Starke Robert M, Komotar Ricardo J, Otten Marc L, Hahn David K, Fischer Laura E, Hwang Brian Y, Garrett Matthew C, Sciacca Robert R, Sisti Michael B, Solomon Robert A, Lavine Sean D, Connolly E Sander, Meyers Philip M
Department of Neurosurgery, Columbia University, 710 West 168th Street, Room 428, Neurological Institute, New York, NY 10032, USA.
Stroke. 2009 Aug;40(8):2783-90. doi: 10.1161/STROKEAHA.108.539775. Epub 2009 May 28.
The purpose of this study was to assess the frequency, severity, and predictors of neurological deficits after adjuvant embolization for cerebral arteriovenous malformations.
From 1997 to 2006, 202 of 275 patients with arteriovenous malformation received embolization before 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. New neurological deficits after embolization were defined as minimal (no change in overall modified Rankin Scale), moderate (modified Rankin Scale < or =2), or significant (modified Rankin Scale >2).
Two hundred two 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. Postembolization deficits resolved in a significant number of patients over time (P<0.0001). Five patients had 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 after embolization: complex arteriovenous malformation with treatment plan specifying more than one embolization procedure (OR, 2.7; 95% CI, 1.4 to 8.6), diameter <3 cm (OR, 3.2; 95% CI, 1.2 to 9.1), diameter >6 cm (OR, 6.2; 95% CI, 1.0 to 57.0), deep venous drainage (OR, 2.7; 95% CI, 1.1 to 6.9), or eloquent location (OR, 2.4; 95% CI, 1.0 to 5.7). These variables were weighted and used to compute an arteriovenous malformation 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 postembolization 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 usefulness of this technique in carefully selected patients.
本研究旨在评估脑动静脉畸形辅助栓塞术后神经功能缺损的发生率、严重程度及预测因素。
1997年至2006年,275例动静脉畸形患者中有202例在显微手术(n = 176)或放射外科手术(n = 26)前接受了栓塞治疗。在血管内栓塞术前、术后及临床随访(平均43.4±34.6个月)时对患者进行检查。结果根据改良Rankin量表进行分类。栓塞后新出现的神经功能缺损被定义为轻微(改良Rankin量表总分无变化)、中度(改良Rankin量表≤2)或重度(改良Rankin量表>2)。
202例患者接受了377次栓塞手术。栓塞后共出现29例新的临床缺损(占手术的8%;占患者的14%),其中19例为中度或重度。随着时间推移,大量患者的栓塞后缺损得到缓解(P<0.0001)。5例患者因栓塞出现持续性神经功能缺损(占手术的1.3%;占患者的2.5%)。多因素分析显示,以下变量可显著预测栓塞后新的神经功能缺损:治疗计划为多次栓塞的复杂动静脉畸形(比值比[OR],2.7;95%置信区间[CI],1.4至8.6)、直径<3 cm(OR,3.2;95% CI,1.2至9.1)、直径>6 cm(OR,6.2;95% CI,1.0至57.0)、深部静脉引流(OR,2.7;95% CI,1.1至6.9)或功能区位置(OR,2.4;95% CI,1.0至5.7)。对这些变量进行加权并用于计算每位患者的动静脉畸形栓塞预后风险评分。评分为0预测无新缺损,评分为1预测新缺损率为6%,评分为2预测新缺损率为15%,评分为3预测新缺损率为21%,评分为4预测新缺损率为50%(P<0.0001)。
大小、功能区位置、深部静脉引流以及需要多次栓塞手术的复杂血管解剖结构是栓塞后即刻出现神经功能缺损的危险因素。然而,大量与治疗相关的神经功能缺损患者随着时间推移有所改善。永久性神经功能缺损的低发生率凸显了该技术在精心挑选患者中的实用性。