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Full length article| Volume 112, ISSUE 2, P246-276, January 15, 1972

Two patterns of perinatal brain damage and their conditions of occurrence

  • Ronald E. Myers
    Affiliations
    Laboratory of Perinatal Physiology, National Institute of Neurological Diseases and Stroke, National Institutes of Health, United States Public Health Service, Department of Health, Education, and Welfare Bethesda, Maryland, USA
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DOI:https://doi.org/10.1016/0002-9378(72)90124-X
Two patterns of perinatal brain damage and their conditions of occurrence
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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

      DOI: https://doi.org/10.1016/0002-9378(72)90124-X

      Copyright

      © 1972 Published by Elsevier Inc.

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