Introduction

Giant intracranial aneurysms (maximum diameter ≥ 25 mm) of the posterior circulation represent approximately 20 to 40% of all giant aneurysms. Professor Charles Drake pioneered the surgical treatment of giant posterior circulation aneurysms (GPCA) beginning in the 1960s. Despite the significant innovations in microsurgical and endovascular technologies and techniques, GPCAs remain a formidable therapeutic challenge. Although the rates of treatment-related morbidity and mortality for GPCAs have gradually declined over time, the aneurysms remain among the most challenging. The natural history of GPCAs is extremely poor, with high rates of death secondary to subarachnoid hemorrhage (SAH), ischemic events, or pseudotumoral syndromes. The pathogenesis, therapeutic strategies, and outcomes differ between saccular versus nonsaccular (e.g., fusiform or dolichoectatic) GPCAs; therefore, we discuss these aneurysm subtypes separately.

Major controversies in decision making addressed in this chapter include:

1. 
   

   Whether treatment is indicated.

   
   
2. 
   

   Microsurgical versus endovascular treatment for ruptured and unruptured GIAs.

   
   
3. 
   

   Management of GIAs that present with hematomas requiring urgent evacuation.

   
   
4. 
   

   When should adjuvant microsurgical techniques (e.g., bypass, aneurysmorrhaphy, and local or systemic circulatory arrest) be utilized?

Whether to Treat

The natural history of giant aneurysms is dismal. Peerless and Wallace reported mortality rates of 68% at 2 years and 85% at 5 years for unruptured giant aneurysms, and survivors suffered significant morbidity ( 1 , 2, 3 in algorithm ). Posterior circulation aneurysm location confers an even worse prognosis. The prospective arm of the International Study of Unruptured Intracranial Aneurysms (ISUIA) found a 5-year rupture risk of 50% for GPCAs, compared to a 40% for giant anterior circulation aneurysms. Michael reported a mortality rate of 100% at 1 year in six patients with untreated GPCAs. Similarly, Bull reported that all eight patients with GPCAs either died or suffered disabling morbidity. Therefore, conservative management of GPCAs should be employed with caution.

Based on several large case series, 13 to 41% of GPCAs are located on the posterior cerebral artery (PCA), 22 to 67% at the basilar apex (▶ Fig. 44.1 and ▶ Fig. 44.2 ), 5 to 17% on the superior cerebellar artery (SCA), 12 to 47% on the basilar trunk (▶ Fig. 44.3 ), 6 to 33% at the vertebrobasilar junction (VBJ), and 5 to 36% in the vertebral artery (VA) or posterior inferior cerebellar artery (PICA). Overall, approximately 70% of GPCAs are located in the vicinity of the basilar quadrification. In the series by Lawton and Spetzler, 77% of GPCAs were surgically treated with clipping, and Nurminen et al found that 66% of GPCAs had a saccular morphology based on the angiographic analysis. Thus, the incidence of saccular GPCAs is approximately 70%, a lower rate compared to giant anterior circulation aneurysms. Fusiform giant aneurysms develop three times more frequently in the posterior circulation compared to the anterior circulation. Approximately 80% of the 120 fusiform giant aneurysms reviewed by Drake were located in the posterior circulation. In this series, 32% were located on the PCA, 5% near the basilar apex, 2% on the SCA, 34% on the basilar trunk, 11% at the VBJ, and 17% on the VA or PICA. The most common location for fusiform GPCAs is the basilar trunk.

Unfortunately, current classification schemes for these aneurysms are somewhat limited due to significant clinical heterogeneity. Giant dolichoectatic vertebrobasilar aneurysms in young patients are more commonly of the dissecting type and atherosclerosis is more commonly involved in those elderly patients. Incomplete classification and understanding of the pathophysiology of these aneurysms makes determination of the natural history and optimal treatment strategies more difficult.

Pathophysiology

Saccular giant aneurysms are believed to develop from the progressive enlargement of smaller saccular aneurysms, which tend to develop at arterial bifurcations as an accumulated effect of chronic hemodynamic stress. Expansion of a saccular aneurysm is prevented by sufficient wall tension as governed by Laplace′s law. In some cases, wall weakening and elastic thinning secondary to local fluid vibrations and pulsations result in continued aneurysmal dilation or potential eruption. More commonly, endothelial damage results in fibroblast invasion and platelet aggregation, causing intraluminal fibrous deposition and clotting, respectively. The latter phenomenon generates increased flow turbulence, which exacerbates endothelial damage. These chronic cycles of damage and repair to the endothelium and internal elastic lamina can result in gradual aneurysmal enlargement. The observation that thrombosed aneurysms contain numerous intrathrombotic vascular channels as well as continue to grow and that giant aneurysms typically have a laminated, onionskin structure supports yet another developmental theory. Specifically, a series of recurrent intramural hemorrhages and resultant hypervascularization and scarring cause the aneurysm to grow, much like an encapsulated intracranial hematoma. Unlike their saccular counterparts, fusiform, dolichoectatic, and serpentine giant aneurysms typically develop away from arterial branch points. They form as a consequence of an atherosclerotic, degenerative, or traumatic process that induces intimal damage (e.g., atherosclerotic plaque formation, connective tissue disease, arterial dissection), often in the setting of hypertension. Damage to the arterial wall induces an inflammatory response, resulting in fibrin, collagen, and hyaline deposition that replaces elastin. Thus, the arterial segment dilates and becomes rigid, generally with severe atherosclerotic changes and organized intramural thrombus.

Workup

Treatment

The treatment of GPCAs requires an individualized approach, including consideration of patient- and aneurysm-specific factors ( 4–9 in algorithm ). Microsurgery and endovascular therapy can be employed individually, or in combination, for the goal of aneurysm obliteration. The adjunctive use of adenosine-induced cardiac arrest, neuroprotective anesthetic agents (e.g., isoflurane, barbiturates), intraoperative angiography, and electrophysiological neuromonitoring should also be considered, particularly for patients undergoing surgical aneurysm treatment.

Cerebrovascular Management—Operative Nuances

Selection of an appropriate skull base approach is crucial to optimizing surgical treatment of GPCAs, including visualization of the aneurysm dome and neck, parent and branch vessel anatomy, and relevant perforators, which frequently supply critical adjacent structures, such as the thalamus and brainstem. The orbitozygomatic (OZ) craniotomy can be utilized for basilar apex and SCA aneurysms in which the basilar quadrifurcation is above the level of the posterior clinoid process (PCP) (▶ Fig 44.4 a, b ) ( 3, 8, 9 in algorithm ). The OZ craniotomy is useful for high-riding basilar aneurysms (i.e., aneurysm neck is >1 cm superior to the PCP). When approaching a posterior circulation aneurysm with a midposition basilar quadrifurcation (i.e., within 1 cm of the PCP), drilling of the PCP is frequently necessary to obtain proximal control of the upper basilar trunk and dissect the neck of the aneurysm. The pretemporal transcavernous approach is an extension of the OZ craniotomy which allows access to the upper one-third of the posterior fossa by a combination of an extradural anterior clinoidectomy, intradural posterior clinoidectomy, partial exposure of the cavernous sinus, and lateral mobilization of the oculomotor nerve. Basma et al found that all patients who underwent a transcavernous approach experienced an oculomotor nerve palsy, but 97% completely recovered its function by 9 months of follow-up. Division of the posterior communicating artery (PCoM) close to the P1–P2 junction and resection of the uncus can further increase the operative view from a transsylvian corridor.

Basilar apex and SCA aneurysms can also be treated from a subtemporal approach, particularly in cases in which the basilar quadrifurcation is below the level of the PCP ( 3, 8, 9 in algorithm ). The posteriorly directed perforators from the basilar apex and ipsilateral branch arteries are better visualized from a subtemporal approach, and division of the tentorium may facilitate proximal control. However, the contralateral branch arteries and neck anatomy are difficult to visualize, and considerable temporal lobe retraction may be necessary to maintain the operative corridor. Cerebrospinal fluid drainage from a lumbar drain is necessary for the subtemporal approach, but patients remain vulnerable to temporal lobe injury secondary to retraction and/or vein of Labbe occlusion.

Additional approaches are utilized for GPCAs below the proximal to the basilar apex. An anterior, posterior, or combined petrosectomy can be performed to access GPCAs of the midbasilar trunk or anterior inferior cerebellar artery (AICA) ( 2, 6, 7 in algorithm ); however, drilling of the labyrinth (i.e., for a posterior or combined petrosectomy) sacrifices hearing on that side. The retrosigmoid approach can also be utilized for GPCAs of the midbasilar region.

The far-lateral approach allows access to GPCAs of the lower basilar trunk, VBJ, VA, and PICA ( 1 , 4, 5 in algorithm ). Distal PICA aneurysms may not require drilling of the occipital condyle (i.e., as is necessary for a far-lateral approach), and may be accessed with a lateral or midline suboccipital craniotomy, depending on the location of the lesion. The aforementioned approaches can be combined to further expand the operative corridor. For example, a combined supratentorial OZ and infratentorial transpetrosal approach can be employed to visualize the full extent of the brainstem. A number of authors have reported combining the transsylvian and subtemporal approaches (otherwise known as a half-and-half or extended lateral transsylvian approach) for basilar apex aneurysms.

Vascular control in the posterior fossa is difficult to achieve, and this is particularly the case for GPCAs. GPCAs are located along the skull base, where maneuverability may be limited. Additionally, the vascular anatomy, including that of the parent, branch, and perforator arteries, is complex and often obscured by the aneurysm. Crucial midbasilar perforators supplying the brainstem are particularly vulnerable to transient ischemia during temporary clipping. Furthermore, obtaining both proximal and/or distal control for GPCAs may be challenging from a single approach. Revascularization of the posterior circulation using extracranial–intracranial or intracranial–intracranial bypasses requires tremendous technical skill in many cases, due to the deep location of the recipient artery (exceptions including bypasses to the distal PICA, which has a relatively superficial location; ▶ Fig. 44.5 ). And even a technically successful bypass does not ensure physiologically adequate blood supply.

For basilar apex aneurysms that fail other treatment strategies or cannot be treated with direct microsurgical clipping, microsurgical basilar clip ligation just proximal to the SCA is another option if there are adequate collaterals from the PCoAs ( 7, 8, 9 in algorithm ). This treatment allows continued blood flow into the perforators and SCAs without direct hemodynamic jet into the aneurysm and can allow for progressive aneurysm thrombosis. In these cases, we perform a balloon test occlusion first.

Related posts:

37 Vertebral Artery Aneurysms 38 Midbasilar Artery Aneurysms 39 Basilar Artery Apex Aneurysms 47 Traumatic Intracranial Aneurysms of the Posterior Circulation 42 Anterior Inferior Cerebellar Artery Aneurysms 46 Dissecting Intracranial Aneurysms of the Posterior Circulation

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