Diagnosis of Venous Sinus Thrombosis

In most patients, the D-dimer level in the blood is increased, reflecting increased blood clotting. Radiologic brain imaging studies are required to establish the diagnosis of cerebral venous sinus thrombosis, suspected on clinical grounds. Direct visualization of the thrombosed sinus or vein conclusively confirms the definitive diagnosis.

Initial evaluation commonly uses plain computerized axial tomography (CT) scanning of the brain. Plain CT may show evidence of brain swelling and edema, or venous infarctions, which tend to be hemorrhagic with large surrounding edema and not conforming to well-defined arterial vascular territories (see Plates 9-13 and 9-21 to 9-23). However, plain CT scan may only show subtle and nonspecific abnormalities in the absence of venous infarction. Contrast administration may increase the sensitivity of CT scan in diagnosing cerebral venous sinus thrombosis. Magnetic resonance imaging (MRI) is superior to CT scan and is the imaging modality of choice.

The major cerebral sinuses and veins can be reliably imaged by magnetic resonance venography (MRV), CT venography (CTV), or conventional catheter-based angiography. Plate 9-35, D depicts a normal MRV showing all major sinuses and veins, whereas Plate 9-35, B depicts MRV showing absence of flow in the posterior portion of the superior sagittal sinus and some of the neighboring cortical veins. Conventional angiography with a prolonged venous phase is the gold standard for diagnosing cerebral sinus or vein thrombosis (see Plate 9-35, C), and its use is usually reserved for cases with high suspicion where MRV and CTV are negative or equivocal.

The specific treatment of cerebral venous sinus thrombosis depends on the underlying etiology. Most patients without contraindications for anticoagulation are initially treated either with body weight–adjusted subcutaneous low-molecular-weight heparin or doseadjusted intravenous heparin and transitioned to oral anticoagulation to avoid thrombus extension and to prevent pulmonary embolism. The optimal duration of oral anticoagulation is uncertain and varies from 3 to 12 months in idiopathic cases or those provoked by thrombogenic drugs to lifelong anticoagulation in those with thrombophilia.

Local thrombolysis may be occasionally used in patients who deteriorate despite anticoagulation and in whom other causes of deterioration have been excluded. Symptomatic treatment includes the management of increased intracranial pressure, use of antiepileptic drugs, and analgesics for headache.

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