 82

Children of alcoholic mothers are at increased risk for various social and metabolic problems. They are also likely to develop fetal alcohol syndrome: a variable pattern of growth retardation, mental retardation, neurologic dysfunction and congenital dysmorphology. Linear growth is retarded more than weight. Craniofacial anomalies, including microcephaly, are most common. Malformations appear to be related to heavy ethanol intake during the first trimester of pregnancy.
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PMID:Fetal alcohol syndrome. 738 48


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