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Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia


Periventricular leukomalacia is a form of white matter injury in premature neonates. The leukoencephalopathy leads to the formation of periventricular cysts and cavitation. This condition falls within the continuum of periventricular leukoencephalopathy and subcortical leukomalacia. It affects preterm infants and is most common among those that are less than 34 weeks gestation and weigh less than 1500 grams at birth. It can result in cerebral palsy or other intellectual disabilities.

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Periventricular leukomalacia is more common in premature or low birth weight babies. It affects approximately 20,000 to 30,000 premature babies. Approximately 7,000 will go on to develop cerebral palsy. Periventricular leukomalacia causes tight, swollen muscles and is linked to a greater risk of developing learning disabilities and cerebral palsy. A child suffering from this disorder will need treatment throughout his or her lifetime.

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Early diagnosis is important for children suffering from periventricular leukomalacia. In very young infants, symptoms of the condition may not be noticeable until a few months after birth. The condition may progress to other parts of the body. If not diagnosed, it can impact a child's ability to move freely. In addition to the brain damage, it can result in vision loss and hearing loss. Fortunately, the condition can be treated with specialized therapies.

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Despite the fact that the exact cause of periventricular leukomalacia is not known, it is commonly seen in premature infants. Approximately two percent of premature infants will develop some form of PVL. During birth, it can cause brain damage when the brain receives insufficient oxygen. When the membranes rupture too early, the risk of PVL is greater. Early rupture of the membranes and an infection inside the uterus are two other factors that are associated with the development of PVL.

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There are several causes of PVL, including inadequate oxygen and blood flow in the brain. A decrease in oxygen and blood flow may cause the death of glial cells that support the neurons in the nervous system. This damage may lead to white matter lesions in the brain. In some cases, this condition may be fatal, but it can be treated. With the proper treatment, PVL can be treated and even prevented.

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Approximately 7 infants born in the United States develop periventricular leukomalacia, a brain injury affecting the periventricular white matter. This area is filled with fluid and contains important nerve fibers that carry messages from the brain to the muscles. In addition to intellectual disability, the condition can cause spasticity and other cognitive impairments. It can also result in mental retardation, spasticity, and even vision problems.

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Symptoms of periventricular leukomalacia are often not noticeable until the baby is five or seven weeks of age. However, early detection can help to prevent periventricular leukomalacia. Early ultrasounds and clinical exams may be able to identify infants who are at risk for the disease, such as mothers with a family history of the disorder. Infants who are diagnosed with periventricular leukomalacia will require special care after leaving the hospital.

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The main neurologic handicap caused by periventricular leukomalacia is cerebral palsy. Children with the condition have extreme impairments in their daily lives. Sometimes, however, they do not have any symptoms at all. The severity of the impairments depends on the extent of damage to the white matter. This condition may even cause death. Therefore, proper diagnosis and treatment of periventricular leukomalacia is crucial for the care of the infant.

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The specific mode of cell death in periventricular WM injury may provide insights into the mechanisms of cellular injury in the periventricular leukomalacia. Cell death in early differentiating OLs results in apoptosis and necrosis, respectively. The latter type of cell death is most likely related to the degree of ischemia in PVL. In addition to the cell death mediated by cytokines, this damage can also be mediated by an endotoxin.

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Often, cystic lesions are incorporated into the lateral ventricles by the time a child reaches term-equivalent age. This results in a characteristic squared-off appearance of the posterior horns. This condition is associated with the development of neurodevelopmental and degenerative problems. This disorder can also affect brain development. It has the potential to cause brain damage. It can also lead to the death of myelinated axons.

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