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Effects of very low birthweight on brain structure in adulthood

Published online by Cambridge University Press:  10 December 2003

Matthew Allin
Affiliation:
Department of Psychiatry, Institute of Psychiatry, King's College, London, UK.
Max Henderson
Affiliation:
Department of Psychiatry, Institute of Psychiatry, King's College, London, UK.
John Suckling
Affiliation:
Department of Psychiatry, University of Cambridge, Cambridge, UK.
Chiara Nosarti
Affiliation:
Department of Psychiatry, Institute of Psychiatry, King's College, London, UK.
Teresa Rushe
Affiliation:
University of Ulster, Jordanstown, Northern Ireland, UK.
Paul Fearon
Affiliation:
Department of Psychiatry, Institute of Psychiatry, King's College, London, UK.
Ann L Stewart
Affiliation:
Perinatal Brain Research Group, Department of Paediatrics, University College London Medical School, UK.
ET Bullmore
Affiliation:
University of Cambridge, Cambridge, UK.
Larry Rifkin
Affiliation:
Department of Psychiatry, Institute of Psychiatry, King's College, London, UK.
Robin Murray
Affiliation:
Department of Psychiatry, Institute of Psychiatry, King's College, London, UK.
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Abstract

Very-low-birthweight (VLBW) individuals are at high risk of brain injury in the perinatal period. We wished to determine how such early brain lesions affect brain structure in adulthood. Thirty-two VLBW adults (20 female, 12 male) and 18 term, normal birthweight sibling control individuals (nine female, nine male) underwent structural MRI at a mean age of 23 years 4 months (range 17 to 33 years; SD 3.4). Images were analyzed using an automated tissue segmentation algorithm in order to estimate whole brain tissue class volumes in native space. Images were then warped to a template image in standard space. There was no significant between-group difference in whole brain, grey matter, white matter, or total cerebral spinal fluid (CSF) volumes. However, lateral ventricular volume was significantly increased by 41% in those with VLBW. The ratio of grey to white matter was also significantly increased (by 10%) in those with VLBW. Group comparison maps showed widespread changes in the distribution of grey and white matter, and relative excess of ventricular CSF, in the brains of VLBW individuals. Increased ventricular volume predicted decreased grey matter in subcortical nuclei and limbic cortical structures, and decreased periventricular white matter. We conclude that these diffuse abnormalities of grey and white matter are a consequence of the interaction of perinatal brain injury and ongoing neurodevelopmental processes.

Type
Original Articles
Copyright
© 2004 Mac Keith Press

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