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Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia

Often, periventricular leukomalacia is the cause of a number of motor, cognitive, and behavioral problems in premature children. This condition can be caused by medical negligence. As a parent, you may have the right to pursue legal justice for your child's condition. By completing a free case review, you can determine if your child has periventricular leukomalacia.

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A condition called periventricular leukomalacia involves damage to the white matter of the brain, which carries messages from the brain to the muscles. Premature babies are especially susceptible to developing this condition, and it can have devastating consequences. Patients with PVL may face delayed mental development, coordination problems, and vision impairment. PVL is treatable, but it should be addressed as soon as possible. If it's detected at an early stage, the disease may lead to other, more severe complications.

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The condition has been linked to cerebral palsy in as many as 4 to 6% of premature infants. Of the babies who survive, however, as much as 50% do, they will have significant motor and sensory deficits. Periventricular leukomalacia is the most common cause of cerebral palsy in premature infants. The symptoms of this condition are similar to those of other brain disorders, including cerebrovascular accident.

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The symptoms of periventricular leukomalacia include spasticity, intellectual disability, and developmental delay. In children, this condition affects the periventricular white matter, which houses the nerve fibers called axons. Damage to the white matter affects motor function, vision, and cognitive development. Children with PVL may experience spastic movements and cognitive problems, as well as problems with balance and coordination.

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The cause of PVL is unknown, but it is linked to decreased blood flow and oxygen to the brain. This causes damage to glial cells that support neurons throughout the nervous system. Among these cells are those in the cerebrum and in the cerebellum. These cells interact with neurons and become damaged by decreased blood flow. This sequence of events eventually leads to white matter lesions in the brain. In some cases, PVL is accompanied by cerebral palsy.

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In an effort to understand the cause of PVL, scientists have identified three factors that may contribute to the development of the disease. First, maternal/fetal infection may trigger the death of OL precursors. Second, bacterial lipopolysaccharide activates the innate immune system. The third factor concerns the vulnerability of OL precursors to ischemia and other insults. This has implications for the treatment of PVL.

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Another condition associated with periventricular leukomalacia is adrenalleukodystrophy. It results from a mutation in the PLP gene that causes the peripheral accumulation of very long-chain fatty acids. These fatty acids eventually build up in the brain, resulting in progressive demyelination. Another disorder linked to peroxisomal dysfunction is metachromatic leukodystrophy, which results from mutations in a lipid enzyme.

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Upon diagnosis of PVL, a cystic lesion is required to be present. These lesions usually develop within two to six weeks following the onset of injury. These cysts can be observed on sonograms as localized lesions. Further, periventricular leukomalacia can progress to end stage symptoms including ventriculomegaly, loss of periventricular white matter, and thinning of the corpus callosum.

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