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The Pathogenesis of
Cerebral Injury in the Newborn
Phillip B James Wolfson Hyperbaric Medicine Unit
The University of Dundee, Scotland, UK.
Birth involves the transfer of the function of oxygenation, the most
critical factor in life support from the placental circulation to
breathing. This transfer oroxygenation to the lungs of the neonate
requires major changes to the neonatal circulation. During labor,
placental blood flow is inevitably compromised by uterine contractions,
and if oxygenation falls below a critical level, then brain damage may
occur at this time. Prystowsky has suggested that mothers should breathe
100% oxygen during labor as a preventative measure, because of the
increased gradient for the delivery of oxygen to tissue. Premature
placental separation may also severely compromise fetal oxygenation and
delivery may also be associated with fetal brain tissue. In the last few
weeks of intrauterine life the cerebral circulation of the fetus matures
in preparation for birth. The changes are most prominent in the mid-brain
with increased vascularisation and maturation of the blood-brain barrier.
If delivery is premature the neonate is at special risk of damage because
these critical changes have not yet taken place. Ultrasonic imaging
through the anterior fontanelle allowed damage to the mid0brain to be
detected. Global oxygen deprivation may result in brain atrophy leading to
Microcephaly, but lesser degrees of hypoxia cause cerebral edema,
particularly in the midbrain where the nutrition of some the tissue is
dependent on the venous drainage. The increased tissue water content
reduces oxygen transport and if the edema is not resolved the basal ganlia
and the critical areas of the midbrain can undergo cystic degeneration.
The blood-brain barrier failure may also be associated with hemorrhage.
Damage to the internal capsules in cerebral medulla leads often involves
the internal capsules severing the pyramidal tracts. However, in many
cases the tracts continue to function for some time but myelination is
prevented leaving the axis cylinders exposed. This is associated with a
delay in the development of spasticity which may be as long as two years.
The additional gradient for the transport of oxygen that is provided by
breathing oxygen under Hyperbaric conditions may be able to prevent brain
damage in many children as Magnetic Resonance Spectroscopy can detect
hypoxia inferred from the presence of lactate it is possible to screen
infants at birth to identify those at risk. Even after a delay, the use of
hyperbaric -oxygen therapy may be beneficial by resolving the edema. This
may allow the completion of myelination and prevent the development of
spasticity.
A special
thankyou to the countless Drs and children whom have made this research
possible. All information contained within these pages are the sole
property of the Dr.s and experts that have spent the countless hours
researching for OUR CHILDREN. Please read each page of content and please
contact your local congressmen and appropriate government officials today.
Thankyou.
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Last updated
03/24/03
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