Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Levine, S. R.
Right arrow Articles by Welch, K.M.A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Levine, S. R.
Right arrow Articles by Welch, K.M.A.
NEUROLOGY 1989;39:515
© 1989 American Academy of Neurology

Intraluminal clot in the vertebrobasilar Circulation

Clinical and radiologic features

S. R. Levine, MD, D. J. Quint, MD, M. S. Pessin, MD, R. S. Boulos, MD and K.M.A. Welch, MD

Center for Cerebrovascular Dissase Research, Department of Radiology, Henry Ford Hospital, Detroit, MI (DR. Levine and Welch)
Department of Neurology, Department of Radiology, Henry Ford Hospital, Detroit, MI (Drs. Levine and Welch)
Division of Neuroradiology, Department of Radiology, Henry Ford Hospital, Detroit, MI (Drs. Quint and Bolos)
Department of Neurology, Tufts University School of Medicine, New England Medical Center, Boston, MA (Dr. Pessin).

We studied 15 patients with angiographically documented intraluminal clot in the vertebrobaeilar (VB) circulation and ischemic stroke. Progressive brainetem signs were the most common presentation; the neurologic deficit was maximum at stroke onset in 4. Seven experienced their first symptom during sedentary activities. Thirteen of the initial 15 CTs revealed infarcts in the VB temtory, 7 with multiple foci. Intraluminal clot was present in the vertebral artery in 7 patients (2 bilateral), bash artery in 7, posterior cerebral artery in 5, and superior cerebellar artery in 1. Multiple clots were seen in 5 patients. Stroke risk factors were present in the majority of cases. Although cardiac source embolism was the moat common single etiology (4 patients), most patients had other causes including migraine, coagulopathy associated with malignancy and nephritic syndrome in systemic lupus erythematosus, vertebral artery dissection with local embolism, delayed irradiation arteriopathy, and a bursiform, ectatic bask artery. Six (40%) died within 5 months of follow-up. Intraluminal clot in the posterior circulation is a marker for multiple stroke mechanism, not all of which are embolic. Intraluminal clot should prompt investigations into occult risk factors when no cause appears obvious.

Address correspondence and reprint requests to Dr. Levine. Center for Stroke Research. Department of Neurology, K-11, Henry Ford Hospital, 2799 W. Grand Blvd., Detroit, MI 48202.

Supported in part by NIH grant # NS23393 and the American Heart Association of Michigan (S.R.L.).

Presented in part at the fortieth annual meeting of the American Academy of Neurology, Cincinnati, OH, April 1988.

Received August 23, 1988. Accepted for publication in final form October 18, 1988.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by AAN Enterprises, Inc.