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

Hunger and malnutrition in Africa have been on the increase since the 1960s. During the 1970s, it is estimated that 30 million people were directly affected by famine and malnutrition. About 5 million children died in 1984 alone. In Mozambique during the 1983-84 famine, about 100,000 people perished. In Ethiopia, Sudan, Somalia, Liberia, and Angola armed conflicts compound the problem. Ethiopia alone had 9 million famine victims in 1983. The most common form of malnutrition in Africa is protein energy deficiency affecting over 100 million people, especially 30-50 million children under 5 years of age. Almost another 200 million are at risk. Iron deficiency, commonly called anemia, also affects 150 million people, mostly women and children. Iodine deficiency leads to disorders like mental retardation, cretinism, deafness, abortion, low resistance to disease, and goiter and this affects 60 million with about 150 million more at risk. Vitamin A deficiency causes blindness and low resistance to disease and affects about 10 million. Protein energy deficiency is treated by using donated foods in hospitals, rehabilitation centers, day care centers, and feeding centers. There are no community programs for anemia, or vitamin A or iodine deficiencies. Vaccines for preventing and drugs for treating diseases that cause malnutrition are imported. Therefore, African food and nutrition professionals met in 1988 and created the Africa Council for Food and Nutrition Sciences (AFRONUS) to eliminate famine and malnutrition in Africa. Activities have started in: 1) developing contacts between the workers in food and nutrition; 2) assessing the situation of food and nutrition in Africa; 3) developing an action plan; 4) implementing the plan; and 5) monitoring progress. Food and Nutrition Policy Guidelines have also been prepared by AFRONUS for food and nutrition workers. Africa has enough natural resources to solve the problem of hunger and malnutrition, but these resources have to be harnessed.
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PMID:Hunger and malnutrition: the determinant of development: the case for Africa and its food and nutrition workers. 139 7

Nutritional iodine deficiency and endemic goiter are widely prevalent in developing countries, affecting an estimated 1 billion people. Recent studies in India, using radioimmunoassay methods, have shown that the incidence of neonatal hypothyroidism in endemic goiter regions is more than a hundredfold higher than the incidence in nonendemic regions. This knowledge has given a new momentum to the iodine prophylactic program in the country, resulting in the protection of hundreds of thousands of newborns from mental retardation.
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PMID:Neonatal hypothyroidism in India. 157 62

5-15% of all 3-15 year old children in the world are mentally impaired. In fact, 0.4-1.5% (10-30 million) are severely mentally retarded and an additional 60-80 million children are mildly or moderately mentally retarded. Birth asphyxia and birth trauma account for most cases of mental retardation in developing countries. 1.2 million newborns survive with severe brain damage and an equal number die from moderate or severe birth asphyxia. Other causes of mental retardation can also be prevented or treated such as meningitis or encephalitis associated with measles and pertussis; grave malnutrition during the 1st months of life, especially for infants of low birth weight; hyperbilirubinemia in neonates which occurs frequently in Africa and countries in the Pacific; and iodine deficiency. In addition, iron deficiency may even slow development in infants and young children. Current socioeconomic and demographic changes and a rise in the number of employed mothers may withhold the necessary stimulation for normal development from infants and young children. Primary health care (PHC) interventions can prevent many mental handicaps. For example, PHC involves families and communities who take control of their own care. Besides traditional birth attendants, community health workers, nurse midwives, physicians, and other parents must also participate in prevention efforts. For example, they should be trained in appropriate technologies including the risk approach, home risk card, partograph, mouth to mask or bag and mask resuscitation of the newborn, kick count, and ictometer. WHO has field tested all these techniques. These techniques not only prevent mental handicaps but can also be applied at home, health centers, and day-care centers.
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PMID:Prevention of mental handicaps in children in primary health care. 178 28

The occurrence of congenital deafness, mutism and goitre unassociated with cretinism or mental retardation in euthyroid patients is known as Pendred's Syndrome. It has been estimated that 4-10 % of children with congenital deafness suffer from this condition. The perceptive hearing loss is considered to be present at birth although it is frequently not recognized for several years. The cause of the hearing defect is a congenital bilateral malformation of the cochlea of the Mondini type. The goitre is not recognized clinically at birth or in early childhood. It becomes apparent in the pre-pubertal years when it presents as a colloid enlargement progressing to a nodular goitre. The thyroid defect has been shown to be a partial defect in iodine organification leading to the underproduction of thyroxine and subsequent thyroid hyperplasia. The syndrome is caused by a single mutant recessive gene responsible for both the deafness and goitre. Its autosomal mechanism gives an equal incidence in both sexes, unusual in thyroid disease. This article reviews the current aspects of pathogenesis and treatment of this syndrome and reports its occurrence in two Sudanese siblings.
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PMID:Goitre and deaf-mutism. 181 81

1. An insufficient dietary supply of iodine results in the development of a variety of disorders of thyroid function and development of the fetus and young infants, grouped under the general heading of Iodine Deficiency Disorders, IDD. Endemic goiter constitutes the most spectacular disorder from the clinical and epidemiological point of view. However, the most serious consequence of iodine deficiency is the impact on neuro-intellectual development at a population level, varying from endemic mental retardation to the complete picture of endemic cretinism. 2. Considering that mental retardation due to iodine deficiency represents the longterm consequence of hypothyroidism occurring during the perinatal period, it is presently recognized that the target groups to the effects of iodine deficiency at a population level are, by order of priority, the fetus, the newborn, the pregnant woman, the child and, finally, the adult. 3. The newborn is more susceptible than the adult to the effects of iodine deficiency. Consequently, systematic screening for congenital hypothyroidism in endemic areas is a particularly sensitive index for detecting the presence and action of goitrogens in the environment and for monitoring the effects of programs of iodine prophylaxis. 4. IDD are particularly prevalent in developing countries. However, large areas or even countries in Europe are still obviously iodine deficient. For example, the iodine intake in adults in Belgium is 50 to 70 micrograms/day which is lower than the recommended dietary allowance for iodine (at least 100 micrograms/day). 5. IDD should be corrected on a world scale, including in Europe. Special attention should be devoted to the protection of mother and child. Within this framework, the iodine content of formula milk should be increased in Europe. 6. Finally, correction of iodine deficiency in Europe would decrease the avidity of the thyroid for iodide and, consequently, would constitute the most efficient preventive measure in case of nuclear fallout.
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PMID:[Disorders due to iodine deficiency]. 196 55

Endemic cretinism is the most severe manifestation of dietary iodine deficiency. Two forms of the syndrome are traditionally described: neurological and myxoedematous. Although this classification highlights the important neurological sequelae of the disorder it implies that myxoedematous cretins have an alternative mechanism. Further, the nature of the neurological deficit associated with both types of endemic cretinism has received scant attention in recent times considering that it remains a common disorder in many parts of the world. The nature and extent of the neurological deficit found in endemic cretinism was investigated in 104 cretins from a predominantly myxoedematous endemia in western China and in 35 cretins from central Java, Indonesia, a predominantly neurological endemia. We found a similar pattern of neurological involvement in nearly all cretins from both endemias, regardless of type (myxoedematous or neurological), and of current thyroid function. Hallmarks of the neurological features included mental retardation, pyramidal signs in a proximal distribution and extrapyramidal signs. Many patients exhibited a characteristic gait. This probably reflected pyramidal and extrapyramidal dysfunction, although joint laxity and deformity were important contributing factors. Other frequently encountered clinical features were squint, deafness, and primitive reflexes. Cerebral computerized tomography (CT) revealed basal ganglia calcification in 15 of 50 subjects. The presence of basal ganglia calcification was confined to cretins with severe hypothyroidism. Otherwise, cerebral CT scanning demonstrated only minor abnormalities which did not contribute to the localization of the clinical deficits. We conclude that the same neurological disorder is present in both types of endemic cretinism reflecting a diffuse insult to the developing fetal nervous system. These clinical findings support the concept of maternal and fetal hypothyroxinaemia, arising from severe iodine deficiency, as the primary pathophysiological event in endemic cretinism. Differences between the two types of cretinism may be explained by continuing postnatal thyroid hormone deficiency in the myxoedematous type, which results in impaired growth, skeletal retardation and sexual immaturity.
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PMID:The neurology of endemic cretinism. A study of two endemias. 204 52

A case of 25-year-old woman with glycogen storage myopathy is reported here. She was hospitalized for acute heart failure after alcohol drinking. The electrocardiogram on admission showed marked ST elevation. Laboratory data showed elevated levels of serum myogenic enzymes but no rise in cardiomyogenic enzyme: CK 3862 IU/l CK-MB 35 IU/l, LDH 427 IU/l, GOT 203 IU/l. After several days, she recovered from acute heart failure and could walk without supporting. ST elevation in ECG and elevated myogenic enzymes were also normalized. The occurrence of acute myocardial infarction was ruled out because a coronary angiogram and 99 Tcm scintigram were normal. Physical examination revealed proximal muscular weakness and mental retardation (WAIS, total 72). Venous lactate response was normal after semi-ischemic forearm exercise. PAS staining of muscle specimen showed an excess deposit of glycogen. Ragged-red fibers were not seen on Gomori-trichrome stain. By electron microscopy, a large amount of glycogen particles were demonstrated in the subsarcolemma, but there were no abnormal mitochondrial changes. Biochemical analysis showed accumulation of glycogen in muscles: 28.7 mg/g muscle (normal 11.4 +/- 4.2 mg/g muscle). The activities of enzyme in the pathway of glycogen and glycogenosis (alpha-glucosidase, amylo-1,6-glucosidase, phosphorylase a, phosphorylase kinase, phosphofructokinase, etc.) were within normal limits. The spectrum of glycogen iodine complex was normal. Our case was different from any type of muscle glycogen storage disease previously reported. The etiology of an excess of glycogen deposit in muscles is unknown.
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PMID:[A case of glycogen storage myopathy with acute heart failure]. 220 34

The clinical manifestations of various degrees of mental retardation, spastic diplegia, and deaf mutism are known as the neurologic type of endemic cretinism (EC), occurring in countries with high goiter endemicity. Maternal iodine deficiency has been established as the major cause in EC, whereas a genetic predisposition has not been well-documented. Genetic data on 70 families with EC from Highland Ecuador are reported. A segregation analysis of 49 fully classified families yielded an estimate of P = 0.245 (var [P] = 0.00167). Half-sibs were all unaffected and no significant birth order effect was observed among 101 probands. The data indicate an autosomal recessive predisposition as a major etiological factor. Because the neurologic type of EC represents a defined section of the spectrum of iodine deficiency disorders (IDD), the term fetal iodine deficiency disorder (FIDD) rather than cretinism is suggested. The clinical findings in 70 patients were used to delineate the minimal diagnostic criteria of FIDD.
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PMID:Clinical pattern and the genetics of the fetal iodine deficiency disorder (endemic cretinism): results of a field study in Highland Ecuador. 230 74

Both animal and vegetable life depend for their existence on appropriate amounts of various trace elements, albeit in very small amounts. This paper lists some of these trace elements and the ailments in which they play an important role. The elements discussed are gold, platinum, copper, lead, zinc, aluminium, silica, mercury, cadmium, selenium, arsenic, and iodine. The diseases involved range from multiple sclerosis, various cancers, arthritis, goitre, Down's Syndrome, and mental retardation. Less well known are Keshan, Alzheimer's, Itai-Itai, and Minamata diseases. Of particular interest in the latter part of the twentieth century is the discovery that serious deficiencies of either copper or zinc in the diet of animals may break down their immune defence mechanisms. The ability of certain plants selectively to concentrate particular heavy metals in their tissues and pollen is discussed.
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PMID:Geology, trace elements and health. 268 20

Disorders caused by iodine deficiency continue to be a major health problem in many underdeveloped areas of the world. The most significant is the impaired mental and physical development which occurs as a result of iodine deprivation early in life. Individuals in affected communities show a spectrum of abnormalities which can be attributed to two interacting pathological processes. Fetal hypothyroidism in the first and early second trimester predominantly affects the developing nervous system causing deaf-mutism and mental retardation. If hypothyroidism occurs in the early postnatal period the main abnormalities are growth stunting and related somatic abnormalities. Subclinical deficits of intellectual and motor development may also be found in apparently normal individuals living in affected areas. Although dietary iodine deficiency is clearly the major aetiological factor in both endemic goitre and cretinism, cofactors such as goitrogens, other trace element deficiencies and immunological mechanisms may greatly modify the expression of these disorders. Iodine supplementation programmes form the basis of the public health strategy in combatting these disorders. Where the iodization of foodstuffs is not feasible, an alternative is the use of iodine containing oil which can be given orally or intramuscularly to provide a long-lasting supply of iodine.
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PMID:Endemic goitre and iodine deficiency disorders--aetiology, epidemiology and treatment. 306 26


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