Epidemiology of Infantile Hydrocephalus in Sweden
Identifieur interne : 006638 ( Main/Exploration ); précédent : 006637; suivant : 006639Epidemiology of Infantile Hydrocephalus in Sweden
Auteurs : E. Fernell ; B. Hagberg ; G. Hagberg ; L. Von Wendt [Suède]Source :
- Acta Pædiatrica [ 0803-5253 ] ; 1987-05.
Abstract
ABSTRACT. The aetiology of infantile hydrocephalus (IH) was studied in a population‐based series of 141 children with IH, born at term in southwestern Sweden 1967–82. A prenatal aetiology was present in 81 children (57%), a pre‐ and perinatal in 6(4%), a perinatal in 27(19%), and a postnatal in 8(6%); the origin in 19 children (13%) remained untraceable. A variety of aetiologies were revealed or indicated among prenatal conditions. The dominant intrauterine infection was toxoplasmosis. The predominant perinatal condition was posthaemorrhagic IH. The broad outline of outcome differed between pathogenetic groups. Children with a clear prenatal onset of IH were found to be at high risk for early death or multiple neurological impairments. Thirteen of 63(21%) within this group had died before 2 years of age and 34 of the 50(68%) survivors showed major neurological dysfunction. This contrasted to the incidences of 3% deaths and 30% sequelae in children with IH of other onset.
Url:
DOI: 10.1111/j.1651-2227.1987.tb10491.x
Affiliations:
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Von Wendt</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>The Regional Habilitation Institution for Motorhandicapped, Bräcke Östergård, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Acta Pædiatrica</title><title level="j" type="alt">ACTA PAEDIATRICA</title><idno type="ISSN">0803-5253</idno><idno type="eISSN">1651-2227</idno><imprint><biblScope unit="vol">76</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="411">411</biblScope><biblScope unit="page" to="417">417</biblScope><biblScope unit="page-count">7</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1987-05">1987-05</date></imprint><idno type="ISSN">0803-5253</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0803-5253</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">ABSTRACT. The aetiology of infantile hydrocephalus (IH) was studied in a population‐based series of 141 children with IH, born at term in southwestern Sweden 1967–82. A prenatal aetiology was present in 81 children (57%), a pre‐ and perinatal in 6(4%), a perinatal in 27(19%), and a postnatal in 8(6%); the origin in 19 children (13%) remained untraceable. A variety of aetiologies were revealed or indicated among prenatal conditions. The dominant intrauterine infection was toxoplasmosis. The predominant perinatal condition was posthaemorrhagic IH. The broad outline of outcome differed between pathogenetic groups. Children with a clear prenatal onset of IH were found to be at high risk for early death or multiple neurological impairments. Thirteen of 63(21%) within this group had died before 2 years of age and 34 of the 50(68%) survivors showed major neurological dysfunction. This contrasted to the incidences of 3% deaths and 30% sequelae in children with IH of other onset.</div></front></TEI><affiliations><list><country><li>Suède</li></country></list><tree><noCountry><name sortKey="Fernell, E" sort="Fernell, E" uniqKey="Fernell E" first="E." last="Fernell">E. Fernell</name><name sortKey="Hagberg, B" sort="Hagberg, B" uniqKey="Hagberg B" first="B." last="Hagberg">B. Hagberg</name><name sortKey="Hagberg, G" sort="Hagberg, G" uniqKey="Hagberg G" first="G." last="Hagberg">G. Hagberg</name></noCountry><country name="Suède"><noRegion><name sortKey="Von Wendt, L" sort="Von Wendt, L" uniqKey="Von Wendt L" first="L." last="Von Wendt">L. Von Wendt</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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