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Abstract
Term monkey fetuses may be subjected to episodes of total asphyxia characterized by complete stoppage of respiratory gas exchange. Such animals,
after resuscitation and extended survival, exhibit damage to structures in their brainstems.
This injury pattern fails to resemble that found after perinatal damage in the human
being. Term monkey fetuses subjected to episodes of partial asphyxia, on the other hand, exhibit injury to structures in the hemispheres. This
damage, when severe, may consist of a total bilateral hemispheral necrosis. With less
severe injury, the necrosis may be restricted to the middle third of the paracentral
region and/or to the basal ganglia. After prolonged survival, areas of necrosis are
transformed into areas of nodular cortical atrophy, white matter sclerosis, and status
marmoratus of the basal ganglia. These eventual long-term, static lesions closely
compare to the lesions of human perinatal injury or cerebral palsy. Episodes of in
utero fetal partial asphyxia may be brought about in a variety of ways, many of which,
in one fashion or another, reduce maternal blood flow through the placenta. Retardation
of placental intervillous space perfusion, in turn, diminishes the net exchange of
respiratory gases between the mother and the fetus and leads to varying degrees of
hypoxia, hypercarbia, and acidosis. Episodes of fetal bradycardia and hypotension
following uterine contractions (Type II dips) may appear with severe asphyxia. Such
hypotensive episodes may be associated with impairments of cerebral perfusion which,
when repeated, may contribute to fetal brain injury. Maternal stimulation with exogenous
or endogenous catecholamines leads to fetal asphyxia by producing maternal visceral
vasoconstriction, thereby reducing maternal blood flow to the uterus. The tendency
for perinatal asphyxia to be associated with myocardial injury and heart failure is
emphasized. More babies die of cardiovascular failure secondary to myocardial injury
than survive less severe disturbances in heart action to exhibit brain damage.
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Article Info
Publication History
Received:
August 6,
1971
Footnotes
☆Invited address delivered at the 2nd Congress of the International Association for the Scientific Study of Mental Deficiency, August 1970, in Warsaw, Poland.
Identification
Copyright
© 1972 Published by Elsevier Inc.