Dural venous sinus thrombosis is a subset of cerebral venous thrombosis, often coexisting with cortical or deep vein thrombosis, and presenting in similar fashions, depending mainly on which sinus is involved.
As such, please refer to cerebral venous sinus thrombosis.
Any age, however, women on the contraceptive pill are over-represented.
Presentation is variable, and can range from asymptomatic to coma and death. Typically patients complain of headache nausea and vomiting. Neurological deficits are variable. Pathology
Superior sagittal sinus or the dominant transverse sinus thrombosis can affect the arachnoid granulations absorption of cerebrospinal fluid; consequently increase of cerebral swelling may occur 4. The subsequent venous hypertension can lead to oedema, and even haemorrhage.
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, infections (especially mastoid sinus - dural sinus occlusive disease), head injury (especially skull fractures that extends to a dural venous sinus)
Systemic illness, e.g. dehydration, sepsis, malignancy, connective tissue disorders
Any of the dural sinuses can be affected, in isolation or combined/continuous with one another:
Superior sagittal sinus thrombosis
Straight sinus thrombosis
Transverse sinus thrombosis
Sigmoid sinus thrombosis (including dural sinus occlusive disease -DSOD)
Cavernous sinus thrombosis
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. Multiplanar reformatted CT venography has been reported with a sensitivity of 95% for this diagnosis 4. Signs on contrast CT include:
empty delta sign (specific to a superior sagittal sinus thrombosis) gyral enhancement prominent intramedullary veins
In the blunt head trauma setting, there are findings that correlate with increase risk of dural venous sinus thrombosis and thereby promote CTV confirmation:
skull fractures that extend to a dural venous sinus skull base fractures that involve the groove for the sigmoid sinus dural sinus hyperdensity intrasinus gas
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 the detection of dural venous sinus thromboses. 3D T1WI GRE is the most sensitive and specific MRI sequence in detection of DVST; MRV will demonstrate a 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
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 includes microcatheter thrombolysis or thromboplasty.
Dural arteriovenous fistula and increased CSF pressure have been reported as possible complications after dural venous sinus thrombosis.
asymmetric anatomy: hypoplasia or atresia of the transverse sinus. The right transverse sinus is larger than the left in most patients. If the sinus is small or absent, then the ipsilateral sigmoid sinus and jugular fossa should also be small.
arachnoid granulations: usually characterised as well-defined focal filling defects within the dural venous sinuses (measuring 2–9 mm in diameter). 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 the transverse or sigmoid sinus can mimic a dural venous thrombosis
infarction in a non-arterial location, especially when bilateral or haemorrhagic
cortical or peripheral haemorrhage, especially when heterogeneous and gyriform
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.
A 35-year-old woman developed associated complications of cranial sinus thrombosis that included intracranial hypertension caused by an expanding intracranial hematoma, pulmonary embolism treated by placement of filters in superior and inferior vena cava to eliminate intra- and extracranial sources of emboli, and procedure-related retroperitoneal hematoma that necessitated peripheral vascular intervention. After the failure of several common devices during mechanical thrombolysis, a thrombectomy catheter (typically for peripheral vascular intervention to aide in the clot removal) was used. This case highlights the fine balance of anticoagulation and thrombolysis and the proactive, aggressive approach used by our multispecialty team to manage concurrent factors 1).