Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia

Periventricular leukomalacia (PVL) is a condition in which the white matter of the brain becomes damaged. White matter is the inner layer of the brain that transmits signals between nerve cells and the spinal cord. When this material is damaged, the child develops problems in their movements and coordination. Some children will develop epilepsy or cerebral palsy as a result of PVL.

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Premature infants have a lowered ability to regulate their blood flow and may experience hemorrhages. Insufficient blood flow can damage white matter in the brain. The spine and eyes may be affected, depending on the cause of the injury. Insufficient oxygen in the blood is one cause of PVL. Some children develop severe symptoms and others do not. Treatment depends on the specifics of each case.

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Periventricular leukomalacia is a condition in which there is an ischemic insult to the white matter of the brain. This damage results in periventricular cysts and cavitation. It corresponds to the continuous disease spectrum of subcortical leukomalacia. Most cases occur in premature infants who weigh less than 1500 grams at birth. It can cause intellectual and developmental disabilities, visual dysfunction, and spastic diplegia.

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There are several causes of PVL, and certain types of maternal infections may increase the risk of the condition. In some cases, the condition can be fatal and affect the development of the child's brain. However, medical professionals take preventative measures to reduce the risk of PVL in children by implementing therapeutic hypothermia. Further, pregnant women may reduce the risk of PVL by avoiding certain drugs, alcohol, or infections during pregnancy. Moreover, their overall health should be closely monitored and tested to determine if they are at risk for the condition.

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While there are no proven treatments for PVL, it is important to be aware of its complications, as early diagnosis is crucial. A physician must closely monitor infants who have been diagnosed with PVL to ensure that their progress is normal. In most cases, patients may experience some or all of these deficits. The prognosis of periventricular leukomalacia depends on the extent of white matter damage and the extent of motor impairment.

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The brain has a thin-walled structure, which makes hypoxia and ischemia a possibility. The thin walls of the fetal blood vessels do not have the ability to maintain sufficient blood flow during hypoxia-ischemic episodes. Cesarean section births may result in hypotension. Such episodes may damage the blood brain barrier, which contains endothelial cells. If the BBB is damaged, greater hypoxia and ischemia can occur.

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The development of PVL generally occurs within the uterus. Occasionally, it develops after the birth, but only when the infant is born prematurely or if the child has abnormal blood levels. The most common time for PVL to occur is during the infant's development, between 26 weeks and 34 weeks. This is because the brain continues to develop over time. The specific area affected by the condition depends on which side of the brain is injured.

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The pathogenesis of PVL shows a central role for OL death. In early developmental stages, premyelinating oligodendroglia are prone to free radical attack. Activation of microglia during this developmental window is associated with focal necrosis and apoptosis. The presence of an infectious agent may also cause the development of PVL. And apoptosis and inflammation are associated with PVL.

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There is no cure for PVL, but some experts believe that the lack of blood in the brain is one of the major causes. This may happen before, during, or after birth. Infants with PVL are preterm, and the risk of infection around the time of delivery is increased. Infection in the uterus may also contribute to the development of PVL. A premature infant's risk for developing PVL is higher when the baby was born before 32 weeks.

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PVL occurs in two primary components. A focal component, affecting the end zone of the cerebral WM, is characterized by localized necrosis and cyst formation. A diffuse component is characterized by injury to OL precursors, which develop into mature OLs and produce myelin in the cerebral WM. Acute or chronic condition of PVL is characterized by a decrease in cerebral blood flow and the emergence of a ventriculomegaly.