46 Dissecting Intracranial Aneurysms of the Posterior Circulation
Abstract
Posterior circulation dissecting aneurysms, sometimes referred to as “pseudoaneurysms,” are relatively uncommon. Management of these lesions is controversial. Furthermore, due to their location, morphology, small perforators to the brainstem arising from their wall, and involvement of the branch vessels such as posterior inferior cerebellar artery and anterior spinal artery, they are challenging to treat. Conservative treatment with anticoagulation or antiplatelet therapy might be considered for unruptured asymptomatic dissecting aneurysms. Ruptured dissecting and symptomatic unruptured dissecting aneurysms need to be treated surgically or endovascularly or in combination. The treatment options can be broadly divided into (1) surgical reconstruction or occlusion with or without bypass strategies and (2) endovascular reconstructive options with stent-assisted coiling (SAC), coiling alone or flow diverting (FD) stents, or internal trapping with or without proximal vessel occlusion (PVO). Endovascular treatment is emerging as the first-line treatment because of its less invasive nature and the high incidence of surgery-associated morbidities. The morphology of the aneurysm, location of the aneurysm along the posterior circulation, and locoregional hemodynamics are considered in making the treatment decision. Internal trapping of the aneurysm with PVO affords the highest chances of successfully treating the dissecting aneurysm. For fusiform aneurysms involving the branch vessels for which occlusion strategies can pose a significant risk, reconstruction strategies including FD stent or SAC are favored options. For ruptured aneurysms where involvement of branching vessels does not permit endovascular treatment or when further surgical interventions are anticipated due to the need of antiplatelet agents with endovascular management, surgical occlusion with bypass is performed.
Introduction
Dissecting aneurysms of the posterior circulation constitute a relatively uncommon subgroup of aneurysms. These aneurysms are sometimes known as “pseudoaneurysms” and represent around 28% of the posterior circulation aneurysms and 3.3% of all intracranial aneurysms. Dissecting aneurysms of the posterior inferior cerebellar artery (PICA) account for 0.5 to 0.7% of all intracranial aneurysms. Posterior circulation dissecting aneurysms account for 3 to 7% of cases of nontraumatic subarachnoid hemorrhage (SAH). These are now recognized as a common cause of stroke and SAH in otherwise healthy young adults. Management of these lesions is still controversial. Prevention of rebleeding of ruptured dissecting aneurysms of the posterior circulation is an essential cornerstone of treatment.
Major controversies in decision making addressed in the chapter include:
Whether treatment is indicated.
Does clinical presentation stroke/SAH dictate different treatment?
Open versus endovascular treatment for ruptured and unruptured dissecting aneurysms of the posterior circulation.
Whether to Treat
The guidelines for endovascular treatment of unruptured dissecting aneurysms presenting with ischemia, headache, and incidental findings remain controversial. The relatively benign clinical course and outcome reported for unruptured minimally symptomatic posterior circulation dissecting aneurysms have resulted in conservative treatment such as anticoagulation being recommended. Also for patients presenting with a PICA infarct, conservative treatment can be recommended if there are no obvious angiographic risk factors for hemorrhage such as a pseudoaneurysm.
Ruptured fusiform and dissecting aneurysms of the posterior circulation typically have a poor prognosis if left untreated. The rebleeding rate is particularly high in the range of 25 to 30% with a mortality rate of around 50% in untreated patients. Rebleeding generally occurs within the first 24 hours after rupture onset and is associated with a poor clinical outcome. Considering the aggressive behavior of ruptured vertebral dissecting aneurysms, such aneurysms warrant urgent treatment ( 1 , 2, 3, 4, 5 in algorithm ).
Conservative Treatment
Conservative treatment with anticoagulation or antiplatelet therapy can be considered for unruptured minimally symptomatic or asymptomatic posterior circulation dissecting aneurysms ( 2 in algorithm ). Ruptured dissecting aneurysms should be treated surgically or endovascularly on an urgent basis.
Anatomical Pathology
Histologic characteristics of the cerebral vessels include a deficient external elastic lamina, thinner adventitia, thicker internal elastic lamina, and fewer elastic fibers in the media in addition to lack of vasa vasorum. Histopathologically, these lesions have been classified into two types:
Dissections resulting from disruption of the intima and collection of blood in the subintimal space. This results in subintimal hematoma and can lead to ischemic events from vessel lumen occlusion. Extension of this initial dissection forms a false lumen, which can recommunicate with the true lumen distally, depending on the plane of dissection (▶ Fig. 46.1 ).
When the plane of dissection extends through the media and elastica to the subadventitial space, a “dissecting aneurysm” is formed.
When blood ruptures through the adventitia and partial thrombosis of extravasated blood occurs to contain the rupture, a “pseudoaneurysm” results. Based on this sequence of events and the extent of mural tear, patients can present with ischemic and/or hemorrhagic complications.
Pathophysiology
Most cases of dissecting aneurysm are idiopathic in origin; however, numerous causes have been reported in the literature including trauma, hypertension, syphilis and other arteritis, fibromuscular dysplasia, and polyarteritis nodosa. Acute dissecting aneurysms, which involve a disruption of the internal elastic lamina and intramural hemorrhage, typically present with SAH or ischemia secondary to compromise of the vessel lumen. Chronic fusiform aneurysms arise from various vascular abnormalities that cause a defect in the arterial media. These gradually enlarging aneurysms may result from congenital, acquired, or iatrogenic causes; atherosclerosis and hypertension are thought to play a role in their development. Chronic dissections with recurrent intramural hemorrhage may slowly lead to an enlargement of the intramural thrombi and expansion of the arterial segment involved. Such dissections may evolve to fusiform or dolichoectatic aneurysms, causing symptoms through compression, ischemia, or less commonly rerupture.
Anatomical Considerations
Vertebral Artery Dissecting Aneurysms
The vertebral arteries (VAs) travel a short distance after piercing the dura prior to their anastomosis at the vertebrobasilar junction (VBJ). V1 (origin to C6 transverse foramen) and V3 (C2 transverse foramen to foramen magnum) represent the most mobile segments, while V2 (C6 transverse foramen to C2 transverse foramen) and V4 (foramen magnum to VBJ) are relatively fixed in place. Due to its location at the skull base, V4 region is likely to be subject to a higher degree of traumatic forces secondary to head rotation and flexion resulting in VA dissection (▶ Fig. 46.2 ). The intracranial portion of the VA gives rise to three major branches: the PICA, the anterior spinal artery (ASA), and the lateral spinal artery. Perforating arteries arise most frequently between PICA origin and VBJ, which are of the short circumflex type and terminate on the anterior and lateral surfaces of the medulla. ASA arises near the end of the VA and descends anterior to the medulla oblongata to unite with the other ASA from the opposite side at the midmedullary level. A posterior spinal artery usually arises from the PICA but may come directly from the VA, near the medulla oblongata.
Attempts are generally made to occlude the dissecting aneurysm if the lesion does not incorporate a branch such as the anterior inferior cerebellar artery (AICA), PICA, or ASA. However, if the dissected segment incorporates important branches such as AICA, PICA, or ASA, proximal occlusion is preferentially performed without internal or external trapping of the aneurysm itself to prevent branch-related infarct ( 8, 9, 10, 15 in algorithm ).
Posterior Cerebral Artery Dissecting Aneurysms
Posterior cerebral artery (PCA) P2 (most common) and P1 segments are the common sites of PCA dissecting aneurysms. P2 segment of the PCA has an intimate anatomic relationship with the tentorial edge because the PCA enters the middle incisural space between the cerebral peduncle and uncus at the P2 segment. This close relation of P2 segment to the tentorial edge predisposes the arterial wall of P2 segment to dissection from any trauma or stress. One should be mindful of the anatomy of the PCA and its perforators during treatment, as in many instances, PCA-dissecting aneurysms have an indistinguishable neck and ill-defined dissecting segment; thus, only proximal vessel occlusion (PVO) with or without revascularization can be used to treat them. Any decrease or obstruction of blood flow in the main PCA branches and/or perforators can cause cerebral infarction with significant morbidity. The clinical presentations of PCA-dissecting aneurysms depend on the affected PCA segment and the structures of the arterial wall: they vary markedly from SAH to ischemic symptoms and mass effects due to the enlarged aneurysm.
Posterior Inferior Cerebellar Artery Aneurysms
PICA originates from the intracranial portion of VA in 80 to 95% of patients, approximately 8.6 mm above the foramen magnum and 1 cm proximal to the VBJ. The intracranial course of PICA can be divided into five segments; they are named according to their course along the medulla and cerebellar tonsils and cerebellar suboccipital surface.
When aneurysms are located beyond the origin, in the more distal course of the PICA, they are usually fusiform; such aneurysms are most often caused by vessel wall dissections. Probably the most important issue in the management of PICA-dissecting aneurysms is their site. There is evidence that patients with distal dissections have better clinical outcome than those with proximal lesions. Perforating arteries usually arise from the first three segments of PICA, which run close to the medulla. The facts that occlusion of PICA beyond the first three segments is unlikely to result in brain stem injury and distal PICA dissections have a low propensity to bleed or rebleed due to relatively low rate of recanalization make PVO with or without internal trapping a suitable choice for managing distal PICA aneurysms ( 12, 13, 14 in algorithm ).
Workup
Clinical Evaluation
Symptoms of posterior circulation dissecting aneurysms depend on a multitude of factors, such as subintimal or subadventitial plane of dissection, size and location of the aneurysm, and whether the lesion is intradural or extradural, and the regional hemodynamics, such as the presence of collaterals, dominance of VA, and small PICA. Typical presentations include SAH, thromboembolic events, and cranial neuropathy from mass effect. Usually, depending on the dissecting plane, manifestations relate to ischemic events and/or SAH. In general, dissecting aneurysms of the posterior circulation present more frequently with SAH caused by rupture, rather than with an ischemic event caused by stenosis or occlusion. While proximal PICA dissections tend to cause infarctions, peripheral lesions tend to give rise to SAH. Nevertheless, symptomatic patients may complain of nonspecific symptoms, including headache, vertigo, nausea/vomiting, tinnitus, double vision, hearing loss, dysesthesia, and dysphasia.
Imaging
Digital Subtraction Angiography
Diagnosis of a true intracranial dissecting aneurysm can be challenging and requires a high degree of clinical suspicion. The gold standard in diagnostic imaging is still represented by digital subtraction angiography (DSA). Classical findings are as follows:
“Pearl and String” sign with dilatation proximal and/or distal to stenosis.
“Double lumen” sign: visualizing both true and false channels.
“String” sign: a narrow tapered lumen.
A more fusiform or rosette (multilobulated aneurysm) appearance of the involved segment which sometimes evolve into a serpentine luminal channel.
Angiograms, although invasive, provide valuable information such as size, shape, and location of the dissecting aneurysm with respect to the major branches and collaterals important in decision making in choosing the intervention. Each lesion is examined for evidence of extension of the dissection into adjacent arterial segments and relationship to perforators to the brain stem or cranial nerves.
Noninvasive Techniques
Computed Tomographic Imaging
CT angiography (CTA) can provide information about vessel caliber, false lumens, fusiform dilatations, and pseudoaneurysms. The advantages over conventional angiography include large noninvasive nature and large number of projections that can be obtained from one data acquisition. However, it does not provide the valuable information such as small perforators and collateral supply, and the evaluation of actual lumen might be difficult to discern from CTA due to calcification artifact. This knowledge can only be provided by conventional angiograms.
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