- Email: [email protected]
Dissecting Intracranial Aneurysms
C H A P T E R
35 Dissecting Intracranial Aneurysms Yahia M. Lodi*, Justin G. Thomas†, Richard D. Fessler‡ *
Comprehensive Stroke and NeuroEndovascular Center at UHS Wilson Medical Center, Upstate Medical University, Johnson City, NY, United States † Department of Surgery, Michigan State University College of Human Medicine, East Lansing; Providence-Providence Park Hospitals, Southfield, MI, United States ‡ Division of Neurological Surgery, Department of Surgery, St. John Hospital & Medical Centers, Detroit, MI, United States
O U T L I N E 35.1 Introduction
630
35.2 Etiology and Pathophysiology
632
35.3 Classification 35.3.1 Anatomic Location
633 633
35.4 Clinical Presentations of ID Aneurysms
Intracranial Aneurysms https://doi.org/10.1016/B978-0-12-811740-8.00059-9
634
35.5 Radiographic Evaluation and Diagnosis of DIA
635
35.6 Management of DIA 35.6.1 Pediatric DIA
636 640
35.7 Conclusion
641
References
641
629
# 2018 Elsevier Inc. All rights reserved.
630
35. DISSECTING INTRACRANIAL ANEURYSMS
35.1 INTRODUCTION The occurrence of dissecting intracranial aneurysms (DIA) is relatively rare, comprising roughly 3% of all intracranial aneurysms (Santos-Franco, Zenteno, & Lee, 2008). The identification of a DIA depends on the clinical presentation of the patient (Fig. 35.1). The ruptured DIA is diagnosed during the evaluation of a presenting subarachnoid hemorrhage (SAH),
FIG. 35.1 (A, B) Noncontrast CT head of a 56-year-old female presenting with subarachnoid hemorrhage, Hunt-Hess grade IV, and Fisher 4. Cerebral angiography (C,D) revealed a 5.8-mm dissecting right vertebral artery aneurysm (arrow). The aneurysm is just below the PICA (arrowhead).
VI. ATYPICAL ANEURYSMS
35.1 INTRODUCTION
631
whereas the unruptured DIA is typically an incidental finding during the investigation of a transient ischemic attack (TIA), ischemic stroke (IS), or suspected intracranial dissection (ID). There are numerous case series and case reports regarding dissecting vertebrobasilar aneurysms compared to anterior circulation lesions. This may be due to a higher incidence of DIA in the posterior circulation versus the anterior circulation. Reports of unruptured DIA in the internal carotid and vertebral artery distributions suggest that SAH is a relatively rare occurrence (Byoun et al., 2016; Meling et al., 2008; Nakatomi, Nagata, Kawamoto, & Shiokawa, 1997). However, more recent case series suggest that the natural history of DIA that present with hemorrhage carries a profound mortality of up to 80% of untreated cases within 5 years (Santos-Franco et al., 2008). There is growing evidence that the risk of early hemorrhage is comparable to that of ruptured saccular aneurysms (Byoun et al., 2016). Therefore, it has been recommended that patients with ruptured dissecting intracranial aneurysms (rDIA) should undergo early repair of the aneurysm either by an endovascular approach (Fig. 35.2) or by
FIG. 35.2 Lateral cerebral angiogram (A) and native view (B) of the right vertebral artery undergoing deconstructive endovascular repair of the aneurysm by coil embolization (C) just below the origin of right PICA. Injection of the left vertebral artery (D) demonstrated filling of the right PICA through the vertebrobasilar artery junction.
VI. ATYPICAL ANEURYSMS
632
35. DISSECTING INTRACRANIAL ANEURYSMS
open surgery as evidence supports that an unsecured and untreated rDIA is associated with poor outcome (Mizutani et al., 1995; Nakatomi et al., 1997; Yamaura, Watanabe, & Saeki, 1990). DIA of the vertebral artery are unusual, with an incidence of 0.001%–0.0015% in the general population (Santos-Franco et al., 2008; Schievink, 2001). rDIA of the vertebral artery account for 3% of all spontaneous SAH (Lylyk, Ceratto, Hurvitz, & Basso, 1998; Yamaura et al., 1990). Recurrent SAH in DIA of the vertebral artery could be as high as 71.4% with mortality rates as high as 46.7%–80% after a recurrent hemorrhage (Mizutani et al., 1995; Santos-Franco et al., 2008). As with all ruptured aneurysms, the risk of recurrent SAH is highest during the first 24 h and up to 7 days after the initial ictus if not treated. Thus, it is important to initiate therapy in rDIA of the vertebral artery to obviate future events in an attempt to maximize the opportunity to achieve a favorable outcome (Hamada et al., 2003; Iihara et al., 2002; Ramgren et al., 2005; Santos-Franco et al., 2008). Several case reports and series on childhood DIA exist. In one case series, the majority of DIA presented with mass effect, TIA, or IS (similar to adult giant aneurysms). In fact, most were DIA of the vertebral artery and most of them were large or giant aneurysms (Zhang et al., 2016). This is significantly different than the morphology typically encountered in the adult population with DIA.
35.2 ETIOLOGY AND PATHOPHYSIOLOGY Congenital and acquired abnormalities of the arterial media and elastic tissue—for example, Ehlers-Danlos syndrome and especially fibromuscular dysplasia—do render patients more vulnerable to dissection. Yet most patients with dissections do not have concurrent clinically diagnosable connective tissue disorders. A few patients, particularly those with a family history of dissections, have alpha antitrypsin deficiency, or mutations in genes that affect collagen. Migraine is particularly common among patients with dissections, possibly because edema of the vessel wall during a migraine attack makes the involved artery more vulnerable to tearing. In most cases, however, dissections are related to sudden or unusual stretching of arteries, both in the neck and in the head, regardless of whether there is an underlying abnormality in the connective tissue architecture of the arteries involved. Other common etiologies include both extrinsic and intrinsic physiologic abnormalities such as defective repair mechanisms, risk factors such as hypertension, smoking, inflammatory diseases, genetic predisposition, fibromuscular dysplasia, collagen disease, and trauma. Symptoms in patients with ID (Table 35.1) can be related to the mass effect, ischemia, or SAH (Linden, Chou, Furlan, & Conomy, 1987; Wolman, 1959). Angiographic findings (Table 35.3) consistent with arterial dissection include: (1) the double-lumen sign; (2) stenosis with dilatation (the pearl and string sign); (3) stenosis without dilatation (the string sign); (4) tapered occlusion; (5) extensive stenosis but not segmental stenosis on initial angiography; (6) resolution of stenosis or occlusion seen on follow-up angiography; and (7) dilatation without stenosis (contrast stasis within an aneurysmal dilatation due to intramural hematoma) (Byoun et al., 2016; Uhl, Schmid-Elsaesser, & Steiger, 2003).
VI. ATYPICAL ANEURYSMS
35.3 CLASSIFICATION
TABLE 35.1
633
Clinical Presentation of Dissecting Intracranial Aneurysms
Presentation
Clinical Features
Asymptomatic
Incidental on imaging
Symptomatic
Ischemia: TIA/stroke Hemorrhage: SAH Mass effect: elevated intracranial pressure, hydrocephalus, seizure Headache
Histologically, the extracranial and intracranial vessels are different. Intracranial arteries possess a tunica media and tunica adventitia which are only one-third as thick as their extracranial counterparts, with the vast majority of elastic fibers located in a subendothelial elastic lamina. This fundamental difference accounts for the markedly different natural history of intracranial artery dissection when compared to extracranial dissection. When a tear breaches the intracranial subendothelial elastic layer, there is little tissue to prevent extension into the subarachnoid space. In addition, the media and internal layer of intracranial arteries lack vasa vasorum. These changes occur at the level of the skull base in the carotid artery and 1 cm proximal to the dural perforation of the vertebral artery. Histopathological characterization of an arterial dissection includes sudden disruption of the endothelium and internal elastic lamina with penetration of circulating blood through the intima. Dissecting blood propagates longitudinally within the artery wall, extending between the internal elastic lamina and media, within the media, or between the media and the adventitia, creating a pseudolumen. The pseudolumen may then reenter the true lumen of the artery, end blindly within the artery wall, or rupture through the adventitia (Linden et al., 1987; Wolman, 1959). These histopathological patterns have clinical correlates. With a dissection plane between the intima and media, subintimal accumulation of thrombus may exert a mass effect on the true arterial lumen. This effect can result in hemodynamic stress from (1) stenosis of the parent artery or (2) embolization from thrombus formation, either from within the pseudolumen or from the stenosed true lumen. Ultimately, the predominant clinical manifestation in these instances is brain ischemia. By contrast, a dissection plane between the media and adventitia likely results in bulging of the adventitia with fusiform aneurysmal dilatation of the artery, or rupture through the adventitia. Rupture will cause SAH if the artery is surrounded by cerebrospinal fluid (Wolman, 1959).
35.3 CLASSIFICATION DIA can be classified based on the anatomical distributions, radiographic characteristics, and clinical presentations (Table 35.2).
35.3.1 Anatomic Location DIA are either of anterior or posterior circulation origin. Most commonly, dissecting aneurysms of the internal carotid artery occur at the skull base, cervical-petrous, followed by
VI. ATYPICAL ANEURYSMS
634
35. DISSECTING INTRACRANIAL ANEURYSMS
TABLE 35.2
Mechanism and Angiographic Features of Dissecting Intracranial Aneurysms
Etiology
Mechanism
Radiographic Features
Spontaneous
Unknown
Fusiform dilation
Traumatic
Penetrating or blunt trauma: GSW, knife wound, MVA, etc. Valsalva maneuvers (weight lifting, snow shoveling, etc.) Neck manipulation
Pearl-and-string sign Bleb-like lesion Subintimal flap Irregular luminal stenosis
FIG. 35.3 Cerebral angiogram of a 55-year-old healthy female presenting with a sudden onset of right-sided paresthesias during a ski trip. Cerebral angiography revealed a left ICA dissecting aneurysm (A) with newly diagnosed moderate fibromuscular dysplasia. Reconstructive endovascular therapy was performed with intravascular stentassisted coiling. Four-week follow-up (B) shows complete obliteration and normalization of the parent vessel.
petrous-cavernous, and then para-ophthalmic segments in order (Fig. 35.3). However, dissecting aneurysms of the middle cerebral artery and anterior cerebral artery can and do occur (Hashimoto, Iida, Shin, Hironaka, & Sakaki, 1999; Kunze & Schiefer, 1971). Common locations for dissecting aneurysms of the vertebrobasilar system include the dural segment of the vertebral artery, the basilar trunk, the vertebrobasilar junction, the basilar apex with the first segment of the posterior cerebral artery (PCA) and posterior inferior cerebellar artery (PICA). Posterior circulation dissecting aneurysms represented roughly 90% of the dissecting aneurysms treated in one series. In the pediatric populations, ID aneurysms are present more frequently in the basilar artery trunk and the PCA, both of which are more rare in adults (de Barros Faria et al., 2011).
35.4 CLINICAL PRESENTATIONS OF ID ANEURYSMS DIA tend to present with SAH, IS/TIA, and headache (Uhl et al., 2003). As always, clinical signs and symptoms vary according to the morphology and anatomic location of the aneurysm. Table 35.1 provides a list of the typical symptoms at presentation in adults along with patients who are either asymptomatic or symptomatic. Children usually present with mass
VI. ATYPICAL ANEURYSMS
35.5 RADIOGRAPHIC EVALUATION AND DIAGNOSIS OF DIA
635
effect as they typically have large and giant aneurysms (Zhang et al., 2016). The most common nonfocal clinical presentation of ID aneurysms is headache. An important consideration is the presence or absence of known trauma or a clinical/physiologic event. Often, an asymptomatic, unruptured ID aneurysm is identified as an incidental finding during cerebral imaging for the evaluation of other routine neurologic conditions. In a study by Kobayshi et al., 113 patients with unruptured vertebral artery dissecting aneurysms without IS/TIA at presentation were followed for a mean of 3 years and there was 3% morbidity at follow-up. Two patients in the study deteriorated due to the mass effect and one patient had an IS with SAH including enlargement of the DIA (Kobayashi et al., 2014). The morbidity of a ruptured DIA based on the anatomical location is not entirely clear. There are literature reports of patients presenting with worse Hunt Hess grades in ruptured vertebrobasilar artery disecting aneurysm (VBADA) (Byoun et al., 2016) and others (Yonekawa, Zumofen, Imhof, Roth, & Khan, 2008) claim that the ruptured dissecting aneurysm in the anterior circulation presents with poorer Hunt-Hess grades. Recurrent SAH is more frequently observed in the rVBADA compared to rDIA in the anterior circulation (Rabinov, Hellinger, Morris, Ogilvy, & Putman, 2003). Recurrent bleeding in rDIA occurs in up to 71.4% of patients (Mizutani et al., 1995) and was associated with poor H&H grades and uncontrolled blood pressure (Byoun et al., 2016; Ohkuma, Nakano, Manabe, & Suzuki, 2002; Sakata et al., 2000).
35.5 RADIOGRAPHIC EVALUATION AND DIAGNOSIS OF DIA Most dissecting aneurysms are diagnosed as incidental findings on imaging modalities performed for other reasons related to neurological illness. These modalities include MRI, MRA, CT, and CT angiography (CTA). The diagnosis or clinical suspicion of an intracranial aneurysm typically leads to appropriate referral and subsequent workup via catheter based cerebral angiography. Digital subtraction angiography (DSA) in conjunction with 3D reconstruction techniques continues to be the gold standard for diagnosis and therapeutic planning. In patients presenting with SAH on CT scan, DSA represents the definitive modality to establish the diagnosis of an ID aneurysm and angiographic findings are listed in Table 35.3. DSA enables evaluation of the collateral circulation, the aneurysm itself, and potential involvement of adjacent vasculature including perforators to guide the management TABLE 35.3 Angiographic Features of Dissecting Intracranial Aneurysms Angiographic Features of Dissecting Intracranial Aneurysms Fusiform dilatation along the vessel Pearl-and-string sign Irregular luminal stenosis Subintimal flap Bleb-like lesion
VI. ATYPICAL ANEURYSMS
636
35. DISSECTING INTRACRANIAL ANEURYSMS
TABLE 35.4 Magnetic Resonance Imaging Features of Dissecting Intracranial Aneurysms MRI Features of Dissecting Intracranial Aneurysms Intramural hematoma (61%) Double lumen (50%) Intimal flap (42%)
plan. The most common finding on DSA imaging is an area of vessel dilatation (67%), followed by dilatation and stenosis (26%), with an area of vessel stenosis alone comprising only 7% of cases. The remaining two cases demonstrated intramural thrombus without luminal changes. Magnetic resonance imaging findings, using 3 T high-resolution imaging, in cases of DIA (Table 35.4) include intramural hematoma (61%), double lumen sign (50%), and intimal flap (42%) (Wang et al., 2014).
35.6 MANAGEMENT OF DIA The remainder of this chapter focuses on the management of a DIA from an endovascular perspective (Figs. 35.4–35.9). However, surgical approaches should always be kept within one’s armamentarium when warranted. In the event of SAH, optimization of medical management with implementation of standard SAH protocols should occur concurrently with planning of definitive aneurysm repair. In the case of a DIA, recurrent SAH can occur in up to 71.4% of patients within the first 24 h (Rabinov et al., 2003). Thus, expeditious evaluation is warranted in all cases of suspected DIA presenting with SAH. Rabinov et al. reported the 30-day mortality for ruptured posterior circulation DIA to be 50% in the conservative
FIG. 35.4 A 67-year-old male with symptomatic right ICA stenosis and a spontaneous dissecting aneurysm (A). The patient was treated with simple self expandable carotid stenting (B, immediate postprocedure). Three month follow-up cerebral angiogram shows complete resolution of aneurysm (C).
VI. ATYPICAL ANEURYSMS
35.6 MANAGEMENT OF DIA
637
FIG. 35.5
A 25-year-old female with headache postmotor vehicle accident. Digital subtraction angiography of the common carotid artery (A) revealed a right ICA traumatic dissecting pseudoaneurysm (arrow). The patient was treated with self-expandable carotid stent (B) and 4-year follow-up revealed complete resolution (C).
FIG. 35.6 A 44-year-old male who underwent treatment of for dissecting stenosis developed a dissecting aneurysm at the proximal landing zone of the stent (left image, arrow). Subsequently patient was treated with reconstructive endovascular therapy with stent assisted coiling (right imaging, arrow).
management group compared to 20% in the endovascular treatment group. Furthermore, mortality rates ranged from 47% to as high as 80% after a recurrent hemorrhage (Mizutani et al., 1995; Santos-Franco et al., 2008). Ergo, we advocate rapid endovascular assessment and treatment of patients with DIA. Prior to the endovascular era, repair of DIA relied on control of hydrocephalus secondary to SAH and surgical intervention. The mainstays of open neurosurgical intervention included: traditional clipping, trapping (segmental occlusion), wrapping (muslin, cotton, etc.), and parent vessel occlusion with or without bypass. Today, technical success can be achieved with either open craniotomy or endovascular treatment. With the advent of intracranial stents and other novel techniques, the preferred initial treatment approach to DIA is trending to
VI. ATYPICAL ANEURYSMS
638
35. DISSECTING INTRACRANIAL ANEURYSMS
FIG. 35.7 A 54-year-old male developed a recurrent right ICA skull base dissecting aneurysm (A, arrowhead). He also developed a proximal ICA dissection with fusiform aneurysm (A, arrow). The skull base dissecting aneurysm was treated with reconstructive endovascular therapy with stent assisted coiling (B, arrowhead). The proximal cervical ICA was surgically repaired. Follow up MRA shows complete resolution (C, arrowheads).
FIG. 35.8 A 38-year-old female with a dissecting aneurysm of the cavernous ICA ((A) precoiling and (B) postinitial stent-coiling) demonstrating recurrence of a dissecting pseudoaneurysm (C) after stent assisted repair. The patient underwent treatment with a flow diverter and resulted in complete resolution (D).
endovascular management. Numerous reports suggest that endovascular techniques for treating DIA result in lower morbidity and mortality rates (Gonzalez et al., 2014; Kocaeli, Chaalala, Andaluz, & Zuccarello, 2009; Ohkuma et al., 2002) compared to open surgical approaches. High morbidity in the treatment of DIA (especially posterior circulation lesions) is due to the complexity of the surgical approach (i.e., via eloquent corridors or failure to achieve complete obliteration), potential for regrowth and rehemorrhage, and maintenance of flow from collateral circulation following sacrifice operations (e.g., proximal vertebral artery or carotid occlusion) that exclude trapping or trapping and bypass (Ahn et al., 2005; Chen et al., 2013; Kitanaka et al., 1994; Kurata et al., 2001; Uhl et al., 2003).
VI. ATYPICAL ANEURYSMS
35.6 MANAGEMENT OF DIA
639
FIG. 35.9 A 31-year-old male developed a symptomatic right vertebral artery dissecting intracranial aneurysm (left, arrow) which was treated with a flow diverting stent (center, between arrowheads) and resulted in complete resolution of the aneurysm during follow-up imaging (right).
Endovascular therapy has essentially emerged as the treatment of choice for DIA due to perceived lower rates of treatment related complications and overall success in treatment. Endovascular therapies have long been used for the proximal occlusion or trapping of ID aneurysms due to less morbid access and rapid transition to definitive treatment after diagnostic angiography (Hamasaki, Ikawa, Hidaka, Kurokawa, & Yonezawa, 2014). However, with the advent of stent assisted techniques (Lanzino et al., 1999), parent vessels were preserved in the majority of cases. With the relatively recent development of dedicated intracranial stents and now flow diverters (devices that maintain laminar flow through the parent vessel while disrupting flow in a surrounding lesion, ultimately leading to obliteration of the lesion), parent artery preservation techniques have become the preferred treatment for ID aneurysms. Endovascular therapy can be conceived as deconstructive or reconstructive. Deconstructive techniques rely on parent vessel occlusion, whereas reconstructive techniques preserve parent vessels. Deconstructive techniques are considered when adequate collateral circulation is available (i.e., occlusion of dissecting aneurysm of the vertebral artery with preservation of the contralateral V4 segment) and terminal eloquent vessels (i.e., perforators) are not involved in the treatment segment of the parent vessel. Deconstructive techniques should also be considered when patients are resistant to antiplatelet therapy or in cases of rupture in which antiplatelet therapy is counterproductive to overall management (e.g., ventriculostomy management, anticipated ventriculoperitoneal shunt placement, tracheostomy, etc.). In fact, risk of intracranial hemorrhage is over 3 times more likely in patients needing cranial procedures concurrent with endovascular therapies requiring dual antiplatelet therapy (Kung et al., 2011; Mahaney et al., 2013) than those without. However, reconstructive techniques are always preferred if possible to maintain parent vessel patency. Other reasons to maintain the parent vessel include protection of perforators and/or the absence of collateral circulation (Fig. 35.1). A recent systemic review and metaanalysis on deconstructive and reconstructive techniques in the treatment of VBADAs (S€ onmez, Brinjikji, Murad, & Lanzino, 2015)
VI. ATYPICAL ANEURYSMS
640
35. DISSECTING INTRACRANIAL ANEURYSMS
included 17 studies with 478 patients. Endovascular treatment was associated with high rates of long-term occlusion (87.0%; 95% CI: 0.74–0.94), low rates of recurrence (7.0%; 95% CI: 0.05–0.10), and low rates of retreatment (3.0%; 95% CI: 0.02–0.06). Good neurological outcome (defined as a modified Rankin Scale score of 2) was observed in 84.0% of patients (95% CI: 0.65–0.94) in the long term. Both deconstructive and reconstructive techniques were associated with high rates of good neurological outcome (86.0%; 95% CI: 0.68–0.95 versus 92.0%; 95% CI: 0.86–0.95; P ¼ 0.10). However, deconstructive techniques were associated with higher rates of long-term complete occlusion compared with reconstructive techniques (88.0%; 95% CI: 0.35–0.99 versus 81.0%; 95% CI: 0.64–0.91; P < .0001). The authors concluded that either endovascular technique is an acceptable option for treatment of ID aneurysms of the posterior circulation with deconstructive techniques having higher occlusion rates. There appears to be no statistical difference in the neurological outcomes between the two treatment approaches. Overall, for all patients with VBADAs, deconstructive techniques were associated with higher rates of immediate (88.0% versus 53.0%, P < .001) and long-term (88.0% versus 81.0%, p < 0.0001) obliteration. However, perioperative morbidity was lower in the reconstructive group compared to the deconstructive group (4.0% versus 12.0%, P ¼ .04) and mortality trended lower in the reconstructive group (4.0% versus 10.0%, P ¼ .11), in addition to a trend toward better outcome in the reconstructive group (92.0% versus 86.0%, p ¼ 0.10) (S€ onmez et al., 2015). In ruptured ID vertebrobasilar aneurysms, deconstructive techniques were associated with higher immediate (94.0% versus 43.0%, P < 0.0001) and long-term (95.0% versus 83.0%, P ¼ .02) aneurysm occlusion compared with reconstructive techniques. No statistical significance in perioperative morbidity (14.0% versus 7.0%, P ¼ .82) and mortality (13.0% versus 7.0%, P ¼ 0.82) was observed between the two groups. In addition, rehemorrhage rates (9.0% versus 7.0%, P ¼ .75) and clinical outcomes (83.0% versus 88.0%, P ¼ .19) were similar in both groups. In patients with unruptured aneurysms, deconstructive techniques had higher immediate (94.0% versus 57%, P .0001) and long-term occlusion rates (97% versus 68%, P ¼ 0.02) compared to reconstructive techniques. Perioperative morbidity (7.0% versus 7.0%, P ¼ .57) and mortality (4.0% versus 5.0%, P ¼ 1.00) were similar between the two groups. Long-term neurological outcomes were also similar between the deconstructive and reconstructive groups (93.0% versus 94.0%, P ¼ 1.0) (S€ onmez et al., 2015). DIA which are incidental are typically treated. A case series by Kobayashi et al. followed 113 patients for a mean of 3 years with incidental DIA without stroke or TIA. Aneurysms were found to have enlarged in five cases with two patients having morbidity secondary to mass effect and one patient suffering an IS coincident with SAH. Overall, there were no deaths and a 3% morbidity rate related to aneurysm progression or rupture. Owing to its relatively limited size, the study is only relevant to a region of Japan and should not be generalized to other populations (Kobayashi et al., 2014). Nonetheless, treatment should be considered for incidental DIA to prevent growth, rupture, or ischemic attack.
35.6.1 Pediatric DIA As with adult ID aneurysms, surgical and endovascular therapies are offered on a case-bycase basis with treatment trending toward endovascular therapy with indications similar to
VI. ATYPICAL ANEURYSMS
REFERENCES
641
those in the adult population. There is also a preference for endovascular treatment versus open surgical treatment because of the lower morbidity associated with endovascular access and lower overall morbidity compared to surgery. Numerous case reports and small series exist (Ahn et al., 2006; Debette et al., 2015; Fischer et al., 2014; Nass, Hays, & Chutorian, 1982; Rizzi et al., 2012; Saraf, Shrivastava, Siddhartha, & Limaye, 2012; Songsaeng et al., 2009; Zhang et al., 2016). In a recent case series by Zhang et al., 26 pediatric patients with 31 ID aneurysms underwent endovascular, open surgical therapy, or conservative management. The majority of patients were male and 65% of the aneurysms were large or giant-sized. Fourteen patients underwent deconstructive treatment versus six on whom reconstructive therapy was performed. Similar to the adult series, there was no difference regarding morbidity or mortality. However, 33% of the reconstructive cohort had recurrence versus 7% in the parent vessel occlusion group. However, with respect to angiographic outcome, two out of six patients in the reconstructive group had evidence of recurrence versus one out of the 14 patients in the deconstructive treatment group.
35.7 CONCLUSION DIA, while rare, should be included in the differential diagnosis of patients who present with SAH, TIA/IS, and ID. They are best divided into lesions involving the anterior or posterior intracranial circulation. When confirmed, treatment of DIA should be carried out via deconstructive or reconstructive neuroendovascular techniques, with open surgery reserved for patients who are unable to undergo neuroendovascular care or for neuroendovascular treatment failures. Treatment should also be prompt in patients presenting with SAH, as their morbidity, mortality, and risk of rehemorrhage are similar to those who present with aneurysmal SAH. An argument can be made for observation in cases of incidentally diagnosed DIA; however, the authors typically advocate treatment to reduce the risk of growth, rupture, or future ischemic attacks.
References Ahn, J. Y., Chung, S. S., Lee, B. H., Kim, S. H., Yoon, P. H., Joo, J. Y., et al. (2005). Treatment of spontaneous arterial dissections with stent placement for preservation of the parent artery. Acta Neurochirurgica, 147(3), 265–273 [discussion 273]. https://doi.org/10.1007/s00701-004-0436-8. Ahn, J. Y., Han, I. B., Kim, T. G., Yoon, P. H., Lee, Y. J., Lee, B.-H., et al. (2006). Endovascular treatment of intracranial vertebral artery dissections with stent placement or stent-assisted coiling. AJNR. American Journal of Neuroradiology, 27(7), 1514–1520. Byoun, H. S., Yi, H. J., Choi, K. S., Chun, H. J., Ko, Y., & Bak, K. H. (2016). Comparison of endovascular treatments of ruptured dissecting aneurysms of the intracranial internal carotid artery and vertebral artery with a review of the literature. Journal of Korean Neurosurgical Society, 59(5), 449–457. https://doi.org/10.3340/jkns.2016.59.5.449. Chen, Y.-A., Qu, R.-B., Bian, Y.-S., Zhu, W., Zhang, K.-P., & Pang, Q. (2013). Stent placement to treat ruptured vertebral dissecting aneurysms. Interventional Neuroradiology: Journal of Peritherapeutic Neuroradiology, Surgical Procedures and Related Neurosciences, 19(4), 479–482. https://doi.org/10.1177/159101991301900412. de Barros Faria, M., Castro, R. N., Lundquist, J., Scrivano, E., Ceratto, R., Ferrario, A., et al. (2011). The role of the pipeline embolization device for the treatment of dissecting intracranial aneurysms. AJNR. American Journal of Neuroradiology, 32(11), 2192–2195. https://doi.org/10.3174/ajnr.A2671.
VI. ATYPICAL ANEURYSMS
642
35. DISSECTING INTRACRANIAL ANEURYSMS
Debette, S., Compter, A., Labeyrie, M.-A., Uyttenboogaart, M., Metso, T. M., Majersik, J. J., et al. (2015). Epidemiology, pathophysiology, diagnosis, and management of intracranial artery dissection. The Lancet. Neurology, 14(6), 640–654. https://doi.org/10.1016/S1474-4422(15)00009-5. Fischer, S., Perez, M. A., Kurre, W., Albes, G., B€azner, H., & Henkes, H. (2014). Pipeline embolization device for the treatment of intra- and extracranial fusiform and dissecting aneurysms: initial experience and long-term follow-up. Neurosurgery, 75(4), 364–374 [discussion 374]. https://doi.org/10.1227/NEU.0000000000000431. Gonzalez, A. M., Narata, A. P., Yilmaz, H., Bijlenga, P., Radovanovic, I., Schaller, K., et al. (2014). Blood blister-like aneurysms: single center experience and systematic literature review. European Journal of Radiology, 83(1), 197–205. https://doi.org/10.1016/j.ejrad.2013.09.017. Hamada, J., Kai, Y., Morioka, M., Yano, S., Todaka, T., & Ushio, Y. (2003). Multimodal treatment of ruptured dissecting aneurysms of the vertebral artery during the acute stage. Journal of Neurosurgery, 99(6), 960–966. https://doi.org/10.3171/jns.2003.99.6.0960. Hamasaki, O., Ikawa, F., Hidaka, T., Kurokawa, Y., & Yonezawa, U. (2014). Treatment of ruptured vertebral artery dissecting aneurysms. A short report. Interventional Neuroradiology: Journal of Peritherapeutic Neuroradiology, Surgical Procedures and Related Neurosciences, 20(3), 304–311. https://doi.org/10.15274/INR-2014-10024. Hashimoto, H., Iida, J., Shin, Y., Hironaka, Y., & Sakaki, T. (1999). Subarachnoid hemorrhage from intracranial dissecting aneurysms of the anterior circulation. Two case reports. Neurologia Medico-Chirurgica, 39(6), 442–446. Iihara, K., Sakai, N., Murao, K., Sakai, H., Higashi, T., Kogure, S., et al. (2002). Dissecting aneurysms of the vertebral artery: a management strategy. Journal of Neurosurgery, 97(2), 259–267. https://doi.org/10.3171/ jns.2002.97.2.0259. Kitanaka, C., Sasaki, T., Eguchi, T., Teraoka, A., Nakane, M., & Hoya, K. (1994). Intracranial vertebral artery dissections: clinical, radiological features, and surgical considerations. Neurosurgery, 34(4), 620–626 [discussion 626-7]. Kobayashi, N., Murayama, Y., Yuki, I., Ishibashi, T., Ebara, M., Arakawa, H., et al. (2014). Natural course of dissecting vertebrobasilar artery aneurysms without stroke. AJNR. American Journal of Neuroradiology, 35(7), 1371–1375. https://doi.org/10.3174/ajnr.A3873. Kocaeli, H., Chaalala, C., Andaluz, N., & Zuccarello, M. (2009). Spontaneous intradural vertebral artery dissection: a single-center experience and review of the literature. Skull Base: Official Journal of North American Skull Base Society ... [et al.], 19(3), 209–218. https://doi.org/10.1055/s-0028-1114296. Kung, D. K., Policeni, B. A., Capuano, A. W., Rossen, J. D., Jabbour, P. M., Torner, J. C., et al. (2011). Risk of ventriculostomy-related hemorrhage in patients with acutely ruptured aneurysms treated using stent-assisted coiling. Journal of Neurosurgery, 114(4), 1021–1027. https://doi.org/10.3171/2010.9.JNS10445. Kunze, S., & Schiefer, W. (1971). Angiographic demonstration of a dissecting aneurysm of the middle cerebral artery. Neuroradiology, 2(4), 201–206. Kurata, A., Ohmomo, T., Miyasaka, Y., Fujii, K., Kan, S., & Kitahara, T. (2001). Coil embolization for the treatment of ruptured dissecting vertebral aneurysms. AJNR. American Journal of Neuroradiology, 22(1), 11–18. Lanzino, G., Wakhloo, A. K., Fessler, R. D., Hartney, M. L., Guterman, L. R., & Hopkins, L. N. (1999). Efficacy and current limitations of intravascular stents for intracranial internal carotid, vertebral, and basilar artery aneurysms. Journal of Neurosurgery, 91(4), 538–546. https://doi.org/10.3171/jns.1999.91.4.0538. Linden, M. D., Chou, S. M., Furlan, A. J., & Conomy, J. P. (1987). Cerebral arterial dissection. A case report with histopathologic and ultrastructural findings. Cleveland Clinic Journal of Medicine, 54(2), 105–114. Lylyk, P., Ceratto, R., Hurvitz, D., & Basso, A. (1998). Treatment of a vertebral dissecting aneurysm with stents and coils: technical case report. Neurosurgery, 43(2), 385–388. Mahaney, K. B., Chalouhi, N., Viljoen, S., Smietana, J., Kung, D. K., Jabbour, P., et al. (2013). Risk of hemorrhagic complication associated with ventriculoperitoneal shunt placement in aneurysmal subarachnoid hemorrhage patients on dual antiplatelet therapy. Journal of Neurosurgery, 119(4), 937–942. https://doi.org/ 10.3171/2013.5.JNS122494. Meling, T. R., Sorteberg, A., Bakke, S. J., Slettebø, H., Hernesniemi, J., & Sorteberg, W. (2008). Blood blister-like aneurysms of the internal carotid artery trunk causing subarachnoid hemorrhage: treatment and outcome. Journal of Neurosurgery, 108(4), 662–671. https://doi.org/10.3171/JNS/2008/108/4/0662. Mizutani, T., Aruga, T., Kirino, T., Miki, Y., Saito, I., & Tsuchida, T. (1995). Recurrent subarachnoid hemorrhage from untreated ruptured vertebrobasilar dissecting aneurysms. Neurosurgery, 36(5), 905–911 [discussion 912-3]. Nakatomi, H., Nagata, K., Kawamoto, S., & Shiokawa, Y. (1997). Ruptured dissecting aneurysm as a cause of subarachnoid hemorrhage of unverified etiology. Stroke, 28(6), 1278–1282. Nass, R., Hays, A., & Chutorian, A. (1982). Intracranial dissecting aneurysms in childhood. Stroke, 13(2), 204–207.
VI. ATYPICAL ANEURYSMS
REFERENCES
643
Ohkuma, H., Nakano, T., Manabe, H., & Suzuki, S. (2002). Subarachnoid hemorrhage caused by a dissecting aneurysm of the internal carotid artery. Journal of Neurosurgery, 97(3), 576–583. https://doi.org/10.3171/ jns.2002.97.3.0576. Rabinov, J. D., Hellinger, F. R., Morris, P. P., Ogilvy, C. S., & Putman, C. M. (2003). Endovascular management of vertebrobasilar dissecting aneurysms. AJNR. American Journal of Neuroradiology, 24(7), 1421–1428. Ramgren, B., Cronqvist, M., Romner, B., Brandt, L., Holta˚s, S., & Larsson, E.-M. (2005). Vertebrobasilar dissection with subarachnoid hemorrhage: a retrospective study of 29 patients. Neuroradiology, 47(2), 97–104. https://doi.org/ 10.1007/s00234-005-1346-z. Rizzi, M., De Benedictis, A., Marras, C. E., Palma, P., Desiderio, F., & Rollo, M. (2012). Ruptured dissecting vertebrobasilar aneurysm in childhood: what is the therapeutic strategy? Pediatric Neurosurgery, 48(5), 313–318. https://doi.org/10.1159/000351578. Sakata, N., Takebayashi, S., Kojima, M., Masawa, N., Suzuki, K., & Takatama, M. (2000). Pathology of a dissecting intracranial aneurysm. Neuropathology: Official Journal of the Japanese Society of Neuropathology, 20(1), 104–108. Santos-Franco, J. A., Zenteno, M., & Lee, A. (2008). Dissecting aneurysms of the vertebrobasilar system. A comprehensive review on natural history and treatment options. Neurosurgical Review, 31(2), 131–140 [discussion 140]. https://doi.org/10.1007/s10143-008-0124-x. Saraf, R., Shrivastava, M., Siddhartha, W., & Limaye, U. (2012). Intracranial pediatric aneurysms: endovascular treatment and its outcome. Journal of Neurosurgery. Pediatrics, 10(3), 230–240. https://doi.org/10.3171/2012.5. PEDS1210. Schievink, W. I. (2001). Spontaneous dissection of the carotid and vertebral arteries. The New England Journal of Medicine, 344(12), 898–906. https://doi.org/10.1056/NEJM200103223441206. Songsaeng, D., Srivatanakul, K., Toulgoat, F., Saliou, G., Ozanne, A., & Lasjaunias, P. (2009). Repair process in spontaneous intradural dissecting aneurysms in children: report of eight patients and review of the literature. Child’s Nervous System: ChNS: Official Journal of the International Society for Pediatric Neurosurgery, 25(1), 55–62. https://doi. org/10.1007/s00381-008-0698-1. € Brinjikji, W., Murad, M. H., & Lanzino, G. (2015). Deconstructive and reconstructive techniques in treatS€ onmez, O., ment of Vertebrobasilar dissecting aneurysms: a systematic review and meta-analysis. AJNR. American Journal of Neuroradiology, 36(7), 1293–1298. https://doi.org/10.3174/ajnr.A4360. Uhl, E., Schmid-Elsaesser, R., & Steiger, H.-J. (2003). Ruptured intracranial dissecting aneurysms: management considerations with a focus on surgical and endovascular techniques to preserve arterial continuity. Acta Neurochirurgica, 145(12), 1073–1083 [discussion 1083-4]. https://doi.org/10.1007/s00701-003-0122-2. Wang, Y., Lou, X., Li, Y., Sui, B., Sun, S., Li, C., et al. (2014). Imaging investigation of intracranial arterial dissecting aneurysms by using 3 T high-resolution MRI and DSA: from the interventional neuroradiologists’ view. Acta Neurochirurgica, 156(3), 515–525. https://doi.org/10.1007/s00701-013-1989-1. Wolman, L. (1959). Cerebral dissecting aneurysms. Brain: A Journal of Neurology, 82, 276–291. Yamaura, A., Watanabe, Y., & Saeki, N. (1990). Dissecting aneurysms of the intracranial vertebral artery. Journal of Neurosurgery, 72(2), 183–188. https://doi.org/10.3171/jns.1990.72.2.0183. Yonekawa, Y., Zumofen, D., Imhof, H. G., Roth, P., & Khan, N. (2008). Hemorrhagic cerebral dissecting aneurysms: surgical treatments and results. Acta Neurochirurgica. Supplement, 103, 61–69. Zhang, Y.-S., Wang, S., Wang, Y., Tian, Z.-B., Liu, J., Wang, K., et al. (2016). Treatment for spontaneous intracranial dissecting aneurysms in childhood: a retrospective study of 26 cases. Frontiers in Neurology, 7, 224. https://doi. org/10.3389/fneur.2016.00224.
VI. ATYPICAL ANEURYSMS
35 Dissecting Intracranial Aneurysms Yahia M. Lodi*, Justin G. Thomas†, Richard D. Fessler‡ *
Comprehensive Stroke and NeuroEndovascular Center at UHS Wilson Medical Center, Upstate Medical University, Johnson City, NY, United States † Department of Surgery, Michigan State University College of Human Medicine, East Lansing; Providence-Providence Park Hospitals, Southfield, MI, United States ‡ Division of Neurological Surgery, Department of Surgery, St. John Hospital & Medical Centers, Detroit, MI, United States
O U T L I N E 35.1 Introduction
630
35.2 Etiology and Pathophysiology
632
35.3 Classification 35.3.1 Anatomic Location
633 633
35.4 Clinical Presentations of ID Aneurysms
Intracranial Aneurysms https://doi.org/10.1016/B978-0-12-811740-8.00059-9
634
35.5 Radiographic Evaluation and Diagnosis of DIA
635
35.6 Management of DIA 35.6.1 Pediatric DIA
636 640
35.7 Conclusion
641
References
641
629
# 2018 Elsevier Inc. All rights reserved.
630
35. DISSECTING INTRACRANIAL ANEURYSMS
35.1 INTRODUCTION The occurrence of dissecting intracranial aneurysms (DIA) is relatively rare, comprising roughly 3% of all intracranial aneurysms (Santos-Franco, Zenteno, & Lee, 2008). The identification of a DIA depends on the clinical presentation of the patient (Fig. 35.1). The ruptured DIA is diagnosed during the evaluation of a presenting subarachnoid hemorrhage (SAH),
FIG. 35.1 (A, B) Noncontrast CT head of a 56-year-old female presenting with subarachnoid hemorrhage, Hunt-Hess grade IV, and Fisher 4. Cerebral angiography (C,D) revealed a 5.8-mm dissecting right vertebral artery aneurysm (arrow). The aneurysm is just below the PICA (arrowhead).
VI. ATYPICAL ANEURYSMS
35.1 INTRODUCTION
631
whereas the unruptured DIA is typically an incidental finding during the investigation of a transient ischemic attack (TIA), ischemic stroke (IS), or suspected intracranial dissection (ID). There are numerous case series and case reports regarding dissecting vertebrobasilar aneurysms compared to anterior circulation lesions. This may be due to a higher incidence of DIA in the posterior circulation versus the anterior circulation. Reports of unruptured DIA in the internal carotid and vertebral artery distributions suggest that SAH is a relatively rare occurrence (Byoun et al., 2016; Meling et al., 2008; Nakatomi, Nagata, Kawamoto, & Shiokawa, 1997). However, more recent case series suggest that the natural history of DIA that present with hemorrhage carries a profound mortality of up to 80% of untreated cases within 5 years (Santos-Franco et al., 2008). There is growing evidence that the risk of early hemorrhage is comparable to that of ruptured saccular aneurysms (Byoun et al., 2016). Therefore, it has been recommended that patients with ruptured dissecting intracranial aneurysms (rDIA) should undergo early repair of the aneurysm either by an endovascular approach (Fig. 35.2) or by
FIG. 35.2 Lateral cerebral angiogram (A) and native view (B) of the right vertebral artery undergoing deconstructive endovascular repair of the aneurysm by coil embolization (C) just below the origin of right PICA. Injection of the left vertebral artery (D) demonstrated filling of the right PICA through the vertebrobasilar artery junction.
VI. ATYPICAL ANEURYSMS
632
35. DISSECTING INTRACRANIAL ANEURYSMS
open surgery as evidence supports that an unsecured and untreated rDIA is associated with poor outcome (Mizutani et al., 1995; Nakatomi et al., 1997; Yamaura, Watanabe, & Saeki, 1990). DIA of the vertebral artery are unusual, with an incidence of 0.001%–0.0015% in the general population (Santos-Franco et al., 2008; Schievink, 2001). rDIA of the vertebral artery account for 3% of all spontaneous SAH (Lylyk, Ceratto, Hurvitz, & Basso, 1998; Yamaura et al., 1990). Recurrent SAH in DIA of the vertebral artery could be as high as 71.4% with mortality rates as high as 46.7%–80% after a recurrent hemorrhage (Mizutani et al., 1995; Santos-Franco et al., 2008). As with all ruptured aneurysms, the risk of recurrent SAH is highest during the first 24 h and up to 7 days after the initial ictus if not treated. Thus, it is important to initiate therapy in rDIA of the vertebral artery to obviate future events in an attempt to maximize the opportunity to achieve a favorable outcome (Hamada et al., 2003; Iihara et al., 2002; Ramgren et al., 2005; Santos-Franco et al., 2008). Several case reports and series on childhood DIA exist. In one case series, the majority of DIA presented with mass effect, TIA, or IS (similar to adult giant aneurysms). In fact, most were DIA of the vertebral artery and most of them were large or giant aneurysms (Zhang et al., 2016). This is significantly different than the morphology typically encountered in the adult population with DIA.
35.2 ETIOLOGY AND PATHOPHYSIOLOGY Congenital and acquired abnormalities of the arterial media and elastic tissue—for example, Ehlers-Danlos syndrome and especially fibromuscular dysplasia—do render patients more vulnerable to dissection. Yet most patients with dissections do not have concurrent clinically diagnosable connective tissue disorders. A few patients, particularly those with a family history of dissections, have alpha antitrypsin deficiency, or mutations in genes that affect collagen. Migraine is particularly common among patients with dissections, possibly because edema of the vessel wall during a migraine attack makes the involved artery more vulnerable to tearing. In most cases, however, dissections are related to sudden or unusual stretching of arteries, both in the neck and in the head, regardless of whether there is an underlying abnormality in the connective tissue architecture of the arteries involved. Other common etiologies include both extrinsic and intrinsic physiologic abnormalities such as defective repair mechanisms, risk factors such as hypertension, smoking, inflammatory diseases, genetic predisposition, fibromuscular dysplasia, collagen disease, and trauma. Symptoms in patients with ID (Table 35.1) can be related to the mass effect, ischemia, or SAH (Linden, Chou, Furlan, & Conomy, 1987; Wolman, 1959). Angiographic findings (Table 35.3) consistent with arterial dissection include: (1) the double-lumen sign; (2) stenosis with dilatation (the pearl and string sign); (3) stenosis without dilatation (the string sign); (4) tapered occlusion; (5) extensive stenosis but not segmental stenosis on initial angiography; (6) resolution of stenosis or occlusion seen on follow-up angiography; and (7) dilatation without stenosis (contrast stasis within an aneurysmal dilatation due to intramural hematoma) (Byoun et al., 2016; Uhl, Schmid-Elsaesser, & Steiger, 2003).
VI. ATYPICAL ANEURYSMS
35.3 CLASSIFICATION
TABLE 35.1
633
Clinical Presentation of Dissecting Intracranial Aneurysms
Presentation
Clinical Features
Asymptomatic
Incidental on imaging
Symptomatic
Ischemia: TIA/stroke Hemorrhage: SAH Mass effect: elevated intracranial pressure, hydrocephalus, seizure Headache
Histologically, the extracranial and intracranial vessels are different. Intracranial arteries possess a tunica media and tunica adventitia which are only one-third as thick as their extracranial counterparts, with the vast majority of elastic fibers located in a subendothelial elastic lamina. This fundamental difference accounts for the markedly different natural history of intracranial artery dissection when compared to extracranial dissection. When a tear breaches the intracranial subendothelial elastic layer, there is little tissue to prevent extension into the subarachnoid space. In addition, the media and internal layer of intracranial arteries lack vasa vasorum. These changes occur at the level of the skull base in the carotid artery and 1 cm proximal to the dural perforation of the vertebral artery. Histopathological characterization of an arterial dissection includes sudden disruption of the endothelium and internal elastic lamina with penetration of circulating blood through the intima. Dissecting blood propagates longitudinally within the artery wall, extending between the internal elastic lamina and media, within the media, or between the media and the adventitia, creating a pseudolumen. The pseudolumen may then reenter the true lumen of the artery, end blindly within the artery wall, or rupture through the adventitia (Linden et al., 1987; Wolman, 1959). These histopathological patterns have clinical correlates. With a dissection plane between the intima and media, subintimal accumulation of thrombus may exert a mass effect on the true arterial lumen. This effect can result in hemodynamic stress from (1) stenosis of the parent artery or (2) embolization from thrombus formation, either from within the pseudolumen or from the stenosed true lumen. Ultimately, the predominant clinical manifestation in these instances is brain ischemia. By contrast, a dissection plane between the media and adventitia likely results in bulging of the adventitia with fusiform aneurysmal dilatation of the artery, or rupture through the adventitia. Rupture will cause SAH if the artery is surrounded by cerebrospinal fluid (Wolman, 1959).
35.3 CLASSIFICATION DIA can be classified based on the anatomical distributions, radiographic characteristics, and clinical presentations (Table 35.2).
35.3.1 Anatomic Location DIA are either of anterior or posterior circulation origin. Most commonly, dissecting aneurysms of the internal carotid artery occur at the skull base, cervical-petrous, followed by
VI. ATYPICAL ANEURYSMS
634
35. DISSECTING INTRACRANIAL ANEURYSMS
TABLE 35.2
Mechanism and Angiographic Features of Dissecting Intracranial Aneurysms
Etiology
Mechanism
Radiographic Features
Spontaneous
Unknown
Fusiform dilation
Traumatic
Penetrating or blunt trauma: GSW, knife wound, MVA, etc. Valsalva maneuvers (weight lifting, snow shoveling, etc.) Neck manipulation
Pearl-and-string sign Bleb-like lesion Subintimal flap Irregular luminal stenosis
FIG. 35.3 Cerebral angiogram of a 55-year-old healthy female presenting with a sudden onset of right-sided paresthesias during a ski trip. Cerebral angiography revealed a left ICA dissecting aneurysm (A) with newly diagnosed moderate fibromuscular dysplasia. Reconstructive endovascular therapy was performed with intravascular stentassisted coiling. Four-week follow-up (B) shows complete obliteration and normalization of the parent vessel.
petrous-cavernous, and then para-ophthalmic segments in order (Fig. 35.3). However, dissecting aneurysms of the middle cerebral artery and anterior cerebral artery can and do occur (Hashimoto, Iida, Shin, Hironaka, & Sakaki, 1999; Kunze & Schiefer, 1971). Common locations for dissecting aneurysms of the vertebrobasilar system include the dural segment of the vertebral artery, the basilar trunk, the vertebrobasilar junction, the basilar apex with the first segment of the posterior cerebral artery (PCA) and posterior inferior cerebellar artery (PICA). Posterior circulation dissecting aneurysms represented roughly 90% of the dissecting aneurysms treated in one series. In the pediatric populations, ID aneurysms are present more frequently in the basilar artery trunk and the PCA, both of which are more rare in adults (de Barros Faria et al., 2011).
35.4 CLINICAL PRESENTATIONS OF ID ANEURYSMS DIA tend to present with SAH, IS/TIA, and headache (Uhl et al., 2003). As always, clinical signs and symptoms vary according to the morphology and anatomic location of the aneurysm. Table 35.1 provides a list of the typical symptoms at presentation in adults along with patients who are either asymptomatic or symptomatic. Children usually present with mass
VI. ATYPICAL ANEURYSMS
35.5 RADIOGRAPHIC EVALUATION AND DIAGNOSIS OF DIA
635
effect as they typically have large and giant aneurysms (Zhang et al., 2016). The most common nonfocal clinical presentation of ID aneurysms is headache. An important consideration is the presence or absence of known trauma or a clinical/physiologic event. Often, an asymptomatic, unruptured ID aneurysm is identified as an incidental finding during cerebral imaging for the evaluation of other routine neurologic conditions. In a study by Kobayshi et al., 113 patients with unruptured vertebral artery dissecting aneurysms without IS/TIA at presentation were followed for a mean of 3 years and there was 3% morbidity at follow-up. Two patients in the study deteriorated due to the mass effect and one patient had an IS with SAH including enlargement of the DIA (Kobayashi et al., 2014). The morbidity of a ruptured DIA based on the anatomical location is not entirely clear. There are literature reports of patients presenting with worse Hunt Hess grades in ruptured vertebrobasilar artery disecting aneurysm (VBADA) (Byoun et al., 2016) and others (Yonekawa, Zumofen, Imhof, Roth, & Khan, 2008) claim that the ruptured dissecting aneurysm in the anterior circulation presents with poorer Hunt-Hess grades. Recurrent SAH is more frequently observed in the rVBADA compared to rDIA in the anterior circulation (Rabinov, Hellinger, Morris, Ogilvy, & Putman, 2003). Recurrent bleeding in rDIA occurs in up to 71.4% of patients (Mizutani et al., 1995) and was associated with poor H&H grades and uncontrolled blood pressure (Byoun et al., 2016; Ohkuma, Nakano, Manabe, & Suzuki, 2002; Sakata et al., 2000).
35.5 RADIOGRAPHIC EVALUATION AND DIAGNOSIS OF DIA Most dissecting aneurysms are diagnosed as incidental findings on imaging modalities performed for other reasons related to neurological illness. These modalities include MRI, MRA, CT, and CT angiography (CTA). The diagnosis or clinical suspicion of an intracranial aneurysm typically leads to appropriate referral and subsequent workup via catheter based cerebral angiography. Digital subtraction angiography (DSA) in conjunction with 3D reconstruction techniques continues to be the gold standard for diagnosis and therapeutic planning. In patients presenting with SAH on CT scan, DSA represents the definitive modality to establish the diagnosis of an ID aneurysm and angiographic findings are listed in Table 35.3. DSA enables evaluation of the collateral circulation, the aneurysm itself, and potential involvement of adjacent vasculature including perforators to guide the management TABLE 35.3 Angiographic Features of Dissecting Intracranial Aneurysms Angiographic Features of Dissecting Intracranial Aneurysms Fusiform dilatation along the vessel Pearl-and-string sign Irregular luminal stenosis Subintimal flap Bleb-like lesion
VI. ATYPICAL ANEURYSMS
636
35. DISSECTING INTRACRANIAL ANEURYSMS
TABLE 35.4 Magnetic Resonance Imaging Features of Dissecting Intracranial Aneurysms MRI Features of Dissecting Intracranial Aneurysms Intramural hematoma (61%) Double lumen (50%) Intimal flap (42%)
plan. The most common finding on DSA imaging is an area of vessel dilatation (67%), followed by dilatation and stenosis (26%), with an area of vessel stenosis alone comprising only 7% of cases. The remaining two cases demonstrated intramural thrombus without luminal changes. Magnetic resonance imaging findings, using 3 T high-resolution imaging, in cases of DIA (Table 35.4) include intramural hematoma (61%), double lumen sign (50%), and intimal flap (42%) (Wang et al., 2014).
35.6 MANAGEMENT OF DIA The remainder of this chapter focuses on the management of a DIA from an endovascular perspective (Figs. 35.4–35.9). However, surgical approaches should always be kept within one’s armamentarium when warranted. In the event of SAH, optimization of medical management with implementation of standard SAH protocols should occur concurrently with planning of definitive aneurysm repair. In the case of a DIA, recurrent SAH can occur in up to 71.4% of patients within the first 24 h (Rabinov et al., 2003). Thus, expeditious evaluation is warranted in all cases of suspected DIA presenting with SAH. Rabinov et al. reported the 30-day mortality for ruptured posterior circulation DIA to be 50% in the conservative
FIG. 35.4 A 67-year-old male with symptomatic right ICA stenosis and a spontaneous dissecting aneurysm (A). The patient was treated with simple self expandable carotid stenting (B, immediate postprocedure). Three month follow-up cerebral angiogram shows complete resolution of aneurysm (C).
VI. ATYPICAL ANEURYSMS
35.6 MANAGEMENT OF DIA
637
FIG. 35.5
A 25-year-old female with headache postmotor vehicle accident. Digital subtraction angiography of the common carotid artery (A) revealed a right ICA traumatic dissecting pseudoaneurysm (arrow). The patient was treated with self-expandable carotid stent (B) and 4-year follow-up revealed complete resolution (C).
FIG. 35.6 A 44-year-old male who underwent treatment of for dissecting stenosis developed a dissecting aneurysm at the proximal landing zone of the stent (left image, arrow). Subsequently patient was treated with reconstructive endovascular therapy with stent assisted coiling (right imaging, arrow).
management group compared to 20% in the endovascular treatment group. Furthermore, mortality rates ranged from 47% to as high as 80% after a recurrent hemorrhage (Mizutani et al., 1995; Santos-Franco et al., 2008). Ergo, we advocate rapid endovascular assessment and treatment of patients with DIA. Prior to the endovascular era, repair of DIA relied on control of hydrocephalus secondary to SAH and surgical intervention. The mainstays of open neurosurgical intervention included: traditional clipping, trapping (segmental occlusion), wrapping (muslin, cotton, etc.), and parent vessel occlusion with or without bypass. Today, technical success can be achieved with either open craniotomy or endovascular treatment. With the advent of intracranial stents and other novel techniques, the preferred initial treatment approach to DIA is trending to
VI. ATYPICAL ANEURYSMS
638
35. DISSECTING INTRACRANIAL ANEURYSMS
FIG. 35.7 A 54-year-old male developed a recurrent right ICA skull base dissecting aneurysm (A, arrowhead). He also developed a proximal ICA dissection with fusiform aneurysm (A, arrow). The skull base dissecting aneurysm was treated with reconstructive endovascular therapy with stent assisted coiling (B, arrowhead). The proximal cervical ICA was surgically repaired. Follow up MRA shows complete resolution (C, arrowheads).
FIG. 35.8 A 38-year-old female with a dissecting aneurysm of the cavernous ICA ((A) precoiling and (B) postinitial stent-coiling) demonstrating recurrence of a dissecting pseudoaneurysm (C) after stent assisted repair. The patient underwent treatment with a flow diverter and resulted in complete resolution (D).
endovascular management. Numerous reports suggest that endovascular techniques for treating DIA result in lower morbidity and mortality rates (Gonzalez et al., 2014; Kocaeli, Chaalala, Andaluz, & Zuccarello, 2009; Ohkuma et al., 2002) compared to open surgical approaches. High morbidity in the treatment of DIA (especially posterior circulation lesions) is due to the complexity of the surgical approach (i.e., via eloquent corridors or failure to achieve complete obliteration), potential for regrowth and rehemorrhage, and maintenance of flow from collateral circulation following sacrifice operations (e.g., proximal vertebral artery or carotid occlusion) that exclude trapping or trapping and bypass (Ahn et al., 2005; Chen et al., 2013; Kitanaka et al., 1994; Kurata et al., 2001; Uhl et al., 2003).
VI. ATYPICAL ANEURYSMS
35.6 MANAGEMENT OF DIA
639
FIG. 35.9 A 31-year-old male developed a symptomatic right vertebral artery dissecting intracranial aneurysm (left, arrow) which was treated with a flow diverting stent (center, between arrowheads) and resulted in complete resolution of the aneurysm during follow-up imaging (right).
Endovascular therapy has essentially emerged as the treatment of choice for DIA due to perceived lower rates of treatment related complications and overall success in treatment. Endovascular therapies have long been used for the proximal occlusion or trapping of ID aneurysms due to less morbid access and rapid transition to definitive treatment after diagnostic angiography (Hamasaki, Ikawa, Hidaka, Kurokawa, & Yonezawa, 2014). However, with the advent of stent assisted techniques (Lanzino et al., 1999), parent vessels were preserved in the majority of cases. With the relatively recent development of dedicated intracranial stents and now flow diverters (devices that maintain laminar flow through the parent vessel while disrupting flow in a surrounding lesion, ultimately leading to obliteration of the lesion), parent artery preservation techniques have become the preferred treatment for ID aneurysms. Endovascular therapy can be conceived as deconstructive or reconstructive. Deconstructive techniques rely on parent vessel occlusion, whereas reconstructive techniques preserve parent vessels. Deconstructive techniques are considered when adequate collateral circulation is available (i.e., occlusion of dissecting aneurysm of the vertebral artery with preservation of the contralateral V4 segment) and terminal eloquent vessels (i.e., perforators) are not involved in the treatment segment of the parent vessel. Deconstructive techniques should also be considered when patients are resistant to antiplatelet therapy or in cases of rupture in which antiplatelet therapy is counterproductive to overall management (e.g., ventriculostomy management, anticipated ventriculoperitoneal shunt placement, tracheostomy, etc.). In fact, risk of intracranial hemorrhage is over 3 times more likely in patients needing cranial procedures concurrent with endovascular therapies requiring dual antiplatelet therapy (Kung et al., 2011; Mahaney et al., 2013) than those without. However, reconstructive techniques are always preferred if possible to maintain parent vessel patency. Other reasons to maintain the parent vessel include protection of perforators and/or the absence of collateral circulation (Fig. 35.1). A recent systemic review and metaanalysis on deconstructive and reconstructive techniques in the treatment of VBADAs (S€ onmez, Brinjikji, Murad, & Lanzino, 2015)
VI. ATYPICAL ANEURYSMS
640
35. DISSECTING INTRACRANIAL ANEURYSMS
included 17 studies with 478 patients. Endovascular treatment was associated with high rates of long-term occlusion (87.0%; 95% CI: 0.74–0.94), low rates of recurrence (7.0%; 95% CI: 0.05–0.10), and low rates of retreatment (3.0%; 95% CI: 0.02–0.06). Good neurological outcome (defined as a modified Rankin Scale score of 2) was observed in 84.0% of patients (95% CI: 0.65–0.94) in the long term. Both deconstructive and reconstructive techniques were associated with high rates of good neurological outcome (86.0%; 95% CI: 0.68–0.95 versus 92.0%; 95% CI: 0.86–0.95; P ¼ 0.10). However, deconstructive techniques were associated with higher rates of long-term complete occlusion compared with reconstructive techniques (88.0%; 95% CI: 0.35–0.99 versus 81.0%; 95% CI: 0.64–0.91; P < .0001). The authors concluded that either endovascular technique is an acceptable option for treatment of ID aneurysms of the posterior circulation with deconstructive techniques having higher occlusion rates. There appears to be no statistical difference in the neurological outcomes between the two treatment approaches. Overall, for all patients with VBADAs, deconstructive techniques were associated with higher rates of immediate (88.0% versus 53.0%, P < .001) and long-term (88.0% versus 81.0%, p < 0.0001) obliteration. However, perioperative morbidity was lower in the reconstructive group compared to the deconstructive group (4.0% versus 12.0%, P ¼ .04) and mortality trended lower in the reconstructive group (4.0% versus 10.0%, P ¼ .11), in addition to a trend toward better outcome in the reconstructive group (92.0% versus 86.0%, p ¼ 0.10) (S€ onmez et al., 2015). In ruptured ID vertebrobasilar aneurysms, deconstructive techniques were associated with higher immediate (94.0% versus 43.0%, P < 0.0001) and long-term (95.0% versus 83.0%, P ¼ .02) aneurysm occlusion compared with reconstructive techniques. No statistical significance in perioperative morbidity (14.0% versus 7.0%, P ¼ .82) and mortality (13.0% versus 7.0%, P ¼ 0.82) was observed between the two groups. In addition, rehemorrhage rates (9.0% versus 7.0%, P ¼ .75) and clinical outcomes (83.0% versus 88.0%, P ¼ .19) were similar in both groups. In patients with unruptured aneurysms, deconstructive techniques had higher immediate (94.0% versus 57%, P .0001) and long-term occlusion rates (97% versus 68%, P ¼ 0.02) compared to reconstructive techniques. Perioperative morbidity (7.0% versus 7.0%, P ¼ .57) and mortality (4.0% versus 5.0%, P ¼ 1.00) were similar between the two groups. Long-term neurological outcomes were also similar between the deconstructive and reconstructive groups (93.0% versus 94.0%, P ¼ 1.0) (S€ onmez et al., 2015). DIA which are incidental are typically treated. A case series by Kobayashi et al. followed 113 patients for a mean of 3 years with incidental DIA without stroke or TIA. Aneurysms were found to have enlarged in five cases with two patients having morbidity secondary to mass effect and one patient suffering an IS coincident with SAH. Overall, there were no deaths and a 3% morbidity rate related to aneurysm progression or rupture. Owing to its relatively limited size, the study is only relevant to a region of Japan and should not be generalized to other populations (Kobayashi et al., 2014). Nonetheless, treatment should be considered for incidental DIA to prevent growth, rupture, or ischemic attack.
35.6.1 Pediatric DIA As with adult ID aneurysms, surgical and endovascular therapies are offered on a case-bycase basis with treatment trending toward endovascular therapy with indications similar to
VI. ATYPICAL ANEURYSMS
REFERENCES
641
those in the adult population. There is also a preference for endovascular treatment versus open surgical treatment because of the lower morbidity associated with endovascular access and lower overall morbidity compared to surgery. Numerous case reports and small series exist (Ahn et al., 2006; Debette et al., 2015; Fischer et al., 2014; Nass, Hays, & Chutorian, 1982; Rizzi et al., 2012; Saraf, Shrivastava, Siddhartha, & Limaye, 2012; Songsaeng et al., 2009; Zhang et al., 2016). In a recent case series by Zhang et al., 26 pediatric patients with 31 ID aneurysms underwent endovascular, open surgical therapy, or conservative management. The majority of patients were male and 65% of the aneurysms were large or giant-sized. Fourteen patients underwent deconstructive treatment versus six on whom reconstructive therapy was performed. Similar to the adult series, there was no difference regarding morbidity or mortality. However, 33% of the reconstructive cohort had recurrence versus 7% in the parent vessel occlusion group. However, with respect to angiographic outcome, two out of six patients in the reconstructive group had evidence of recurrence versus one out of the 14 patients in the deconstructive treatment group.
35.7 CONCLUSION DIA, while rare, should be included in the differential diagnosis of patients who present with SAH, TIA/IS, and ID. They are best divided into lesions involving the anterior or posterior intracranial circulation. When confirmed, treatment of DIA should be carried out via deconstructive or reconstructive neuroendovascular techniques, with open surgery reserved for patients who are unable to undergo neuroendovascular care or for neuroendovascular treatment failures. Treatment should also be prompt in patients presenting with SAH, as their morbidity, mortality, and risk of rehemorrhage are similar to those who present with aneurysmal SAH. An argument can be made for observation in cases of incidentally diagnosed DIA; however, the authors typically advocate treatment to reduce the risk of growth, rupture, or future ischemic attacks.
References Ahn, J. Y., Chung, S. S., Lee, B. H., Kim, S. H., Yoon, P. H., Joo, J. Y., et al. (2005). Treatment of spontaneous arterial dissections with stent placement for preservation of the parent artery. Acta Neurochirurgica, 147(3), 265–273 [discussion 273]. https://doi.org/10.1007/s00701-004-0436-8. Ahn, J. Y., Han, I. B., Kim, T. G., Yoon, P. H., Lee, Y. J., Lee, B.-H., et al. (2006). Endovascular treatment of intracranial vertebral artery dissections with stent placement or stent-assisted coiling. AJNR. American Journal of Neuroradiology, 27(7), 1514–1520. Byoun, H. S., Yi, H. J., Choi, K. S., Chun, H. J., Ko, Y., & Bak, K. H. (2016). Comparison of endovascular treatments of ruptured dissecting aneurysms of the intracranial internal carotid artery and vertebral artery with a review of the literature. Journal of Korean Neurosurgical Society, 59(5), 449–457. https://doi.org/10.3340/jkns.2016.59.5.449. Chen, Y.-A., Qu, R.-B., Bian, Y.-S., Zhu, W., Zhang, K.-P., & Pang, Q. (2013). Stent placement to treat ruptured vertebral dissecting aneurysms. Interventional Neuroradiology: Journal of Peritherapeutic Neuroradiology, Surgical Procedures and Related Neurosciences, 19(4), 479–482. https://doi.org/10.1177/159101991301900412. de Barros Faria, M., Castro, R. N., Lundquist, J., Scrivano, E., Ceratto, R., Ferrario, A., et al. (2011). The role of the pipeline embolization device for the treatment of dissecting intracranial aneurysms. AJNR. American Journal of Neuroradiology, 32(11), 2192–2195. https://doi.org/10.3174/ajnr.A2671.
VI. ATYPICAL ANEURYSMS
642
35. DISSECTING INTRACRANIAL ANEURYSMS
Debette, S., Compter, A., Labeyrie, M.-A., Uyttenboogaart, M., Metso, T. M., Majersik, J. J., et al. (2015). Epidemiology, pathophysiology, diagnosis, and management of intracranial artery dissection. The Lancet. Neurology, 14(6), 640–654. https://doi.org/10.1016/S1474-4422(15)00009-5. Fischer, S., Perez, M. A., Kurre, W., Albes, G., B€azner, H., & Henkes, H. (2014). Pipeline embolization device for the treatment of intra- and extracranial fusiform and dissecting aneurysms: initial experience and long-term follow-up. Neurosurgery, 75(4), 364–374 [discussion 374]. https://doi.org/10.1227/NEU.0000000000000431. Gonzalez, A. M., Narata, A. P., Yilmaz, H., Bijlenga, P., Radovanovic, I., Schaller, K., et al. (2014). Blood blister-like aneurysms: single center experience and systematic literature review. European Journal of Radiology, 83(1), 197–205. https://doi.org/10.1016/j.ejrad.2013.09.017. Hamada, J., Kai, Y., Morioka, M., Yano, S., Todaka, T., & Ushio, Y. (2003). Multimodal treatment of ruptured dissecting aneurysms of the vertebral artery during the acute stage. Journal of Neurosurgery, 99(6), 960–966. https://doi.org/10.3171/jns.2003.99.6.0960. Hamasaki, O., Ikawa, F., Hidaka, T., Kurokawa, Y., & Yonezawa, U. (2014). Treatment of ruptured vertebral artery dissecting aneurysms. A short report. Interventional Neuroradiology: Journal of Peritherapeutic Neuroradiology, Surgical Procedures and Related Neurosciences, 20(3), 304–311. https://doi.org/10.15274/INR-2014-10024. Hashimoto, H., Iida, J., Shin, Y., Hironaka, Y., & Sakaki, T. (1999). Subarachnoid hemorrhage from intracranial dissecting aneurysms of the anterior circulation. Two case reports. Neurologia Medico-Chirurgica, 39(6), 442–446. Iihara, K., Sakai, N., Murao, K., Sakai, H., Higashi, T., Kogure, S., et al. (2002). Dissecting aneurysms of the vertebral artery: a management strategy. Journal of Neurosurgery, 97(2), 259–267. https://doi.org/10.3171/ jns.2002.97.2.0259. Kitanaka, C., Sasaki, T., Eguchi, T., Teraoka, A., Nakane, M., & Hoya, K. (1994). Intracranial vertebral artery dissections: clinical, radiological features, and surgical considerations. Neurosurgery, 34(4), 620–626 [discussion 626-7]. Kobayashi, N., Murayama, Y., Yuki, I., Ishibashi, T., Ebara, M., Arakawa, H., et al. (2014). Natural course of dissecting vertebrobasilar artery aneurysms without stroke. AJNR. American Journal of Neuroradiology, 35(7), 1371–1375. https://doi.org/10.3174/ajnr.A3873. Kocaeli, H., Chaalala, C., Andaluz, N., & Zuccarello, M. (2009). Spontaneous intradural vertebral artery dissection: a single-center experience and review of the literature. Skull Base: Official Journal of North American Skull Base Society ... [et al.], 19(3), 209–218. https://doi.org/10.1055/s-0028-1114296. Kung, D. K., Policeni, B. A., Capuano, A. W., Rossen, J. D., Jabbour, P. M., Torner, J. C., et al. (2011). Risk of ventriculostomy-related hemorrhage in patients with acutely ruptured aneurysms treated using stent-assisted coiling. Journal of Neurosurgery, 114(4), 1021–1027. https://doi.org/10.3171/2010.9.JNS10445. Kunze, S., & Schiefer, W. (1971). Angiographic demonstration of a dissecting aneurysm of the middle cerebral artery. Neuroradiology, 2(4), 201–206. Kurata, A., Ohmomo, T., Miyasaka, Y., Fujii, K., Kan, S., & Kitahara, T. (2001). Coil embolization for the treatment of ruptured dissecting vertebral aneurysms. AJNR. American Journal of Neuroradiology, 22(1), 11–18. Lanzino, G., Wakhloo, A. K., Fessler, R. D., Hartney, M. L., Guterman, L. R., & Hopkins, L. N. (1999). Efficacy and current limitations of intravascular stents for intracranial internal carotid, vertebral, and basilar artery aneurysms. Journal of Neurosurgery, 91(4), 538–546. https://doi.org/10.3171/jns.1999.91.4.0538. Linden, M. D., Chou, S. M., Furlan, A. J., & Conomy, J. P. (1987). Cerebral arterial dissection. A case report with histopathologic and ultrastructural findings. Cleveland Clinic Journal of Medicine, 54(2), 105–114. Lylyk, P., Ceratto, R., Hurvitz, D., & Basso, A. (1998). Treatment of a vertebral dissecting aneurysm with stents and coils: technical case report. Neurosurgery, 43(2), 385–388. Mahaney, K. B., Chalouhi, N., Viljoen, S., Smietana, J., Kung, D. K., Jabbour, P., et al. (2013). Risk of hemorrhagic complication associated with ventriculoperitoneal shunt placement in aneurysmal subarachnoid hemorrhage patients on dual antiplatelet therapy. Journal of Neurosurgery, 119(4), 937–942. https://doi.org/ 10.3171/2013.5.JNS122494. Meling, T. R., Sorteberg, A., Bakke, S. J., Slettebø, H., Hernesniemi, J., & Sorteberg, W. (2008). Blood blister-like aneurysms of the internal carotid artery trunk causing subarachnoid hemorrhage: treatment and outcome. Journal of Neurosurgery, 108(4), 662–671. https://doi.org/10.3171/JNS/2008/108/4/0662. Mizutani, T., Aruga, T., Kirino, T., Miki, Y., Saito, I., & Tsuchida, T. (1995). Recurrent subarachnoid hemorrhage from untreated ruptured vertebrobasilar dissecting aneurysms. Neurosurgery, 36(5), 905–911 [discussion 912-3]. Nakatomi, H., Nagata, K., Kawamoto, S., & Shiokawa, Y. (1997). Ruptured dissecting aneurysm as a cause of subarachnoid hemorrhage of unverified etiology. Stroke, 28(6), 1278–1282. Nass, R., Hays, A., & Chutorian, A. (1982). Intracranial dissecting aneurysms in childhood. Stroke, 13(2), 204–207.
VI. ATYPICAL ANEURYSMS
REFERENCES
643
Ohkuma, H., Nakano, T., Manabe, H., & Suzuki, S. (2002). Subarachnoid hemorrhage caused by a dissecting aneurysm of the internal carotid artery. Journal of Neurosurgery, 97(3), 576–583. https://doi.org/10.3171/ jns.2002.97.3.0576. Rabinov, J. D., Hellinger, F. R., Morris, P. P., Ogilvy, C. S., & Putman, C. M. (2003). Endovascular management of vertebrobasilar dissecting aneurysms. AJNR. American Journal of Neuroradiology, 24(7), 1421–1428. Ramgren, B., Cronqvist, M., Romner, B., Brandt, L., Holta˚s, S., & Larsson, E.-M. (2005). Vertebrobasilar dissection with subarachnoid hemorrhage: a retrospective study of 29 patients. Neuroradiology, 47(2), 97–104. https://doi.org/ 10.1007/s00234-005-1346-z. Rizzi, M., De Benedictis, A., Marras, C. E., Palma, P., Desiderio, F., & Rollo, M. (2012). Ruptured dissecting vertebrobasilar aneurysm in childhood: what is the therapeutic strategy? Pediatric Neurosurgery, 48(5), 313–318. https://doi.org/10.1159/000351578. Sakata, N., Takebayashi, S., Kojima, M., Masawa, N., Suzuki, K., & Takatama, M. (2000). Pathology of a dissecting intracranial aneurysm. Neuropathology: Official Journal of the Japanese Society of Neuropathology, 20(1), 104–108. Santos-Franco, J. A., Zenteno, M., & Lee, A. (2008). Dissecting aneurysms of the vertebrobasilar system. A comprehensive review on natural history and treatment options. Neurosurgical Review, 31(2), 131–140 [discussion 140]. https://doi.org/10.1007/s10143-008-0124-x. Saraf, R., Shrivastava, M., Siddhartha, W., & Limaye, U. (2012). Intracranial pediatric aneurysms: endovascular treatment and its outcome. Journal of Neurosurgery. Pediatrics, 10(3), 230–240. https://doi.org/10.3171/2012.5. PEDS1210. Schievink, W. I. (2001). Spontaneous dissection of the carotid and vertebral arteries. The New England Journal of Medicine, 344(12), 898–906. https://doi.org/10.1056/NEJM200103223441206. Songsaeng, D., Srivatanakul, K., Toulgoat, F., Saliou, G., Ozanne, A., & Lasjaunias, P. (2009). Repair process in spontaneous intradural dissecting aneurysms in children: report of eight patients and review of the literature. Child’s Nervous System: ChNS: Official Journal of the International Society for Pediatric Neurosurgery, 25(1), 55–62. https://doi. org/10.1007/s00381-008-0698-1. € Brinjikji, W., Murad, M. H., & Lanzino, G. (2015). Deconstructive and reconstructive techniques in treatS€ onmez, O., ment of Vertebrobasilar dissecting aneurysms: a systematic review and meta-analysis. AJNR. American Journal of Neuroradiology, 36(7), 1293–1298. https://doi.org/10.3174/ajnr.A4360. Uhl, E., Schmid-Elsaesser, R., & Steiger, H.-J. (2003). Ruptured intracranial dissecting aneurysms: management considerations with a focus on surgical and endovascular techniques to preserve arterial continuity. Acta Neurochirurgica, 145(12), 1073–1083 [discussion 1083-4]. https://doi.org/10.1007/s00701-003-0122-2. Wang, Y., Lou, X., Li, Y., Sui, B., Sun, S., Li, C., et al. (2014). Imaging investigation of intracranial arterial dissecting aneurysms by using 3 T high-resolution MRI and DSA: from the interventional neuroradiologists’ view. Acta Neurochirurgica, 156(3), 515–525. https://doi.org/10.1007/s00701-013-1989-1. Wolman, L. (1959). Cerebral dissecting aneurysms. Brain: A Journal of Neurology, 82, 276–291. Yamaura, A., Watanabe, Y., & Saeki, N. (1990). Dissecting aneurysms of the intracranial vertebral artery. Journal of Neurosurgery, 72(2), 183–188. https://doi.org/10.3171/jns.1990.72.2.0183. Yonekawa, Y., Zumofen, D., Imhof, H. G., Roth, P., & Khan, N. (2008). Hemorrhagic cerebral dissecting aneurysms: surgical treatments and results. Acta Neurochirurgica. Supplement, 103, 61–69. Zhang, Y.-S., Wang, S., Wang, Y., Tian, Z.-B., Liu, J., Wang, K., et al. (2016). Treatment for spontaneous intracranial dissecting aneurysms in childhood: a retrospective study of 26 cases. Frontiers in Neurology, 7, 224. https://doi. org/10.3389/fneur.2016.00224.
VI. ATYPICAL ANEURYSMS