Sinus Thrombosis jugular6c

Cerebral Venous Thrombosis. (Left) T1-weighted axial MRI; (Middle) T2-weighted axial MRI, (Right) Flair axial MRI. Note the lesion in the left temporal / parietal areas. The lesion is isointense to dark on T1-weighted MRI, and dark on T2-weighted MRI. This is the picture of an acute hemorrhage (dark signal on T1- and T2-weighted MRI is deoxyhemoglobin). In this case, this is a hemorrhagic venous infarct. The surrounding bright signal on T2-weighted and Flair MRI is vasogenic edema.

Cerebral venous thrombosis (CVT) is an uncommon cause of stroke. As venous outflow is impeded, patients develop venous infarctions which are often hemorrhagic. The etiology of CVT is diverse but most often includes the following:

● Genetic hypercoagulable states (e.g., protein S and C deficiencies, antithrombin III deficiency, Leiden factor V mutation)
● Oral contraceptives
● Pregnancy / puerperium
● Collagen vascular diseases (especially Systemic Lupus Erythematosus)
● Antiphospholipid antibody syndrome
● Malignancy
● Adjacent infectious processes (e.g., otitis, mastoiditis, sinusitis)

Patients typically present with a prominent headache. In addition, thrombosis of the superior sagittal sinus classically presents with bilateral leg weakness, as the superior sagittal sinus is midline. Depending on what other sinuses are thrombosed, there can be a multitude of other focal neurological deficits. Seizures are not uncommon. In addition, blockage of venous outflow commonly results in intracranial hypertension. Papilledema may be seen. CVT can mimic the syndrome of idiopathic increased intracranial pressure (so-called pseudotumor cerebri). CVT is an important diagnosis to recognize, as anticoagulation is indicated to prevent further clot formation. The prognosis of CVT varies, from complete recovery, to residual neurological deficits, to death.

Cerebral Venous Thrombosis - Case 6