PATHOLOGY OF CEREBRAL INFARCTION, WITH SPECIAL

Abstract

In 31 cases of cerebral infarction (24 cases of the infarction of the thalamus and the basal ganglia and 7 cases of that of the cerebral cortex), the cerebral arteries, especially those supplying the infarcts were investigated histologically in order to elucidate arterial lesions which are considered to be the cause of the infarction. Further, morphogenesis of these arterial lesions were discussed.1) Out of 84 infarcts in the thalamus and the basal ganglia, 62 (74%) were resulted from stenosed cerebral arteries owing to arteriosclerosis and 22 (26%) were derived from thrombosis at the site of angionecrosis (fibrinoid degeneration of cerebral arteries), or from the so-called “nodular lesions of the arteries”.On the other hand, 5 of 8 infarcts in the cerebral cortex were resulted from occlusion by thrombi which were formed on atherosclerotic plaques of meningeal arteries, and the remaining 3 (38%) were caused by arteriosclerotic stenosis without thrombosis.2) Cerebral arteriosclerosis (atherosclerosis, intimal lipoidosis and intimal fibrosis) in arteries with diameters of above 150μ were resulted from insudation of plasma protein and lipid into cellulofibrous intimal thickening at the bifurcation (bifurcation-pad). In smaller arteries with diameters of below 150μ, arteriosclerosis was started by insudation of plasma into the intima without predilection either for the bifurcation or for other. That is the development of arteriosis, which was followed by the secondary prolifelation of subendothelial cells and became to be arteriosclerosis.3) Atherosclerosis of the cerebral arteries were classified into two types, α and β. In the former, the atheroma was formed as the result of destruction of increased intimal collagenous fibers showing fatty swelling, while in the latter it was resulted from necrosis and destruction of aggregated intimal form cells. The β type atherosclerosis was predominant in the cerebral arteries.4) Pseudocalcification in the wall, especially in the media of the arteries running through the globus pallidus, induced or enhanced intimal lesions (intimal edema, intimal fibrosis and atherosclerosis), and was the common cause of the infarction of the globus pallidus.5) Angionecrosis of the cerebral arteries, which is the cause of hypertensive intracerebral hemorrhage, was seen in the 91. 7% of the cases of infarction of the thalamus and of the basal ganglia. There was multiple occurrence of this lesion in the lenticulostriate arteries and the thalamic arteries.6) The angionecrosis was commonly found in the intracerebral arteriosclerotic arteries about 150μ in diameter, and when the change was severe, the arteries exhibited aneurysmal dilatation with hemorrhage into the arterial walls. This suggests that in the course of cerebral infarction, cerebral hemorrhage is apt to be induced.7) The so-called k nodular lesions of the arteries were produced when the thrombi formed on the angionecrotic walls were organized together with fibrinoid substance in the arterial walls.8) Multiple occurrence of angionecrosis was seen not only in cerebral infarction cases with hypertension but also in those without hypertension (27%). Because arterial lumina were stenosed by arteriosclerotic changes at many bifurcations on the proximal side of the angionecrotic arteries, it is considered that not only hypertension but also hypoxidosis resulting from decreased blood flow would participate in the morphogenesis of the angionecrosis in cerebral infarction.