Of nontraumatic subarachnoid hemorrhages, approximately 80% are due to a ruptured berry aneurysm.

Rupture of arteriovenous malformations (AVMs) is the second most identifiable cause of SAH, accounting for
10% of cases of SAH. Most of the remaining cases result from rupture of the following types of pathologic
entities:

Mycotic aneurysm
Angioma
Neoplasm
Cortical thrombosis
SAH may reflect a secondary dissection of blood from an intraparenchymal hematoma (eg, bleeding from
hypertension or neoplasm).
Both congenital and acquired factors are thought to play a role in SAH. Evidence supporting the role of
congenital causes in aneurysm formation includes the following:

Clusters of familial occurrence, such as in Finland, where the incidence of familial cerebral aneurysm
is 10%
Significant incidence of multiple aneurysms in patients with SAH (15%)
The association of aneurysms with specific congenital diseases (eg, coarctation of the aorta, Marfan
syndrome, Ehlers-Danlos syndrome, fibromuscular dysplasia, polycystic kidney disease)
Familial cases of AVM are rare, and the problem may result from sporadic abnormalities in embryologic
development. AVMs are thought to occur in approximately 4-5% of the general population, of which 10-15% are
symptomatic. Congenital defects in the muscle and elastic tissue of the arterial media in the vessels of the
circle of Willis are found in approximately 80% of normal vessels at autopsy. These defects lead to
microaneurysmal dilation (< 2 mm) in 20% of the population and larger dilation (>5 mm) and aneurysms in 5%
of the population.
Acquired factors thought to be associated with aneurysmal formation include the following:

Atherosclerosis
Hypertension
Advancing age
Smoking
Hemodynamic stress
Less common causes of SAH include the following:

Fusiform and mycotic aneurysms

Fibromuscular dysplasia
Blood dyscrasias
Moyamoya disease
Infection
Neoplasm
Trauma (fracture at the base of the skull leading to internal carotid aneurysm)
Amyloid angiopathy (especially in elderly people)
Vasculitis

Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by recurrent thunderclap headaches

and reversible segmental multifocal cerebral artery narrowing, and it results in SAH in more than 30% of cases.
Muehlschlegel and colleagues found that clinical and imaging findings can differentiate RCVS with SAH from
other causes of SAH.[8, 9]
After analyzing clinical and imaging features of 38 patients with RCVS-SAH, 515 patients with aneurysmal
SAH, and 93 patients with cryptogenic (angiogram negative) SAH, Muehlschlegel et al identified clinical
characteristics and radiological findings that can differentiate RCVS-SAH from aneurysmal SAH or cryptogenic
SAH. These researchers concluded that these differences may be useful for improving diagnostic accuracy,
clinical management, and resource utilization. [8, 9]

Risk factors
Although risk factors for SAH have been evaluated extensively, little conclusive evidence has been derived.
Smoking appears to be a significant risk factor, as does heavy alcohol consumption. The risk of AVM rupture is
greater during pregnancy. Data regarding the relationship between hypertension and SAH are conflicting.
Previously documented acute severe hypertension with diastolic pressure over 110 mm Hg has been linked to
SAH.
The following do not appear to be significant risk factors for SAH:

Use of oral contraceptives

Hormone replacement therapy
Hypercholesterolemia
Vigorous physical activity