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Query: UMLS:C0917816 (mental retardation)
 15,867 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a review of some of the literature dealing with the relationship between parity and several indices of child health and child survival in India. The indices covered are: stillbirth, neonatal mortality, maternal health, prematurity and birth weight, physical growth of children, intelligence and mental deficiency, effect on child care, and influence on diseases. Stillbirth rates are highest for 1st pregnancy and rise again after the 3rd or 4th birth with marked increases following the 5th birth. Multiparous women have been found to have higher incidences of premature birth and other complications of pregnancy. Children from higher parity families develop slower both mentally and physically. Malnutrition diseases occur more often in larger families. Other factors having an important, though lesser, effect on child survival rates are maternal age at birth, race, and socioeconomic status of the family.
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PMID:Paediatric aspects of family planning. 57 83

The physician who looks after children and teenagers is often confronted with the problem of short stature or growth failure. Common causes of growth failure include genetic background, intrauterine disease, malnutrition, chronic illness and hormonal disorders; some cases are attributed to mental retardation or primary central nervous system disease. A major concern in the evaluation of these patients is when, and how extensively, to investigate the problem. From a practical standpoint assessment can be related to height percentiles. The aims of treatment are a) to identify and treat appropriately the patients in whom there is an organic cause and b) to provide psychologic counselling and support.
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PMID:An approach to solving problems of growth retardation in the child and teenager. 85 6

Sixteen children with anomalies of the auricle and/or middle ear who presented malformations of the face, mouth, upper airway, spine, limbs, heart, gastrointestinal (GI), and/or genitourinary (GU) systems, were described. While clusters of anomalies suggested syndromes such as the oculo-auriculo-vertebral syndrome of Goldenhar, hamifacial microsomia, mandibulo-facial dysostosis (Treacher Collins syndrome), Pierre Robin, Klippel-Feil, Moebius, Duane, and/or VATER syndromes, many children did not fit what are usually considered even minimal criteria for these syndromes. Several children had malformations which fit the description of more than one syndrome. The importance of investigating the children for unsuspected anomalies, especially of the GU system, was emphasized. Life threatening problems in this group consisted of airway problems, congenital heart disease, and major anomalies of the GI and GU systems. Better management of sucking, swallowing and airway problems might have decreased the early morbidity and mortality (3/16) in this group. Children with multiple defacing anomalies may not be mentally retarded so that aggressive management of their visceral anomalies and hearing problems, and early educational intervention are mandatory. Delay in development may be due to hearing loss, vestibular impairment, ataxia, the consequences of early malnutrition, and multiple hospitalizations rather than to mental retardation. A pessimistic attitude in infancy is unwarranted since it is impossible to predict which children will end up competitive individuals.
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PMID:Patterns of anomalies in children with malformed ears. 96 14

In the underdeveloped areas of the world malnutrition frequently starts "in utero" as indicated by a high proportion of low birth weight babies. These "small for date" babies have a high risk of death and contribute significantly to the high infant mortality rates observed in these populations. After birth inadequate physical growth is the most frequent manifestation of malnutrition. It is not yet clear if the observed mental retardation is directly related to malnutrition or more to psycho-social deprivation, but is is anyhow an important problem. The effects of transculturization resulting in early weaning is complicating the situation even more by producing severe malnutrition at earlier ages.
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PMID:Nutritional problems of children. 99 May 72

The high prevalence of intestinal parasitic infections as an index of underdevelopment, especially in tropical countries, is related to poverty, poor housing, lack of sanitation, malnutrition, and ignorance. The effects are lowered work capacity, physical and mental retardation, leading to recurrences and exacerbations of the parasitism and malnutrition. The most prevalent parasites, methods of detection by specific tests in patients in clinical trials involving antiparasitic drugs are dealt with. How and by whom investigations of new drugs should be undertaken, the need for a basic knowledge of parasitology and techniques of the discipline, of biostatistics, and use of such controls as randomized allotment to treatment groups, placebo administration, and double-blind assessments are emphasized. The justification for undertaking an evaluation of an antiparasitic drug is predicated on the demonstration of safety in exhaustive in vitro and animal studies and of the drug's potential superiority as to efficacy and lower incidence of unwanted side effects, as compared with existing agents. Tolerance and dose-range studies should be conducted in male adult hospitalized patients under close supervision. The evaluation of amebicides in clinical trials, as well as of anthelmintics, is considered in terms of differentiation and reproductive habits of specific causative agents and tests for detecting their elimination to determine improvement under drug therapy. The problem of reinfection, particuarly of nonhospitalized patients under the adverse conditions of life, is stressed.
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PMID:Clinical trial methodology in intestinal parasitic diseases. 126 2

The hyperphenylalaninemias are caused by the defect of either phenylalanine hydroxylase (PAH) or tetrahydrobiopterin (BH4) cofactor. The former is diagnosed as phenylketonuria (PKU) or benign hyperphenylalaninemia, based on the serum phenylalanine values. The latter, so called malignant hyperphenylalaninemia, includes three enzyme defects, dihydropteridine reductase (DHPR), 6-pyruvoyl tetrahydropterin synthase (PT PS) and guanosine triphosphate cyclohydrolase (GTP-CH). Excess phenylalanine and its metabolites cause brain damage before 6 years of age. Deficiency of BH4 impairs two other hydroxylases (tyrosine and tryptophan), and severe neurological symptoms develop because of the lack of neurotransmitters. Tyrosinemia I, II, and III are different enzyme defects, fumarylacetoacetate hydrolyase (FAH), hepatic tyrosine aminotransferase (TAT), and 4-hydroxyphenylpyruvate acid oxidase, respectively. Tyrosinemia I is associated with severe involvement of the liver, kidney and central nervous system. Tyrosinemia II has mental retardation, palmar hyperkeratosis and corneal ulcers. Tyrosinemia III has mild mental retardation but no eye or skin manifestations.
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PMID:[The metabolic basis of the hyperphenylalaninemias and tyrosinemia]. 135 1

8 microcephalic children, mean age 3.06 years, with head circumferences -3.5 SD to -6 SD, achieved IQ scores of 79-115 on the Thermann, WPPSI, WISC-R, and/or Columbia tests. They had no dysmorphic features nor congenital anomalies, and their fundi were normal. 7 had congenital microcephaly, associated with proven autosomal dominant heritage in 3, 1 had suspected autosomal recessive heritage, 1 had intrauterine growth retardation (overall smallness), 1 had cerebral palsy, and in 1 there was an unknown prenatal cause. 6 of these children had 1 or 2 developmental disabilities, including neurosensory deafness, cerebral palsy, short attention span, perceptual dysfunctions, and learning disability. Microcephaly, most probably secondary to malnutrition in early infancy, was diagnosed in 1 child without developmental disabilities. However, our data support the concept that some microcephalic children with significantly small head circumference, who function without mental retardation, have a high incidence of other developmental disabilities.
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PMID:[Microcephalic children without mental retardation]. 138 36

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

Three enzymes of purine metabolism, adenylosuccinate synthetase, adenylosuccinate lyase and AMP deaminase, have been proposed to form a functional unit, termed the purine nucleotide cycle. This cycle converts AMP into IMP and reconverts IMP into AMP via adenylosuccinate, thereby producing NH3 and forming fumarate from aspartate. In muscle, the purine nucleotide cycle has been shown to function during intense exercise; the metabolic flux through the cycle has been proposed to play a role in the regeneration of ATP by pulling the adenylate kinase reaction in the direction of formation of ATP, and by providing Krebs cycle intermediates. In kidney, the purine nucleotide cycle was shown to account for the release of NH3 under the normal acid-base status, but not under acidotic conditions. In brain, the purine nucleotide cycle might function under conditions that induce a loss of ATP, and thereby contribute to its recovery. There is no evidence that the purine nucleotide cycle operates in liver. Deficiency of muscle AMP deaminase is an apparently frequent disorder, which might affect approximately 2% of the general population. The observation that it can be found in clinically asymptomatic individuals suggests, paradoxically, that the ATP-regenerating function which has been attributed to the purine nucleotide cycle is not essential for muscle function. Further work should be aimed at identifying the conditions under which AMP deaminase deficiency becomes symptomatic. Adenylosuccinate lyase deficiency provokes psychomotor retardation, often accompanied by autistic features. Its clinical heterogeneity justifies systematic screening in patients with unexplained mental deficiency. Additional studies are required to determine the mechanisms whereby this enzyme defect results in psychomotor retardation.
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PMID:The purine nucleotide cycle and its molecular defects. 152 4

This study was undertaken to determine the profile of migraine in Nigerian children, as earlier reports on migraine from Africa dealt mostly with the adult population. Migraine constituted 5.7% of all new referrals seen in the Child Neurology Clinic over a 44 month period. The overall profile is not different from that reported for other racial groups. Haemoglobin AS was found to be more frequent among children with migraine than in the general population, although this difference did not attain statistical significance. Childhood migraine is probably commoner than this study indicates. This may be partly due to the fact that practitioners in the less developed countries have to deal with the more pressing problems of malnutrition, infections, chronic motor handicaps, mental retardation and epilepsy.
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PMID:Migraine in Nigerian children--a study of 51 patients. 176 24


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