Intracranial aneurysms: Diagnosis and therapy

While management of intracranial aneurysms has been the domain of neurosurgeons, relatively recent advances in endovascular therapy highlight the importance of radiologists in the diagnosis and treatment of cerebral aneurysms. The author reviews the clinical management of patients with intracranial aneurysms and discusses the imaging considerations and therapeutic options.

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Intracranial aneurysms are relatively common, occurring in approximately 1% of the general population. Prevalence of aneurysms may be increased in patients with first-degree relatives with aneurysms and those with polycystic kidney disease and connective tissue disorders. Aneu-rysms may be recognized after spontaneous rupture, through mass effect on adjacent nerves, or may be noted incidentally on CT or MR imaging performed for other reasons. Historically, management of these aneurysms has been the domain of neurosurgeons; however, relatively recent advances in endovascular therapy highlight the importance of radiologists in the diagnosis and treatment of cerebral aneurysms.

Clinical management

Patients presenting with ruptured aneurysms present little dilemma regarding management. In essentially all cases of ruptured aneurysms, primary therapy is aimed at reducing or eradicating the risk of rehemorrhage, which approaches 50% at 6 months. Patients presenting with aneurysms causing mass effect present a more complex management scheme. Many of these aneurysms occur in the region of the cavernous sinus, and these aneurysms present little risk for subsequent rupture. Because of the relatively low risk of subarachnoid hemorrhage in these patients, management in many cases may be expectant, with symptoms of double vision ameliorated using an eye patch.

In contrast to giant aneurysms of the cavernous sinus, incidently noted aneurysms around the Circle of Willis represent an extremely challenging clinical algorithm. Although recent data suggests an extremely low rate of spontaneous hemorrhage in small aneurysms, aneurysms located at the anterior communicating artery or the basilar tip, and/or a family history of ruptured aneurysm may prompt more aggressive management. Many other small aneurysms may be managed with follow-up imaging alone.

Ruptured aneurysms

For ruptured aneurysms, therapy aimed at closure of aneurysm cavity is mandatory, since the rehemorrhage rate for ruptured aneurysms approaches 20% at 2 weeks and 50% at 6 months following initial hemorrhage. Regardless of initial deficit, rehemorrhage is devastating in the majority of cases.

Endovascular therapy-Endovascular therapy of aneurysms can be broadly divided into two types: deconstructive (obliteration of the parent artery along with the aneurysm) and reconstructive (intrasaccular occlusion of the aneurysm cavity with preservation of adjacent vessel). Deconstructive therapy is primarily related to therapy for giant aneurysms, which will be described in detail below. Reconstructive therapy is the endovascular approach of choice for small aneurysms.

Reconstructive, endovascular therapy-Although several modes of intrasaccular therapies for aneurysms were developed in the past several decades (including balloons, glues, and various coils), the advent of the Guglielmi detachable coil (GDC, Target Therapeutics, Fremont, CA) has revolutionized the endovascular approach to reconstructive cerebral aneurysm therapy.2,3 The GDC was developed in the early 1990s and received FDA approval in 1995. The GDC is manufactured in numerous sizes and shapes, and is constructed of a soft platinum wire. The platinum renders the coil extremely radiopaque under fluoroscopic imaging, and is also soft, atraumatic, and relatively non-thrombogenic. The platinum coil is welded to a stainless steel pusher wire. The coil can be advanced out of the catheter for positioning within the aneurysm, and can be retracted if positioning is suboptimal, usually as a result of protrusion into the parent artery. Once satisfactory coil positioning is achieved, a current is passed through the device and electrolytic detachment occurs several minutes following application of the current.

The precise coil used to begin embolization is based on the size and shape of the aneurysm cavity. The diameter of the initial coil should nearly approximate the diameter of the aneurysm cavity. The coil is then placed so that coil winds occupy the periphery of the aneurysm cavity and cross the aneurysm neck. Subsequent coils are typically smaller in diameter and/or shorter, and are used to fill in the spaces along the interior of the initial coil. While coils in numerous sizes, shapes, and softness characteristics are available, this technique is used in nearly all cases. Coil embolization continues with the addition of subsequent coils until the aneurysm is densely packed with platinum. Then the catheter is removed and control angio-graphy is performed (figures 1 and 2).

Surgery versus endovascular therapy-The choice between surgical or endovascular therapy is complex, and is based on aneurysm size, geometry, and location. Many practitioners use coil embolization as a first-line therapy in basilar tip aneurysms, given the relatively high surgical mortality associated with these lesions. Conversely, middle cerebral artery aneurysms are generally more appropriate for surgical therapy, given the relatively low rates of surgical complications and the complex anatomy associated with these aneurysms that makes coil embolization difficult.

Complications of GDC embolization-For ruptured aneurysms, the overall complication rate of GDC embolization approaches 5% to 7%.4 Most often, such complications are related to thromboembolic events, which can be minimized by using systemic anticoagulation. Aneurysm perforation can occur in up to 2% of ruptured aneurysms, although this rate is lower in unruptured aneurysms. Parent artery compromise may occur from damage to the coil or protrusion of coil loops into the parent artery.

Outcomes-Radiographic outcome for coil embolization of cerebral aneurysms is graded in reference to the degree of aneurysm occlusion. Although numerous semi-quantitative scales are available, most scales are divided into complete occlusion, subtotal occlusion, or partial occlusion. For small aneurysms (< 10 mm diameter), total or near total occlusion is achieved in most cases. Conversely, for aneurysms 3 5 mm in diameter, the minority of cases are termed completely or nearly completely occluded.

For ruptured aneurysms, the rate of rehemorrhage following GDC embolization is approximately 1% to 2% at 6 months, as compared with the 50% rehemorrhage rate for untreated ruptured aneurysms. Because the background spontaneous rupture rate for unruptured aneurysms is extremely low, significant decreases in spontaneous rupture rate after coil embolization have not yet been proven.

Rate of recanalization is related not only to aneurysm size but also to the diameter of the aneurysm neck. For large aneurysms or wide-neck aneurysms (typically aneurysm necks

> 4 mm), occurrence rates are significantly higher compared with small- or

narrow-neck aneurysms. For small- and narrow-neck aneurysms, recanalization rates at 3 months are approximately 15%. At the other end of the spectrum, recannalization for giant aneurysms (3 25 mm in diameter) is on the order of 75% (figure 3). For this reason, most practitioners will not attempt reconstructive therapy of giant aneurysms, leaving this to direct surgical therapy or to deconstructive therapy.9

Follow-up imaging-The platinum used in the GDC makes follow-up MRI imaging quite safe. Indeed, the degree of susceptibility artifact from these coils is surprisingly low. Most practitioners recommend catheter angiography at 6 months following coil embolization, at which time recurrent aneurysm remnants may be coiled.

Deconstructive, endovascular therapy-Deconstructive therapy, otherwise known as parent artery occlusion or Hunterian ligation, is typically used for large or giant carotid and basilar aneurysms. The typical aneurysm treated with deconstructive therapy is along the carotid artery, either in the cavernous carotid artery, which is extradural, or the supraclinoid internal carotid artery (ICA), which is intradural. Precise localization of the aneurysm is extremely important in determining the patient's prognosis. If the aneurysm is present in an extradural location, the risk of intracranial hemorrhage is extremely low. Clinical consequences of these extradural aneurysms include cranial nerve palsies from mass effect resulting in double vision, carotid cavernous fistulae resulting from spontaneous decompression of the aneurysm into the adjacent cavernous sinus, or epistaxis. Patients presenting with isolated sixth-nerve palsy in the presence of a large or giant cavernous aneurysm frequently are managed conservatively with an eye patch. More aggressive therapies may be applied in cases of rapid growth, erosion into the sphenoid sinus, or multiple cranial nerve palsy.

Imaging considerations-It is extremely important for the imager to localize the origin of aneurysms precisely along the distal carotid artery. Cavernous carotid aneurysms, which are extradural in location and thus of low or negligible risk for intracranial hemorrhage, are located along the horizontal portion of the carotid siphon, and are directed laterally. Medial projections of these aneurysms typically occur only after the aneurysms have grown to extremely large size laterally. Conversely, intradural aneurysms along the distal ICA carry prognostic features identical to those for berry aneurysms around the Circle of Willis. Intracranial aneurysms along the distal ICA are generally termed "ophthalmic segment aneurysms." These intradural aneurysms can arise at the origin of the ophthalmic artery or may be more distal in location than the ophthalmic artery, yet not as distal as the origin of the posterior communicating arteries. The aneurysms between the ophthalmic and posterior communicating arteries are called "superior hypophyseal aneurysms." Unlike cavernous aneurysms that are typically directed laterally, the superior hypophyseal aneurysms are often directed medially. Smaller aneurysms at the superior hypophyseal artery typically project anteromedially into the region of the carotid cave. Larger superior hypophyseal aneurysms frequently project above the sella. Ophthalmic aneurysms usually project anterosuperiorly, and are relatively easily discerned from cavernous aneurysms.

Therapeutic approach-Deconstructive therapy is relevant for large and giant aneurysms of the distal ICA. Smaller aneurysms of the distal ICA may be treated with reconstructive approaches as described above. For giant aneurysms, Hunterian ligation is preferred. The general approach of deconstructive therapy is to effect occlusion of the aneurysm cavity. In most cases, occlusion of the proximal parent artery will achieve occlusion of the aneurysm cavity. This almost always applies for cavernous aneurysms, since occlusion of the ICA proximal aneurysm will achieve closure of the internal artery up to the origin of the ophthalmic artery, which is distal to the aneurysm sack. Therapy for ophthalmic and superior hypophyseal giant aneurysms is more problematic. Occlusion of the ICA proximal to the aneurysm, without occlusion of the aneurysm sack itself, may allow persistent flow into the aneurysm from retrograde flow through the ophthalmic artery in approximately 50% of cases. For these reasons, we often combine intrasaccular, loose coil embolization with proximal parent artery occlusion for such aneurysms.

Parent artery occlusion is tolerated in the vast majority of patients. Test occlusion of the involved artery is mandatory. At our institution, a non-detachable balloon is inflated in the target artery for up to 30 minutes. During this time, the patient's blood pressure is maintained in the normal range, and a detailed neurologic examination is performed. At the end of this test occlusion, the temporary balloon is removed, and, if the patient has tolerated the test, permanent balloon occlusion is performed. No provocative testing, such as hypotension challenge, or any functional imaging, such as SPECT imaging, are performed during the test occlusion. Most often, permanent occlusion of the parent artery is achieved using balloons, either latex or silicone. In some cases, it may be preferred to perform coil embolization of the involved parent artery.

Complications-Regardless of diagnostic maneuvers used during test occlusion, the stroke risk associated with parent artery occlusion approaches 5%. These strokes may result from hypoperfusion or thromboembolic complications, and may occur up to 30 days following the procedure. These complications may be diminished using systemic anticoagulation in the periprocedural period, as well strict bed rest for 24 to 48 hours following balloon occlusion.

Follow up imaging-No specific follow up imaging is performed after parent artery occlusion.

Conclusion

Management of patients with intracranial aneurysms, whether presenting with subarachnoid hemorrhage, mass effect, or incidentally, requires detailed understanding of the therapeutic options for these cases. Small, incidental aneurysms as well as large cavernous aneurysms may managed expectantly. Frequently, small aneurysms presenting with subarachnoid hemorrhage are treated with intrasaccular coil embolization. Giant aneurysms remain the domain of parent artery occlusion. AR

References

1. The International Study of Unruptured Intracranial Aneurysms Investigators: Unruptured intracranial aneurysms: Risks of rupture and risks of surgical intervention. N Engl J Med 339:1725-1733, 1998.

2. Eskridge JM, Song JK: Endovascular embolization of 150 basilar tip aneurysms with guglielmi detachable coils-Results of the Food and Drug Administration multicenter clinical trial. J Neurosurg 89(1):81-86, 1998.

3. Malisch TW, Guglielmi G, Vinuela F, et al: Intracranial aneurysms treated with the Guglielmi detachable coil-Midterm clinical results in a consecutive series of 100 patients. J Neurosurg 87(2):176-183, 1997.

4. Vineula F, Duckwiler G, Mawad M: Gugliemi detachable coil embolization of acute intracranial aneurysm: Perioperative anatomical and clincial outcome in 403 patients. J Neurosurg 86:475-482, 1997.

5. Gruber A, Killer M, Bavinzski G, Richling B: Clinical and angiographic results of endosaccular coiling treatment of giant and very large intracranial aneurysms: A 7-year, single-center experience. Neurosurgery 45:793-803, 1999.

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