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Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia

Although the symptoms of periventricular leukomalacia are generally mild, some children with the disorder experience severe and permanent disabilities. Children with periventricular leukomalacia may develop epilepsy or cerebral palsy. While the symptoms of periventricular leukomalacia may not be obvious immediately after birth, they can develop months after birth. The most common symptom is cerebral palsy, characterized by stiff muscles in the legs, difficulty with movement, and developmental and learning disabilities. Hearing loss and vision problems are also possible. Treatment for periventricular leukomalacia is usually based on the severity of the disease.

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Premature babies are particularly susceptible to periventricular leukomalacia because their bodies lack the ability to regulate blood flow. During delivery, insufficient blood is delivered to the brain, causing hemorrhage. Insufficient blood oxygenates the white matter, leading to cognitive, motor, and vision impairment in babies with periventricular leukomalacia. In addition, premature babies are at risk for a variety of conditions including spastic quadriplegia and developmental delays.

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The pathogenesis of periventricular leukomalacia is unknown, but early differentiation of OLs is particularly vulnerable to free radical-mediated cell death. Both types of insult result in neuronal death via apoptosis and necrosis. The mode of cell death in periventricular leukomalacia depends on the severity of the insult. In moderate cases, OLs die from apoptosis, while severe damage causes necrosis.

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Premature infants are at higher risk for developing periventricular leukomalacia than full-term infants. Although the causes of PVL are not fully understood, the disease often occurs before or during pregnancy. Infection inside the uterus and premature rupture of membranes are also risk factors. If periventricular leukomalacia occurs, medical treatment is essential to help prevent the development of disabilities and the loss of life.

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The most common neuropathologic cause of infant brain damage, periventricular leukomalacia (PVL) is a leading cause of cerebral palsy and other cognitive disabilities in premature infants. Magnetic resonance imaging-based neuroimaging techniques (MRI) are particularly useful for PVL diagnosis, as they are more sensitive than head ultrasonography. MRI can also document involvement of telencephalic gray matter and long tracts, in addition to periventricular white matter. Furthermore, microglial activation and free radicals are hallmarks of PVL.

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In some severe cases, PVL is accompanied by hemorrhage in the periventricular-intraventricular region. This hemorrhage can lead to cerebral palsy. A thorough physical examination will help your doctor diagnose the disease. Your child may need further testing. Additional tests may include brain tissue images and cranial ultrasounds. If a diagnosis is made, you may need to undergo further testing.

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The underlying cause of periventricular leukomalacia is unknown. Researchers have identified a genetic variant of the peroxisome enzyme (PLP) that causes fatty acid accumulation in the brain. This mutation results in peripheral accumulation of very long-chain fatty acids in the brain, resulting in progressive demyelination. In addition, mutations in lipid enzymes in the brain can also cause adrenoleukodystrophy and metachromatic leukodystrophy.

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The earliest stage of PVL is grade I. This stage is usually characterized by limited cystic lesions that appear in the frontoparietal white matter. Acute insults may manifest as an echogenic region near the ventricular septum. The later stages represent total tissue necrosis, and may be characterized by Swiss-cheese-like patterns of multicystic leukoence.

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In infants with PVL, the risk for cerebral palsy increases significantly. Between 60 percent and 100% of these children will be diagnosed with cerebral palsy. Although the cause of PVL is unknown, the lack of blood and oxygen to the brain during delivery may contribute to the development of the disease. The premature infants with this disease are at increased risk for intraventricular hemorrhage, which increases the chance of developing PVL.

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