Cerebral (Brain) Aneurysms
- A bulge or dilatation of a brain artery, present in 2–3% of people
- Most are never noticed and never cause a problem
- A rupture (subarachnoid haemorrhage) is a medical emergency
- Treatment balances the lifetime risk of rupture against the risk of treatment
- All cases are discussed in a multidisciplinary cerebrovascular meeting
A brain aneurysm (also known as a “cerebral”, “berry” or “saccular” aneurysm) is a bulge or dilatation of an artery within the brain. These arteries are high pressure vessels surrounded by cerebrospinal fluid (CSF), which bathes your brain and is known as the subarachnoid space. There are four main arteries that supply blood to the brain, and aneurysms typically form at weak areas of one of these arteries, typically where the artery splits into two or ‘bifurcates’. Aneurysms typically become evident between the ages of 45 and 65 due to various risk factors (see below). They occur in approximately 3% of the adult population, and the vast majority are unrecognised and never cause a problem.1 Of those people that have an aneurysm, approximately 20% will have more than one aneurysm.1
- Age — increased age, especially > 50 years old
- Gender — females are at increased risk (up to twice that of men after age 50)
- Smoking — significant increase of both formation and rupture
- Hypertension — untreated high blood pressure
- Family History — two or more direct family members with an aneurysm
- Connective tissue disorders — autosomal dominant polycystic kidney disease (ADPKD), vascular Ehlers-Danlos syndrome and fibromuscular dysplasia; a possible but less well-established association also exists with Marfan’s syndrome
- Excessive alcohol — excessive daily alcohol intake
- Drug use — especially cocaine and amphetamines
All ruptured aneurysms are urgently treated to prevent re-bleeding and worsened outcomes.
However, as most incidental aneurysms never rupture, treatment is not necessarily required. Ultimately, a person’s lifetime risk of rupture must be balanced against the risk of treatment. Averaged across all incidental aneurysms, the annual risk of rupture is low — on the order of 1% per year — though it varies considerably with aneurysm and patient characteristics.4 Many factors are taken into consideration:
- Patient age — younger patients are more likely to be treated
- Aneurysm size — often smaller aneurysms (< 5 mm) are simply monitored. Rupture risk rises steeply with size. For small aneurysms (under 7 mm), estimates range from roughly 0–0.5% per year in North American data to around 1% per year in Finnish and Japanese cohorts, rising further with risk factors such as smoking and high blood pressure. Larger aneurysms carry substantially higher annual risks, up to several percent per year for the largest.5-7
- Aneurysm location — different aneurysm locations carry different risk; posterior circulation and anterior communicating artery aneurysms carry a higher risk of rupture5
- Aneurysm shape — irregular shape or the presence of a daughter sac is associated with higher rupture risk
- Prior aneurysm rupture — prior SAH from a separate aneurysm increases overall risk
- Risk of aneurysm treatment — not all aneurysms carry the same treatment risk
- Patient wishes — patient anxiety and quality of life are treatment factors
To assist in estimating rupture risk, validated scoring tools such as the PHASES score (Population,
Hypertension, Age, Size of aneurysm, Earlier SAH, Site) can provide a 5-year rupture risk estimate based on individual patient and aneurysm characteristics.4 This is a useful aid in multidisciplinary discussion, though it does not replace the need for clinical judgement.
All patients should be discussed in a multidisciplinary meeting with a neurosurgeon, interventional neuroradiologist (INR) and sometimes a neurologist, to ensure a consensus opinion on both treatment requirement and best treatment modality.3 When treatment risk is deemed less than the lifetime risk of the aneurysm itself, treatment is typically offered.
Rebleeding. As the small clot preventing continued bleeding is extremely delicate, there is a high risk of re-rupture — reported at approximately 9–17% within the first 72 hours if left untreated, and up to 50% within the first 6 months. Mortality approximately doubles if rebleeding occurs.8,9
Hydrocephalus. Brain pressure elevation from the SAH is often compounded by a build-up of CSF within the fluid spaces (ventricles), known as hydrocephalus. This occurs in approximately 20–30% of patients with SAH.9,10 It is treated by placing a small rubber catheter known as an external ventricular drain (EVD) into the ventricle and diverting fluid into an attached bag. This remains in place until the brain self-regulates fluid once more; occasionally a permanent EVD is required, where the catheter is tunnelled from the brain into the abdomen, known as a ventriculo-peritoneal shunt (VPS).
Vasospasm and Delayed Cerebral Ischaemia. Blood within the subarachnoid space often causes the brain’s blood vessels to narrow, limiting blood supply to vital areas. Cerebral vasospasm typically develops 3–14 days after rupture and is a leading cause of secondary morbidity and mortality. It affects 20–45% of patients and, if severe enough, may lead to stroke and permanent disability despite optimal management.9,10
Altered sodium levels. SAH can disrupt the sodium balance within the blood, potentially causing brain swelling and increased brain pressure.
Seizures. SAH may cause seizures either at the time of the initial bleed or in a delayed fashion. These may be clinically silent and require specialised brain monitoring (EEG) to detect them. If left uncontrolled, they may cause permanent brain damage.
Microsurgical clipping of a cerebral aneurysm involves shaving a small amount of hair, followed by a skin incision and creating a hole in the skull known as a craniotomy. A microscope is then used to carefully expose the aneurysm and surrounding arteries. One or more alloy clips (always MRI compatible) are used to pinch off the aneurysm from the brain circulation, ensuring that the arteries leading to and from it are not narrowed or blocked. This is confirmed using a combination of visual inspection, Doppler ultrasound and intraoperative angiogram. This is a very technically demanding procedure that should only be performed by an experienced cerebrovascular neurosurgeon who regularly performs this type of surgery.
The risk of a serious complication (stroke, major neurological deficit or death) for an elective aneurysm clipping is typically 2–4%.<sup>5</sup> Other less serious complications include brain haemorrhage requiring repeat surgery (<1%), brain infection (1%), wound healing problems (1%), seizures (1–2%) and incomplete aneurysm clipping (<5%). For ruptured cases, these figures are higher — at least twice those of unruptured cases.
Whilst clipping is initially a more invasive procedure than coiling, if an aneurysm is adequately clipped it will very rarely recur and requires significantly less frequent imaging follow-up.
Link to aneurysm clipping: https://www.youtube.com/watch?v=8WSZUtC9oi0&feature=youtu.be
Performed by either an interventional neuroradiologist (INR) or INR-trained neurosurgeon, this is a less invasive treatment whereby a small catheter is inserted into the groin and guided up into the brain vessels using live X-ray imaging. Often referred to as “coiling”, one established method packs the aneurysm with small platinum coils. Increasingly, intrasaccular devices — small braided baskets placed within the aneurysm sac (such as the WEB or Artisse devices) — are used, as are stents and flow diverters (alloy mesh sleeves) placed across the aneurysm neck.3 These devices promote clot formation within the aneurysm, blocking it from the main arterial circulation.
The major risks of endovascular treatment are comparable to those of clipping, with serious complication (stroke, major neurological deficit or death) rates of approximately 2–4%.3 Blood-thinning agents such as aspirin and/or clopidogrel are often needed for a period of 3–12 months. Less serious risks include contrast reaction affecting kidney function and access-site complications in the groin. A rare but specific complication is contrast-induced encephalopathy — a temporary disturbance of brain function caused by a reaction to the contrast dye, which may produce confusion, visual disturbance (including temporary blindness), weakness or seizures; it usually resolves completely within a few days.11
Aneurysm recurrence, though rarely presenting with rebleeding, is more common with this technique and occasionally requires retreatment. Imaging follow-up is therefore more frequent than after clipping.
Link to aneurysm coiling: https://www.youtube.com/watch?v=5Ss-IOmFyeA&feature=youtu.be
- 1. Vlak MHM, Algra A, Brandenburg R, Rinkel GJE. Prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: a systematic review and meta-analysis. Lancet Neurol. 2011;10(7):626-636. doi:10.1016/S1474-4422(11)70109-0
- 2. Brisman JL, Song JK, Newell DW. Cerebral aneurysms. N Engl J Med. 2006;355(9):928-939. doi:10.1056/NEJMra052760
- 3. Etminan N, de Sousa DA, Tiseo C, et al. European Stroke Organisation (ESO) guidelines on management of unruptured intracranial aneurysms. Eur Stroke J. 2022;7(3):V. doi:10.1177/23969873221099736
- 4. Greving JP, Wermer MJH, Brown RD Jr, et al. Development of the PHASES score for prediction of risk of rupture of intracranial aneurysms: a pooled analysis of six prospective cohort studies. Lancet Neurol. 2014;13(1):59-66. doi:10.1016/S1474-4422(13)70263-1
- 5. Wiebers DO, Whisnant JP, Huston J, et al. Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet. 2003;362(9378):103-110. doi:10.1016/s0140-6736(03)13860-3
- 6. Morita A, Kirino T, Hashi K, et al.; UCAS Japan Investigators. The natural course of unruptured cerebral aneurysms in a Japanese cohort. N Engl J Med. 2012;366(26):2474-2482. doi:10.1056/NEJMoa1113260
- 7. Korja M, Lehto H, Juvela S. Lifelong rupture risk of intracranial aneurysms depends on risk factors: a prospective Finnish cohort study. Stroke. 2014;45(7):1958-1963. doi:10.1161/STROKEAHA.114.005318
- 8. Ohkuma H, Tsurutani H, Suzuki S. Incidence and significance of early aneurysmal rebleeding before neurosurgical or neurological management. Stroke. 2001;32(5):1176-1180. doi:10.1161/01.str.32.5.1176
- 9. Hoh BL, Ko NU, Amin-Hanjani S, et al. 2023 Guideline for the Management of Patients With Aneurysmal Subarachnoid Hemorrhage: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2023;54(7):e314-e370. doi:10.1161/STR.0000000000000436
- 10. Busl KM, Bogossian EG, Claassen J, et al. Beyond the bleed: complications after aneurysmal subarachnoid hemorrhage. Crit Care. 2025;29(1):414. doi:10.1186/s13054-025-05640-z
- 11. Quintas-Neves M, Araújo JM, Xavier SA, et al. Contrast-induced neurotoxicity related to neurological endovascular procedures: a systematic review. Acta Neurol Belg. 2020;120(6):1419-1424. doi:10.1007/s13760-020-01508-x
A cerebrovascular subspecialist
Mr Russell heads the Austin Hospital cerebrovascular service and is dual-fellowship trained at Toronto Western.
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