Abstract
The most skilled stonemasons cannot construct a cathedral without an ample supply of fine granite blocks. Likewise, the human brain cannot be built properly if stocks of neuroglial progenitors (the building blocks of the brain) are depleted by injury during the critical period of progenitor cell proliferation and migration, as occurs in germinal matrix haemorrhage in prematurity. The article by Prof. Marc Del Bigio (2011), representing the analysis of a career-spanning autopsy cohort of preterm infants with and without germinal matrix haemorrhage, he addresses a persistent clinical concern facing paediatric specialists caring for survivors of prematurity: what are the consequences of germinal matrix haemorrhage on normal brain development at the microanatomic level, and do they explain observed neurodevelopmental and neuroimaging outcome data? As a serious complication of prematurity, germinal matrix haemorrhage and its frequent accompaniment, intraventricular haemorrhage, have been recognized in the medical literature since the turn of the last century (Corvelaire, 1903). In the period from 1940 to 1970, population studies identified the maternal, obstetric and neonatal risk factors for development of germinal matrix haemorrhage, including vaginal delivery, low birth weight, low Apgar scores, hypoxia and hypercapnea (Bassan, 2009; Ballabh, 2010). Improvements since the 1970s in neonatal intensive care have reduced the incidence of cardiorespiratory complications and increased survival following preterm delivery; however, the overall incidence of intraventricular haemorrhage in very low birth weight infants has remained static over the last two decades (Jain et al. , 2009). Thus, intraventricular haemorrhage is still a significant problem affecting >12 000 infants per year in the USA …
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