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

The concept of developmental disabilities as a group of problems with origins in the stages of human development has been broadened by recent legislation to include mental retardation, cerebral palsy, epilepsy, autism, dyslexia, and other neurological impairments. The debate continues on whether or not specific disability categories should be named, but the functional aspects of the problems seem to be generally accepted. Potential implications of this legislation for occupational therapy are discussed in this paper. Numerous programs supported by a variety of governmental units and private agencies will need qualified professionals. This paper concludes with a brief list of six developmental disability programs of the University of Michigan University Affiliated Facility and an outline of three models of field placement in developmental disabilities for occupational therapy students.
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PMID:Developmental disabilities. 7 85

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

In the differential diagnosis as well as in the rehabilitation of hearing impaired children other disorders affecting language aquisition and speech development need to be taken into account. The rehabilitation programme is highly dependent on the early diagnosis of these additional disorders such as dysphasia, mental retardation of various degrees, cognitive disorders such as dyslexia and dysgraphia, dyspractic and dysarthric disorders of speech production, cleft palate and other anomalies of articulatory organs, autism and other abnormal features of psychic and personality development. In addition children with multiple disorders like malformations, visual disorders, epilepsy, CP and other diseases and handicaps, even though they may not influence language and speech development directly, may still be deprived of possibilities to aquire adequate verbal stimulation. The paper presents a material of 200 children whose hearing loss was diagnosed at the preschool age. Major associated handicaps were found in 35.5% of cases and in 26% they were complicating rehabilitation and development of the child. The frequency of associated disorders and their effect on language and speech development, learning ability and social development is being more closely analysed and discussed.
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PMID:Associated handicaps in children with hearing loss. 322 82

The corpus callosum (CC), the main structure subserving hemispheric collaboration, that is necessary for efficient cognitive functioning, undergoes developmental processes such as axonal retraction and myelination. Callosal growth therefore is vulnerable for adverse events such as perinatal asphyxia, but there are also genetic and epigenetic factors that determine form and thickness. MRI scans of 110 children, either with specific learning disabilities (LD), i.e. dysphasia/dyslexia, or with several degrees of general LD, showed callosa that were highly variable in size. The callosal size corrected for brain size did not vary significantly according to the severity of the LD, although it tended to be smaller in severe LD, i.e. mental retardation. Callosal size varied however, due to the likely presence of genetic influences or of adverse perinatal events. Children with familial dysphasia/dyslexia, had a thicker CC, possibly reflecting a poorly understood neurodevelopmental mechanism that inhibits the establishment of cerebral dominance. LD children (all subgroups together) with perinatal adverse events had a smaller CC than the familial cases, suggesting CC damage. Despite a multitude of developmental factors influencing the final size, this study suggests that total callosal size, supposedly linked to interhemispheric function, may contribute to the pathophysiological mechanisms that give rise to LD.
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PMID:Callosal size in children with learning disabilities. 753 Sep 64

Four-layered microgyria is associated with many developmental disorders, including mental retardation, epilepsy, and developmental dyslexia. Freezing lesions to the newborn rodent neocortex result in the formation of four-layered microgyria. Previous research had suggested this type of injury acts as an hypoxic/ischemic event to the developing cortical plate. The current study examines the effectiveness of the non-competitive N-methyl-D-aspartate receptor antagonist dizocilpine (MK-801) in protecting against freezing injury to the newborn rat cortical plate. Three groups of rats received freezing injury to the cortical plate on the first day of life (postnatal day 1). Two groups were treated with MK-801 (1 or 2 mg/kg) 0.5 h before the lesion and 6 and 14 h after, while one group received saline injections. A fourth group received MK-801 injections, but did not have a freezing lesion. The volume of neocortical abnormality was determined for all three groups in rats killed after postnatal day 7. Treatment with the higher dose of MK-801 (3 x 2 mg/kg) dramatically reduced the effects of freezing injury but also resulted in over 50% mortality in both lesioned and unlesioned groups. Animals in the lesioned group, however, had a decreased volume of abnormal cortex, and there were fewer animals with microsulci than in the untreated group. This is the first demonstration of a significant anatomical neuroprotective effect in newborns leading to a reduction of cortical malformation.
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PMID:The neuroprotective effects of MK-801 on the induction of microgyria by freezing injury to the newborn rat neocortex. 863 9

Sex differences in intelligence is among the most politically volatile topics in contemporary psychology. Although no single finding has unanimous support, conclusions from multiple studies suggest that females, on average, score higher on tasks that require rapid access to and use of phonological and semantic information in long-term memory, production and comprehension of complex prose, fine motor skills, and perceptual speed. Males, on average, score higher on tasks that require transformations in visual-spatial working memory, motor skills involved in aiming, spatiotemporal responding, and fluid reasoning, especially in abstract mathematical and scientific domains. Males, however, are also over-represented in the low-ability end of several distributions, including mental retardation, attention disorders, dyslexia, stuttering, and delayed speech. A psychobiosocial model that is based on the inextricable links between the biological bases of intelligence and environmental events is proposed as an alternative to nature-nurture dichotomies. Societal implications and applications to teaching and learning are suggested.
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PMID:Sex differences in intelligence. Implications for education. 932 93

The molecular characterization of single-gene disorders or chromosomal abnormalities that result in a cognitive abnormality (predominantly mental retardation) and of the genetic variants responsible for variation in intellectual abilities (such as IQ, language impairment and dyslexia) is expected to provide new insights into the biology of human cognitive processes. To date this hope has not been realized. Success in finding mutations that give rise to mental retardation has not been matched by advances in our understanding of how genes influence cognition. In contrast, the use of engineered mutations in mice to study models of learning and memory has cast new light on the molecular basis of memory. A comparison of studies of human and mouse mutations indicates the limitations of current genetic approaches to the understanding of human cognition. It is essential to interpret a mutation's effect within a well-characterized neural system; mutations can be used to define gene function only when the mutation has an effect on a system whose constituents form a serial causal chain, such as the molecular components of a signal transduction pathway. Typically, however, genetic mutations with a cognitive and behavioural phenotype are characterized by specific effects on different systems whose inter-relationships are unknown. Genetic approaches are currently limited to exploring neuronal function; it is not yet clear whether they will throw light on how neuronal connections give rise to cognitive processes. We need a much greater integration of different levels of understanding of cognition in order to exploit the genetic discoveries. In short, a rapprochement between molecular and systems neuroscience is required.
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PMID:The genetic basis of cognition. 1054 88

Family and adoption studies indicate that genetic factors play a role in the development of many psychiatric disorders. A variable number of possible interacting genes predisposing to the diseases is likely. The genetic dissection has been hampered by genetic complexity as well as by difficulties in defining the phenotypes. Genetic mapping efforts using sib pairs, twins and individual large families has revealed preliminary or tentative evidence for susceptibility loci for a number of psychiatric disorders. Illnesses include the prion disease familial fatal insomnia (FFI), alcoholism, anorexia nervosa, autism, bipolar affective disorder, dyslexia, enuresis nocturnal, epilepsia, obsessive-compulsive disorders (OCD), schizophrenia, as well as the dementias, Alzheimer's disease and frontal lobe dementia, and mental retardation. The genes and proteins related to the newly discovered transmitter in the central nervous system, nitric oxide (NO), and its genes and proteins are also reviewed. The number of mapped human genes now exceeds 30,000 of the estimated total number of 60,000 to 100,000 genes. This rapid development will facilitate gene mapping, as well as efforts to isolate and identify the genes responsible for symptom susceptibility in many of the etiologically unclear psychiatric diseases with complex genetic origin.
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PMID:[Mental disease a heritage. New genetic knowledge can reveal "public diseases" such as autism, dyslexia, alcoholism, anorexia, schizophrenia]. 1070 80

The Colorado MRRC was one of the original MRRCs funded and has maintained its focus on genetic and nutritional causes of mental retardation and developmental disabilities. Significant discoveries of the center have included a number of metabolic disorders, including glutaric academia types I and II, electron transport flavoprotein (ETF) deficiency, ETF dehydrogenase deficiency, glycerol kinase deficiency, sphingolipidoses, genetic linkages in dyslexia, phonological deficits in dyslexia, and the importance of the trace mineral Zn in early development. Current research at the center is supported by program of projects grants on inborn errors of metabolism, Down syndrome (DS), autism, and dyslexia.
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PMID:The Colorado mental retardation and developmental disabilities research center. 1217 65

Cortical malformations resulting from aberrant brain development can be associated with mental retardation, dyslexia, and intractable forms of epilepsy. Despite emerging interest in the pathology and etiology of cortical malformations, little is known about the phenotype of cells within these lesions. In utero exposure to the DNA methylating agent methylazoxymethanol acetate (MAM) during a critical stage in neurodevelopment results in animals with distinct clusters of displaced neurons in hippocampus, i.e. nodular heterotopia. Here we examined the molecular and electrophysiological properties of cells within hippocampal heterotopia using rats exposed to MAM during gestation. Molecular analysis revealed that heterotopic cells do not express mRNA markers normally found in hippocampal pyramidal cells or dentate granule cells (SCIP, Math-2, Prox-1, neuropilin-2). In contrast, Id-2 mRNA, normally abundant in Layer II-III supragranular neocortical neurons but not in CA1 pyramidal neurons, was prominently expressed in hippocampal heterotopia. Current-clamp analysis of the firing properties of heterotopic neurons revealed a striking similarity with supragranular cortical neurons. In particular, both cells were characterized by small hyperpolarizing 'sag' potentials, high input resistance values, slow spike-train afterhyperpolarizations, and the absence of a depolarizing afterpotential. Normotopic CA1 pyramidal neurons (e.g. pyramidal cells with normal lamination adjacent to a heterotopia) in the MAM brain exhibited molecular and electrophysiological properties that were nearly identical to those of age-matched CA1 pyramidal neurons from control rats. We conclude that neuronal heterotopiae in the hippocampus of MAM-exposed rats are comprised of neurons with a Layer II-III supragranular cortex phenotype. The MAM model, therefore, may serve as a useful tool in examination of the factors influencing aberrant brain development and epilepsy.
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PMID:Hippocampal heterotopia with molecular and electrophysiological properties of neocortical neurons. 1237 51


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