| Research Abstract |
Materials & Methods : The just bleeding arteries of 45 cases of Intracerebral Hemorrhage (ICH) were identified directly during craniotomy, which were resected after hemostasis, fixed with formalin, embedded in paraffin. Serial sections cut 15 micrometer long, and stained with Elastica van Gieson's method. In addition to usual histopathological examinations, necessary serial sections were three-dimensionally reconstructed by a computer program TRI (Ratoc System Engineering Co.).
These 45 patients were showing good prognosis.
Results : 1)Locations of ICHs were 27 cases of putamen, 11 of white matter, 2 of thalamus, 4 of cerebellum, and 1 of pons.
2)Age of the patients at onset was 65.4+/-10.2 SD as a mean. Male suffered at 40s year-old, earlier than female. But after 50 year-old, male and female suffered constantly. This fact suggests us that ICHs might been not related with ageing, and it have to examine by much larger patients of ICHs.
3)As a relation to hypertension before onset, only 60%
… More
of the patients were hypertensive, and 20% were not, in addition, about 20% were unknown.
4)Among 45 cases, 3 cases were only coagulation tissue without any arteries. Excluding these 3 insufficient materials, all the 42 cases showed acute arterial dissections at 115 points. There were no atherosclerosis, medial necrosis (Oneda).
5)In addition, not rupture area of these dissecting arteries showed abnormal internal elastic lamina ( IEL) such as irregular thickening, disconnections, and torn looking like onion slices. But medial smooth muscle layer seemed intact. These abnormal IEL changes were thought to be the cause of acute cerebral arterial dissections resulting in ICHs : elastopathy.
6)By the way, one case revealed a Charcot-Boushard microaneurysm (MA), 700 micrometer in diameter, which was not ruptured but connected with an artery. In this case, ruptured and dissecting arteries were small, 50 micrometer in diameter, running around the MA. This MA consisted of collagen fibers, some of which were parallel running fibrils of collagen. There were no medial smooth muscle layer, no IEL. These were looking like never compensated intimal thickening by hypertension, but an adoventitia of the artery wall. This will be necessary to the further researches, the pathological sequences changing an artery to a MA. By the way, lumen of this MA was empty. We supposed that a MA had been dolichoectatic aneurysms of a basilar artery, but there were no organized thrombi within the lumen and no fragmentation of IEL, so this MA was different from dolichoectatic aneurysms of penetrating arteries.
Conclusion : The direct cause of ICHs is multiple acute arterial dissections of cerebral penetrating arteries. And this based upon the elastopathy. Less
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