Mechanisms of Injury to White Matter Adjacent to a Large Intraventricular Hemorrhage in the Preterm Brain

Eastern Radiologists, Greenville, NC 27834, USA.
Journal of Clinical Ultrasound (Impact Factor: 0.69). 06/2010; 38(5):254-8. DOI: 10.1002/jcu.20683
Source: PubMed


The purpose of this article is to investigate the hyperechoic lesion seen adjacent to a lateral ventricle that contains blood but is not distended. The literature on ependymal barrier dysfunction was reviewed in search of mechanisms of injury to the white matter adjacent to an intraventricular hemorrhage. The clinical literature on the clinical diagnosis of periventricular hemorrhagic infarction was also reviewed to find out how frequently this diagnosis was made. Support was found for the possibility that the ventricular wall does not always function as an efficient barrier, allowing ventricular contents to gain access to the white matter where they cause damage. Hemorrhagic infarction may not be the only or the most frequent mechanism of white matter damage adjacent to a large intraventricular hemorrhage.

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Available from: Sjirk J Westra
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    • "This explanation does not account for large periventricular hyperechoic lesions that are not accompanied by a blood-distended ventricle [4,5]. A third explanation hypothesizes that blood components toxic to white matter move across the ventricular ependyma and injure immature oligodendrocytes and other vulnerable brain cells [4]. This explanation could also account for the diffuse white matter damage that is evident as white matter volume loss and subsequently as ventriculomegaly. "
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    • "This was also found in our experiments, which showed that adult rats had diminished cerebral volume after autologous blood was injected into the periventricular region during the neonatal period (Balasubramaniam et al., 2006). The mechanism of premature brain injury following haemorrhage remains somewhat conjectural with infarction and inflammation presumed to play a role (Kusters et al., 2009; Adler et al., 2010). In addition, autologous blood injection into neonatal mouse brains caused reduced expression of Ki67 protein, a marker of cellular proliferation, in the germinal matrix near the site of the haematoma (Xue et al., 2003). "
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    ABSTRACT: In premature infants, germinal matrix haemorrhage in the brain is a common occurrence. However, cell proliferation and fate determination in the normal human germinal matrix is poorly understood. Human ganglionic eminence samples were collected prospectively from autopsies of premature and term infants with no evidence of pathological process (n=78; dying at post-menstrual age 14-88 weeks). The ganglionic eminence was thickest at 20-26 weeks and involuted by 34-36 weeks. Proliferating cells, detected by Ki67 immunoreactivity, were abundant throughout the ganglionic eminence prior to 18 weeks, after which a sharp boundary between the dorsal and ventral ganglionic eminence appeared with reduced cell proliferation in the dorsal region. Ki67 immunoreactivity persisted in the majority of ventral cells until ∼28 weeks, after which time the proportion of proliferating cells dropped quickly. The expression of cell lineage markers (such as Olig2, SOX2, platelet-derived growth factor receptor alpha) showed partitioning at the microscopic level. The hypothesis that germinal matrix haemorrhage suppresses cell proliferation was then addressed. In comparison to controls, germinal matrix haemorrhage (n=47; born at post-menstrual age 18-34 weeks followed by survival of 0 h to 98 days) was associated with significantly decreased cell proliferation if survival was >12 h. The cell cycle arrest transcription factor p53 was transiently increased and the oligodendroglial lineage markers Olig2 and platelet-derived growth factor receptor alpha were decreased. Cell death was negligible. A low level of microglial activation was detected. Haemorrhage-associated suppression of cell proliferation in premature human infants could partially explain the reduced brain size and clinical effects in children who suffer germinal matrix haemorrhage after premature birth.
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