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J Korean Neurosurg Soc. 1990 Jul;19(7):945-954. Korean. Original Article.
Huh YD , Yim MB , Son EI , Kim DW , Lee JK , Kim IH , Jeon DS .
Department of Neurosurgery, Keimyung University, School of Medicine, Taegu, Korea.
Department of Clinical Pathology, Keimyung University, School of Medicine, Taegu, Korea.
Abstract

It is known that antithrombin III is a potent vasodilator and plasmin is a vasoconstrictor, and some patients with a subarachnoid hemorrhage(SAH) develop clinical vasospasm and some patients do not. Under the hypothesis that the development of clinical vasospasm might depend on the difference of the blood level of antithrombin III in each patient with SAH and that the plasmin might have a role in the development of clinical vasospasm, we repeatedly checked the levels of blood antithombin III with a single radial immunodiffusion method and CSF fibrinogen degradation products(FDP : indirect indicator of plasmin activity) with a latex-test(Thrombo-Wellcotest(R)) during the period between 1-4, 5-11 and 12-24 days after a SAH in 29 patients. 10 patients with diseases except those with a SAH were selected as a control group. First, we analyzed the difference of the average of blood antithrombin III and CSF FDP between aneurysmal SAH patients and control patients and then, between patients with clinical vasospasm(8 cases) and patients without clinical vasospasm(21 cases). Secondly, we also analyzed the difference of these data between patients with clinical vasospasm and patients without clinical vasospasm according to the sampling day after a SAH. As a result, there was no statistical difference between the average blood level of antithrombin III in control and in SAH patients(29.06+/-3.04 vs. 25.61+/-6.95, respectively), and in patients with clinical vasospasm and in patients without clinical vasospasm(26.59+/-7.65 vs. 23.67+/-7.40, respectively). The average CSF levels of FDP is higher in SAH patients than in control patients(18.16+/-14.36 vs. 1.00+/-3.16, respectively : p<0.01). It is also higher in patients with clinical vasospasm than in patients without clinical vasospasm. However, there is no statistical significance(28.75+/-9.91 vs. 21.75+/-12.07, respectively : p>0.05). In the analysis of the average CSF levels of the FDP according to the sampling day after a SAH, even though the average levels is higher in patients with clinical vasospasm than in patients without clinical vasospasm(1-4 days : 31.43+/-14.64 vs. 27.33+/-16.24, 5-11 days : 23.75+/-17.68 vs. 18.10+/-16.32, 12-24 days : 32.50+/-13.89 vs. 18.82+/-16.54, respectively), a statistical significant difference was noticed only in levels which were checked between 12 and 24 days after a SAH(p<0.05). This study concludes that the blood level of antithrombin III shows no difference between the control and SAH patients, and patients with clinical vasospasm and patients without clinical vasospasm. Although it suggests a causal relationship between the FDP itself or plasmin in CSF and the development of clinical vasospasm, it does not justify any valid conclusion.

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