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Brain/Spine » Neonatal Brain
Periventricular leukomalacia
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Presentation Premature infant delivered at 29 weeks gestational age. Clinical course complicated by respiratory distress syndrome and hypotension.
 
 
 
Caption: Coronal image through anterior fontanelle
Description: Moderate ventricular dilitation is present with cystic changes in the periventricular white matter adjacent to the lateral ventricles.
 
 
 
Caption: Coronal image through anterior fontanelle.
Description: Moderate ventricular dilitation is shown with cystic changes in the periventricular white matter. A moderate subdural effusion is present over the convexity.
 
 
 
Caption: Semiaxial scan through anterior fontanelle.
Description: Cystic changes of PVL are present in the perventricular white matter adjacent to the lateral ventricles.
 
 
 
Caption: Sagittal scan of left lateral ventricle
Description: Subtle increase in periventricular echogenicity is seen at the trigone with a few small areas of cystic change.
 
 
 
Caption: Sagittal view left; lateral to ventricle.
Description: Cystic changes of periventricular leukomalacia are present in the white matter just lateral to the trigone of the left lateral ventricle.
 
 
 
Caption: Sagittal scan right lateral ventricle.
Description: Increased parenchymal echogenicity and cystic changes of PVL are present in the periventricular white matter.
 
Differential Diagnosis Periventricular leukomalacia 
Periventricular hemorrhage
 
Final Diagnosis Periventricular leukomalacia
 
Discussion Periventricular leukomalacia (PVL) is the result of an hypoxic - ischemic insult, occurs in 4 to 15% of very low birth weight infants and is a common finding at autopsy in prematurity. Many premature infants have both PVL and intracranial hemorrhage (ICH). Unlike periventricular hemorrhage, PVL is usually bilateral and symmetrical.

Sonographic findings in early stages consist of increased parenchymal echogenicity in the region of the optic radiations in the periventricular white matter near the trigones of the lateral ventricles. These changes may be subtle and may not be seen initially. Ultrasound reportededly has a sensitivity of only about 25-30% in the identification of acute changes of PVL.

In 15-20% of affected neonates, cavitary necrosis develops producing increased periventricular echogenicity and periventricular cystic changes. Ventricular dilatation due to atrophy may also develop. The majority of infants with PVL will later develop signs of cerebral palsy, with spastic diplegia being the most common form.
 
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