About 75-80% of cases of non-traumatic SAH are due to rupture of a saccular aneurysm in the cerebral circulation [12].
Incidence
These aneurysms are found in approximately 2-3% of the population and are more common in older people [13].
Only 2% of relatives of patients with SAH are similarly affected and an increased risk is only attributed if two or more first degree relatives are involved [14].
The genetic predisposition to form intracerebral aneurysms has been studied with links found with polycystic kidney disease [15] and, rarely, with other connective tissue diseases.
Risk factors
Modifiable risk factors include [16]:
These are much more important in the causation of SAH than any genetic predisposition which is implicated in only 10% of cases [17].
Aneurysm sites
Fig 1: Anterior communicating artery aneurysm (click to enlarge)
Cerebral aneurysms principally develop at sites of turbulent blood flow (often bifurcations) due to intravascular shear stresses.
About 80-90% of aneurysms are found in the anterior carotid circulation (Fig 1) or communicating arteries of the Circle of Willis [7] and in a quarter of affected individuals these are multiple [7].
As aneurysms increase in size, wall tension rises and compliance reduces leading to an increased tendency to rupture. When an aneurysm exceeds 2 cm in diameter, it is referred to as a giant aneurysm. However, most aneurysms that rupture are <1 cm in diameter [18].
Learning Bite
Many more people have intracerebral aneurysms than develop SAH and most ruptured aneurysms are small [12-14].