Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia
Periventricular leukomalacia is a brain disorder affecting premature babies. It is caused by inadequate blood and oxygen supply to the inner brain tissue. It occurs most commonly in infants who are born prematurely and have hemorrhage in the brain. It can also occur in babies with ruptured amniotic sacs. Toxins in the blood, amniotic fluid, and brain tissue cause the membranes around the fetus to rupture prematurely.
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This condition can cause significant cognitive, sensory, and behavioral deficits in a few cases. The majority of premature infants survive, but five to ten percent develop severe motor and cognitive deficits. Among premature infants who die, periventricular leukomalacia is the most common cause of cerebral palsy. This condition has a wide range of clinical manifestations and has no cure. However, it has a genetic basis and a variety of treatments.
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Symptoms of periventricular leukomalacia are often difficult to notice. They depend on the severity of the damage. While the symptoms may vary from child to child, children with PVL frequently exhibit spastic diplegia, a form of cerebral palsy characterized by rigid movement. The condition can occur months after birth, requiring ongoing therapy. It is important to note that the condition can cause severe developmental delays and may lead to epilepsy.
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The symptoms of periventricular leukomalacia can vary, ranging from mild to severe. Mild cases may show no signs at all. More severe cases may appear months or years after birth. The most common symptom of PVL is cerebral palsy, which causes stiff muscles in the legs and affects development and learning. Other symptoms include vision loss and hearing loss. Fortunately, most cases of periventricular leukomalacia can be successfully treated with specialized therapies.
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When a child suffers from periventricular leukomalacia, it is not uncommon for the white matter of the cerebral cortex to be injured. The resulting damage to the cerebral white matter is characterized by microscopic necrosis and can be either focal or diffuse. A significant proportion of premature infants with PVL develop cerebral palsy, a disability that causes developmental problems. The condition can also lead to intellectual disability and cerebral palsy.
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In the neonatal period, cranial ultrasonography is able to detect focal PVL, but diffuse PVL is harder to diagnose. MRI may be helpful in identifying diffuse PVL, although more research is needed to determine the sensitivity of this technique. Conventional brain imaging is used for ventriculomegaly and myelin depletion. However, most of the available qualitative imaging data points toward diffuse PVL being more common than focal PVL.
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Although the prevalence of periventricular leukomalacia has declined to less than three percent of preterm infants, it is still an important risk factor for cerebral palsy. Infants with cystic PVL may have severe impairments or no symptoms at all. In some cases, the cell death in the periventricular leukomalacia may be so small that it is not even noticeable.
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The white matter that surrounds the periventricular regions of the brain is heavily involved in motor control. Therefore, those with the disease may exhibit a variety of motor problems, ranging from impaired balance to spasticity. Symptoms of PVL are difficult to detect early in development, although they may be obvious after initial diagnosis. The symptoms may not be immediately obvious at the onset of the condition, but they will develop over time.
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In early differentiation, OLs are vulnerable to free radical-mediated cell death. The specific mode of cell death may provide further insight into the molecular mechanisms of periventricular WM injury. In PVL, moderate insult causes apoptosis in the periventricular region, while severe insult results in focal necrosis. The first two factors may contribute to the development of PVL, while the third factor is related to the vulnerability of OL precursors to ischemia and other insults.
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While the exact cause of PVL remains unknown, the condition is thought to develop when blood flow to the brain is inadequate. The condition may occur during or after delivery. Although most cases of PVL occur in preterm infants, early rupture of the membranes and infection of the uterus are associated with the condition. Preterm infants are at increased risk of developing PVL because they have thinner brain tissue. And as the disease worsens with age, it is a significant cause of cerebral palsy.
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Although there is no specific cure for PVL, early detection can help avoid serious complications and potentially life-threatening outcomes. Often, PVL is not visible on ultrasound until about 8 weeks after birth. During this time, infants may not show any symptoms at all. The doctor may use a combination of methods to screen for the disease. This means that the doctor may have to perform an emergency c-section to deliver the baby.