, Nima Etminan1 and Daniel Hänggi1, 2
(1)
Neurochirurgische Klinik, Universitätsklinikum Düsseldorf, Düsseldorf, Germany
(2)
Medical Art Christine Opfermann-Rüngeler, Zentrum für Anatomie Heinrich Heine Universität, Düsseldorf, Germany
9.1 General Considerations
Aneurysms of the posterior cerebral circulation account for only about 15 % of all intracranial aneurysms, and surgical treatment of these aneurysms was demanding until the introduction of endovascular therapy. The surgery-related morbidity and mortality—about 10 % in the best published series—was correspondingly high. One must assume that in the average series, the surgery-related morbidity and mortality may have been about 30 % or higher. Part of the high complication rate can be linked to the relative rarity of these aneurysms, because the particular approaches and techniques require special skills and awareness of specific pitfalls. Another reason for the unsatisfactory results of microsurgical treatment, however, has certainly been the highly eloquent territory supplied by the parent arteries of these aneurysms—that is, the brainstem. Drake and Peerless from London, Ontario, acquired the world’s largest experience in the surgical treatment of aneurysms of the posterior circulation [1].
The difficult surgical therapy for aneurysms of the basilar artery led to the acceptance of endovascular therapy as the treatment of first choice prior to the general acceptance of endovascular coiling. In the late 1990s, it was shown that the treatment-related morbidity and mortality after endovascular treatment was lower than after microsurgical operation. Thus, the endovascular treatment of basilar artery aneurysms was established 3–4 years before the general acceptance of endovascular therapy for ruptured aneurysms in the wake of the International Subarachnoid Aneurysm Trial (ISAT), the results of which were first published in 2002.
The acceptance of the superiority of endovascular treatment techniques applies not to all aneurysms in the posterior circulation, but particularly to aneurysms of the basilar artery. Of all ruptured and unruptured aneurysms of the posterior circulation, the aneurysms of the basilar bifurcation account for approximately 50 %. The next most common locations are the origin of the superior cerebellar artery (SCA) and the origin of the posterior inferior cerebellar artery (PICA), each with about 15 %. Other sites of saccular and fusiform aneurysms of the posterior circulation are the junction of the vertebral arteries and the origin of the anterior inferior cerebellar artery (AICA). Aneurysms occur rarely at the origin of the posterior communicating artery from the posterior cerebral artery, as well as in the peripheral portions of the posterior cerebral artery and the peripheral portions of the SCA, AICA, and PICA. These latter groups each account for a few percent of all aneurysms of the posterior circulation. Special situations are dissecting aneurysms, especially of the vertebral artery, fusiform vertebrobasilar aneurysms in the context of arterial ectasia and elongation (megadolichobasilar artery), and aneurysms of the feeder arteries of posterior fossa arteriovenous malformations. Each of these special situations accounts also for a few of all aneurysms of the posterior circulation.
Endovascular treatment of aneurysms of the basilar bifurcation and aneurysms at the origin of the SCA and AICA has become so well established that microsurgical competence has been lost and microsurgical therapy is no longer available as an alternative for these aneurysms. The situation for saccular aneurysms at the origin of the PICA from the vertebral artery is different; both endovascular and microsurgical therapies currently appear to be equivalent [2]. It remains unclear which treatment modality provides better short-term and long-term results, on the average. Finally, endovascular treatment of peripheral aneurysms is currently difficult. From the endovascular side, only obliteration of the carrier artery may be offered, which generally results in territorial cerebellar infarction. Therefore, peripheral aneurysms remain the domain of microsurgery.
9.1.1 PICA Aneurysms
The PICA is characterized by a highly variable origin: In 90 % of individuals, it originates from the so-called intradural V4 segment of the vertebral artery, and in about 10 % it originates extracranially from the extradural V3 segment of the vertebral artery, or from the basilar artery. Anatomically, the PICA runs in a tortuous way around the lateral medulla oblongata at the level of the caudal cranial nerves (IX–XII). At the anterior aspect of the cerebellar tonsil, it forms the caudal loop. In its further course, the PICA runs between the dorsal aspect of the medulla oblongata and the tonsils and forms the cranial loop. The distal portion divides into two main branches to supply the vermis and cerebellar hemisphere [3].
In principle, the PICA is divided into five sections: (1) anteromedullary, (2) lateromedullary, (3) tonsillomedullary, (4) telovelotonsillary, and (5) the cortical segment. The rami perforantes arise from the first three segments to supply the posterolateral medulla. The first three segments are also referred to as the proximal PICA; segments four and five are the distal PICA. About 2 % of all intracranial aneurysms are associated with the PICA. Clinically, PICA aneurysms may present with rupture and consecutive subarachnoid hemorrhage (SAH), or conversely with signs of ischemia or as an expression of a mass, with symptoms such as hiccups, dysphagia, and other paralytic caudal cranial nerve failures.
PICA-origin aneurysms are most common. As mentioned, both endovascular and surgical treatment modalities are currently used for optimal care. Details of the surgical management are given in a subsequent section.
9.1.2 AICA Aneurysms
The AICA originates anatomically from the lower third of the basilar artery, in the prepontine region of the cerebellopontine angle. It is surrounded by numerous caudal cranial nerves and the arterial perforators of the brain stem. Less than 1 % of all intracranial aneurysms may be associated with the AICA. Most AICA aneurysms become symptomatic with SAH, but giant aneurysms (>2.5 cm) represent a significant proportion and become symptomatic by signs of brainstem compression.
Aneurysms with AICA origin are difficult to access surgically, which is the main reason that endovascular therapy has been accepted as the first treatment choice.
9.1.3 Dissecting Aneurysms of the Vertebral Artery
Anatomically, the vertebral artery runs anteriorly from the transverse foramen of the atlas, ascending dorsally and medially to the atlanto-occipital joint and entering the subarachnoid space at the level of the occipital condyle. Intracranial dissecting aneurysms occur preferentially at the proximal intradural vertebral artery. Mechanical stress is considered to be a pathophysiological factor. Dissecting aneurysms occur more frequently in the vertebrobasilar territory than in the carotid artery.
Dissecting aneurysms can result in ischemia by vascular occlusion or thromboembolism, compression of surrounding structures, or rupture with SAH. Because of the generally good collateral circulation of the brainstem, with inflows of both vertebral arteries and connections to the carotid artery by the posterior communicating arteries, dissection of a vertebral artery leads only in exceptional cases to direct hemodynamic compromise, but thromboembolic complications can lead to basilar thrombosis or embolic occlusion of the posterior cerebral arteries.
Thromboembolic complications today can be effectively prevented pharmacologically, and the prognosis of dissecting aneurysms with nonhemorrhagic manifestation appears relatively good. The prognosis for ruptured dissecting aneurysms with SAH, on the other hand, must be regarded as highly critical; the rate of rerupture is higher than with saccular aneurysms.
The typical angiographic feature of a dissecting aneurysm is the “pearl and string” sign—a dilated arterial segment next to a narrowed segment—but sometimes only discrete changes of arterial caliber are evident. These changes often are detectable only with catheter angiography, as the resolution of CT angiography or MR angiography is not sufficient to detect such small changes in caliber. Definition of intramural hematoma on MRI is the key finding for diagnosis of an extradural arterial dissection, but attempts to use this feature to identify intradural dissections have been disappointing, particularly in the context of SAH.