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Dural venous sinus thrombosis

Dural venous sinus thrombosis is a subset of cerebral venous thrombosis, often coexisting with cortical or deep vein thrombosis, and presenting in similar fashion, depending mainly on which sinus is involved. 

As such please refer to the cerebral venous thrombosis article for a general discussion. 


Any age however women on the contraceptive pill are over represented.

Clinical presentation

Presentation is variable, and can range from asymptomatic to coma and death. Typically patients complain of headache nausea and vomiting. Neurological deficits are variable. The subsequent venous hypertension can lead to oedema, and even haemorrhage.


Risk factors
  • hormones, e.g. oral contraceptive pill, pregnancy, puerperium, steroids
  • prothrombotic haematological conditions, e.g. protein S deficiency, polycythaemia
  • local factors, e.g. skull abnormalities/trauma, infections (especially mastoid sinus - dural sinus occlusive disease (DSOD))
  • systemic illness, e.g. dehydration, sepsis, malignancy, connective tissue disorders
  • idiopathic: ~12.5%

Radiographic features

Any of the dural sinuses can be affected, in isolation or combined/continuous with one another. 


In a non-contrast CT, when not associated with venous haemorrhage or infarction it can be a subtle finding, relying on hyperdensity of the sinus being identified. Potential findings include:

  • cord sign
  • dense vein sign
    • a potential pitfall is interpreting the distal superior sagittal sinus as being hyperdense near the torcular herophili. The walls at this location can be thick, measuring upto 2-3 mm
  • cerebral oedema: secondary to venous hypertension
  • cortical/cerebral swelling
  • unilateral or bilateral venous haemorrhage

With contrast administration, especially with a CT venogram, then a filling defect in a sinus is sought. When in the superior sagittal sinus it is referred to as the empty delta sign. Signs on contrast CT include:


MRI is able to both visualise the clot as well as the sequelae. The clot acutely is isodense on T1 and hypointense on T2 (this can mimic a flow void), with subacute clot becoming hyperintense on T1. All the findings listed in the CT section are also seen on MRI.

MRV will demonstrate lack of flow.

Staging severity
  • type 1: no imaging abnormality
  • type 2: high T2
  • type 3: high T2 with enhancement
  • type 4: haemorrhage or infarction

Treatment and prognosis

Medical, with heparin and warfarin. Anticoagulation is usually required even in the setting of venous haemorrhage (see cerebral venous infarction).

Interventional management include microcatheter thrombolysis or thromboplasty. 

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