Dural venous sinuses

Sinus durae matris
Also: Superior sagittal sinus · Cavernous sinus · Transverse sinus · Sigmoid sinus · Straight sinus · Cerebral venous sinus thrombosis · Cavernous sinus thrombosis
VeinHigh-yielddraftCardio

Valveless venous channels between the layers of the dura that drain the brain into the internal jugular veins. Thrombosis of the sagittal or cavernous sinus is an important, easily missed cause of headache and cranial nerve palsies.

Core anatomy

Formation

Endothelium-lined spaces between the periosteal and meningeal layers of the dura (see cranial meninges and intracranial hemorrhage); they receive the cerebral, cerebellar, diploic and emissary veins and CSF from the arachnoid granulations.

Course

Superior sagittal sinus (along the attached border of the falx; receives CSF via arachnoid granulations) and straight sinus (formed by the inferior sagittal sinus and the great cerebral vein of Galen) meet at the confluence of sinuses (near the internal occipital protuberance) → transverse sinuses → sigmoid sinuses (grooving the mastoid part of the temporal bone) → internal jugular vein at the jugular foramen. The cavernous sinuses on each side of the sella drain via the superior and inferior petrosal sinuses.

Tributaries
  • Superior cerebral veins (bridging veins) → superior sagittal sinus
  • Great cerebral vein (of Galen) → straight sinus
  • Superior and inferior ophthalmic veins → cavernous sinus (connecting it with the facial veins)
  • Emissary veins (scalp ↔ sinuses) and diploic veins
Drains into

Internal jugular vein (via the sigmoid sinus and inferior petrosal sinus).

Relations

Cavernous sinus contents: internal carotid artery and CN VI run through the sinus; CN III, IV, V1 and V2 run in its lateral wall (see oculomotor nerve (CN III), trochlear nerve (CN IV), trigeminal nerve (CN V), abducens nerve (CN VI)); the pituitary gland lies medially.

Notes

The valveless facial veins (angular → ophthalmic) connect the "danger triangle" of the face (nose and upper lip) with the cavernous sinus; scalp emissary veins connect scalp infections with the intracranial sinuses (see scalp).

Flow of cerebrospinal fluid and the causes of hydrocephalusCerebrospinal fluid is made mainly by the choroid plexus, about 500 mL a day. It flows from the lateral ventricles through the interventricular foramina of Monro into the third ventricle, through the cerebral aqueduct into the fourth ventricle, and out through the median aperture of Magendie and the lateral apertures of Luschka into the subarachnoid space and cisterns. It is absorbed through the arachnoid granulations into the superior sagittal sinus and drains via the transverse and sigmoid sinuses to the internal jugular vein. A block within the ventricular system causes noncommunicating hydrocephalus: a colloid cyst at the foramen of Monro, aqueductal stenosis, or a posterior fossa tumor, Chiari II or Dandy–Walker malformation at the fourth ventricle. Failed absorption at the arachnoid granulations, after subarachnoid hemorrhage or meningitis or in normal pressure hydrocephalus, causes communicating hydrocephalus.Choroid plexusmakes about 500 mL a dayLateral ventriclesThird ventricleFourth ventricleSubarachnoid spaceand cisterns (and central canal)Superior sagittal sinusInternal jugular veinvia the transverse and sigmoid sinusessecretes intoInterventricular foramina (Monro)Cerebral aqueduct (Sylvius)Median (Magendie) and lateral (Luschka) aperturesArachnoid granulationsdrains toColloid cyst of the third ventricle(positional headache, drop attacks)Aqueductal stenosis: lateral and thirdventricles dilated, fourth normalPosterior fossa tumor, Chiari II,Dandy–WalkerAfter subarachnoid hemorrhage ormeningitis; normal pressure hydrocephalusNoncommunicating (obstructive)block inside the ventriclesCommunicatingabsorption fails✕ = where hydrocephalus starts

Swipe sideways to see the whole diagram →

Flow of cerebrospinal fluid. Lateral ventricles → foramina of Monro → third ventricle → cerebral aqueduct → fourth ventricle → Magendie and Luschka → subarachnoid space → arachnoid granulations → superior sagittal sinus. A block anywhere inside the ventricles causes noncommunicating (obstructive) hydrocephalus, with the ventricles dilated upstream of the block; failed absorption at the granulations causes communicating hydrocephalus.
Original schematic, created for this atlas.
Sagittal view of the skull showing the falx cerebri with the superior and inferior sagittal sinuses, straight sinus and the confluence of sinuses (torcular Herophili)
The superior and inferior sagittal, straight and transverse sinuses and the confluence.
Henry Vandyke Carter, Gray's Anatomy of the Human Body, 20th ed. (1918), Fig. 568. Source · Public domain (Public domain in the US: published before January 1, 1931 (per Wikimedia Commons))
Section of the cavernous sinus showing the internal carotid artery and abducent nerve within the sinus, and the oculomotor, trochlear, ophthalmic and maxillary nerves in its lateral wall, beside the sphenoidal sinus
Section through the cavernous sinus.
Henry Vandyke Carter, Gray's Anatomy of the Human Body, 20th ed. (1918), Fig. 786. Source · Public domain (Public domain in the US: published before January 1, 1931 (per Wikimedia Commons))
View from above with the skull cap removed showing the superior sagittal sinus, venous lacunae and dural veins
The superior sagittal sinus and venous lacunae.
Henry Vandyke Carter, Gray's Anatomy of the Human Body, 20th ed. (1918), Fig. 566. Source · Public domain (Public domain in the US: published before January 1, 1931 (per Wikimedia Commons))

Clinical correlations

Cerebral venous sinus thrombosis PANCE

Mechanism / lesion

Prothrombotic states — oral contraceptives, pregnancy and postpartum, thrombophilias, cancer, dehydration, infection (mastoiditis → sigmoid/transverse sinus).

Classic presentation

Headache (often progressive, worse lying down), papilledema, seizures, focal deficits, altered consciousness; venous (often hemorrhagic) infarcts not matching arterial territories. Diagnose with MR or CT venography (empty delta sign on contrast CT). Treat with anticoagulation (heparin) even if there is hemorrhage.

Cavernous sinus thrombosis PANCE

Mechanism / lesion

Septic thrombosis spreading from the face (danger triangle), sphenoid/ethmoid sinusitis, orbit or teeth; usually S. aureus.

Classic presentation

Fever, headache, proptosis, chemosis, periorbital edema, ophthalmoplegia (CN VI often first), reduced sensation in V1/V2, and spread to the other eye. IV antibiotics ± anticoagulation; MRI/CT venography.

Carotid–cavernous fistula

Mechanism / lesion

Abnormal connection between the ICA (or its branches) and the cavernous sinus — trauma or ruptured cavernous aneurysm.

Classic presentation

Pulsatile exophthalmos, orbital bruit, chemosis, arterialized conjunctival veins, ophthalmoplegia; endovascular repair.

High-yield PANCE pearls

  • Headache + papilledema + seizures in a woman on OCPs or postpartum → venous sinus thrombosis → MRV → heparin (even with hemorrhage).
  • Facial/sinus infection → proptosis + chemosis + ophthalmoplegia + fever → cavernous sinus thrombosis.
  • CN VI is the first/most affected nerve in the cavernous sinus.
  • Pulsatile exophthalmos + bruit → carotid–cavernous fistula.
  • Sinus drainage: superior sagittal → confluence → transverse → sigmoid → IJV.

Imaging anatomy

CT

Noncontrast CT may show a hyperdense sinus ("cord sign") or venous infarcts; CT venography shows filling defects (empty delta sign).

MRI

MRI with MR venography — the test of choice for venous sinus thrombosis; contrast MRI of the orbits and cavernous sinus.

Key views & landmarks
  • MR venography
  • CT venography

Physical exam

Strength / function testing

Fundoscopy (papilledema), eye movements (CN III, IV, VI), corneal reflex and V1/V2 sensation, proptosis and chemosis, facial skin and sinuses for an infective source.

Self-quiz

Q1.

A 29-year-old woman 2 weeks postpartum has a worsening headache for 5 days, blurred vision and a seizure. Fundi show bilateral papilledema. CT shows a small hemorrhagic infarct in the left parietal lobe. What is the most likely diagnosis?

Show answer

B

Postpartum hypercoagulability, headache, papilledema, seizures and a hemorrhagic venous infarct suggest cerebral venous sinus thrombosis. Confirm with MR/CT venography; treat with anticoagulation despite the hemorrhage.

Q2.

A 35-year-old squeezed a boil on the side of his nose. Three days later he has fever, proptosis, chemosis and cannot abduct the right eye. Which structure is involved?

Show answer

B

Infection from the danger triangle spreads through the valveless facial and ophthalmic veins to the cavernous sinus. CN VI, which runs freely within the sinus, is often affected first.

Q3.

MR venography confirms cerebral venous sinus thrombosis in a postpartum woman with a small hemorrhagic venous infarct. What is the appropriate treatment?

Show answer

D

Venous sinus thrombosis is treated with anticoagulation (heparin) even when there is a hemorrhagic venous infarct, because restoring venous outflow is key.

Q4.

Weeks after a head injury, a patient has a pulsating, protruding eye with an audible orbital bruit and arterialized conjunctival vessels. What is the most likely diagnosis?

Show answer

B

A carotid–cavernous fistula (an abnormal connection between the ICA and the cavernous sinus, after trauma or a ruptured cavernous aneurysm) causes pulsatile exophthalmos, an orbital bruit, chemosis and ophthalmoplegia.

Q5.

What is the usual order of venous drainage from the superior sagittal sinus?

Show answer

A

The superior sagittal and straight sinuses meet at the confluence, then drain through the transverse and sigmoid sinuses to the internal jugular vein at the jugular foramen.

Flashcards

See also