Aneurysm

1. Intracranial Extradural Aneurysms [CAROTID-CAVERNOUS
ANEURYSMS]
Almost all of the lesions in the extradural group are cavernous carotid aneurysms.the lesions are saccular in type
and congenital in origin, presumably arising in connection with the numerous intracavernous minor branchings
of the internal carotid artery. In approximately one-fourth of the cases, cavernous carotid aneurysms are bilateral.
figure [1] carotid cavernous aneurysm
If such an aneurysm ruptures, a carotid-cavernous fistula results. In the absence of trauma, the spontaneous
rupture of a saccular aneurysm is the most common cause of an arteriovenous fistula in this location. After a fistula
has developed, it may be difficult or impossible to demonstrate the original sacculation by angiography because of
surrounding dural sinus opacification, unless the arterial aneurysm had attained considerable size prior to rupture.
The second principal manifestation of a cavernous carotid aneurysm is its mass effect. Occasionally, symptoms may
develop because of blockage of the cavernous sinuses. Some cavernous aneurysms become extremely large. This is
possible because as they expand, usually upward, they are covered by the dural wall of the sinus which helps prevent
early rupture. Rarely, they may act as an extracerebral subfrontal tumor in the anterior fossa . More often, they
expand into the suprasellar cistern; an aneurysm must always be included in the differential diagnosis of suprasellar
tumors .Less frequently, such a lesion may extend laterally and backward. Also, infrequently, the expansion
of such aneurysms may so thin the overlying dura that they rupture intracranially to produce a subarachnoid
hemorrhage or intracerebral hematoma. In many cases, a large portion of the aneurysmal lumen may be filled by
organized thrombus, and a shell of calcium about its periphery may allow diagnosis from plain skull films .
Inspite of the organized thrombus and calcification, many such lesions continue to enlarge slowly throughout life.
Erosions of the superior orbital fissure, the lateral aspect of the sella turcica, and of the clinoid processes are
sometimes found.
Cranial nerves are often compressed because of the expanding mass of a cavernous-carotid aneurysm.The larger
lesions extending into the suprasellar cistern may compress the optic nerves and chiasm producing visual
impairment.These originate usually from the carotid system but may also arise from the basilar artery

2. Within the cavernous sinus, the internal carotid artery lies chiefly below and medial to the oculomotor nerve .A
rather similar relationship pertains to the trochlear nerve, whereas the abducent nerve is very close to the lateral wall
of the carotid qrtery, along the transverse course of the vessel in the cavernous sinus. Extraocular movements
and other functions may be impaired by compression of one or more of these cranial nerves by a cavernous
aneurysm. A medially projecting aneurysm is occasionally seen to encroach upon the cavity of the sella turcica.
Intracranial Intradural Aneurysms
VASCULAR ECTASIA
Fusiform lesions resulting from atherosclerosis were
among the earlist intracranial aneurysms described and,
although they are not nearly as common as
congenital saccular lesions, they are occasionally
encountered in the course of examination of older
individuals.The major vessels at the base of the brain,
particularly the basilar artery, are most commonly
affected. The basilar artery is frequently found to be
ectatic to a marked degree; the vessel is also usually
elongated and tortuous . As noted earlier, the
increased mass of
the artery may produce indentation of the floor of the third ventricle and interference with the circulation of
cerebrospinal fluid.Occasionally, the vertebral artery may undergo aneurysmal atherosclerotic dilatation. A greatly
elongated and ectatic vertebral artery may press upon cranial nerves and even simulate a cerebellopontine angle
tumor clinically and at CT scan and MRI
Basilar and vertebral fusiform aneurysms may displace the brainstem backward and upward; it may also be displaced
laterally by eccentric aneurysmal dilatation of an elongated S-shaped basilar artery and some lesions indent and
compress the brain stem. They seldom rupture, but there are often symptoms of ischemia.

3. figure [2] thrombosed ectatic basilar artery
Apparently the orifices of branch vessels
become occluded by the intimal disease.
At times, the carotid siphon is grossly
ectatic and tortuous.The enlargement may
extend into the proximal segments of the
main branches of the internal carotid and
basilar arteries and elements of the circle of
Willis may be involved.
Figure [3] vertebrobasilar ectasia
True saccular aneurysms of principal arteries atthe base of the brain produce mass effects, when they become
large without rupturing, even more often than fusiform aneurysms, which may be silent. A large supraclinoid
aneurysm of the carotid siphon frequently extends medially and upward to compress the optic chiasm and
hypothalamus . There may even be obstruction at the foramen of Monro. In many instances, a large portion of the
aneurysm is filled by mural thrombus so that there is much more vascular displacement than can be accounted for by
the size of the opacified lumen at angiography.
Occasionally, an aneurysm arising at the origin of the ophthalmic artery may be encountered. Such a lesion
may arise either intradurally or extradurally. Similarly, its expansion may occur within the subarachnoid space or
extradurally along the course of the vessel toward the optic foramen. In the latter instance, erosion of the inner
end of the optic canal may be visible on plain skull radiographs. Such an aneurysm can compress the optic nerve
against the bony edge of its canal.
Surprisingly large aneurysms can develop along the course of the middle cerebral artery. Although many middle
cerebral aneurysms bleed when they are relatively small,occasional aneurysms along the course of this vessel over
the anterior perforated substance and between the temporal lobe and insula become sufficiently enlarged to act as
tumors.
Saccular aneurysms of the basilar artery may become very large. Their massive proportions are probably
related to the frequent development of a large organized thrombus about the periphery of the lumen. Circulation in
the lumen of the lesion may constitute a relatively small part of its total volume
At angiography, an estimation of the true size of the mass may be gained from the displacements of adjacent
vessels and the circumferential course of the basilar arterial branches around the lesion and the displaced and
deformed brainstem. Basilar artery aneurysms often imbed themselves deeply in the anterior or anterolateral
aspect of the brainstem. Long tract signs are frequently produced. The aqueduct of Sylvius may be displaced far
backward and narrowed, and the floor of the posterior part of the third ventricle may be invaginated. Narrowing
of the aqueduct frequently produces hydrocephalus involving the lateral and third ventricles

4. There also may be interference with cerebrospinal fluid circulation at the tentorial incisura. Such a large basilar
artery aneurysm occasionally ruptures into the brainstem, even after having been present for very Prolonged periods
of time, during which it has acted as a slowly expanding anterior extra-axial mass.
Some of the larger aneurysms can be identified by computerized tomography. With this technique, increased
radiation absorption may be caused by a calcified shell, a densely organized mural thrombus, blood, or a blood clot in
the lesion; or the density of an unclotted aneurysm may be enhanced by contrast enhancement techniques.