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Abnormal cortical development after premature birth shown by altered allometric scaling of brain growth.

Kapellou, O; Counsell, SJ; Kennea, N; Dyet, L; Saeed, N; Stark, J; Maalouf, E; Duggan, P; Ajayi-Obe, M; Hajnal, J; et al. Kapellou, O; Counsell, SJ; Kennea, N; Dyet, L; Saeed, N; Stark, J; Maalouf, E; Duggan, P; Ajayi-Obe, M; Hajnal, J; Allsop, JM; Boardman, J; Rutherford, MA; Cowan, F; Edwards, AD (2006) Abnormal cortical development after premature birth shown by altered allometric scaling of brain growth. PLoS Medicine, 3 (8). e265 (1382) -e265 (1390). ISSN 1549-1676 https://doi.org/10.1371/journal.pmed.0030265
SGUL Authors: Kennea, Nigel

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Abstract

BACKGROUND: We postulated that during ontogenesis cortical surface area and cerebral volume are related by a scaling law whose exponent gives a quantitative measure of cortical development. We used this approach to investigate the hypothesis that premature termination of the intrauterine environment by preterm birth reduces cortical development in a dose-dependent manner, providing a neural substrate for functional impairment. METHODS AND FINDINGS: We analyzed 274 magnetic resonance images that recorded brain growth from 23 to 48 wk of gestation in 113 extremely preterm infants born at 22 to 29 wk of gestation, 63 of whom underwent neurodevelopmental assessment at a median age of 2 y. Cortical surface area was related to cerebral volume by a scaling law with an exponent of 1.29 (95% confidence interval, 1.25-1.33), which was proportional to later neurodevelopmental impairment. Increasing prematurity and male gender were associated with a lower scaling exponent (p < 0.0001) independent of intrauterine or postnatal somatic growth. CONCLUSIONS: Human brain growth obeys an allometric scaling relation that is disrupted by preterm birth in a dose-dependent, sexually dimorphic fashion that directly parallels the incidence of neurodevelopmental impairments in preterm infants. This result focuses attention on brain growth and cortical development during the weeks following preterm delivery as a neural substrate for neurodevelopmental impairment after premature delivery.

Item Type: Article
Additional Information: ©2006 Kapellou et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Keywords: Biometry, Brain, Cerebral Cortex, Cohort Studies, Developmental Disabilities, Female, Gestational Age, Humans, Infant, Newborn, Infant, Premature, Magnetic Resonance Imaging, Male, Models, Neurological, Sex Factors
SGUL Research Institute / Research Centre: Academic Structure > Institute of Medical & Biomedical Education (IMBE)
Academic Structure > Institute of Medical & Biomedical Education (IMBE) > Centre for Clinical Education (INMECE )
Journal or Publication Title: PLoS Medicine
ISSN: 1549-1676
Dates:
DateEvent
1 August 2006Published
PubMed ID: 16866579
Web of Science ID: 16866579
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URI: http://openaccess.sgul.ac.uk/id/eprint/400
Publisher's version: https://doi.org/10.1371/journal.pmed.0030265

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