Epidemiology and pathophysiology of cerebral aneurysms

Dr Roger Traill

Department of Anaesthetics, RPAH, Sydney, Australia

A Cerebral Aneurysm is a balloon like weakness of a cerebral blood vessel usually occurring at a branch point. They are important due to their propensity to rupture (sub-arachnoid haemorrhage - SAH) leading to high morbidity and mortality. About a third of patients will die at the time of the bleed and of the remaining patients who make it to hospital ,a further third will die, a third will have some deficit and only a third will have no deficit!
They are broadly classified into:
Saccular (like a "sac")
Fusiform - like an abdominal aortic aneurysm and are associated with atherosclerosis
If the aneurysm is greater than 2.5cm in diameter it is called a giant aneurysm.
Most aneurysms arise sporadically but occasionally they may be: dissecting (resulting from a luminal endothelial tear), traumatic (usually within 2-3 weeks after severe head injury) or mycotic (as a result of embolism of infected material)
Saccular Aneurysms are mostly due to a pre-existing vascular weakness however the relative roles of genetics and other factors are not clearly elucidated. It is clear however that there is a familial relationship to cerebral aneurysms as studies have shown that siblings (RR 6:1) and first-degree relatives (RR 3-7:1) have a higher incidence than the background population. There have also been relatively small numbers of families described with a Mendelian dominant inheritance. No single gene has been found so far to be responsible for cerebral aneurysms.
A number of conditions are associated with cerebral aneurysm formation. The most important of these is the presence of an AVM. Another important association is the presence of the autosomal dominant type of polycystic kidneys that has a 5-40% incidence. Screening for aneurysms is recommended for these patients by CT or MRI angiography. Other conditions with an increased incidence are; fibromuscular dysplasia, Marfan's syndrome and Ehlers-Danlos syndrome (type IV).
Other causative factors are hypertension, smoking, cocaine use and "heavy" alcohol use.
90% of Aneurysms occur in the anterior circulation (30% Internal Carotid Artery, 40% Anterior Cerebral or Anterior Communicating Artery, 20% Middle Cerebral Artery) and 10% in the Posterior Circulation (Vertebro-Basilar systems).
The risk of rupture is greater (per year) the larger the aneurysm is but 90% of aneurysms that rupture are <12mm in size.
La Places Law (T=2PR) would explain a linear increase in the risk of rupture as size increases however there is also thinning of the aneurysm wall that occurs as they expand and the aneurysm wall is not uniform in size. This leads to the risk being greater than La Place's Law would predict, one study indicating that the risk of rupture is related to the third power of the aneurysm radius.
The overall prevalence of aneurysms is unclear as it can only be determined by autopsy studies or screening of the normal population with cerebral angiography or one of the less invasive alternatives (CT or MRI angiography).
Several autopsy and screening studies have found rates between 0.2 and 9.9%. It may be higher in Japan and Finland and the average prevalence of all these studies is about 2%.
It is estimated that there is an average risk of rupture is 1-2% per year but this varies greatly on the size and location of the aneurysm. It is estimated that between 50-80% will never rupture.
The incidence of Sub-Arachnoid Haemorrhage is about 10 per 100,000 per year in Western Europe and the US. The rate is higher in Japan and Finland (about 15 per 100,000 per year)
The International Study of Unruptured Intracranial Aneurysms (ISUIA) looked at a retrospective analysis of cerebral aneurysms as well as a prospective analysis. The initial, retrospective analysis, indicated minimal risk of rupture if the aneurysm is <10mm in size but subsequent prospective analysis has revealed that only if the aneurysm is <7mm in size, is located in the anterior circulation and their have been no previous SAHs is the risk minimal, location in the Anterior circulation, larger size and previous SAH increases the likelihood of rupture.
The decision to treat however depends on an individual assessment of the risks of bleeding versus the risks of treatment (surgery or endovascular). The risks of treatment must be considered in the light of the success and complication rate of the treating centre. In many cases high risk of bleeding is associated with a high risk of treatment.
Bibliography:
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