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

Water-lead levels were measured in the homes occupied during the first year of life by 77 mentally retarded children aged two to six years and 77 non-retarded matched controls, and in the homes occupied by their mothers during pregnancy. The water-lead content was significantly higher in the retarded group, and the probability of mental retardation was significantly increased when water lead exceeded 800 mug. per litre. Blood-lead levels were also significantly higher in the retarded group. It is concluded that lead contamination of water may be one factor in the multifactorial aetiology of mental retardation and that every effort should be made to reduce the lead content of drinking-water.
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PMID:Role of chronic low-level lead exposure in the aetiology of mental retardation. 4 43

A study of the neurological and intellectual sequelae of childhood near-drowning is reported. Results are from a total population study, without selection, of all freshwater immersion accidents in which consciousness was lost in the water. Such accidents affected 56 children in the city of Brisbane and environs over the period 1971-75. 54 of these children have been re-examined medically and psychometrically. Over 95 per cent of children who survived such accidents were neurologically normal. The median i.q. of survivors was 110 (range 90-137), which is higher than that of the general population. There is a suggestion that visualmotor (performance)) skills are particularly vulnerable to freshwater immersion hypoxia. In 20 per cent of survivors subscale disparities between verbal and performance skills exceeded 15 i.q. points. No correlation between the post-immersion I.Q. and either estimated immersion-time or water temperature was demonstrated in this study. No long-term emotional or personality disorders were encountered. Uncommon gross clinical sequelae of prolonged immersion in fresh water included spastic quadriplegia and gross mental retardation. All children in this study were apparently dead at the moment of rescue; despite this, the prognosis of near-drowning in childhood is excellent
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PMID:Neurological and phychometric studies in children surviving freshwater immersion accidents. 6 99

Blood-lead concentrations were measured retrospectively in the blood contained on cards used for testing for phenylketonuria in the first two weeks of life. Cards which belonged to 80 of a group of 77 children with mental retardation of unknown aetiology and 77 controls were identified. Of 77 usable cards, 41 were from mentally retarded children and 36 were from controls; 24 mental-retardation/control pairs were found. There was a highly significant trend towards higher blood-lead concentrations in the mentally retarded children. Water-lead concentrations in the maternal home during pregnancy correlated with blood-lead concentrations in the mentally retarded children. These results reinforce the probable association between lead exposure during pregnancy and the development of mental retardation of otherwise unknown aetiology.
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PMID:A retrospective analysis of blood-lead in mentally retarded children. 6 17

Thyroid hormone exerts a powerful influence on CNS growth and maturation. Hypothyroidism early in life has long been known to cause disturbances in innate behavior, motor performance, severe and frequently irreversible mental retardation. In this deficiency, depressed caudate neurogenesis, cell migration and neuropil development during the rapid period of CNS growth may contribute to the clinical picture of perceptual handicaps often seen in cretins. Light microscopic and Golgi studies of the developing caudate nucleus in thyroid deficiency have been carried out to help attain insights into the mechanisms whereby the extrapyramidal system regulates motor function. The ultrastructural study of caudate nuclear cytogenesis and synaptogenesis in normal and hypothyroid states provides more detailed information for further analysis of the problem. Hypothyroidism was induced from birth by adding prophylthiouracil to the food and drinking water of lactating dams. Linear development of the caudate nucleus of both normal and hypothyroid rats at ages 8, 14, 20, 30 and 42 days was studied by electron microscopy. Thyroid glands were examined by light microscopy to assess the normal and deficient states. Immature cells, primitive processes and synapses were the characteristic features of the 8-day-old normal caudate nucleus. Distinctively wide cisternae of the rough endoplasmic reticulum, loosley packed Golgi apparatus and chromatin clumps throughout the nuclei of the neurons were significant early morphologic variations. The dramatic cytoarchitectural maturation in the 14- and 20-day normal caudate neuropil points to the rapidity of developmental rate. After the growth spurt of the first three weeks a maturational plateau occurs which is characterized by well-formed neuronal cytoplasmic organelles, myelinated and non-myelinated axons, axon terminals, dendrites and their spines, and synapses. Thyroid deficiency causes a marked maturational delay of approximately 7 days in caudate neuronal proliferation, the elaboration of neuronal networks and the attainment of mature synaptic contents and membranes. This delay is evidenced by comparison of the structural similarities between 8-day-old normal and 14-day-old deficient rats; and additional comparisons between the 14-day-old normal and 20-day-old hypothyroid rats. A rapid "catch up" process in fine structural morphogenesis takes place in the period between days 14 and 30 in the deficient animals. Repression of thyroid function does not entirely prevent development of the caudate nucleus but allows a fairly extensive, though critically incomplete degree of maturation. This imperfection is manifested by a decrease in the number of synaptic contacts that persists even after the rapid "catch up" phenomenon of caudate synaptogenesis.
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PMID:An electron microscopic study of the developing caudate nucleus in euthyroid and hypothyroid states. 86 26

We report on oral ketamine for the preinduction of 3 patients who aggressively refused the commonly used induction of anaesthesia, due to young age or mental retardation. One child and two mentally retarded patients aged 30 and 31 years who were to undergo dental surgery aggressively refused the induction of anaesthesia, either by inhalation or rectal, intramuscular, or intravenous application of drugs. One of them previously injured the medical personnel and destroyed the interior equipment of a gynaecologist, who tried to perform an examination. After having received 6 to 8 mg/kg body weight ketamine in 10 ml water, which they accepted well, probably because of the long lasting fluid restriction (about 12 hours), they tolerated the induction of anaesthesia by inhalation (2 patients) or intravenously (1 child). Two patients remained awake, but calm, one fell deeply asleep. After several hours of surgery in inhalation anaesthesia they could be extubated within several minutes and discharged the same day. We conclude that 5 to 10 mg/kg oral ketamine in water which has a bioavailability of approximately 20% is a useful agent for the preinduction of patients who aggressively refuse medical treatment. Because deep sleep states cannot be excluded, we recommend a careful supervision after the application of ketamine. Nevertheless, we could discharge our patients on the same day even after long lasting surgical procedures; this makes this method useful in day case surgery.
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PMID:[Oral ketamine as preferred preanesthetic medication of uncooperative patients]. 145 Mar 15

To protect against reactive oxygen species, prokaryotic and eukaryotic cells have developed an antioxidant defence mechanism where O2- is converted to H2O2 by superoxide dismutase (Sod), and in a second step, H2O2 is converted to H2O by catalase (Cat) and/or glutathione peroxidase (Gpx). If Sod levels are increased without a concomitant Gpx increase, then the intermediate H2O2 accumulates. This intermediate could undergo the Fenton's reaction, generating hydroxyl radicals which may lead to lipid peroxidation in cells. In this study, we investigate the expression of Sod1, Gpx1 and susceptibility to lipid peroxidation during the aging process in mouse brains. We demonstrate that the mRNA levels and enzyme activity of Sod1 are higher in brains from adult mice compared to neonatal mice. Furthermore, we show that a linear increase in Sod1 mRNA and enzyme activity occurs with aging (1-100 weeks). On the contrary, we find that the mRNA and enzyme activity for Gpx1 does not increase with aging in mouse brains. In addition, our results demonstrate that the susceptibility of murine brains to lipid peroxidation increases with aging. The data in this study are consistent with the notion that reactive oxygen species may contribute to the aging process in mammalian brains. These results are discussed in relation to the normal aging process in mammals, and to the premature aging and mental retardation in Down syndrome.
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PMID:Cu/Zn superoxide dismutase mRNA and enzyme activity, and susceptibility to lipid peroxidation, increases with aging in murine brains. 159 44

Screening urine for inherited and acquired organic acidurias in newborns has the potential of preventing severe disease, mental retardation, and death. A method for screening dried urine filter paper samples for acidic markers of at least 20 different metabolic conditions has been developed. These conditions include, among others, maple syrup urine disease; methylmalonic, propionic, isovaleric, glutaric, and hydroxymethylglutaric acidurias; methylcrotonylglycinuria; medium-chain acyl-CoA dehydrogenase deficiency; inherited vitamin responsive disorders B12, biotin, B2), and acquired deficiencies of these vitamins. The preparation of the urine extract is identical to the method we use to screen infants for neuroblastoma. Screening is based on a highly sensitive and specific determination of eight organic acid markers by an automated computerized gas chromatography mass spectrometry system using selected ion monitoring. The markers used for screening are methylmalonic acid, 2-hydroxyisocaproic acid, glutaric acid, propionylglycine, isovalerylglycine, 3-methylcrotonylglycine, hexanoylglycine, and 3-phenylpropionylglycine. The extraction efficiencies of these acids from dried filter paper were similar to extraction from water, ranging from about 40% to 80%, except for propionylglycine which showed a low extraction efficiency of 11-13%. The stability of these acids on filter paper exposed to room air and temperature over a period of 15 d was adequate for the use of this collection method for organic aciduria screening. Normal levels, adjusted to urinary creatinine, were established for these acids in 519 urine filter paper samples obtained from 3-wk-old newborns. This screening method was tested on samples obtained from 12 patients with known organic acidurias including stored urine filter paper collected at 3-wk of age from two infants later found to have organic acidurias.
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PMID:Screening newborns for multiple organic acidurias in dried filter paper urine samples: method development. 195 13

The toxicities of many metals, such as mercury and lead, are known to man since the dawn of civilization. Organic compounds of some heavy metals are known to have a particular toxic impact on the central nervous system. Organomercury, particularly alkyl-mercuric compounds (e.g. methylmercury), has a selective effect on the granule cells of the cerebellum, the nerve cells of the calcarine cortex, and the sensory neurons in the dorsal root ganglia. The well known Minamata Bay disease is the result of a massive epidemic episode of human exposure to alkylmercury contaminated food sources. Mental retardation and other developmental defects are also known to be a consequence of exposure to this toxic metal. Organic lead compounds have been employed as gasoline additives and in other industrial purposes. Unlike its inorganic counterpart, organolead compounds have a more prominent impact on the central nervous system. Pathological changes of the brain stem neurons have been described. Organotin compounds have been used in plastic industries and as agricultural chemicals. Both trimethyl and triethyl tin compounds are found to be extremely neurotoxic. Despite the similarity of their chemical structures, trimethyl and triethyl tins have a diversely different toxic property and effects. While triethyl tin is myelinotoxic, producing edematous and vacuolar changes in the central myelin, trimethyl tin is neurotoxic, producing prominent toxic changes in the neurons of the limbic system (hippocampus, entorhinal cortex, etc.). The factors which determine the specificity and selectivity of the neurotoxic impacts by various organometals are still unknown. In view that most of the organometals are still widely employed by many countries for industrial and for agricultural purposes, caution must be made for their proper handling and disposure to avoid undesirable exposures to workers and environmental contamination of water sources and food-chain for the common public. Since organometals are difficult to eliminate from the central nervous system, injuries usually lead to permanent neurological deficits, such tragedies are frequently long lasting and create not only a medical problem, but also a social economical problem for the society.
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PMID:The neurotoxicology and pathology of organomercury, organolead, and organotin. 210 Mar 18

There are differences between young and adult organisms regarding toxokinetic aspects and clinical manifestations of heavy metal intoxications. Chronically, toxic Cd intake causes a microcytotic hypochromic anemia in young rats at lower exposure levels and after shorter exposure periods than in adult animals. Cd absorption is increased by co-administration of milk and in conjunction with iron deficiency. After long exposure periods toxic Cd concentrations accumulate in the kidney cortex; this process starts very early in life. In 3-year-old children Cd concentrations in the kidney can reach up to one-third of those found in adults. Hg++ and methyl-Hg can cause Hg encephalopathia, and frequently cause mental retardation in adults. Correspondingly, Hg++ accumulation in the brains of suckling rats is approx. 10 times higher than in grown animals. Milk increases the bioavailability of Hg++. In suckling rats Hg is bound to a greater extent to ligands in the erythrocytes. Methyl-Hg concentrations in breast milk reach 5% of those in maternal plasma and that is a severe hazard for breastfed children of exposed mothers. Toxic Pb concentrations can lead to Pb encephalopathia. A high percentage of surviving children have seizures and show signs of mental retardation. Anemia and reduced intelligence scores were recently observed in children after exposure to very low levels of Pb. Pb absorption is increased in children and after co-administration of milk. There are no definite proofs for carcinogenesis or mutagenesis after oral exposure to Cd, Hg, and Pb in man. Heavy metal concentrations were found in the same order of magnitude in commercial infant formulas and in breast milk. When infant formulas are reconstituted with contaminated tap water, however, Pb and Cd concentrations can be much higher. The average heavy metal uptake from such diets exceeds the provisional tolerable weekly intake levels set by the WHO for adults, calculated on the basis of an average food intake and a downscaled body weight. These considerations do not even provide for differences in absorption and distribution or for the increased sensitivity of children to heavy metal exposure. However, dilution effects for essential heavy metals were observed in fast-growing young children; this effect might be extrapolated to toxic metals. These theoretical considerations are compared with epidemiological evidence. A health statistic from Baltimore shows a decline of Pb intoxications in infants. This observation correlates with a simultaneous decline in exposure to Pb which was due, for example, to decreased use of lead dyes in house paints and the abolition of tin cans for infant food.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The toxicological estimation of the heavy metal content (Cd, Hg, Pb) in food for infants and small children]. 218

This overview of health programs and conditions in India reveals that health is related to economic development antipoverty measures, food production and distribution, drinking water supply, sanitation, housing, environmental protection, and education. There are urgent requirements for effective intersectorial coordination. Unprecedented growth of 1 million a year has resulted in slums and shanties--a place of epidemics; urbanization has contributed to environmental pollution impacting on health, and water pollution to water-born diseases. Health services are still insufficient to meet the needs. Sanitation practices contribute to cholera, dysentery, diarrhea, enteric fevers, and malaria. Indian Systems of Medicine and Homeopathy must be active in preventive and health care. Accomplishments include in 1987/8 a decline in leprosy cases attributed to the existence of leprosy control units. 40 AIDS Surveillance Units are actively treating and screening. The Naval Goitre Control Programme's goal is replacement of iodized salt for edible salt by 1992, thereby reducing mental retardation and low birth weight babies. The Family Welfare Programme, targets a New Production Rate of Unity before 2000. A National Technology Mission on immunization and the Universal Immunization Programme plans to be operational in all districts by 1990. Oral rehydration therapy programs dispense free packets to fill the needs of 1 million children under 5 who suffer from diarrhea 3 times a year with 3 million facing death. The Primary Health Care Programme provides iron and folic acid to women with nutritional anemia and Vitamin A to children. Health service developments have been increased.
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PMID:Status of health in India and its future prospects. 226 69


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