Periventricular leukomalacia

Periventricular leukomalacia
Classification and external resources
Specialty	pediatrics
ICD-10	P91.2
ICD-9-CM	779.7
DiseasesDB	9868
MedlinePlus	007232
eMedicine	ped/1773
MeSH	D007969
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Periventricular leukomalacia (PVL) is a form of white-matter brain injury, characterized by the necrosis (more often coagulation) of white matter near the lateral ventricles. It can affect newborns and (less commonly) fetuses; premature infants are at the greatest risk of the disorder. Affected individuals generally exhibit motor control problems or other developmental delays, and they often develop cerebral palsy or epilepsy later in life.

This pathology of the brain was described under various names ("encephalodystrophy", "ischemic necrosis," "periventricular infarction", "coagulation necrosis", "leukomalacia," "softening of the brain," "infarct periventricular white matter", "necrosis of white matter", "diffuse symmetrical periventricular leukoencephalopathy"), and more often by German scientists, but the worldwide dissemination was the term «periventricular leukomalacia», introduced in 1962 B. A. Banker and J. C. Larroche. The term can be misleading, as there is no softening of the tissue in PVL. V. V. Vlasyuk and V. P. Tumanov in 1985 published the world's first monograph devoted to PVL. Vlasyuk (1981) first revealed the high incidence of optic radiation lesions and demonstrated that PVL - a persistent process that the old necrosis can join a new, foci of PVL may be at different stages of development. In the process of morphogenesis focuses PVL pass through three stages: 1) necrosis, 2) resorption, and 3) the formation gliosis scars or cysts. Cysts occur when large and confluent focuses of PVL, with mixed necrosis (kollikvacia in the center and coagulation rim at the periphery). Around the foci is generally defined area of other lesions of the brain white matter - the death of prooligodendrocytes, proliferation mikrogliocytes and astrocytes, swelling, bleeding, loss of capillaries, and others (the so-called "diffuse component PVL"). However, diffuse lesions without necrosis are not PVL.

Those generally considered to be at greatest risk for PVL are premature, very low birth-weight infants. It is estimated that approximately 3-4% of infants who weigh less than 1,500 g (3.3 lb) have PVL, and 4-10% of those born prior to 33 weeks of gestation (but who survive more than three days postpartum) have the disorder. Gestational CMV infection also produces PVL in neonates.

Two major factors appear to be involved in the development of PVL: (1) decreased blood or oxygen flow to the periventricular region (the white matter near the cerebral ventricles) and (2) damage to glial cells, the cells that support neurons throughout the nervous system. These factors are especially likely to interact in premature infants, resulting in a sequence of events that leads to the development of white matter lesions.

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