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Biomedical subjects

M Mizukami

Publications and source records attributed to M Mizukami.

17 recordsLinked to original sources
PubMed1979

[Arterial occlusion following cerebral vasospasm (author's transl)].

1. The present study analysed the clinical course, the serial angiograms and the CT scans of the patients with angiographic arterial occlusion following vasospasm after subarachnoid hemorrhage. The occlusion was observed in 6 out of 84 patients with vasospasm. 2. The angiograms which showed this phenomenon were obtained between the 11th and the 30th day of the illness. The affected vessels were the branches of middle cerebral artery. 3. Thrombus formed on the intima which had been injured by vasospasm is suspected to be a genesis of this arterial occlusion. The pathological findings of a case in this series support this concept. 4. The surgical procedure during the direct aneurysmal operation performed in the period of "smooth narrowing" seems to be a contributing factor to the arterial occlusion. There was no correlation between antifibrinolytic therapy and this phenomenon except in one case. 5. Fibrinolytic therapy after clipping of aneurysm may be a treatment of choice for this arterial occlusion following vasospasm.

Cerebral Angiography↗
PubMed1978

Fibromuscular dysplasia of the cervico-cephalic arteries.

Six cases of fibromuscular dysplasia of the cervical and cephalic portions of the internal carotid arteries, including their intracranial branches are reported. It should perhaps be pointed out that one of the cases was from the Sudan. As far as we know, the condition has never before been reported in a male African. The condition was associated with an intracranial aneurysm in four of our cases. To our knowledge only three autopsied cases of fibromuscular dysplasia involving intracranial arteries are on record. In our six cases the diagnosis was based on angiographic evidence, and three of the cases, two with intracranial involvement, were verified post mortem.

Adult↗
PubMed1976

Is angiographic spasm real spasm?

Systematic 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 intimal 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.

Acute Disease↗
PubMed1976

[Communicating hydrocephalus following the rupture of intracranial aneurysm (author's transl)].

It is well recognized that the communicating hydrocephalus following the rupture of intracranial aneurysms is one of the factors which cause the disturbance of consciousness in acute stage and the impairment of mental functions in chronic stage. In this report we analyzed the surgical experience with this complication and discussed the mechanisms which cause the ventricular dilatation. 1. The communicating hydrocephalus following the rupture of intracranial aneurysms is devided into the acute form and the chronic form. 2. Acute communicating hydrocephalus may develop with 24 hours after the onset and the incidence is about 10% (6 out of 66 cases). 3. Intraventicular pressure is high in acute communicating hydrocephalus and becomes normal in chronic stage. 4. The incidence of the chronic communicating hydrocephalus is about 10% (6 out of 66 cases). 5. There are two types of chronic communicating hydrocephalus. One develops from acute form and another develops gradually after onset. Among 6 chronic communicating hydrocephalus, 3 developed from acute form, 2 showed slowly progressive ventricular dilatation and 1 admitted with hydrocephalus at chronic stage resepctively. 6. The intraventricular pressure of the acute form is high and the chronic form shows high pressure in acute stage, intermittent high pressure wave lasting 20-30 minutes in subacute stage and normal pressure in chronic stage when the ventricle is dilated. 7. The mechanisms of ventricular dilatation in normal pressure hydrocephalus are discussed on the basis of the continuous monitoring of intraventricular pressure in cases with rupture of intracranial aneurysm. 8. Indication of shunting procedures whould be determined by combination of clinical pictures, ventriculocranial index, findings of cisternography and EEG. Our operative criteria are presented.

Acute Disease↗
PubMedDate not supplied

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 cerebral infraction. The mean numbers of smooth muscle cells per unit area in the patient with cerebral hemorrhage were less than those in cerebral infraction. 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.

Adult↗