Intracranial Aneurysms

Prevalence is estimated at 0.2% to 5%; slight predominance among females

80% to 90% arise in anterior carotid circulation, with anterior communicating, posterior communicating, and middle cerebral arteries being most common

Multiple aneurysms in 15% to 30% of patients

Associated with polycystic kidney disease, fibromuscular dysplasia, arteriovenous malformations, moyamoya disease, connective tissue diseases, and familial intracranial aneurysm syndrome

Most common presenting symptom is sudden-onset, severe headache resulting from acute subarachnoid hemorrhage (“worst headache of life”)

Meningismus, focal neurologic deficit, and obtundation may also occur

Peak age of rupture is 55 to 60 years

Large unruptured aneurysms may cause cranial neuropathies, headaches, or seizures

SAH is associated with 50% mortality rate

Treatment options: craniotomy with surgical clipping or endovascular coil embolization

Vasospasm may occur 4 to 14 days after SAH, resulting in cerebral ischemia and stroke

On noncontrast CT, aneurysmal SAH appears as hyperdense material within the basilar cisterns

Aneurysms appear as outpouchings of vessels at branching points on CT angiography or cerebral angiography

Aneurysms are round or lobulated sacs that have a constricted “neck” at sites of origin from arterial branch points

Subarachnoid, intraventricular, or intraparenchymal hemorrhage present if the aneurysm ruptured

The wall may be thick or thin; calcification or thrombus may be palpable

Multiple aneurysms may be found

Aneurysm wall typically shows medial disorganization and myointimal hyperplasia

No internal elastic lamina is visible; endothelium may be absent

Wall thickness may vary from very thick, because of disorganized myointimal hyperplasia, to a very thin hypocellular wall with extensive underlying luminal thrombus

Masson trichrome stain will highlight fibrosis of the aneurysm wall

Loss of the internal elastic lamina well demonstrated by Verhoeff-Van Gieson elastin stain