Abstract
The pattern of neonatal brain lesions associated with hypoxia-ischemia depends not only on the severity of the event but also on gestational age at birth. The immature brain of preterm babies reacts to hypoxia-ischemia differently than does the brain of full-term babies [1, 2]. White matter lesions are mainly observed in premature babies, whereas gray matter lesions are predominant in full-term babies. Germinal matrix and intraventricular hemorrhage, parenchymal venous hemorrhagic infarction (PVHI), post-hemorrhagic hydrocephalus, and periventricular leuko-malacia (PVL) with a focal necrotic and a diffuse component represent the spectrum of lesions responsible for the encephalopathy of prematurity [2]. Parasagittal watershed infarcts, injury to the basal ganglia, and the perirolandic cortex or more extensive lesions associated with macrocystic encephalomalacia comprise the spectrum of lesions following hypoxia-ischemia in the full-term baby [3–5]. Stroke is an important cause of mortality and morbidity in the neonatal period [6, 7]. Neonatal stroke is less common than adult stroke but more common than that in childhood, and the carotid artery territory is most commonly affected [6, 7].
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© 2012 Springer-Verlag Italia
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Argyropoulou, M.I. (2012). Hemorrhage, Stroke, and Ischemia of the Neonatal Brain. In: Hodler, J., von Schulthess, G.K., Zollikofer, C.L. (eds) Diseases of the Brain, Head & Neck, Spine 2012–2015. Springer, Milano. https://doi.org/10.1007/978-88-470-2628-5_37
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DOI: https://doi.org/10.1007/978-88-470-2628-5_37
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