Adjuvant embolization with N-butyl cyanoacrylate in the treatment of cerebral arteriovenous malformations: outcomes, complications, and predictors of neurologic deficits.

Adjuvant embolization with N-butyl cyanoacrylate in the treatment of cerebral arteriovenous malformations: outcomes, complications, and predictors of neurologic deficits.
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DOI:
10.1161/strokeaha.108.539775
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发表时间:
2009-08
期刊:
影响因子:
8.3
通讯作者:
Meyers PM
Meyers PM
中科院分区:
医学1区
文献类型:
--
作者:
Starke RM;Komotar RJ;Otten ML;Hahn DK;Fischer LE;Hwang BY;Garrett MC;Sciacca RR;Sisti MB;Solomon RA;Lavine SD;Connolly ES;Meyers PM

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评估脑动静脉畸形 (AVM) 辅助栓塞术后神经功能缺损的频率、严重程度和预测因素。从 1997 年到 2006 年,275 名 AVM 患者中有 202 名在显微手术 (n=176) 或放射外科 (n=26) 之前接受了栓塞治疗。患者在血管内栓塞术前后以及临床随访(平均 43.4±34.6 个月)时接受检查。根据改良Rankin量表(mRS)对结果进行分类。栓塞后新出现的神经功能缺损被定义为最小(总体 mRS 无变化)、中度(mRS≤2)或显着(mRS>2)。 202 名患者接受了 377 次栓塞手术。栓塞后总共出现 29 例新的临床缺陷(8% 的手术;14% 的患者),其中 19 例为中度或显着。随着时间的推移,大量患者的栓塞后缺陷得到解决(p<0.0001)。 5 名患者因栓塞而出现持续性神经功能缺损(手术的 1.3%;患者的 2.5%)。在多变量分析中,以下变量显着预测栓塞后新的神经功能缺损:复杂AVM,治疗计划指定不止一种栓塞程序(OR=2.7;95% CI,1.4-8.6),直径<3cm(OR=3.2;95%,CI 1.2-9.1),直径>6cm(OR=6.2;95% CI,1.0-57.0),深静脉引流(OR=2.7;95% CI,1.1-6.9)或雄辩位置(OR=2.4;95% CI,1.0-5.7)。对这些变量进行加权并用于计算每位患者的 AVM 栓塞预后风险评分。 0 分预测没有新赤字,1 分预测新赤字率为 6%,2 分预测新赤字率为 15%,3 分预测新赤字率为 21%,4 分预测新赤字率为 50% (p<0.0001)。大小、位置、深静脉引流以及需要多次栓塞手术的复杂血管解剖结构是发生栓塞后立即神经功能缺损的危险因素。然而,随着时间的推移,大量患有与治疗相关的神经功能缺损的患者得到了改善。永久性神经功能缺损的低发生率强调了该技术在精心挑选的患者中的实用性。
To assess the frequency, severity, and predictors of neurologic deficits following adjuvant embolization for cerebral arteriovenous malformations (AVMs). From 1997-2006, 202 of 275 AVM patients received embolization prior to microsurgery (n=176) or radiosurgery (n=26). Patients were examined before and after endovascular embolization, and at clinical follow-up (mean 43.4±34.6 months). Outcome was classified according to the modified Rankin Scale (mRS). New neurological deficits after embolization were defined as minimal (no change in overall mRS), moderate (mRS≤2), or significant (mRS>2). 202 patients were treated in 377 embolization procedures. There were a total of 29 new clinical deficits after embolization (8% of procedures; 14% of patients), of which 19 were moderate or significant. Post-embolization deficits resolved in a significant number of patients over time (p<0.0001). Five patients suffered persistent neurological deficits due to embolization (1.3% of procedures; 2.5% of patients). In multivariate analysis, the following variables significantly predicted new neurological deficit following embolization: complex AVM with treatment plan specifying more than one embolization procedure (OR=2.7; 95% CI, 1.4-8.6), diameter <3cm (OR=3.2; 95%, CI 1.2-9.1), diameter >6cm (OR=6.2; 95% CI, 1.0-57.0), deep venous drainage (OR=2.7; 95% CI, 1.1-6.9) or eloquent location (OR=2.4; 95% CI, 1.0-5.7). These variables were weighted and used to compute an AVM Embolization Prognostic Risk Score for each patient. A score of 0 predicted no new deficits, a score of 1 predicted a new deficit rate of 6%, a score of 2 predicted a new deficit rate of 15%, a score of 3 predicted a new deficit rate of 21%, and a score of 4 predicted a new deficit rate of 50% (p<0.0001). Small and large size, eloquent location, deep venous drainage, and complex vascular anatomy requiring multiple embolization procedures are risk factors for the development of immediate post-embolization neurological deficits. Nevertheless, a significant number of patients with treatment-related neurological deficits improve over time. The low incidence of permanent neurological deficits underscores the utility of this technique in carefully selected patients.