No description available.

Providing adequate nutrition to children with severe neurological disabilities is extremely difficult due to the high prevalence of oral-motor dysfunction in this group. Short stature and light weight for height are common in disabled children and undernutrition is believed to play a role in this poor growth. This programme of study investigated the effect of gastrostomy-tube feeding in disabled children with oral-motor dysfunction and evaluated the energy balance and body composition of disabled children fed both orally and via gastrostomy-tube over twelve months. The Quality of Life of the children and their carers was also evaluated. Energy intake was measured using three-day dietary diaries and energy expenditure with indirect calorimetry and doubly labelled water. Total body water using oxygen-18 dilution was used to evaluate body composition along with standard anthropometry. Improved growth, nutritional status and general health were seen at six and twelve months after gastrostomy-tube placement. The Quality of Life of the children and their carers also significantly increased. Both energy intake and energy expenditure were found to be lower than reference standards, but energy balance was positive indicating that inadequate nutrition was not the sole cause of poor growth. Body composition was also found to be significantly different from reference. Fat-free mass was significantly low for age and for height. Fat mass was higher in gastrostomy-tube fed children, but lower or normal in disabled children fed orally. Physical activity levels were low for the entire group of disabled children yet the gastrostomy-tube fed children displayed much higher levels of disability. Gastrostomy-tube feeding has a positive impact upon the growth, health and Quality of Life of disabled children and their carers. Careful follow-up is critical in order to optimize health and body composition.

To investigate the relationship between birth asphyxia and neurological impairment a cohort of 184 infants with a low (≤3) one-minute Apgar score was studied. All were singletons, apparently normally formed, and born at term (≥37 weeks' gestation) in the John Radcliffe Hospital, between January 1984 and September 1985. The 181 cohort survivors were traced at the age of five years; 159 were assessed by a paediatrician on a battery of neurodevelopmental tests, and information about a further eight was obtained from other sources. Three infants in the cohort died neonatally with a diagnosis of birth asphyxia, and three had spastic quadriplegia, profound developmental delay and visual impairment. Examination of the perinatal histories of these six children, including their fetal heart rate patterns in labour and acid-base status at delivery, found convincing evidence of birth asphyxia. Only one other child in the cohort exhibited similar signs of birth asphyxia; he was unimpaired at the age of five. To assess the impact of birth asphyxia on the overall rate of cerebral palsy, all cases of cerebral palsy born to Oxford residents in the study period were identified. Of 30 cases of cerebral palsy, the three identified in the follow-up study were the only ones whose impairment could be attributed to birth asphyxia in a full-term birth. Birth asphyxia therefore accounted for 10% of all cases of cerebral palsy, a fraction that agrees with previous estimates. The frequency of cerebral palsy due to birth asphyxia was estimated as 1 in 3800 full-term livebirths. A detailed analysis of the test scores of the 159 children assessed by the paediatrician failed to show any association between their acid-base values at delivery and test scores, or between their fetal heart rate patterns in labour and test scores. These results conform with the view that birth asphyxia has an "all or nothing" effect, and that it presents as a cluster of abnormal neonatal signs, including persistent cerebral depression, severe acidaemia, neonatal encephalopathy, and multiorgan dysfunction.

No description available.

Thesis (M.S.)--University of Oregon, 2004. / Includes bibliographical references (leaves 56-58). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Thesis (doctoral)--Göteborg University, 1996. / Added t.p. with thesis statement inserted.

Thesis (doctoral)--Göteborg University, 1996. / Added t.p. with thesis statement inserted.

Thesis (Ph.D.) - University of Queensland, 2005. / Includes bibliography.

Thesis--Wisconsin. / Includes bibliographical references (leaves 66-69).

Thesis (M.S.)--University of Oregon, 2004. / Includes bibliographical references (leaves 56-58).