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Stroke. 2008;39:2385-2387
Published online before print June 12, 2008, doi: 10.1161/STROKEAHA.107.505420
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(Stroke. 2008;39:2385.)
© 2008 American Heart Association, Inc.


Research Letters

Early Disruption of the Blood–Brain Barrier After Thrombolytic Therapy Predicts Hemorrhage in Patients With Acute Stroke

Andreas Kastrup, MD; Klaus Gröschel, MD; Thomas M. Ringer, MD; Christoph Redecker, MD; Robert Cordesmeyer, MD; Otto W. Witte, MD Christoph Terborg, MD

From the Department of Neurology (A.K., K.G., R.C.), University of Göttingen, Göttingen, Germany; and the Department of Neurology (A.K., K.G., T.M.R., C.R., O.W.W., C.T.), University of Jena, Jena, Germany.

Correspondence to Andreas Kastrup, MD, Department of Neurology, University of Göttingen, Robert-Koch-Str 40, 37075 Göttingen, Germany. E-mail andreas.kastrup{at}medizin.uni-goettingen.de

Background and Purpose— Leaks of the blood–brain barrier can be detected on postcontrast-enhanced T1-weighted MRIs. Although early disruptions of the blood–brain barrier appear to be an important risk factor for tissue plasminogen activator-related hemorrhages in rodents, little is known about their incidence and consequences in human stroke.

Methods— This is a retrospective analysis of a prospectively collected stroke database over the past 6 years. In 52 patients, multimodal MRI (including diffusion-weighted, perfusion-weighted, and postcontrast-enhanced T1-weighted MRI to detect blood–brain barrier changes) had been performed immediately before systemic thrombolysis and in 48 patients within a median of 30 minutes (interquartile range: 30 to 60 minutes) after recombinant tissue plasminogen activator treatment. The incidence of symptomatic hemorrhage (SICH), defined as any parenchymal hemorrhage leading to deterioration in the patient’s clinical condition, was related to several clinical and imaging variables, including early blood–brain barrier changes.

Results— Overall, SICH was detected in 9 (9%) patients and among these, 2 died. Although no blood–brain barrier changes were detectable before thrombolysis, 3 of 48 patients (6.25%) had a parenchymal gadolinium enhancement in the areas of initial infarction after tissue plasminogen activator treatment. All 3 patients developed SICHs at sites corresponding to the areas of enhancement. The presence of a parenchymal enhancement was significantly associated with SICH (P<0.01), whereas other clinical and imaging variables did not predict SICH in this series.

Conclusion— Early parenchymal enhancement after intravenous tissue plasminogen activator is significantly associated with subsequent SICH and could therefore become a useful imaging sign for the rapid initiation of preventive strategies in the future.


Key Words: thrombolytic therapy • hemorrhage • magnetic resonance imaging