The rationale for routine cerebral ultrasound in premature infants.

Abstract

Premature birth is associated with brain lesionsmostly resulting from hypoxia-ischaemia and haemorrhage [1, 2]. Hypoxiaischaemia may give rise to periventricular leukomalacia (PVL) in either the focal form or the diffuse form [3]. Focal PVL is characterized by necrosis of all cell elements in the periventricular white matter, with the formation of cysts that progressively coalesce, resulting in ventricular enlargement with irregular outlines of the lateral ventricles and thinning of the periventricular white matter [3, 4]. Diffuse PVL is characterized by apoptotic cell death of the oligodendroglial precursors, resulting in hypomyelination and ventricular enlargement with regular outlines [3, 5]. An increased incidence (50%) of periventricular leukomalacia is reported in very-low-birthweight (≤1,500 g) premature infants, with the most severe cystic form representing only 5% [6]. Haemorrhagic lesions take the form of a continuum of germinal matrix haemorrhage, intraventricular haemorrhage and periventricular venous haemorrhagic infarction. The factors underlying the development of germinal matrix haemorrhage, which is apparently of venous origin, are increased vascularity, vascular immaturity and deficient autoregulation of cerebral blood flow [7]. Germinal matrix haemorrhage may progress to intraventricular haemorrhage, with or without ventricular dilatation. Periventricular haemorrhagic infarction is almost always associated with intraventricular haemorrhage, and compression of the paraventricular veins belonging to the deep Galenic system of drainage is thought to be the underlying cause [1, 2]. Germinal matrix haemorrhage with intraventricular haemorrhage occurs in 20% of very-low-birth-weight premature infants, while intraventricular haemorrhage associated with periventricular haemorrhagic infarction occurs in less than 5% of cases [6]. An increased incidence of periventricular haemorrhagic infarction is observed in infants with birth weight less than 750 g [6]. Post-haemorrhagic hydrocephalus, which can be communicating or non-communicating, is another complication of intraventricular haemorrhage [1, 2]. The incidence of posthaemorrhagic ventricular dilation is 36%, and this resolves in approximately 65% of cases [1]. Cerebellar abnormalities, mainly haemorrhage, infarction and underdevelopment, are being increasingly recognized and these have been associated with very low birth weight [4, 8]. Hemispheric haemorrhage, which is the most common cerebellar haemorrhagic lesion, is usually unilateral, starting in the external granular layer [8]. The less common vermian haemorrhage starts in the germinal matrix of the fourth ventricle [8]. The incidence of cerebellar haemorrhage is 17% in infants weighing less than 750 g and 2% in infants more than 750 g at birth [8]. Cerebellar infarction has been associated with supratentorial periventricular leukomalacia, and its reported incidence in an unselected population is 10–15% [9]. Underdevelopment is the most common cerebellar abnormality, for which the predisposing factors are extreme prematurity, very low birth weight, haemosiderin blood products, severe hypotension, large patent ductus arteriosus and transynaptic trophic effects [3]. Other acquired lesions of the premature brain are punctate white matter hyperintensities, perforator stroke and infectious lesions [10–12]. Punctate white matter hyperintensities are relatively common lesions (incidence 20%), occurring in the preterm period and decreasing in number at term-equivalent age [10]. Perforator stroke occurs in the distribution of lenticulostriate arteries, and in preterm neonates it is often subclinical [12]. Viral or fungal infections can affect the brain M. I. Argyropoulou (*) Department of Radiology, University of Ioannina Medical School, 45110 Ioannina, Greece e-mail: margyrop@cc.uoi.gr