Arteriovenous malformation

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

Workup

• 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

Sources

• Friedlander, Robert. Arteriovenous Malformations of the Brain. The New England Journal of Medicine. June 2007; 356: 2704-12.
• Greenberg, Mark. Handbook of Neurosurgery. New York: Thieme, 2006. 835-838.