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Part 2 book “Decision making in neurovascular disease” has contents: Superior cerebellar artery aneurysms, posterior inferior cerebellar artery aneurysm, mycotic intracranial aneurysms, pediatric intracranial aneurysms, spinal aneurysms, brainstem arteriovenous malformations,… and other contents.
32 Fusiform Aneurysms of the Anterior Circulation Leonardo B.C Brasiliense, Pedro Aguilar-Salinas, Douglas Gonsales, Andrey Lima, Eric Sauvageau, and Ricardo A Hanel Abstract The estimated prevalence of intracranial aneurysms (IA) in the general population ranges between and 4% Although fusiform aneurysms are more commonly found in the vertebrobasilar circulation, these challenging lesions can occur in the anterior circulation with a prevalence ranging from 0.1 to 0.3% Fusiform aneurysms are complex lesions that involve more than 50% of the arterial circumference and are typically characterized by a lack of discernible neck In general, this subset of lesions is associated with worse outcomes, higher rates of complications, and death In this chapter, we discuss their anatomical features and explore pathophysiological mechanisms as well as current evidence in surgical and endovascular options Microsurgery remains an adequate treatment option and some of the vascular reconstructions include trapping, wrapping, bypass, and excision and induction of aneurysm thrombosis by proximal clipping Endovascular options for fusiform aneurysms are typically associated with the use of stents or flow diverters with or without the use of adjuvant coiling Overall, these procedures have demonstrated a safe and effective profile favoring this option over microsurgery However, in some instances, a combined approach can be done Although there is no consensus for the optimal management of fusiform aneurysms in the anterior circulation, the decision is made on a case-by-case basis assessing the patient’s hemorrhagic risk over an estimated life span in contrast to neurosurgeon’s perceptions of potential complications, particularly major neurological morbidity and loss of functional independence Keywords: intracranial aneurysm, fusiform aneurysm, surgery, endovascular Introduction Intracranial aneurysms are estimated to occur in approximately 2.8% of the general population and giant aneurysms (≥25 mm in largest diameter) represent an infrequent subset of lesions representing only to 5% of intracranial aneurysms These lesions are often also categorized into saccular and fusiform based on their morphology and appearance on imaging studies Saccular aneurysm implies that a discernible neck is present, which typically occurs following a localized defect in the arterial wall In contrast, fusiform aneurysms are complex lesions involving more than 50% of the arterial circumference and typically characterized by no discernible neck, which has important treatment implications Although fusiform aneurysms are more commonly found in the vertebrobasilar circulation, these challenging lesions also occur in the anterior circulation with an estimated prevalence ranging from 0.1 to 0.3% Within the anterior circulation, the majority of fusiform aneurysms occur in the internal carotid artery (ICA) Fusiform aneurysms involving the anterior cerebral arteries (ACAs) and middle cerebral arteries (MCAs) are rarely seen Fusiform aneurysms in the supraclinoid segment of the ICA have a higher rate of rupture (~40–50% over years) compared to aneurysms located in the cavernous segment (10% over the same period) The former lesions are also associated with worse outcomes, higher rates of complications, recanalization, and death In the past, some authors have suggested that fusiform aneurysms may have an atherosclerotic component in their etiology However, other pathogenic factors unrelated to atherosclerosis have been previously demonstrated to increase the risk of aneurysm enlargement over time and bleeding Age of the patient is a very good indicator of lesion pathogenesis Young patients often develop these aneurysms in the context of vessel dissection or underlying vasculopathy, while older patients (older than 45 years) are more likely to develop these lesions in association with vessel atherosclerosis Major controversies in decision making addressed in this chapter include: Imaging surveillance versus treatment Microsurgical treatment versus endovascular techniques Long-term durability of current treatment strategies State-of-the-art endovascular devices Whether to Treat Compared to saccular aneurysms, the natural history and risk of rupture for fusiform aneurysms in the anterior circulation remains a topic only marginally understood and an area that would benefit greatly from further studies As with other intracranial aneurysms, factors to aid in the treatment algorithm include (1) aneurysm size, (2) recent growth on imaging studies, (3) previous subarachnoid hemorrhage (SAH), and (4) patient preference Smaller asymptomatic lesions can be safely monitored with serial imaging and rarely demonstrate further growth (1 in algorithm) The decision to treat should always take in consideration the estimated risks associated with treatment weighted against the natural history Anatomical Considerations Intracranial aneurysms are more likely to occur in certain segments of the artery, which has generally been based on regional differences in blood flow Similarly, fusiform aneurysms tend to occur between areas of vessel bifurcation in both proximal and distal segments of major intracranial arteries The majority of fusiform aneurysms in the anterior circulation are found in the cavernous segment of the ICA (~42%), followed by the remaining ICA (23–39%), MCA bifurcation (32–41%), and rarely ACA (0.2–1.0%) Fusiform aneurysms involving the ACA are usually restricted to the A1 segment and similarly, these lesions are more likely to occur at the M1 segment when the MCA is involved Pathophysiology The events leading to the development of fusiform aneurysms are often unknown; atherosclerosis has been postulated as a potential mechanism due to disruption of the internal elastic lamina (IEL) It has also been hypothesized that these lesions may arise from arterial microdissections with intramural hemorrhage between the intima and the media leading to progressive dilatation and tortuosity As previously mentioned, dissection or nonatherosclerotic vasculopathy is more likely to occur in younger patients, and atherosclerosis occurs more often in older patients In addition, turbulent flow within the aneurysm lumen has been shown to create nonphysiological transmural pressures and shear stress on the vessel wall, which may induce changes in smooth muscle cell homeostasis and loss of endothelial integrity Fusiform aneurysms often have unique underlying pathological features on autopsy including calcified walls, onion skin pattern in the vessel wall, partial aneurysm thrombosis, and absence of aneurysm neck Although uncommon, infection involving the vessel has been found to predispose the arterial wall to fusiform dilation, which has been correlated with medial fibrosis, loss of smooth muscle layer, destruction of the IEL, and intimal hyperplasia Tumor cell infiltration of intracranial vessels via the vasa vasorum has also been associated with pseudoaneurysm formation and fusiform dilatations with partial destruction of the vessel wall, microvascular occlusion by the tumor, and direct invasion of the arterial wall Rare cases of fusiform aneurysm formation have been reported in patients with X-linked lymphoproliferative (XLP) syndrome in which the immune system is unable to mount an adequate response to viral infections, 212 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 32 Fusiform Aneurysms of the Anterior Circulation Algorithm 32.1 Decision-making algorithm for fusiform aneurysms in the anterior circulation SAH, subarachnoid hemorrhage; TIA, transient ischemic attack 213 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Aneurysms—Anterior Circulation particularly by the Epstein–Barr virus, which may result in diffuse necrotizing vasculitis affecting major intracranial arteries Fibromuscular dysplasia may also facilitate aneurysm formation by causing various degrees of collagen hyperplasia, IEL rupture, and disorganization of the medial layer, which can result in dilatation of the artery Classification From an angiographic and pathological standpoint, these lesions can be classified into the following: • Type 1: classic dissecting aneurysms Angiographic features of a fusiform aneurysm with irregular wall and irregular stenotic portion near the proximal or distal end Pathological features include widespread disruption of the IEL without intimal thickening, and the presence of a pseudolumen, which is filled with thrombus • Type 2: segmental ectasia Angiographic features of a fusiform aneurysm with a smooth contour and typically associated with other cerebrovascular diseases Pathological features such as stretched or fragmented IEL, moderately thickened intima, and no evidence of thrombi • Type 3: dolichoectatic dissecting aneurysm Angiographic features of tortuous fusiform appearance with irregular contrast opacification caused by intraluminal thrombus Pathological features include fragmentation of IEL combined with multiple dissections of thickened intima, and organized laminar thrombi • Type 4: saccular aneurysm arising from arterial trunk Angiographic features of saccular aneurysms unrelated to the branching zones Pathological features of a mixed type such as IEL pattern resembling a type lesion without a discernible pseudolumen or organized thrombus as well as absence of IEL at the dome of the aneurysm with distended fragile adventitia Workup Clinical Evaluation Fusiform aneurysms arising in the anterior circulation often present with symptoms of mass effect such as headaches, cranial neuropathy (especially visual symptoms) as well as transient ischemic attacks (TIAs) or stroke SAH occurs less often and similar to saccular aneurysms; the majority of fusiform aneurysms (nearly 60%) are found incidentally Visual deficits due to optic nerve compression are more frequently associated with fusiform aneurysm located in the ACA (2 in algorithm) Skull base erosion with massive epistaxis has been reported with these lesions although the true incidence is unknown Imaging Imaging of fusiform aneurysms is similar to its saccular counterpart and should evaluate the aneurysm wall, lumen, and flow Magnetic resonance imaging (MRI) based techniques are clearly the best modality for wall imaging since these provide important information about wall thickness, the presence of intramural thrombus, and the extent of mass effect Lumen imaging can be assessed with multislice helical computed tomography angiogram (CTA) and has become the primary modality for noninvasive imaging Time-of-flight (TOF) magnetic resonance angiography (MRA) is a reasonable alternative in patients with severe renal disease or in patients requiring repeated imaging, with the caveat that MRA TOF can provide misleading information such as apparent vessel stenosis or occlusion However, the “gold standard” modality remains digital subtraction angiography (DSA) because it provides real-time imaging of blood flow inside the parent vessel and aneurysm as well as accurate vessel measurements, which are essential for endovascular strategies Catheter-based imaging also allows us to perform better assessment of collateral flow, very often useful for treatment of these lesions Balloon test occlusion for the carotid artery or superselective into the MCA and ACA (with newer low-profile balloons) often provides valuable therapeutic guidance Differential Diagnosis The differential diagnosis of fusiform aneurysms in the anterior circulation is broad and includes nonvascular processes such as intracranial tumors, demyelinating diseases, intracranial infections, and other vascular events such as acute ischemic stroke, vasculitis, and sinus thrombosis Treatment In general terms, treatment of fusiform aneurysms remains an individualized assessment of patient’s hemorrhage risk over an estimated life span in contrast to the neurosurgeon’s perceptions of potential complications, particularly major neurological morbidity and loss of functional independence As with other intracranial aneurysms, the patient’s age, pretreatment functional status, aneurysm size, location, and relationship to arterial branches and perforators are important aspects to be evaluated Management of fusiform aneurysms in the anterior circulation remains a formidable challenge and is frequently incompatible with conventional surgical and/or endovascular techniques For instance, fusiform cavernous aneurysms with intramural thrombus, highly calcified aneurysms, dissecting aneurysms, and aneurysms with major branches originating in the dome are often not amenable to conventional microsurgical techniques Treatment of fusiform ICA aneurysms frequently requires cerebral revascularization of the distal territory with aneurysmal and/or parent artery occlusion through direct surgical or endovascular approaches Goals of treatment include preservation of emerging perforator arteries and the parent vessel Partial occlusion may result in complete thrombosis of the aneurysm, but recanalization is not a rare event Endovascular options for fusiform aneurysms are typically associated with the use of stents or flow diverters with or without use of adjuvant coiling Unless therapeutic sacrifice is the goal, simple coiling of fusiform aneurysms is usually unfeasible or unsafe and may place the parent vessel at unnecessary risks Stent-assisted coiling as a primary treatment for fusiform aneurysms has been reported to have high rates of recanalization, ranging from 19 to 50% Constructs overlapping multiple stents have also been used with variable success rates Flow diverters represent a landmark in the management of fusiform aneurysms because these stentlike devices are the first stand-alone option to reconstruct the disease segment of the parent vessel by redirecting blood flow away from the aneurysm (4 in algorithm) Increased experience with these devices has expanded their use to include complex anterior circulation aneurysms such as fusiform lesions in the ICA and MCA It has been demonstrated that aneurysm thrombosis following placement of flow diverters is a dynamic process that can be manipulated with different techniques of device placement including telescoping or deployment of loose coils inside the aneurysm prior to device placement Overall, flow diverters could be considered the first-line endovascular treatment for fusiform aneurysms following several studies that demonstrated their safety, effectiveness, and durability (4 in algorithm) Microsurgery remains an adequate treatment option for fusiform aneurysms involving the ICA or its branches with the caveat that it requires complex techniques for vascular reconstruction Some of the goals of the vascular reconstruction are trapping, excision, and induction of aneurysm thrombosis by proximal clipping Aneurysm trapping and resection are usually unfeasible in the distal anterior circulation due to perforators originating from the aneurysmal segment Aneurysm wrapping has fallen out of favor, especially with refinements in microsurgical techniques and endovascular devices Bypass surgery either in situ or with extracranial anastomosis continues to be an important surgical option in the neurosurgeon’s armamentarium Depending on flow patterns in the donor vessel, these reconstructive procedures may be divided into lowflow and high-flow bypasses High-flow bypass is usually performed for fusiform aneurysms in the ICA where a saphenous vein or radial artery must be harvested to provide approximately 50 mL/min of blood flow for adequate distal perfusion In situ bypass is an elegant solution that 214 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 32 may be performed for MCA or ACA aneurysms after careful assessment for size match and length between vessels Interposition grafts may also be employed in these lesions prior to parent vessel occlusion or surgical trapping Although recent innovations in aneurysm treatment have limited the indications for bypass surgery, it remains an essential skill for cerebrovascular neurosurgeons who intend to treat these lesions Conservative Management When a decision is made for aneurysm observation, aspirin therapy is generally recommended, although it lacks the support of clinical studies The anti-inflammatory properties of aspirin can potentially decrease the risk of progression and hemorrhage It is prudent to maintain close surveillance of these lesions with the first repeat imaging at months to document aneurysm stability (3 in algorithm) As previously mentioned, other aspects to consider prior to treatment include age, baseline functional status, severity of symptoms, and comorbid conditions Cerebrovascular Management—Operative Nuances In preparation for open reconstructive procedures, patients typically undergo ICA balloon test occlusion to assess collateral flow and tolerance to proximal occlusion Hunterian ligation remains a viable option for giant fusiform aneurysms with a relatively simple surgical technique that has been used to divert flow away from the aneurysm and induce aneurysm thrombosis Of note, fusiform aneurysm proximal to the anterior clinoid may be amenable to proximal occlusion alone, whereas supraclinoid aneurysms are generally better managed with trapping techniques, especially to alleviate symptoms of mass effect When considering microanastomotic techniques, the superficial temporal artery (STA) is a very versatile donor for these lesions, allowing for simple or double barrel, or in association with a high-flow graft For in situ grafts, the internal maxillary artery (IMA) is also a useful alternative For ICA lesions, high-flow revascularization with the radial artery or saphenous vein (~18–20 cm of graft) is necessary The cervical ICA is exposed using a standard anterior approach and a pterional or orbitozygomatic craniotomy for intracranial exposure Exposure of the external carotid artery for an extracranial–intracranial (EC–IC) bypass, end-toend, or end-to-side anastomosis is performed between the graft and the ECA distal to the lingual artery Clip application is performed parallel to the branch vessels to avoid narrowing of the parent artery Perforating or branch arteries emerging from the fusiform aneurysm of the anterior circulation are important determinants of the timing and degree of occlusion after revascularization as hemodynamic alteration by flow diversion and acute thrombosis may result in serious adverse effects Postoperatively, the pulsations of the graft in the subcutaneous tunnel are monitored with palpation and Doppler for the first 24 hours Graft occlusion within the first 24 hours should prompt immediate bypass surgery with a new graft Heparin (5.000 units) is administered every hours for days in addition to 81 mg of aspirin daily for approximately year MR perfusion and CTA are performed on postoperative day to confirm revascularization and graft patency Follow-up MRA or CTA are recommended at months and then annually ►Figs 32.1 and ►32.2 illustrate the management of complex fusiform aneurysms Endovascular Management—Operative Nuances Patients are preloaded with dual-antiplatelet therapy, aspirin (325 mg daily), and clopidogrel (75 mg daily) or ticagrelor (90 mg twice a day) week prior to the intervention Steroids (dexamethasone 10 mg bolus or mg every hours) are used for giant fusiform aneurysms and patients with symptoms of mass effect and continued for approximately 10 days Fusiform Aneurysms of the Anterior Circulation A French (6F) or 8F-long sheath is placed using a standard femoral access and a guide catheter with an intermediate catheter (e.g., Navien; 058 Navien; ev3, Irvine, CA) is navigated to the cervical ICA A microcatheter and microwire are maneuvered under road–map guidance proximal to the aneurysm in preparation for a device to be deployed A number of intracranial stents are currently available, for example, Neuroform or Atlas Neuroform (Stryker Neurovascular, Fremont, CA), LVIS or LVIS Jr (Microvention, Tustin, CA) Multiple flow diverters are currently available or under development, but we typically prefer to use the pipeline embolization device (PED) or PED FLEX (PED; ev3-Covidien, Irvine, CA) due to increased experience and positive evidence in the literature In general, flow diverters are considered excellent treatment options for fusiform aneurysms, especially in the anterior circulation where their use appears to be associated with fewer number of thromboembolic events In brief, arterial access is obtained (more often femoral, occasionally radial/brachial/axillary) with a 6F- or 8F-long sheath and the intermediate catheter (058 Navien; ev3) is navigated selectively in the distal ICA under road-map guidance A Marksman (ev3), Phenom 27 (Phenom), or an XT-27 (Stryker Neurovascular) microcatheter is advanced distal to the landing zone and the device is deployed across the neck of the aneurysm Expansion of the PED is closely monitored with fluoroscopy and Xpert CT angiography after final deployment (►Fig 32.3) When the device seems inadequately opposed to the vessel wall, it can be manipulated with a wire and catheter or balloon angioplasty (Hyperglide or Hyperform; ev3 Neurovascular, Irvine, CA) can be performed Complication Avoidance Complications of open revascularization include occlusion of the graft, which can best be prevented by meticulous surgical techniques and adequate sizing prior to implantation Stroke may occur after inadvertent placement of the aneurysm clip over adjacent perforators, which has been greatly reduced with routine use of intraoperative indocyanine green (ICG) angiography Other complications include intraoperative aneurysm rupture and SAH, injury to cranial nerves, and chemical meningitis from intradural drilling of the anterior clinoid and sphenoid bone Ischemic events are one of the most frequent complications with endovascular procedures With flow diverters, the rate of ischemic events ranges from to 8%, most likely because these devices have a higher metal density compared to intracranial stents and the procedures require more extensive catheter manipulation Other uncommon complications include acute device thrombosis, vessel dissection, vasospasm, and delayed aneurysm rupture Long-term complications include device stenosis, spontaneous bleeding from dual-antiplatelet therapy, and stent migration Outcome As mentioned in the earlier sections, the choice of treatment should be made on a case-by-case basis The available data on outcomes are lacking and have been obtained mostly from retrospective case series partially due to the low prevalence of anterior fusiform aneurysms, which makes it difficult to compare outcomes between microsurgical and endovascular techniques In general, microsurgical strategies have estimated rates of clinical improvement between 58 and 84% (modified Rankin Scale [mRS] score 0–3) but rates of mortality ranging from 14 to 22% In contrast, endovascular strategies such as flow diverters have shown excellent outcomes with rates of clinical improvement in up to 90% (mRS 0–2) of patients and acceptable rates of aneurysm occlusion ranging from 60 to 78% (supports algorithm step 4) A recently published series of 323 intracranial dissecting and/or fusiform aneurysms were classified based on a modified imaging classification in dissecting (type I), segmental ectasia (type II), dolichoectatic dissecting aneurysm (type III), and large bleeding mural ectasia (type IV) A logistic regression was done to find predictors of outcome Of the 323, 66.8% was treated with stent-assisted coiling, 14.5% with internal trapping, and 18.6% with sole stenting Clinical follow-up was available for 309 patients with a mean of 10.4 months (range 3–60 months) Imaging 215 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Aneurysms—Anterior Circulation Fig 32.1 Case illustration A 48-year-old female patient with previous subarachnoid hemorrhage presenting with enlarging complex fusiform dilatation of the left middle cerebral artery (MCA) aneurysm demonstrated on computed tomography angiography (CTA; a,b) Cerebral angiogram showed a complex fusiform aneurysm extending from M1 to superior M2 division (c,d) Note areas of stenosis at the origin of the inferior division on three-dimensional (3D) reconstruction (e) Our initial plan consisted in performing a superficial temporal artery–middle cerebral artery (STA–MCA) bypass to the superior division with clipping of the M1-inferior division lesion Prior to treatment, the stenotic segment of the M1–M2 inferior division was stented (f,g) The STA–MCA bypass was performed 30 days later (h) A remnant M1-inferior division aneurysm could not be clipped (i) The patient was later treated with coiling of the remaining aneurysm sac (j) and persistent aneurysm occlusion at 5-year follow-up 216 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 32 Fusiform Aneurysms of the Anterior Circulation Fig 32.2 Case illustration A 34-year-old male patient presented with seizures Brain magnetic resonance imaging (MRI; a,b) demonstrated a giant thrombosed aneurysm of the anterior cerebral artery (ACA) Cerebral angiogram with anteroposterior (c–e) and lateral (f–h) views showed a giant serpentine aneurysm on the left ACA with delayed transit time compared to middle cerebral artery (MCA) territory Balloon test occlusion performed under local anesthesia with balloon placed at distal left A2 (i) demonstrated adequate A3–A4 collaterals from posterior circulation branches (j) The patient underwent a craniotomy for clip trapping of the lesion and a possible A3–A3 bypass Intraoperative angiography posttrapping confirmed presence of collaterals (k) and a decision was made for trapping only with evacuation of the aneurysm content The patient was seizure free with persisted aneurysm occlusion at 6-month follow-up (l,m) follow-up was available for 262 patients only; there was a recurrence rate of 9.16% The only independent predictor factor was aneurysm type; types III and IV had a significant unfavorable outcome Reconstructive endovascular treatment using conventional stents did not resolve the mass effect and had a higher recurrence rate compared to the cases that had reconstruction using flow diverter stents (supports algorithm step 4) Clinical and Radiographic Follow-Up Following treatment of fusiform aneurysms, patients are best managed with clinical evaluation at month to identify early signs of open or endovascular complications such as TIAs and worsening cranial neuropathy Vascular imaging is usually obtained at months using noninvasive tests and at months with DSA, followed by yearly thereafter following endovascular procedures A DSA-based scale is used to determine aneurysm occlusion (Raymond–Roy) Expert Commentary Fusiform aneurysms of the anterior circulation are some of the most challenging lesions we face in cerebrovascular surgery The natural history for these lesions remains less defined compared to saccular ones A thorough risk-versus-benefit analysis should be made prior to making a decision to treat Careful analysis with MRI-based images and catheter-based angiography, including balloon test occlusion, and collateral flow assessment are paramount The advent of improved stent technology, especially flow diverters, has provided a significant upgrade to endovascular tools The decision for endovascular versus microsurgical or combined approaches should be done on a case-bycase basis Ricardo A Hanel, MD Baptist Neurological Institute, Jacksonville, FL 217 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Aneurysms—Anterior Circulation Fig 32.3 Case illustration A 55-year-old female patient with previous history of subarachnoid hemorrhage and clipped right middle cerebral artery aneurysm She presented with headaches and workup demonstrated a fusiform aneurysm in the right M1 trunk (a,b) We decided to treat it with a flow diverter A single pipeline embolization device (PED; × 35 mm) was used, oversized to decrease mesh density over the M1 perforators covered with the PED (c) Contrast stasis in the aneurysm was noticed after device placement (d) Intraoperative cone beam computed tomography (CT) demonstrates device in adequate position (e) A 6-month follow-up angiogram demonstrates complete aneurysm occlusion and preservation of perforators (f,g) Editor Commentary Fusiform aneurysms come in many varieties, and each demands its own solution These lesions are almost certainly the result of earlier dissection and can be found incidentally or can become symptomatic from thrombus formation, mass effect, or SAH Asymptomatic lesions may best be treated with continued observation, while those that present symptomatically may require the entire endovascular and surgical armamentarium Flow diverters, vessel occlusion, bypass, clip reconstruction, and circumferential wrapping are all options depending on the specific lesion Peter Nakaji, MD and Robert F Spetzler, MD Barrow Neurological Institute, Phoenix, AZ Suggested Reading Anson JA, Lawton MT, Spetzler RF Characteristics and surgical treatment of dolichoectatic and fusiform aneurysms J Neurosurg 1996;84(2):185–193 Darsaut TE, Darsaut NM, Chang SD, et al Predictors of clinical and angiographic outcome after surgical or endovascular therapy of very large and giant intracranial aneurysms Neurosurgery 2011;68(4):903–915, discussion 915 Drake CG, Peerless SJ, Ferguson GG Hunterian proximal arterial occlusion for giant aneurysms of the carotid circulation J Neurosurg 1994;81(5):656–665 218 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 32 Kashimura H, Mase T, Ogasawara K, Ogawa A, Endo H Trapping and vascular reconstruction for ruptured fusiform aneurysm in the proximal A1 segment of the anterior cerebral artery Neurol Med Chir (Tokyo) 2006;46(7):340–343 Mizutani T, Miki Y, Kojima H, Suzuki H Proposed classification of nonatherosclerotic cerebral fusiform and dissecting aneurysms Neurosurgery 1999;45(2): 253–259, discussion 259–260 Monteith SJ, Tsimpas A, Dumont AS, et al Endovascular treatment of fusiform cerebral aneurysms with the pipeline embolization device J Neurosurg 2014;120(4):945–954 Nurminen V, Lehecka M, Chakrabarty A, et al Anatomy and morphology of giant aneurysms—angiographic study of 125 consecutive cases Acta Neurochir (Wien) 2014;156(1):1–10 Fusiform Aneurysms of the Anterior Circulation Shokunbi MT, Vinters HV, Kaufmann JC Fusiform intracranial aneurysms Clinicopathologic features Surg Neurol 1988;29(4):263–270 Spetzler RF, Selman W, Carter LP Elective EC-IC bypass for unclippable intracranial aneurysms Neurol Res 1984;6(1–2):64–68 Thompson BG, Brown RD Jr, Amin-Hanjani S, et al; American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, and Council on Epidemiology and Prevention American Heart Association American Stroke Association Guidelines for the management of patients with unruptured intracranial aneurysms: a guideline for healthcare professionals from the American Heart Association/American Stroke Association Stroke 2015;46(8):2368–2400 219 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 33 Dissecting Intracranial Aneurysms of the Anterior Circulation Stephen R Lowe, Jan Vargas, Alejandro Spiotta, and Raymond D Turner, IV Abstract Dissecting intracranial aneurysms are anatomically unique and thus are not easy to classify in the same way that saccular aneurysms have been in the neurosurgical literature These lesions are dynamic and may present with both hemorrhagic (i.e., subarachnoid hemorrhage) and ischemic symptoms These are complex anatomical lesions and generally require some form of neurosurgical intervention Neurosurgical intervention may be both an open surgical procedure or endovascular vessel reconstruction, or vessel sacrifice In cases where endovascular reconstruction is feasible, it is generally preferred However, given the variability in location and morphology of these lesions, treatment must be individualized as much as possible In this chapter, we present the relevant natural history, prognosis, anatomy, pathophysiology, workup, and management of dissecting intracranial aneurysms of the anterior circulation We will also discuss blister-type aneurysms, a special subset of dissecting aneurysms with a unique physiology, natural history, and treatment algorithm Keywords: dissecting intracranial aneurysm, dissecting pseudoaneurysm, blister-type aneurysm, subarachnoid hemorrhage, clip reconstruction, flow diversion Introduction Dissecting intracranial aneurysms (DIAs) represent a unique challenge to the cerebrovascular surgeon These rare lesions must be addressed carefully and thoughtfully to ensure a safe and durable treatment for the patient Their friable anatomy makes them technically complex lesions to treat, either by open or by endovascular techniques More significantly, these are lesions that not conform to the typical saccular morphology seen with aneurysms described in the large International Subarachnoid Aneurysm Trial (ISAT) and International Study of Unruptured Intracranial Aneurysms (ISUA) series Due to this lack of high-quality randomized and observational data, and due to the relative paucity of reports in the literature regarding the natural history, prognosis, and treatment of these lesions, developing a well-validated treatment algorithm for these lesions is challenging We aim to describe the classification, natural history, pathogenesis, and treatment considerations for DIA of the anterior circulation For the purposes of this chapter, we will consider dissecting pseudoaneurysms (i.e., those that arise either spontaneously or secondary to trauma or iatrogenic causes), which we will term DPA, separately from a unique group of dissecting aneurysms, which we will term blister-type aneurysms (BTAs) The abbreviation “DIA” will refer to DPAs and BTAs collectively Major controversies in decision making addressed in this chapter include: Whether or not treatment is indicated Open versus endovascular management for DIAs Advanced strategies for open reconstruction of DIAs Advanced strategies for endovascular reconstruction of DIAs Whether to Treat DIAs are uncommon lesions with an ill-defined incidence in the literature While BTAs are reported to represent 0.3 to 2% of all intracranial aneurysms, DPAs of the anterior circulation are even more unusual, with less than 100 reports of spontaneous DPAs in the literature and less than 50 reports of DIA secondary to trauma reported in the literature Unlike the more common saccular or “berry” aneurysm, where long-term rates of rupture are well defined, the natural history of DIAs is not well defined due to their infrequent presentation and lack of observational studies The large majority of these lesions in the literature are described in the setting of subarachnoid hemorrhage (SAH), suggesting a malignant natural history (1, 2, in algorithm) Additionally, many retrospective studies have shown these lesions to be dynamic in nature (particularly for BTAs), demonstrating rapid growth and rapid change in the conformation of the aneurysm, even in short intervals of follow-up Rapid growth and change in these lesions is even observed after attempted treatment, particularly with BTAs In the setting of SAH, patients with DIAs tend to have worse outcomes than those with a ruptured saccular aneurysm history (2 in algorithm) As noted earlier, the natural history of these lesions is not well documented BTAs are almost always described in the ruptured setting, and short-interval follow-up vascular imaging suggests that these lesions are dynamic, demonstrating rapid conformational change suggestive of instability and a malignant natural history DPAs were historically implicated as a rare cause of ischemic symptoms in young patients; however, recent reports suggest that they are more commonly associated with SAH When presenting with SAH, DIAs have been reported to have a higher rate of rebleeding (44%) compared to saccular aneurysms (14%), and as such the prognosis is worse in these patients As such, when a DIA is diagnosed in the setting of SAH, it should be treated aggressively and promptly (1, 2, in algorithm) DPAs with ischemic symptoms, on the other hand, can have a more benign course Compared to dissecting aneurysms of the vertebral artery, DPAs of the internal carotid artery (ICA) tend to persist longer, but carry little risk of recurrent ischemic events Patients with recurrent ischemic symptoms may warrant definitive treatment, but in the light of the good prognosis of these lesions, medical management to prevent thromboemboli is usually first-line treatment before subjecting a patient to invasive treatments (4, 12 in algorithm) Despite the associated higher risk of treatment, the aggressive course of DIA seen in the literature suggests that these lesions should be treated aggressively when presenting with SAH Treatment should be offered to all patients with evidence of a ruptured DIA In patients with an incidentally discovered DPA with ischemic symptoms, conservative management is appropriate, unless the patient suffers recurrent ischemic events DIA secondary to trauma should be given strong consideration for treatment in the unruptured setting given they likely have an aggressive natural history The natural history of incidentally discovered BTAs is not well documented, but the malignant natural history of these lesions suggests that conservative management is not appropriate and these lesions must be treated aggressively despite clear risks of treatment Anatomical Considerations Dissecting Pseudoaneurysms The majority of dissections occur in the extracranial ICA, and most spontaneous DPA arise in the same location DPAs that originate at the skull base, however, are more challenging to access and treat, both with open microsurgery and endovascular techniques These lesions tend to have large, irregular domes with irregular and variable neck segments, and generally arise from nonbranching segments of their parent vessel DPAs secondary to trauma are generally seen arising from distal branches of the anterior cerebral artery However, traumatic dissections can be seen in any location involved with a penetrating trauma or iatrogenic injury, including in association with malpositioned ventriculostomy catheters or intracranial pressure monitors Traumatic DPA can 220 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 33 Dissecting Intracranial Aneurysms of the Anterior Circulation Algorithm 33.1 Decision-making algorithm for dissecting intracranial aneurysms of the anterior circulation 221 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Hypervascular Tumors Fig 70.2 Juvenile nasal angiofibroma (JNA) Transarterial approach: lateral digital subtraction angiogram (DSA) from the external carotid artery (a) demonstrates hypervascular tumor blush of the JNA supplied by the sphenopalatine artery Lateral fluoroscopy postembolization (b) demonstrates the Onyx cast of the sphenopalatine artery and the distal internal maxillary artery achieved via a transarterial approach Fig 70.1 Neck tumor metastasis (a) Computed tomography (CT) with contrast demonstrating a large metastatic tumor at the left supraclavicular region (b) Left thyrocervical trunk angiogram demonstrating a hypervascular tumor blush (c) Postembolization CT scan demonstrating the Onyx cast within the tumor and the thyrocervical trunk branches (d) Immediate postembolization angiogram of the thyrocervical trunk demonstrating successful devascularization of tumor (Images courtesy of Leonardo Rangel-Castilla, MD, Mayo Clinic, Rochester, MN.) which is observed or manipulated during surgical exposure (►Fig 70.3) Delivery of particle embolic agents has not been described in direct puncture techniques There may be limited by the ability to propagate upstream against capillary flow The liquid embolic agents have been well described with transarterial techniques and are increasingly described with the direct puncture technique Direct puncture also obviates catheter entrapment by the liquid embolic agent because the delivery is achieved via a rigid needle However, the slowly diffuse nature of injection via direct puncture makes application of NBCA, which polymerizes relatively quickly, difficult in comparison to Onyx embolization Reflux of NBCA into the intracranial supply has been reported both intraprocedurally due to unexpectedly low resistance, and in a delayed fashion following completion of embolization due to delayed polymerization With gradual centripetal polymerization and diffusely infiltrative spread of the agent into low resistance channels, Onyx can be effectively delivered throughout the hypervascular capillary network via a single direct puncture and intervals of injection In addition to varying viscosity of liquid embolic agents, variation in needle caliber used for direct puncture may alter the embolic penetration The liquid embolic agents are delivered with nonionic solutes In comparing the liquid embolic agents, NBCA is mixed with Ethiodol (Savage Laboratories), which is radiopaque and conveys viscosity to the agent, while Onyx is delivered in dimethyl sulfoxide (DMSO), which has been reported to cause vasospasm and discomfort when delivered quickly However, NBCA polymerizes more quickly and is at higher risk of trapping the catheter and due to its adhesive nature In contrast, Onyx delivery can be started and stopped on the order of several minutes at a time due to a slower precipitating reaction, and Onyx is cohesive in nature and therefore less likely to cause catheter retention The Apollo detachable-tip catheter (Covidien Medtronic) is also designed to minimize complication from catheter tip trapping by the embolic agents Although some groups hesitate to deploy a retained catheter device in addition to embolic agents, this catheter can be particularly useful in preoperative embolizations since the mass itself will be resected shortly thereafter Furthermore, the Onyx cast is more brittle and there are reports of complications with monopolar electrocautery due to conductivity of the tantalum radio-opaque agent However, NBCA can be delivered with a larger variety of catheters, including highly navigable catheters such as the Magic (Balt), while the DMSO solvent for Onyx is restricted to use in specifically designed catheters Consider the following example and decisions of embolization technique A patient with JNA presents with recurrent epistaxis and supplied by multiple branches from bilateral internal maxillary arteries, which also supplies significant transethmoidal collateral supply to the ipsilateral choroidal blush In such a case, the number of arterial pedicles that must be catheterized to achieve successful devascularization of the tumor and the risk of embolizing an “en passant” vessel with retinal embolization may lead one to use a direct puncture approach with Onyx This can be accomplished via a percutaneous or an endonasal–transmucosal–endoscopic-guided approach The ability to penetrate diffuse hypervascularity from multiple arterial sources would enable cerebral embolization, while the controlled distribution and high visibility of Onyx decrease the risk of off-target embolization Complications Avoidance Risk of embolization is associated with generic procedural risks, with risks of endovascular access, with risks of off-target embolization, and with risks of postembolization tumor changes To better visualize the distribution of the embolic agents and to minimize discomfort during embolization, many interventionists prefer general anesthesia during embolization Medical comorbidity represents a significant risk factor not related to the tumor itself Nonvascular operative risks are related to the tumor size and location and include cranial nerve palsy and incomplete tumor resection with attendant recurrence In contrast with these nonmodifiable risks, tumor hypervascularity can be mitigated via preoperative embolization Hemorrhage can also obscure the operative field, complicating tumor resection and protection of normal anatomy Embolization may reduce hemorrhage and reduce operative time and complexity (►Fig 70.3) Meta-analysis demonstrated significant decreases in blood loss with pre-operative embolization; primary literature reports a range of 500 mL compared with 2.5 L without preoperative embolization In addition to the risk of multiple superselective catheterizations, visible and occult anastomoses may expose eloquent vascular territories to thromboembolic complications or unintended embolization As the head and neck is supplied via the vertebral and carotid arteries, embolization of extracranial tumors may still involve thromboembolism in the cerebral 512 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 70 Extracranial Vascular Tumors the tumor may result in changes in the activity of secretory tumors A postembolization hypertensive crisis has been reported following embolization prior to resection Prophylactic beta-blockade may be an appropriate consideration in secreting tumors, while alpha adrenergic antagonists should be avoided in the periembolization and perioperative periods Outcome and Durability Fig 70.3 Carotid body tumor Lateral plane digital subtraction angiogram (DSA) (a) of the carotid bifurcation demonstrating tumor hypervascularity and displacement of the proximal internal and external carotid arteries Lateral projection DSA (b) with direct tumor puncture and contrast injection demonstrating hypervascular tumor blush and normal venous outflow Lateral DSA with right common carotid artery injection (c) during tumor embolization and (d) after completion of tumor embolization with resolution of hypervascular tumor blush Lateral (e) and anterior–posterior (f) projection DSA with faint contrast injection from the right common carotid artery after tumor embolization demonstrating liquid embolic cast of the carotid body tumor after direct puncture access for embolization Intraoperative (g,h) images of dissected tumor The left side is rostral, and the right side is caudal Vessel loops encircle the internal carotid artery (left inferior loop) and the external carotid artery (superior loop) A hemostat displaces the internal jugular vein posterolaterally Although the tumor demonstrates some dark discoloration from the embolic agent, the discoloration of the carotid bifurcation is from coagulation There is excellent hemostasis with the assistance of preoperative embolization The resected tumor (i) is approximately 4.5 cm in length arterial supply In tumors of the thoracolumbar spine, the spinal medullary supply is intricately involved in and dependent on the segmental arterial supply Transarterial access of spinal and paraspinal lesions is also associated with a risk of spinal neurologic thromboembolic complications Embolization for head and neck hemorrhage is associated with a 2% risk of complications from transarterial access, while cases series in tumor embolization reported complication rates from access of to 10% However, percutaneous access may be associated with an increased risk of injury to the local structures, such as the trachea or esophagus Delivery of embolic agent is associated with risk of unintended embolization In the head and neck territory collateralization between the internal and external carotid arteries can result in embolization of the ophthalmic artery, the vasa nervosum of cranial nerves, muscular branches so the vertebral artery, or the cerebral pial vasculature There is a similar risk in the spinal vascular supply, where segmental arteries anastomosis with the spinal cord vasculature via radiculomedullary arteries Pre-embolization diagnostic angiography can determine the extent of these risks to guide the aggressiveness of embolization and selection of embolic agent In particular, with glomus tumors, close proximity to a shared vascular supply with cranial nerves is associated with a relatively high rate of permanent cranial nerve palsy, estimated at one in five Successful and precisely targeted delivery of embolic agent may still be complicated by adverse tumor reactivity to altered hemodynamics Laryngeal or tracheal compression may compromise respiratory function, while compression of the thecal sac may result in peripheral neurological dysfunction Tumor swelling may also alter the dissection plane Although devascularization of the tumor may make the boundaries more distinct from the surrounding normal tissue, tumor edema may also blur the distinction Furthermore, acute necrosis of A recent publication by Torrealba et al included 30 patients with 32 carotid bifurcation tumors The most frequent presentation was an asymptomatic neck swelling or palpable mass at the carotid triangle (87%) Of the 32, 30 underwent surgical resection, 28 (93%) of the tumors were confirmed paragangliomas, and (7%) were diagnosed as schwannomas Only two patients underwent preoperative embolization Five (17%) required simultaneous carotid revascularization Transient extracranial nerve deficit was observed in seven (23%) patients One patient underwent a planned en bloc excision of the vagus nerve There was no perioperative mortality or procedure-related stroke No malignancy or tumor recurrences were observed during follow-up (supports algorithm step 2) Rangel-Castilla et al presented their results of 100 consecutive cases of head, neck, and spinal tumors embolized with Onyx liquid embolic agent Tumors included 30 meningiomas, 23 metastases, 16 paragangliomas, juvenile nasal angiofibromas, giant cell bone tumors, Ewing’s sarcomas, hemangiomas, hemangioblastomas, multiple myelomas, and osteoblastomas All patients were embolized and all embolizations were completed in a single session No mortality or major complications were observed Minor complications were observed in 11 patients Only 85 patients underwent surgical resection (supports algorithm steps 2, 5, and 6) Thiex et al presented their experience in 71 extracranial embolizations with Onyx liquid embolic material The diagnoses included: 18 cervicofacial arteriovenous malformations, traumatic fistulas, and vessel laceration Embolic material was delivered transarterially in 67 procedures and percutaneously in procedures Clinical goals included amelioration of pain and bleeding control Cessation of acute bleeding was achieved in 13 of 14 cases Control of subacute bleeding episodes and pain was achieved for all patients Surgeons reported high satisfaction with intraoperative handling properties of Onyx Transient swelling, local tenderness, or numbness was encountered after seven (10%) procedures There were no entrapped catheters, vessel dissections, or vessel ruptures and no skin discoloration (supports algorithm steps 2, 5, and 6) In the publication by Zähringer et al demonstrated the role of percutaneous endovascular embolization for cervicofacial neoplasms and hemorrhages This 8-year retrospective analysis included 85 patients with tumor bleeding and epistaxis Outcome of the preoperative embolized patients was defined as successful if intraoperative bleeding was < 500 mL and/or postinterventional angiogram showed complete occlusion of all tumor-feeding or bleeding vessels Complete preoperative tumor embolization was achieved in 83.5% of the patients Partial embolization was possible in 10.5% All tumor bleedings refractory to conservative therapy and bleedings from epistaxis showed a successful outcome The authors concluded that preoperative percutaneous embolization improves surgical outcome, reduces intraoperative blood loss, and facilitates tumor resectability (supports algorithm steps 2, 5, and 6) Clinical and Radiographic Follow-up Patients with benign tumors who undergo complete surgical resection were seen in follow-up every months for the first year, and annually thereafter for at least 10 years after surgical resection For patients with malignant tumors, surveillance needs to be more rigorous Skull base tumors treated primarily with radiation require a different longer follow-up because they tend to recur after even longer time periods, and because there is a tendency for secondary radiation-induced malignancy in later years For instance, aggressive growth of meningiomas can be seen even 14 years after radiation treatment; this highlights the importance of long-term radiological surveillance after radiation 513 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Hypervascular Tumors Expert Commentary In distinction with tumors without hypervascularity, extracranial vascular tumors represent an opportunity to modify operative risks using preoperative embolization When the open surgical approach may struggle to achieve hemostasis due to deep arterial supply, preoperative embolization may decrease the overall risk of treating the lesion The cumulative risk of the combined approach includes the addition of a second procedure, often under general anesthesia, risk of endovascular access, and risk of off-target embolization Percutaneous and transarterial access each have appropriate applications and delivering embolic agents Likewise embolic particles and liquid embolic agents have distinct niches of optimal application, and sometimes combinations of these are needed for safe and effective embolization Although the available techniques and walls for embolization continue to evolve, preoperative embolization is likely best applied in specific situations with well-defined goals for embolization Mohammad Ali Aziz-Sultan, MD Brigham and Women’s Hospital, Boston, MA Editor Commentary Management of the patient presenting with an extracranial vascular tumor begins with identification of the pathology and concern for hypervascularity If there is concern of increased operative risk due to hypervascularity, the vascular supply should be further defined with diagnostic angiography The goal of embolization should be clearly defined, whether this involves devascularization of the entirety of the parenchyma, or specific embolization of a deep arterial pedicle which is particularly challenging for the surgeon to control The surgical exposure is often able to manage superficial arterial supply and embolization of the entire parenchymal capillary that work may simplify operative resection, but be associated with a higher risk of unintended embolization The total risk of embolization and risk of surgery must be less than that of the risk of surgery alone In designing the preoperative embolization for an extracranial vascular tumor, multiplicity of arterial supply or complexity of arterial access may suggest a direct puncture approach However, this may not achieve the needed goals; embolization and transarterial access may offer a better complement to the open surgical approach Multiple microcatheters and liquid embolic material can be used For extracranial neck and head hypervascular tumors, proper anesthesia is a must if the procedure is performed with patient under conscious sedation Arterial branches from the external carotid artery are very sensitive and go into vasospasm easily; therefore, delicate microwire and microcatheter maneuvers are advised Severe vasospasm can prevent arterial and tumor access and a successful embolization Leonardo Rangel-Castilla, MD Mayo Clinic, Rochester, MN Suggested Reading Casasco A, Houdart E, Biondi A, et al Major complications of percutaneous embolization of skull-base tumors AJNR Am J Neuroradiol 1999;20(1):179–181– Available Elhammady MS, Wolfe SQ, Ashour R, et al Safety and efficacy of vascular tumor embolization using Onyx: is angiographic devascularization sufficient? J Neurosurg 2010;112(5):1039–1045 Gaynor BG, Elhammady MS, Jethanamest D, Angeli SI, Aziz-Sultan MA Incidence of cranial nerve palsy after preoperative embolization of glomus jugulare tumors using Onyx J Neurosurg 2014;120(2):377–381 Gore P, Theodore N, Brasiliense L, et al The utility of Onyx for preoperative embolization of cranial and spinal tumors Neurosurgery 2008;62(6):1204–1211, discussion 1211–1212 Gupta AK, Purkayastha S, Bodhey NK, Kapilamoorthy TR, Kesavadas C Preoperative embolization of hypervascular head and neck tumours Australas Radiol 2007;51(5):446–452 Hayes SB, Johnson JN, Most Z, Elhammady MS, Yavagal D, Aziz-Sultan MA Transarterial embolization of intractable nasal and oropharyngeal hemorrhage using liquid embolic agents J Neurointerv Surg 2015;7(7):537–541 Jackson RS, Myhill JA, Padhya TA, McCaffrey JC, McCaffrey TV, Mhaskar RS The effects of preoperative embolization on carotid body paraganglioma surgery: a systematic review and meta-analysis Otolaryngol Head Neck Surg 2015;153(6):943–950 Rangel-Castilla L, Shah AH, Klucznik RP, Diaz OM Preoperative Onyx embolization of hypervascular head, neck, and spinal tumors: experience with 100 consecutive cases from a single tertiary center J Neurointerv Surg 2014;6(1):51–56 Torrealba JI, Valdés F, Krämer AH, Mertens R, Bergoeing M, Mariné L Management of carotid bifurcation tumors: 30-year experience Ann Vasc Surg 2016;34:200–205 Thiex R, Wu I, Mulliken JB, Greene AK, Rahbar R, Orbach DB Safety and clinical efficacy of Onyx for embolization of extracranial head and neck vascular anomalies AJNR Am J Neuroradiol 2011;32(6):1082–1086 Zähringer M, Guntinas-Lichius O, Gossmann A, Wustrow J, Krüger K, Lackner K Percutaneous embolization for cervicofacial neoplasms and hemorrhages ORL J Otorhinolaryngol Relat Spec 2005;67(6):348–360 514 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 71 Spinal Vascular Tumors Yoshua Esquenazi, Mark H Bilsky, Ilya Laufer, and Athos Patsalides Abstract The primary treatment modalities for metastatic spinal tumors are radiotherapy and surgery; the goals are palliative and include neurological preservation or improvement, mechanical spinal stability, and local tumor control The treatment decision-making process can be broken down into four fundamental considerations referred to as NOMS: Neurological (N) includes the degree of myelopathy and the degree of radiographic spinal cord compression; Oncologic (O) primarily reflects the known radiosensitivity of the tumor; Mechanical instability (M) is broadly defined as movement-related pain and is level dependent; and Systemic disease (S) includes both the extent of disease and the medical comorbidities Approximately 95% of the patients with spinal metastases will demonstrate epidural disease As chemotherapy is usually ineffective in providing local control in the spine, radiotherapy and/or surgery is most often used in the treatment of spinal tumors Preoperative embolization of hypervascular tumors significantly reduces intraoperative blood loss and improves the surgeon’s ability to decompress the spinal cord and maximize tumor resection Spinal tumors previously considered unresectable due to the potential for catastrophic blood loss can be effectively addressed following tumor embolization With the advent of microcatheters, and new embolic agents, as well as advances in digital substraction imaging over the past two decades, embolization of spinal tumors has become a standard and safe procedure Keywords: separation surgery, spine metastases, hypervascular, embolization, radiotherapy, endovascular, angiography Introduction Spinal metastases (SM) complicate the courses of to 10% of cancer patients The primary treatment modalities for metastatic spinal tumors are radiotherapy and surgery; the goals are palliative and include neurological preservation or improvement, mechanical spinal stability, and local tumor control The treatment decision-making process can be broken down into four fundamental considerations referred to as NOMS: Neurological (N) includes the degree of myelopathy and the degree of radiographic spinal cord compression; Oncologic (O) primarily reflects the known radiosensitivity of the tumor; Mechanical instability (M) is broadly defined as movement-related pain and is level dependent; and Systemic disease (S) includes both the extent of disease and the medical comorbidities Approximately 95% of the patients with SM will demonstrate epidural disease, mainly affecting the vertebral body and the pedicle regions Symptomatic spinal cord compression occurs more frequently in the thoracic spine, followed by cervical and then lumbar As chemotherapy is usually ineffective in providing local control in the spine, radiotherapy and/or surgery is most often used in the treatment of spinal tumors The treatment of primary spinal tumors involves a similar decision process as well as considerations regarding curative resection that are pathology and case dependent Preoperative embolization of hypervascular tumors significantly reduces intraoperative blood loss and improves the surgeon’s ability to decompress the spinal cord and maximize tumor resection Furthermore, it also aims to reduce operative time and improve visualization of the operative field Spinal tumors previously considered unresectable due to the potential for catastrophic blood loss can be effectively addressed following tumor embolization Curative embolization is occasionally the goal in patients with certain benign primary tumors, such as giant cell tumors and aneurysmal bone cysts (►Fig 71.1) Arterial embolization of bone tumors was first described in 1975 Since then, there have been several reports in the literature describing embolization of spinal tumors prior to surgical resection With the advent of microcatheters, and new embolic agents, as well as advances in digital substraction imaging over the past two decades, embolization of spinal tumors has become a standard and safe procedure Major controversies in decision making addressed in this chapter include: Whether or not treatment is indicated Indications for diagnostic spinal angiography Case selection for preoperative endovascular embolization and adequate timing for surgery after embolization Potential complications of endovascular embolization and technical nuances Whether to Treat The optimal clinical management of these patients requires integrated decisions by an interdisciplinary cancer team comprised medical and radiation oncologist and spine surgeons, as well as all other health care professionals and involved medical specialties The decision to refer a patient for angiography and preoperative embolization is based on both tumor histology and magnetic resonance imaging (MRI) findings (1, in algorithm) Traditional MRI criteria suggestive of tumor hypervascularity include flow voids, intratumoral hemorrhage, and diffuse contrast enhancement The presence of these findings is an indication of hypervascularity; however, many tumors are hypervascular on angiogram even in the absence of these findings Recently, dynamic contrast-enhanced MR (DCE-MR) imaging has been used to differentiate tumor vascularity and may be more accurate compared with standard MRI Unfortunately, this is not currently a standard imaging sequence Thus, tumor histology is used as an independent predictor of hypervascularity (2 in algorithm) Tumor histologies that are commonly hypervascular and benefit from embolization include benign lesions such as hemangioma, aneurysmal bone cyst, and giant cell tumors; primary malignant tumors (Ewing’s sarcoma and hemangiopericytoma), metastatic tumors (renal cell carcinoma, papillary and follicular thyroid carcinoma, cholangiocarcinoma, and angiosarcoma), neuroendocrine tumors such as carcinoid, pheochromocytoma, and paraganglioma of the spine (3 in algorithm) Most of the common solid tumor malignancies, such as breast, lung, and colon carcinoma are relatively avascular and not require preoperative embolization Conversely, multiple myeloma, melanoma, and hepatocellular carcinoma are potentially hypervascular, but not typically benefit from embolization because the vascularity is derived from small capillary feeders, rather than major segmental arteries Fig 71.1 Imaging studies from a 35-year-old woman with progressive low back pain and evidence of an expansile L3 cystic lesion with a fluid/fluid level consistent with an aneurysmal bone cyst She underwent selective arterial embolization with improvement in her back pain She has been followed up closely with no further treatment 515 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Hypervascular Tumors Algorithm 71.1 Decision-making algorithm for spinal vascular tumors 516 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 71 Spinal Vascular Tumors In addition, any histology in which the word “angio” or “hemangio” is part of the tumor or if the organ of origin is vascular should also be evaluated with angiography (i.e., cholangiocarcinoma, angiosarcoma, and hemangioma) For this reason, it is critical to recognize that solitary fibrous tumor was initially called hemangiopericytoma, and is commonly found to be among the most hypervascular tumors (3 in algorithm) MR characteristics for preoperative angiography and embolization include intratumoral flow voids, hemorrhage, and avid contrast enhancement (4 in algorithm) Anatomical Considerations The arterial supply to the spinal column, spinal cord, dura, nerve roots, and the paraspinal soft tissues comes from the segmental arteries The segmental arteries originate from the vertebral arteries and the thyrocervical or costocervical trunk in the cervical region, the aorta in the thoracic and upper lumbar spine, and the internal iliac or median sacral artery in the lower lumbar spine and the sacrum The segmental arteries give rise to the radiculomeningeal arteries that supply the dura and nerve roots and the anterior and posterior radiculomedullary arteries that supply the anterior and posterior spinal arteries, respectively The radiculomeningeal arteries exist at every vertebral level, but the radiculomedullary arteries exist only at some levels with great variability The anterior spinal artery runs in the groove of the anterior median fissure from the level of the foramen magnum to the conus medullaris and supplies blood to the anterior two-thirds of the spinal cord The two posterior spinal arteries run parallel to each other on the posterolateral surface of the spinal cord and supply blood to the posterior one-third of the spinal cord The most cephalic portion of the anterior spinal artery is formed by small branches from one or both vertebral arteries The blood supply to the most cephalad portion of the posterior spinal arteries arises from small branches of either the vertebral or the posterior inferior cerebellar arteries There are to anterior radiculomedullary arteries that make functional connections to the anterior spinal artery and 11 to 16 posterior radiculomedullary arteries that supply the posterior spinal arteries At the cervical level, the radiculomedullary arteries arise from the vertebral artery and the ascending and deep cervical arteries At the thoracolumbar level, the radiculomedullary arteries arise from the supreme intercostal, posterior intercostal, and lumbar arteries The great anterior radiculomedullary artery, better known as the artery of Adamkiewicz, is the largest radiculomedullary artery in the thoracolumbar region and is the major supplier of blood to the anterior spinal artery at the lower thoracic and upper lumbar levels It characteristically makes a sharp hairpin turn caudally as it joins the anterior spinal artery (►Fig 71.2) In 75% of individuals, it arises at the T9 to T12 vertebral level, most often on the left side The blood supply of the sacrum and the cauda equina is via the lateral sacral and the iliolumbar arteries from the internal iliac artery, and the median sacral artery off the aorta Each segmental artery is often connected to the neighboring segmental artery via intersegmental anastomoses along the anterolateral aspect of the vertebral body and adjacent to the transverse process Thus, the anastomotic network around the spine needs investigation of the adjacent vertebral levels above and below the tumor to exclude a potential shunt between the segmental artery targeted for embolization and a spinal artery Classification Vascularity can be graded as normal (0, same as the normal adjacent vertebral body), mildly increased (1, slightly more prominent than the normal vertebral body blush; Case illustration 1), moderately increased (2, considerable tumor blush without early arteriovenous shunting), or severely increased (3, intense tumor blush with early arteriovenous shunting; Case illustration 2) The degree of embolization is considered complete if there is grade or less of residual vascularity, near-complete if there is grade or residual vascularity, and partial when grade or residual vascularity Workup Clinical Evaluation NOMS consists of four fundamental assessments: Neurological, Oncologic, Mechanical Instability, and Systemic Disease Considering these four assessments, the interdisciplinary team can determine the optimal treatment consisting of radiation therapy, surgery, systemic therapy, or a combination of these In the NOMS decision framework, the neurological assessment principally reflects the degree of epidural spinal cord compression (ESCC) as well as the presence or absence of myelopathy and/or functional radiculopathy Spinal cord compression is based on a validated scoring system using MR axial T2-weighted images This scoring system is used to differentiate no or minimal ESCC (0–1c) from high-grade spinal ESCC 2–3 (►Fig 71.3) The oncologic consideration is predicated of the known cytotoxicity and the durability of the response to current treatment modalities such as external beam radiation therapy, stereotactic radiosurgery, chemotherapy, immunotherapy, hormones, or biologics Mechanical instability has recently been defined for neoplastic disease and a scoring system, and spinal instability neoplastic score has been developed to aid in this assessment An unstable spine will not respond to radiation and/or chemotherapy but requires spinal stabilization The extent of systemic disease, medical comorbidities, and expected survival, which all impact the decision to offer not only surgical treatment but also radiation or systemic therapy From the oncologic perspective, radiation is the mainstay of therapy for tumor control With few exceptions, such as myeloma and lymphoma, systemic therapy has little impact in this regard Fig 71.2 (a) Selective angiogram at the T12 level showing normal vertebral body enhancement and the great anterior radiculomedullary artery (artery of Adamkiewicz) supplying the anterior spinal artery (b) Selective angiogram at the level of the lesion (L3) showing abnormal tumor enhancement (Grade 1) consistent with the MRI findings (c) Selective angiogram after embolization showing obliteration of the tumoral blush The embolization was performed after coils were deployed to divert PVA particles to the tumor 517 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Hypervascular Tumors Fig 71.3 A six-point grading system by the Spine Oncology Study Group uses axial T2-weighted images at the site of most severe compression to describe the degree of ESCC: tumor is confined to bone only; 1, tumor extension into the epidural space without deformation of the spinal cord; 2, spinal cord compression but cerebrospinal fluid is visible; and 3, spinal cord compression without visible cerebrospinal fluid The grade delineation is further subdivided into 1a to 1c: 1a, epidural impingement but no deformation of the thecal sac; 1b, deformation of the thecal sac but without spinal cord abutment; and 1c, deformation of the thecal sac with spinal cord abutment but without compression Imaging MR is the imaging modality of choice for SM evaluation Typically sagittal screening of the entire spinal axis is undertaken to assess for occult lesions outside the symptomatic area that may bear on decision-making The most important sequences for sagittal screening are T1-weighted and short inversion time recovery images in which tumor is hypointense and hyperintense, respectively The degree of spinal cord compression is predicated on axial T2-weighted sequences (►Fig 71.4) Most commonly images are obtained with and without gadolinium contrast to further evaluate the degree of spinal cord compression and to rule out leptomeningeal and intramedullary tumors Preprocedure imaging is indispensable in planning the spinal angiography and embolization Findings on plain radiographs, such as the destruction of pedicles or ribs, help determine the specific areas to be evaluated during angiography Computed tomography (CT) and MRI determine the locations and extent of the tumor as well as involvement of the spinal canal Contrast-enhanced CT and/or MRI may also provide information about the vascularity of the tumor, the tumor-feeding arteries, and the radiculomedullary and spinal arteries and their origins MRI scans also demonstrate the displacement of the spinal cord, which must be taken into account when evaluating the angiogram for anterior and posterior spinal arteries Recent studies have compared DCE-MR perfusion with digital substraction angiography (DSA) in determining the vascularity of spinal tumors A significant correlation between cerebral blood flow ratio and DSA has been found suggesting that DCE-MR perfusion can serve as a surrogate to DSA for determining tumor vascularity in patients with extramedullary SM This can enable clinicians to select candidates for endovascular embolization in a noninvasive way Treatment The treatment of metastatic and primary spinal tumors is comprised of a combination of surgical resection and reconstruction, radiation therapy, and chemotherapy The ultimate goal is to achieve local tumor control while minimizing morbidity Preoperative and palliative embolization of spinal tumors are an effective procedure It reduces intraoperative blood loss, palliates pain, and improves neurological symptoms Fig 71.4 Imaging studies from a 69-year-old man The patient had renal cell cancer metastatic to L2 resulting in back pain and mechanical radiculopathy The tumor had extension into the right pedicle with extension into the ventral epidural space (Grade I) The tumor encroached upon the right L2–L3 neural foramen Endovascular Management—Operative Nuances The criteria for embolization include the presence of significant tumor vascularity (grade or higher) and the ability to perform the embolization safely without inadvertent embolization of the brain or spinal cord (5 in algorithm) The presence of a spinal cord artery feeder (anterior or posterior spinal artery) arising from the same segmental artery as the tumor feeder and the presence of a dangerous anastomosis between adjacent segmental arteries are absolute contraindications for embolization of that particular feeder Angiograms are performed using standard interventional neuroradiology techniques using French (5F) catheters via a transfemoral arterial access Most thoracic procedures are performed with general anesthesia to achieve the best possible quality of images with transient apnea (►Fig 71.5) Lumbar procedures are typically performed with moderate sedation, unless the patient is unable to tolerate being recumbent due to severe back pain Diagnostic angiography should include evaluation of the segmental arteries at the level(s) of the tumor as well as at least one contiguous level above and below the tumor For every lower thoracic and upper lumbar lesion, identification of the artery of Adamkiewicz is always attempted For L4 and L5 level lumbar tumors and sacral tumors, angiography should include evaluation of the common, external, and internal iliac arteries and their branches, as well as selective angiogram of the median and lateral sacral arteries For upper thoracic and cervical tumors, angiography should include evaluation of the vertebral arteries, subclavian arteries, thyrocervical trunks, costocervical trunks, and supreme intercostal arteries Postembolization angiography should assess the artery embolized, the contralateral segmental artery at the same level, and ipsilateral segmental arteries at least one level above and one below In the largest published series of preoperative embolization of hypervascular thoracic and lumbar spinal column tumors published in 2013 from our institution, two main methods of embolization were used The first method involved selective catheterization of the posterior (dorsal) branch of the segmental artery using a microcatheter and injection of polyvinyl alcohol (PVA) particles directly into the tumor feeder The second method was employed when the tumor feeder could not be selectively catheterized In these cases, the anterior (ventral) branch of the segmental artery was selectively catheterized with a microcatheter and then occluded with detachable coils (6 in algorithm) The microcatheter was then retracted into the segmental artery, where PVA particles were injected with flow directed toward the posterior (dorsal) branch Occlusion of the anterior (ventral) 518 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 71 Spinal Vascular Tumors Fig 71.5 Preoperative embolization was performed Selective catheterization at the L2 level shows the classic appearance of a grade hypervascular mass (a) Early phase of catheter angiography, showing hypertrophic segmental artery (b) Intense tumor blush (c) Arteriovenous shunt and early venous drainage (d) Postembolization angiogram shows no residual tumor blush and contrast stasis in the segmental artery Right L2 hemilaminectomy, L2–L3 facetectomies, transpedicular resection of ventral epidural tumor, and L1–L3 posterolateral instrumentation and fusion were performed Postoperatively, the patient received 2,400 cGy in one single fraction branch of the segmental artery was used to divert particles into the posterior (dorsal) branch In both methods, PVA particles were injected until stasis and absence of residual tumoral blush from the particular feeder Embolization of cervical spinal column tumors is more complex due to the additional risk of inadvertent embolization of intracranial vasculature via the vertebral artery or through anastomoses with the carotid artery (►Fig 71.6) Although the basic techniques are similar for cervical spine and thoracic/lumbar spinal tumor embolizations, additionally, care must be taken in the cervical spine region in order to avoid devastating complications Occlusion of one of the vertebral arteries can be necessary in some cases, in order to achieve effective embolization of the tumor while preventing embolization of intracranial vessels In our institution, vertebral occlusion is always preceded by a balloon test occlusion and is considered in the following circumstances: (1) significant tumor vascularity from the vertebral artery branches with risk of reflux of the embolic material into the vertebral artery despite selective catheterization of tumor feeder, (2) the presence of anastomoses from tumor feeders to the vertebral artery, (3) significant tumor involvement of the vertebral artery (►Fig 71.6), and (4) codominant vertebral arteries or a contralateral dominant vertebral artery Complication Avoidance Liquid embolic materials (N-butyl cyanoacrylate [NBCA]) were considered for use as an adjunct in cases of extreme hypervascularity and prominent arteriovenous shunting that did not improve significantly after particle embolization These agents have historically been difficult to control because of their liquid nature, which may render them dangerous because of the risk of nontargeted embolization Embolization with liquid agents requires experience and technical expertise Otherwise, the procedure may result in neurologic complications and skin or muscle necrosis Technical failure of embolization can occur if superselective catheterization of a small tumor feeder and/or stable catheter position is not achieved Embolization in these cases is not performed due to the risk of embolic complications Provocative testing with a barbiturate or anesthetic or intraoperative neurophysiologic monitoring is not routinely done Outcome Our experience reported in 2013 by Nair et al included a total of 228 spinal angiography procedures performed in 199 patients with 40 different tumor types The most common primary tumor type was renal cell carcinoma (44.2%) followed by thyroid carcinoma (9.2%) and leiomyosarcoma (6.6%) Mean vascularity score of all lesions was 1.69 Hemangiopericytoma had the highest mean vascularity (2.6) of all tumor types followed by renal cell carcinoma (2.0) and thyroid (2.0) PVA particles were used in all cases Detachable platinum coils were used in 51.6% of cases Complete, near-complete, and partial embolizations were achieved in 86.1, 12.7, and 1.2% of all cases, respectively There were no new postprocedure neurological deficits or other complications with long-term morbidity and the mean intraoperative blood loss for these tumors was 1,745 mL The encouraging results of this study suggest that preoperative embolization of hypervascular thoracic, lumbar, and sacral spine tumors can be performed with high success rates and Fig 71.6 A 40-year-old woman with neck pain and a hypervascular C2 vertebral body tumor (a) Sagittal MRI with gadolinium demonstrating an enhancing C2 vertebral tumor (b) Left vertebral artery (VA) angiography demonstrating tumor “blush” from direct branches of the VA (c) Microangiography of the tumor The embolizing microcatheter is within the tumor and a balloon is positioned in the VA to prevent Onyx reflux into the VA (d) Postembolization VA angiography demonstrating successful tumor embolization (Images courtesy of Leonardo Rangel-Castilla, MD, Mayo Clinic, Rochester, MN.) a high degree of safety in experienced hands (supports algorithm steps 4, 6, 7) While spinal tumor embolization is a relatively safe procedure, catastrophic complications such as spinal cord ischemia and post-embolization paralysis have been reported Additionally, minor complications such as groin hematomas and cardiac events secondary to anesthesia have also been reported Durability and Rate of Recurrence The available data on preoperative embolization of spinal tumors come from retrospective series and case reports Randomized prospective studies are needed to determine the exact efficacy of the procedure; however, it would be unethical to design a study in which patients randomly or not receive embolization because spinal tumor surgery without preoperative embolization is associated with excessive hemorrhage and morbidity Repeat embolization can be done in cases of tumor recurrence requiring repeat surgery In our prior series, 16 patients had 18 repeat embolization procedures and the great majority (94%) of repeat embolizations for local recurrence followed complete embolization of the original lesion (supports algorithm steps 4, 6, 7) Clinical and Radiographic Follow-up A neurological examination should be performed immediately after embolization to identify possible complications After embolization, patients should be admitted to the neurosurgical service to monitor their neurologic status closely because tumor swelling and spinal cord compression can occur after embolization Some patients may experience a postembolization syndrome with low-grade fever, pain, nausea, vomiting, and an elevated white blood cell count This self-limiting syndrome generally lasts a few days and can be managed with conservative treatment Although the embolization is generally effective for to 10 days, surgical resection with or without spinal stabilization is typically performed within 48 hours of the procedure to minimize possible tumor 519 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Hypervascular Tumors revascularization via collaterals (supports algorithm steps 4, 6, 7) Many retrospective studies have indicated that intraoperative blood loss is significantly lower in patients who undergo preoperative embolization than in patients who not Although estimated blood loss represents the most commonly used method to evaluate the efficacy of preoperative embolization in patients with spinal tumors, the exact quantification of intraoperative bleeding is difficulty Expert Commentary Preoperative embolization of hypervascular tumors of the spine aims to reduce intraoperative blood loss and improve qualitative variables for the surgeon such as visibility and resectability As this is an adjunct treatment, safety is paramount Preoperative embolization of spinal tumors can be performed safely and with great success in experienced hands with proper knowledge of the vascular anatomy Meticulous evaluation of pre-embolization angiography is essential to identify and therefore, protect radiculomedullary and spinal arteries The presence of an artery supplying the spinal cord from the same segmental artery as arteries supplying the spinal cord, or the presence of a dangerous anastomosis between segmental arteries should not be missed, to avoid devastating and usually irreversible neurological complications of spinal cord ischemia The decision on whether to embolize any or all feeders must be made based on the results of pre- and intraembolization angiography and the risk/benefit ratio which must be determined on a case-by-case basis Yoshua Esquenazi Levy, MD University of Texas Health Science Center, Houston, TX Editor Commentary Vascular spinal tumors such as hemangioblastoma, hemangioma, aneurysmal bone cyst, giant cell tumor, osteoblastoma, and metastatic deposits from renal cell carcinoma or thyroid gland are considered difficult to operate Patients can lose significant amount blood during the surgical resection of these tumors Angioembolization has been increasingly employed for preoperative devascularization Although most studies on this topic lack a control arm, preoperative embolization is widely accepted to reduce the intraoperative blood loss Subsequently, extent of disease, number of involved vertebral levels, and bleeding during surgical approach to the lesion can still cause significant intraoperative blood loss A detailed digital subtraction spinal angiogram should be performed in all suspected cases of vascular spinal tumors Vascular supply of the tumor and normal spinal cord must be visualized It is often necessary to catheterize arteries at least two levels above and below the level of pathology For cervical tumors, vertebral arteries, external carotids, thyrocervical trunk, costocervical trunk, and extreme intercostal arteries must be visualized by angiography Similarly, both internal iliac arteries and median sacral artery must be visualized in addition to assessing segmental vessels in case of lumbosacral tumors The artery of Adamkiewicz and feeding arteries with concomitant medullary supply or en passant vessels must also be recognized If surgical access to feeding arteries can be achieved safely and adequately, preoperative embolization is not necessary and may in fact increase the risk of harm These considerations are important to avoid serious complications such as spinal cord ischemia and infarction If angioembolization is required, we prefer liquid embolic agents such as Onyx or NBCA Particle embolization is seldom used anymore Surgical management of spinal tumors depends on the location of the tumor (intramedullary, extramedullary, intradural, or extradural), extent of the lesion, age, and comorbid conditions of the patient We recommend performing the surgery within 48 hours of embolization Vertebral body tumors would require corpectomy and replacement with implant, correction of deformity (if present), and fusion This often requires a combined anterior and posterior approaches, titanium cage, and autologous bone graft To perform anterior approaches, assistance from a thoracic surgeon or urologist is often useful as the exposure cannot be compromised Two approaches can be staged or performed in the same setting Most tumors within the spinal canal can be removed through posterior approach The laminectomy should involve a level above and below the level of pathology Extradural tumors should be devascularized and removed in piecemeal fashion Intramedullary tumors such as hemangioblastoma are approached with midline durotomy With the help of the preoperative angiogram, feeding vessels are identified and divided, and the tumor is carefully dissected from the surrounding gliotic tissue before the division of drainage veins Tumor should be removed as a single piece In selected cases laminoplasty can also be performed especially in cervical spine However, exposure is key to the successful removal of vascular tumors and should not be compromised Adequate blood products should be available before surgery and transfused in case of significant blood loss A postoperative MRI is obtained within 48 hours of surgery to evaluate the extent of resection Postoperative X-rays and CT scan are required for cases of spinal instrumentation Longterm management involves oncology, clinical, and radiological follow-up Elad I Levy, MD, MBA University at Buffalo, Buffalo, NY Leonardo Rangel-Castilla, MD Mayo Clinic, Rochester, MN Suggested Reading Berkefeld J, Scale D, Kirchner J, Heinrich T, Kollath J Hypervascular spinal tumors: influence of the embolization technique on perioperative hemorrhage AJNR Am J Neuroradiol 1999;20(5):757–763 Bilsky MH, Laufer I, Burch S Shifting paradigms in the treatment of metastatic spine disease Spine 2009;34(22, Suppl):S101–S107 Djindjian R, Cophignon J, Théron J, Merland JJ, Houdard R Embolization in vascular neuroradiology Technic and indications apropos of 30 cases [in French] Nouv Presse Med 1972;1(33):2153–2158 Fisher CG, DiPaola CP, Ryken TC, et al A novel classification system for spinal instability in neoplastic disease: an evidence-based approach and expert consensus from the Spine Oncology Study Group Spine 2010;35(22):E1221–E1229 George B, Laurian C Surgical approach to the whole length of the vertebral artery with special reference to the third portion Acta Neurochir (Wien) 1980;51 (3-4):259–272 Hilal SK, Michelsen JW Therapeutic percutaneous embolization for extra-axial vascular lesions of the head, neck, and spine J Neurosurg 1975;43(3):275–287 Laufer I, Rubin DG, Lis E, et al The NOMS framework: approach to the treatment of spinal metastatic tumors Oncologist 2013;18(6):744–751 Manke C, Bretschneider T, Lenhart M, et al Spinal metastases from renal cell carcinoma: effect of preoperative particle embolization on intraoperative blood loss AJNR Am J Neuroradiol 2001;22(5):997–1003 Mazura JC, Karimi S, Pauliah M, et al Dynamic contrast-enhanced magnetic resonance perfusion compared with digital subtraction angiography for the evaluation of extradural spinal metastases: a pilot study Spine 2014;39(16): E950–E954 Nair S, Gobin YP, Leng LZ, et al Preoperative embolization of hypervascular thoracic, lumbar, and sacral spinal column tumors: technique and outcomes from a single center Interv Neuroradiol 2013;19(3):377–385 Olerud C, Jónsson H Jr, Lưfberg AM, Lörelius LE, Sjöström L Embolization of spinal metastases reduces peroperative blood loss 21 patients operated on for renal cell carcinoma Acta Orthop Scand 1993;64(1):9–12 Ozkan E, Gupta S Embolization of spinal tumors: vascular anatomy, indications, and technique Tech Vasc Interv Radiol 2011;14(3):129–140 Prabhu VC, Bilsky MH, Jambhekar K, et al Results of preoperative embolization for metastatic spinal neoplasms J Neurosurg 2003;98(2, Suppl):156–164 Robial N, Charles YP, Bogorin I, et al Is preoperative embolization a prerequisite for spinal metastases surgical management? Orthop Traumatol Surg Res 2012;98(5):536–542 Santillan A, Nacarino V, Greenberg E, Riina HA, Gobin YP, Patsalides A Vascular anatomy of the spinal cord J Neurointerv Surg 2012;4(1):67–74 Sundaresan N, Choi IS, Hughes JE, Sachdev VP, Berenstein A Treatment of spinal metastases from kidney cancer by presurgical embolization and resection J Neurosurg 1990;73(4):548–554 520 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Index Note: Page references followed by f or t indicate material in figures or tables, respectively A Abla, A A., 393–394 ACA aneurysms – anatomical considerations, 183, 184f – characterization, 183 – classification, 183–185, 185f – clinical evaluation, 185 – complication avoidance, 187 – conservative management, 183, 184f, 185–186 – endovascular treatment, 184f, 186f, 187–188 – follow-up, 187 – imaging, 185, 185–186f – outcome, 187 – recurrent (see recurrent/residual aneurysms) – ruptured blebs, dissections, 188 – surgical management, 186–187 – treatment indications, 183, 184f – treatment options, 184–185f, 185, 187–188 AChA aneurysms – anatomical considerations, 156 – cerebrovascular management, 158, 158f, 160f – characterization, 156 – classification, 156–158 – clinical evaluation, 158 – complication avoidance, 160–161 – conservative management, 158 – differential diagnosis, 158, 160f, 162 – durability, 161 – endovascular management, 159f, 160, 161 – follow-up, 161 – imaging, 158, 158–160f – intracerebral hematoma influences, 158 – outcome, 161 – recurrence rate, 161 – treatment indications, 156, 157f – treatment options, 157f, 158, 161–162 ACoA aneurysms – adjacent anatomy, 191 – adjuncts, 192–193f, 194 – anatomical considerations, 189, 191f – cerebrovascular management, 190f, 192f, 193–196 – characterization, 189 – clinical evaluation, 191 – complication avoidance, 192–193f, 194–195 – conservative management, 190f, 191 – embolization, 192f, 194 – endovascular management, 190f, 192f, 194 – endovascular vs open microsurgery, 190f, 192, 193f – follow-up, 195 – imaging, 191, 192–193f – intracerebral hematoma influences, 190f, 192, 193f – outcome, 195 – perforators, 191 – ruptured, 189, 190f, 193f, 195 – treatment indications, 189, 190f – unruptured, 189, 190f, 191, 192f acute ischemic stroke see large vessel occlusion; small vessel disease AICA aneurysms – anatomical considerations, 283–285, 285f – AVM associated with, 291 – balloon remodeling coiling/stent-assisted coiling, 284f, 289 – cerebrovascular management, 284f, 288, 288f – characterization, 283, 291 – classification, 284f, 285 – clinical evaluation, 285 – complication avoidance, 289–290 – – – – conservative management, 287 differential diagnosis, 285 durability, 290 endovascular management, 284f, 289, 291 – far-lateral suboccipital craniotomy/ posterior petrosectomy, 288–289 – follow-up, 290 – fusiform aneurysm concurrent with, 284f, 289, 290f – imaging, 285 – intracerebral hematoma influence, 288 – meatal location, 284f, 289, 291 – outcome, 290 – pathophysiology, 283–285, 286–287t – postmeatal, 284f, 289, 290f, 291 – premeatal location, 284f, 288, 288f, 291 – recurrence rate, 290 – subtemporal craniotomy/anterior petrosectomy (Kawase approach), 289 – treatment indications, 283, 284f – treatment options, 288, 291 Allcock test, 259 Anson, J A., 308 anterior inferior cerebellar artery see AICA aneurysms Arnold, M., 98 arteriovenous malformations, 355, 363, 377t see also spinal artery aneurysms; specific AVMs by type ARUBA trial, 370–372, 425 aspirin, 6, 20 Asymptomatic Carotid Surgery Trial (ACST), 36 ataxic hemiparesis, Ausman, J L., 52 B Badhiwala, J H., 491 Barber, S M., 442 basal ganglia cavernous malformations see thalamic/basal ganglia cavernous malformations BASICS study, 25, 26t basilar apex aneurysms – anatomical considerations, 263–265 – cerebrovascular management, 265–266f, 265–267, 302 – characterization, 263 – complication avoidance, 267 – conservative management, 264f, 265 – dissecting, 313f, 317 – durability, 267–268 – endovascular management, 264f, 266–267, 267f – follow-up, 268 – outcome, 267–268, 304, 330 – recurrent, anatomical considerations, 326–328, 327–328f – stent-assisted coiling, 266–267 – treatment indications, 263, 264f – treatment options, 268, 302 – workup, 265, 265f basilar artery occlusion (acute) – ADAPT approach, 25, 25f – anatomical considerations, 22–24, 27 – anesthesia, 24–25 – antithrombotic therapy, 25, 26t – cerebrovascular management, 24 – characterization, 22 – clinical evaluation, 24, 24t – complication avoidance, 25 – conservative management, 22 – differential diagnosis, 24 – durability, 27 – endovascular management, 24–25 – follow-up, 27 – functional outcome, 26–27 – hemorrhage, 25 – imaging, 24, 24f – ischemia, 25 – outcome, 24t, 25–26 – peripheral artery disease and, 27–28 – recanalization rates, 26 – recurrence rate, 27 – rescue therapy, 25 – stent retrievers, 26 – treatment indications, 22, 23f – treatment options, 24, 26t – treatment timing, 26, 26t blister-type aneurysms see also blood blister aneurysms – anatomical considerations, 222 – characterization, 220 – complication avoidance, 224 – durability, 225 – outcome, 224–225 – pathophysiology, 222, 222–223f – recurrence rate, 221f, 225 – treatment indications, 220, 221f blood blister aneurysms see also blister-type aneurysms – anatomical considerations, 344 – cerebrovascular management, 345–346f, 346–347 – characterization, 344 – clinical evaluation, 344 – complication avoidance, 345f, 348 – differential diagnosis, 346 – durability, 348 – endovascular management, 345f, 347–348, 347f – flow diversion, 345f, 347–349, 347f – follow-up, 348 – imaging, 344–346, 348 – outcome, 345f, 348, 349f – pathophysiology, 344 – recurrence rate, 348 – treatment indications, 344, 345f – treatment options, 346, 349 Borhani, Haghighi A., 111 brainstem AVMs – anatomical considerations, 395–402, 396f, 399–403f – basilar paramedian perforating artery supply, 396f, 399–402, 402–403f – cerebrovascular management, 399–402f, 403–404 – characterization, 395, 397–398t, 405 – clinical evaluation, 402–403 – craniotomies, surgical approaches, 377t – differential diagnosis, 403 – diffuseness, 402, 403f – durability, 405 – endovascular management, 404–406 – follow-up, 405 – hematoma cavity, 402, 403f – imaging, 403, 403f – microsurgery timing, 403f, 404 – outcome, 398t, 405 – radiosurgery, 396f, 404, 405 – radiosurgery grading, 395 – recurrence rate, 405 – Spetzler–Martin grading, 395 – surgical resection, diagram, 399–402f, 404 – treatment indications, 395, 396f brainstem cavernous malformations – anatomical considerations, 477, 480–481f – cerebrovascular management, 478f, 479 – characterization, 477, 486 – classification, 477–479, 479t – clinical evaluation, 479 – complication avoidance, 485 – conservative management, 478f, 479 – differential diagnosis, 479 – durability, 485–486 – extended retrosigmoid approach, 482–483, 484t – far-lateral approach, 480–481f, 483f, 484t, 485 – follow-up, 486 – imaging, 479, 480–483f – medial transpetrosal approach, 483, 484t – medulla, surgical approaches, 480–481f, 483f, 484t, 485 – midbrain, surgical approaches, 480–481f, 481–482, 484t – operative planning, 480–481, 480–483f – outcome, 485 – pons, surgical approaches, 480–481f, 483–485, 484t – recurrence rate, 485–486 – suboccipital-transventricular approach, 480–481f, 483–484, 484t – supracerebellar-infratentorial approach, 480–481f, 481–482, 484t – supratonsillar approach, 480–481f, 484t, 485 – surgery, timing of, 478f, 479 – surgical resection principles, 481, 484t, 486 – telovelar approach, 480–481f, 483–484, 484t – transpontomedullary sulcus approach, 480–481f, 484, 484t – transsylvian approach, 480–481f, 482, 484t – treatment indications, 477, 478f BRAT trial – ACoA aneurysms, 195 – basilar apex aneurysms, 268 – MCA aneurysms, 175 – ophthalmic artery aneurysms, 145 – PCA aneurysms, 275 – PCoA aneurysms, 154, 155 – PICA aneurysms, 297 – recurrent/residual aneurysms, 232, 330 – SHA aneurysms, 138 Britz, G W., 52–53 C CADASIL, CADISS trial, 92, 98 Canhão, P., 111 carotid aneurysms see cave carotid aneurysms; cavernous carotid aneurysms; cervical carotid aneurysms carotid cave aneurysms see cave carotid aneurysms carotid-cavernous fistulas anatomical considerations, 437 – cerebrovascular management, 440 – characterization, 437 – classification, 439, 439f – clinical examination, 439–440 – complication avoidance, 442 – differential diagnosis, 440 – endovascular management, 438–439f, 440–442 – imaging, 440, 441f – manual compression, 440 – outcome, 442 – pathophysiology, 437 – pipeline device, 442 – radiosurgery, 440 – treatment indications, 437, 438f – treatment options, 438f, 440, 442–443 carotid injury/dissection see also ICA dissection – anatomical considerations, 74, 76t – cerebrovascular management, 75f, 76–77 – characterization, 74 – clinical evaluation, 75f, 76, 78 – complication avoidance, 77–78 – conservative management, 75f, 76 – differential diagnosis, 76 – durability, 77–78 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 521 Index – endovascular management, 75f, 77, 77–78f – follow-up, 78 – grading scale, 76t – imaging, 75f, 76, 77–78f – outcome, 77–78 – pathophysiology, 74 – recurrence rate, 77–78 – treatment indications, 74, 75f – treatment options, 76 CASANOVA study, 36 CAVATAS trial, 46 cave carotid aneurysms – anatomical considerations, 129 – characterization, 129 – classifications, 129–131 – clinical evaluation, 131 – clipping, 133 – coiling, 130f, 131–132 – conservative management, 130f, 131 – durability, 133 – endovascular management, 130f, 131–134, 132–133f – follow-up, 133 – imaging, 131 – outcome, 132–133 – recurrence rate, 133 – surgical management, 130f, 131, 133 – treatment indications, 129, 130f – treatment options, 130f, 131 cavernous carotid aneurysms – anatomical considerations, 122 – cerebrovascular management, 123f, 124 – characterization, 122 – clinical evaluation, 122 – clipping, 124 – coiling, stent-assisted coiling, 124 – complication avoidance, 126 – conservative management, 123f, 124 – differential diagnosis, 124 – durability, 126, 127f – endovascular management, 123f, 124–126 – endovascular parent artery occlusion, 123f, 124–125 – flow diversion, 123f, 125, 126f – follow-up, 126 – Hunterian ligation, 123f, 124, 125f – imaging, 122–124 – intracerebral hematoma influences, 123f, 124 – PED deployment, 125–126 – recurrence rate, 126, 127f – treatment indications, 122, 123f – treatment options, 123f, 124, 127–128 cerebellar AVMs – anatomical considerations, 407–410, 409–410f – cerebrovascular management, 409–410f, 411 – characterization, 407, 412 – classification, 407, 409t – clinical evaluation, 410 – complication avoidance, 411 – craniotomies, surgical approaches, 377t – durability, 412 – elderly patients, 410 – endovascular embolization, 411 – follow-up, 412 – imaging, 410 – intracerebral hematoma influence, 408f, 410 – outcome, 411–412 – radiosurgery, 412 – recurrence rate, 412 – treatment indications, 407, 408f – treatment options, 408f, 410, 412 cerebral amyloid angiopathy, 5, 5f cerebral cavernous malformations – anatomical considerations, 465 – cerebrovascular management, 467–468, 467–468f – characterization, 465, 469 – clinical evaluation, 467 – complication avoidance, 468 522 – conservative management, 466f, 467–468 – differential diagnosis, 467 – durability, 468 – follow-up, 468 – imaging, 467, 467–468f – insular/basal ganglia, 468 – outcomes, 468 – pathophysiology, natural history, 465, 466f – radiosurgery, 468–469 – recurrence rate, 468 – treatment indications, 465, 466f cerebral venous thrombosis/occlusion – anatomical considerations, 106, 108f – anticoagulation therapy, 111 – characterization, 106 – clinical evaluation, 108 – complication avoidance, 111 – conservative management, 106 – differential diagnosis, 110 – elevated ICPs, medical treatment of, 111 – endovascular management, 110–111 – follow-up, 112 – imaging, 108–110, 109f – microsurgical management, 110 – outcomes, 111–112 – pathophysiology, 106–108 – recurrence rates, 112 – Solumbra technique, 111 – treatment indications, 106, 107f – treatment options, 107f, 110, 112 cervical carotid aneurysms – anatomical considerations, 118, 120 – cerebrovascular management, 119 – characterization, 115, 115f, 117f – classification, 118, 118f – clinical evaluation, 116f, 119 – conservative management, 116f, 119 – differential diagnosis, 119 – endovascular management, 116f, 119, 120f – follow-up, 120 – imaging, 116f, 119 – outcome, 119–120 – pathophysiology, 118, 118f – recurrence rate, 120 – treatment indications, 116f, 118 – treatment options, 116f, 119, 120 CHARISMA trial, choroid plexus tumors, 499–500 clopidogrel, 6, 48 Cognard, C., 427, 429–430, 434–435 COSS study, 104 CREST trial, 39, 46–47 D Daou, B., 98 Day, J D., 442 deep AVMs, 377t DHC, 111 dissecting intracranial aneurysms – anatomical considerations, 220–222 – cerebrovascular management, 221f, 223–224, 223f – characterization, 220 – classification, 214 – complication avoidance, 224 – durability, 225 – endovascular management, 221f, 223f, 224 – follow-up, 225 – outcome, 224–225 – pathophysiology, 222, 222–223f – recurrence rate, 221f, 225 – treatment indications, 220, 221f – treatment options, 223, 225 dissecting pseudoaneurysms – cerebrovascular management, 221f, 223–224, 223f – durability, 225 – outcome, 224 – pathophysiology, 222, 222f – recurrence rate, 221f, 225 – treatment indications, 220, 221f – treatment options, 223 distal anterior cerebral artery (DACA) see PcaA aneurysms distal MCA aneurysms – anatomical considerations, 177, 179–180f – cerebrovascular management, 178f, 180–181 – characterization, 177, 181 – classification, 177 – clinical evaluation, 177 – complications avoidance, 181 – conservative management, 178f, 180 – differential diagnosis, 179–180 – durability, 181 – endovascular management, 178f, 181 – follow-up, 181 – imaging, 179, 179–180f – intracerebral hematoma influences, 178f, 180 – outcome, 181 – recurrence rate, 181 – treatment indications, 177, 178f – treatment options, 178f, 180, 181 dolichoectatic dissecting, classification, 214 Drake, C G., 411 Dumont, T M., 52, 304 dural AVFs – angioplasty, 428f, 433 – anterior cranial fossa, 428f, 432f, 434 – arterial embolization, 430f, 432f, 433 – cavernous/coronal sinus, 434 – cerebrovascular management, 434 – characterization, 427, 435–436 – classification, 427 – clinical evaluation, 427–432, 429t – complication avoidance, 430–431f, 434 – conservative management, 433 – dementia, 429, 431f – durability, 435 – endovascular management, 428f, 430–431f, 433 – hemorrhage, 428f, 429–430 – imaging, 432–433 – intracranial hypertension, 428f, 429–430 – myelopathy, 430–432, 432f – ocular symptoms, 429 – outcome, 434–435 – pathophysiology, 427, 428f – pulsatile tinnitus, 429, 430–431f – radiosurgery, 434 – sinus occlusion/coils, 430f, 433 – sinus recanalization, 428f, 433 – stents, 428f, 433 – tentorial, 434 – transarterial sinus occlusion/NALEA, 430–432f, 433 – treatment indications, 427, 428f – treatment options, 435–436 – venous embolization, 432f, 433–434 – venous infarction, 428f, 429–430 dysarthria–clumsy hand syndrome, E eptifibatide, ICA occlusion, 20 ESCAPE trial, 14 ESPRIT study, 38 ESPS-2 trial, 6, 38 esthesioneuroblastoma, 504, 506, 507 extracranial vascular tumors – characterization, 509, 514 – clinical evaluation, 509, 520 – complications avoidance, 512–513, 513f – durability, 513 – embolization objective, 511, 512f – endovascular management, 511–512, 512–513f – follow-up, 513 – imaging, 509–511, 510f, 520 – metastatic, 509 – outcome, 513 – treatment indications, 509, 510f – treatment options, 511, 514, 520 F Flickinger, J C., 388 frontal AVMs, 377t Fukushima, T., 442 fusiform aneurysms – AICA aneurysms, concurrent with, 284f, 289, 290f – anatomical considerations, 212 – cerebrovascular management, 213f, 215, 216–217f – characterization, 212 – classification, 214, 260 – clinical evaluation, 212f, 214 – complication avoidance, 215 – conservative management, 213f, 215 – differential diagnosis, 214 – durability, 318 – endovascular management, 214, 215, 218f – flow diverters, 213f, 214 – follow-up, 217 – imaging, 214, 217 – outcome, 215–217 – pathophysiology, 212–214, 314 – posterior circulation (see posterior circulation fusiform aneurysms) – treatment indications, 212, 213f – treatment options, 213f, 214–215, 218 G giant intracranial aneurysms – anatomical considerations, 203–205 – cerebrovascular management, 206–207, 206–208f – characterization, 203, 209–210 – classification, 251–253 – clinical evaluation, 205, 210 – complication avoidance, 208–209 – conservative management, 203, 204f – differential diagnosis, 205 – durability, 209 – endovascular management, 207–208, 209f – follow-up, 209 – imaging, 204f, 205, 207, 210 – intracerebral hematoma influences, 205–206 – outcomes, 209 – recurrence rate, 209 – treatment indications, 203, 204f – treatment options, 204f, 205–206, 208f, 210 giant posterior circulation aneurysms – cerebrovascular management, 300f, 301–302, 302–303f – characterization, 299, 304 – clinical evaluation, 301 – durability, 302–304 – endovascular management, 302, 304f – flow-diverting stents, 304 – follow-up, 304 – imaging, 299f, 301, 301f – outcomes, 302–304 – pathophysiology, 301 – treatment indications, 299, 299–301f – treatment options, 300f, 301 H hemangioblastoma – anatomical considerations, 495 – classification, 495 – clinical evaluation, 495–497 – differential diagnosis, 497 – follow-up, 497 – imaging, 495f, 497 – pathophysiology, 495 – treatment indications, 495, 495–496f – treatment options, 495f, 497 hemangiopericytoma, 497–498, 502, 505, 506 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Index Henkes, H., 268 heparin, 111 Hetts, S W., 353 Huang, J., 353 Hui, F K., 202 Hwang, P Y., 86 I ICA bifurcation aneurysms – anatomical considerations, 163, 165f – arachnoid dissection, 166 – cerebrovascular management, 166–167, 167f – characterization, 163, 169 – classification, 165 – clinical evaluation, 164f, 166 – complication avoidance, 167 – conservative management, 166 – distal, internal, 163–165 – durability, 168–169 – endovascular management, 164f, 167, 168f, 169 – follow-up, 169 – general approach, 166 – imaging, 166 – intracranial hemorrhage, 163f – lateral lenticulostriate arteries, 165 – medial lenticulostriate arteries, 165 – neck preparation, 167, 167f – outcome, 167–168 – patient position, 166 – proximal ACA, 165 – proximal MCA, 165 – recurrence rate, 168–169 – recurrent artery of Heubner, 165 – treatment indications, 163, 164f – treatment options, 164f, 166 – WEB device, 168 ICAD see intracranial atherosclerotic disease ICA dissection see also carotid injury/ dissection – acute endovascular intervention, 89f, 92–93 – anatomical considerations, 88, 90f – aneurysms, endovascular treatment of, 89f, 91f, 93 – anticoagulation vs antiplatelets, 89f, 92 – cerebrovascular management, 92 – characterization, 88 – clinical evaluation, 88–90, 89f – complication avoidance, 89f, 93 – conservative management, 89f, 92 – differential diagnosis, 89f, 92 – durability, 93 – endovascular management, 89f, 92–93 – follow-up, 89f, 93 – imaging, 89f, 90–92, 90f – intravenous t-PA, 89f, 92 – prognosis, 93 – recurrence rate, 93 – treatment indications, 88, 89f – treatment options, 89f, 92, 93 ICA occlusion – anatomical considerations, 14–16, 17f – cerebrovascular management, 15f, 16 – characterization, 14 – classification, 16 – complication avoidance, 19 – conservative management, 16 – endovascular management, 19 – extratracranial, 16, 19 – follow-up, 20 – imaging, 16, 17–18f – intracranial, 16, 17–18f, 19 – outcome, 19–20 – pathophysiology, 16 – tandem lesions, 16, 18f, 19–20 – treatment indications, 14, 15f – treatment options, 16 ICA occlusion (chronic) – anatomical considerations, 100, 101f – cerebrovascular management, 103 – characterization, 100 – clinical evaluation, 102, 104–105 – complication avoidance, 103–104, 103f – conservative management, 103 – differential diagnosis, 102–103 – durability, 104, 104f – EC-IC bypass, 103, 104 – endovascular management, 103 – follow-up, 104 – imaging, 101–102f, 102 – pathophysiology, 100–102 – recurrence rate, 104 – STA-MCA bypass, 103, 104 – treatment indications, 100, 101–102f – treatment options, 103–105 ICA stenosis (extracranial asymptomatic) – anatomical considerations, 36 – carotid artery stenting, 39, 40f – carotid endarterectomy, 37f, 38–40, 39f – characterization, 36 – clinical evaluation, 38 – complication avoidance, 39–40 – conservative management, 37f, 38 – cranial nerve injury, 40 – durability, 40 – follow-up, 40 – hyperperfusion syndrome, 40 – imaging, 37f, 38 – infections, 39–40 – ischemia, 40 – outcome, 39–40 – recurrence rate, 40 – treatment indications, 36, 37f – treatment options, 38 ICA stenosis (extracranial symptomatic) – anatomical considerations, 43–44f, 44 – carotid artery stenting/angioplasty, 46–47 – carotid endarterectomy, 46 – cerebrovascular management, 45 – characterization, 42 – clinical evaluation, 43–44f, 44 – complication avoidance, 46 – conservative management, 42, 43f – endovascular management, 43–44f, 45–46 – evidence-based decision making, 46 – follow-up, 46 – hyperperfusion syndrome, 46 – imaging, 43–44f, 44–45 – outcome, 46 – stents, 47 – treatment indications, 42, 43f – treatment options, 43f, 45 – treatment timing, 42–44 internal carotid artery see ICA occlusion intracranial aneurysms see also fusiform aneurysms anatomical considerations, 212 – characterization, 212 – pediatric (see pediatric intracranial aneurysms) – recurrent (see recurrent/residual aneurysms) intracranial atherosclerotic disease – anatomical considerations, 29 – cerebrovascular management, 30f, 31 – characterization, 29 – classification, 29 – clinical evaluation, 31 – complication avoidance, 32–34 – conservative management, 31 – differential diagnosis, 31 – durability, 34 – endovascular management, 30f, 31–32, 33f – follow-up, 34 – imaging, 31, 32f – outcome, 34–35 – pathophysiology, 29 – restenosis rate, 34 – treatment indications, 29, 30f – treatment options, 31, 35 intracranial hemorrhage, 7, 12 intracranial vascular tumors – choroid plexus, 499–500 – hemangioblastoma, 495–496f, 495–497 – hemangiopericytoma, 497–498, 502, 505, 506 – meningiomas (see meningiomas) – metastatic, 500 – treatment indications, 495, 496f, 500–501 intravascular lymphoma, ISAT trial, 138, 220, 232, 254, 255, 266, 326 ISUA series trials, 220, 251, 254, 263 IVSCT study, 111 J Jahromi, B S., 209 JET study, 32 JR-NET1/JR-NET2, 317–318 juvenile nasopharyngeal angiofibroma, 502–507, 509–512 K Kalani, M Y., 308, 418 Krings, T., 418 Krisht, A F., 268 L large vessel occlusion – ADAPT FAST, 12 – anatomical considerations, 10 – ASPECTS score, 10 – cerebrovascular management, 12 – characterization, – clinical evaluation, 9f, 10 – complication avoidance, 12 – conservative management, 10 – differential diagnosis, 10 – durability, 12 – endovascular management, 11f, 12 – follow-up, 12 – imaging, 10, 11–12f – outcome, 12 – recurrence rate, 12 – treatment indications, 8, 9f – treatment options, 10 Lasjaunias, P L., 460 Lehecka, M., 193 Levrier, O., 435 lipohyalinosis, Liu, L., 52 Lozier, A P., 268 Lunardini, D J., 86 LVO see large vessel occlusion lymphoma, intravascular, M MACE study, 36 MATCH trial, Matsukawa, H., 189 MCA aneurysms – anatomical considerations, 171 – cerebrovascular management, 172f, 173–174, 173f – characterization, 171, 175–176 – classification, 171–173 – clinical evaluation, 173, 176 – complication avoidance, 174–175 – conservative management, 173 – distal (see distal MCA aneurysms) – durability, 175 – endovascular management, 174 – follow-up, 175 – imaging, 173 – intracerebral hematoma influence, 172–174f, 173 – outcome, 175 – pathophysiology, 171–173 – treatment indications, 171, 172f – treatment options, 173, 173–174f, 175–176 medulla, surgical approaches, 480–481f, 483f, 484t, 485 meningiomas – characterization, 498–499, 498–499f, 505 – differential diagnosis, 504f, 505 – durability, outcome, recurrence rate, 507 – imaging, 504f, 505 – skull base, 502–507, 503–504f – treatment indications, options, 498–499, 498–499f, 505 metastatic vascular tumors, 500 Meyers, P M., 442 midbasilar aneurysms – anatomical considerations, 257–259, 259–260f – cerebrovascular management, 260 – characterization, 257 – classification, 259 – clinical evaluation, 259 – complication avoidance, 261 – conservative management, 257, 258f – differential diagnosis, 259 – endovascular management, 258f, 260–262, 260f – flow diversion, 261 – follow-up, 261 – imaging, 259, 260f – intracerebral hematoma influences, 260 – outcomes, 261 – pathophysiology, 259 – treatment indications, 257, 258f – treatment options, 260–262 midbrain, surgical approaches, 480–481f, 481–482, 484t Mitha, A P., 491 Monteith, S J., 308–309 Moon, K., 195, 370–371 Moon, T H., 230 Morton, R P., 442 Moyamoya disease (adult) – cerebrovascular management, 70–72 – characterization, 68 – classification, 68–70 – clinical evaluation, 69f, 70 – complication avoidance, 72 – direct STA-MCA bypass, 70–71, 71f – durability, 72 – endovascular treatment, 72 – follow-up, 72–73 – imaging, 70 – indirect extracranial–intracranial bypass, 71–72, 72f – outcome, 72 – pathophysiology, 60 – recurrence rate, 72 – screening, patient selection, 68, 69f – treatment indications, 68, 69f – treatment options, 69f, 70, 73 Moyamoya disease (pediatric) – anatomical considerations, 60, 60f – cerebral perfusion deficits, 66 – cerebrovascular management, 62–66 – characterization, 60 – clinical evaluation, 61f, 62 – complication avoidance, 66 – conservative management, 62 – differential diagnosis, 62 – direct revascularization technique, 62f, 63 – durability, 62–63f, 66 – endovascular management, 63–66 – follow-up, 66 – imaging, 60–63f, 62 – indirect revascularization technique, 62–63, 64–65f – OA-to-PCA bypass technique, 63 – outcome, 62–63f, 66 – pathophysiology, 60 – STA-ACA bypass technique, 63 – STA-MCA bypass technique, 63 – treatment indications, 60, 61f – treatment options, 62 MR CLEAN trial, 14 mycotic aneurysms – anatomical considerations, 335 – cerebrovascular management, 336f, 337 – characterization, 335 – classification, 335–337 – clinical evaluation, 337 – complication avoidance, 339 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 523 Index – – – – – – – – – – – – – – conservative management, 336f, 337 differential diagnosis, 337 durability, 340–342 endovascular management, 336f, 337–338, 338–341f flow diversion, 340 follow-up, 342 imaging, 337 intracerebral hematoma influences, 337 outcome, 340 pathophysiology, 335–337 pediatric, 342 recurrence rate, 340–342 treatment indications, 335, 336f treatment options, 336f, 337, 342–343 N NALEA, 432 NASCET trial, 29 O olfactory neuroblastoma, 504, 506, 507 ophthalmic artery aneurysms – anatomical considerations, 140–142 – cerebrovascular treatment, 142, 142–143f – characterization, 140 – clinical evaluation, 141f, 142 – complication avoidance, 141f, 144 – conservative management, 140, 141f – differential diagnosis, 142 – durability, 145 – endovascular treatment, 141f, 142–143, 143–144f, 145–146 – flow-diverting stents, 144–145 – follow-up, 145 – imaging, 142 – outcomes, 144–145 – treatment indications, 140, 141f P paraganglioma, 502, 505–507 parieto-occipital AVMs, 377t PAVFs see pial AVFs PcaA aneurysms – anatomical considerations, 197–199 – cerebrovascular management, 199–200, 200f, 202 – characterization, 197 – classification, 199 – clinical evaluation, 199 – complication avoidance, 201 – conservative management, 198f, 199 – dissection, 200 – endovascular management, 200–202, 201f – follow-up, 202 – imaging, 199, 202 – intracerebral hematoma influences, 199 – outcome, 201–202 – treatment indications, 197, 198f – treatment options, 198f, 199 PCA aneurysms – anatomical considerations, 270–272, 272f – cerebrovascular management, 271f, 272–273 – characterization, 270 – clinical evaluation, 272 – complex, revascularization for, 271f, 273 – complication avoidance, 271f, 274 – conservative management, 270, 271f, 272 – dissecting, anatomical considerations, 314, 314f – durability, 275 – endovascular management, 271f, 273–274, 273–274f – follow-up, 275 – imaging, 272 524 – – – – outcome, 274–275 recurrence rate, 275 STA–PICA bypass, 316 surgical classification approach, 271f, 272–273 – treatment indications, 270, 271f – treatment options, 271f, 272, 273–274f, 275–276, 324 PCFAs see posterior circulation fusiform aneurysms PCoA aneurysms – anatomical considerations, 147–149, 149f – cerebrovascular management, 148f, 150–151, 153f – characterization, 147 – clinical evaluation, 150, 154 – complication avoidance, 152–153 – conservative management, 147, 148f – differential diagnosis, 150 – durability, 154 – endovascular management, 148f, 151–152, 152f, 154–155 – follow-up, 154 – imaging, 150, 259 – intracerebral hematoma influences, 150 – outcome, 153–154 – recurrence rate, 154 – recurrent (see recurrent/residual aneurysms) – third nerve palsy, 152–153 – treatment indications, 147, 148f – treatment options, 148f, 150, 151–152f, 154–155 pediatric AVFs see pial AVFs pediatric intracranial aneurysms – anatomical considerations, 350 – cerebrovascular management, 352–353 – characterization, 350 – classification, 350–352 – clinical evaluation, 352 – conservative management, 352 – differential diagnosis, 352 – durability, 353–354 – endovascular management, 353 – follow-up, 354 – hemodynamic stress-related, 350 – idiopathic, 350 – imaging, 352 – infectious/mycotic, 352 – mycotic, 342 – noninfectious inflammatory, 352 – oncotic, 352 – outcome, 353 – pathophysiology, 350–352 – radiation dose, 352 – traumatic, 350 – treatment indications, 350, 351f – vasculopathic, 352 pericallosal artery aneurysms see PcaA aneurysms Pham, M H., 98 pial AVFs – anatomical considerations, 420, 422–424f – cerebrovascular management, 421f, 425 – characterization, 420, 426 – clinical evaluation, 421f, 422 – complication avoidance, 425–426 – conservative management, 425 – differential diagnosis, 424 – endovascular management, 421f, 425 – imaging, 421f, 422–424, 424f – outcomes, 426 – pathophysiology, 420 – radiosurgery, 425 – treatment indications, 420, 421f PICA aneurysms – anatomical considerations, 292, 294f – angle of attack, 294f, 295–296 – bypass techniques, 293f, 296 – cerebrovascular management, 294f, 295, 321f, 322–323 – characterization, 292, 298 – clinical evaluation, 294 – complication avoidance, 293f, 296–297 – conservative management, 292 – craniotomy planning, 294f, 295 – differential diagnosis, 294 – dissecting, anatomical considerations, 314–315, 314f – dissecting, cerebrovascular management, 327–328f, 329 – dissection, clip placement, 296 – distal, 296, 298, 302 – durability, 297 – endovascular management, 293f, 295f, 296 – follow-up, 297–298 – imaging, 294, 295f, 321 – operative windows, 294f, 295–296 – outcome, 297 – pathophysiology, 292 – recurrence rate, 297 – recurrent, cerebrovascular management, 327–328f, 329 – ruptured, 297, 298 – treatment indications, 292, 293f – treatment options, 293f, 294, 298 – unruptured, 297, 298 Pollock, B E., 388 Ponce, F A., 304 pons, surgical approaches, 480–481f, 483–485, 484t posterior circulation dissecting aneurysms – anatomical considerations, 314–315, 314f – anatomical pathology, 312–314, 312f – cerebrovascular management, 315–316 – characterization, 312, 318 – clinical evaluation, 315 – complication avoidance, 317–318 – conservative treatment, 312, 313f – deconstructive procedures, 313f, 316–317 – durability, 318 – endovascular management, 313f, 316–317 – flow diversion, 313–314f, 317, 318 – follow-up, 318 – imaging, 315 – OA–PICA bypass, 316 – outcomes, 317–318 – pathophysiology, 314 – PICA–PICA bypass, 316 – proximal vessel occlusion, 313f, 316 – reconstructive procedures, 313f, 317 – STA–PICA bypass, 316 – surgical trapping/resection, 316 – treatment indications, 312, 313f – treatment options, 315, 318 posterior circulation fusiform aneurysms – AICA aneurysms, concurrent with, 284f, 289, 290f – anatomical considerations, 306 – cerebrovascular management, 308, 308f – characterization, 306 – classification, 306, 308f – clinical evaluation, 306–308 – complications avoidance, 309 – durability, 310 – endovascular management, 308, 309f – follow-up, 310 – imaging, 308 – intracerebral hematoma influence, 308 – outcomes, 309 – recurrence rate, 310 – treatment indications, 306, 307f – treatment options, 308, 310 posterior inferior cerebellar artery see PICA aneurysms prasugrel (Effient), 48 PRoFESS trial, pseudoaneurysms see posterior circulation dissecting aneurysms pure motor hemiparesis, pure sensory stroke, R radiosurgery – brainstem AVMs, 395, 396f, 404, 405 – carotid-cavernous fistulas, 440 – cerebellar AVMs, 412 – cerebral cavernous malformations, 468–469 – dural AVFs, 434 – pial AVFs, 425 – skull base vascular tumors, 507 – Spetzler–Martin grade 1/2 AVMs, 370, 371 – Spetzler–Martin grade 4/5 AVMs, 393 – spinal AVMs, 418 – thalamic/basal ganglia cavernous malformations, 471 Rangel-Castilla, L., 230–231, 513 Rashad, S., 418–419 recurrent/residual aneurysms (anterior) – anatomical considerations, 232–233, 234–235f, 242, 244f – balloon-assisted coiling, 236 – cerebrovascular management, 232f, 236, 237f, 238, 244–245, 245f – characterization, 232, 240 – classification, 240t, 241f, 242–243 – clinical evaluation, 233, 243 – compaction ratio, 238 – complication avoidance, 238, 246 – conservative management, 241f 243–244 – de novo aneurysms, 241f, 242 – detection immediately post-surgery, 241f, 242, 243f – differential diagnosis, 235, 243, 244f, 246f – double-microcatheter technique, 236–237 – durability, 238, 246 – endovascular management, 236–238, 245–246, 246f – flow diversion, 237–238 – follow-up, 238, 246 – imaging, 235, 241f, 242, 243 – intracerebral hematoma influences, 232f, 234–235f, 235–236 – known residual aneurysms, 241f, 242 – outcome, 238, 246 – pathophysiology, 242 – prevention, 238 – recurrence rate, 238–239, 246 – rupture/hemorrhage risk, 242t – stent-assisted coiling, 237 – treatment indications, 232, 232–233f, 238, 240–242, 240t, 241f, 242t – treatment options, 232f, 234–235f, 235–236, 238–239, 246–247 recurrent/residual aneurysms (posterior) – anatomical considerations, 326–328, 327–328f – cerebrovascular management, 327–328f, 329 – characterization, 326 – classification, 328 – clinical evaluation, 328 – clipping data outcomes, 330 – coiling data outcomes, 330 – complication avoidance, 330 – conservative management, 327–328f, 329 – endovascular management, 327f, 329, 329–330f – imaging, 327f, 328–329 – outcomes, 330–331 – pathophysiology, 328 – treatment indications, 326, 327f – treatment options, 331 S saccular aneurysms – classification, 214, 259 – midbasilar, 259, 262 – pathophysiology, 259, 301 – treatment indications, 212, 213f Sairanen, T., 26t Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license Index SAMMPRIS trial, 31, 32, 35, 48 Sanai, N., 353 SAPPHIRE trial, 39, 46 sarcoidosis, SCA aneurysms – anatomical considerations, 277–279 – cerebrovascular management, 279f, 280 – characterization, 277, 282 – classification, 279 – clinical evaluation, 279 – complication avoidance, 281 – durability, 281 – endovascular management, 280–281, 280f – follow-up, 282 – imaging, 279, 279–280f, 282 – intracerebral hematoma influences, 279–280 – outcome, 281, 281t – recurrence rates, 282 – treatment indications, 277, 278f – treatment options, 278f, 279–280, 282, 302 Schramm, J., 393 segmental ectasia, 214 Sekhar, L N., 268 SHA aneurysms – anatomical considerations, 135, 136f – cerebrovascular management, 137, 137f – characterization, 135 – classification, 135 – clinical evaluation, 135 – complication avoidance, 138 – conservative management, 136f, 137 – differential diagnosis, 135 – durability, 138 – endovascular management, 137–139, 138f – follow-up, 138–139 – imaging, 135 – intracerebral hematoma influences, 136f, 137 – outcome, 138 – recurrence rate, 138 – treatment indications, 135, 136f – treatment options, 136f, 137, 139 Sharma, B S., 209 Siddiqui, A H., 261, 304 Singer, O C., 26t skull base vascular tumors – cerebrovascular management, 503f, 506 – characterization, 502, 507–508 – classification, 504–505 – clinical evaluation, 505 – complication avoidance, 506–507 – conservative management, 502, 503f – differential diagnosis, 505 – durability, 507 – dural metastases, 506 – endovascular management, 503f, 506 – esthesioneuroblastoma, 504, 506, 507 – follow-up, 507 – foramen magnum, 504f – hemangiopericytoma, 497–498, 502, 505, 506 – imaging, 503–504f, 505 – juvenile nasopharyngeal angiofibroma, 502–507, 509–512 – outcome, 507 – paraganglioma, 502, 505–507 – pathophysiology, 504–505 – radiosurgery, 507 – reconstruction, 507 – recurrence rate, 507 – treatment indications, 502, 503f small vessel disease – antiplatelet agents, – bleeding risk, – characterization, – classification, – clinical evaluation, – complication avoidance, 6–7 – confluent, – differential diagnosis, 5–6, 5f – dyslipidemia management, – follow-up, – hyperacute management, – hypertension management, – imaging, 3–5, 5f – lifestyle modifications, – monitoring, – outcomes, 6–7 – pathophysiology, – screening, – treatment indications, 3, 4f – treatment options, SPACE trial, 46 SPARCL trial, 38 Spetzler–Martin grade 1/2 AVMs – anatomical considerations, 365, 366–369f – cerebrovascular management, 368f, 369–370 – characterization, 363, 371 – classification, 365, 366–367f, 368t – clinical considerations/evaluation, 365 – complication avoidance, 370 – conservative management, 364f, 369, 371 – endovascular management, 368–369f, 370 – follow-up, 371 – imaging, 365 – outcome, 370–371 – radiosurgery, 370, 371 – ruptured, 365 – treatment indications, 363, 364f – treatment options, 368, 371–372 – treatment timing, 363–365, 364f Spetzler–Martin grade AVMs – anatomical considerations, 373–376, 375–376f – cerebrovascular management, 377–379, 377t, 378–383f – characterization, 373 – classification, 373, 383–384 – clinical evaluation, 376, 384 – complication avoidance, 380–381 – conservative management, 377 – differential diagnosis, 376 – durability, 383 – endovascular management, 379–380 – follow-up, 383 – imaging, 376 – intracerebral hematoma influences, 375–376f, 376–377 – outcome, 381–382 – recurrence rate, 383 – treatment indications, 373, 374f – treatment options, 375–376f, 376–377, 384 Spetzler–Martin grade 4/5 AVMs – anatomical considerations, 388, 389–390f – cerebrovascular management, 392 – characterization, 386 – classification, 388–391 – clinical evaluation, 391 – complication avoidance, 393 – conservative management, 386–388, 387f, 391 – differential diagnosis, 391 – endovascular classification, 391 – endovascular management, 387f, 392–393 – follow-up, 394 – imaging, 391, 392f – intracerebral hematoma influence, 387f, 391 – multimodal treatments, 393 – outcome, 393–394 – radiosurgery, 393 – treatment indications, 386, 387f – treatment options, 387f, 391, 394 – spinal artery aneurysms – anatomical considerations, 355 – cerebrovascular management, 356f, 358 – characterization, 355, 359 – clinical evaluation, 355–357, 359 – complication avoidance, 358 – conservative management, 356f, 357 – differential diagnosis, 357 – – – – – durability, 359 endovascular management, 356f, 358 follow-up, 359 imaging, 357, 357–358f, 359 intracerebral hematoma influence, 356f, 357 – outcome, 358 – pathophysiology, 355 – recurrence rate, 359 – treatment indications, 355, 356f – treatment options, 356f, 357 spinal AVFs – anatomical considerations, 444, 446–447f – cerebrovascular management, 445–446f, 447, 448f – characterization, 444, 450–451 – classification, 444–446, 445f, 448–449f – clinical evaluation, 446 – complication avoidance, 449 – conservative management, 447 – differential diagnosis, 446 – durability, 450 – endovascular management, 447–449, 451, 451f – follow-up, 450 – imaging, 446, 446–447f, 450f – outcome, 449–450, 451–452t – pathophysiology, 444–446, 445f, 448–449f – recurrence rate, 450 – treatment indications, 444, 445f – treatment options, 445f, 447, 450–451 spinal AVMs – anatomical considerations, 413 – cerebrovascular management, 414f, 417 – characterization, 413, 419 – classification, 413, 414f, 415–417f – clinical evaluation, 413–417 – complication avoidance, 418 – differential diagnosis, 417, 419 – durability, 419 – endovascular management, 417, 418 – follow-up, 419 – imaging, 417, 419 – outcome, 418–419 – radiosurgery, 418 – recurrence rate, 419 – subtypes, 417 – treatment indications, 413, 414f spinal cavernous malformations – anatomical considerations, 487, 489–490f – cerebrovascular management, 488–489f, 490–491 – characterization, 487, 491 – clinical evaluation, 487 – complication avoidance, 491 – conservative management, 488f, 489 – differential diagnosis, 489 – durability, 491 – follow-up, 491 – imaging, 487–489, 490f – pathophysiology, 487, 488f – recurrence rate, 491 – surgical management, 489–490 – treatment indications, 487, 488f spinal vascular tumors – anatomical considerations, 517, 517f – characterization, 515, 515f – classification, 517 – clinical evaluation, 517, 518f – complication avoidance, 519 – durability, 519 – endovascular management, 516f, 518–519, 519f – follow-up, 519–520 – imaging, 518, 518f – outcome, 519 – recurrence rate, 519 – treatment indications, 515–517, 516f – treatment options, 518 SSYLVIA study, 32, 58 Stam, J., 111–112 stereotactic radiosurgery see radiosurgery Sturiale, C L., 201–202 SUAVe study, 197 Suh, S H., 287t, 290 superior cerebellar artery see SCA aneurysms superior hypophyseal artery see SHA aneurysms supratentorial cavernous malformation see cerebral cavernous malformations Susac’s disease, 5–6 SVAD see vertebral artery dissection (spontaneous) SVD see small vessel disease SWIFT PRIME trial, 14 T temporal AVMs, 377t thalamic/basal ganglia cavernous malformations – anatomical considerations, 471, 472f – anteroinferior region management, 472f, 474 – cerebrovascular management, 472f, 474–475 – characterization, 471, 476 – clinical evaluation, 473 – complication avoidance, 472f, 475–476 – conservative management, 472f, 473–474, 473f, 475f – differential diagnosis, 473 – durability, 476 – endovascular management, 475 – follow-up, 476 – imaging, 472f, 473, 473–474f – lateral region management, 472f, 474 – outcomes, 472f, 476 – pathophysiology, 473 – posterosuperior region management, 472–473f, 474–475, 475f – radiosurgery, 471 – recurrence rate, 476 – treatment indications, 471, 472f – treatment timing, 471, 472f THERAPY trial, 14 Thiex, R., 513 ticagrelor (Brilinta), 48 TICAs (anterior) – anatomical considerations, 227, 229f – characterization, 227, 231 – classification, 227–229 – clinical evaluation, 229 – complication avoidance, 229f, 230 – conservative management, 227, 228f – differential diagnosis, 230 – durability, 231 – follow-up, 231 – imaging, 228f, 229–231 – outcome, 230–231 – pathophysiology, 227–229, 228–229f – recurrence rates, 231 – treatment indications, 227, 228–229f – treatment options, 228f, 230–231 TICAs (posterior) – anatomical considerations, 320 – cerebrovascular management, 321f, 322–323, 323f – characterization, 320 – clinical evaluation, 320 – complication avoidance, 323 – conservative management, 321f, 322 – covered stents, 324 – differential diagnosis, 322 – dissecting, 320, 324 – durability, 324 – follow-up, 324 – iatrogenic, 324 – imaging, 320–322 – intracerebral hematoma influence, 322 – outcome, 323–324 – penetrating injuries, 324 – recurrence rate, 324 – treatment indications, 320, 321f – treatment options, 321f, 322, 324 TO-ACT trial, 112 traumatic intracranial aneurysms see under TICAs Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license 525 Index U UCAS Japan study, 197 UCSF Brain AVM study, 370 V vascular dementia, vein of Galen malformations – anatomical considerations, 453 – Bicetre score, 455t – characterization, 453 – classification, 455, 456–457f – clinical evaluation, 455 – complication avoidance, 458–459 – conservative management, 454f, 458, 460f – differential diagnosis, 457 – durability, 461 – endovascular management, 454f, 458 – follow-up, 461 – imaging, 455–457, 457–460f – outcomes, 459–461 – pathophysiology, 455, 456–457f – recurrence rate, 461 – treatment indications, 453, 454f, 455t – treatment options, 454f, 457, 457–459f, 461 ventricular/periventricular AVMs, 377t VerifyNow assay, 48 VERiTAS trial, 35 vertebral artery aneurysms – anatomical considerations, 251 – cerebrovascular management, 253, 253f – characterization, 251, 255 – classification, 251–253 – clinical evaluation, 253 – complication avoidance, 254 – conservative management, 251 526 – differential diagnosis, 253 – dissecting, anatomical considerations, 314, 314f – durability, 255 – ELITE approach, 253, 254 – endovascular management, 253–255, 254f – flow diversion, 254–255, 254f – follow-up, 255 – imaging, 253 – OA–PICA bypass, 316 – outcomes, 254–255, 304, 317–318 – PICA–PICA bypass, 316 – recurrence rate, 255 – treatment indications, 251, 252f – treatment options, 252f, 253, 255, 302 vertebral artery dissection – anatomical considerations, 95f, 97 – characterization, 95 – clinical evaluation, 95–96f, 97–99 – complication avoidance, 98 – endovascular management, 95–96f, 98 – extradural, 95–96f, 97 – follow-up, 98 – imaging, 95–96f, 97 – intradural, 95–96f, 97 – outcomes, 98 – pathophysiology, 95–97, 95f – treatment indications, 95, 95–96f, 98–99 – treatment options, 95–96f, 97–99 vertebral artery injury – anatomical considerations, 80–82, 81–82f – case studies, 81f, 83–86, 84–85f – cerebrovascular management, 81f, 83 – characterization, 80 – clinical evaluation, 82 – complication avoidance, 86–87 – – – – conservative management, 81f, 83 differential diagnosis, 83 durability, 86 endovascular management, 81f, 83–84 – follow-up, 86 – imaging, 82–83 – outcome, 86 – pathophysiology, 80–82, 81–82f – subarachnoid hemorrhage, 86–87 – surgical anatomy, 82 – thromboembolism, 86 – treatment indications, 80, 81f, 86 – treatment options, 83 vertebral artery ostium stenosis – anatomical considerations, 54 – cerebrovascular management, 55f, 56 – characterization, 54 – classification, 54 – clinical evaluation, 54 – complication avoidance, 57, 58 – conservative management, 55f, 56 – differential diagnosis, 56 – durability, 58 – endovascular management, 55f, 56–58 – follow-up, 58 – imaging, 54–56, 56–57f – outcome, 55f, 57 – pathophysiology, 54 – restenosis rate, 58 – stenting, 58 – treatment indications, 54, 55f, 58 – treatment options, 56 vertebrobasilar stenosis, insufficiency – anatomical considerations, 48–50, 50f – cerebrovascular management, 50–51 – characterization, 48 – clinical evaluation, 50 – complication avoidance, 51–52, 51–52f – conservative treatment, 48, 49f – durability rates, 53 – endovascular treatment, 48, 49f, 51 – follow-up, 53 – imaging, 50 – outcome, 52–53 – restenosis rates, 53 – treatment indications, 48, 49f – treatment options, 50, 51–52f Veterans Affairs Cooperative Study Group, 36 VOGMs see vein of Galen malformations W WASID trial, 35, 48 Watanabe, Y., 131 Webb, S., 26t Wermer, M J., 330 WILLIS stent, 442 X Xavier, A R., 193 Xianjun, H., 92–93 Y Yamazaki, T., 193 Z Zähringer, M., 513 Zhang, L., 491 Zhang, Y S., 354 Zhiming, Z., 92–93 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68420-057-3), copyright © 2018 Thieme Medical Publishers All rights reserved Usage subject to terms and conditions of license ... definitive diagnosis and to prepare for treatment (►Figs 33 .2 and ►33.3) If catheter angiography including three-dimensional (3D) reconstructions 22 2 Rangel-Castilla et al Decision Making in Neurovascular. .. safety of pipeline embolization device in patients with ruptured carotid blister aneurysms Neurosurgery 20 14;75(4):419– 429 , discussion 429 22 6 Rangel-Castilla et al Decision Making in Neurovascular. .. Algorithm 34.1 Decision- making algorithm for traumatic intracranial aneurysms of the anterior circulation 22 8 Rangel-Castilla et al Decision Making in Neurovascular Disease (ISBN 978-1-68 420 -057-3),