BACKGROUND- The ependyma, the lining providing a protective barrier and filtration system separating brain parenchyma from cerebrospinal fluid, is still inadequately known in humans. In this study we aimed to define, by morphological and immunohistochemical methods, the sequence of developmental steps of the human ependyma in the brainstem (ventricular ependyma) and thoracic spinal cord (central canal ependyma) of a large sample of fetal and infant death victims, aged from 17 gestational weeks to 8 postnatal months. Besides we investigated a possible link between alterations of this structure, sudden unexplained fetal and infant death and maternal smoking. RESULTS- Our results demonstrated that in early fetal life the human ependyma shows a pseudostratified cytoarchitecture including many tanycytes and ciliated cells together with numerous apoptotic and reactive astrocytes in subependymal layer. The ependyma results fully differentiated, with a monolayer of uniform cells, by 32-34 gestational weeks. We observed a wide spectrum of ependymal pathological changes in sudden death victims, such as desquamation, clusters of ependymal cells in subventricular zone, radial glial cells, and the unusual presence of neurons within and over the ependymal lining. These alterations were significantly related to maternal smoking in pregnancy. CONCLUSIONS- We conclude that in smoking mothers, nicotine and its derivatives easily reach the cerebrospinal fluid in the fetus, immediately causing ependymal damages. Consequently, we suggest that the ependyma should be as first examined in depth in victims of sudden fetal or infant death with smoker mothers.

Ependymal alterations in sudden intrauterine unexplained death and sudden infant death syndrome: possible primary consequence of prenatal exposure to cigarette smoking / AM. Lavezzi, MF. Corna, L. Matturri. - In: NEURAL DEVELOPMENT. - ISSN 1749-8104. - 5:17(2010 Jul 19), pp. 17.1-17.9. [10.1186/1749-8104-5-17]

Ependymal alterations in sudden intrauterine unexplained death and sudden infant death syndrome: possible primary consequence of prenatal exposure to cigarette smoking

A. Lavezzi
Primo
;
M. Corna
Secondo
;
L. Matturri
Ultimo
2010

Abstract

BACKGROUND- The ependyma, the lining providing a protective barrier and filtration system separating brain parenchyma from cerebrospinal fluid, is still inadequately known in humans. In this study we aimed to define, by morphological and immunohistochemical methods, the sequence of developmental steps of the human ependyma in the brainstem (ventricular ependyma) and thoracic spinal cord (central canal ependyma) of a large sample of fetal and infant death victims, aged from 17 gestational weeks to 8 postnatal months. Besides we investigated a possible link between alterations of this structure, sudden unexplained fetal and infant death and maternal smoking. RESULTS- Our results demonstrated that in early fetal life the human ependyma shows a pseudostratified cytoarchitecture including many tanycytes and ciliated cells together with numerous apoptotic and reactive astrocytes in subependymal layer. The ependyma results fully differentiated, with a monolayer of uniform cells, by 32-34 gestational weeks. We observed a wide spectrum of ependymal pathological changes in sudden death victims, such as desquamation, clusters of ependymal cells in subventricular zone, radial glial cells, and the unusual presence of neurons within and over the ependymal lining. These alterations were significantly related to maternal smoking in pregnancy. CONCLUSIONS- We conclude that in smoking mothers, nicotine and its derivatives easily reach the cerebrospinal fluid in the fetus, immediately causing ependymal damages. Consequently, we suggest that the ependyma should be as first examined in depth in victims of sudden fetal or infant death with smoker mothers.
ependyma ; SIDS ; SIUD ; maternal smoking
Settore MED/08 - Anatomia Patologica
19-lug-2010
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/164806
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