Abstract
A total of 21 cases diagnosed a "cerebral embolism" at autopsy were studied, Nine of 21 cases were softening and 12 were massive hemorrhage, The lesions and the arteries leading into the lesions were examined in detail by serial sections in an attempt to clarify the mechanism of softening and hemorrhage. The following are observed. 1) The cause of so-called "embolic cerebral softening" is not always "mechanical obstruction" of an artery by embolus, and so-called "embolic hemorrhage" is not diapedetic, but principally rhexisbleeding. 2) In both embolic softening and hemorrhage, the chief role is played by some small or chemical inflammatory agents carried from the heart or other sites to the meningeal and/ or intracerebral artery and inciting first a localized arteritis, and it is the arteritis which is the direct cause of the obstruction or rupture. 3) When the "localized arteritis" under-goes a proliferative or thrombusforming process, a stenosis or obstruction of the vessel and hence softening occurs. When it undergoes a exsudative or destructive process, a rupture and massive hemorrhage occurs. Sometimes both softening and hemorrhage can occur together in different parts of the same brain. 4) The arteritis causing obstruction or rupture appears most frequently in a. cerebri media and its branches. 5) The rupture in case of embolic hemorrhage occurs usually in "meningeal" arteries larger than 1.0mm in average diameter. It is essentially different from arterial rupture in hypertensive cerebral hemorrhage in which the rupture is caused by angionecrosis of "intracerebral" mall arteries measuring 200μ or less in diameter.
