Hindbrain regional growth in preterm newborns and its impairment in relation to brain injury

Premature birth globally affects about 11.1% of all newborns and is a risk factor for neurodevelopmental disability in surviving infants. Histology has suggested that hindbrain subdivisions grow differentially, especially in the third trimester. Prematurity‐related brain injuries occurring in this p...

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Published in:	Human brain mapping 2016-02, Vol.37 (2), p.678-688
Main Authors:	Kim, Hosung, Gano, Dawn, Ho, Mai-Lan, Guo, Xiaoyue M., Unzueta, Alisa, Hess, Christopher, Ferriero, Donna M., Xu, Duan, Barkovich, A. James
Format:	Article
Language:	eng
Subjects:	Adult Brain Diseases - etiology Brain Diseases - pathology Female hindbrain regional growth Humans Imaging, Three-Dimensional Infant Infant, Premature - growth & development Intensive Care, Neonatal Magnetic Resonance Imaging Male neonatal brain MRI Organ Size preterm newborns Rhombencephalon - growth & development Rhombencephalon - pathology Severity of Illness Index surface-based morphometry
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Summary:	Premature birth globally affects about 11.1% of all newborns and is a risk factor for neurodevelopmental disability in surviving infants. Histology has suggested that hindbrain subdivisions grow differentially, especially in the third trimester. Prematurity‐related brain injuries occurring in this period may selectively affect more rapidly developing areas of hindbrain, thus accompanying region‐specific impairments in growth and ultimately neurodevelopmental deficits. The current study aimed to quantify regional growth of the cerebellum and the brainstem in preterm neonates (n = 65 with individually multiple scans). We probed associations of the regional volumes with severity of brain injury. In neonates with no imaging evidence of injury, our analysis using a mixed‐effect linear model showed faster growth in the pons and the lateral convexity of anterior/posterior cerebellar lobes. Different patterns of growth impairment were found in relation to early cerebral intraventricular hemorrhage and cerebellar hemorrhage (P < 0.05), likely explaining different mechanisms through which neurogenesis is disrupted. The pattern of cerebellar growth identified in our study agreed excellently with details of cerebellar morphogenesis in perinatal development, which has only been observed in histological data. Our proposed analytic framework may provide predictive imaging biomarkers for neurodevelopmental outcome, enabling early identification and treatment of high‐risk patients. Hum Brain Mapp 37:678–688, 2016. © 2015 Wiley Periodicals, Inc.
ISSN:	1065-9471 1097-0193