Adjuvant Endovascular Management of Brain Arteriovenous Malformations

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CHAPTER 386 Adjuvant Endovascular Management of Brain Arteriovenous Malformations

Robert M. Starke, Sean D. Lavine, Philip M. Meyers, E. Sander Connolly, Jr.

Clinical Significance and Treatment Plan

Currently, there are four major treatment options for brain arteriovenous malformations (AVMs). The lesion can be monitored expectantly with the acceptance that the patient has a risk for hemorrhage, neurological deficit, or seizure. The goal of AVM intervention is to eliminate the risk for hemorrhage and to preserve or improve functional neurological status. Microsurgery, radiosurgery, and embolization have all been used successfully in various combinations. Each modality has been used as the sole treatment or in combination with the others. Treatment efficacy is a critical outcome parameter (total/permanent angiographic obliteration of the lesion), as is delay in or failure of obliteration of the lesion. Although combination therapy allows treatment of lesions previously considered untreatable, the patient is subject to the combined risk associated with each treatment. In some cases, however, multimodality therapy may decrease the overall risk related to the treatment plan rather than subjecting a patient to an aggressive approach with one modality. For each patient, a unique treatment plan with specific goals and potential risks and benefits must be established and understood by the treating team of health professionals, the patient, and family. The natural history of each lesion must be analyzed along with the ability of the various treatment options to satisfy the goals of treatment while assessing the risks associated with the intervention plan. The natural history and classification of brain AVMs are discussed elsewhere in this textbook, and other chapters address surgical and radiosurgical management.

This chapter focuses on the endovascular management of brain AVMs. Currently, embolization may be used (1) as adjuvant therapy before definitive microsurgery or radiosurgery, (2) as palliative therapy for inoperable or otherwise incurable AVMs, or (3) as curative therapy (i.e., without surgical resection or radiotherapy). Primary curative embolization of AVMs is discussed elsewhere in this textbook.

To formulate the best treatment plan for AVMs, a complete analysis of each patient is required, including knowledge of the clinical history and present clinical status, cross-sectional imaging characteristics, and the angioarchitecture of the AVM and normal brain circulation. The angioarchitecture of the AVM often determines the approach to the lesion and the probability of reaching the therapeutic goal. Treatment of a particular patient with an AVM should be considered if therapy could result in an improved outcome in comparison to the expected natural history of the lesion. Risk factors specific to each patient must be considered. Most commonly, the goal is curative treatment. Under certain circumstances, however, treatment may be palliative because a complete cure may not be possible or indicated.

Treatment of AVMs often requires a multidisciplinary approach with a team consisting of an interventional neuroradiologist, a vascular neurosurgeon, a vascular neurologist, and a stereotactic radiosurgeon.1–5 Such a team provides a balanced approach to management of the AVM.

Patient Selection

The discovery of an AVM in a patient does not represent an immediate indication for treatment. Each AVM does not carry the same risk for future hemorrhage.6 An incidentally discovered cortical micro-AVM in a young patient does not have the same prognosis and natural history as a large thalamic AVM in a young patient with a progressive neurological deficit or hemorrhage.

An important part of the management of incidentally discovered AVMs is to educate the patient and provide information regarding the natural history and influencing factors that may apply to the specific situation inasmuch as the true natural history of asymptomatic AVMs is not fully defined. Treatment options and associated risks encountered in the treating team’s experience must be explained.

In summary, a complete clinical and morphologic analysis of each patient is required to determine whether and when treatment is indicated and which treatment modalities will best serve the patient with the lowest risk of morbidity.

Clinical Analysis

Age

In general, the younger the patient at the time of diagnosis, the more likely treatment should be considered. Diagnosis at a young age represents an early imbalance between the patient (i.e., host) and the AVM, and the patient has a greater number of years at risk for hemorrhage. Increasing age and age older than 60 years have also been found to be risk factors for hemorrhage.6,7 Older patients likewise have a greater risk for hemorrhage-associated morbidity and mortality than younger individuals do; therefore, treatment may even be warranted in the elderly.

Gender

The gender of the patient should not influence the decision to treat a brain AVM. Although there has been controversy about the risk for hemorrhage or other symptoms in women, especially during pregnancy, this association has not been well established. The majority of studies demonstrate that pregnancy or delivery does not seem to increase the risk for hemorrhage or the risk for progression of neurological symptoms.8–11

Lifestyle and Occupation

The decision to treat a patient with an AVM should include an analysis of lifestyle and the impact of symptoms and potential complications of therapy in trying to achieve cure. Consideration of hemispheric dominance, stage of education, and occupation should have a role in therapeutic decisions.

Initial Symptoms

The initial symptoms play a significant role in the timing of treatment and choice of treatment modality. AVM patients tend to initially be seen at a younger age and with fewer medical conditions than do patients requiring other types of vascular surgery, but they may have serious comorbidity because of the AVM itself. The estimated risk for intracranial hemorrhage or rebleeding is the highest priority. In patients with significant comorbid conditions precluding general anesthesia and microsurgery, a less invasive approach may be warranted, such as radiosurgery or, in select circumstances, embolization. In patients with a significant risk for hemorrhage or recurrent hemorrhage, embolization may be a consideration for select AVMs, in which case embolization may be curative.

Hemorrhage

Although some controversy exists regarding the rebleeding rate during the first year after hemorrhage, it is generally believed to be similar to or just slightly higher than the natural history risk of 2% to 4% per year.12–20 Each episode of hemorrhage is associated with a 10% risk for mortality and a 30% to 50% morbidity rate.35 A study by Ondra and coworkers analyzed the outcome of symptomatic AVMs. They reported a severe morbidity rate of 1.7%, annual mortality rate of 1%, and a mean rebleeding interval of greater than 6 years.18

There is seldom a need for urgent treatment after AVM hemorrhage, and a treatment strategy can be planned accordingly. Treatment of an AVM is generally an elective procedure in a stable patient. In contrast, patients with intracranial hemorrhage and hydrocephalus secondary to life-threatening hematoma may require emergency surgery. Clot evacuation and external ventricular drainage may avert the need for emergency AVM resection, thus allowing the patient time to recover, as well as time to obtain additional imaging studies such as catheter angiography to better delineate all elements of the lesion. Early surgical resection of an AVM at the time of emergency clot evacuation is usually done only for superficial AVMs when the anatomy can be fully elucidated.

When the benefits of treatment outweigh the risks associated with treatment in patients with a history of AVM hemorrhage, the angioarchitecture of the AVM is meticulously analyzed in search of areas of anatomic weakness. The pattern of hemorrhage may correspond with a particular feature, such as a feeding artery or perinidal aneurysm. If such an abnormality is discovered, targeted embolization can be performed (Figs. 386-1 to 386-3).8,21 If the source of hemorrhage can be occluded by embolization, surgical resection may be deferred to allow more complete recovery. If embolization of high-risk or causative malformations is technically impossible or unsuccessful, early surgical resection may be necessary. Although treatment philosophies vary depending on local expertise, the universal goal should be to reduce or eliminate the risk for future hemorrhage with acceptable treatment-associated risk.

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FIGURE 386-1 Targeted embolization in a patient with a left, high cerebellar micro–arteriovenous malformation and an off-midline, low cerebellar parenchymal hematoma. A, Lateral and magnified lateral views of a left vertebral angiogram demonstrate the malformation’s small nidus (small arrow), left posterior inferior cerebellar artery (PICA) pial supply with a proximal irregular aneurysm (arrow) anatomically correlated with the hematoma, and indirect left superior cerebellar pial supply. B, Superselective angiographic study performed through a microcatheter (arrowheads) in the left PICA. Notice the PICA branch with mild irregularity and the proximal aneurysm leading to the malformation (arrow). Normal cortical branches are seen posteriorly. C, Angiographic superselective study before embolization with N-butyl-2-cyanoacrylate. The microcatheter (arrowheads) was navigated to the irregular aneurysm entrance. Embolization of the distal nidus (small arrow) with obliteration of the proximal aneurysm (arrow) is the goal to prevent an early repeat hemorrhage. D, Lateral and anteroposterior views during left vertebral angiography after embolization. Notice the obliteration of the PICA aneurysm and preservation of the normal cerebellar cortical branches and small residual nidus (arrow) supplied by the left superior cerebellar distal branches. This residual malformation was resected surgically.

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FIGURE 386-2 Targeted embolization of a symptomatic right insular arteriovenous malformation. A, Anteroposterior angiographic views of the right internal carotid artery (ICA) in the arterial and venous phases show an insular malformation with predominantly cortical venous drainage. Notice the distal arterial aneurysm (arrow). B, In the magnified early arterial phases of the anteroposterior and lateral views of a global right ICA angiogram, notice the large, distal arterial aneurysm at the entrance to the nidus (arrow) and the proximal, small flow-related aneurysms (arrowheads). C, The lateral view of a superselective angiographic study performed through a microcatheter (arrowheads) positioned at the level of the aneurysm (arrow) shows high-flow fistulization distal to the aneurysm in combination with a proximal nidus. Occluding this area of angioarchitectural weakness was a high priority. D, A lateral subtracted fluoroscopic image shows a combination of microcoils and acrylic obliterating the base of the aneurysm and the leading pedicle (arrow), as well as a portion of the nidus (small arrow). E, In the anteroposterior view of a control angiographic study of the right ICA, notice the elimination of the large aneurysm and occlusion of the lateral portion of the nidus. The patient underwent second-stage embolization before radiosurgery.

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FIGURE 386-3 Palliative targeted embolization of a large basal ganglia and thalamic arteriovenous malformation (AVM) causing recurrent hemorrhages and hemipareses. A, The anteroposterior view of a vertebral angiogram shows multiple, enlarged, right posterior thalamic perforators and posterior choroidal arteries supplying the malformation in the posterior thalamic region and draining to the aneurysmally dilated vein of Galen. B, The anteroposterior and lateral views of a right internal carotid artery angiogram show multiple, enlarged, medial and lateral lenticulostriate arteries supplying the widespread AVM in the basal ganglia and draining into the aneurysmally dilated vein of Galen and straight sinus. C, Axial computed tomography (CT) and coronal T1-weighted magnetic resonance imaging (MRI) were completed a short period after the patient was noted to have combined parenchymal and intraventricular hemorrhage with neurological deterioration. Notice the acrylic cast (arrow) from previous embolization procedures. D and E, Anteroposterior views of the superselective angiographic studies were obtained through a microcatheter (arrowheads) positioned distally in two separate lateral lenticulostriate arteries supplying a malformation in the basal ganglia in the territory of the hematoma seen on CT and MRI. Notice the arterial pseudoaneurysms (long arrows) and intranidal pseudoaneurysm (short arrow), which could not be identified in the global angiographic studies. F, The anteroposterior view of a subtracted fluoroscopic study shows the acrylic cast deposited after the superselective study in E. Notice the obliteration of the arterial (long arrow) and the intranidal (short arrow) pseudoaneurysm with acrylic. G, An anteroposterior skull radiograph demonstrates the radiopaque acrylic cast in the malformation after the last embolization stage. Multiple stages were performed as part of a prolonged palliative treatment targeting weaknesses in the angioarchitecture and reduction of malformation size and flow.

Seizures

Many patients initially seen with a seizure disorder can be treated successfully with antiepileptic medications and rarely require immediate intervention. Patients with seizures carry the same future risk for hemorrhage as those with other symptomatic AVMs. Seizures do not alter the risk for future hemorrhage.18 When indicated, both microsurgery and radiosurgery have demonstrated similar results in reducing the incidence of seizures attributable to AVMs and the need for anticonvulsant therapy.22–24 Embolization has little role in the specific treatment algorithm of patients with seizures, except as an adjuvant to definitive treatment planning.

Headaches

Headache is a nonspecific symptom. Some patients with AVMs that have a dural or posterior cerebral artery supply complain of headaches that resolve or improve after embolization.25 Other patients with parietal lobe AVMs complain of worsening headache after embolization of anterior and middle cerebral artery feeders if there is a compensatory increased supply through the posterior cerebral arteries. Headaches by themselves do not represent an indication for treatment of patients with AVMs because the risk for hemorrhage is not changed from that of the general population.

Neurological Deficit

Up to 40% of patients with AVMs have neurological deficits,26 but neurological deficits are uncommon in patients without history of hemorrhage. In our experience and in the reports of others, neurological deficits are present in more than half of patients.25 Although arterial steal and mass effect have been implicated as possible causes,27 venous congestion and ischemia are also probable mechanisms (Fig. 386-4).25 Magnetic resonance imaging (MRI) has demonstrated changes in the venous drainage patterns of adjacent brain tissue with associated edema and partial thrombosis of draining veins of the AVM. If treated by partial embolization, these changes may be reversible in lobar AVMs causing progressive neurological deficits. Partial embolization of deep thalamic and basal ganglia AVMs in patients with progressive neurological deficits has been reported to result in stabilization in 27% and reversal of symptoms in 64% (see Fig. 386-3).28 Further definitive therapy should be carried out to completely obliterate the AVM and remove the risk for future hemorrhage, when possible.

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FIGURE 386-4 Palliative embolization of a left frontal and basal ganglia arteriovenous malformation in a patient with hemipareses and uncontrolled seizures. A, On axial T2-weighted magnetic resonance imaging (MRI), notice the malformation and the large draining veins. B, In the early and late phases of the lateral view of the left internal carotid angiogram, notice the malformation nidus (curved arrow) and multiple venous aneurysms (arrows, correlated with the MRI scan) in the deep venous drainage into the basal vein of Rosenthal and in the superficial drainage pathway into the sylvian vein leading through the vein of Trolard to the superior sagittal sinus. C, Axial T2-weighted MRI shows the area after multistage embolization. Notice the marked reduction in the size of the nidus and the venous outflow structures (compare with A). D, In lateral views of the venous phases of repeated carotid angiograms, notice the progressive reduction in size of the venous aneurysm in the basal vein of Rosenthal (arrow), the reduction in size of the venous aneurysm close to the nidus (arrow), and the reduction in size of the vein of Trolard. After palliative treatment, the patient showed clinical improvement with medical control of his seizures.

Architecture of the Arteriovenous Malformation

The vascular architecture of an AVM is an important consideration when planning treatment. Along with a thorough clinical examination, all AVM patients need detailed preoperative radiographic clarification of AVM anatomy, architecture, and associated aneurysms with MRI and high–frame rate digital subtraction angiography. The angiogram must delineate the characteristics of the AVM, including its arterial feeders, venous drainage, internal angioarchitecture, and associated vascular lesions, and it must define the collateral circulation and venous drainage pathways of the normal brain tissue. After a comprehensive evaluation has been performed, decisions can be made regarding the best management approach by comparing the natural history of the lesion with the intervention-related morbidity and mortality.

Determination of the accessibility of an AVM nidus starts with the patient’s past medical history and comorbid conditions. The extracranial or intracranial vasculature in patients with a history of congenital aortic or great-vessel malformations or occlusive disease may impair or preclude access of the microcatheter to the AVM. Further assessment during angiography is imperative because embolization in patients with AVM feeders that cannot be catheterized superselectively carries an increased risk for inadvertent occlusion of nontarget vessels and subsequent stroke. If nidal embolization is not performed, embolization often remains incomplete. In addition to the angioarchitecture of the nidus and feeders, determination of the hemodynamic properties of an individual AVM nidus is crucial for successful endovascular embolization. The number, morphology, and velocity of the arteriovenous shunting determine whether embolic material can be deposited selectively and safely in the nidus.

A decision to treat depends, in part, on the demonstration of areas of weakness in the angioarchitecture indicating potential instability. If there is an associated arterial aneurysm on the feeding pedicle or in the nidus, evidence of venous thrombosis, restriction of outflow, venous hypertension, venous pouches or dilations, venous pseudoaneurysm, or compromised venous outflow, treatment may be indicated and can achieve cure in certain circumstances, or targeted treatment as an adjuvant to definitive treatment may be beneficial (Fig. 386-5; see also Figs. 386-1 to 386-4).

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FIGURE 386-5 Angiographic studies were undertaken to define safe embolization in a right parietal arteriovenous malformation. A, The lateral view of a superselective angiogram was obtained with a microcatheter (arrowheads) introduced through the left vertebral artery to the right posterior cerebral artery and into a distal parietal occipital cortical branch. Normal branching arteries supply the cortex with a normal parenchymal blush (arrow). The angiogram shows the distal supply to the malformation (curved arrow). Acrylic embolization will induce ischemia in the surrounding normal cortex. B, The microcatheter was navigated distally, directly to the vessel leading to the malformation (curved arrow) beyond the normal cortex. There is no parenchymal blush. Embolization of the nidus was performed without neurological deficit or diffusion abnormality, as assessed by follow-up magnetic resonance imaging. Precise anatomic studies may eliminate the need for functional testing before the deposition of acrylic. C and D, On lateral vertebral angiograms before (C) and after (D) embolization, notice the obliteration of the whole posterior compartment of the malformation, preservation of normal cortical branches (as in A), and immediate regression of collateral circulation to the nidus (arrow).

A number of radiologic variables have been associated with an increased risk for hemorrhage, including small AVM size, elevated feeding artery pressure, periventricular or intraventricular location, basal ganglia location, deep venous drainage, impaired venous drainage, single draining vein, intranidal aneurysm, multiple aneurysms, and vertebrobasilar blood supply.15,29–36

Data from the New York Islands AVM Hemorrhage Study, an ongoing, prospective, population-based survey to determine the incidence of AVM-related hemorrhage and the associated rates of morbidity and mortality in a zip code–defined population of 10 million people, showed that increasing age (hazard ratio [HR], 1.05; 95% confidence interval [CI], 1.03 to 1.08), initial hemorrhagic AVM manifestation (HR, 5.38; 95% CI, 2.64 to 10.96), deep brain location (HR, 3.25. 95% CI, 1.30 to 8.16), and exclusive deep venous drainage (HR, 3.25; 95% CI, 1.01 to 5.67) were independent predictors of subsequent hemorrhage. Annual hemorrhage rates on follow-up ranged from 0.9% in patients without a hemorrhagic AVM manifestation, deep AVM location, or deep venous drainage to as high as 34.4% in those harboring all three risk factors.6,12,20 The authors also studied predictors of residual dysplastic vessels on cerebral angiography after AVM treatment. The number of patients showing angiographic evidence of dysplastic vessels was significantly associated with increasing size of the AVM, and symptomatic postoperative intracerebral hemorrhage was associated with dysplastic vessels on the postoperative angiogram.37

Location, Size, and Deep Venous Drainage

Although the location, size, and deep venous drainage of a malformation are important factors in determining the risks associated with microsurgical or radiosurgical therapy,38 these factors are of lesser concern in the endovascular treatment of AVMs. In performing embolization of AVMs, meticulous technique is important to prevent embolization of nontarget tissue and stroke (see Fig. 386-5).

Associated Lesions

Aneurysms are associated with AVMs in 10% to 40% of patients.39–42 Such aneurysms may be flow related (i.e., proximal or distal on a feeder vessel), intranidal, or remote and apparently unrelated (Figs. 386-6 and 386-7; see also Fig. 386-2).39–42 This weakness represents a marker for future hemorrhage and increases the risk for hemorrhage from 3% to 7%.13 Patients with subarachnoid hemorrhage, intracerebral hemorrhage, or both and an angiographically demonstrated AVM with an associated aneurysm should have therapy directed first toward the lesion that is suspected to be the source of hemorrhage. In the presence of acute subarachnoid hemorrhage, the source of hemorrhage is often a feeding artery aneurysm. When an intracerebral hematoma exists, the more likely source of hemorrhage is the AVM, including nidal and perinidal locations (see Fig. 386-3). Enlarging pseudoaneurysms represent an unstable situation and deserve special attention to prevent early hemorrhage. Ventricular hemorrhage or parenchymal hemorrhage may be venous in origin.

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FIGURE 386-6 Preoperative embolization of a right frontal arteriovenous malformation (AVM) with a proximal left superior hypophysial aneurysm. A, Anteroposterior angiographic views of the right and left internal carotid arteries (ICAs) demonstrate the malformation. A large, proximal venous aneurysm (arrow) and pial supply by the left anterior cerebral artery (ACA) and left middle cerebral artery (MCA) (curved arrows) cortical branches are seen. B, On the lateral angiographic view of the left common carotid, notice the left superior hypophysial aneurysm (arrow) and the left MCA pial supply (curved arrow). C, A road map lateral view was obtained during endovascular occlusion of the aneurysm with Guglielmi detachable coils (GDCs) (arrow). D, A live fluoroscopic, subtracted anteroposterior oblique view demonstrates the acrylic cast (arrowhead) achieved by embolizing the malformation through a left ACA feeding cortical branch. E, The final radiopaque acrylic cast (arrowhead) is seen on a radiograph of the skull. Notice the GDCs in the aneurysm (arrow). F, The lateral angiographic view of the left ICA after embolization but before surgery shows a small, residual malformation (open arrow) supplied by MCA frontal branches. The left hypophysial aneurysm is completely obliterated by the coils. G, The patient underwent uneventful microsurgical resection of the residual AVM. A follow-up lateral angiogram of the left ICA confirms complete removal and stable occlusion of the aneurysm.

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FIGURE 386-7 Left, posterior-frontal arteriovenous malformation (AVM) and a large, proximal aneurysm. Combined endovascular occlusion of the aneurysm and AVM nidus was achieved before radiosurgery. A, On coronal T1-weighted magnetic resonance imaging (MRI), notice the high-flow cortical-gyral AVM. B, On global and magnified views of the anteroposterior angiogram of the left internal carotid artery (ICA), notice the proximal middle cerebral artery (MCA) aneurysm (arrow) and the cortical wedge shape of the malformation supplied by the left MCA and anterior cerebral artery distal branches. C, On the anteroposterior skull radiograph obtained after the last endovascular procedure, notice the radiopaque acrylic cast in the nidus (curved arrow) and coils in the proximal aneurysm (arrow). D, On the anteroposterior angiogram of the left ICA after the last endovascular procedure, notice the small, residual nidus deep within the white matter that drains to the deep venous system (small arrow). Complete occlusion of the MCA aneurysm (large arrow) was achieved, and the patient was treated by radiosurgery for the residual malformation. E, Postembolization coronal T1-weighted MRI shows the acrylic casting of the nidus as a bright signal secondary to Lipiodol in the acrylic mixture. F, In the follow-up study after radiosurgery, the anteroposterior arterial and venous phases of a left ICA angiogram show complete obliteration.

High blood flow to an AVM may induce aneurysms to form on feeding arteries. Such “flow-related” aneurysms may regress after complete or partial obliteration of the AVM by endovascular embolization, and regression is more likely to occur the closer the aneurysm is to the nidus of the AVM.41 If the aneurysm is located close to the AVM, it should be obliterated at the time of embolization. If the aneurysm is within the planned resection field, it may be clipped at the time of microsurgery. If on follow-up angiography 6 to 12 months after AVM embolization there is no regression of the associated aneurysm, active treatment of the aneurysm should be considered. We recommend treating large, irregular, proximal aneurysms early as part of a global treatment plan (see Figs. 386-4 and 386-5). However, the treatment-associated morbidity must be low to justify the procedure in light of the unknown natural history of the aneurysm in the absence of the AVM.

Treatment Goals

Endovascular embolization is most commonly used as an adjunct to surgical resection or stereotactic radiosurgery. Embolization can be performed as the sole treatment (curative or palliative) in carefully selected patients, or it may result in excessive complications.43

Curative Embolization

Curative embolization is discussed in greater detail elsewhere in this textbook. The prerequisite for curing an AVM with endovascular embolization techniques alone is angioarchitecture that permits solid casting of the AVM nidus with permanent embolization material. Curative embolization is complete anatomic obliteration of the malformation by endovascular embolization, occlusion of the nidus, and early venous shunting, and it therefore requires the use of a permanent, nonbiodegradable embolic agent to form a cast within the pathologic angioarchitecture (Fig. 386-8). Particles or resorbable agents should not be used for curative embolization.

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FIGURE 386-8 Right temporal micro–arteriovenous malformation (micro-AVM) in a patient with a large parenchymal hematoma. A, On the early arterial and capillary phases of a lateral angiogram of the right internal carotid artery (ICA), notice the posterior temporal micro-AVM (small arrow) with early cortical venous drainage (large arrows). B, On the early and late phases of a lateral superselective angiogram performed through a microcatheter (arrowheads) in a minimally enlarged superior temporal branch, notice the normal proximal cortical branches with a parenchymal blush and the distal cortical supply to the malformation (arrow). C, The early and late arterial phases of a lateral postembolization angiogram of the right ICA show that complete obliteration was achieved without residual nidus or early venous shunting.

In addition to the immediate postembolization angiogram, 6-month and, preferably, 12- to 24-month postprocedural angiograms are useful to confirm the durability of treatment. Long-term angiographic follow-up is needed to detect small remnants that may not have been appreciated on the immediate postembolization angiogram and to exclude recanalization caused by the radiopaque embolic material mixing with nonopaque autologous blood at the time of embolization.44–46

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