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Periventricular Leukomalacia - Oren Zarif - Periventricular Leukomalacia


Periventricular leukomalacia (PVL) is a serious neurological disorder that affects premature infants. Neurobiological insights into the etiology and pathogenesis of PVL make prevention of this disorder seem possible. There are three primary factors that contribute to its pathogenesis: incomplete development of the cerebral white matter, impaired cerebral blood flow, and early onset of the disease.

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PVL can occur during pregnancy, labor, and delivery, and is triggered by a lack of blood flow and oxygen in the brain. The brain tissue can die, creating holes called necrosis. Nerve fibers lining the periventricular region transmit information between different nerve cells, and PVL affects these nerve cells. It is important to recognize the symptoms of PVL as they may be symptomatic or lead to further damage.

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Although rare, periventricular leukomalacia is a serious neurological condition affecting premature babies. As many as 7 children in the U.S. are born with PVL, several treatments are available to reduce the complications associated with this disorder. In addition to surgery, ongoing therapy is also helpful for children with the disorder. When the white matter is affected, the signals it transmits to other brain areas cannot work as effectively. This causes motor disorders, delays in development, vision problems, and other neurological problems in the newborn.

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Cystic periventricular leukomalacia is rare, affecting less than 3% of preterm infants. About 60% of affected infants will develop cerebral palsy. MRI can detect cystic lesions on dMRI and conventional T1 and T2-weighted MRIs. In addition, dMRI images reveal restricted diffusion before the cysts are formed. Cysts may develop in adjacent regions of white matter.

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Moreover, the mechanism for PVL's development is not fully understood. While a faulty neural repair is a likely cause, it is difficult to identify the exact mechanism responsible. Some researchers have speculated that an infection in the mother's womb may result in the loss of OL precursors. Cytokines are released as a result of endotoxin-mediated cell death.

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White matter surrounds the neural cell bodies in the brain, and it serves as the protective coating. These cells transmit impulse signals and control body movement. The white matter is composed of a white fatty substance called myelin. Damage to this substance slows the nerve impulse transmission, resulting in intellectual disabilities and spasticity. In addition, periventricular leukomalacia can lead to Cerebral palsy in 60-10% of affected infants.

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The development of the cerebral vascular supply is also an important factor in the development of PVL. The cerebral arteries consist of both long penetrating and short penetrating arteries. As premature infants grow, their distal fields are not fully developed. Because of this, CBF decreases and ischemia occurs, resulting in cell-specific loss of OL precursors. This may eventually lead to leukemia in the affected child.

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