Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia
Despite the presence of numerous symptoms, periventricular leukomalacia is rarely diagnosed in newborns. The disease causes a range of developmental and intellectual impairment, and can also be a cause of spastic diplegia. Its causes are unknown, but certain maternal infections can cause it. Toxins released into the amniotic fluid can damage membranes surrounding the fetus, specifically injuring the developing brain. As a result, the membrane can prematurely rupture, leading to an early birth and other life-threatening complications.
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The white matter of the brain plays a vital role in transporting impulses from the spinal cord to the gray matter cells. Periventricular leukomalacia causes the cells of this region of the brain to die and impair their functions. It is common among infants and children with cerebral palsy, and can cause spasticity and intellectual impairment. As the white matter dies, the lateral ventricles begin to fill with fluid.
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Damage to periventricular leukomalacia is a leading cause of cerebral palsy in premature infants. In fact, 75% of premature infants who died shortly after birth had it. Toxins from intrauterine infections can selectively injure the brain's developing layers and cause premature membrane rupture. These toxins can occur at any time in a fetus' development, but researchers have isolated a number of critical stages.
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The first diagnosis for periventricular leukomalacia is a cerebral hemorrhage. Insufficient blood flow in premature infants causes hemorrhage. As a result, the white matter becomes deprived of oxygen. The condition may also lead to acidosis or hypocarbia, both conditions affecting the nervous system. The condition may be life-threatening or even fatal.
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Identifying a child with periventricular leukomalacia requires a thorough medical history. Testing for the disease can begin four to eight weeks after birth. Diagnostic tests include cranial ultrasounds and magnetic resonance imaging. While there is no definitive cure for periventricular leukomalacia, early detection of the disorder is important to preventing it from progressing further. It is important to remember that a diagnosis is often made only after numerous developmental assessments and tests have been performed.
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Although the cause of PVL is not entirely understood, symptoms of this disease include spasticity and cerebral palsy. A MRI will show areas of T1 hyperintensity in the periventricular white matter. Further testing may reveal cysts. The most important sonographic marker for cerebral palsy is cystic PVL. A patient with this condition is prone to cerebral palsy, but it is not always life-threatening.
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Treatment for PVL is dependent on the severity of the symptoms and the extent of white matter damage. Initially, the disease will cause a significant impairment in motor skills. In some cases, the symptoms of PVL will not show until the child has reached adolescence. However, if the disease is detected early enough, the child may be cured. But if they develop, the problem can still recur and the symptoms may be reversible.
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Besides the specific cause, the disease is associated with various genetic risks. Free radicals cause cell death in early differentiating OLs. The mode of cell death may provide insights into the molecular mechanisms of periventricular leukomalacia. However, the severity of the ischemia that causes OL death varies between mild and severe. A moderate insult, such as cerebral ischemia, results in apoptosis, while a severe insult results in focal necrosis.
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The symptoms of PVL are unique to each child. In most cases, they appear gradually, over time. The main reason for PVL is lack of blood flow to the brain's ventricles. Premature babies, however, have particularly fragile brain tissue, which makes them more susceptible to injury. Consequently, children with PVL are more likely to develop symptoms than healthy newborns. However, the severity of these symptoms is dependent on the side of the brain in which they were injured.