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

Borderline and mildly retarded children attending the hospital developmental evaluation clinic were divided into two groups on the basis of the presence or absence of a pred with a paediatric control group using blood-lead concentration as the independent variable. Children with a history of diagnosed lead posisoning were excluded from the study. The group of mentally retarded children "aetiology unknown" had statistically significantly raised blood-lead concentrations but the mentally retarded sample with "probable aetiology" showed no significant difference in lead concentrations from those of the normal controls. It is concluded that the association between lead and mental retardation extends over a much wider range than hitherto suspected and that the nature of this association is independent of a history of "encephalopathic" lead poisoning. It is suggested that physicians should consider raised lead levels in their examination of all children suspected of mental retardation and that the numerical definition of lead toxicity should be re-evaluated.
Lancet 1976 Dec 25
PMID:Low lead levels and mental retardation. 6 49

Hepatitis-Associated (Australia) Antigen (HAA) was detected in 13 (5.8%) of 223 patients with Down's syndrome and in 14 (3.7%) of 378 patients with other forms of mental retardation. The frequency of HAA was 2.4 per cent in 127 noninstitutionalized patients with Down's syndrome, and 10.4 per cent in 96 institutionalized patients. The frequency of HAA with Down's syndrome was lower on the average in Japan than in the United States or Germany. HAA was detected in one (1.3%) of 78 mothers of infants with Down's syndrome. Our study suggests that maternal exposure to HAA, as reflected by the presence of either HAA or anti-HAA, was not associated with the subsequent birth of an infant with Down's syndrome.
Clin Pediatr (Phila) 1975 Dec
PMID:Hepatitis-associated (Australia) antigen and Down's syndrome. 12 83

Trisomy-22 was confirmed with both Q- and G-banding in two sibs. Growth and mental retardation plus various dysmorphic features of this syndrome are described and compared with previous reports. Cytogenetic studies reveal a morphologically atypical No. 22 in cells of the phenotypically normal mother (46,XX) and in both affected children. The variant G chromosome is identified as No. 22 by Q- and G-banding and is interpreted as a product of a pericentric inversion on the basis of general length, arm ratio (1.4), and anomalous satellite association frequency. Repeated nondisjunction for No. 22 is considered to have resulted from asynapsis caused by interference of an inversion loop configuration which, though short, comprised a major part of chromosome 22.
J Med Genet 1976 Dec
PMID:Abnormal chromosome 22 and recurrence of trisomy-22 syndrome. 13 42

A small-for-dates male infant with mental retardation, microcephaly, malformed ears, preauricular sinuses, epicanthal folds, micrognathia, congenital heart diseases, micropenis, and micropolygyria of the parietal and occipital lobes of the cerebral cortex was shown to have a 47,XY,+22 karyotype by trypsin-giemsa banding. Review of reported cases confirms that there may be distinctive trisomy 22 syndrome.
J Med Genet 1976 Dec
PMID:Confirmation of trisomy 22 by trypsin-giemsa staining. 13 43

Tuberous sclerosis is a rare disease in which hamartomas may be found in the brain, the retina, the skin and in other internal organs. The classic form of the disease showing mental retardation, epilepsy and adenoma sebaceum is easily recognised. Incomplete forms, however, can provide considerable diagnostic difficulties. Angiographically, appearances are found which cannot be differentiated with certainty from those of malignant tumours. Malignant tumours are very rare in this condition. Nephrectomy can be avoided if the diagnosis is made at an early stage. Two female patients are reported, in one of whom the diagnosis was made by renal angiography. Despite the presence of large tumours in both kidneys, these organs could be preserved by surgery. In the second patient there were also bilateral renal hamartomas, but surgery was not carried out. Both cases showed typical changes in the fingers and toes as well as intracerebral calcification, and in one the lungs were affected.
Rofo 1978 Dec
PMID:[The place of radiology in tuberous sclerosis (author's transl)]. 15 82

A population of young people who are mentally retarded is described in terms of the frequency of various kinds and degrees of impairment--intellectual, physical and behavioural. The population consisted of all those born in 1951--1955 who were resident in a city in 1962 and who at any time during the school years had been placed in any mental retardation service. The prevalence of the mentally retarded as defined is sixteen per 1000. Age specific prevalence rates for the same population rise from age five, reach a plateau of fourteen per 1000 from ages ten to fifteen and then drop sharply for the post-school period to a rate of five to six per 1000. Classifications of physical impairment, seizure histories and behaviour disturbances are described. Percentages are given separately for those with each impairment and in combination for each individual. For the survivors at age twenty-two, 44 per cent had physical impairments, 26 per cent had a history of seizures and 46 per cent had experienced behaviour disturbances. Results are discussed in relation to service needs.
J Ment Defic Res 1979 Dec
PMID:Some characteristics of a population of mentally retarded young adults in a British city. A basis for estimating some service needs. 16 26

A case of Feuerstein-Mims syndrome (naevus sebaceous, convulsions and mental retardation) is described in association with vitamin D resistant reckets.
Pediatr Radiol 1976 Dec 15
PMID:Feuerstein and Mims syndrome with resistant rickets. 18 80

A large kindred is described in which 22 males and 3 females show non-specific mental retardation with impaired speech. An X-linked recessive is the most likely mode of inheritance of this condition. Similar families have been described in the literature, characteristic physical abnormalities are absent and performance I.Q. tends to be higher than verbal I.Q. This possible heterogenous condition may be a major individual cause of mental deficiency in males, and may account for the excess of male retardates in the population.
Ann Genet 1977 Dec
PMID:X-linked recessively inherited non-specific mental retardation. Report of a large family. 30 54

This report describes an infant with fatal congenital heart disease, cleft palate, brain malformations, and trisomy 8p resultant from the paternal balanced reciprocal translocation, rcp(8;15) (p11;p11). Review of six previously reported trisomy 8p patients (resultant from parental balanced translocation in each instance) revealed severe mental retardation in five, short stature in all, and a variety of brain, skeletal, and cardiac defects. The features of the seven trisomy 8p patients reviewed here are not sufficiently similar to suggest a distinct dysmorphic syndrome. In addition the features differ from those in the trisomy 8 mosaicism syndrome, in which the mental retardation and malformations are generally less severe.
Ann Genet 1978 Dec
PMID:Report of a trisomy 8p infant with carrier father. 31 58

A sibship originally reported by Friedman and Roy as showing severe mental retardation, strabismus, hyperactive tendon reflexes, lalling speech, and foot deformities was restudied. Three major additional findings were noted. The cerebrospinal fluid protein concentration was increased two to three times above normal in four siblings who were available for study. Radiographs of cranial structures in three siblings showed identical pathologic intracranial calcifications which correspond in distribution to the choroid plexus. The choroid plexus was not demonstrable in one patient when radiolabeled 99m-Tc-pertechnetate was injected without perchlorate. Neuropathologic findings in one sibling included small subcortical heterotopias and atrophy of the choroid plexus with encasement by glial fibrils. These findings denote a new heredofamilial neurologic syndrome associated with mental retardation and a disorder of choroid plexus.
Neurology 1979 Dec
PMID:Familial amentia, unusual ventricular calcifications, and increased cerebrospinal fluid protein. 31 25


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