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Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia


When a baby is born prematurely, a condition known as periventricular leukomalacia (PVL) may occur. It can affect the brain's white matter, which sends messages to the spinal cord and nerve cells. The affected part of the brain can cause the child to have difficulty with movement and balance. A child suffering from PVL is at risk for developing learning and physical disabilities such as cerebral palsy.

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In a premature baby, the body cannot regulate blood flow, so there can be hemorrhage. Insufficient blood can also cause oxygen-deprived white matter. In addition, the spine, ears, and eyes can be affected. The body's pH levels are affected, leading to acidosis and hypocarbia, which are conditions characterized by lack of carbon dioxide. These conditions can be life-threatening for a baby.

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The symptoms of periventricular leukomalacia depend on the severity of the condition. Mild cases can go unnoticed and cause no impairment. More severe cases may manifest months after birth. The most common symptom is cerebral palsy, resulting in stiffness in the legs and other movement problems. Children with this disorder may also develop visual dysfunction, hearing loss, and spastic diplegia.

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If the brain is injured during the pregnancy, there may be an increased risk of periventricular leukomalacia. The periventricular area of the brain contains important nerve fibers that carry signals from the brain to the muscles. Premature babies are especially at risk for developing this condition. Lack of oxygen and blood flow can result in brain tissue death. If PVL is left untreated, the baby may suffer from motor problems, vision impairment, and delayed mental development.

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While there is no cure for PVL, early detection is important for monitoring and treatment. A physician can identify if a child has the condition by looking at their medical history and performing physical exams. Further testing may include cranial ultrasounds, brain and spinal cord tissue images, and magnetic resonance imaging (MRI), which uses radio waves to create images of the brain and spinal cord. These procedures are essential for diagnosing this condition.

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An ischemic condition in which oxygen-rich blood is unable to reach the brain causes a lack of cytokine production in the PVL WM. This condition is also associated with maternal/fetal infection and inflammatory processes. A series of studies suggest that an inflammatory environment during pregnancy causes cytokine release. In addition to maternal/fetal infection, a series of studies have suggested that endotoxin is also responsible for the development of PVL.

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The first MR images of patients with PVL typically show only limited cystic lesions in the periventricular white matter. Grade II lesions usually occur in the frontoparietal white matter and coalesce into spastic diplegia. On follow-up scans, cysts can also develop. However, cystic PVL is considered the most accurate sonographic marker for cerebral palsy.

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Premature babies are at a higher risk for developing PVL than full-term infants. The major cause of PVL is not known, but it is thought to result from changes in blood flow to the area surrounding the ventricles of the brain, which is prone to injury before 32 weeks of gestation. Another risk factor is infection in the uterus at the time of delivery. While the exact causes of PVL remain unclear, it is known that it is more common in premature infants, as well as those with a history of intraventricular hemorrhage, and among preterm babies.

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If the damage to the white matter is severe, PVL can lead to extensive brain damage. Children with extreme cases of the condition may be quadriplegic or suffer from high muscle tone. Some patients also suffer from progressive loss of vision, especially in the eyes. In severe cases, a baby may be born blind and eventually become completely blind. Eventually, the brain may develop a new function, but the symptoms of PVL often go away on their own.

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