Acute cerebral venous thrombosis, a typical case.

67-year-old woman with a personal history of Lupus and autoimmune thrombocytopenic purpura, attending to the emergency room due to speech reduction and behavior alteration since the previous day. On neurological examination, she presents with mixed aphasia and obeys simple but not complex orders. First, we perform an unenhanced head CT that shows hyperdensity of the left sigmoid and transverse sinuses, straight sinus, internal cerebral veins and vein of Galen with extension to the cortical Labbé vein draining into the transverse sinus. We completed the study with an IVC head CT, finding extensive filling defects in the same locations. As for the findings in the cerebral parenchyma, hemorrhagic infarction in subcortical region of the left temporal lobe, with signs of perilesional edema.

Our diagnosis was cerebral venous thrombosis (CVT). This entity is often underdiagnosed because it is an uncommon disease, clinical presentation is often nonspecific, and diagnostic imaging features can be subtle. There are multiple causes of CVT, can be classified as local (trauma, infection ...) or systemic, as in the case of our patient, typically due to hypercoagulability states such as Lupus. In 20–35% of cases, the cause remains unknown, therefore, one should remain suspicious, even in the absence of known risk factors. The most typical locations are the transverse and sigmoid sinuses. Direct signs of CVT on unenhanced CT are hiperdensity of dural sinus “dense clot sign”, and linear hyperdensity, of thrombosed cortical vein, “cord sign”. Indirect signs, include diffuse brain edema or decreased ventricular size. Venous infarction is the most specific indirect sign on unenhanced CT. Direct evidence of CVT on contrast-enhanced CT includes a filling defect (thrombus) in the dural sinus. In 10–30% of cases of CT findings are negative. Infarction not conforming to a major arterial vascular territory, involvement of a subcortical region, and extension over more than one arterial distribution, is highly suspicious for a venous cause and we should perform contrast-enhanced CT to rule out CVT.

CVT is a relatively uncommon but serious neurologic disorder. The clinical presentation is nonspecific. To avoid a delay in diagnosis, radiologists need to be aware of the various imaging features of CVT, which can be subtle. Prompt and appropriate medical therapy is important because brain parenchymal alterations and venous thrombus formation are potentially reversible. Unfortunately in our case after 24 hours, the hemorrhagic infarction had progressed due toanticoagulant therapy.

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