Role of Multiple Cerebral Microthrombosis in Symptomatic Cerebral Vasospasm: With a Case Report

Neurosurgery ◽  
1983 ◽  
Vol 13 (2) ◽  
pp. 199-203 ◽  
Author(s):  
Shigeharu Suzuki ◽  
Mikio Suzuki ◽  
Takashi Iwabuchi ◽  
Yoshimasa Kamata

Abstract In our studies of the pathogenesis of cerebral vasospasm, we have been emphasizing that microthrombosis may play an important role in the induction of cerebral ischemic symptoms or cerebral infarction. In this report, multiple microthrombi are demonstrated histologically to be a major cause of cerebral infarction in the autopsied brain of a 63-year-old woman who died from typical cerebral vasospasm that occurred after the rupture of an anterior communication artery aneurysm. We discuss the significance of thrombus formation and subarachnoid perivascular acidosis in vasospasm.

2017 ◽  
Vol 20 (3) ◽  
pp. 098
Author(s):  
Lu He ◽  
Ge-sheng Cheng ◽  
Ya-juan Du ◽  
Yu-shun Zhang

Patent foramen ovale (PFO) and pulmonary arteriovenous fistula (PAVF) have been both proposed as a mechanism for cerebral infarction. However, there are only a few reports on how to distinguish the role of the two factors in cerebral infarction.


Medicina ◽  
2016 ◽  
Vol 52 (6) ◽  
pp. 378-388 ◽  
Author(s):  
Eglė Sukockienė ◽  
Kristina Laučkaitė ◽  
Antanas Jankauskas ◽  
Dalia Mickevičienė ◽  
Giedrė Jurkevičienė ◽  
...  

Nosotchu ◽  
2011 ◽  
Vol 33 (1) ◽  
pp. 160-163 ◽  
Author(s):  
Hideo Saito ◽  
Hideki Matsuura ◽  
Takahiro Kohji ◽  
Tatsumi Yamanome ◽  
Kuniaki Ogasawara ◽  
...  

Neurosurgery ◽  
1981 ◽  
Vol 9 (6) ◽  
pp. 679-685 ◽  
Author(s):  
Shigeharu Suzuki ◽  
Eiji Sobata ◽  
Takashi Iwabuchi

Abstract The results of our previous experimental and clinical studies led us to the hypothesis that, in the pathogenesis of cerebral vasospasm, subarachnoid focal acidosis resulting from anaerobic changes of subarachnoid clots may be a factor upsetting the balanced synthesis of both thromboxane A2 and prostaglandin I2 from prostaglandin endoperoxides on the inner surface of cerebral arteries. Thus, there is a higher concentration of thromboxane A2, a prostanoid that causes arterial contraction and platelet aggregation. We tested the administration of trapidil, an antagonist and selective synthesis inhibitor of thromboxane A2, in a series of 20 cases for the prevention of cerebral vasospasm and cerebral ischemia after aneurysmal rupture. Vasospasm was demonstrated by angiography in 9 of these cases, but only 2 of the 9 showed mild signs of cerebral ischemia. Of the 20 patients, 15 were discharged from the hospital as cured and 3 had a neurological deficit at discharge. Our findings suggest the significance in symptomatic vasospasm of thrombus formation by platelet aggregation and the effectiveness of trapidil as a preventive.


2014 ◽  
Vol 75 (S 02) ◽  
Author(s):  
S. Heredero ◽  
J. Solivera ◽  
A. Romance ◽  
A. Dean ◽  
J. Lozano

1999 ◽  
Vol 81 (04) ◽  
pp. 601-604 ◽  
Author(s):  
Hiroyuki Matsuno ◽  
Osamu Kozawa ◽  
Masayuki Niwa ◽  
Shigeru Ueshima ◽  
Osamu Matsuo ◽  
...  

SummaryThe role of fibrinolytic system components in thrombus formation and removal in vivo was investigated in groups of six mice deficient in urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA), or plasminogen activator inhibitor-1 (PAI-1) (u-PA-/-, t-PA-/- or PAI-1-/-, respectively) or of their wild type controls (u-PA+/+, t-PA+/+ or PAI-1+/+). Thrombus was induced in the murine carotid artery by endothelial injury using the photochemical reaction between rose bengal and green light (540 nm). Blood flow was continuously monitored for 90 min on day 0 and for 20 min on days 1, 2 and 3. The times to occlusion after the initiation of endothelial injury in u-PA+/+, t-PA+/+ or PAI-1+/+ mice were 9.4 ± 1.3, 9.8 ± 1.1 or 9.7 ± 1.6 min, respectively. u-PA-/- and t-PA-/- mice were indistinguishable from controls, whereas that of PAI-1-/- mice were significantly prolonged (18.4 ± 3.7 min). Occlusion persisted for the initial 90 min observation period in 10 of 18 wild type mice and was followed by cyclic reflow and reocclusion in the remaining 8 mice. At day 1, persistent occlusion was observed in 1 wild type mouse, 8 mice had cyclic reflow and reocclusion and 9 mice had persistent reflow. At day 2, all injured arteries had persistent reflow. Persistent occlusion for 90 min on day 0 was observed in 3 u-PA-/-, in all t-PA-/- mice at day 1 and in 2 of the t-PA-/-mice at day 2 (p <0.01 versus wild type mice). Persistent patency was observed in all PAI-1-/- mice at day 1 and in 5 of the 6 u-PA-/- mice at day 2 (both p <0.05 versus wild type mice). In conclusion, t-PA increases the rate of clot lysis after endothelial injury, PAI-1 reduces the time to occlusion and delays clot lysis, whereas u-PA has little effect on thrombus formation and spontaneous lysis.


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