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Published Online
on September 17, 2009

Stroke. 2009
Published online before print September 17, 2009, doi: 10.1161/STROKEAHA.109.563080
A more recent version of this article appeared on December 1, 2009
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Submitted on July 23, 2009
Revised on August 17, 2009
Accepted on August 19, 2009

Hypoplasia or Occlusion of the Ipsilateral Cranial Venous Drainage Is Associated With Early Fatal Edema of Middle Cerebral Artery Infarction

Wengui Yu MD, PhD*; Joanna Rives RN; Babu Welch MD; Jonathan White MD; Edward Stehel MD; and Duke Samson MD

From the Departments of Neurological Surgery (W.Y., J.R., B.W., J.W., D.S.), Neurology (W.Y.), and Radiology (B.W., E.S.), University of Texas Southwestern Medical Center, Dallas, Texas.

* To whom correspondence should be addressed. E-mail: Wengui.Yu{at}UTSouthwestern.edu.

Background and Purpose—Thrombosis of the cerebral venous sinus may cause venous congestion, cerebral edema, and infarction. The role of cerebrovenous disorders in arterial ischemic stroke is unknown. The objective of this study was to examine the contribution of ipsilateral cranial venous abnormalities to the development of cerebral edema in middle cerebral artery infarction.

Methods—This is a retrospective study of consecutive patients with large middle cerebral artery infarction admitted to our neurocritical care unit from January 2007 to October 2008. Medical records, laboratory data, and imaging of cerebral edema and cranial venous sinuses were analyzed.

Results—Of the 14 patients identified to have large middle cerebral artery infarction and images of cranial venous drainages, 5 (35.7%) had fatal edema with clinical signs of transtentorial herniation. Four of the 5 patients developed fatal edema within 48 hours of ictus and were found to have abnormal ipsilateral cranial venous drainage, including atresia of the transverse sinus (one), occlusion of the internal jugular vein (one), and hypoplasia of the transverse sinus and internal jugular vein (2). The fifth patient had symmetrical bilateral cranial venous drainages and fatal edema at Day 5. Of the 9 patients with nonmalignant middle cerebral artery infarction, all had ipsilateral dominant or symmetrical bilateral venous drainages.

Conclusions—In this small case series, we demonstrated that only the patients with hypoplasia or occlusion of the ipsilateral cranial venous drainage developed early fatal edema after large middle cerebral artery infarction. Our results suggest a role of cranial venous outflow abnormalities in the development of brain edema after arterial ischemic stroke.


Key words: fatal edema • cranial venous sinus • MCA infarction