Cranial magnetic resonance imaging and school performance in very low birth weight infants in adolescence
AIM To determine whether neurological deficits are associated with structural anomalies of the brain in very low birthweight (VLBW) infants with subsequent learning disorders but without cerebral palsy, or whether other factors, such as poor early growth, are responsible. METHODS Eighty seven VLBW i...
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Published in | Archives of disease in childhood. Fetal and neonatal edition Vol. 81; no. 2; pp. F116 - F121 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
London
BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health
01.09.1999
BMJ BMJ Publishing Group LTD BMJ Group |
Subjects | |
Online Access | Get full text |
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Summary: | AIM To determine whether neurological deficits are associated with structural anomalies of the brain in very low birthweight (VLBW) infants with subsequent learning disorders but without cerebral palsy, or whether other factors, such as poor early growth, are responsible. METHODS Eighty seven VLBW infants and eight term controls who had been examined at school between the ages of 12 and 13 years, had cranial magnetic resonance imaging (MRI) scans at 15–17 years of age. RESULTS Thirty seven (42.5%) of the VLBW children had abnormalities reported on their scans (two porencephaly, 28 periventricular leucomalacia, 24 ventricular dilatation, and 15 thinning of the corpus callosum). No significant differences in intelligence quotient, motor clumsiness, or frequency of attention deficit / hyperactivity disorder were observed between those children with MRI lesions and those with normal scans. Quantitative measurements showed the VLBW infants had smaller brains, and a relatively smaller corpus callosum compared with controls. No association between brain measurements and school performance was observed among the VLBW infants. CONCLUSIONS The difficulties experienced by VLBW children at school are unlikely to be the result of perinatal brain injury, but they might to be attributable to the effects of poor postnatal growth. |
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Bibliography: | local:fetalneonatal;81/2/F116 istex:1DD94517885C5DAA82A9ADEEFB3F3A2D6AABF380 ark:/67375/NVC-D6090K79-5 href:fetalneonatal-81-F116.pdf PMID:10448179 Dr R Cooke. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1359-2998 1468-2052 |
DOI: | 10.1136/fn.81.2.F116 |