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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

More than 30,000 Norwegians are mentally retarded and about 50% of them are severely retarded and often multihandicapped. Before 1975 the majority of the severely retarded resided in large institutions. New legislation has led to an increasing emphasis on decentralization and integration in local communities. Mental retardation is caused by prenatal brain damage in 90% of the cases. Chromosomal aberrations like Down and Fragile-X syndromes are the most common causes. A high proportion of individuals with autism, cerebral palsy, epilepsy and sensory defects are mentally retarded, and the most common additional diagnoses in mental retardation are speech defects, epilepsy, cerebral palsy, congenital heart disease, sight and hearing impairment and hydrocephalus. Almost 1/3 of the mentally retarded adults have developed psychiatric disturbances. Families with mentally retarded children are affected emotionally, socially and economically, and the burden increases as the mentally retarded individual grows older.
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PMID:[The mentally retarded dental patients. Who are they?]. 183 92

Thirty-five children with autistic disorder and 17 with autistic-like conditions underwent an exhaustive neurobiological evaluation, and the findings were contrasted with those obtained from various comparison groups. Almost 90 per cent of the children with autistic disorder and autistic-like conditions had major indications of brain damage or dysfunction. Some of those who did not show such abnormalities had a first-degree relative with Asperger syndrome. The rate of abnormality was similar to that of severely mentally retarded children, but in excess of that of normal children. Within the autism group, abnormality rate did not correlate with degree of mental retardation. It is concluded that autism has multiple biological aetiologies and that autistic symptoms in a child should always prompt a thorough medical/neurobiological evaluation.
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PMID:Neuropsychiatric assessment of children with autism: a population-based study. 186 76

The neuropsychological performances, outcome of epilepsy and MRI topography of tubers of 23 children with tuberous sclerosis were reviewed. Seven children had normal intelligence, 10 had mental retardation, and six mental retardation and autism. An adverse association was found between the number of lesions and IQ, behaviour and severity of epilepsy. Posterior lesions, in addition to frontal-lobe dysfunction, were observed in children with autism. Tuberous sclerosis with well-defined cerebral lesions may represent a model for the relationship between different neuropsychiatric problems.
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PMID:Neuropsychological aspects of tuberous sclerosis in relation to epilepsy and MRI findings. 191 24

Immune abnormalities in autistic children led us to study for indirect evidence of immune activation as measured by the serum analysis of soluble interleukin-2 (sIL-2), interleukin-2 receptor (sIL-2R), T8 antigen (sT8), and interleukin-1 (sIL-1). The serum concentration of these soluble antigens was quantitated by enzyme-linked immunosorbent assays. The concentration of sIL-2 and sT8, but not of sIL-2R and sIL-1, antigens was significantly (P less than 0.05) increased in the sera of autistic children over that in the control healthy children or children with mental retardation (non-Down's syndrome). This finding indirectly indicates that the activation of a subpopulation of T cells occurs in some children with autism.
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PMID:Changes of soluble interleukin-2, interleukin-2 receptor, T8 antigen, and interleukin-1 in the serum of autistic children. 193 32

Brainstem auditory evoked potentials were compared in 109 children with infantile autism, 38 with autistic condition, 19 with mental retardation, and 20 normal children. Children with infantile autism or autistic condition had significantly longer brainstem transmission time than normal (p less than .001). Autistic features, rather than age, sex, or lower mentality, correlated with brainstem transmission time (p less than .0001). The autistic characteristics may be related to dysfunction of the brainstem which affects the processing of the sensory input through the auditory pathway. The brainstem lesion may be part of a generalized process of neurological damage that accounts for the deviant language, cognitive, and social development in the spectrum of autistic disorder.
J Autism Dev Disord 1991 Sep
PMID:Brainstem auditory evoked potential study in children with autistic disorder. 193 78

Autism is a chronic, nonprogressive developmental disability with a unique triad of abnormalities in socialization, communication and behavior. Most, but not all, children with autism have some degree of mental retardation, and many develop epilepsy. No single biomedical etiology has been found, but a significant number of medical disorders occur in association with autism. The medical evaluation is directed toward finding underlying or associated neurologic, metabolic, genetic or infectious diseases. Psychoeducational and behavioral therapies are the most successful approaches to the treatment of autism. Community-based and structured programs that emphasize socialization, communication and family training are the most effective. Medical management focuses on treatment of underlying or associated diseases. Pharmacotherapy is sometimes beneficial, but no drug acts specifically on this complex of symptoms. Family physicians can provide early identification, continuing medical care and support to the child and the family.
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PMID:Autism: early identification and management in family practice. 195 Sep 71

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

Of 135 autistic and/or mentally retarded youngsters, 30 with pervasive developmental disorders and 2 with nonautistic mental retardation showed school refusal according to its modified definition. School refusal was significantly more frequent in other PDDs than in nonautistic mental retardation. The intellectual level was significantly higher in PDD children with school refusal than those without it. A certain level of mental development and obsessive tendency appear necessary for PDD children to develop school refusal. In order to treat school refusal in PDD, it is important to make school a pleasant place to go and to encourage the child to attend.
J Autism Dev Disord 1991 Mar
PMID:School refusal in pervasive developmental disorders. 203 46

The Aberrant Behavior Checklist (ABC; Aman, Singh, Stewart, & Field, 1985a, 1985b) is a 58-item third-party informant rating scale originally developed for institutionalized, low-functioning adolescents and adults. The present study investigated the appropriateness of the scale for youngsters with dual diagnosis of mental retardation and psychiatric disturbance. Over a period of 2 1/2 years, 204 patients (199 after data reduction) from a child psychiatry unit were rated twice daily by direct care staff. Data analysis addressed internal consistency, interrater reliability, criterion validity, and robustness of the factor structure. Internal consistency was satisfactory with alpha coefficients ranging from .82 to .94. Interrater reliability varied between subscales but was relatively low (Pearson correlations between .39 to .61). In terms of its criterion validity, the ABC was sensitive to psychiatric diagnoses and age and the original 5-factor structure was robust (congruence coefficients ranged between .80 to .89). Yet, only a relatively small proportion of the variance (31.5%) was explained by factor analysis indicating possible limitations of the ABC for this population. Given the paucity of assessment instruments for this particular population and the difficulty involved in developing new population-specific instruments, the ABC can be recommended for children and adolescents with dual diagnosis.
J Autism Dev Disord 1991 Mar
PMID:The Aberrant Behavior Checklist with children and adolescents with dual diagnosis. 203 47

Two behavior genetic research strategies have been utilized to understand gene influences in autism. There is overwhelming evidence for gene involvement, although an exact mode of inheritance has not yet been elucidated. Family and twin studies illustrate that the clinical phenotype of autism is not sufficient to characterize the underlying genotype(s) involved. Exactly what should be included in the phenotype remains elusive. Cognitive and social deficits are indicated as milder variants of the autism phenotype, but precisely how to define these deficits requires further research. Furthermore, more complex models of inheritance (e.g., two-locus models--multifactorial and major gene) may be necessary to explain gene influences in autism. Genetic heterogeneity is indicated in autism, with an X-linked disorder, fragile X, and an autosomal dominant disorder, tuberous sclerosis, together accounting for perhaps 8% to 11% or more of cases of autism. Differences in family patterns (i.e., recurrence risks) of neuropsychiatric disorders between autism with and without mental retardation or other clinically defined groups (e.g., males and females) are suggested. Whether these differences represent genetic heterogeneity or multifactorial inheritance with varying thresholds (e.g., of severity or sex differences) cannot be distinguished on the basis of the data available to date. Autosomal recessive inheritance is suggested in a subgroup of families with autism, but the proportion of all autism that may be accounted for by autosomal recessive inheritance is unknown. Evidence exists that stoppage occurs in families with autism, however, and this can affect accurate estimates of segregation ratios when not taken into account. Future family studies need to report (1) exact ascertainment schemes and specification of probands and (2) sex and birth order of affected siblings, including sibship size, so that data may be pooled and such effects can be tested. Investigations of populations with fragile X or tuberous sclerosis as well as those with autism (without known genetic disorders) will identify the etiologic basis of these associations. Such associations may be due to linkage of genes underlying autism and those underlying the known genetic disorders (i.e., linkage disequilibrium) or shared brain pathophysiology or merely shared overt behaviors. Until such mechanisms are elucidated, we can use only empiric risk figures in genetic counseling situations of autism, assuming that no known genetic or environmental cause is identified. Pooling available data from family and twin studies, the following empiric risks are suggested for genetic counseling purposes. An average sibling risk (frequency of affected siblings among all siblings) based on pooled data is 3% (i.e., 57/1698).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetic influences in autism. 204 27


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