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?