or torn veins. Blood can also extend into the SASs from
parenchymal hemorrhage that ruptures through the cortex
and pia, spilling into the adjacent SAS.
Trauma, "burst" aneurysm, vascular malformations, and
amyloid angiopathy are potential causes of subarachnoid
hemorrhage (SAH). The most common cause of SAH is trauma.
Traumatic SAH (tSAH) occurs when hemorrhage from
contused brain or lacerated cortical vessels extends into sulci
Aneurysmal SAH (aSAH): Nontraumatic "spontaneous" SAH
represents about 5% of all acute "strokes." The most common
cause of nontraumatic SAH is a ruptured intracranial saccular
("berry") aneurysm (aSAH). Because most saccular aneurysms
(SAs) are located either on the circle of Willis or at the middle
cerebral artery bifurcation, the most common locations for
aSAH are the suprasellar cistern and sylvian fissures.
aSAH can be focal or diffuse. Attempts to determine the
precise anatomic location of a suspected intracranial
aneurysm based on the distribution of SAH are necessarily
imprecise. Anterior interhemispheric aSAH is typically
associated with rupture of a superiorly directed anterior
communicating artery aneurysm. aSAH seen primarily in the
posterior fossa cisterns &/or 4th ventricle suggests a posterior
Perimesencephalic nonaneurysmal SAH (pnSAH): An
uncommon but important cause of SAH, pnSAH, is a clinically
benign variant that is probably venous in origin. pnSAH is
confined to the cisterns around the midbrain and anterior to
Convexal SAH (cSAH): An uncommon subset of nontraumatic
SAH occurs over the dorsolateral surface ("convexity") of the
cerebral hemispheres. The basal and perimesencephalic
cisterns are typically spared. cSAH typically affects just 1 sulcus
or a grouping of adjacent sulci. Common etiologies in older
adults are amyloid angiopathy or vasculitis, whereas vasculitis
and reversible cerebral vasoconstriction syndrome are
common causes in patients < 60 years old. Cortical vein
occlusion with cSAH occurs at all ages.
Superficial siderosis (SS): Chronic, recurrent SAH results in
hemosiderin deposition on the pia and cranial nerves. The
brain, brainstem, cerebellum, and spinal cord can all be
affected, although the posterior fossa is most commonly
The classic clinical presentation of SS is in an adult with a
history of trauma or surgery, who presents with ataxia and
bilateral sensorineural hearing loss. A history of aSAH is
uncommon. SS is best identified on T2* (GRE or SWI).
Aneurysms and Arterial Ectasias
Terminology and overview: The word "aneurysm" comes
from the combination of 2 Greek words meaning "across" and
"broad." Hence, brain arterial aneurysms are widenings or
dilatations of intracranial arteries.
Intracranial aneurysms are generally classified by their
phenotypic appearance. Saccular or "berry" aneurysms are the
most common type. Fusiform aneurysms are focal dilatations
that involve the entire circumference of a vessel and extend
for relatively short distances. Ectasias refer to generalized
arterial enlargement without focal dilatation and are not true
Saccular aneurysm (SA): As the name implies, SAs are focal
sac- or berry-like arterial dilatations. The vast majority are
acquired lesions, the result of an underlying genetically based
susceptibility plus superimposed mechanical stresses on
vessel walls. SAs lack the 2 strongest layers of blood vessel
walls, the internal elastic lamina and the muscular layer. The
aneurysm sac itself consists of only intima and adventitia.
Most SAs arise at major blood vessel bifurcations, where
hemodynamic stresses are highest. The vast majority of
intracranial aneurysms are located on the circle of Willis plus
the middle cerebral artery bi- or trifurcation. 90% are "anterior
circulation" aneurysms, i.e., on the internal carotid artery and
its branches. The posterior communicating artery is
considered part of the anterior circulation; the vertebrobasilar
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