Description

• Abnormal, localized dilation or outpouching of cerebral artery wall:
  • Occurs in 5–10% of population
• Rupture of saccular aneurysms account for 5–15% of strokes
• Of those that rupture:
  • 40% occur at anterior communicating artery (ACA)
  • 30% at internal carotid (IC)
  • 20% in middle cerebral artery (MCA)
  • 5–10% in vertebrobasilar artery (VBA) system

Etiology

• Asymptomatic in 3.2% of population
• “Congenital,” saccular, or berry aneurysms most common (90%):
  • Develop at weak points in arterial wall and bifurcations of major cerebral arteries
  • Incidence increases with age
  • Multiple in 20–30%
  • Increased incidence:
    • Polycystic kidney disease
    • Cerebral arteriovenous malformation
    • Type III collagen deficiency
    • Fibromuscular dysplasia
    • Ehlers–Danlos syndrome
    • Marfan syndrome
    • Pseudoxanthoma elasticum
    • Neurofibromatosis
    • Moyamoya syndrome
    • Coarctation of the aorta
    • Tuberous sclerosis
    • Sickle cell disease
    • Osler–Weber–Rendu syndrome
    • α1-antitrypsin deficiency
    • Systemic lupus erythematosus
    • Glucocorticoid remediable hyperaldosteronism
• Arteriosclerotic, fusiform, or dolichoectatic (7%):
  • More common in peripheral arteries
• Inflammatory (mycotic):
  • 10% of patients with bacterial endocarditis
• Traumatic, associated with severe closed head injury
• Neoplastic, embolized tumor fragments
• Familial correlation: First-degree relative with history of aneurysm essentially doubles lifetime risk

• Although rare in children, more likely to be giant (>25 mm)
• Occur in the posterior circulation