Fact-sheet: Dural sinus thrombosis
Updated on 09/30/2019 at 4:38 PM
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Definition
Thrombus of cortical veins, venous sinuses, or deep veins
1) Etiology: Multiple++
- Predisposing conditions: genetic or acquired prothrombotic state, hematologic disease, malignancy, systemic and inflammatory disease
- Precipitating factors: infection, pregnancy, contraceptives, postoperative state, central catheters, treatment (L-asparaginase)
- Undetermined in 30% of cases
2) Natural history:
- Obstruction of venous outflow and elevation of venous pressure
- Disruption of the blood-brain barrier with vasogenic edema, hemorrhage
- Venous infarction with cytotoxic edema
Clinical features
Variable onset: acute (30%) / subacute (50%) / chronic (20%)
Female predominance
- Headache +++, nausea, vomiting
- Isolated intracranial hypertension: papilledema +/- sixth nerve palsy
- Focal neurological deficit
- Seizures
- Impaired consciousness, encephalopathy
- Cavernous sinus involvement: chemosis, ptosis, painful ophthalmoplegia
Prognosis - Course:
- Complete recovery without sequelae (60%)
- Moderate to severe disability (5%)
- Late complications: epilepsy (10%), recurrent thrombosis (5%), cerebral arteriovenous fistula
CT
- Spontaneous hyperdensity of the thrombus: "cord sign" or "dense triangle sign"
- Cerebral CT venography: "empty delta sign"
- Indirect signs: cerebral edema, intraparenchymal Hematoma, subarachnoid hemorrhage, ischemic lesions with suggestive topography (bithalamic, subcortical parietal)
MRI
Note: thrombus signal varies over time and according to the sequence used
- T1 SE: loss of flow void, thrombus iso- to hyperintense
- T2 FSE: thrombus hypo- to isointense in the acute stage, then hyperintense. Edema
- T2 GRE: marked hypointensity – magnetic susceptibility effect. High sensitivity for cortical veins. Superior sensitivity with SWI
- Diffusion: thrombus hyperintense. Predictive of poor recanalization (P. Favrole, Stroke 2004), ischemic lesions with decreased ADC
- Post-contrast T1: volumetric acquisition. Intraluminal filling defect. MR venography preferred
- MR venography (with or without contrast): defines the occlusion
- Value of SWI imaging to increase sensitivity for thrombus visualization when not seen on T2*, particularly for cortical vein thrombosis
Parenchymal impact:
- Venous infarction: corticosubcortical vasogenic edema not corresponding to an arterial vascular territory, complicated by hemorrhage in 50% of cases (typically a large area of edema with +/- limited central hemorrhagic transformation)
- In deep venous system thrombosis = bilateral FLAIR hyperintensity (DWI = increased ADC) of the thalami +/- striatum
NOTE: unilateral involvement is possible: pseudotumoral appearance (-> consider deep venous thrombosis) - Intraparenchymal Hematoma or subarachnoid hemorrhage
Vascular intervention
X-Ray Angiography:
- Venous occlusion – absence of opacification
- Circulatory delay – stasis
- Collateral circulation: cortical, transcerebral, extracerebral veins
Management
- Antithrombotic treatment: Heparin ++ even in cases of hemorrhagic venous infarction
- Symptomatic treatment: anti-epileptics, corticosteroids/edema
- Etiologic treatment
Differential diagnosis
- Intrasinus Pacchionian granulation: rounded, more focal appearance
- Venous anatomical variant
- Venous sinus hypoplasia (dominant right transverse sinus in 60% of cases)
- Flow-related artifact (TOF, T1 GRE...)
- Bithalamic lesions: ischemic due to artery of Percheron? Gayet-Wernicke?