| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 2008;39:741.)
© 2008 American Heart Association, Inc.
Editorials |
From the Department of Neuroradiology (M.B.), University of Würzburg, Germany; and the Department of Neurosurgery (B.M.), Technical University of Munich, Germany.
Correspondence to Bernhard Meyer, Department of Neurosurgery, Technical University of Munich, Ismaningerstr 22, 81675 München, Germany. E-mail bernhard.meyer@lrz.tum.de
Key Words: AVM
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
See related article, pages 878–885.
Cerebral arteriovenous malformations (AVM) represent a heterogeneous entity, and a multitude of classifications for this rare disorder exists. Moreover, data on different treatment regimens are controversial.1
In this issue of Stroke, Lasjaunias et al2 present a group of vascular malformations which they consider a distinct entity separate from other brain AVM and classify them as cerebral proliferative angiopathy. Criteria for this classification were predefined almost 20 years ago and included angiomorphological, cross-sectional imaging and in one case also histopathological data. In a large patient cohort of >1400 patients 49 patients (3.4%) were found to meet these criteria. Clinical signs included seizures, headaches and nonhemorrhagic neurological deficits. Angiography demonstrated a diffuse nidus, stenosis of the proximal arteries in almost 40% and a transdural supply in almost 60% of the cases. This angiographic appearance was considered as typical for this disorder. In 1 case with a histopathological work-up the authors found normal-appearing neural tissue in between pathological AVM vessels.
Notwithstanding the authors vast experience, one must recognize that the conclusions are derived from a retrospective analysis of a huge database installed primarily for clinical quality management reasons and not for this particular study purpose. This alone introduces a definite element of bias. Furthermore, only the clinical data of both classical AVM and cerebral proliferative angiopathy were compared, and it remains unclear how frequently angiographic and histological findings considered as typical for cerebral proliferative angiopathy were also present in classic AVM. In this respect one must
Related Article:
Stroke 2008 39: 878-885.
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2008 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |