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From the Service de Neurologie Pédiatrique et Laboratoire de Neurologie du Développement (Drs. Kadhim, Tabarki, and Sébire, and A.-M. Rona); the Service de Néonatologie (Dr. Verellen), Cliniques Universitaires Saint Luc, Université Catholique de Louvain; and Unité de Neuropathologie (Drs. Kadhim and De Prez), Service d’Anatomopathologie, CHU Brugmann, Université Libre de Bruxelles, Brussels, Belgium.
Address correspondence and reprint requests to Dr. Hazim Kadhim, Neurologie Pédiatrique, Cliniques Universitaires Saint Luc, Avenue Hippocrate 10, 1200 Brussels, Belgium; e-mail: Hazim.Kadhim{at}nepe.ucl.ac.be
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-1ß and -6, tumor necrosis factor 
[TNF]), 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 TNF and to a lesser extent interleukin-1ß; 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: TNF immunoreactivity was significantly lower than the PVL group.
CONCLUSIONS: An immune-mediated inflammatory process may play a role in PVL. TNF, a myelinotoxic factor, may be the major mediator.
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