Loading…
Ependymal Changes in Sudden Infant Death Syndrome
The ependyma may befall a variety of pathogenic noxae during fetal life, resulting in histological changes which may persist after birth but are without clinical manifestations. Eight of a series of 19 children who died suddenly and unexpectedly, where no explanation as to the cause of death was fou...
Saved in:
Published in: | Journal of neuropathology and experimental neurology 1996-03, Vol.55 (3), p.348-356 |
---|---|
Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | The ependyma may befall a variety of pathogenic noxae during fetal life, resulting in histological changes which may persist after birth but are without clinical manifestations. Eight of a series of 19 children who died suddenly and unexpectedly, where no explanation as to the cause of death was found at autopsy, were shown to have diverse histological features involving the ependyma. Five μm paraffin-embedded brain tissue sections including frontal, temporal, occipital, and ventricular horns as well as the fourth ventricle were stained with hematoxylin-eosin (H&E) and luxol fast blue (LFB). Immunohistochemical stains using antibodies to glial fibrillary acidic protein (GFAP), vimentin and S-100 were also performed. Findings included areas of denuded and/or desquamated ependyma, rosettes in different stages of formation, vacuoles and/or pseudocysts, inflammatory changes consisting in macro- and microglial nodules in the subependymal layer, and gliosis. Chronic brain edema was seen in 4 cases. Our findings indicate that ependymal changes in sudden infant death syndrome (SIDS) cases belong to the prenatal or early postnatal period, thus providing, indirectly, a morphological substrate for the previous existence of a noxa that may also affect other CNS areas, and thus being in the position to produce cardiorespiratory control dysfunction |
---|---|
ISSN: | 0022-3069 1554-6578 |
DOI: | 10.1097/00005072-199603000-00010 |