Hemangiomas and Dural Fistulas

Louis J. Kim, Michael R. Levitt, Iman Feiz-Erfan, and Robert F. Spetzler

♦ Cavernous Malformations

Cavernomas or cavernous malformations of the central nervous system are uncommon pathologic entities, accounting for approximately 16% of all intracranial vascular lesions.¹ Histologically, they are composed of a dilated, single endothelial cell layer and sinusoidal veins with little or no intervening neural tissue (Fig. 10.1).² Ultrastructural studies have demonstrated that the absence of tight junctions between endothelial cells may account for the propensity of cavernous malformations to leech blood products into adjacent tissue.³ These lesions are usually angiographically occult because of their slow flow, which belies their proclivity for hemorrhage. Their magnetic resonance imaging (MRI) appearance is uniquely characteristic. T2-weighted images exhibit a dark, hemosiderin-stained rim and mixed-age blood products composing the nidus of the lesion. Patchy enhancement is observed occasionally, but otherwise cavernous malformations seldom enhance. Contrast administration usually unveils an associated venous angioma.

Posterior fossa cavernous malformations account for approximately 9 to 35% of intracranial cavernous malformations.⁴^–⁶ In order of decreasing frequency, the most common locations involving these lesions are the cerebellum, pons, midbrain, and medulla.⁷ On rare occasion, cavernous malformations of the cranial nerves are discovered (Fig. 10.2).⁸ Symptomatic annualized event rates for brainstem cavernous malformations have been reported to range from 0.25 to 22.9%.⁹^–¹¹ It is believed that hemorrhage rates rise significantly after the initial hemorrhage, with rebleed rates reported as high as 30 to 60% per patient per year.^7,12 Posterior fossa cavernous malformations, particularly in the brainstem, are associated with a significantly worse clinical course than lesions in supratentorial locations.⁵ In the analysis of our institutional series, which is based on the assumption that the lesions were present since birth, the retrospective hemorrhage rate was 5%.⁷ In another prospective study, the annual event rate for deep lesions was 10.6%.⁹ Hemorrhage rates have been reported higher in women, implicating estrogen as a risk factor.¹²^–¹⁵ With the widespread availability of MRI, posterior fossa cavernous malformations are being detected more frequently and often incidentally.

Because they are usually located in exquisitely eloquent parenchyma, posterior fossa cavernous malformations present a particularly challenging tactical quandary for neurosurgeons. The stochastic nature of brainstem cavernoma hemorrhages is problematic. A phenomenon known as “temporal clustering” of brainstem cavernomas refers to the clustering of hemorrhagic events in a relatively short time period, flanked by longer periods of relative quiescence. These active periods involving multiple hemorrhages can produce a significant stepwise decline in neurologic function.^16,17 Hence, an untreated patient who suffers repeated hemorrhages should be strongly considered for surgery. However, surgical intervention risks iatrogenic neurologic deficits and poses a daunting technical challenge in this unforgiving region of the brain. Hence, the treatment algorithm for posterior fossa cavernous malformations can be unclear.

In our experience, we base the decision to operate on the presence of the following factors: (1) neurologic symptoms directly attributable to repeated hemorrhages; (2) documented intra-or extralesional hemorrhage associated with mass effect; and (3) posterior fossa cavernous malformations that approach a pial surface, are exophytic, or are adjacent to non-eloquent parenchyma that serves as a surgical avenue. Surgical intervention on acute or subacute hemorrhagic lesions can take advantage of the plane created by the hematoma between the cavernous malformation and parenchyma, thus favoring early operation. However, patients are often referred after significant or even complete recovery from initial deficits. Therefore, the timing of surgery has varied, depending on the severity of a patient’s clinical presentation and on referral patterns.

Because the natural history of posterior fossa cavernous malformations is not completely understood and symptoms can change dramatically over time, a careful discussion of treatment options with patients and family members is mandatory. The option of expectant observation must be explicitly addressed.¹⁸ Asymptomatic lesions or previously symptomatic patients who have recovered from initial deficits may be followed nonsurgically, particularly if the cavernous malformation is deep-seated or minute in size. If surgery is recommended, patients and family should be informed that direct intervention typically mimics the course of a hemorrhagic event. That is, patients should expect to suffer transient, mild but discernible, neurologic deficits following surgery. Most patients, however, return to their baseline preoperative function during follow-up.⁷

Fig. 10.1 Histology demonstrates dilated, sinusoidal veins and the absence of smooth muscle layers. (Courtesy of Barrow Neurological Institute.)

♦ Surgical Approach

Once the decision to pursue surgery has been made, the surgical approach is chosen by using the two-point method (Fig. 10.3).^7,19 Extending a line from the center of the lesion through the nearest point of contact with a pial surface or surgical corridor demonstrates the optimal surgical approach. This method maximizes exposure and minimizes transit through eloquent brain tissue. For posterolateral midbrain lesions, we prefer either a subtemporal or supracerebellar-infratentorial approach.^20,21 Anterior pontine lesions are accessible through a transsylvian, orbitozygomatic, or retrosigmoid corridor. Lower brainstem lesions are approached via a midline suboccipital or far-lateral craniotomy depending on their precise location (Fig. 10.4).

Fig. 10.2 Cavernous malformation involving the seventh and eighth cranial nerve complex was confirmed histologically. Numerous other cavernous malformations were present throughout the brain. Cavernous malformations involving the cranial nerves can have the typical heterogenous appearance on magnetic resonance imaging (MRI). Alternatively, as in this case, they can enhance and mimic a neoplastic process. (Courtesy of Barrow Neurological Institute.)

♦ Microsurgical Technique

After the appropriate approach has been selected, several important technical issues involving microdissection of posterior fossa cavernous malformations must be considered. For lesions that reach a pial surface, the malformation is easily visualized before surgical manipulation. A simple corticectomy can be performed directly over the lesion, followed by microdissection around its borders. We favor microdissectors (Synergetics USA, St. Louis, MO) that offer a variety of instrument angles and microcurette tip sizes to facilitate resection. It is imperative to maintain the plane around the lesion itself without violating the thin-walled, sinusoidal veins of the posterior fossa cavernous malformation or disrupting normal adjacent (usually hemosiderin-stained) brain tissue.

For lesions just beneath the pial surface or buried by overlying parenchyma, we routinely use neuronavigation (Stealth Station; Medtronic SNT, Louisville, CO) as an essential adjunctive tool for locating the lesion. Preoperative diffusion tensor imaging (DTI), which visualizes major white matter tracts, can aid in the selection of a surgical approach by determining which tracts are at risk during dissection and lesion removal.22,23 This technology can also be applied to intraoperative neuronavigation, with the hope of reducing postoperative neurologic deficits.²⁴ Intraoperative nerve stimulation of the cranial nerve VII can be useful when treating lesions adjacent to the floor of the fourth ventricle.

Fig. 10.3 Two-point method. A line connects the center of the lesions with the nearest point on the surface. This trajectory determines the optimal approach for resection. (Courtesy of Barrow Neurological Institute.)

For posterior fossa cavernous malformations deep to the pial surface, a fundamental understanding of access zones in the brainstem is required to enter lesions adjacent to eloquent brainstem structures while minimizing residual deficits (Fig. 10.5).²⁵ We advocate an extralesional dissection and excision of the lesion when possible. If a cavernoma is entered inadvertently, the thin walls of the lesion will collapse, which renders them difficult to identify and dissect from the walls, and risks leaving residual malformation. Once the lesion has been resected, a thorough final inspection of the walls ensures that no residual remains. Bipolar cauterization for hemostasis is used only sparingly to minimize tissue damage. Procoagulant agents such as Nu-Knit (Johnson & Johnson, Arlington, TX) or FloSeal (Baxter Healthcare, Fremont, CA) are preferred.

Frequently, a venous angioma is encountered during microdissection (Fig. 10.6). This association is well described,²⁶ and a popular theory places cavernous malformations, venous angiomas, and capillary telangiectasias along the same pathophysiologic spectrum.²⁷ It is imperative to distinguish this entity from the cavernous malformations itself. Inadvertent injury or resection can lead to devastating venous infarction.

Typically, we obtain postoperative MRIs to serve as a baseline for future comparisons. A 1-year postoperative MRI is followed by regular scans at increasing intervals to monitor for the rare possibility of recurrence. After 10 years of follow-up, patients are advised to obtain imaging studies only if symptoms recur.

Our previously published surgical experience⁷ with 100 patients with brainstem cavernous malformations yielded 87% favorable outcomes, 9% worsening of neurologic deficits, and 4% mortality. These results are consistent with data from other series.^4,28^–³⁰ Comparatively, our untreated cohort of 83 brainstem cavernous malformations have fared worse, with 65% favorable, 33% worse than at presentation, and 2% mortality.²¹ Permanent complications have ranged from 12 to 70%.^6,7,29,31 These data stress the importance of careful patient selection before exercising surgical options. The surgical risks also must be weighed against the poor natural clinical history of brainstem cavernous malformations when compared with supratentorial lesions. Using judicious inclusion criteria and careful microsurgical technique, these lesions can be resected with acceptable results (Fig. 10.7).

♦ Radiosurgery

The effect of stereotactic radiosurgery on cavernous malformations remains controversial. Several studies have demonstrated a potential beneficial effect of radiation therapy, stereotactic proton-beam therapy, or stereotactic radiosurgery on the hemorrhage rate associated with cavernous malformations.^29,32,33 Hasegawa et al³⁴ documented a dramatic reduction in hemorrhage rate from 33.9% per year before gamma knife radiosurgery (GKRS; mean pre-GKRS follow-up of 4.33 years) to 12.3% per year in the first 2 years after GKRS. This rate dropped to 0.76% per year during the 2nd through 12th years of follow-up. In this series, the radiosurgical morbidity rate was 13.4%. Similarly, Pollock et al³⁵ reported a significant reduction in the annual hemorrhage rate from 40% to 2.9% after 2 years of follow-up. However, their rate of treatment morbidity was 41%. Finally, a large series by Lunsford et al³⁶ showed that patients with hemorrhagic or symptomatic lesions in deep or highly eloquent structures treated with GKRS had a significant reduction in hemorrhage rate from 32.5% to 10.8% per year for the first 2 years after treatment. The rate was reduced to 1.06% annually thereafter with up to 20 years of follow-up. Treatment morbidity was 13.5%.

Whether GKRS really affects cavernous malformations is confounded by multiple variables, including the effect of temporal clustering of hemorrhages on outcome after GKRS, relatively short follow-up periods, population or referral selection biases toward GKRS, and the lack of histologic evidence of radiation-induced changes. It is important to recognize that radiosurgery, particularly in the posterior fossa, subjects patients to a modest but significant risk of morbidity, whereas the effect on the lesion itself is only poorly understood. Future long-term follow-up studies may better elucidate the potential benefits of radiosurgery. Based on current evidence and our clinical experience, we do not recommend radio-surgery as a primary treatment option to our patients.

Fig. 10.4 Surgical approaches to the . brainstem. (Courtesy of Barrow Neurological Institute.)

Fig. 10.5 Annotated lines indicate relative safe entry zones into the brainstem when cavernomas lie beneath the pial surface. (A) Lateral view. (B) Posterior view. (Courtesy of Barrow Neurological Institute.)

Fig. 10.6 MRI of a classic venous angioma associated with a cavernous malformation (arrow). (Courtesy of Barrow Neurological Institute.)

Fig. 10.7 Mesencephalic brainstem cavernous malformation. Two-point method favors either a subtemporal or lateral supracerebellar infratentorial approach; the latter was used in this case. A safe entry zone in the posterolateral midbrain, lateral to the tectal plate, was chosen as the entry point. (Courtesy of Barrow Neurological Institute.)

♦ Dural Fistulas of the Posterior Fossa

Like cavernous malformations, dural arteriovenous fistulas (dAVFs) are uncommon entities of the posterior fossa that can manifest incidentally, secondary to neurologic symptoms, or due to frank hemorrhage. They account for 10 to 15% of all intracranial vascular lesions.37^–⁴¹ The transverse-sigmoid sinus (38%) is the most common location of dAVFs, followed by the cavernous sinus (34%). Less common locations include the superior sagittal sinus (5%), ethmoidal sinus (4%), superior and inferior petrosal sinuses (5% and 3%, respectively), and marginal sinus (4%).^42,43

The most common symptom at presentation is headache. However, bruits, visual symptoms, venous infarction, and intracranial hemorrhage are well described.^44,45 dAVFs are also associated with trauma, chronic venous hypertension, middle ear infections, surgery of the venous sinus, or sinus occlusion.⁴² Dural sinus thrombosis is strongly correlated with the pathophysiology of dAVF formation and persistence. Once the venous system is subjected to arterialized pressures from the fistula, ensuing venous hypertension can lead to leptomeningeal venous drainage, venous varices, and subsequent risk for hemorrhagic or ischemic events. The link with angiogenic growth factors has been described in animal models,32,46 the inhibition of which might serve as a potential treatment avenue in the future. Nonetheless, most patients have no antecedent history to explain the formation of the lesion.

A multivariate analysis of more than 100 cases^47,48 demonstrated that leptomeningeal or galenic (deep) venous drainage pattern and venous varix formation significantly correlated with aggressive behavior and poor outcome. Using angioarchitectural features, grading scales have been formulated to predict the risk of neurologic symptoms or hemorrhage.⁴⁹^–⁵² The University of California–San Francisco (UCSF) scale describes four grades of dAVFs.⁴⁹ Grade 1 lesions exhibit anterograde drainage via normal sinus pathways. Grade 2 lesions demonstrate antero-and retrograde venous drainage with or without cortical venous drainage. Grade 3 lesions have retrograde venous drainage related to an occluded sinus. Grade 4 lesions have only cortical venous drainage. According to the UCSF data, hemorrhage occurred in 31% of grade 3 and in 100% of grade 4 lesions.

The Cognard classification describes five types of dAVFs delineating location, direction of flow, and drainage patterns.⁵⁰ Type 1 lesions have antegrade drainage into a dural venous sinus. Type 2 lesions are divided into three subtypes: type 2A lesions have direct retrograde drainage into a dural sinus; type 2B lesions flow antegrade into a dural sinus with retrograde cortical venous drainage; and type 2A+B lesions have retrograde flow into a dural sinus with retrograde cortical drainage. Type 3 lesions drain directly into nonectatic cortical veins. Type 4 lesions have direct ectatic cortical venous drainage. Type 5 lesions have retrograde drainage into spinal perimedullary veins and are classified further as spinal dAVFs.⁵³

Borden et al⁵¹ classified dAVFs into three types based on patterns of venous drainage. Type I lesions drain antegrade directly into a major venous dural sinus. Type II lesions drain into the venous dural sinus with retrograde drainage into subarachnoid veins. Type III lesions drain retrograde into cortical veins. Types II and III are associated with significant venous hypertension and are considered at high risk for hemorrhage. We typically use the Borden classification system and refer to dAVFs using this classification in this chapter’s discussion.

♦ Natural History and Treatment Algorithm

The decision to treat dAVFs can depend on a several factors, including the patient’s symptoms, presence of hemorrhage, location of the fistula, its angiographic features, and changes in the lesion over time.^{39,40,42,49,51,54}^–⁵⁶ Borden type I dAVFs are thought to have a benign natural history, with one series⁵⁷ showing only one hemorrhage in 68 untreated patients followed for at least 27 months. However, type I lesions carry a 2% risk of progression to a higher grade.^57,58 This progression is not always heralded by new symptoms.

Higher-grade dAVFs are considered more dangerous. Van Dijk et al⁵⁹ followed 20 patients with type II or III dAVFs over a total of 87 patient-years, calculating an 8% risk of hemorrhage and 10% risk of death on an annual basis. This and other studies have justified the aggressive treatment of type II or III lesions, especially when symptomatic.^56,60,61 Study of asymptomatic patients with high-risk angiographic features, such as cortical venous drainage (CVD) with distal sinus stenosis or deep venous drainage, demonstrated a high annualized risk of hemorrhage.^59,62,63 However, recent natural history data from Strom et al⁶⁴ of type II or III dAVFs demonstrated that lesions exhibiting asymptomatic CVD follow a more benign course than similar lesions with symptomatic CVD (1.4% versus 19% per year event rate). Similarly, Söderman et al⁶⁰ followed 85 patients with dAVF and CVD and found the annual risk of hemorrhage varied depending on hemorrhage at presentation: 7.5% per year for patients presenting with hemorrhage, and only 1.5% per year for patients without. The presence of high-risk features requires careful consideration when determining treatment strategy.

Patients with low-risk dAVFs and no associated neurologic symptoms can be observed and should undergo regular angiographic follow-up. Low-risk dAVFs associated with flow-related headaches, orbital symptoms, or bruits that impair the quality of life may be treated with carotid compressive therapy^45,65^–⁶⁸ or palliative transarterial embolization. The goal of treatment of high-risk dAVFs is complete obliteration; however, high-grade lesions with complex or inaccessible features are sometimes treated with surgical or endovascular disconnection of the cortical venous drainage.^69,70 This leaves the fistula intact, converting a high-risk dAVF to a more benign lesion, although this outcome is not as favorable as complete resection or obliteration. As with cavernous malformations, treatment recommendations should be based on both clinical presentation and angiographic features.

♦ Surgical Approach and Microsurgical Technique

The key to successful surgical management of posterior fossa dAVFs is appropriate angiographic identification of the fistulous connection. Careful evaluation of the primary source on angiographic images enables the surgeon to identify the exact point at which arterial blood flow from the extracranial circulation enters the venous circulation. Knowing this exact location, the fistula can be localized within the posterior fossa (i.e., transverse-sigmoid junction, torcular Herophili, superior petrosal sinus, etc.). Once the location is determined, the appropriate surgical approach can be chosen. Almost all posterior fossa dAVFs can be accessed through a retrosigmoid, supratentorial-infratentorial, or lateral suboccipital craniotomy (Figs. 10.8 and 10.9).⁷¹

Intraoperatively, careful exploration allows the artery feeding the fistula to be identified. At this point, simple ligation of the fistula is performed with arteriovenous malformation (AVM) clips. Numerous tiny arterial feeding branches may be observed in the vicinity of the fistula. These branches may be ligated at surgery, but disruption of the main fistula is sufficient to obliterate the entire lesion.^72,73 If multiple small-to-medium feeders that cannot be reached easily are present, preoperative transarterial embolization is helpful. When external ligation is not technically feasible, direct embolization of the fistula with muslin packing is a useful technique. Intraoperative angiography is extremely useful to confirm complete obliteration before closure. Close clinical and angiographic follow-up is warranted to check for recurrences.

Fig. 10.8 (A) Torcular dural arteriovenous fistula (dAVF) approached via suboccipital craniotomy. (B) Postoperative obliteration of the dAVF by direct clipping of the fistulous connection. (Courtesy of Barrow Neurological Institute.)

♦ Endovascular Treatment

At our institution, endovascular treatment options for dAVFs are usually explored first. Careful patient selection for endovascular therapy is paramount. Even with contemporary techniques, specific angiographic features make some dAVFs better suited for stand-alone endovascular treatment and others better suited for combined endovascular, surgical, and/or radiosurgical treatment. If a fistula has normal anterograde sinus drainage, every effort must be made to maintain the patency of the parent sinus. Inadvertent occlusion of the parent dural sinus may be poorly tolerated and can lead to severe venous outflow obstruction and venous infarction. Caragine et al 74 presented a series of patients with transverse-sigmoid junction dAVFs associated with a venous pouch parallel to the parent sinus. By recognizing this separate, parallel channel, the endovascular surgeon can safely embolize the venous pouch, preserve the parent sinus, and cure the patient.

Lesions with parent sinus occlusion distal to the fistula can be obliterated with coiling of the sinus at the fistulous connection because there is a lower risk of losing important distal venous drainage. Local venous anatomy must be delineated for each case before executing parent sinus embolization. Alternatively, if the venous route to the dAVF is blocked by occlusion or if there is direct communication between the dAVF and a cortical vein, it is usually preferable to surgically obliterate the fistula directly.⁷⁵ In such cases intraoperative direct puncture embolization of the fistula is another option.⁷⁶

Prior to the advent of nonadhesive liquid embolic agents (such as Onyx; see below), endovascular treatment of dAVFs typically involved staged transarterial embolization of dAVF feeders followed by transvenous coiling. Smaller feeding branches could be obliterated with liquid adhesives agents such as N-butyl cyanoacrylate (NBCA), whereas larger arterial feeders were left intact for “road-mapping” purposes and for angiographic verification that subsequent transvenous coiling or surgical ligation has obliterated the fistula. This technique is still commonly used as primary treatment in many centers and in cases where curative transarterial Onyx embolization is not feasible.⁷⁷

Onyx (ev3 Endovascular, Plymouth, MN), a nonadhesive liquid embolic agent originally approved for the endovascular occlusion of arteriovenous malformations, is an emerging endovascular treatment for dAVFs. Onyx is cohesive, rather than adhesive, and is considered a more controllable and less rapid form of embolization compared with NBCA. Stiefel et al⁷⁸ treated 28 patients with dAVFs of various grades, achieving angiographic cure in 21. Similar results were obtained by Cognard et al⁷⁹ in their series of 30 patients. Several other series have described excellent short-and long-term cure rates with Onyx treatment of dAVF.⁸⁰^–⁸² Long-term angiographic and clinical follow-up of such treatments is needed to confirm the durable efficacy of Onyx embolization.

♦ Surgical Treatment

For those dAVFs where definitive endovascular occlusion cannot be safely obtained, surgical ligation is necessary. Similar to multimodality treatment in arteriovenous malformations,⁸³ preoperative embolization of arterial connections, particularly in surgically inaccessible areas, can facilitate the surgeon’s task of dissecting and ligating the main fistula (Fig. 10.10). If a combined approach is warranted, embolization of arteries with significant scalp supply (superficial temporal, occipital, posterior auricular) is avoided to prevent possible skin necrosis after surgery.⁸⁴ Instead, middle meningeal artery feeders are targeted and embolized.

Fig. 10.9 Anteroposterior (A) and lateral (B) angiograms showing a tentorial dAVF. (C) Postoperative angiogram after retrosigmoid craniotomy and direct clipping of the fistulous connection shows excellent obliteration of the lesion. (Courtesy of Barrow Neurological Institute.)

Surgical obliteration of dAVFs has a high success rate. The best surgical approach is matched to the location of the lesion. Meticulous skeletonization of the associated dural sinus is required, including disconnection of feeders from the tentorium and falx where applicable. In 23 patients with highgrade dAVFs treated with surgery with or without preoperative embolization, Liu et al 72 reported complete angiographic obliteration and no perioperative complications or further clinical events with up to 84 months of follow-up. Another series of 17 patients with high-grade dAVFs treated with surgery alone showed angiographic cure in 16.⁸⁵ Collice et al⁸⁶ described complete angiographic cure in 34 patients treated with surgery with or without embolization. Overall, surgery is considered a safe and effective treatment for dAVFs, particularly when embolization is not feasible or curative.

Fig. 10.10 (A) Left transverse-sigmoid sinus region dAVF with primary cortical venous drainage and obstruction of transverse sinus outflow. (B) Scout film after preoperative embolization. (C) Postembolization angiogram shows significant reduction of several of the occipital artery feeders. Residual feeders are present due to endovascular inaccessibility. (Courtesy of Barrow Neurological Institute.)

♦ Radiosurgery

Recent data have suggested that GKRS, either with or without tandem transarterial embolization, may provide therapeutic relief of symptoms and potentially promote the obliteration of fistulas.87^–⁸⁹ Pan et al⁸⁷ reported that over a median follow-up of 19 months, 58% of patients were angiographically cured after GKRS at a dose of 16.5 to 19 Gy at the 50 to 70% isodose line. Friedman et al⁸⁸ described 25 radiosurgery patients, 22 of whom also received transarterial embolization. Of these patients, 17 ultimately underwent angiographic follow-up, and 11 patients demonstrated “total or near total (>90%) obliteration.” All but one patient experienced immediate relief of symptoms. Söderman et al⁹⁰ studied GKRS in 53 patients with dAVFs and reported an angiographic cure rate of 68% at 2 years. Wu et al⁹¹ studied GKRS in 81 patients with dAVFs and found complete or partial symptomatic relief in 75 after treatment. However, angiographic cure at 24 months was only 50% and was slightly less in patients with high-grade lesions. Although the clinical outcome of patients treated with GKRS seems to be better than the natural history of untreated patients, relief of symptoms is not directly comparable to a surgical or endovascular cure. Nonetheless, this modality is recognized as a useful adjuvant or stand-alone treatment of dAVFs. Posterior fossa dAVFs commonly recruit feeding arteries from petrosal and tentorial collaterals. The former typically derive from branches of the neuromeningeal branch of the ascending pharyngeal artery. These are usually unsafe for embolization due to well-known collateral branches to the cranial nerves. The latter can have significant contributions from the tentorial branch of the meningohypophyseal trunk. Typically, due to the high tortuosity of this vessel, embolization is not feasible. Therefore, GKRS is ideally suited for high-risk transpetrosal or skull-based dAVFs that cannot be safely treated with embolization due to potential collateral arterial feeders to the posterior circulation and cranial nerves or that are poorly accessible surgically.