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| 2. |
- Bågenholm, Andriette, et al.
(författare)
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Psychosocial effects on siblings of children with autism and mental retardation: a population-based study.
- 1991
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Ingår i: Journal of Mental Deficiency Research. - 0022-264X. ; 35 (Pt4), s. 291-307
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Tidskriftsartikel (refereegranskat)abstract
- The probands of this study were 60 children and young adults between 5 and 20 years of age, 20 of whom had siblings with autism, 20 of whom had siblings with mental retardation, and 20 of whom had siblings who were free of handicap. The three proband groups were matched for gender, birth order and socioeconomic status. The children were questioned about their sibling relationships and about particular problems they faced concerning their handicapped brothers or sisters and about problems concerning themselves. Parents were interviewed about the healthy child's behaviour and social adjustment. Mothers completed the Eysenck Personality Inventory concerning themselves. Siblings of handicapped children and especially siblings of children with autism were more concerned about the future. They also felt lonely more often and many of them had peer problems. They often regarded their handicapped siblings as a burden. They tended to have only one sibling. Siblings often did not know why their handicapped brother or sister was different from other children. There were more behaviour disturbances in the siblings of handicapped children and mothers with a child with autism reported more 'stressful events'. There were no differences as regards the personality of the mothers and the self-concept of the children between the three groups.
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| 3. |
- Drugge, Ulf
(författare)
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Fragile-X syndromet i gången tid
- 1991
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Ingår i: Forskning om utvecklingsstörning och omsorger inför 90-talet. - Stockholm : Sävstaholmsföreningen. ; , s. 37-43
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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| 4. |
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| 5. |
- Fernell, Elisabeth, 1948, et al.
(författare)
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Autistic symptoms in children with infantile hydrocephalus.
- 1991
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Ingår i: Acta Paediatrica Scandinavica. - 0001-656X. ; 80:4, s. 451-457
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Tidskriftsartikel (refereegranskat)abstract
- From a population-based series of children with Infantile Hydrocephalus (IH) 69 patients (mean age 11.7 years) were examined with respect to the occurrence of autistic symptoms. Autistic symptomatology was evaluated according to a modified short Swedish version of the so-called Autism Behavior Checklist. Sixteen of the 69 IH children (23%) reached a score which was considered indicative of autistic symptoms (AS) in the child. This group was compared with the remaining 53 IH children without autistic symptoms (non AS). Significant differences were found between these two groups with respect to aetiological and clinical data. In the AS group 44% were born preterm as compared to 9% in the non AS group. CT scan showed major abnormalities in 64% of the AS children while this was present in 28% in the non AS group. The occurrence of major neuroimpairments--epilepsy, mental retardation and cerebral palsy--was 50%, 88% and 50% in the AS group as compared to 9%, 23% and 19% respectively in the non AS group. It was concluded that the more severe the brain damage in children with IH the more likely that autistic symptomatology would ensue. This implies that specific neuropsychiatric services to these families are required.
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| 6. |
- Fernell, Elisabeth, 1948, et al.
(författare)
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Behavioural problems in children with infantile hydrocephalus.
- 1991
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Ingår i: Developmental Medicine and Child Neurology. - : Wiley. - 0012-1622 .- 1469-8749. ; 33:5, s. 388-395
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Tidskriftsartikel (refereegranskat)abstract
- The occurrence of behavioural problems in a population-based series of children with infantile hydrocephalus (non-spina bifida) was analysed, using parent questionnaires. Children with both infantile hydrocephalus and mental retardation had significantly more behavioural problems compared with those with no mental retardation and controls. Inattentiveness and hyperactivity were particularly typical. No differences were found between children with infantile hydrocephalus and no mental retardation and the control group.
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| 7. |
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| 8. |
- Gillberg, Christopher, 1950
(författare)
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Outcome in autism and autistic-like conditions.
- 1991
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Ingår i: Journal of the American Academy of Child and Adolescent Psychiatry. - : Elsevier BV. - 0890-8567. ; 30:3, s. 375-382
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Tidskriftsartikel (refereegranskat)abstract
- Autism carries a very variable prognosis; there might be a slight increase in mortality in the first 30 years of life. A small, but not negligible, minority of people with autism lead productive, self-supporting adult lives, but about two-thirds will remain dependent on others throughout life. The risk of epilepsy is very high, both in early childhood and adolescence. An important minority deteriorate in adolescence. Outcome in autistic-like conditions is even more variable, ranging from excellent in many cases of so-called Asperger syndrome to gloomy in most cases of so-called disintegrative disorders.
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| 9. |
- Gillberg, Christopher, 1950
(författare)
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The treatment of epilepsy in autism.
- 1991
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Ingår i: Journal of Autism and Developmental Disorders. - 0162-3257. ; 21:1, s. 61-77
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Tidskriftsartikel (refereegranskat)abstract
- Autism is associated with epilepsy. One third of the population of people with autism have developed seizures in early adult life. In spite of this well-known association, little is known about the treatment of epilepsy in autism. This paper reviews the sparse literature and reports a systematic case-record study of the treatment of epilepsy in autism. Some practical guidelines for clinicians are provided. Research in the field of epilepsy in autism is highly warranted.
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| 10. |
- Reuterdahl, C, et al.
(författare)
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Characterization of platelet-derived growth factor beta-receptor expressing cells in the vasculature of human rheumatoid synovium
- 1991
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Ingår i: Laboratory Investigation. - 1530-0307. ; 64:3, s. 321-329
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Tidskriftsartikel (refereegranskat)abstract
- Platelet-derived growth factor (PDGF) beta-receptor expression in normal and rheumatoid synovia was investigated by double immunofluorescence staining of frozen sections and by in situ hybridization. In the inflamed synovia, PDGF beta-receptor mRNA was present in vascular cells, as well as in discrete stromal cells. PDGF beta-receptor expressing cells in rheumatoid synovia were characterized by double immunofluorescence staining using the PDGFR-B2 monoclonal antibody at a concentration at which this antibody merely stained granular accumulations of PDGF beta-receptors. Granular accumulations of PDGF beta-receptors were articulate in blood vessel cells, but also appeared in discrete stromal cells. Thus, the overall distribution of cells having granular accumulations of PDGF beta-receptors was similar to the distribution of cells expressing PDGF beta-receptor mRNA. Double immunofluorescence stainings showed that: (a) a majority (greater than 90%) of resident macrophages did not express granular PDGF beta-receptor staining, but macrophages were often juxtaposed to PDGF beta-receptor-positive cells; (b) T lymphocytes did not express PDGF beta-receptors, but these cells were frequently found in the proximity of cells stained by PDGFR-B2; (c) in some blood vessels both HLA-DR expressing cells and PDGF beta-receptor expressing cells could be visualized, whereas in other blood vessels, cells expressing only one of these activation markers could be detected; (d) smooth muscle cells in blood vessels contained PDGF beta-receptors; and (e) capillary endothelial cells in the inflamed synovia recurrently displayed granular PDGF beta-receptor staining. The granular accumulations of PDGF beta-receptors may reflect internalization of the receptor as a result of paracrine or autocrine ligand stimulation. In support of such a possibility are the findings that elevated levels of PDGF B chain mRNA were detected by in situ hybridization in the inflamed synovia, and that cells expressing PDGF B chain mRNA were distributed similarly to cells expressing PDGF beta-receptor mRNA. Taken together, the results indicate that PDGF has a role in the inflammatory process in rheumatoid synovitis, most likely by stimulating proliferative events in the vasculature.
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