(Stroke. 2002;33:1816.)
© 2002 American Heart Association, Inc.
Original Contributions |
From the Stroke Center, Neurological Institute, New York Presbyterian Hospital, New York (A.H., C.S., R.R.S., J.P.M., H.C.S., H.M.); Department of Interventional Neuroradiology, Columbia University, College of Physicians and Surgeons, New York, NY (A.H., J.P.-S.); Stroke Unit, Department of Neurology, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Berlin, Germany (A.H., C.S.); and Schlaganfallzentrum Halle, Stroke Unit, Berufsgenossenschaftliche Kliniken, Bergmannstrost, Halle, Germany (A.F., H.C.S., H.M.).
Correspondence to Andreas Hartmann, MD, Stroke Unit, Neurologische Klinik, Universitätsklinikum Benjamin Franklin, Hindenburgdamm 30, 1200 Berlin, Germany. E-mail ahart{at}zedat.fu-berlin.de
Background and Purpose Independently assessed data on frequency, severity, and determinants of neurological deficits after endovascular treatment of brain arteriovenous malformations (AVMs) are scarce.
Methods From the prospective Columbia AVM Study Project, 233 consecutive patients with brain AVM receiving
1 endovascular treatments were analyzed. Neurological impairment was assessed by a neurologist using the Rankin Scale before and after completed endovascular therapy. Multivariate logistic regression models were used to identify demographic, clinical, and morphological predictors of treatment-related neurological deficits. The analysis included the components used in the Spetzler-Martin risk score for AVM surgery (AVM size, venous drainage pattern, and eloquence of AVM location).
Results The 233 patients were treated with 545 endovascular procedures. Mean follow-up time was 9.6 months (SD, 18.1 months). Two hundred patients (86%) experienced no change in neurological status after treatment, and 33 patients (14%) showed treatment-related neurological deficits. Of the latter, 5 (2%) had persistent disabling deficits (Rankin score >2), and 2 (1%) died. Increasing patient age [odds ratio (OR), 1.04; 95% confidence interval (CI), 1.01 to 1.08], number of embolizations (OR, 1.41; 95% CI, 1.16 to 1.70), and absence of a pretreatment neurological deficit (OR, 4.55; 95% CI, 1.03 to 20.0) were associated with new neurological deficits. None of the morphological AVM characteristics tested predicted treatment complications.
Conclusions From independent neurological assessment and prospective data collection, our findings suggest a low rate of disabling treatment complications in this center for endovascular brain AVM treatment. Risk predictors for endovascular treatment differ from those for AVM surgery.
Key Words: arteriovenous malformations embolization, therapeutic outcome
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