Pathogenesis of Hemorrhagic Infarction of the Brain

Introduction The pathogenic mechanism of the hemorrhagic or red cerebral infarct, as opposed to the pale or ischemic infarct, remains controversial. Clinical and pathologic observations have emphasized the close association that exists between cerebral hemorrhage and systemic arterial hypertension.¹However, cerebral hemorrhage is a different syndrome from that of hemorrhagic infarction, which frequently cannot be differentiated clinically from ischemic infarction. The demonstration of meningeal cortical anastomoses,²as well as radiologic evidence supporting the functional availability of such anastomotic channels in the presence of clinically obstructive vascular lesions,³points up the necessity for investigation of the exact role of collateral circulation in acute cerebral infarction. It is the purpose of this communication to report upon the experimental investigation of two major factors in the pathogenesis of the hemorrhagic cerebral infarct: first, the role of systemic arterial hypertension; and second, the role of meningeal cortical anastomoses in this mechanism.