Cerebral Venous Thrombosis - Case 4

A 34 year-old woman presented with headaches and a mild receptive aphasia, two weeks following labor and delivery.

Show the Missing Transverse and Sigmoid Sinuses   Show the Clot within the Transverse Sinus   Show the Venous Infarction

Cerebral Venous Thrombosis. (Left) Magnetic Resonance Venogram (MRV); (Middle) T1-weighted coronal MRI; (Right) T2-weighted axial MRIs. In the MRV, note the absence of the left transverse and sigmoid sinuses. In the coronal scan, note the clot within the left transverse sinus. In the right image, note the bright signal seen in the left posterior temporal lobe, indicating a subacute hemorrhage, the cause of the patient's receptive aphasia.

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.


Revised 11/29/06.
Copyrighted 2006. David C Preston