Periventricular leukomalacia

The human brain has many parts, including the cerebral ventricles. The lateral ventricles belong to a category of cerebral ventricles, and the lateral ventricles also include white matter. These are all useful tissues for the human body, and they are also very important and indispensable. If there is a problem, it will cause very serious consequences to our body and affect our daily life, so we need to be extra careful. So what should we do if the white matter of the lateral ventricles softens?

It is a late change of hypoxic-ischemic encephalopathy and the main cause of cerebral palsy in premature infants (mainly spastic paraplegia or quadriplegia). PVL is a secondary leukoencephalopathy seen in premature infants and surviving children of postnatal asphyxia. Due to hypoxic-ischemic brain parenchyma damage, periventricular white matter softening occurs, leading to bilateral spastic hemiplegia, quadriplegia, and mental retardation. It is generally believed that PVL is related to ischemia, hypoxia and infection. PVL mainly damages axons and oligodendrocytes, but the pathogenesis is still unclear.

PVL is more common in premature infants, which may be related to the different brain damage mechanisms at different developmental stages. Brain abnormalities in the early and middle stages of pregnancy are mostly developmental malformations, while those in the late stage (last 3 months) are mostly cerebrovascular changes. The periventricular blood supply comes from the terminal arteries of the ventricular zone and the distal ventricular zone respectively. The collateral circulation of the deep branches of the terminal arteries of immature infants has not yet been established. This part is sensitive to ischemia and hypoxia at the beginning of the late pregnancy. The cortex is only affected when the lesion is very extensive. Therefore, PVL is more common in premature infants. By the late stage to the end of pregnancy, collateral circulation has been established and the sensitive areas have changed to the cortex, subcortical white matter and basal ganglia. Ischemic and hypoxic brain damage in full-term infants is more common in the above-mentioned areas.

Clinical diagnosis: PVL can lead to cerebral palsy (mainly spastic paraplegia and quadriplegia), mental retardation, convulsions, and various eye abnormalities such as nystagmus, strabismus, decreased vision, etc. Its clinical symptoms are closely related to CT and MRI changes. Its typical CT manifestations are: the body and triangular part of the lateral ventricle are enlarged and irregular in shape; the white matter around the triangular part and body is significantly reduced, and in severe cases, the white matter in the center of the semioval is also significantly reduced; the sulci and fissures are widened and deepened, and the subcortical gray matter directly approaches the ventricular wall, with almost no white matter components in between. MRI is more sensitive than CT, and its main manifestations are: high signal in periventricular white matter T2WI; enlargement of the body and triangular part of the lateral ventricle, with irregular shape; a significant decrease in white matter around the triangular part and body, and in severe cases, a significant decrease in white matter in the centrum semiovale; widening and deepening of cerebral sulci and fissures, and subcortical gray matter directly approaching the ventricular wall, with almost no white matter components in between.