Leech R W, Alvord E C
Arch Neurol. 1977 Feb;34(2):109-13. doi: 10.1001/archneur.1977.00500140063013.
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.
尽管人类脑干被认为相对不易受缺血性缺氧影响，但对16例出生时或出生后单次急性窒息发作的病例评估表明，这种受累情况是婴儿缺氧性脑病常见且具有特征性的方面。除1例婴儿外，其余所有婴儿的脑干均存在缺血性细胞改变、神经元丢失以及核或网状结构胶质增生。缺氧性脑病至少存在两种拓扑模式：（1）易损性递减的头尾模式，其中大脑皮层最敏感，脑干最不敏感；（2）脑干和丘脑损伤模式。在这两种模式中，后一种模式似乎在人类新生儿和婴儿的大多数急性窒息发作后出现。
