Cerebral venous drainage receives less attention than arterial supply in clinical neurology, but venous disease — sinus thrombosis, cortical vein thrombosis, jugular foramen obstruction — produces distinctive and often serious syndromes. The venous system is also clinically important because of its relationship to spreading infection (from face into cavernous sinus), to chemotherapy toxicity, to oral contraceptives and procoagulant states, and to the management of intracranial hypertension. This page covers the dural venous sinuses, the cortical and deep cerebral veins, and the major venous syndromes.

The Dural Venous Sinuses

The dural venous sinuses are channels between the layers of the dura, draining blood from the brain to the internal jugular veins. They are valveless and rigid (because of their dural walls), which makes them resistant to collapse but also makes thrombosis more dangerous because pressure increases cannot be relieved by venous distensibility.

Superior Sagittal Sinus (SSS)

Runs in the upper margin of the falx cerebri from front to back. Drains most of the cortical veins of the upper convexity. Receives CSF via the arachnoid granulations. Thrombosis of the SSS produces bilateral parasagittal infarcts (often with hemorrhagic transformation), headache, papilledema, seizures, and altered consciousness.

Inferior Sagittal Sinus

Runs in the lower margin of the falx cerebri. Joins the great cerebral vein to form the straight sinus.

Straight Sinus

Lies at the junction of falx and tentorium. Drains the deep cerebral veins (great vein of Galen) and inferior sagittal sinus. Joins the SSS at the torcular Herophili (confluence of sinuses).

Transverse Sinuses

Run laterally in the tentorium from the confluence of sinuses outward. Receive drainage from the cerebellar hemispheres and inferior occipital lobes. Often asymmetric, with right typically larger.

Sigmoid Sinuses

Continuations of the transverse sinuses, curving downward and forward to exit the skull at the jugular foramen as the internal jugular veins.

Cavernous Sinuses

Paired sinuses on either side of the sella turcica. Unique in containing important structures within them: CN III, IV, V₁, V₂, VI, the internal carotid artery, and the sympathetic plexus. Drained anteriorly by the ophthalmic veins (from the face and orbit) and posteriorly by the superior and inferior petrosal sinuses.

Cavernous sinus thrombosis is a feared complication of facial and sinus infection, producing painful ophthalmoplegia, V₁ and V₂ sensory loss, proptosis, chemosis, and Horner syndrome. Emergency.

Petrosal Sinuses

Connect cavernous sinus to sigmoid sinus (superior petrosal) or to jugular bulb (inferior petrosal).

Cortical Veins

Drain the cerebral cortex into the dural venous sinuses. Three major groups:

  • Superior (ascending) cortical veins: drain into SSS. Include the named vein of Trolard (superior anastomotic vein, connecting Sylvian fissure to SSS).
  • Middle (lateral) cortical veins: drain into Sylvian region or cavernous sinus. Include the superficial middle cerebral vein.
  • Inferior cortical veins: drain into transverse sinus. Include the vein of Labbé (inferior anastomotic vein, connecting Sylvian to transverse sinus).

Cortical vein thrombosis can occur without sinus thrombosis (less common). Cortical vein thrombosis produces focal infarction or hemorrhage in the affected cortical region.

Deep Cerebral Veins

Drain the deep gray matter, white matter, and ventricular system:

  • Internal cerebral veins: paired veins in the roof of the third ventricle, draining caudate, thalamus, lateral ventricle choroid plexus.
  • Basal vein of Rosenthal: drains the medial temporal lobe and parts of the basal ganglia.
  • Great cerebral vein of Galen: short, large midline vein formed by union of internal cerebral veins and basal veins. Drains into the straight sinus.

Thrombosis of the deep cerebral venous system (internal cerebral veins, vein of Galen, straight sinus) produces bilateral thalamic infarcts with severely altered consciousness — a particularly dramatic presentation.

Cerebral Venous Sinus Thrombosis (CVST)

An important diagnosis to recognize because:

  • Presentation is variable — headache, seizures, focal deficits, encephalopathy, isolated intracranial hypertension.
  • It can affect young patients without conventional vascular risk factors.
  • Treatment with anticoagulation reduces morbidity and mortality.

Risk Factors

  • Procoagulant states: oral contraceptives, pregnancy and puerperium, factor V Leiden, prothrombin G20210A, antiphospholipid syndrome, malignancy, nephrotic syndrome.
  • Infection: sinusitis, mastoiditis, meningitis, otitis.
  • Trauma to head or neck.
  • Dehydration.
  • Chemotherapy.
  • Idiopathic (about 15-20%).

Clinical Presentations

  • Isolated intracranial hypertension picture: headache, papilledema, sometimes visual loss. Can mimic IIH.
  • Focal deficits with or without seizures: from venous infarction. Bilateral parasagittal infarcts in SSS thrombosis; temporal lobe infarction in transverse/sigmoid thrombosis (vein of Labbé).
  • Encephalopathy: with extensive sinus involvement or deep cerebral venous thrombosis.
  • Cavernous sinus thrombosis: painful ophthalmoplegia, V₁/V₂ sensory loss, proptosis, chemosis. Often septic.
  • Deep cerebral vein thrombosis: bilateral thalamic infarcts with profoundly altered consciousness, vertical gaze palsy, often coma.

Imaging

CT venography or MR venography are the imaging modalities of choice. CT can show hyperdense thrombus in the sinus (especially SSS). MRI shows absent flow void in the affected sinus on routine sequences and confirmed by venography.

Treatment

Anticoagulation (heparin acutely, transitioning to oral anticoagulant) for several months, even in the presence of hemorrhagic venous infarction (this is one of the few situations where anticoagulation is indicated despite intracranial hemorrhage). Mechanical thrombectomy is being investigated for severe cases. Treatment of underlying cause (infection if present, removal of OCPs).

Idiopathic Intracranial Hypertension (IIH)

Elevated intracranial pressure without mass lesion or ventricular dilatation. Predominantly young women with elevated BMI. Increasingly recognized to be associated with transverse sinus stenosis in many patients — possibly a cause, possibly a consequence. Treatment includes weight loss, acetazolamide, sometimes CSF shunting or transverse sinus stenting in refractory cases.

Pitfalls and Pearls

  • Cerebral venous sinus thrombosis can present in many ways — headache, papilledema, seizures, focal deficits, encephalopathy.
  • Consider CVST in young patients with stroke or headache without conventional risk factors.
  • Procoagulant states are important risk factors — OCPs, pregnancy, thrombophilia.
  • Anticoagulation is indicated in CVST even with hemorrhagic infarction.
  • Cavernous sinus thrombosis is a feared complication of facial infection. Painful ophthalmoplegia with V₁/V₂ sensory loss and proptosis is the picture. Emergency.
  • Deep cerebral vein thrombosis produces bilateral thalamic infarcts with severely altered consciousness — easily mistaken for metabolic encephalopathy.
  • Vein of Labbé thrombosis can produce temporal lobe infarction.
  • IIH is associated with transverse sinus stenosis in many patients.
  • CT/MR venography is the imaging of choice for CVST.

References

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  2. Stam J. Thrombosis of the cerebral veins and sinuses. N Engl J Med. 2005;352(17):1791-1798.
  3. Friedman DI, Liu GT, Digre KB. Revised diagnostic criteria for the pseudotumor cerebri syndrome. Neurology. 2013;81(13):1159-1165.
  4. Bousser MG, Ferro JM. Cerebral venous thrombosis: an update. Lancet Neurol. 2007;6(2):162-170.
  5. Standring S, ed. Gray’s Anatomy. 42nd ed. Elsevier; 2021.