HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Aminoff, M. J. Search for Related Content PubMed PubMed Citation Articles by Aminoff, M. J.

Treatment of unruptured cerebral arteriovenous malformations

Department of Neurology, University of California, San Francisco, CA.

The presence of a cerebral AVM is a potential risk to a patient's life or quality of life. Pharmacologic maneuvers or partial obliteration of an AVM by non-operative means will help most of its nonhemorrhagic manifestations but do not influence the threat of intracranial bleeding, which is the major cause of morbidity and mortality. This risk is eliminated if the AVM is removed. Surgical treatment, however, also carries a risk, and it is therefore important to determine how this risk compares to that of conservative management before surgery is recommended in patients with unruptured AVMs. The present analysis suggests that the surgical mortality and morbidity, although considerably reduced in recent years, still generally precludes surgery for unruptured AVMs. The most favorable figures for surgery are properly applicable to small, superficial AVMs located in clinically silent areas of the brain in young and otherwise well patients who are to be operated upon by surgeons especially experienced in treating AVMs. Even using these favorable figures, however, there is no clear advantage to surgical excision over conservative management over a 20-year period unless AVMs have ruptured once, following which the risks of further episodes of hemorrhage are increased.

Address correspondence and reprint requests to Dr. Aminoff, Box 0114, Room 794-M, Department of Neurology, University of California, San Francisco, CA 94143.

Received March 10, 1987. Accepted for publication in final form March 12, 1987.

This article has been cited by other articles:

				T. Haitjema, C. J. J. Westermann, T. T. C. Overtoom, R. Timmer, F. Disch, H. Mauser, and J.-W. J. Lammers Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu Disease) New Insights in Pathogenesis, Complications, and Treatment Arch Intern Med, April 8, 1996; 156(7): 714 - 719. [Abstract] [PDF]