engleski

Diagnosing venous stroke: tips and tricks with neurological-radiological correlation

Introduction/Objectives: Venous infarct is a rare form of stroke usually caused by occlusion of venous channels in cranial cavity. It accounts for 0.5% of all cerebrovascular diseases and usually affects younger population. Variable clinical presentation with a range of non-specific symptoms and often subtle imaging findings on initial computed tomography (CT) make diagnosis a challenge. The aim of this paper is to review role of the neuroradiological imaging in setting proper and timely diagnosis of venous stroke. Participants, Materials/Methods: We describe the most common radiological signs of venous stroke seen on CT and magnetic resonance imaging (MRI) on the example of three patients who were diagnosed at our department. Non-enhanced CT (NECT) and contrast-enhanced CT (CECT) are mandatory initial examination. MRI allows differentiation between newly formed, subacute and chronic thrombus based on signal intensities on T1 weighted images (T1W1) and T2 weighted images (T2WI) that depend on oxygenation state of hemoglobin and location of red blood cells. Fluid attenuated inversion recovery (FLAIR) sequence and T2WI are used to depict white matter edema. Results: Although unspecific, symptoms that were most frequently reported in our patients were headache, seizures occuring for the first time, suddenly altered mental state and nausea. First imaging modality performed in all patients was CT. Sign suggesting stroke of venous rather than arterial origin was vasogenic edema usually associated with hemorrhage in areas of brain which do not correspond to a typical arterial territory. Location of the infarction depended on the venous structure being occluded. Patients showed in this paper suffered from thrombosis of superior saggital sinus with consequent bilateral parasagittal occurence of stroke, occlusion of internal cerebral veins with stroke in both thalami or occlusion of inferior anastomotic vein (vein of Labbe) with infarction affecting temporal lobe. Given the presence of vasogenic edema it was important to consider other possible differential diagnosis besides venous thrombosis such as expansive lesions, posterior reversible encephalopathy syndrome (PRES), white matter edema surrounding intracerebral hematoma etc. In some cases obstruction of venous flow eventually led to cytotoxic edema as brain swelling caused compression on cerebral arteries, turning venous stroke into ischemia. Thrombus inside venous structures was visualized on NECT as hyperdense dural sinus or vein. Thrombosed confluence of sinuses showed a special appearance named delta sign on NECT and empty- delta sign on CECT. To confirm diagnosis, imaging was followed with MRI which more clearly showed intraluminal clot whose signal intensity was high on T1WI, implying subacute thrombosis. A lack of flow was observed on T2WI ( loss of „flow-void“ ) and more precisely on 2D time-of-flight (TOF) venography. Another sequence used to directly visualise the clot was susceptibility-weighted-imaging (SWI) which showed „blooming-artifacts“ representing hemosiderin deposits. Conclusions: Natural course of cerebral venous thrombosis can range from complete recovery to fatal outcome. Regardless of associated hemorrhage, it is the condition that requires administration of anticoagulation therapy. Neuroradiological imaging has a key role in diagnostic algorithm of venous stroke, with MRI being the most sensitive and specific modality.

stroke, thrombosis

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