Hiroshi Mihara

Is angiographic spasm real spasm

SummarySystematic morphological study of the cerebral arteries was made in six autopsy cases of ruptured aneurysms. The time course of the arterial luminal narrowing was observed by repeated angiograms, and segments of the narrowed arteries were studied histologically.Various histological changes were found consistent with the angiographic findings. We have devided these into three stages according to the duration of the disease.In the acute stage (less than one day) the contraction of the medial smooth muscle cells may be the main cause of the luminal narrowing. In the subacute stage, arteries showed a reduction in lumen size with medial thickening, marked corrugation of the internal elastic lamina, and thrombus formation attached to the endothelial surface. If vasoconstriction remained localized to the same segment for several days, the intimai or medial thickening and thrombus might produce the luminal narrowing consistent with the angiographic narrowing. In the chronic stage (more than two weeks), most cases showed dilatation of the arterial lumen on angiography. These arteries showed frank necrosis of the smooth muscle cells histologically. In a case which demonstrated progressive luminal narrowing on angiograms over 2 weeks, the arterial wall showed luminal narrowing with cellulofibrous thickening of the intima and organization of the thrombus.The presence of these structural changes in the narrowed arteries seen at angiography seems to be very important for proper understanding and treatment of vasospasm.

Arteriographically Visualized Extravasation in Hypertensive Intracerebral Hemorrhage

Seven cases are reported in which extravasation of contrast medium from the lateral lenticulostriate artery was observed on cerebral angiography performed in the early stage of hypertensive intracerebral hemorrhage. We advance the theory that continuous bleeding from the ruptured artery with mechanical destruction and displacement of cerebral tissue is the cause of massive hematoma formation, and discuss the possibility of surgical treatment of the acute stage of hypertensive intracerebral hemorrhage.

Cerebral angiographic study on C.V.D. in Japan.

have more C.N.S. vascular lesion, but less heart diseases than the other countries.1 In Japan, death rate from C.N.S. vascular lesion per 100.000 population, is increasing year by year, shown in Table 2, but death rate from malignant tumors was 107.2, and from heart diseases was 69.5 in 1964. However, C.N.S. vascular lesion, which is the largest cause of death in Japan, has not attracted its proportional share of interest and research funds, as have heart and cancer in Japan, as in United States.2 2

Surgical treatment of primary intracerebral hemorrhage- Part 1: new angiographical classification.

A new angiographical classification of primary intra* cerebral hemorrhage is presented. We have clarified the predilection sites of intracerebral hemorrhage and the advancing direction of the hematoma by studying autopsy cases. Furthermore, we tried to detect the presence or absence of destruction of the internal capsule and ventricular ventricular rupture by means of angiography. Our classification, introducing the idea of dynamic changes of hematoma advancement from localized to advanced type, can be applied to clinical practice. This classification, along with the patients level of consciousness, is felt to be the most important indication for operation.

Comparative angiographic and histological evaluations of intracranial atherosclerosis in hypertensive and normotensive subjects.

Cerebral atherosclerosis without luminal narrowing has been found macroscopically and by angiographic examinations in some patients with cerebral hemorrhage. In order to clarify the histology of non-stenotic atherosclerosis of the cerebral vessels, we examined cleared specimens and serial sections of the main trunks of the cerebral arteries. The middle cerebral artery was selected in 20 cases of cerebral hemorrhage and 7 cases of cerebral infarction. Non-stenotic atherosclerosis was found frequently in cases of cerebral hemorrhage, while most patients with cerebral infarction showed stenotic cerebral atherosclerosis. We counted the numbers of medial smooth muscle cells in 10 autopsied cases of cerebral hemorrhage and 6 of cerebralinfarction. The mean numbers of smooth muscle cells per unit area in the patientwith cerebral hemorrhage were less than those in cerebral infarction. In cerebral hemorrhage, the main trunks of the cerebral arteries were dilated, probably as a result of the damage to medial muscle cells and higher blood pressure during the course of intimal thickening. It is considered that arterial hypertension spreads to the peripheral, small arteries through the main trunks without luminal narrowing of the cerebral vessels.