Periventricular leukomalacia (PVL) is a form of white-matter brain injury, characterized by the necrosis (more often coagulation) of white matter near the lateral ventricles.
[1][2] It can affect newborns and (less commonly) fetuses; premature infants are at the greatest risk of neonatal encephalopathy which may lead to this condition.
Affected individuals generally exhibit motor control problems or other developmental delays, and they often develop cerebral palsy or epilepsy later in life.
[1] Cysts occur when large and confluent focuses of PVL, with mixed necrosis (kollikvacia in the center and coagulation rim at the periphery).
Around the foci is generally defined area of other lesions of the brain white matter - the death of prooligodendrocytes, proliferation mikrogliocytes and astrocytes, swelling, bleeding, loss of capillaries, and others (the so-called "diffuse component PVL").
Some of the most frequent signs include delayed motor development, vision deficits, apneas, low heart rates, and seizures.
Those with white matter injury often exhibit "tight coupling" of leg joints (all extending or all flexing) much longer than other infants (premature and full-term).
Infants with PVL often exhibit decreased abilities to maintain a steady gaze on a fixed object and create coordinated eye movements.
[9] Seizures are typically seen in more severe cases of PVL, affecting patients with greater amounts of lesions and those born at lower gestational ages and birth weights.
It is estimated that approximately 3-4% of infants who weigh less than 1,500 g (3.3 lb) have PVL, and 4-10% of those born prior to 33 weeks of gestation (but who survive more than three days postpartum) have the disorder.
[9] These factors are especially likely to interact in premature infants, resulting in a sequence of events that leads to the development of white matter lesions.
[2] Additionally, hypotension resulting from fetal distress or cesarean section births can lead to decreased blood and oxygen flow to the developing brain.
"[13] In a study described by Miller, of 41 full-term newborns with congenital heart disease, 13 infants (32%) exhibited white matter injury.
Diffuse white matter lesions of the cerebral hemispheres of the brain, accompanied by softening and spreading to the central and subcortical areas are more likely DFL, PHI and ME.
Common methods for preventing a premature birth include self-care techniques (dietary and lifestyle decisions), bed rest, and prescribed anti-contraction medications.
Because white matter injury in the periventricular region can result in a variety of deficits, neurologists must closely monitor infants diagnosed with PVL in order to determine the severity and extent of their conditions.
Additionally, motor deficits and increased muscle tone are often treated with individualized physical and occupational therapy treatments.
Because neural structures are still developing and connections are still being formed at birth, many medications that are successful for treatment and protection in the adult central nervous system (CNS) are ineffective in infants.
Researchers have begun to examine the potential of synthetic neuroprotection to minimize the amount of lesioning in patients exposed to ischemic conditions.
Minor white matter damage usually is exhibited through slight developmental delays and deficits in posture, vision systems, and motor skills.
[20] Many of these affected patients exhibit some seizures, as well as spastic diplegia or more severe forms of cerebral palsy, before a diagnosis of epilepsy is made.
[21] On a large autopsy material without selecting the most frequently detected PVL in male children with birth weight was 1500-2500 g., dying at 6–8 days of life.