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Anoxic-Ischemic Encephalopathy in the Human Neonatal PeriodThe Significance of Brain Stem Involvement
Richard W. Leech, MD;
Ellsworth C. Alvord, Jr, MD
Arch Neurol. 1977;34(2):109-113.
Abstract
Although the human brain stem is considered relatively invulnerable to ischemic anoxia, evaluation of 16 cases of a single acute asphyxial episode either at or following birth indicates that such involvement is a frequent and characteristic aspect of anoxic encephalopathy in the infant. Ischemic cell change, neuronal loss, and nuclear or reticular formation gliosis were present in the brain stem of all but one infant. At least two topographic patterns of anoxic encephalopathy exist: (1) a rostrocaudal pattern of decreasing vulnerability, with the cerebral cortex being most sensitive and the brain stem least sensitive, and (2) a pattern of brain stem and thalamic damage. Of the two, the latter pattern appears to follow most acute asphyxial episodes in the human neonate and infant.
Author Affiliations
From the Department of Neuroscience (Neuropathology) (Dr Leech), University of North Dakota School of Medicine, Fargo, and the Laboratory of Neuropathology (Dr Alvord), Department of Pathology, University of Washington School of Medicine, Seattle.
Footnotes
Accepted for publication May 13, 1976.
Read before the 51st annual meeting of the American Association of Neuropathologists, New York, June 1, 1975.
Reprint requests to Department of Neuroscience (Neuropathology), University of North Dakota School of Medicine, 700 First Ave S, Fargo, ND 58102 (Dr Leech).
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