The pattern of distribution of impaired smallvessel reperfusion within the brain following varying lengths of circulatory arrest was studied in juvenile rhesus monkeys by means of a colloidal carbon perfusion. The brains of the animals perfused without prior circulatory stasis exhibited complete perfusion. Following ten minutes of circulatory arrest, discrete bilaterally symmetrical areas of non perfusion appeared in the inferior colliculus, in the region of the third and fourth cranial nerve nuclei, and in the putamen and thalamus. Periods of stasis of thirty and fifty minutes led to a striking, bilaterally symmetrical pattern of nonperfusion affecting chiefly the paracentral and anterior temporal cortices, as well as to more extensive confluent zones of no-reflow in the putamen, thalamus, and brainstem. Seventy minutes of circulatory arrest led to smaller zones of nonperfusion than occurred following stasis of thirty or fifty minutes. The tendency for the no-reflow process to focus primarily on the paracentral cortex resembles the tendency for a like distribution of injury following a variety of insults, including partial asphyxia in newborn monkeys. In addition, the occurrence of discrete areas of no-reflow centering on the inferior colliculus and third and fourth cranial nerve nuclei suggests a possible etiologic relationship of this process to the distribution of damage following episodes of total asphyxia in the newborn rhesus monkey or following total circulatory arrest in the juvenile monkey.
ASJC Scopus subject areas
- Clinical Neurology