Intracranial dural arteriovenous fistulas with spinal venous drainage: relation between clinical presentation and angiographic findings.

PURPOSETo investigate why some patients with an intracranial dural arteriovenous fistula (DAVF) with spinal venous drainage have myelopathy and others do not.METHODSWe reviewed the clinical and radiologic data for 12 patients who had a DAVF with spinal venous drainage diagnosed at our institutions from 1982 to 1995.RESULTSSix patients had progressive spinal cord indications of disease (patients with myelopathy) and six others (patients without myelopathy) had cerebral indications (five had intracranial hemorrhage and one had a seizure). Cerebral angiography showed a posterior fossa DAVF with spinal venous drainage in all cases. The clinical presentation of DAVFs with spinal venous drainage was compared with the extent of the drainage. In patients without myelopathy, the spinal venous drainage exited the intradural canal via the cervical medullary-radicular veins and was therefore limited to the cervical perimedullary veins. In patients with myelopathy, no medullary-radicular vein was seen, and the venous drainage descended along the perimedullary veins of the entire spinal cord toward the conus medullaris.CONCLUSIONWe found an exact relation between clinical presentation and venous drainage of DAVFs with spinal venous drainage. Patients had no myelopathy when the venous drainage was limited to the cervical cord; myelopathy was present when the venous drainage descended toward the conus medullaris.     

Quantifying the Cerebral Hemodynamics of Dural Arteriovenous Fistula in Transverse Sigmoid Sinus Complicated by Sinus Stenosis: A Retrospective Cohort Study

BACKGROUND AND PURPOSE:Sinus stenosis occasionally occurs in dural arteriovenous fistulas. Sinus stenosis impedes venous outflow and aggravates intracranial hypertension by reversing cortical venous drainage. This study aimed to analyze the likelihood of sinus stenosis and its impact on cerebral hemodynamics of various types of dural arteriovenous fistulas.MATERIALS AND METHODS:Forty-three cases of dural arteriovenous fistula in the transverse-sigmoid sinus were reviewed and divided into 3 groups: Cognard type I, type IIa, and types with cortical venous drainage. Sinus stenosis and the double peak sign (occurrence of 2 peaks in the time-density curve of the ipsilateral drainage of the internal jugular vein) in dural arteriovenous fistula were evaluated. “TTP” was defined as the time at which a selected angiographic point reached maximum concentration. TTP of the vein of Labbé, TTP of the ipsilateral normal transverse sinus, trans-fistula time, and trans-stenotic time were compared across the 3 groups.RESULTS:Thirty-six percent of type I, 100% of type IIa, and 84% of types with cortical venous drainage had sinus stenosis. All sinus stenosis cases demonstrated loss of the double peak sign that occurs in dural arteriovenous fistula. Trans-fistula time (2.09 seconds) and trans-stenotic time (0.67 seconds) in types with cortical venous drainage were the most prolonged, followed by those in type IIa and type I. TTP of the vein of Labbé was significantly shorter in types with cortical venous drainage. Six patients with types with cortical venous drainage underwent venoplasty and stent placement, and 4 were downgraded to type IIa.CONCLUSIONS:Sinus stenosis indicated dysfunction of venous drainage and is more often encountered in dural arteriovenous fistula with more aggressive types. Venoplasty ameliorates cortical venous drainage in dural arteriovenous fistulas and serves as a bridge treatment to stereotactic radiosurgery in most cases.

Dural arteriovenous fistulas (DAVFs) account for 10%–15% of intracranial vascular malformations.^1,2 The most common location of an intracranial DAVF is the cavernous sinus, followed by the transverse-sigmoid sinus.^1–3 Major DAVF classification systems, such as the Cognard and Borden systems, grade DAVFs on the basis of venous drainage patterns, in which the presence of retrograde cortical venous drainage (CVD) indicates a higher risk of hemorrhage.^4–7 Cases of venous outlet obstruction playing a role in transforming benign (without CVD) into malignant DAVFs (with CVD) have been reported in the literature.⁸ Sinus stenosis (SS) is frequently associated with idiopathic intracranial hypertension.^9,10 Nevertheless, the incidence of SS and its association with DAVFs have not been thoroughly explored. SS can be found in DAVFs with retrograde or antegrade sinus flow, but its impact on cerebral hemodynamics has rarely been discussed. Theoretically, stenotic and thrombosed sinuses impede the venous outflow, and a DAVF itself increases overall blood volume in the affected sinus; the combination of the 2 hemodynamic disorders adversely affects venous flow and subsequently increases intracranial pressure and the risk of intracranial hemorrhage.Current treatment strategies for DAVFs in the transverse sinus include microsurgery, endovascular treatment, stereotactic radiosurgery (SRS), or their combinations.^11–13 Endovascular treatment has been the treatment of choice for DAVFs with CVD because it provides immediate curative results and minimizes the risk of hemorrhage.^14–16 Nevertheless, the complication rate of endovascular treatment is higher than that of SRS.^14,17,18 By contrast, SRS has hardly any periprocedural risks and achieves DAVF cure rates of between 58% and 73%. Although SRS can reduce the bleeding rate from 20% to 2% after shunting has been totally closed,¹⁹ the latent period for SRS ranges from 1 to 3 years and carries a 4.1% hemorrhagic rate in DAVFs with CVD.^3,20 Therefore, SRS is usually preferred for cases without CVD, and endovascular treatment is more suitable for immediately minimizing the risk of hemorrhage.Several studies have proposed a reconstructive method by using venoplasty and stent placement in combination with transarterial embolization to ameliorate or even cure DAVFs with venous outlet obstruction.^21–23 We wondered whether this approach could downgrade DAVFs with CVD—that is, to restore their normal cortical venous drainage and make them eligible for SRS, thereby minimizing the risk of hemorrhage during the latent period. Therefore, the purpose of the current study was to clarify the following: 1) the incidence of SS in different grades of DAVF in the transverse sigmoid sinus, 2) the impact of SS on DAVF hemodynamics by using quantitative DSA, and 3) the initial treatment results of venoplasty and/or stent placement followed by SRS.     

Dural arteriovenous fistulas with cortical venous drainage: incidence, clinical presentation, and treatment

BACKGROUND AND PURPOSE: Our purpose was to report our experience with intracranial dural arteriovenous fistulas (DAVFs) with cortical venous drainage during a 12-year period. PATIENTS AND METHODS: Between January 1994 and January 2006, 91 patients with intracranial DAVFs presented at our institution, and 29 (32%) had cortical venous drainage. There were 5 women and 24 men (mean age, 53.9 years; range, 24-77). Clinical presentation was intraparenchymal or subarachnoid hemorrhage in 18 patients (62%), seizures in 4 patients (14%), visual symptoms in 2 patients (7%), pulsatile bruit in 1 patient (3%), and the DAVF (14%) was incidentally discovered in 4 patients. RESULTS: In 2 patients, the DAVF had been obliterated spontaneously at the time of scheduled embolization 10 and 2 months after hemorrhage, respectively. Five patients with an anterior fossa DAVF underwent successful surgery. In 14 patients, the DAVF was completely occluded with embolization alone, and in 7 patients, embolization was followed by surgery. Altogether, complete occlusion was angiographically confirmed in 28 of 29 DAVFs; the result of radiosurgery of 1 DAVF is pending. There were no complications of surgery; embolization was complicated by postembolization hemorrhage in 1 patient (3%). CONCLUSION: Most DAVFs with cortical venous drainage have an aggressive clinical course. Treatment by a neurovascular team by using surgery, embolization, or a combination resulted in cure in all cases, with a very low complication rate.     

Progressive versus Nonprogressive Intracranial Dural Arteriovenous Fistulas: Characteristics and Outcomes

BACKGROUND AND PURPOSE:A minority of intracranial dural arteriovenous fistulas progress with time. We sought to determine features that predict progression and define outcomes of patients with progressive dural arteriovenous fistulas.MATERIALS AND METHODS:We performed a retrospective imaging and clinical record review of patients with intracranial dural arteriovenous fistula evaluated at our hospital.RESULTS:Of 579 patients with intracranial dural arteriovenous fistulas, 545 had 1 fistula (mean age, 45 ± 23 years) and 34 (5.9%) had enlarging, de novo, multiple, or recurrent fistulas (mean age, 53 ± 20 years; P = .11). Among these 34 patients, 19 had progressive dural arteriovenous fistulas with de novo fistulas or fistula enlargement with time (mean age, 36 ± 25 years; progressive group) and 15 had multiple or recurrent but nonprogressive fistulas (mean age, 57 ± 13 years; P = .0059, nonprogressive group). Whereas all 6 children had fistula progression, only 13/28 adults (P = .020) progressed. Angioarchitectural correlates to chronically elevated intracranial venous pressures, including venous sinus dilation (41% versus 7%, P = .045) and pseudophlebitic cortical venous pattern (P = .048), were more common in patients with progressive disease than in those without progression. Patients with progressive disease received more treatments than those without progression (median, 5 versus 3; P = .0068), but as a group, they did not demonstrate worse clinical outcomes (median mRS, 1 and 1; P = .39). However, 3 young patients died from intracranial venous hypertension and intracranial hemorrhage related to progression of their fistulas despite extensive endovascular, surgical, and radiosurgical treatments.CONCLUSIONS:Few patients with dural arteriovenous fistulas follow an aggressive, progressive clinical course despite treatment. Younger age at initial presentation and angioarchitectural correlates to venous hypertension may help identify these patients prospectively.

Intracranial dural arteriovenous fistulas (DAVFs) are rare arteriovenous shunts involving the epidural space and adjacent dura mater, which receive arterial supply from meningeal vessels and drain directly to dural venous sinuses or cortical veins.¹ In the early days of cerebral angiography, DAVFs were considered a subset of AVMs: Newton and Cronqvist² classified AVMs by arterial supply as pure dural, mixed pial-dural, or pure pial malformations. Unlike brain AVMs, however, DAVFs are most often thought to be acquired (as opposed to congenital), and DAVFs lack a nidus of vessels in the brain parenchyma. DAVF is also distinguished from nongalenic pial arteriovenous fistula by its fistula location in the dura.Management of a DAVF is based on its expected clinical course: Fistulas demonstrating cortical venous drainage (CVD) generally warrant curative therapy to prevent intracranial hemorrhage, and fistulas without CVD are managed for either symptom palliation or cure.^3–6 Treatment modalities include transarterial or transvenous endovascular embolization to occlude the arteriovenous fistula site, microsurgical interruption of the fistula site, stereotactic radiosurgery, or multimodality therapy. Endovascular procedures are used to treat a most DAVFs and are the treatment of choice for lesions accessible to catheterization.^5,6A small number of patients with DAVFs respond poorly to conventional therapies and demonstrate progressive neurologic and angiographic deterioration with enlargement of existing fistulas, formation of de novo fistulas, and development of features that increase the risk of intracranial hemorrhage.⁷ Reports of such rapidly progressive “runaway” DAVFs are scarce. Only a few cases have been published in the past 15 years; therefore, the pathogenesis, presentation, clinical course, and treatment remain unclear.^4,8–12 The purpose of this single-institution retrospective cohort study was to compare the clinical characteristics, angioarchitecture, and treatment outcomes of patients with progressive (enlarging fistulas or developing de novo fistulas) versus nonprogressive (recurrent original fistula or the presence of multiple unchanging fistulas) intracranial DAVFs.     

Preliminary experience with onyx embolization for the treatment of intracranial dural arteriovenous fistulas

BACKGROUND AND PURPOSE: Onyx was recently approved for the treatment of pial arteriovenous malformations, but its use to treat dural arteriovenous fistulas (DAVFs) is not yet well established. We now report on the treatment of intracranial DAVFs using this nonadhesive liquid embolic agent.MATERIALS AND METHODS: We performed a retrospective analysis of 12 consecutive patients with intracranial DAVFs who were treated with Onyx as the single treatment technique at our institution between March 2006 and February 2007.RESULTS: A total of 17 procedures were performed in 12 patients. In all of the cases, transarterial microcatheterization was performed, and Onyx-18 or a combination of Onyx-18/Onyx-34 was used. Eight patients were men. The mean age was 56 ± 12 years. Nine patients were symptomatic. There was an average of 5 feeders per DAVF (range, 1–9). Cortical venous reflux was present in all of the cases except for 1 of the symptomatic patients. Complete resolution of the DAVF on immediate posttreatment angiography was achieved in 10 patients. The remaining 2 patients had only minimal residual shunting postembolization, 1 of whom appeared cured on a follow-up angiogram 8 weeks later. The other patient has not yet had angiographic follow-up. Follow-up angiography (mean, 4.4 months) is currently available in 9 patients. There was 1 angiographic recurrence (asymptomatic), which was subsequently re-embolized with complete occlusion of the fistula and its draining vein. There was no significant morbidity or mortality.CONCLUSION: In our experience, the endovascular treatment of intracranial DAVFs with Onyx is feasible, safe, and highly effective with a small recurrence rate in the short-term follow-up.

Dural arteriovenous fistulas (DAVFs) are acquired abnormal arteriovenous connections within the dura that account for 10%–15% of all intracranial arteriovenous malformations (AVMs).¹ The origin of these malformations is not entirely understood but has been associated with several conditions including venous thrombosis, intracranial surgery, tumor, puerperium, and trauma.² DAVFs may be asymptomatic or present with symptoms that range from tinnitus to intracranial hemorrhage (ICH) and severe neurologic deficits. Their behavior is fundamentally determined by the venous drainage pattern. Retrograde leptomeningeal or cortical venous drainage has a strong correlation with adverse clinical events: such patients are thought to have an annual risk of aggressive neurologic presentation of 15% resulting in an annual mortality of 10.4%.³ Moreover, rebleeding rates may be as high as 35% over the first 2 weeks after the initial hemorrhage.⁴ Thus, the DAVFs that have these features require treatment.The current management of DAVFs includes endovascular, surgical, and radiosurgical treatments, either alone or in combination. Endovascular therapy is typically performed with cyanoacrylate, ethyl alcohol, coils, and/or particles. Onyx (ev3, Irvine, Calif), an ethylene vinyl alcohol copolymer preparation, was recently approved for the treatment of pial AVMs, but its use to treat DAVFs is not yet well established. We report our preliminary experience with the endovascular treatment of intracranial DAVFs using this nonadhesive liquid embolic agent.     

Regional cerebral blood flow after acetazolamide challenge in patients with dural arteriovenous fistula: simple way to evaluate intracranial venous hypertension

BACKGROUND AND PURPOSE: Because venous hypertension determines the clinical severity of dural arteriovenous fistulas (DAVFs), evaluation of intracranial venous pressure is important in making decisions concerning treatment. We determined whether intracranial venous hypertension could be quantified by using an acetazolamide test in a manner that indicates whether treatment of the DAVF is necessary. METHODS: We enrolled 21 untreated patients: 11 with a sigmoid and/or transverse DAVF, six with a cavernous DAVF, two with an anterior cranial fossa DAVF, and two with a superior sagittal sinus DAVF. Cerebral hemodynamics were studied with stable-xenon CT. Patients were angiographically classified into three groups, and regional cerebral blood flow (rCBF) after acetazolamide challenge was compared between angiographic groups, between patients with and those without symptoms attributable to intracranial venous hypertension, and between preembolization and postembolization examinations. RESULTS: A high angiographic grade was associated with decreased resting rCBF and a blunted response to acetazolamide. Response to acetazolamide was more sensitive to venous hypertension, as angiographically assessed, than decreased resting rCBF. Resting rCBF and the increase in rCBF associated with acetazolamide were significantly lower in the symptomatic group than in the asymptomatic group. Treatment of the DAVF significantly enhanced the increased rCBF due to the acetazolamide challenge. CONCLUSION: Cerebral venous hypertension in DAVF reduced the response to acetazolamide, as shown on stable-Xe CT. Therefore, a patient with DAVF and a reduced rCBF response to acetazolamide requires treatment irrespective of his or her symptoms.     

MR imaging of dural arteriovenous fistulas draining into cerebellar cortical veins

BACKGROUND AND PURPOSE: Retrograde leptomeningeal venous drainage (RLVD) in a dural arteriovenous fistula (DAVF) is associated with intracerebral hemorrhage, nonhemorrhagic neurologic deficit, or death, and recognizing the presence of this drainage is important. We investigated the MR findings of DAVFs draining into cerebellar cortical veins and compared these findings with those of conventional angiography. METHODS: The MR and angiographic findings of six patients (five men, one woman; mean age, 73.4 years) with DAVF with RLVD into cerebellar cortical veins were reviewed retrospectively. Signal intensity characteristics, contrast material enhancement, topography of the lesion, and presence of signal voids were evaluated on MR images. Site of the shunt, feeding arteries, and draining veins were evaluated on angiograms. RESULTS: In all patients, MR images showed high signal intensity on T2-weighted images and peripheral enhancement on gadolinium-enhanced T1-weighted images at the inferior aspect of the cerebellar hemisphere. A combination of posterior meningeal and occipital arteries was the most frequent blood supply (83%) for these DAVFs. In all six patients, the inferior hemispheric vein was the primary draining vein. CONCLUSION: The characteristic MR findings of DAVF draining into cerebellar cortical veins represent venous congestive encephalopathy in the territory of the involved cortical vein.     

Intracranial dural arteriovenous fistulas: classification, imaging findings, and treatment

Intracranial DAVFs are pathologic dural-based shunts and account for 10%-15% of all intracranial arteriovenous malformations. These malformations derive their arterial supply primarily from meningeal vessels, and the venous drainage is either via dural venous sinuses or through the cortical veins. DAVFs have a reported association with dural sinus thrombosis, venous hypertension, previous craniotomy, and trauma, though many lesions are idiopathic. The diagnosis is dependent on a high level of clinical suspicion and high-resolution imaging. Cross-sectional imaging techniques by using CT and MR imaging aid in the diagnosis, but conventional angiography remains the most accurate method for complete characterization and classification of DAVFs. The pattern of venous drainage observed on dynamic vascular imaging determines the type of DAVF and correlates with the severity of symptoms and the risk of hemorrhage.     

Embolization of intracranial dural arteriovenous fistulas with Onyx-18

Background and purpose

The use of Onyx in the treatment of AVMs has been reported in the literature, but experience in the treatment of DAVF is lacking. We report the clinical outcome obtained in the treatment of dural arteriovenous fistulas (DAVFs) using a new liquid embolic agent, Onyx-18.

Methods

The present series included 21 patients; 9 had DAVFs draining directly into the cortical veins, 6 had DAVFs draining directly into the dural sinus, 4 had DAVFs draining through the ophthalmic veins and 2 had DAVFs involving the dural sinus with leptomeningeal retrograde venous drainage Clinical data were extracted from hospital files and all patients were followed.

Results

In 14 patients (70%) there was complete angiographic elimination of the shunts and resolution of the symptoms. The remaining 7(30%) patients was not cured with residual shunts. Adverse events occurred in 6(30%) of 21 patients with 1 DAVF located at the transverse sigmoid sinus, 2 at tentorium, and 3 at the cavernous sinus. Cranial deficits occurred in 3(15%) patients, brain infarction in 1(5%) patient and microcatheter gluing in 1(3.2%) patient. At final follow up, 20 patients were asymptomatic with 1 showed clinical improvement.

Conclusion

Definitive cure may be attained effectively with Onyx in dural arteriovenous fistulas and adjunctive to surgery and radiotherapy. Location of the DAVFs affected the outcome of transarterial embolization.     

Enhanced cervical MRI in identifying intracranial dural arteriovenous fistulae with spinal perimedullary venous drainage

Diagnosis of an intracranial dural arteriovenous fistula (DAVF) with spinal perimedullary venous drainage is challenging because the presenting symptoms are usually related to dysfunction of the spine, not of the brain. Repeated spinal angiograms are usually performed before the diagnosis is finally made by cerebral angiography. We report two cases of intracranial DAVFs with spinal perimedullary venous drainage. In both cases contrast-enhanced cervical MRI demonstrated dilated lower brainstem and upper spinal veins, which, we believe, is a good indicator of the existence of such drainage. We suggest that, in cases with perimedullary serpentine enhancement on thoracic or lumbar MR images, additional Gd-enhanced cervical spinal MR imaging should be performed. The simple process of tracing the veins upwards may avoid a lot of unnecessary examinations and delay in the diagnosis. Received: 3 July 1997 Accepted: 6 August 1997     

Pial Artery Supply as an Anatomic Risk Factor for Ischemic Stroke in the Treatment of Intracranial Dural Arteriovenous Fistulas

BACKGROUND AND PURPOSE:Although intracranial dural arteriovenous fistulas are principally supplied by dural branches of the external carotid, internal carotid, and vertebral arteries, they can also be fed by pial arteries that supply the brain. We sought to determine the frequency of neurologic deficits following treatment of intracranial dural arteriovenous fistulas with and without pial artery supply.MATERIALS AND METHODS:One hundred twenty-two consecutive patients who underwent treatment for intracranial dural arteriovenous fistulas at our hospital from 2008 to 2015 were retrospectively reviewed. Patient data were examined for posttreatment neurologic deficits; patients with such deficits were evaluated for imaging evidence of cerebral infarction. Data were analyzed with multivariable logistic regression.RESULTS:Of 122 treated patients, 29 (23.8%) had dural arteriovenous fistulas with pial artery supply and 93 (76.2%) had dural arteriovenous fistulas without pial arterial supply. Of patients with pial artery supply, 4 (13.8%) had posttreatment neurologic deficits, compared with 2 patients (2.2%) without pial artery supply (P = .04). Imaging confirmed that 3 patients with pial artery supply (10.3%) had cerebral infarcts, compared with only 1 patient without pial artery supply (1.1%, P = .03). Increasing patient age was also positively associated with pial supply and treatment-related complications.CONCLUSIONS:Patients with dural arteriovenous fistulas supplied by the pial arteries were more likely to experience posttreatment complications, including ischemic strokes, than patients with no pial artery supply. The approach to dural arteriovenous fistula treatment should be made on a case-by-case basis so that the risk of complications can be minimized.

Intracranial dural arteriovenous fistulas (DAVFs) are vascular malformations that connect meningeal arteries to dural venous sinuses or cortical veins. DAVFs account for 10%–15% of all intracranial arteriovenous shunting lesions.^1–14 DAVFs are often thought to be acquired, sometimes in the setting of hypercoagulability.¹⁵ DAVF venous drainage determines the natural history risk of spontaneous intracranial hemorrhage. Thus, venous drainage is incorporated into the most commonly used grading systems of DAVF natural history risk: the Borden-Shucart and Cognard grading scales.^2,3 Drainage to cortical veins is the highest risk category because pressurization of these thin-walled venous structures frequently leads to rupture. Although venous angioarchitecture is a key determinant of natural history risk, the risk of endovascular and/or surgical treatment of DAVFs in the modern era related to underlying lesion angioarchitecture is not well-known.Although DAVFs are most commonly fed by dural branches of the internal carotid, external carotid, and vertebral arteries, they can also have pial artery supply. Pial arteries lie on the surface of the brain. They then branch into penetrating arteries and parenchymal arterioles that lie within and supply the brain parenchyma. The mechanism of pial feeder formation is not well-understood but is believed to be like that of dural feeders, with increased vascular endothelial growth factor secretion from the venous sinus and abnormal angiogenesis.^16–24 Embolization of pial AVFs has been suggested to lead to the development of subsequent DAVFs in up to 25% of cases.^25,26 The inflammatory reaction within the DAVF vessel wall after embolization may also lead to angiogenesis.²⁷Transarterial embolization of DAVFs with pial artery supply with agents that can migrate retrograde (ie, from the dural arteries to the pial arteries) could thus block blood supply to the associated brain parenchyma and cause ischemia. Surgical or endovascular point occlusion of DAVFs with pial artery supply at the fistula site might also result in retrograde thrombosis of feeding pial arteries due to decreased flow. We hypothesized that patients with DAVFs with pial artery supply have a higher risk of postoperative stroke than those who do not have pial supply.     

The anterior medullary–anterior pontomesencephalic venous system and its bridging veins communicating to the dural sinuses: normal anatomy and drainage routes from dural arteriovenous fistulas

Introduction  We evaluated the normal venous anatomy of the anterior medullary/anterior pontomesencephalic venous (AMV/APMV) system and bridging veins connected to the dural sinuses using magnetic resonance (MR) imaging and demonstrated cases of dural arteriovenous fistulas (DAVFs) with bridging venous drainage. Materials and methods  MR images obtained using a 3D gradient echo sequence in 70 patients without lesions affecting the deep or posterior venous channels were reviewed to evaluate the normal anatomy of the AMV/APMV system and bridging veins. MR images and digital subtraction angiography in 80 cases with intracranial or craniocervical junction DAVFs were reviewed to evaluate the bridging venous drainage from DAVFs. Results  MR images clearly revealed AMV/APMV in 35 cases. Fifteen cases showed a direct connection between AMV and APMV, while 15 cases showed an indirect communication via the transverse pontine vein or the bridging vein. In the five remaining cases, the AMV and APMV end separately to the bridging vein or the transverse pontine vein. Bridging veins were identified in 34 cases, connecting to the cavernous sinus in 33, to the suboccipital cavernous sinus in 11, and the inferior petrosal sinus in five cases. In 80 DAVF cases, seven of 40 cavernous sinus DAVFs, two craniocervical junction DAVFs, and one inferior petrosal sinus DAVF drained via bridging veins to the brain stem. Conclusion  The AMV/APMV and bridging veins showed various anatomies and frequently showed a connection to the cavernous sinus. Knowledge of the venous anatomy is helpful for the diagnosis and intravascular treatment of DAVFs.     

Doppler sonographic evaluation of shunts in patients with dural arteriovenous fistulas

BACKGROUND: AND PURPOSE: Doppler sonography has been used to assess global cerebral circulation time (CCT) in healthy volunteers and a small number of patients with cerebral arteriovenous malformations. We evaluated the effect of arteriovenous shunts on global CCT in patients with dural arteriovenous fistulas (DAVFs) by using this Doppler echo contrast-bolus tracking test. METHODS: We measured CCT as the time delay in a contrast bolus to the internal carotid artery (ICA) and internal jugular vein (IJV) in 13 patients with DAVF and 30 age-matched control subjects. Mean CCT and mean arterial and venous rise times (Delta t = 80% of total signal-intensity increase) were compared. Posttreatment follow-up measurements were performed in five patients. RESULTS: Mean CCT and venous Delta t were significantly different between patients and controls (CCT, 1.1 +/- 0.9 vs 6.9 +/- 1.2 seconds, P <.0001; venous Delta t, 5.2 +/- 2.0 vs 7.0 +/- 2.6 seconds, P =.024), but arterial Delta t values were not (4.4 +/- 1.8 vs 4.7 +/- 2.0 seconds). Posttreatment follow-up of two occluded fistulas showed CCT normalization. One near-occlusion showed a two-step increase in signal intensity, and incomplete occlusion in two patients left the CCT unchanged. One patient with an extracranial, highly vascularized glomus tumor draining into the IJV had a CCT of 1.8 seconds. CONCLUSION: In DAVF patients, sonographic CCT is significantly shortened. Our test is highly sensitive for arteriovenous shunts but not specific for DAVF alone. Follow-up measurements in DAVF patients are well correlated with results of angiographic treatment. CCT assessment might become an additional tool for evaluating these patients and monitoring their treatment.     

Endovascular treatment of intracranial dural arteriovenous fistulas with cortical venous drainage: new management using Onyx

BACKGROUND AND PURPOSE: DAVFs (dural arteriovenous fistulas) represent one of the most dangerous types of intracranial AV shunts. Most of them are cured by arterial or venous embolization, but surgery/radiosurgery can be required in case of failure. Our goal was to reconsider the endovascular treatment strategy according to the new possibilities of arterial embolization using non polymerizing liquid embolic agent.MATERIALS AND METHODS: Thirty patients were included in a prospective study during the interval between July 2003 and November 2006. Ten of these had type II, 8 had type III, and 12 had type IV fistulas. Sixteen presented with hemorrhage. Five had been treated previously with other embolic materials.RESULTS: Complete angiographic cure was obtained in 24 cases. Of these 24 cures, 20 were achieved after a single procedure. Cures were achieved in 23 of 25 patients who had not been embolized previously and in only 1 of 5 previously embolized patients. Among these 24 patients, 23 underwent a follow-up angiography, which has confirmed the complete cure. Partial occlusion was obtained in 6 patients, 2 were cured after additional surgery, and 2 underwent radiosurgery. Onyx volume injected per procedure ranged from 0.5 to 12.2 mL (mean, 2.45 mL). Rebleeding occurred in 1 completely cured patient at day 2 due to draining vein thrombosis. One patient had cranial nerve palsy that resolved. Two ethmoidal dural arteriovenous fistulas were occluded. All 10 of the patients with sinus and then CVR drainage were cured.CONCLUSION: Based on this experience, we believe that Onyx may be the treatment of choice for many patients with intracranial dural arteriovenous fistula (ICDAVF) with direct cortical venous reflux (CVR). The applicability of this new embolic agent indicates the need for reconsideration of the global treatment strategy for such fistulas.

Several studies have shown an association between intracranial (IC) dural arteriovenous fistula (DAVF) venous drainage patterns and clinical presentation.^1,2 DAVFs draining retrogradely into cortical veins exhibit a much higher incidence of hemorrhage or venous infarction.^3,4 The annual mortality rate for cortical venous reflux (CVR) may be as high as 10.4%, whereas the annual risk for hemorrhage or nonhemorrhagic neurologic deficits during follow-up are 8.1% and 6.9%, respectively, resulting in an annual event rate of 15%.⁴ In subjects presenting with hemorrhage, the risk of rebleeding has been evaluated at 35% in the 2 weeks after the initial hemorrhage.³ Consequently, DAVFs with CVR require treatment aimed at a complete and definitive fistula closure. In general, treatment of such fistulas primarily involves an endovascular approach, and if this fails, surgical or radiosurgical approaches are used. The present prospective study investigated the use of a new nonadhesive liquid embolic agent, Onyx (ev3, Irvine, Calif), in the treatment of DAVF with CVR.     

Venous congestion: an MR finding in dural arteriovenous malformations with cortical venous drainage.

PURPOSETo present the MR findings of intracranial dural arteriovenous malformations with cortical venous drainage, emphasizing the parenchymal changes.METHODSConventional MR and x-ray angiograms in 13 patients with dural arteriovenous malformations and cortical venous reflux were reviewed. The site of the shunt, location of the venous reflux, and presence of venous stenosis were assessed on the angiograms. Parenchymal changes, dilated vessels, and venous occlusive disease were assessed on MR.RESULTSOn MR, 10 of the 13 patients (77%) had dilated pial vessels. Two patients had hydrocephalus. Two patients presented with parenchymal bleeds, one with a subdural component, both remote from the nidus. Two patients presented with subarachnoid hemorrhage. One patient had a parenchymal bleed 9 months after presentation. Venous occlusion was evident on MR in 2 patients. Diffuse white matter edema in the cerebellar or cerebral hemispheres was present on MR in 4 patients and correlated with neurologic deficits. In 2 of these 4 patients, gadolinium enhancement was seen in the periphery of the involved hemisphere.CONCLUSIONSOn MR a surplus of pial vessels suggests a dural arteriovenous malformation with cortical venous drainage. The MR finding of white matter edema deep in the cerebral or cerebellar hemispheres is direct evidence of a venous congestion.     

Recurrence of the cavernous sinus dural arteriovenous fistula at adjacent sinuses following repeated transvenous embolizations: case report and literature review

We present a unique case of a cavernous sinus (CS) dural arteriovenous fistula (DAVF), which recurred at adjacent sinuses following repeated transvenous embolizations (TVEs). A 68-year-old woman presented with progressive left conjunctival chemosis and diplopia. Cerebral angiography revealed a left CS DAVF, which was completely obliterated by TVE via the left inferior petrosal sinus (IPS). Two years later, the DAVF recurred in the left IPS, and again in the left sigmoid sinus (SS) 3 years after the initial treatment in spite of a second TVE. Moreover, the left SS and the left internal jugular vein, which had been previously stenotic, had been occluded. The third TVE resulted in the complete obliteration of the SS DAVF. CS DAVFs may recur at adjacent sinuses even after complete obliteration by TVE. Careful follow-up is necessary to check for the recurrence of DAVFs, especially in cases with venous flow changes, such as sinus occlusion, following endovascular treatment.     

Clinical and angiographic characteristics of cavernous sinus dural arteriovenous fistulas manifesting as venous infarction and/or intracranial hemorrhage

Introduction  Cavernous sinus (CS) dural arteriovenous fistulas (DAVFs) rarely cause venous infarction (VI) and/or intracranial hemorrhage (ICH) despite the presence of cortical venous drainage (CVD). The present study investigated the characteristics of CS DAVFs manifesting as VI/ICH. Materials and methods  Fifty-four patients treated for CS DAVFs were retrospectively studied. Results  Six patients presented with VI/ICH. Two of the three patients presenting with ICH had CVD only to the superficial sylvian vein (SSV) or the deep sylvian vein (DSV). Three patients presenting with VI had multiple drainages, and angiography of these patients showed a varix on the SSV, drainage into the DSV with agenesis of the second and third segment of basal vein of Rosenthal, and thrombosis of the distal petrosal vein. CS DAVF with CVD only carries higher risk of VI/ICH than multiple drainages. Many CS DAVFs presenting with VI, especially those with drainage into the petrosal vein, have multiple drainages in the early stage. Thrombosis of the inferior and superior petrosal sinuses and superior orbital vein gradually increases pressure of the CVD, and then, VI may occur. In contrast, CS DAVFs with CVD only from the beginning, common in the patients with drainage into the SSVs and DSVs, are likely to cause ICH. Conclusion  Angiographic risk factors causing VI/ICH are CVD only, varix formation, agenesis of the second and third segment of basal vein of Rosenthal, and thrombosis of the superior orbital vein, lateral half of the superior petrosal sinus, and distal CVD.     

Alteration in the venous drainage of a dural arteriovenous fistula following angioplasty

The pattern of venous drainage from a dural arteriovenous fistula (DAVF) has been shown to affect the natural history of these lesions. Angioplasty and stent placement of the dural sinuses have been described to improve outflow in venous hypertensive states and may improve the venous drainage pattern from a DAVF. We report the case of a patient with a benign but stenosed type IIa transverse sinus DAVF who underwent angioplasty to improve venous outflow. This resulted in conversion of the DAVF to a more malignant type IIb drainage pattern with reflux into the cortical venous system.     

Selective transvenous embolization of dural fistulas without occlusion of the dural sinus.

Two patients with dural arteriovenous fistulas (DAVFs) and unsuccessful transarterial embolizations were treated with a technique for selective transvenous embolization. A 5F catheter was advanced from a femoral vein access into the internal jugular bulb and a catheter was navigated through the sinus lumen into the involved cortical veins or the parasinusal venous draining channels of the DAVFs. The venous recipients at the nidal level of the DAVFs were occluded by fibered platinum coils. Complete angiographic cure was effected in both patients, with occlusion of the venous recipients and the nidus, although the sinus segments next to the nidus of the DAVFs remained patent. Placement of coils in a transsinusal route into the venous channel of a DAVF yet outside the sinus lumen can result in complete obliteration of the fistula without damage to the physiological function of the dural sinuses.     

Dural arteriovenous fistulas: evaluation with MR imaging

The preangiographic diagnosis of cerebral dural arteriovenous fistula (DAVF) can be difficult. The magnetic resonance (MR) images of 12 patients with angiographically proved DAVF were evaluated to characterize the appearance of these lesions and to identify those patients at increased risk for complications. Patients with DAVF demonstrating venous occlusive disease are at higher risk for complications from the arterialized collateral venous system. This venous occlusive disease is demonstrated best at arteriography. The MR imaging appearance of dilated cortical veins without a parenchymal nidus is suggestive of a DAVF with veno-occlusive disease. Eight of the 12 patients in our series demonstrated this finding at angiography. Complications, including infarction and hemorrhage, were identified at MR imaging in eight patients with MR imaging evidence of veno-occlusive disease. At angiography 42% of these complications were not apparent. In one patient with a DAVF draining into an unobstructed right sigmoid sinus, results of MR study were normal. Although patients with DAVF without veno-occlusive disease may have normal findings at MR imaging, DAVF associated with veno-occlusive disease and dilated pial venous drainage can be documented on MR images. This subset of DAVF patients, many of whom were identified only at MR imaging, is at higher risk for complications due to veno-occlusive disease. These patients are believed to require more urgent therapy. MR imaging is useful in the pretherapeutic planning for patients with DAVF.