Arteriovenous malformation (CNS)

Background

  • Focal abnormal conglomerations of dilated arteries and veins in the brain parenchyma
    • Arterial blood flows directly into draining veins without capillary beds creating high pressure channels
    • May rupture, causing intracerebral hemorrhage +/- intraventricular hemorrhage. Mechanism of rupture incompletely understood.
  • Prevalence 0.14%
  • Congenital lesions
    • Majority are sporadic, not familial
    • Associated with Osler- Weber-Rendu disease and Sturge-Weber syndrome
  • Lifelong risk of bleeding
    • 2-4% per year, cumulative

Clinical Features

  • Hemorrhage (most common)
    • 42-72% of clinically apparent AVMs
    • Usually by age 20-49
  • Seizures
  • Ischemia (by vascular steal – rare)
  • Headaches

Differential Diagnosis

  • Venous angioma
  • Cavernous malformation
  • Capillary telangiectasia

Intracranial Mass

Evaluation

  • CT/CTA
    • CT delineates acute hemorrhage, CTA to show abnormal vasculature
  • MRI/MRA
    • Vessels appear as abnormal flow voids
    • Both better than CT for visualizing structures in relation to AVM
  • Angiography
    • Gold standard to evaluate the architecture including arterial feeding, venous drainage, and AVM-associated aneurysms

Management

  • Surgical Resection
    • Traditionally treatment of choice
  • Radiosurgery (Gamma Knife or CyberKnife)
  • Embolization (usually an adjunct treatment)
  • Combination of above three in some cases
    • Decision is based on AVM size, location, and patient factors

Disposition

  • In cases of acute hemorrhage or neurological decline, obvious need for immediate neurosurgical consultation
  • If patient presents with headache or seizure and lesion is then found, may simply warrant outpatient neurosurgical evaluation

See Also

External Links

References

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