Intracranial Aneurysms, Diagnosis and Treatment

The term aneurysm usually refers to a persistent pathologic dilatation of an arterial wall. In certain diseases, particularly arteriovenous malformations, the possibility of aneurysms affecting venous structures must be considered as well. Arterial aneurysms may be described according to configuration as fusiform, when the whole vessel circumference is involved (Figs. 18-1 and 18-2), or saccular, when the lesion is eccentric. Mild dilatation of a segment of vessel is called ectasia. The point at which diffuse ectasia becomes an extended fusiform aneurysm is often difficult to define objectively. The term pseudoaneurysm is used when the circumferential containment of the lumen by the arterial wall is lost to a substantial degree and is dependent on an improvised barrier of clot, adventitia, or surrounding tissues.

Extradural Aneurysms and Pseudoaneurysms

Extradural aneurysms are unlikely to cause subarachnoid hemorrhage, unless they rupture with particular force against the dura. They are therefore, usually considered to be less immediately life-threatening than subarachnoid aneurysms. The commonest location for true aneurysms of the extradural carotid artery is in the cavernous segment.

Aneurysms of the Petrous and Cervical Segments of the Internal Carotid Artery

Aneurysms of the petrous and cervical segments are uncommon. They are sometimes seen in patients with connective tissue diseases. However, pseudoaneurysms in these areas are encountered more frequently. They can be related to complications of posttraumatic or idiopathic dissection, parapharyngeal infection, infection of the petrous air cells, skull fracture, surgical or traumatic laceration, or tumor invasion. When complications of bleeding or embolic phenomena in the internal carotid artery territory occur, these lesions can constitute a serious risk to life. Bleeding from a petrous aneurysm may occur when erosion of the adjacent supporting bone permits rupture of the aneurysm into the middle ear or sphenoid sinus. These aneurysms or pseudoaneurysms may also present with mass effect as they bulge into adjacent structures, particularly the floor of the middle cranial fossa where they may compress branches of the trigeminal nerve.

Aneurysms of the Cavernous Segment of the Internal Carotid Artery

Aneurysms in this location are relatively common and are seen particularly in older patients. They may be fusiform or have a relatively defined neck. Frequently, there are variable degrees of intraluminal thrombus and atherosclerotic mural changes. They are often giant in size (>25 mm), in which case they are likely to present with mass effect and neuropathy of the paracavernous cranial nerves. They may rupture into the cavernous sinus and establish a carotid-cavernous fistula. It is uncommon for them to rupture into the subarachnoid or subdural spaces.

Cavernous aneurysms projecting medially into the sella turcica are thought to carry a particular risk of subarachnoid hemorrhage if they rupture, but even this phenomenon for aneurysms in this particular location is rare. Additional care is advised for large cavernous aneurysms when the support of the sphenoid sinus wall has become eroded. Rupture of an aneurysm in this direction is life-threatening due to exsanguinating epistaxis, a feature to bear in mind when reading the CT bone windows.

Most small cavernous aneurysms are incidental observations on angiographic or axial examinations. Asymptomatic cavernous aneurysms are usually not treated unless there is compelling evidence of imminent complications.

False Aneurysms of the Intracranial Circulation

Cerebral aneurysms can be classified according to location, size, etiology, or configuration. When classified by
the integrity or otherwise of their mural components, they can be separated into true aneurysms (intima and adventitia intact) or pseudoaneurysms. A pseudoaneurysm is one in which the wall of the artery has been perforated. The apparent lumen of the opacified aneurysm is contained by an organized extraluminal hematoma.

Figure 18-1. Fusiform aneurysm. A fusiform aneurysm (arrows) of the right middle cerebral artery involves the entire circumference of an extended segment of vessel. With an irregular appearance over a long segment of vessel, it is fairly probable that a dissection mechanism played a role in the genesis of this aneurysm.

Figure 18-2. Mild dysplasia. The communicating segment of the supraclinoidal right internal carotid artery in this patient demonstrates mild ectasia (arrowheads) and an alteration in caliber, in contrast to the more proximal internal carotid artery. Infundibular widening (arrow) of the origin of the posterior communicating artery extends posteriorly from this segment.

Postsurgical Pseudoaneurysms

False aneurysms of the proximal or distal intracranial vessels after surgery are rare. They have been seen following vessel injury in the course of open or endoscopic sinus surgery (1,2,3,4), transsphenoidal pituitary procedures (5,6), stereotactic biopsy (7), or craniotomy for a variety of reasons (8).

Traumatic Intracranial Aneurysms

Pseudoaneurysms of the intracranial circulation may be seen as a result of penetrating or nonpenetrating head injuries (9), impaction on the vessel by bone fragments (10), or following surgical injury (11,12). They are typically seen in young males after severe injury to the head (Figs. 18-3 and 18-4), but more than 30% are identified in children (13,14). Posttraumatic lacerations of intracranial major vessels are often fatal, and in the past it would have been unusual for a patient so injured to reach medical attention.

A consistent theme in the literature dealing with posttraumatic pseudoaneurysms is that their discovery depends entirely on the index of suspicion of the managing physician. Without angiography, they frequently elude early detection. They can be present with subacute or delayed rebleeding or other complications, typically after a period of 1 or 2 weeks but possibly as long as months (9,15).

These injuries can be seen in the anterior or posterior circulation (16) and most frequently have a contiguous or related bone injury. Their discovery is usually associated with penetrating injuries in which the missile impact has scattered numerous fragments of bone or metal in diverging trajectories, particularly when fragments are seen close to the skull base (17).

Pseudoaneurysms in the setting of closed head injury have also been seen where no violation of the dura or skull is present (18). Pseudoaneurysms may be seen with closed head injury, particularly in children, when frontolateral shear injuries cause significant impaction of the pericallosal and callosomarginal branches against the falx cerebri, or of the middle cerebral artery against the sphenoid ridge (19). Traumatic aneurysms may account for 14% to 39% of intracranial aneurysms in the pediatric population (20). Traumatic intracranial pseudoaneurysms may be a more significant problem in military experience than in civilian life. While they were described as rare in the Korean and Vietnamese wars (21,22), experience in Lebanon and in the Iran–Iraq wars in the 1970s and 1980s indicates an incidence higher than once supposed (9,17,23,24), a trend that has become even more prominent with the high incidence of blast and penetrating head injuries casualties returning from the Iraq and Afghanistan wars (25,26,27,28). As many as 35% of military casualties from these conflicts who undergo cerebral angiography for vascular problems demonstrate intracranial or extracranial pseudoaneurysms, as well as other cerebrovascular complications such as vasospasm (29), vessel occlusions, or late development of carotid-cavernous fistulas (30).

Intracranial pseudoaneurysms also feature prominently in low-velocity civilian injuries, such as in South Africa where stabbing injuries to the head are more commonplace than in the Occidental urban experience. In stabbing victims, vascular injuries to the head may reach an incidence of

30%, including pseudoaneurysms, dissections, fistulae, and occlusions (31).

Figure 18-3. (A–C) Traumatic intracranial pseudoaneurysm. A: A young adult was shot accidentally behind the left mastoid bone. The bullet traversed the intracranial space and lodged in the left orbit, which it enucleated. A left common carotid arteriogram demonstrates bullet fragments extending from the middle cranial fossa to the orbit. The supraclinoidal left internal carotid artery is attenuated and fills a pseudoaneurysm in the expected region of the posterior communicating artery (arrows). B: Endovascular treatment was planned but delayed because of prolonged sepsis. A left common carotid arteriogram performed 3 weeks after the first study demonstrates change in the contour of the pseudoaneurysm and less filling of the ipsilateral hemispheric circulation. C: The left internal carotid artery was therapeutically occluded using detachable balloons proximal to the pseudoaneurysm. A right internal carotid artery injection following left internal carotid artery occlusion shows no evidence of filling of the aneurysm. The patient recovered with moderate right-sided paretic and language deficits.

Figure 18-4. (A–B) Traumatic dissection and occlusion of the basilar artery. A young adult male involved in a high-velocity motor vehicle accident demonstrates a sagittally oriented fracture of the clivus (arrow in A). His left vertebral artery arteriogram demonstrated complete occlusion of the basilar artery (arrow in B) in its proximal segment, an injury from which no likelihood of a neurologic recovery could be countenanced.

Figure 18-5. (A–B) Carotid cavernous fistula following trauma. Lateral (A) and PA (B) views of the left internal carotid artery injection in a young adult following severe head trauma. There is immediate and profuse opacification of venous structures due to fistulous flow from the cavernous internal carotid artery. Intercavernous connections fill the contralateral cavernous sinus. Although his symptoms were relatively mild, the angiographic appearance of varicose distention of the anterior segment of the basal vein (BV) and opacification of parenchymal veins of the posterior fossa (arrowheads) suggest that complications of venous hypertension may be imminent (SOV, superior ophthalmic vein; SS, straight sinus.)

Complications specifically related to false aneurysms include delayed rupture; mass effect on adjacent brain or cranial nerves; or an associated intraparenchymal, subarachnoid, or subdural hemorrhage. Delayed presentation may be seen months or even years following the initial injury (32). Acute or delayed complications of carotid injuries in the sphenoidal region include carotid cavernous fistulae and massive epistaxis from the sphenoidal sinus (Figs. 18-5 and 18-6).

Posttraumatic aneurysms represent a difficult management problem, as there is a significant risk of profuse bleeding at surgery when the dura is opened. Trapping of the pseudoaneurysm or occlusion of the parent vessel proximal to the laceration by surgical or endovascular means may represent the best therapeutic option in certain circumstances (25,27,33).

Immediate angiography for patients with penetrating head injuries is likely prudent as approximately 12% to 35% of such patients will have an intracranial pseudoaneurysm (29,34). Follow-up angiography may be necessary for patients in whom spasm or other vascular abnormalities preclude adequate evaluation.

Fusiform Intradural Aneurysms

Fusiform aneurysms are frequently associated with vessel tortuosity, hypertension, atherosclerosis, and advancing age. They typically affect the cavernous or supraclinoidal internal carotid artery and the basilar trunk. They often present with symptoms related to mass effect (Fig. 18-7). With large aneurysms, stagnation of blood can lead to thrombus formation, and patients may present with embolic stroke (35,36). Rupture is not common when the condition is mild (37). Surgical management of a ruptured fusiform
segment of vessel can be difficult (38). Techniques, including wrapping, proximal occlusion, or bypassing, must make allowance for preserving important perforator vessels, which might take origin from the dysplastic segment (39). Endovascular treatment with flow-diverting stents, such as Pipeline or Silk, will undoubtedly play more of a role in the treatment of these difficult lesions in the future (40,41,42,43).

Figure 18-6. Remember to examine the venous structures when evaluating penetrating missile injuries. Venous injury may follow penetrating injuries. In this patient, the right transverse sinus has been occluded by bullet fragments lodged in the right mastoid bone.

Figure 18-7. Fusiform dysplasia/aneurysm of the basilar artery. Changes of this degree are frequently associated with a history of long-standing hypertension. Vessel changes may be more extreme than indicated on an angiogram. Circumferential thrombus augments the degree of mass effect on surrounding structures.

When ectasia of the basilar artery reaches bizarre proportions, the terms megadolichobasilar anomaly or giant fusiform aneurysm are used (Fig. 18-8) (36,44). They represent less than 1% of intracranial aneurysms. Although they are classically described as affecting the vertebrobasilar circulation, giant fusiform or serpentine aneurysms are also seen in the anterior circulation (39) (Fig. 18-8). This group of usually elderly patients typically presents with mass effect, brainstem compression, cranial nerve deficits, obstructive hydrocephalus, subarachnoid hemorrhage, and embolic strokes due to stagnation of blood. Underlying, partially healed dissection likely explains the genesis of many of these aneurysms (45). Furthermore, long-term clinical follow-up of this group of patients indicates a poor prognosis due to recurrent subarachnoid hemorrhage or progressive mass effect.

Mycotic and Inflammatory Aneurysms

Mycotic aneurysms are classically described as occurring distally in the cerebral circulation and as being not necessarily related to vessel bifurcation points. They may be subtle in appearance and are frequently best seen in the parenchymal phase of the injection when the arteries are already washing out.

Intracranial aneurysms of inflammatory origin may be of several types: Bacterial; syphilitic (Heubner arteritis); related to angiocentric organisms such as mucormycosis, aspergillus (46), or other fungi; or associated with systemic arteritides such as giant cell arteritis, human immunodeficiency virus (HIV), and polyarteritis nodosa (Fig. 18-9).

In the modern era, an increased incidence of aneurysms related to HIV or its associated infections has been described. This may be primarily due to a necrotizing vasculitis related to the virus itself, particularly in congenital infections, or due to acquired diseases such as tuberculosis or syphilis (47,48,49).

Presentation and Incidence of Mycotic Aneurysms

Mycotic intracranial aneurysms present most commonly with acute subarachnoid hemorrhage or intraparenchymal hematoma developing as a complication of already established septic disease. Occasionally, young patients may present with an embolic neurologic deficit, such as hemiplegia, as the presenting event of bacterial endocarditis (Figs. 18-10 and 18-11) (50). Other common presentations include seizure or focal neurologic signs due to vasculitis or vegetative emboli in an area of the brain distal to a silent aneurysm (51). Direct vessel invasion from adjacent infected paranasal sinuses may also be seen (Figs. 18-12 and 18-13).

Although mycotic aneurysms are typically described as being found in unusual peripheral locations, multiple in number, and not necessarily related to vessel bifurcations, this archetype is not always valid (52). They may be single in presentation and centrally located. Mycotic aneurysms can be seen in the cavernous carotid artery when a systemic illness is complicated by cavernous thrombophlebitis (53). When an aneurysm is seen in an unusual peripheral location, the possibility of an infectious embolic etiology should be considered, but not all mycotic aneurysms are atypical in appearance or location.

Bacterial aneurysms were typically associated with bacterial endocarditis when this disease was more common but can be seen with any septicemic state, particularly with respiratory infections. Older studies suggest that the incidence of intracranial aneurysms in patients with endocarditis varies between 4% and 15% or perhaps higher, and many of these aneurysms remain asymptomatic (53,54).

Mycotic aneurysms are related to impaction of a septic embolus in the intima of a peripheral cerebral artery with development of a resulting arteritis, focal mural necrosis, and aneurysm formation. This explains the friable nature of the wall of these lesions and their propensity to bleed spontaneously or during surgery.

Figure 18-8. (A–D) Megadolichobasilar anomaly and serpentine aneurysm. (Two cases) Townes (A) and lateral (B) projections of a megadolichoectatic basilar artery in an elderly hypertensive patient. A CT scan of the head (C) in a young adult presenting with sudden headache demonstrates a focal collection of blood in the right Sylvian fissure. An oblique RAO view (D) of the right internal carotid artery injection demonstrates an elongated fusiform or “serpentine” aneurysm of the parietal branch of the right middle cerebral artery.

Figure 18-9. (A–B) HIV-associated arteriopathy. A middle-aged patient with advanced complications of HIV and fluctuating neurologic deficits showed subtle pial enhancement on a gadolinium enhancement MRI (not shown) but no confirming evidence of a meningitis or cerebritis could be found. An angiogram of the left internal carotid artery (A) and magnification view of the right internal carotid artery (B) showed diffuse arterial disease characterized by aneurysmal dilatation of multiple segments of arteries through the anterior circulation. In the absence of an identifiable other cause, this arterial disease was assumed to be a direct effect of the HIV virus itself.

Figure 18-10. (A–B) Mycotic aneurysm of the right middle cerebral artery. A young patient with known bacterial endocarditis had a change in mental status and a CT scan (A) demonstrated a hemorrhagic masslike region in the parietal lobe of the right hemisphere. A right common carotid artery angiogram (B) demonstrates a mycotic aneurysm of the parietal branch of the right middle cerebral artery, which was assumed to be embolic from the primary site of endocarditis.

Figure 18-11. (A–B) Mycotic aneurysm of the right middle cerebral artery. This peripheral aneurysm (arrows) in a patient with infective endocarditis is demonstrated on a skewed lateral view (A). The aneurysm has a fusiform, tapered appearance extending into adjacent branches. Small peripheral mycotic aneurysms are frequently best seen on a late arterial phase when the main arterial structures have begun to lose density (B).

Figure 18-12. (A–C) Carotid pseudoaneurysm with aspergillus infection. An elderly patient with intractable aspergillus infection of the left orbital apex extending to the left cavernous sinus, seen on the gadolinium-enhanced MRI image (arrow in A). An angiogram (B) was performed to evaluate for possible pseudoaneurysm formation but was negative. Two weeks later, with a suspicious flow void evident on a follow-up MRI, a rapidly developing pseudoaneurysm was demonstrated on a second angiogram (arrow in C).

Role of Endovascular Intervention in Management of Mycotic Aneurysms

Some inflammatory aneurysms, a third or more in some series, tend to regress with treatment of the primary infection (45,46,47) (55,56,57). Possibly as many as a third of them will resolve spontaneously with medical treatment alone (52,55). Better results are seen in patients with single, unruptured aneurysms. Sequential angiography in patients with infective endocarditis may be reasonable where a high index of suspicion for development of lesions, even in the setting of active treatment, much be maintained. Surgical evacuation of ruptured aneurysms with hematoma and endovascular treatment of unruptured aneurysms are typically necessary when medical management fails (51,58,59,60).

Oncotic Intracranial Aneurysms

Invasion of the intracranial vessel wall with destruction of the internal elastic lamina and cavitation with aneurysm or pseudoaneurysm formation is a rare but well-recognized event from metastatic deposits of atrial myxoma,
choriocarcinoma (61,62), renal cell carcinoma, or bronchogenic carcinoma (63,64,65). Invasion of arteriolar walls by gliomatous tumors may explain the very rare association of false aneurysms with primary brain tumors (66). Features shared by oncotic aneurysms are that they may be delayed at the onset (i.e., they may not be seen on an initial angiogram), may be multiple, may grow rapidly, or may thrombose spontaneously. They may resolve with chemotherapy for the primary lesion (67).

Figure 18-13. (A–C) Myxomatous emboli and aneurysms. A nonenhanced CT (A) examination in a young adult patient with a known cardiac myxoma demonstrates multiple intraparenchymal hemorrhagic foci. Lateral (B) and PA (C) views of the left internal carotid arteriogram demonstrated multiple peripheral areas of pseudoaneurysm formation (arrowheads).

Left atrial myxoma may be complicated by or present with neurologic symptoms related to arterial obstruction by myxomatous emboli or intracranial aneurysmal rupture with subarachnoid or intraparenchymal hemorrhage (Fig. 18-13) (68,69,70). The destructive and invasive nature of the histologic findings with embolization of cardiac myxoma is ascribed to the high degree of elaboration of matrixmetalloproteinases and interleukin-6 by this tumor (71,72). Although this is a rare clinical presentation, it is a treatable disease that can be seen in otherwise healthy young patients. Systemic emboli from myxoma have been reported in up to 45% of patients, one-half of these going to the cerebral circulation (73). The diagnosis may be delayed due to the initially small size of the cardiac tumor (74). Angiographic features described in these patients include intraluminal filling defects, fusiform or saccular peripheral aneurysms, vessel occlusions, and delayed passage of contrast. Some peripheral aneurysms may be extremely subtle and could be missed if not looked for carefully on the late arterial or parenchymal angiographic phase.

Intracranial Dissections and Dissecting Aneurysms

Dissection of intracranial vessels, once considered an extremely rare disease (75), is now a more recognized entity representing as many as 3% to 7% of patients presenting with nontraumatic subarachnoid hemorrhage and possibly as many as 50% of aneurysms in the younger pediatric age group (76,77,78,79,80,81). In general this phenomenon is a devastating disease when the presentation is hemorrhagic with a mortality rate between 17% and 46% or more (78,82). Intracranial dissections are usually clinically idiopathic but have been reported after head trauma, electrocution, with syphilitic and other arteritides of the intracranial vessels, and with conditions such as polyarteritis nodosa, fibromuscular
dysplasia, and migraine (Figs. 18-14–18-17). Before 1950, more than one-half of recognized cases were associated with the meningovascular phase of syphilis (Heubner endarteritis), a disease seen now as a result of the AIDS epidemic. Some cases of intracranial dissection in older patients might be related to rupture of intramural arteriosclerotic plaques, but this is unlikely to be an explanation for this disease in younger patients (83).

Figure 18-14. Intracranial dissection in a child. Dissections (arrows) in children have a predilection for the supraclinoidal internal carotid artery. They may be idiopathic or follow trauma. Hemispheric ischemia is the most common presenting event in this age group.

Intracranial dissections are more common in the posterior than in the anterior circulation (Fig. 18-18). Patients typically present in two different ways, either with an acute subarachnoid hemorrhage related to rupture of the arterial pseudoaneurysm or with nonhemorrhagic complication such as suboccipital headache, mass effect, focal neurologic deficits, or ischemic complications (84). Patients presenting with nonhemorrhagic complications have a much better outcome, whereas those with pseudoaneurysms or subarachnoid bleeding account for most of the mortality associated with this disease. The media and adventitia of the intradural vertebral and carotid arteries are thinner than in the extracranial vessels. Therefore, arterial rupture with subarachnoid hemorrhage as a complication of intracranial dissections is more likely to develop than is the case with extracranial dissections. Intracranial vessels lack an external elastic membrane and have fewer elastic fibers in the media (85). Furthermore, the intracranial arteries are relatively deficient in vasa vasorum (86). Poor healing of intracranial vessels due to the lack of vasa vasorum may be part of the explanation for the greater likelihood of complications in many diseases of these vessels compared with extracranial vessels. In autopsy specimens of intracranial dissection with subarachnoid hemorrhage, extension of clot between the media and adventitia is seen with destruction of all three mural layers (77,87). Intracranial dissections usually affect the major vessel trunks of the circle of Willis, less commonly in the distal vessels (88).

Dissections in the anterior domain of the circle of Willis are less common than in the posterior, and have a predilection for the carotid terminus in children and young adults (76,89,90). Patients may have a variable course after the initial ictus of hemispheric ischemia. Massive infarction and swelling with herniation is the mechanism of death when the deterioration is rapid (91). When vascular occlusion is only partial, patients can survive with variable deficits (Fig. 18-19).

Intracranial dissections can be recognized angiographically by an irregular tapering of the vessel lumen, a linear filling defect within the lumen, retention of contrast within the wall of the vessel, or by the presence of an irregular aneurysm or pseudoaneurysm associated with focal luminal narrowing or irregularity (92,93,94). The angiographic and MRA appearance of the dissected vessel is sometimes described as a “pearl and string” sign, referring to the appearance of fusiform dilatation interrupted by segments of stringlike narrowing (Figs. 18-16 and 18-17). In a small number of patients, a double set of parallel lumens may be seen angiographically (75).

It is important to distinguish dissecting aneurysms from saccular bifurcation aneurysms, as the treatment may be different. Even with good-quality angiography, the signs of intracranial dissection may be subtle. The possibility of a dissection as a source for subarachnoid hemorrhage should be borne in mind during aneurysm search studies. The disease may be bilateral in the vertebrobasilar system in 5% to 10% of cases (95). Optimal treatment for dissecting extradural and intradural aneurysms sometimes involves altering or eliminating, if possible, the flow pattern in the vessel around the pseudoaneurysm. This hemodynamic alteration will suppress the inflow jet. This can be done by surgical clipping of the vessel or vessel reimplantation (96). Endovascular techniques include coiling of the pseudoaneurysm, stenting the vessel, trapping the pseudoaneurysm or occluding the parent vessel proximally, if the patient’s collateral flow will tolerate such a procedure (Fig. 18-20) (97,98,99,100,101,102,103,104,105). It is important to perform this occlusion as close as possible to the aneurysm to eliminate the possibility of continued anterograde flow through collateral vessels (106). Without treatment, dissecting aneurysms with subarachnoid hemorrhage have a rebleed risk reported to be between 30% and 70% (78,107,108,109). Therefore, immediate treatment of intracranial dissecting pseudoaneurysms is advised bearing in mind that ruptured dissecting aneurysms are extremely fragile with a significant risk of intraprocedural rebleeding. The possibility of spasm from subarachnoid hemorrhage related to this disease may affect the efficacy of collateral vessels where vessel occlusion is planned. Dissections without subarachnoid hemorrhage may do well without surgical intervention,

although some of these patients may progress to a chronic fusiform dilatation of the vertebrobasilar system (93) and may ultimately need surgical or endovascular treatment. An important discriminator for the clinical effects of the disease seems to be whether extension to the basilar artery from the vertebral artery occurs. When the disease is more confined and there is no subarachnoid hemorrhage, patients have a far more favorable outcome, and most will resolve their symptoms and angiographic findings within a few months (82,103,110,111).

Figure 18-15. (A–C) Intracranial dissection in a 6-month-old child and the importance of angiographic data in treatment planning. A young infant presented with recurrent episodes of alteration in neurologic status over a 2-week period. Her second CT scan (A) demonstrated a subarachnoid hemorrhage in the suprasellar cistern close to the right internal carotid artery bifurcation, extending toward the right Sylvian region (arrowhead in A). An MRA of the same level (B) confirms the hemorrhage and raises suspicion of an aneurysm in that location (arrow in B). A lateral view of the right common carotid artery angiogram (C) shows an aneurysm (arrow in C) of the distal right internal carotid artery, but its exact origin cannot be discerned. A skewed lateral view (D) shows that the aneurysm is arising above the posterior communicating artery at or above the level of the anterior choroidal artery. Furthermore, the segment of the carotid artery from which the aneurysm arises is narrowed and irregular, virtually pathognomonic for dissection. The left common carotid artery injection (E) shows cross filling via the anterior communicating artery to the right A1 (arrowheads in E), auspicious for the patient being able to tolerate an occlusion of the right internal carotid artery. It can be deduced from the angiogram that the dissection aneurysm is very close to the right A1–M1 junction, meaning that the tolerance for error is very small during an endovascular procedure. Occlusion devices (coils) placed too high would occlude flow to the middle cerebral artery while too low would allow persistent filling of the dissected segment. In an adult patient, one can work around such difficulties with bilateral catheters and repeated test injections of contrast, but in a 6-month-old child, such options do not apply. With hopes of preserving the carotid artery and the anterior choroidal artery, the patient was taken for surgical exploration, but the artery proved itself to be dissected with a mural structure friable and tattered beyond repair. Fortunately, a clip placement just below the A1–M1 junction was feasible with a successful outcome.

Figure 18-16. (A–B) Dissecting aneurysm of the distal left vertebral artery. A middle-aged male presenting with Grade II subarachnoid hemorrhage was found to have a sharply cornered aneurysm (arrowheads) projecting from an irregular segment (arrows) of the vertebrobasilar junction, indicating a dissection. The right vertebral artery did not supply flow to the basilar artery. The patient was treated successfully by balloon occlusion of the left vertebral artery. This resulted in reversal of flow down the basilar artery altering the hemodynamic stress on the ruptured dissection. The procedure jeopardized supply to the left posterior inferior cerebellar artery (P). A right carotid injection during placement of the first balloon in the left vertebral artery (prior to detachment) demonstrated adequate filling of the posterior inferior cerebellar artery, and the patient showed no neurologic deficit to suggest posterior fossa ischemia. Consequently, balloon occlusion of the left vertebral artery was executed. The patient made an excellent recovery.

Figure 18-17. (A–B) Unruptured left vertebral artery dissection. A middle-aged female with complaints of headaches was found to have a suspicious flow void on MRI examination (not shown). A dissection at the vertebrobasilar junction demonstrated a focal area of aneurysmal widening (arrow) associated with extreme narrowing of the proximal basilar artery (arrowhead) above that level (“string and pearl”). The overlapping posterior inferior cerebellar artery (P) made the standard PA and Townes views difficult to interpret. The anatomy of the vertebrobasilar junction was clarified by these obliqued and skewed images.

Figure 18-18. (A–B) Dissecting aneurysm of the right vertebral artery treated by trapping. A middle-aged female patient presented with a severe subarachnoid hemorrhage related to an irregular aneurysm (small arrows in A) of the right vertebral artery. The location and configuration are typical of intracranial dissecting aneurysms. The aneurysm was thought too fragile to withstand stent and coil occlusion. In planning a sacrifice of the right vertebral artery, the absence of a right posterior inferior cerebellar artery on the diseased segment was fortunate, although the status of the anterior spinal artery (small arrowheads in A) had to be considered. Following coil occlusion of the disease segment on the right, a left vertebral artery injection (B) shows reflux into the right vertebral artery stump, but no evidence of penetration into the coil mass. The anterior spinal artery (arrowheads in B) has been preserved. The patient made a promising recovery from the acute presentation and procedure, but eventually succumbed to complications of severe cerebral vasospasm and bowel strangulation.

Figure 18-19. (A–B) Three-month follow-up of an unruptured dissection of the left posterior inferior cerebellar artery. A middle-aged female presented with the worst headache of her life. A workup for subarachnoid hemorrhage was negative, but an angiogram was performed nonetheless. This showed a fusiform, presumed dissection of the left posterior inferior cerebellar artery on the left vertebral artery injection (arrow in A). Distal to the dilatation, the posterior inferior cerebellar artery lumen continues to be irregular and slightly beaded over a short segment, suggesting that the diseased segment is quite long. A decision was made with the patient to take a chance on managing her conservatively. Her symptoms resolved and a follow-up angiogram (B) after 3 months shows a normal appearance with no new symptoms since that time.

Figure 18-20. (A–H) Vertebrobasilar dissection in a teenager presenting with mass effect. A teenager presented with a 3-week history of syncopal episodes, headache, and fluctuating degrees of left-sided hemiparesis and sensory disturbance. The likely diagnosis is that of a dissecting aneurysm of the vertebrobasilar junction. The high-density appearance on the noncontrast CT examination (A) is suggestive of intramural or laminar thrombus, confirmed on the contrast-enhanced CT (B) and MRI (C and D) images with evidence that enhancing lumen is only a small component of the mass formed. The principal concern for this lesion in the acute phase is progression to rupture or extension of the dissection higher in the basilar artery with probable injury to the brainstem. Rupture with subarachnoid hemorrhage from an aneurysm in this location would carry a substantial morbidity and mortality in any circumstance, but the likelihood of further hemorrhage from a dissecting aneurysm is probably higher than that of a berry aneurysm. Surgical or endovascular treatment for a ruptured dissecting aneurysm is probably more hazardous than for a berry aneurysm due to the possibility of disintegration of the aneurysm from any type of manipulation. The fragility of a dissecting aneurysm in this location would probably demand that even angiographic images should be obtained gingerly with gentle hand injections of contrast. In addition to defining the anatomy of the dissected segment, which in this instance extends up from the vertebrobasilar junction to the origin of the left anterior inferior cerebellar artery (arrow in E and F), some of the important findings from this angiogram include the identification of prompt collateral flow from the anterior circulation from the carotid arteries.

In this patient, a test occlusion of the collateral circulation was performed with the plan to preserve flow in the vertebral arteries proximal to the dissection, thus maintaining perfusion of the posterior inferior cerebellar arteries, medullary perforators, and anterior spinal artery below the dissection. The basilar artery above the dissection would then rely on the collateral flow from the anterior circulation for perfusion (straight arrows in G–H post occlusion). Coils within the disease segment are indicated with a corrugated arrow in (H). Furthermore, the preserved segment of the left vertebral artery below the coils (arrowhead in H) is opacified via the occipital artery representing the vital preservation of flow to the left posterior inferior cerebellar artery, lower brainstem, and upper spinal cord.

Saccular (Berry) Aneurysms

The cognomen “berry” for saccular intracranial aneurysms was introduced in 1931 by Collier (112) because of the fanciful resemblance of these aneurysms with their shining coats to berries hanging from the arterial tree. The perfect berry-shaped aneurysm with a spherical contour and confined neck is uncommon. Many aneurysms have a more complex structure, often with more than one distinct compartment or lobule and a neck that can be of variable size. A congenital defect in the arterial media may be one of the explanations for later development of this acquired disease.

Histopathologic examination demonstrates that unruptured small aneurysms have a thin wall measuring 30 to 150 μm in thickness, composed of endothelium and adventitia similar to that of the parent vessel (113). As the aneurysm enlarges, some portions of the wall become collagenized and thickened with endothelial cells, fibroblasts, and elastic fibers. More attenuated portions become points of potential rupture. When an aneurysm ruptures, it is usually assumed that it is the dome that has given way, but this is not always the case. The wall at the neck may sometimes be the most fragile segment. After the aneurysm ruptures and stabilizes, the rupture point is supported by weak fibrin nets for approximately the first 3 weeks. This correlates with the clinically observed period of high risk for rerupture. After 3 weeks, the wall becomes infiltrated with capillaries. Stronger collagen is incorporated into the healing wall with a diminishing risk of rerupture (114).

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