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

Adolescents with developmental disabilities deserve the same sophisticated multidisciplinary evaluation which is now available to younger children. Most of these fit into one of four groupslow normal IQ with poor performance because of psychologic problems, true learning disability, neuromuscular disease, or known mental retardation in need of planning for future care. It is important for the physician dealing with these adolescents to recognize and be ready to deal with the high incidence of emotional problems. He must be able to relate to the adolescents as the primary subject, and to arrange special education, vocational evaluation, and legal counseling. The physician must cultivate professional relationships with a wide range of disciplines since his adolescent patient is likely to need a wide variety of services.
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PMID:Adolescents with developmental disabilities; a survey of their problems and their management. 111 72

The reported incidence of mental retardation in Leber's congenital amaurosis has varied from 10% to 87%. There has been no review of the estimate since it became possible to delineate an increasing number of diagnostic subcategories. In this study, the visual and cognitive development of 38 children with congenital retinal dystrophies has been followed up prospectively. Children with associated disorders in other systems and those with central nervous system malformations or degenerations were significantly more likely to have learning disability than those without additional medical problems. Most subgroups made little or no visual progress with the exception of the group with associated hypoplasia of the cerebellar vermis. The study highlights the importance of using the specialised techniques now available to delineate fully the visual diagnosis and paediatric perspective because of their relevance to cognitive and visual prognosis.
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PMID:Congenital retinal dystrophies: a study of early cognitive and visual development. 137 26

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

Two cases of fragile X-syndrome are presented. Both boys had a family history of learning disability. This syndrome is the most common cause of inherited mental retardation. There are few dysmorphic features in childhood, but in puberty 80% of persons with this syndrome develop macro-orchidism, as presented in our second case. Some of the cases may have large ears, with no folding pinnea (simple pinnae). They may also have long faces, and a prominent forehead and chin. A characteristic of the condition is behavioural dysfunction, including hyperactivity and autism. The author discusses difficulties diagnosing the condition, both clinically and by specialized chromosome analysis.
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PMID:[Fragile X-syndrome and mental retardation]. 155 20

Developmental language and learning disabilities in children can take many different forms and can result from a variety of causes. Research to date has focused primarily on specific disabilities in learning, which are characterized by a significant delay or disorder in one aspect of learning against a background of otherwise normal development. Learning disabilities affecting language and/or reading acquisition (developmental dysphasia and dyslexia) have been studied most thoroughly. Verbal learning disabilities occur more frequently in boys than in girls, and there is a higher than expected incidence of left-handedness among affected children. Although there are many reasons why a child may have delayed or disordered language development, differential diagnosis of specific developmental language or reading disorders calls for ruling out mental retardation, peripheral auditory or visual dysfunction, autism, frank neurological impairments such as hemiplegia or seizure disorder, and severe social deprivation or lack of educational opportunity. The typical profile of a developmentally dysphasic or dyslexic child is one who shows a marked discrepancy between nonverbal (performance) IQ and verbal IQ, with a history of delayed or disordered speech, language and/or reading development. Such a child usually performs quite normally on visual spatial tasks, while demonstrating severe deficits in tasks of auditory temporal processing, motor sequencing, phonological processing and memory, language, reading and spelling. This characteristic neuropsychological profile may suggest left hemisphere dysfunction or a failure to develop normal cerebral lateralization. The etiology of these developmental learning disorders is unknown, but there is evidence of familial aggregation, indicating a potential genetic basis. Although these children respond to remediation, longitudinal studies have shown that the symptoms often persist into adulthood (see Tallal, 1988, for a more detailed discussion).
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PMID:Hormonal influences in developmental learning disabilities. 196 40

We have evaluated 62 fragile X syndrome [fra(X)] individuals (55 males and 7 females) with different degrees of developmental disabilities that were clinically non-progressive and non-focal in character. The mean age for the 55 males was 23.1 years +/- 14.3 SD with a range of 2-70: for the 7 females, the mean age was 15.7 years +/- 3.5 SD with a range of 10-20 years. Mental retardation (MR) was found in 53 males (8/53 [15.1%] mild, 26/53 [49.1%] moderate, 14/53 [26.4%] severe, and 5/53 [9.4%] profound). Learning disabilities were found in 2/55 (3.6%) of males. One of the 7 females had mild and one had moderate MR: the other 5 were learning disabled. Autistic stigmata were present in 10/62 (16%) of the patients. Only 14/62 (23%) had a history of seizures, all of which were controlled with anticonvulsants. In 36/62 cases, an electroencephalogram (EEG) was performed. We compared these data with that of others. Brain stem auditory evoked response (BAER) was performed in 12 cases. Abnormalities were found in only 5/12. Neuroimaging and computerized cranial transaxial tomography (CT scan) were performed on 21/62 (34%) of the patients. Only 8 of these 21 (38%) studies were abnormal. One patient died; neuropathological studies showed mild brain atrophy, with light microscopic and ultrastructural abnormalities. Rapid Golgi dendritic spine patterns showed that the proximal apical segments were abnormally developed. Very thin, long tortuous spines with prominent terminal heads and irregular dilatations were present. Marked reductions in the length of the synapses, as determined on EPTA-postfixed tissue where noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The Fra(X) syndrome: neurological, electrophysiological, and neuropathological abnormalities. 201 89

In 1983-88 period, 206 subjects with a average age of 9 years and 6 months, referred [correction of envoied] to our service for learning disabilities, have been submitted to neuropsychiatric visit with a psychometric evaluation, I.Q. included, by which a neuropsychological diagnosis has been expressed. The distribution curves of I.Q. of different diagnostic groups (neurosis, psychosis, specific learning disability with and without sociocultural deprivation, central neuromotor damage, psychomotor delay, Down syndrome, mental retardation) have been examined. The analysis shows that only subjects with central neuromotor damage, psychomotor delay, Down syndrome, mental retardation have an I.Q. less than or equal to 70. The anamnesis and clinical evaluation consent to assert an "organic" etiopathogenesis in 9 of 20 subjects with mental retardation. Therefore for diagnostic evaluation of children with learning disabilities seems useful to perform always an I.Q. and, when I.Q. less than or equal to 70, to execute an instrumental examination to exclude an "organic" etiopathogenesis.
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PMID:[The diagnostic value of the intelligence quotient in learning disabilities]. 207 99

This study examined the differential influence of an IQ cutoff and standard score or regression-based method for determining a severe discrepancy as eligibility criteria for the identification of black and white students with learning disabilities. Subjects were 218 white and 132 black students referred for possible learning disability services. The results of the study demonstrated that the use of a standard score method for determining a severe discrepancy and the use of an IQ cutoff above the range for mental retardation resulted in the disproportionate underrepresentation of black students meeting eligibility criteria. In contrast, when a regression-based method to determine a severe discrepancy was used, along with the absence of an IQ cutoff, no differences were discerned between the two groups. The implications of these findings for current practice are discussed.
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PMID:Factors influencing the identification of black and white students with learning disabilities. 236 42

It has not been determined whether severity of handicap or other associated factors are more important in determining the age of presentation for developmental disabilities. The relationship between age at presentation and referral source, presenting complaint, diagnosis, and associated factors (medical illness, motor signs, or behavioral disturbances) was examined in 738 consecutive children referred for developmental evaluation during 1982-1983. The nature of the complaint or diagnosis (motor, language, behavioral, or educational) was a far better predictor of age of presentation than the severity of the disorder. The degree of mental retardation did not affect age of presentation. Behavior problems did not affect the age of presentation for school failure or learning disability, but were associated with later presentation for motor delay, language delay, communication disorder, and within all IQ groups. The association of topography of handicap rather than severity with age of presentation should be considered when establishing or evaluating efforts at early identification of developmental disability.
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PMID:Age of presentation in developmental disability. 243 9

Literature data on the harmful effects of smoking during pregnancy are reviewed with special emphasis on the fetal growth retardation and delayed changes in child behavior. Intrauterine growth retardation is one of the major causes of low birth weight. It was shown that the birth weight of neonates in smoking mothers can be decreased by 30-396 g. Mass screening data indicate that smoking during pregnancy also increases perinatal mortality (up to 28%). Intrauterine growth retardation was also observed following passive smoking. Inhalation of tobacco smoke by pregnant women was found to increase the fetal heart rate and inhibit fetal movements. Children born from smoking mothers had the higher incidence of asphyxia, cyanosis and hyperactivity. Mass longitudinal studies of children of smoking mothers indicated learning disability, slight mental retardation and insufficient social adaptation by the age of 7 years. Special neurological follow-up study of 326 children revealed frequent minimal brain dysfunction. Pathogenesis of fetal disorders was shown to be associated with impaired adaptation to pregnancy in smoking women. Majority of the constituents of tobacco smoke are capable to pass through the placental-fetal barrier. The most harmful components for fetal development were found to be nicotine and carbon monoxide, which reduce the placental perfusion and blood flow. Exposure to carbon monoxide was shown to increase the level of carboxyhemoglobin and decrease the level of oxyhemoglobin resulting in reduced oxygen supply to fetal tissues and fetal anoxia.
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PMID:[Pathogenesis of fetal growth retardation and behavioral disorders in the progeny caused by smoking during pregnancy]. 265


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