Saccular cerebral aneurysm

Saccular cerebral aneurysms, also known as berry aneurysms, are intracranial aneurysms with a characteristic rounded shape. They account for the vast majority of intracranial aneurysms and are the most common cause of non-traumatic subarachnoid hemorrhage.

Terminology

Those larger than 25 mm in the maximal dimension are called giant cerebral aneurysms.

Charcot-Bouchard aneurysms are minute aneurysms which develop as a result of chronic hypertension and appear most commonly in the basal ganglia and other areas such as the thalamus, pons, and cerebellum, where there are small penetrating vessels (diameter <300 micrometers).

Epidemiology

Prevalence of saccular cerebral aneurysms in the asymptomatic general population has been reported over a wide range (0.2-8.9%) when examined angiographically, and in 15-30% of these patients, multiple aneurysms are found ⁴.

A familial tendency to aneurysms is also well recognized, with patients who have more than one first-degree relative affected, having a ~30% (range 17-44%) chance of themselves having an aneurysm ⁴.

Pathology

Macroscopically, aneurysms are rounded lobulated focal outpouchings. usually arising at the arterial bifurcations.

Most intracranial aneurysms are true aneurysms. The aneurysmal pouch is composed of thickened hyalinised intima with the muscular wall and internal elastic lamina being absent as the normal muscularis and elastic lamina terminate at the neck of an aneurysm. As an aneurysm grows it may become irregular in outline, and may have mural thrombus. Typically rupture occurs from the dome ⁴.

Associations

Numerous associations have been identified, most relating to abnormal connective tissue. Associations include:

• Ehlers-Danlos syndrome (type IV)
• Marfan syndrome (controversial ³)
• autosomal dominant polycystic kidney disease ¹
• coarctation of aorta ²
• bicuspid aortic valve
• neurofibromatosis type 1 ³
• hereditary hemorrhagic telangiectasia
• alpha 1 antitrypsin deficiency ³
• cerebral arteriovenous malformation: a flow related aneurysm
• fibromuscular dysplasia
• thoracic and abdominal aortic aneurysms ⁷

Location

Cerebral aneurysms typically occur at branch points of larger vessels but can occur at the origin of small perforators which may not be seen on imaging. Approximately 90% of such aneurysms arise from the anterior circulation, and 15-30% of these patients have multiple aneurysms ⁴. 

• anterior circulation: ~90%
  • ACA/ACoA complex: 30-40%
  • supraclinoid ICA and ICA/PCoA junction: ~30%
  • MCA (M1/M2 junction) bi/trifurcation: 20-30%
• posterior circulation: ~10%
  • basilar tip
  • SCA
  • PICA

Radiographic features

Berry aneurysms can be imaged in a variety of methods:

• CT angiography
• MR angiography
• digital subtraction (catheter) angiography

Each of these confers certain advantages and disadvantages, although in general digital subtraction catheter angiography, especially with 3D acquisitions, is considered the gold standard in most institutions.

CT

The appearance depends upon the presence of thrombosis within an aneurysm. An aneurysm appears as a well-defined round, slightly hyperattenuating lesion, most apparent on maximum intensity projection reformatted images.

• calcification can be present
• post contrast
  • patent aneurysm: bright and uniform enhancement
  • thrombosed aneurysm: rim enhancement due to filling defect

MRI

On MRI also the patent and thrombosed aneurysm display different imaging features:

• T1
  • most of the patent aneurysm appears as flow void, or they may show heterogeneous signal intensity
  • in thrombosed aneurysm appearance depends on the age of clot within the lumen
• T2
  • typically hypointense
  • laminated thrombus may show a hyperintense rim

DSA: angiography

It has been reported more sensitivity in 3D DSA over 2D DSA when regarding the detection of small aneurysms ⁶. Attention must be given when measuring the aneurysm neck size as it can be overestimated by the 3D reconstructions. 

Treatment and prognosis

Treatment of large or symptomatic aneurysms should be considered, with either endovascular coiling or surgical clipping. 

Management of small aneurysms is controversial. Less than 7 mm in maximal diameter aneurysms are statistically unlikely to rupture, however, due to their prevalence, anyone working in the area has seen numerous patients with small aneurysms which have ruptured resulting in subarachnoid hemorrhage, often with devastating consequences.

Five-year cumulative risk of rupture of anterior circulation aneurysms ⁵:

• <7 mm: 0%
• 7-12 mm: 2.6%
• 13-24 mm: 14.5%
• >25 mm: 40%

Five-year cumulative risk of rupture of posterior circulation aneurysms ⁵:

• <7 mm: 2.5%
• 7-12 mm: 14.5%
• 13-24 mm: 18.4%
• >25 mm: 50%

As such management will vary according to local experience, the location and appearance of an aneurysm, patient demographics etc.

Endovascular coiling is graded with the Raymond–Roy Occlusion Classification (RROC) scheme.

Differential diagnosis

When the abnormality has been confirmed to be vascular, the differential includes:

• fusiform aneurysm
• infundibulum: usually triangular dilatation with the vessel arising from the apex
• dissecting aneurysm
• mycotic aneurysm
• variant arterial anatomy (see imaging differential diagnosis case)

Practical points

Regardless of the modality used, a number of features need to be assessed to allow a decision in relation to treatment to be made:

• size: ideally three axis maximum size measurements
• neck: maximal width of the neck of an aneurysm
• the shape and lobulation
• orientation: the direction in which the aneurysm points is often important in both endovascular and surgical planning
• any smaller branches in the vicinity of an aneurysm
• any branch taking off from the aneurysm
• the presence of other aneurysms or vascular malformations
• relevant arterial variant anatomy (that may complicate or exclude endovascular treatment)

See also

• aneurysm
• ruptured berry aneurysm
• subarachnoid hemorrhage (SAH)
• vasospasm (post-SAH)