Cerebral Arteriovenous Malformations

Cerebral AVMs are rare: 1–2% cause of CVA in a younger population; mean age of diagnosis is 31 y.

55% of pts are men.

Symptomatic cases: 1:100,000 per y.

Found in 4.3% of population at autopsy.

Of those affected, 45–70% present with hemorrhage, 30% with seizures, 12% with persistent neurologic deficits, and 1% with headaches.

Yearly risk of hemorrhage is 1–3%.

Risk of hemorrhage at embolization is 2–4%.

Intraop blood pressure management is critical.

Postop NPPB occurs as blood is diverted from the AVM to the surrounding brain, presenting risk of cerebral edema or hemorrhage.

Massive intraventricular or intraparenchymal hemorrhage

Seizure

New neurologic deficits

Cerebral edema, hyperemia post resection, or endovascular embolization

Localized arteriovenous shunt comprised of a tangle or “nidus” of abnormally walled vessels, which cause symptoms by rupture, ischemia, and diversion of flow or pressure on adjacent structures; many are detected on routine scans. The majority of AVMs will bleed at least once.

0% are supratentorial, and 4–10% are associated with aneurysms.

Increased risk of rebleed of 6–33% within the first year.

As the result of hemorrhage, 16% of pts are moderately or severely disabled. Hemorrhage leads to mortality in 10–30% of cases.

Vein of Galen malformations are rare congenital lesions with connections between the intracerebral vessels and the great vein of Galen. This disorder in neonates or infants may result in high output CHF or increased ICP from hydrocephalus.

Although congenital in origin, no specific genetic defect has been determined. Sometimes AVMs are associated with hereditary hemorrhagic telangiectasia.