Is the Late Preterm Infant More Vulnerable to Gray Matter Injury than the Term Infant?
Section snippets
Perinatal hypoxic-ischemic injury to the gray matter
The critical consequence of hypoxic-ischemic injury is diminished oxygen supply, with hypoxia-ischemia referring to the two mechanisms of oxygen deficiency (ie, diminished oxygen supply in the blood [hypoxia], and diminished amount of blood perfusing the brain tissue [ischemia]) (Fig. 1). Neuronal cell injury and death is primarily caused by deprivation of oxygen and glucose, the two key energy sources for the brain. Because neither oxygen nor glucose is stored in the brain, deprivation of only
Gray matter development in the late preterm brain
The potential for increased vulnerability of the late preterm brain to injury is underscored by recognition of its substantial overall immaturity relative to the term brain, and the immense growth of the gray matter that occurs from 34 weeks to term. At 34 gestational weeks, the total brain weight is 65% of that at term; there is still 35% of brain weight yet to be obtained to reach term (40 weeks) weight over the ensuing 6 weeks [9]. The question arises, what is the timetable of the fetal
Gray matter injury in the late preterm infant
In essence, the pathology of hypoxia-ischemia in the fetal brain reflects cellular and tissue reactions brought about by a complex interplay of the type, timing, and severity of the insult and its changing developmental vulnerabilities during a period when the brain is at its peak capacity for plasticity and repair. Overall brain development is occurring so rapidly that responses to hypoxia-ischemia vary considerably even from midgestation to term, as witnessed by the preferential injury to
The vulnerability of gray matter regions to hypoxia-ischemia in the late preterm infant
The reasons for selective neuronal vulnerability at different develomental ages are clearly complex and multifactorial. Circulatory factors play a role as evidenced by selective neuronal necrosis in vascular border zones of the middle and anterior cerebral arteries in the term infant [7], [57]. Other factors that have been identified experimentally include developmental differences in anaerobic glycolytic capacity, energy requirements, lactate accumulations, calcium influx, free radical
Summary
Here the authors attempt to answer the question: is the late-preterm infant more vulnerable to gray matter injury than the term infant? The short answer seems to be: “it depends.” It depends upon the particular balance of susceptibility and protective factors in the particular gray matter region and particular neuronal subtype at that particular age. The basis pontis in the late preterm infant, for example, may be more vulnerable to hypoxic-ischemic injury than in the term infant, but the
Acknowledgments
We appreciate the help of Sarah E. Andiman in the preparation of the illustrations and Natalia S. Borenstein for technical assistance with the unpublished GAP-43 western blot data in the developing human cerebral cortex. We thank Dr. Joseph J. Volpe for his critical review of the manuscript.
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2016, Journal of PediatricsCitation Excerpt :The association between lower gestational age and poor school readiness in kindergarten seen in VPT infants may be related to the biological differences in early brain development associated with preterm birth. The third trimester of pregnancy is a period of rapid fetal brain development characterized by growth of gray matter,41 increased myelination,42 and increased synaptogenesis and neural connectivity.43 Underdevelopment of the preterm brain has been associated with poorer educational performance and lower intellectual ability compared with full-term infants,44,45 with these differences most pronounced in children born at earlier gestational ages.
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2015, Revista Chilena de PediatriaMild maturational delay of the brainstem at term in late preterm small-for-gestation age babies
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This work was supported by the National Institute of Neurological Disorders and Stroke (PO1-NS38475); the National Institute of Child Health and Development (P30-HD18655); Children's Hospital Boston Developmental Disabilities Center; and the National Multiple Sclerosis Society.