Regional impairments of cortical folding in premature infants

• DOI: 10.1002/ana.24313
• Publication Date: 2014-11-26T07:42:29Z
• Authors: Erin Engelhardt; Terrie E. Inder; Dimitrios Alexopo...; Donna L. Dierker; Jason Hill; David Van Essen; Jeffrey J. Neil
• Keywords: Cerebral Cortex; Male; Infant, Newborn; Gestational Age; Magnetic Resonance Imaging; Functional Laterality; 03 medical and health sciences; 0302 clinical medicine; Image Processing, Computer-Assisted; Humans; Premature Birth; Female; Research Articles; Infant, Premature

ObjectiveThis study was undertaken to evaluate the influence of preterm birth and other factors on cerebral cortical maturation.MethodsWe have evaluated the effects of preterm birth on cortical folding by applying cortical cartography methods to a cohort of 52 preterm infants (<31 weeks gestation, mild or no injury on conventional magnetic resonance imaging) and 12 term‐born control infants. All infants were evaluated at term‐equivalent postmenstrual age.ResultsPreterm infants had lower values for the global measures of gyrification index (GI; 2.06 ± 0.07 vs 1.80 ± 0.12, p < 0.001; control vs preterm) and cortical surface area (CSA; 316 ± 24 cm2 vs 257 ± 40 cm2, p < 0.001). Regional analysis of sulcal depth and cortical shape showed the greatest impact of preterm birth on the insula, superior temporal sulcus, and ventral portions of the pre‐ and postcentral sulci in both hemispheres. Although CSA and GI are related, CSA was more sensitive to antenatal and postnatal factors than GI. Both measures were lower in preterm infants of lower birth weight standard deviation scores and smaller occipitofrontal circumference at time of scan, whereas CSA alone was lower in association with smaller occipitofrontal circumference at birth. CSA was also lower in infants with higher critical illness in the first 24 hours of life, exposure to postnatal steroids, and prolonged endotracheal intubation.InterpretationPreterm birth disrupts cortical development in a regionally specific fashion with abnormalities evident by term‐equivalent postmenstrual age. This disruption is influenced by both antenatal growth and postnatal course. ANN NEUROL 2015;77:154–162