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  • Writer's pictureOren Zarif

Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia

Periventricular leukomalacia (PVL) is a form of brain injury in which white matter tissues suffer severe damage or death. This type of cerebral palsy is highly associated with the presence of this condition. The extent of the damage and the degree of impairment varies in each child. Children with PVL may have severe impairments or they may be asymptomatic. Cerebral palsy can result from the disease in 60 to 10% of children with PVL.

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The most common symptoms of PvL are developmental and cognitive disabilities. The severity of the symptoms varies, with mild cases not showing any signs of the disease at birth. In more severe cases, the child may have noticeable symptoms months after birth. The most common symptom is cerebral palsy, characterized by stiff muscles in the legs and difficulty moving. Developmental and learning disabilities may also arise. Other symptoms include vision loss, hearing loss, and coordination problems. While no cure exists for periventricular leukomalacia, the condition can be managed with special therapies.

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Premature babies are at increased risk for developing periventricular leukomalacia. The damage to the white matter of the brain may occur during birth or afterward. Premature children are at a higher risk for developing the disorder than normal-born children. The condition typically presents at six to nine months of age, when it is associated with developmental delays and learning disabilities. A child may also experience seizures.

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Treatments for PVL focus on improving the quality of life for the child with the disease.

The definitive diagnosis of PVL depends on the formation of a periventricular cyst. This characteristic may occur two to six weeks after injury and is visible on sonograms as localized lesions. Affected ventricles enlarge due to progressive necrosis of periventricular tissue. The condition progresses to end stage PVL, which includes loss of periventricular white matter and corpus callosum thinning.

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In addition to the lack of oxygen, PVL can be caused by the onset of maternal/fetal infections. This can cause inflammation and cytokine release in the brain and lead to the onset of PVL in premature infants. It can be inherited or acquired. The best way to diagnose PVL is through the help of an experienced doctor. You will need to undergo a detailed physical exam and have the affected area re-examined to ensure proper diagnosis.

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The main cellular target in PVL is the oligodendroglial precursor cell (OL). This type of cell is particularly sensitive to free radical attack, and it should therefore be studied for any possible correlation with this type of brain injury. While apoptosis is a common reaction in PVL, necrosis results from severe injury. If the periventricular leukomalacia is associated with atrophic damage, then a cystic PVL can be a good marker of cerebral palsy.

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The progression of PVL depends on its severity and location. Grade II PVL usually manifests as a limited cystic tumor in the frontoparietal white matter. It can coalesce into spastic diplegia. Meanwhile, Grade III PVL appears around the second or third week after an insult. This form represents total tissue necrosis and is located in the fronto-parieto-occipital region. The cysts tend to grow in size, merging with other tumors and causing irregular cavitation or Swiss-chees pattern.

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