Cavernous sinus thrombosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Pathophysiology

Anatomy

• Anatomy:

  • Cerebral veins --> Dural sinuses --> Internal jugular veins
  • The Cerebral veins include:

    • Superficial cerebral veins

      • Anatomy quite variable

    • Deep cerebral veins
    • Veins of the posterior fossa

  • The Dural sinuses most commonly affected by thrombosis are:

    • Superior sagital sinus

      • Drains most of cortex
      • Also fed by scalp emissary veins
      • Contains most of arachnoid villi responsible for draining CSF – obstruction increases intracerebral pressure
      • Superior sagital sinus thrombosis may only result in massive brain edema.

    • Lateral sinus

      • Drains cerebellum, brain stem, posterior cerebral hemispheres, middle ear
      • Near mastoid and inner ear, and susceptible to infections there

    • Cavernous sinus

      • Drains ophthalmic veins, anterior base of brain
      • Near, and susceptible to infection of face, sphenoid sinuses, teeth, and ear – infection (particularly with Staph aureus, fungus) is leading cause of cavernous sinus thrombosis, and cavernous sinus thrombosis is most common cerebral venous thrombosis.
      • Near oculomotor nerve, ophthalmic nerve, trigeminal nerve, abducens nerve, carotid artery and its surrounding sympathetic plexus.

Pathogenesis

• Cerebral venous thrombosis usually leads to parenchymal infarction, though simple intracranial hypertension may be the only finding.

  • Venous infarction affects both the cortex and adjacent white matter, and are often hemorrhagic.

    • Association with subarachnoid hemorrhage, subdural hemorrhage, intracerebral hematoma
    • Classic presentation is extensive bilateral hemorrhagic infarcts in both superior and internal parts of both hemispheres due to thrombosis of the superior sagital sinus and its cortical veins.

• Incidence is unknown, but is generally uncommon, ~0.08% of autopsies in one study.

• Pathogenetic factors:

  • Venous stasis
  • Hypercoagulability
  • Vessel wall changes
  • Embolization

References

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