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³úµ¿¸Æ·ù¼º ÁöÁÖ¸·ÇÏ ÃâÇ÷¿¡ ´ëÇÑ NimodipineÀÇ Ä¡·á È¿°ú Effects of Nimodipine Treatment on Aneurysmal Subarachnoid Hemorrhage

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Abstract

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1993³â 10¿ùºÎÅÍ 1995³â 6¿ù±îÁö ºÎ»ê´ëÇб³º´¿ø¿¡ ÀÔ¿øÇÏ¿© ³úµ¿¸Æ·ù ÆÄ¿­¿¡ ÀÇÇÑ ³úÁö
ÁÖ¸·ÇÏÃâÇ÷·Î È®ÁøµÇ¾î ¼ö¼ú¹ÞÀº 122·Ê¸¦ ¿¬±¸´ë»óÀ¸·Î nimodipineÀ» Åõ¿© ÇÑ ±º 63·Ê¿Í »ç
¿ëÇÏÁö ¾ÊÀº ±º 59·ÊÀÇ Ä¡·á °á°ú¸¦ ºñ±³ ºÐ¼®ÇÏ¿© ´ÙÀ½°ú °°Àº °á·ÐÀ» ¾ò¾ú´Ù.
1) NimodipineÀÇ Åõ¿©½Ã ÁöÁÖ¸·ÇÏ ÃâÇ÷ȯÀÚÀÇ ÀüüÀûÀÎ ¿¹Èĸ¦ Çâ»ó½ÃÅ°Áö ¸øÇÏ¿´´Ù.
2) Hunt¿Í Hess¿¡ ÀÇÇÑ µî±Þ, Fished CT grade¿¡ µû¸¥ ¾ç±ºÀÇ Ä¡·á °á°ú¸¦ ºñ±³ÇÏ¿´À»
¶§ Åë°èÇÐÀûÀ¸·Î´Â ÀÇ¹Ì ÀÖ´Â ¿¹ÈÄ Â÷À̸¦ ³ªÅ¸³»Áö ¾Ê¾Ò´Ù.
3) Áö¿¬¼º ³úÇãÇ÷ ½Å°æ°á¼ÕÀ¸·Î ÀÎÇÑ »ç¸Á·ü ¹× »ç¸Á¿øÀο¡¼­ niomodipineÅõ¿©±º°ú ´ëÁ¶
±º »çÀÌ¿¡ Åë°èÇÐÀûÀ¸·Î ÀÇ¹Ì ÀÖ´Â Â÷ÀÌ´Â ¾ø¾ú´Ù.
4) °íÇ÷¾ÐÀÌ ÀÖ´Â ±º¿¡¼­µµ nimodipineÀÇ Åõ¿©½Ã ´ëÁ¶±º°ú ºñ±³ÇÏ¿© Ä¡·á°á°ú¸¦ Çâ»ó½ÃÅ°
´Â °á°ú¸¦ ¾òÁö ¸øÇÏ¿´´Ù.
µû¶ó¼­ ³úÁöÁÖ¸·ÇÏÃâÇ÷ȯÀÚ¿¡¼­ nimodipineÀº Åõ¿©±º°ú ´ëÁ¶±º»çÀÌÀÇ Áö¿¬¼º ³úÇãÇ÷ ½Å°æ
°á¼Õ ¹ß»ýÀÇ ¿¹¹æ ¹× ¿¹ÈÄ Çâ»ó¿¡ ÀÇ¹Ì ÀÖ´Â ¿µÇâÀ» ¹ÌÄ¡Áö ¸øÇÏ¿´´Ù.
#ÃÊ·Ï#
Nimodipine, a potent, central active, calcium channel blocker, is known to relieve
vasospasm, increase cerebral blood flow(CBF) and affect positively on clinical outcome
in patients with subarachnoid hemorrhage. Experimentally, the potent effects on both
vascular dilation and increasing CBF were proven. However, there are still controversies
and may debates at present about the actual clinical effects nimodipine in subarachnoid
hemorrhage.
To evaluate the clinical effectiveness of nimodipine on aneurysmal subarachnoid
hemorrhage in our series, we analyzed 122 consecutive patients with ruptured aneurysms
who underwent operations between October, 1993 and June, 1995.
These patients were grouped as follow ; Group ¥° consisted of 63 cases(52%) in
which the patients were treated with nimodipine and Group ¥± consisted of 59
cases(48%) in which the patients were treated conventionally.
Administration of nimodipine was started immediately after the radiological diagnosis
of ruptured aneurysm. The dose of nimodipine was 0.5 §¶/kg/min via continuous
intravenous infusion for 7 to 10 days after the subarachnoid hemorrhage. After a course
of intravenous treatment, oral administration of nimodipine was then continued for up to
21 days after subarachinoid hemorrhage in a dose of 60§· every four hours.
We analyzed two groups based on patient's age, sex, aneurysmal location and size,
timing of surgery, presence of hypertension, Hung-Hess grade, presence of vasospasm
on preoperative angiography and Fisher's CT classification. We also analysed the
incidence of delayed ischemic deficits(DID) and outcome(GOS) in each group.
There were no significant differences in any of these parameters between
nimodipine-treated group and the control group(p>0.05) and also, no significant
differences in the distribution of DID or outcome between two groups(p>0.05).
Based on these results, we conclude that nimodipine does not provide any significant
beneficial effects on the prevention of DID and outcome in the patients with aneurysmal
subarachnoid hemorrhage.

Å°¿öµå

Aneurysmal subarachnoid hemorrhage; Nimodipine; Vasospasm; Delayed ischemic deficit(DID); Outcome.;

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