A Cerebral Aneurysm is a focal abnormality of the wall of an artery that lead to the formation of outpouchings most commonly at the level of arterial bifurcations. Intracranially they are mainly found at the base of the brain, along medium-sized arteries of the circle of Willis. They may be classified according to aetiology, location or morphology.
The great majority of aneurysms are of congenital origin. However, infection may lead to formation of aneurysms (so called mycotic aneurysm in bacterial endocarditis), as well as atherosclerosis or dissection of an artery. Excessive flow, as may be found in arteries leading to arteriovenous malformations, may cause the formation of aneurysms (flow-related).
From a morphological point of view aneurysms are classified into three different groups: "saccular or berry" (Fig.1) (Fig.2), "fusiform" (Fig.3) and "dissecting."
The size of the aneurysm may vary from small (less than 4 mm in diameter), to medium (up to 1 cm in diameter), large and giant.
Not infrequently large and giant aneurysms have partially thrombosed components that reduce the size of the lumen.
The incidence of aneurysms in the population is not precisely known and is estimated to be from 1 to 5%.
Although the aetiology is unknown, congenital factors may play a role; in patients with polycystic kidney disease the incidence of intracranial aneurysms is higher than in the normal population, rising up to 10%. Hypertension, atherosclerosis and other tissue connective disorders may play a role.
Aneurysms may present with acute symptoms of subarachnoid haemorrhage when they rupture, with slowly progressive neurological signs, particularly when they are large or giant, or may be asymptomatic. Cavernous aneurysms, do not rupture in the subarachnoid space; a spontaneous carotid cavernous fistula is the usual result of their rare rupture.
The degree of subarachnoid haemorrhage may vary and produce a clinical syndrome of varying severity, graded according to a widely adopted scale (Hunt and Hess).
Radiologically, the diagnostic protocol varies according to the clinical presentation. In subarachnoid haemorrhage CT examination comes first. CT shows the extravasated blood as hyperdensity within the basal cisterns and subarachnoid spaces. Preferential location, or pooling, of blood may suggest the location of the aneurysm ("sylvian haematoma" suggests rupture of a middle cerebral artery aneurysm; "septal haematoma" is most commonly found in ruptured anterior communicating artery aneurysms; pooling of blood in front of the brain stem suggests basilar artery aneurysms). Nonruptured aneurysms, when large enough, may be seen as round isointense nodules within the basal subarachnoid spaces, sometimes with calcified walls; they intensely enhance following contrast injection.
The second diagnostic procedure, to be performed immediately after emergency CT, is selective cerebral angiography. Both carotid arteries and vertebral arteries must be injected. External carotid arteries should also be visualized, particularly if intracranial angiography is negative, because sometimes subarachnoid haemorrhage may be due to rupture not of an aneurysm but of dural arteriovenous malformations.
Angiography should aim at recognizing the aneurysm, its precise location, size, size of the neck, relationship with the parent vessel and multiplicity. To achieve this goal the ideal procedure is rotational angiography with three-dimensional reconstruction. This is particularly useful if an endovascular occlusive procedure is planned.
CT angiography with three-dimensional reconstruction is also performed in some centres.
MR may be useful only in large and giant aneurysms to better evaluate thrombosed components and the relationship with adjacent nervous structures. Giant aneurysms appear as round structures with different signal intensities related to the presence of old or fresh thrombus and flowing blood. Paramagnetic T2 shortening (hypointense signal) produced by haemosiderin may be found as well as T1 shortening (hyperintense signal) due to methaemoglobin. The flow void produced by flowing blood is reflected by absence of signal in both T1- and T2-weighted images.
MR angiography may be useful for detecting intracranial aneurysms in screening procedures, such as in patients with polycystic kidney disease or in family members. Its resolution, however, does not allow recognition of aneurysms below 2–3 mm in diameter and is definitely not sufficient for surgical or endovascular treatment planning. Angio MR is frequently used in the follow-up of treated patients.
Micotic aneurysms may be suspected when they are not based at the circle of Willis but develop on distal branches of the middle, anterior or posterior cerebral arteries. They are false aneurysms, being produced by an inflammatory process involving the three layers of the vessel wall, and do not have a neck. Their treatment requires sacrifice of the parent artery.
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Aneurysm, cerebral, Fig.1 (a)
Aneurysm, cerebral, Fig.1 (b)
Aneurysm, cerebral, Fig.1 (c)
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Aneurysm, cerebral, Fig.2 (a)
Aneurysm, cerebral, Fig.2 (b)
Aneurysm, cerebral, Fig.2 (c)
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Aneurysm, cerebral, Fig.3 (a)
Aneurysm, cerebral, Fig.3 (b)
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