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AJNR - American Journal of Neuroradiology

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American Journal of Neuroradiology 26:607-613, March 2005
© 2005 American Society of Neuroradiology

BRAIN

Reversible MR Imaging Abnormalities following Cerebral Venous Thrombosis

Carina Röttger^a, Susan Trittmacher^b, Tibo Gerriets^a, Franz Blaes^a, Manfred Kaps^a and Erwin Stolz^a

^a Department of Neurology Justus-Liebig–University, Giessen, Germany
^b Department of Neuroradiology, Justus-Liebig–University, Giessen, Germany

Address reprint requests to Erwin Stolz, MD, Department of Neurology, Justus-Liebig-University, Am Steg 14, D-35385 Giessen, Germany; e-mail: erwin.stolz{at}neuro.med.uni-giessen.de

BACKGROUND AND PURPOSE: Although rare, cerebral venous thrombosis (CVT) is being diagnosed more frequently owing to improved imaging techniques. The venous infarcts caused by CVT in 50% of patients are largely reversible and differ from arterial stroke. Our purpose was to study the time-dependent changes of venous infarcts on MR images and to define the variables that influence lesion volume in humans.

METHODS: MR images and venous angiograms were evaluated in 15 consecutive patients with venous infarcts due to CVT of sinus, cortical, or internal veins. All patients were treated with intravenous dose-adjusted heparin followed by oral anticoagulation for 12 months. Reduction of signal intensity changes on T1- and T2-weighted images was correlated to the degree of recanalization, age, initial absolute lesion size, and hemorrhage.

RESULTS: Within the first 30 days, we found a significant correlation between the volume of the lesion on T1-weighted images and recanalization. However, early recanalization did not influence the final lesion volume after 12 months. Eleven patients showed complete resolution of changes on T1- and T2-weighted images. Age of the patients influenced initial absolute volume of brain damage.

CONCLUSION: In venous stroke, even large parenchymal changes can resolve completely independent from recanalization of the thrombosed veins and sinuses. A plausible hypothesis is that venous infarcts largely consist of a persistent edema and that the lesion volume is influenced by the development of collateral veins. However, further investigations are necessary to understand the underlying abnormal mechanisms.

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