title: Abnormal cortical development after premature birth shown by altered allometric scaling of brain growth.
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.
  
  
  RESULTS
  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.
authors.affiliation: Department of Paediatrics, Imperial College, Hammersmith Hospital, London, United Kingdom.
authors.forename: Olga
authors.initials: O
authors.lastname: Kapellou
authors.forename: Serena J
authors.initials: SJ
authors.lastname: Counsell
authors.forename: Nigel
authors.initials: N
authors.lastname: Kennea
authors.forename: Leigh
authors.initials: L
authors.lastname: Dyet
authors.forename: Nadeem
authors.initials: N
authors.lastname: Saeed
authors.forename: Jaroslav
authors.initials: J
authors.lastname: Stark
authors.forename: Elia
authors.initials: E
authors.lastname: Maalouf
authors.forename: Philip
authors.initials: P
authors.lastname: Duggan
authors.forename: Morenike
authors.initials: M
authors.lastname: Ajayi-Obe
authors.forename: Jo
authors.initials: J
authors.lastname: Hajnal
authors.forename: Joanna M
authors.initials: JM
authors.lastname: Allsop
authors.forename: James
authors.initials: J
authors.lastname: Boardman
authors.forename: Mary A
authors.initials: MA
authors.lastname: Rutherford
authors.forename: Frances
authors.initials: F
authors.lastname: Cowan
authors.forename: A David
authors.initials: AD
authors.lastname: Edwards
mesh_terms: D001699:Biometry; D001921:Brain / Q000033:anatomy & histology / Q000254:growth & development*; D002540:Cerebral Cortex / Q000033:anatomy & histology / Q000254:growth & development*; D015331:Cohort Studies; D002658:Developmental Disabilities / Q000209:etiology*; D005260:Female; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D008279:Magnetic Resonance Imaging; D008297:Male; D008959:Models, Neurological; D012737:Sex Factors