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Abstract
Background: Periventricular leukomalacia (PVL) affects the developing white matter of neonatal brain. Inflammatory and infectious conditions are implicated in the cause of PVL.
Methods: The authors investigated the in situ expression of proinflammatory cytokines (interleukin-1β and -6, tumor necrosis factor α [TNFα]), adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1) and inflammatory cell markers (CD68, leukocyte common antigen, human leukocyte antigen II) in 19 neonatal brains with PVL. The authors compared the findings with matched non-PVL brains.
Results: The inflammatory reaction detected at the early stage of PVL extends until the latest phase of cystic cavitation, though at an attenuated level. There is high expression of TNFα and to a lesser extent interleukin-1β; interleukin-6 remains undetectable. Cytokine immunoreactivity is detected in PVL cases both with and without infection. However, cytokine production was higher with infection. A different pattern of cytokine expression was observed in anoxic brains without PVL: TNFα immunoreactivity was significantly lower than the PVL group.
Conclusions: An immune-mediated inflammatory process may play a role in PVL. TNFα, a myelinotoxic factor, may be the major mediator.
- Received October 26, 2000.
- Accepted January 16, 2001.
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