Diffuse axonal injury in periventricular leukomalacia as determined by apoptotic marker fractin.

Abstract:

:Periventricular leukomalacia (PVL), the major substrate of neurologic deficits in premature infants, is associated with reduced white matter volume. Using immunomarkers of axonal pathology [beta-amyloid precursor protein (beta-APP) and apoptotic marker fractin], we tested the hypothesis that widespread (diffuse) axonal injury occurs in the gliotic white matter beyond the foci of necrosis in PVL, thus contributing to the white matter volume reduction. In a cohort of 17 control cases and 13 PVL cases with lesions of different chronological ages, diffuse axonal damage in PVL was detected by fractin in white matter sites surrounding and distant from acute and organizing foci of necrosis. Using beta-APP, axonal spheroids were detected within necrotic foci in the acute and organizing (subacute) stages, a finding consistent with others. Interestingly, GAP-43 expression was also detected in spheroids in the necrotic foci, suggesting attempts at axonal regeneration. Thirty-one percent of the PVL cases had thalamic damage and 15% neuronal injury in the cerebral cortex overlying PVL. We conclude that diffuse axonal injury, as determined by apoptotic marker fractin, occurs in PVL and that its cause likely includes primary ischemia and trophic degeneration secondary to corticothalamic neuronal damage.

journal_name

Pediatr Res

journal_title

Pediatric research

authors

Haynes RL,Billiards SS,Borenstein NS,Volpe JJ,Kinney HC

doi

10.1203/PDR.0b013e31816c825c

subject

Has Abstract

pub_date

2008-06-01 00:00:00

pages

656-61

issue

6

eissn

0031-3998

issn

1530-0447

pii

00006450-200806000-00012

journal_volume

63

pub_type

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