prospectively examined for periventricular leucomalacia (PVL) by cerebral ultrasound. Neurological PVH without PVL or ventricular dilatation, 10 of whom had. examined after fixation. The ultrasound diagnosis of either periventricular haemorrhage or periventricular leucomalacia was compared with the. the incidence of periventricular leucomalacia (PVL) and haemorrhage. Before collection Twenty one infants developed ventricular dilatation, 12 of whom had .

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It is important to note that both periventricular and subcortical leukomalacia correspond to a continuous disease spectrum. Please refer to the article on patterns of neonatal hypoxic—ischemic brain injury for a relation between perinatal brain maturation process and these lesions.

Ventriculwr likely occurs as a result of hypoxic-ischemic lesions resulting from impaired perfusion at the watershed areas, which in premature infants are located in a periventricular location.

It is likely that infection or vasculitis also play a role in pathogenesis.

The white matter necrosis often occurs in a characteristic leucomalwcia with the pattern being dorsal and lateral to the lateral ventricles and with involvement leeucomalacia the centrum semiovale, the optic trigone and occipital horns and acoustic temporal horn radiations. Cranial ultrasound provides a convenient, non-invasive, relatively low-cost screening examination of the haemodynamically-unstable neonate at the bedside. The examination also imparts no radiation exposure.


Sonography is sensitive for the detection of hemorrhage, periventricular leukomalacia and hydrocephalus. On ultrasound, hyperechoic areas are firstly identified in a distinctive fashion in the periventricular area, more often at the peritrigonal area and in an area anterior and lateral to the frontal horns periventricular white matter should be less echogenic than the choroid plexus.

These are watershed areas that are sensitive to ischemic injury. Follow-up scans in the more severely affected patients may reveal the development of cysts in these areas, known as cystic PVL when cystic PVL is present, it is considered the most predictive sonographic marker for cerebral palsy. Subsequent cavitation and periventricular cyst formation, features that are required for a definitive diagnosis of PVL, develop weeks after injury and are easily seen on sonograms as localized anechoic or hypoechoic lesions.

Progressive necrosis of the periventricular tissue with resulting enlargement of the ventricles is called end-stage PVL.

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Periventricular leucomalacia and intraventricular haemorrhage in the preterm neonate.

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