PERIVENTRICULAR LEUKOMALACIA BRAIN INJURY
Category: Child Health
Abstract : periventricular leukomalacia (ischemic brain injury) Periventricular leukomalacia (PVL) is the most common ischemic brain injury in premature infants. The ischemia occurs in the border zone at the end of arterial vascular distributions. The ischemia of PVL occurs in the white matter adjacent to the lateral ventricles. The diagnostic hallmarks of PVL are periventricular echodensities or cysts de
periventricular leukomalacia (ischemic brain injury)
Periventricular leukomalacia (PVL) is the most common ischemic brain injury in premature infants. The ischemia occurs in the border zone at the end of arterial vascular distributions. The ischemia of PVL occurs in the white matter adjacent to the lateral ventricles. The diagnostic hallmarks of PVL are periventricular echodensities or cysts detected by cranial ultrasonography.
Diagnosing PVL is important because a significant percentage of surviving premature infants with PVL develop cerebral palsy (CP), intellectual impairment, or visual disturbances.
Pathophysiology: The two major theories propounded in the pathophysiology of PVL are: (1) Watershed injury to the periventricular area due to a vascular insult and/or (2) maternal chorioamnionitis or vasculitis with the production of cytokines leading to inflammatory damage to the periventricular area in the developing brain.
PVL is a bilateral white matter lesion of premature infants that may result from hypotension, ischemia, and coagulation necrosis at the border or watershed zones of deep penetrating arteries of the middle cerebral artery. Decreased blood flow affects the white matter at the superolateral borders of the lateral ventricles. The site of injury affects the descending corticospinal tracts, visual radiations, and acoustic radiations. Premature infants on mechanical ventilation may develop hypocarbia. Several studies have linked hypocarbia, particularly in the first few days of life, with the development of PVL. In addition to possible ischemic injury, PVL may be the result of edema fluid and hemorrhage causing compression of arterioles in the white matter. Premature infants have impaired cerebrovascular autoregulation and are susceptible to intracranial hemorrhage (ICH) as well as PVL. Many premature infants have both PVL and ICH detected on ultrasonography.
In a recent 1999 epidemiologic study, Leviton et al provided a detailed careful analysis of maternal infection, placental inflammation, and vasculitis and their relationship to PVL. They observed that fetal inflammatory response, as reflected by fetal vasculitis (polymorphonuclear leukocyte infiltration in the chorionic plate or umbilical cord), and not intra-amniotic infection damages the fetal brain. Maternal infection (as reflected by maternal antibiotic administration) is also associated with fetal brain damage, although not as a result of fetal brain infection. Furthermore, various maternal cytokines have also been implicated in the pathogenesis of PVL.
Following the initial insult, whether ischemia- or cytokine-mediated, white matter damage occurs. The white matter damage may occur because of selective loss of oligodendroglia. However, in 2001, Dammann and coworkers offered support that white matter damage involves axons as well as oligodendrocytes.
Frequency:
• In the US: Incidence of PVL ranges from 4-26% in premature infants in neonatal intensive care units (NICUs). Incidence of PVL is much higher in reports from autopsy studies of premature infants. As many as 75% of premature infants have evidence of PVL on postmortem examination.
Mortality/Morbidity:
• Cerebral palsy: Approximately 60-100% infants with PVL later develop signs of CP. Spastic diplegia is the most common form of CP following mild PVL. Severe PVL is frequently associated with quadriplegia.
• Intellectual impairment: Varying degrees of intellectual impairment, developmental impairment, or both have been reported in association with PVL.
• Visual dysfunction: Fixation difficulties, nystagmus, strabismus, and blindness have been associated with PVL. Some cases of visual dysfunction in association with PVL occur in the absence of retinopathy of prematurity, suggesting damage to optic radiations as causation.
Age: PVL occurs most commonly in premature infants younger than 32 weeks' gestation at birth.
History: PVL occurs most commonly in premature infants born at less than 32 weeks' gestation and less than 1500 g birth weight. Most infants have a history of cardiorespiratory problems, such as respiratory distress syndrome or pneumonia, in association with hypotension or patent ductus arteriosus.
Physical: Initially, most premature infants are asymptomatic. If symptoms occur, they usually are subtle. Symptoms may include the following:
• Decreased tone in lower extremities
• Increased tone in neck extensors
• Apnea and bradycardia events
• Irritability
• Pseudobulbar palsy with poor feeding
• Clinical seizures (may occur in 10-30% of infants)
Causes:
• Mechanically ventilated premature infants born at less than 32 weeks' gestation are at greatest risk for PVL.
• Hypotension, hypoxemia, and acidosis may result in ischemic brain injury and PVL.
• Marked hypocarbia in ventilated premature infants has been associated with increased risk of developing PVL.
• Other associated risk factors include the following:
o Placental vascular anastomoses, twin gestation, antepartum hemorrhage
o Chorioamnionitis and funisitis
o Maternal cocaine abuse
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