What Is Periventricular Leukomalacia?
Periventricular Leukomalacia (PVL) is a late change of ischemic hypoxic encephalopathy in children, and is the main cause of cerebral palsy (mainly spastic lower limb paralysis or quadriplegia) in preterm infants. Secondary leukoencephalopathy, seen in surviving premature infants and postnatal asphyxia children, due to ischemic and hypoxic cerebral parenchymal damage, causes softening of white matter around the ventricle, resulting in bilateral spastic hemiplegia, quadriplegics, and poor intelligence. It is generally believed that PVL is related to ischemia, hypoxia and infection. PVL mainly damages axons and oligodendrocytes, but the pathogenesis is not clear. PVL occurs in premature infants, and the reason may be related to different damage mechanisms of the brain at different developmental stages. Brain abnormalities in early and middle pregnancy are mostly developmental malformations, and most of the late (after 3 months) are cerebrovascular changes. Periventricular blood supply is derived from the terminal arteries of the ventricular and distal ventricular regions. The collateral circulation of the deep branches of the terminal arteries in immature children has not yet been established. This part is sensitive to ischemia and hypoxia at the beginning of the third trimester. Only extensively affected, so PVL is more common in preterm infants. Later to the end of pregnancy, the collateral circulation has been established, and the sensitive area has been changed to the cortex and subcortical white matter and basal ganglia areas. Ischemic and hypoxic brain damage in term infants are more common in the above areas.
Periventricular Leukomalacia in Children
Overview of Periventricular Leukomalacia in Children
- Periventricular Leukomalacia (PVL) is a late change of ischemic hypoxic encephalopathy in children, and is the main cause of cerebral palsy (mainly spastic lower limb paralysis or quadriplegia) in preterm infants. Secondary leukoencephalopathy, seen in surviving premature infants and postnatal asphyxia children, due to ischemic and hypoxic cerebral parenchymal damage, causes softening of white matter around the ventricle, resulting in bilateral spastic hemiplegia, quadriplegics, 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 not clear. PVL occurs in premature infants, and the reason may be related to different damage mechanisms of the brain at different developmental stages. Brain abnormalities in early and middle pregnancy are mostly developmental malformations, and most of the late (after 3 months) are cerebrovascular changes. Periventricular blood supply is derived from the terminal arteries of the ventricular and distal ventricular regions. The collateral circulation of the deep branches of the terminal arteries in immature children has not yet been established. This part is sensitive to ischemia and hypoxia at the beginning of the third trimester. Only extensively affected, so PVL is more common in preterm infants. Later to the end of pregnancy, the collateral circulation has been established, and the sensitive area has been changed to the cortex and subcortical white matter and basal ganglia areas. Ischemic and hypoxic brain damage in term infants are more common in the above areas.
Clinical diagnosis of periventricular leukomalacia in children
- PVL can cause cerebral palsy (mainly spastic bilateral lower limb paralysis, quadriplegia), mental retardation, convulsions, and various eye abnormalities, such as nystagmus, strabismus, and decreased vision. The clinical symptoms are closely related to changes in CT and MRI. The typical CT manifestations are: the lateral ventricle body and triangle are enlarged and the shape is irregular; the white matter of the brain around the triangle and the body is significantly reduced; the white matter in the center of the semi-oval is also significantly reduced; the sulcus and fissures are widened and deepened. Subcortical gray matter directly approaches the ventricular wall, with little white matter in between. MRI is more sensitive than CT and mainly manifests as: T2WI high signal in the white matter around the ventricle; the body and triangle of the lateral ventricle are enlarged and the shape is irregular; the white matter in the triangle and around the body is 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.
Ultrasound diagnosis of periventricular leukomalacia in children
- Early ultrasound of cerebral white matter softening shows enhanced white matter echo around the ventricle, borders are unclear, and there is no placeholder effect. If there is no awareness in this area, it is easy to miss diagnosis at this time. Therefore, during the ultrasound examination of the brain, the sections of each ventricle need to be observed. Whether the white matter echoes in the vicinity of the brain are homogeneous, with or without echo enhancement. With time, the liquid cystic area can be seen, which is easier to be detected by ultrasound! Neonatal ischemic hypoxic encephalopathy and craniocerebral injury are common causes.
- Generally, such children are mostly detected in the neonatal period, and they have a history of intracranial infection, intrauterine infection, or birth injury. During the brain ultrasound examination, pay attention to whether the white matter echo is homogeneous, and the contrast between early lesions and surrounding normal tissues is not very good. Obviously, it is easy to miss diagnosis!