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. Please refer to the generic article for a broad discussion on epidemiology and risk factors: cerebral venous thrombosis.

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.


Superior sagittal sinus or the dominant transverse sinus thrombosis can affect the arachnoid granulations absorption of cerebrospinal fluid, a consequently increase of cerebral swelling may occur 4. The subsequent venous hypertension can lead to oedema, and even haemorrhage.

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

Please refer to the generic article for a broad discussion on pathology: cerebral venous thrombosis.

Radiographic features

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


Unenhanced CT is usually the first imaging investigation performed given the nonspecific clinical presentation in this cases. When not associated with venous haemorrhage or infarction, it can be a subtle finding on CT images, 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 torcula herophili; it is important to appreciate that normal blood within the dural sinuses is usually of slightly increased density relative to brain parenchyma and that true hyperdensity is the key to recognising thrombosis
    • The walls at this location can be thick, measuring up to 2-3 mm
  • cerebral/cortical oedema: secondary to venous hypertension
  • unilateral or bilateral cortical or peripheral venous haemorrhage

With contrast administration, especially with a CT venogram, then a filling defect in a sinus is sought. Multiplayer reformatted CT venography has been reported with a sensitivity of 95% for this diagnosis 4. Signs on contrast CT include:


MRI is able to both visualise the clot as well as the sequelae.

Conventional spin-echo sequences may demonstrate an absence of normal flow void on the dural sinuses. 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. The most sensitive conventional MRI sequence for detection of the clot is susceptibility sequences such as SWI or GRE. Overall, the conventional MRI sequences in combination are very sensitive but relatively non-specific in detection of dural venous sinus thromboses. 3D T1WI GRE is the most sensitive and specific MRI sequence in detection of DVST; MRV will demonstrate lack of flow.

Staging severity

Dural venous thromboses can result in parenchymal oedema and ischemia in its watershed area; the severity of which can be graded as follows:

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

Treatment and prognosis

Systemic anticoagulation (e.g. heparin and warfarin) is still the first-line treatment for dural venous thrombosis. Anticoagulation is usually required even in the setting of venous haemorrhage.

Interventional management include microcatheter thrombolysis or thromboplasty.

Dural arteriovenous fistula and increased CSF pressure have been reported as possible complications after dural venous sinus thrombosis.

For general discussion on treatment please refer to the parent article: cerebral venous thrombosis.

Differential diagnosis

  • asymmetric anatomy: hypoplasia or atresia of the transverse sinus. The right transverse sinus is larger than the left in most patients 5. If the sinus is small or absent, then the ipsilateral sigmoid sinus and jugular fossa should also be small 6.
  • arachnoid granulations: usually characterised as well-defined focal filling defects within the dural venous sinuses (measuring 2–9 mm in diameter) 4. These are more commonly in the lateral aspects of the transverse sinuses and should follow CSF signal intensity of all MRI sequences.
  • asymmetric flow in transverse or sigmoid sinus can mimic a dural venous thrombosis

Practical points

  • infarction in a non-arterial location, especially when bilateral or haemorrhagic
  • cortical or peripheral haemorrhage, especially when heterogeneous and gyriform
  • cortical oedema
  • direct signs of a thrombus (e.g. dense clot sign, cord sign, empty delta sign)
  • anatomy variations commonly occur can mimic sinus thrombosis or occlusion

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