Saccular (Berry) Aneurysms

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Learning objectives

  • What is a saccular aneurysm ?
  • What is there significance and associated risks ?
  • How to manage saccular aneurysms ?

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Saccular aneurysms are inherited developmental abnormalities which are incompletely understood but may be related connective tissue weakness, anatomical defects and abnormal flow patterns. They are not detectable at birth or in childhood but then appear to enlarge and be detectable in later life. They tend to form at certain points later in life and can present with haemorrhagic stroke in the form of subarachnoid haemorrhage (5% of all strokes) or with pressure effects. They are found in 1-2% of the population which in the UK suggests 1.2 million individuals. It is clearly only a minority who present and 90% are less than 10 mm diameter. 15% have multiple aneurysms. The risk of rupture of an asymptomatic intracranial aneurysm is approximately 0.7%


  • Thunderclap headache: Symptomatic SAH who will usually need fast track to neurosurgeon for immediate management. Saccular aneurysms are the most important cause of primary non-traumatic SAH and account for 70-80% of all SAH. Patients present with thunderclap headache. This is dealt with under Subarachnoid Haemorrhage.
  • Asymptomatic aneurysm picked up on imaging for some other reason
  • Pressure symptoms as the aneurysm enlarges. Giant aneurysms can be defined as those over 25 mm and within the skull the pressure effects maybe significant. Examples include the pressure of a Posterior communicating artery or Superior Cerebellar artery Aneurysm on the Ipsilateral IIIrd nerve, a basilar artery aneurysm compressing brainstem, Ophthalmic artery aneurysm causing retro-orbital pain, Hemiparesis or aphasia suggests a middle cerebral artery aneurysm.


Anatomically aneurysms have a neck and a dome and this can be assessed radiographically. They tend to form at the site of arterial bifurcations. 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. if an aneurysm grows it can become irregular in outline, and may have mural thrombus and become paper thin. Rupture occurs from the dome.

Increased Risks

  • Ageing, smoking and hypertension
  • Prior SAH from another aneurysm
  • Basilar apex and posterior communicating artery aneurysm


  • Ehlers-Danlos syndrome (type IV), Marfan syndrome
  • Autosomal dominant polycystic kidney disease (ADPKD)
  • Coarctation of aorta, bicuspid aortic valve, neurofibromatosis type 1 (NF1)
  • Hereditary haemorrhagic telangiectasia, alpha 1 antitrypsin deficiency, cerebral AVM
  • Fibromuscular dysplasia, thoracic and abdominal aortic aneurysms


  • Most arise from the anterior circulation. Approximately 20% have multiple aneurysms

Anterior circulation

  • 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 and PICA


  • Berry aneurysms can be imaged in a variety of methods: Each of these confers certain advantages and disadvantages. DSA tends to exit in tertiary centres where there is intention for active management and is considered the gold standard in most institutions.
  • CT angiography (CTA) the appearance depends upon the presence of thrombosis within an aneurysm. Aneurysm appears as a well-defined round, slightly hyperattenuating lesions. Calcification can be present. Post contrast patent aneurysm: bright and uniform enhancement. Thrombosed aneurysm: rim enhancement due to filling defect
  • MR angiography (MRA) the patent and thrombosed aneurysm display different imaging features: On 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. On T2 typically hypointense laminated thrombus may show a hyperintense rim
  • Digital subtraction (catheter) angiography (DSA): It has been reported more sensitivity in 3D DSA over 2D DSA when regarding the detection of small aneurysms. 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.
  • Those less than 7 mm in maximal diameter artery low risk and unlikely to rupture but there are statistically more of these so there are the rare cases of patients with small aneurysms which have ruptured resulting in subarachnoid haemorrhage, often with devastating consequences.
Five-Year Cumulative Percentage Risk of Rupture of Previously Unruptured Aneurysms According to the ISUIA Study
Aneurysm Size vs. Localisation <7 mm* 7–12 mm 13–24 mm >24 mm
Intracavernous ICA 0 0 3.0% 6.4%
Other ICA, MCA, ACA0 (1.5%) 2.6% 14.5% 40.0%
Posterior circulation and posterior communicating artery2.5% (3.4%)14.5%18.4% 50.0%

Other Aneurysms

Fusiform Aneurysms

  • Elongated spindle shaped aneurysms due to atherosclerosis and ectasia of large arteries. The basilar artery is most affected but it can also affect major branches of circle of Willis (MCA/ACA/PCA).
  • As they enlarge the may compress surrounding structures with focal neurological results, eg as facial pain (Trigeminal), hemifacial spasm (Facial), and hearing loss with vertigo (VIII). They rarely rupture; but if they do, total occlusion is usually required because their stiff walls and shape make surgical clipping difficult.

Mycotic Aneurysms

Most commonly related to endocarditis. as an infected embolism enters distal branch of a cerebral artery to cause a microinfarction or microabscesses. The artery can rupture or arteritis or mycotic aneurysms develop. They can later rupture. Treatment is to treat the endocarditis. Intervention is unusual. Anticoagulation can cause bleeding.