PeriventricularLeukoˉmalacia (PVL) in children is a late change in ischemic-hypoxic encephalopathy and is a major cause of cerebral palsy (mainly spastic hypoparesis or tetraplegia) in preterm infants.PVL is a secondary cerebral white matter disease seen in preterm infants and surviving children with postnatal asphyxia due to ischemic-hypoxic brain parenchymal injury, causing periventricular white matter softening, resulting in bilateral spastic hemiplegia, tetraplegia, and mental retardation. It is now generally believed that PVL is associated with ischemia, hypoxia, and infection, and that PVL mainly damages axonal and oligodendrocytes, but the pathogenesis is not yet clear. PVL is more common in preterm infants, and its causes may be related to different mechanisms of brain damage at different developmental stages, with brain abnormalities in the early and middle stages of pregnancy being developmental malformations, and cerebrovascular changes in the late stages (the second trimester). The periventricular blood supply originates from the terminal arteries in the ventricular and distal ventricular regions, respectively. In immature children, the collateral circulation of the deep branches of the terminal arteries has not been established, and the part is sensitive to ischemia and hypoxia at the beginning of late pregnancy, and the cortex is only involved when the lesion is very extensive, so PVL is mostly seen in preterm infants. At the end of late gestation, the lateral branch circulation has been established, and the sensitive area changes to the cortical and subcortical white matter and basal ganglia areas, and ischemic and hypoxic brain injury in full-term infants is mostly seen in these areas. PVL can lead to cerebral palsy (mainly spastic bilateral lower limb palsy and quadriplegia), intellectual backwardness, convulsions, and various eye abnormalities, such as nystagmus, strabismus, and reduced visual acuity, etc. Its clinical symptoms are closely related to CT and MRI changes. MRI is more sensitive than CT, mainly showing: T2WI high signal in the white matter around the ventricles; enlargement of the body and triangle of the lateral ventricles, and irregular shape; enlargement of the body and triangle of the lateral ventricles. The white matter of the brain around the triangle and the body is significantly reduced, and in severe cases, the white matter in the center of the half-oval is also significantly reduced; the cerebral sulcus and fissure are widened and deepened, and the subcortical gray matter is directly adjacent to the ventricular wall, with little white matter between them. Ultrasound diagnosis fold Brain white matter softening early ultrasound can be seen around the ventricle white matter echogenic enhancement, the boundary is unclear, there is no occupancy effect, if there is no awareness of this, at this time is easy to miss the diagnosis, so in the cranial ultrasound examination, can show each ventricular section are required to observe its nearby brain white matter echogenic whether homogeneous, with or without echogenic enhancement, with the passage of time, its visible liquid cystic area, more easily detected by ultrasound! Neonatal ischemic-hypoxic encephalopathy and craniocerebral injury are common causes. Generally such children are mostly detected in the neonatal period, with a history of intracranial infection, intrauterine infection or birth injury. Cranial ultrasonography requires attention to the homogeneity of the brain white matter echogenicity, and the contrast between the early lesion and the surrounding normal tissue is not very obvious and easy to miss the diagnosis!