Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia

Periventricular leukomalacia (PVL) is an ischemic brain injury in premature neonates. The leukoencephalopathy occurs in the periventricular oligodendrocytes and is associated with a high risk of cerebral palsy and other intellectual disabilities. A periventricular leukomalacia diagnosis can be made through magnetic resonance imaging (MRI).

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The brain is made up of white and gray matter. Gray matter is the body of neural cells that initiate nerve impulses and white matter is the transporting medium between these cells. Periventricular leukomalacia occurs when the white matter in the brain is damaged, causing spasticity and intellectual impairment. Myelin is an important part of white matter, which coats the cell pathways and promotes fast nerve impulse transmission. However, it is not always easy to discern when a child has periventricular leukomalacia.

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Children with PVL are at risk for cerebral palsy if their periventricular leukomalacia has led to damage to the white matter in the brain. Fortunately, there are several treatment options that can minimize the complications of this disease, including surgery and ongoing therapy. In addition to cerebral palsy, there are other complications of PVL, such as vision problems and cognitive impairment. Nevertheless, the benefits of a PVL treatment are worth it for the child.

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PVL is characterized by the presence of cystic and noncystic forms of the disease. The first two forms exhibit macroscopic focal necrosis and evolve to glial scarring. The third type of PVL is called diffuse cerebral white-matter gliosis. Diffuse astrogliosis is a common brain disease in premature infants today. It is the most common form of PVL.

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Periventricular leukomalacia is a devastating condition in premature infants, with cognitive and neurologic deficits. Ninety percent of premature infants with PVL have some cognitive impairment. MRI-based neuroimaging techniques are superior for diagnosing PVL and often demonstrate involvement of telencephalic gray matter and long tracts in addition to the periventricular white matter. In the meantime, PVL is characterized by the loss of subplate neurons, which are essential to early organization of the cortex.

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The symptoms of periventricular leukomalacia vary depending on the severity of the condition. Mild cases may have no symptoms while more severe cases can produce symptoms months after birth. Typical symptoms include cerebral palsy, which leads to stiff muscles in the legs. It can also result in developmental and learning disabilities. Some children also experience vision problems, hearing loss, and spastic diplegia. Fortunately, the disease is treatable.

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The main substrate for cerebral palsy is a condition called periventricular leukomalacia. This condition is characterized by diffuse injury to deep cerebral white matter accompanied by focal necrosis. Classic neuropathology of PVL has generated several hypotheses regarding the cause of the disease, including free radical injury and cytokine toxicity. Other hypotheses have been associated with infection and maternofetum.

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Although there is no definite cause for PVL, researchers have noted a link between low blood flow and the lack of oxygen and blood supply in the brain. It may develop during or after birth, though it is most common in preterm infants. Premature birth and infection in the uterus have also been implicated in the development of this disorder. In addition, premature babies are at a higher risk for PVL than full-term infants.