Preoperative Embolization for Brain Arteriovenous Malformation

Preoperative Embolization for Brain Arteriovenous Malformation

Preoperative embolization has traditionally been regarded as a safe and effective adjunct to cerebral arteriovenous malformation surgery. However, there is currently no high-level evidence to ascertain this presumption.

Sattari et al. from the Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Tehran School of Medicine, Tehran University of Medical Science, Tehran, Iran. compared the outcomes of microsurgery (MS) vs microsurgery with preoperative embolization (E + MS) in patients with cerebral arteriovenous malformation through a systematic review.

They searched MEDLINEPubMed, and Embase. The primary outcome was cerebral arteriovenous malformation obliterationSecondary outcomes were intraoperative bleeding (mL), complications, worsened modified Rankin Scale (mRS), and mortality. The pooled proportions of outcomes were calculated through the logit transformation method. The odds ratio (OR) of categorical data and the mean difference of continuous data were estimated through the Mantel-Haenszel and the inverse variance methods, respectively.

Thirty-two studies met the eligibility criteria. One thousand eight hundred twenty-eight patients were treated by microsurgery alone, and 1088 were treated by microsurgery with preoperative embolization, respectively. The meta-analysis revealed no significant difference in AVM obliteration (94.1% vs 95.6%, OR = 1.15 [0.63-2.11], P = .65), mortality (1.7% vs 2%, OR = 0.88 [0.30-2.58], P = .82), procedural complications (18.2% vs 27.2%, OR = 0.47 [0.19-1.17], P = .10), worsened mRS (21.2% vs 18.5%, OR = 1.08 [0.33-3.54], P = .9), and intraoperative blood loss (mean difference = 182.89 [-87.76, 453.55], P = .19).

The meta-analysis showed no significant difference in AVM obliteration, mortality, complications, worse mRS, and intraoperative blood loss between MS and E + MS groups. For AVMs where MS alone has acceptable results, it is reasonable to bypass unnecessary preoperative embolization given the higher postoperative complication risk 1).

In a meta-analysis, preoperative embolization appears to have substantially reduced the lesional volume with active AV shunting before AVM resection. Anecdotally, preoperative embolization facilitates safe and efficient resection; however, differences in outcomes were not significant. The decision to pursue preoperative embolization remains a nuanced decision based on individual lesion anatomy and treatment team experience 2).

Brosnan et al. performed a systematic review of randomized trials and cohort studies evaluating preoperative embolization of bAVMs published between 01 January 2000 and 31 March 2021 and appraise its role in clinical practice. A MEDLINE search was performed, and articles reporting on outcomes following preoperative embolization, as an adjunct to microsurgery, were eligible for inclusion. PRISMA reporting and Cochrane Handbook guidelines were followed. The primary outcome measure was the risk of complications associated with preoperative embolization. The study was registered with PROSPERO (CRD42021244231). Of the 1661 citations, 8 studies with 588 patients met predefined inclusion criteria. No studies specifically compared outcomes of surgical excision of bAVMs between those with and without preoperative embolization. Spetzler Martin (SM) grading was available in 301 cases. 123 of 298 (41⋅28%) patients presented with hemorrhage. Complications related to embolization occurred in 175/588 patients (29.4%, 95% CI 19.6-40.2). Permanent neurological deficits occurred in 36/541 (6%, 95% CI 3.9-8.5) and mortality in 6/588 (0.41%, 95% CI 0-1.4). This is the first systematic review evaluating the preoperative embolization of bAVMs. Existing studies assessing this intervention are of poor quality. Associated complication rates are significant. Based on published literature, there is currently insufficient evidence to recommend the preoperative embolization of AVMs. Further studies are required to ascertain if there are benefits of this procedure and if so, in which cases 3).

A study included patients with brain AVM who underwent embolization at our hospital between April 2011 and May 2021. Risk factors for peri- and postoperative complications were analyzed.

During the study period, 36 AVMs were treated during 58 embolization sessions. The goal of the embolization was preoperative in 24 (67%), pre-radiosurgical in 9 (25%), and palliative in 3 (8%) cases. The overall complication rate was 43% (25 of 58) per session and 36% (13 of 36) per patient. Ischemic and hemorrhagic complications were observed in 14 (24%) and 14 (24%) cases, respectively. n-Butyl cyanoacrylate (n-BCA) embolization was detected as the significant risk for postoperative hemorrhage in the univariate (79% vs. 36%, P = 0.012; Fisher exact test) and the multivariable analysis (odds ratio 4.90, 95% confidence interval 1.08-22.2, P = 0.039). The number of embolized feeder in a single session also tended to be higher in a hemorrhagic complication group (median 3.5 vs. 2.0, P = 0.11; Mann-Whitney U-test).

The risk of embolization in multimodality treatment for complex brain AVM was substantial. n-BCA embolization may carry a higher risk of postoperative hemorrhage. An accumulation of cases is awaited to investigate the effectiveness of minimal target embolization in the future 4).

A total of 11 patients who underwent 12 preoperative SPE procedures were included for analysis. Five AVMs were ruptured (45%), and the median nidus volume was 3.0 cm3 (range: 1.3-42.9 cm3). The Spetzler-Martin grade was I-II in seven patients (64%) and III-IV in four patients (36%). The degree of nidal obliteration was less than 25% in two procedures (17%), 25-50% in one procedure (8%), 50-75% in eight procedures (67%), and greater than 75% in one procedure (8%). The rates of post-embolization AVM hemorrhage and mortality were 8% and 0%, respectively. The postoperative angiographic obliteration rate was 100%, and the modified Rankin Scale score improved or stable in 91% of patients (median follow-up duration 2 months).

Preoperative AVM SPE affords a reasonable risk-to-benefit profile for appropriately selected patients 5)

Embolization of intracranial arteriovenous malformations (AVMs) is generally a preoperative adjunctive procedure in the USA.

Preoperative embolization may also be a contributing factor with the potential for recurrence of unresected but embolized portions of an AVM. Follow-up angiography at 1 to 3 years appears to be warranted 6).

A total of 107 patients were treated for cAVMs during the study period. Of those patients, 41 underwent cAVM embolizations with Onyx in 82 procedures.

Results: After the embolization, the cAVM diameter was reduced from 3.71 +/- 1.55 cm to 3.06 +/- 1.89 cm (P < .05). Median volume reduction was 75%. Complete occlusion with embolization alone was achieved in 4 (10%) cAVMs. The recurrence rate for completely occluded cAVMs was 50% (2 patients). A total of 71% of the 41 patients treated with Onyx underwent surgery, and 15% underwent radiosurgery. There were 9% who have not yet received definitive treatment of their residual cAVMs. A new permanent neurologic deficit occurred in 5 patients (6.1% per procedure or 12.2% per patient).

A considerable risk for a permanent neurologic deficit remains for cAVM embolization with Onyx. The risk has to be carefully weighted against the benefit of volume reduction in the treatment of cAVMs 7).


Sattari SA, Shahbandi A, Yang W, Feghali J, Xu R, Huang J. Microsurgery versus Microsurgery With Preoperative Embolization for Brain Arteriovenous Malformation Treatment: A Systematic Review and Meta-analysis. Neurosurgery. 2023 Jan 1;92(1):27-41. doi: 10.1227/neu.0000000000002171. Epub 2022 Oct 26. PMID: 36519858.

Park MT, Essibayi MA, Srinivasan VM, Catapano JS, Graffeo CS, Lawton MT. Surgical management outcomes of intracranial arteriovenous malformations after preoperative embolization: a systematic review and meta-analysis. Neurosurg Rev. 2022 Dec;45(6):3499-3510. doi: 10.1007/s10143-022-01860-x. Epub 2022 Sep 27. PMID: 36168072.

Brosnan C, Amoo M, Javadpour M. Preoperative embolisation of brain arteriovenous malformations: a systematic review and meta-analysis. Neurosurg Rev. 2022 Jun;45(3):2051-2063. doi: 10.1007/s10143-022-01766-8. Epub 2022 Mar 9. PMID: 35260972; PMCID: PMC9160113.

Koizumi S, Shojima M, Shinya Y, Ishikawa O, Hasegawa H, Miyawaki S, Nakatomi H, Saito N. Risk Factors of Brain Arteriovenous Malformation Embolization as Adjunctive Therapy: Single-Center 10-Year Experience. World Neurosurg. 2022 Sep 18:S1878-8750(22)01346-8. doi: 10.1016/j.wneu.2022.09.069. Epub ahead of print. PMID: 36130658.

Conger JR, Ding D, Raper DM, Starke RM, Durst CR, Liu KC, Jensen ME, Evans AJ. Preoperative Embolization of Cerebral Arteriovenous Malformations with Silk Suture and Particles: Technical Considerations and Outcomes. J Cerebrovasc Endovasc Neurosurg. 2016 Jun;18(2):90-99. doi: 10.7461/jcen.2016.18.2.90. Epub 2016 Jun 30. PMID: 27790398; PMCID: PMC5081503.

Ivanov AA, Alaraj A, Charbel FT, Aletich V, Amin-Hanjani S. Recurrence of Cerebral Arteriovenous Malformations Following Resection in Adults: Does Preoperative Embolization Increases the Risk? Neurosurgery. 2016 Apr;78(4):562-71. doi: 10.1227/NEU.0000000000001191. PubMed PMID: 26702837.

Hauck EF, Welch BG, White JA, Purdy PD, Pride LG, Samson D. Preoperative embolization of cerebral arteriovenous malformations with onyx. AJNR Am J Neuroradiol. 2009 Mar;30(3):492-5. doi: 10.3174/ajnr.A1376. Epub 2008 Dec 26. PMID: 19112062; PMCID: PMC7051448.

Cerebral arteriovenous malformation (AVM)

Cerebral arteriovenous malformation (AVM)

Intracranial arteriovenous malformation in the brain.

see Cerebral arteriovenous malformation epidemiology.

see Arteriovenous malformation associated aneurysm

Cerebral microarteriovenous malformation

Parafalcine arteriovenous malformation,….

Ruptured cerebral arteriovenous malformation

Unruptured cerebral arteriovenous malformation

AVMs that occur in the coverings of the brain are called dural arteriovenous malformation.

Deep arteriovenous malformation.

Motor area arteriovenous malformation.

Pediatric Cerebral arteriovenous malformation.

Cerebral Arteriovenous Malformation Grading.

Cerebral arteriovenous malformation rupture risk.

Significant progress in the understanding of their pathogenesis has been made during the last decade, particularly using whole genome sequencing and biomolecular analysis 1)

Cerebral arteriovenous malformation pathophysiology

Cerebral Arteriovenous Malformation Clinical Features.

Primary lobar hemorrhages (usually due to cerebral amyloid angiopathy) are typically seen in elderly. Younger patients may also develop lobar haemorrhages, but in such cases they usually have an underlying lesion (e.g. cerebral arteriovenous malformation).

see Cerebral arteriovenous malformation treatment.

Cerebral arteriovenous malformation outcome.

Cerebral arteriovenous malformation complications.

Cerebral arteriovenous malformation case series.

Bhanot et al. presented a patient with intraparenchymal hemorrhage due to cerebral arteriovenous malformation (AVM) who exhibited acute ST segment myocardial infarction (STEMI) after neurosurgery. Serial cardiac biomarkers and echocardiograms were performed which did not reveal any evidence of acute myocardial infarction. The patient was managed conservatively from cardiac stand point with no employment of anticoagulants, antiplatelet therapyfibrinolytic agents, or angioplasty and recovered well with minimal neurological deficit. This case highlights that diffuse cardiac ischemic signs on the ECG can occur in the setting of an ICH after neurosurgery, potentially posing a difficult diagnostic and management conundrum 2).


Vetiska S, Wälchli T, Radovanovic I, Berhouma M. Molecular and genetic mechanisms in brain arteriovenous malformations: new insights and future perspectives. Neurosurg Rev. 2022 Oct 11. doi: 10.1007/s10143-022-01883-4. Epub ahead of print. PMID: 36219361.

Bhanot RD, Kaur J, Sriwastawa S, Bell K, Suchdev K. Postoperative ‘STEMI’ in Intracerebral Hemorrhage due to Arteriovenous Malformation: A Case Report and Review of Literature. Case Rep Crit Care. 2019 Apr 22;2019:9048239. doi: 10.1155/2019/9048239. PMID: 31231576; PMCID: PMC6507120.

Borden type I intracranial dural arteriovenous fistula

Borden type I intracranial dural arteriovenous fistula

Type I dural arteriovenous fistulas are supplied by a meningeal artery or arteries and drain into a meningeal vein or dural venous sinus. The flow within the draining vein or venous sinus is anterograde.

Equivalent to Cognard type I and IIa, with a favorable natural history 1) 2).

Type Ia – simple dural arteriovenous fistulas have a single meningeal arterial supply

Type Ib – more complex arteriovenous fistulas are supplied by multiple meningeal arteries The distinction between Types Ia and Ib is somewhat specious as there is a rich system of meningeal arterial collaterals. Type I dural fistulas are often asymptomatic, do not have a high risk of bleeding and do not necessarily need to be treated

A small number of Type I DAVFs will convert to more aggressive DAVFs with CVD over time. This conversion to a higher-grade DAVF is typically heralded by a change in patient symptoms. Follow-up vascular imaging is important, particularly in the setting of recurrent or new symptoms. 3).

A comparative meta-analysis was completed to evaluate the outcomes of intervention versus observation of Borden type I intracranial dural arteriovenous fistula. Outcome measures included: grade progression, worsening symptoms, death due to dural arteriovenous fistula, permanent complications other than death, functional independence (mRS 0-2), and rate of death combined with permanent complication, were evaluated. Risk differences (RD) were determined using a random effects model.

Three comparative studies combined with the authors’ institutional experience resulted in a total of 469 patients, with 279 patients who underwent intervention and 190 who were observed. There was no significant difference in dAVF grade progression between the intervention and observation arms, 1.8% vs. 0.7%, respectively (RD: 0.01, 95% CI: -0.02 to 0.04, P = 0.49), or in symptom progression occurring in 31/279 (11.1%) intervention patients and 11/190 (5.8%) observation patients (RD: 0.03, CI: -0.02 to 0.09, P = 0.28). There was also no significant difference in functional independence on follow-up. However, there was a significantly higher risk of dAVF-related death, permanent complications from either intervention or dAVF-related ICH or stroke in the intervention group (11/279, 3.9%) compared to the observation group (0/190, 0%) (RD: 0.04, CI: 0.1 to 0.06, P = 0.007).

CoIntervention of Borden Type I dAVF results in a higher risk of death or permanent complication, which should be strongly considered when deciding on the management of these lesions 4).

From April 2013 to March 2016, consecutive patients with DAVF were screened at 13 study institutions. We collected data on baseline characteristics, clinical symptoms, angiography, and neuroimaging. Patients with Borden type I DAVF received conservative care while palliative intervention was considered when the neurological symptoms were intolerable, and were followed at 6, 12, 24, and 36 months after inclusion.

Results: During the study period, 110 patients with intracranial DAVF were screened and 28 patients with Borden type I DAVF were prospectively followed. None of the patients had conversion to higher type of Borden classification or intracranial hemorrhage during follow-up. Five patients showed spontaneous improvement or disappearance of neurological symptoms (5/28, 17.9%), and 5 patients showed a spontaneous decrease or disappearance of shunt flow on imaging during follow-up (5/28, 17.9%). Stenosis or occlusion of the draining sinuses on initial angiography was significantly associated with shunt flow reduction during follow-up (80.0% vs 21.7%, p = 0.02).

Conclusion: In this 3-year prospective study, patients with Borden type I DAVF showed benign clinical course; none of these patients experienced conversion to higher type of Borden classification or intracranial hemorrhage. The restrictive changes of the draining sinuses at initial diagnosis might be an imaging biomarker for future shunt flow reduction 5)


Davies MA, TerBrugge K, Willinsky R, Coyne T, Saleh J, Wallace MC. The validity of classification for the clinical presentation of intracranial dural arteriovenous fistulas. J Neurosurg. 1996 Nov;85(5):830-7. doi: 10.3171/jns.1996.85.5.0830. PMID: 8893721.

Strom RG, Botros JA, Refai D, Moran CJ, Cross DT 3rd, Chicoine MR, Grubb RL Jr, Rich KM, Dacey RG Jr, Derdeyn CP, Zipfel GJ. Cranial dural arteriovenous fistulae: asymptomatic cortical venous drainage portends less aggressive clinical course. Neurosurgery. 2009 Feb;64(2):241-7; discussion 247-8. doi: 10.1227/01.NEU.0000338066.30665.B2. PMID: 19190453.

Shah MN, Botros JA, Pilgram TK, Moran CJ, Cross DT 3rd, Chicoine MR, Rich KM, Dacey RG Jr, Derdeyn CP, Zipfel GJ. Borden-Shucart Type I dural arteriovenous fistulas: clinical course including risk of conversion to higher-grade fistulas. J Neurosurg. 2012 Sep;117(3):539-45. doi: 10.3171/2012.5.JNS111257. Epub 2012 Jun 22. PMID: 22725983.

Schartz D, Rahmani R, Gunthri A, Kohli GS, Akkipeddi SMK, Ellens NR, Romiyo P, Kessler A, Bhalla T, Mattingly TK, Bender MT. Observation versus intervention for Borden type I intracranial dural arteriovenous fistula: A pooled analysis of 469 patients. Interv Neuroradiol. 2022 Sep 13:15910199221127070. doi: 10.1177/15910199221127070. Epub ahead of print. PMID: 36113111.

Nishi H, Ikeda H, Ishii A, Kikuchi T, Nakahara I, Ohta T, Sakai N, Imamura H, Takahashi JC, Satow T, Okada T, Miyamoto S. A multicenter prospective registry of Borden type I dural arteriovenous fistula: results of a 3-year follow-up study. Neuroradiology. 2022 Apr;64(4):795-805. doi: 10.1007/s00234-021-02752-5. Epub 2021 Oct 10. PMID: 34628528; PMCID: PMC8907088.

Vertebro-vertebral arteriovenous fistula

Vertebro-vertebral arteriovenous fistula

Vertebro-vertebral arteriovenous fistula (VV-AVF) is a rare vascular disorder with an abnormal shunt between the extracranial vertebral artery (VA), its muscular or radicular branches, and adjacent vein1)

Trauma is the most common cause, including stab wounds, gunshot wound, and blunt trauma. Most VV-AVF patients have lesions that are spontaneous or caused by neck trauma 2) Some patients with VV-AVF are asymptomatic. Others may have tinnitus or neurologic deficit because of high flow arteriovenous shunting, steal phenomenon, or compression mass effect from enlarged venous pouches 3) 4) 5) 6).

The location of VVAVF is also variable with most cases above the C2 vertebra or below the C5 vertebra 7).

Surgical ligation or endovascular closure of the high-flow arteriovenous fistula is the main goal of treatment for VV-AVF 8) 9) 10)11).

Chen et al. presented two female NF-1 patients with a diagnosis of VV-AVF treated with endovascular approach. The fistula was completely obliterated with balloon assisted embolization and covered stent separately and VA patency was preserved in both cases. Reviewing the literature with a focus on endovascular treatment, endovascular occlusion of VV-AVF in NF-1 patients is safe and effective. To preserve the parent VA patency and obliterate the fistula simultaneously is challenging generally, but feasible in some cases 12).

Yeh et al. presented the experience of VV-AVF treatment with covered stents in three patients and detachable coils in two patients. One patient with a fistula at the V3 segment had rapid fistula recurrence one week after covered stent treatment. The possible causes of failed treatment in this patient are discussed. The currently available treatment modalities for VV-AVF are also summarized after a literature review. At the end of this article, we propose a new concept of anatomically based approach for endovascular treatment of VV-AVF. Fistula in the V1-2 segments of vertebral artery could be treated safely and effectively by covered stent with the benefit of preserving VA patency. Embolization with variable embolizers should be considered first for fistula in the V3 segment because of the tortuous course and flexibility of the VA in this segment 13).

Briganti et al. describe endovascular approaches for occlusion of vertebro-vertebral arteriovenous fistula (VV-AVF) in a series of three cases and a review of the literature. Complete neuroimaging assessment, including CT, MR and DSA was performed in three patients (two female, one male) with VV-AVF. Based on DSA findings, the VV-AVF were occluded by endovascular positioning of detachable balloons (case 1), coils (case 2), or a combination of both (case 3) with parent artery patency in two out of three cases. In this small series, endovascular techniques for occlusion of VV-AVF were safe and effective methods of treatment. To date, there are no guidelines on the best treatment for VV-AVF. Detachable balloons, endovascular coiling, combined embolization procedures could all be considered well-tolerated treatments 14).

Vertebro-vertebral arteriovenous fistula involving the vertebral artery segment V3 is a rare vascular pathology that is either spontaneous or traumatic in origin. Furtado et al. described a post-operative traumatic vertebro-vertebral fistula in a 47-year-old lady with NF-1. They reviewed reported cases of V3 segment vertebrovertebral fistula for their incidence, etiology, clinical presentation, treatment, and outcomes using an illustrative case. Traumatic V3 segment vertebrovertebral fistula is predominantly managed with parent vessel occlusion. Per the algorithm presented, we suggest endovascular management of non-traumatic fistula be based on the anatomical variance of the contralateral vertebral artery 15).

A vertebral AVF was detected by carotid duplex ultrasonography, and endovascular treatment was successfully performed in a 72-year-old woman with 1-year history of hemodialysis 16)

A 72-year-old woman was admitted with a complaint of bilateral leg weakness. A cervical magnetic resonance image showed compression of the spinal cord by a large vascular lesion. Right vertebral angiogram showed a vertebro-vertebral fistula draining into ectatic epidural veins. From a transfemoral arterial approach, the fistula site was selected with a microcatheter, and embolization was performed by placement of several Guglielmi detachable coils until flow arrest was obtained. The patient made a full recovery, and a long-term angiographic follow-up demonstrated a complete cure 17).


Halbach VV, Higashida RT, Hieshima GB. Treatment of vertebral arteriovenous fistulas. AJR Am J Roentgenol. 1988 Feb;150(2):405-12. doi: 10.2214/ajr.150.2.405. PMID: 3257333.
2) , 3) , 8)

Beaujeux RL, Reizine DC, Casasco A, Aymard A, Rüfenacht D, Khayata MH, Riché MC, Merland JJ. Endovascular treatment of vertebral arteriovenous fistula. Radiology. 1992 May;183(2):361-7. doi: 10.1148/radiology.183.2.1561336. PMID: 1561336.
4) , 9)

Herrera DA, Vargas SA, Dublin AB. Endovascular treatment of traumatic injuries of the vertebral artery. Am J Neuroradiol. 2008;29(8):1585–1589. doi: 10.3174/ajnr.A1123.

Vinchon M, Laurian C, George B, et al. Vertebral arteriovenous fistulas: a study of 49 cases and review of the literature. Cardiovasc Surg. 1994;2(3):359–369.

Ito O, Nishimura A, Ishido K, et al. Spontaneous vertebral arteriovenous fistula manifesting as radiculopathy. No Shinkei Geka. 2011;39(8):775–781.

Desouza RM, Crocker MJ, Haliasos N, Rennie A, Saxena A. Blunt traumatic vertebral artery injury: a clinical review. Eur Spine J. 2011 Sep;20(9):1405-16. doi: 10.1007/s00586-011-1862-y. Epub 2011 Jun 16. PMID: 21674212; PMCID: PMC3175894.
10) , 14)

Briganti F, Tedeschi E, Leone G, Marseglia M, Cicala D, Giamundo M, Napoli M, Caranci F. Endovascular treatment of vertebro-vertebral arteriovenous fistula. A report of three cases and literature review. Neuroradiol J. 2013 Jun;26(3):339-46. doi: 10.1177/197140091302600315. Epub 2013 Jul 16. PMID: 23859293; PMCID: PMC5278851.

Ishiguro T, Kawashima A, Yoneyama T, et al. Two cases of iatrogenic vertebral arteriovenous fistulas successfully treated by surgery. No Shinkei Geka. 2011;39(3):269–274.

Chen C, Wu Y, Zhao K, Duan G, Liu J, Huang Q. Endovascular treatment of vertebro-vertebral arteriovenous fistula in neurofibromatosis type I: A report of two cases and literature review with a focus on endovascular treatment. Clin Neurol Neurosurg. 2021 Aug;207:106806. doi: 10.1016/j.clineuro.2021.106806. Epub 2021 Jul 14. PMID: 34293658.

Yeh CH, Chen YL, Wu YM, Huang YC, Wong HF. Anatomically based approach for endovascular treatment of vertebro-vertebral arteriovenous fistula. Interv Neuroradiol. 2014 Dec;20(6):766-73. doi: 10.15274/INR-2014-10072. Epub 2014 Dec 5. PMID: 25496689; PMCID: PMC4295251.

Furtado SV, Vasavada P, Baid A, Perikal PJ. Endovascular management of V3 segment vertebro-vertebral fistula: case management and literature review. Br J Neurosurg. 2022 May 3:1-5. doi: 10.1080/02688697.2022.2071416. Epub ahead of print. PMID: 35502703.

Tenjin H, Kimura S, Sugawa N. Coil embolization of vertebro-vertebral arteriovenous fistula: a case report. Surg Neurol. 2005 Jan;63(1):80-3; discussion 83. doi: 10.1016/j.surneu.2004.01.026. PMID: 15639536.

Dural arteriovenous fistula

Dural arteriovenous fistula

Dural arteriovenous fistulas (DAVFs) are pathologic vascular connections that shunt dural arterial flow directly to dural venous drainage.

DAVFs comprise 10–15% of all intracranial AVMs 1). 61–66% occur in females, and patients are usually in their 40 s or 50 s. They occur rarely in children, and when they do they tend to be complex, bilateral dural sinus malformations 2)

Dural arteriovenous fistulas can occur at any dural sinus but are found most frequently at the cavernous or transverse sinus.

Intracranial dural arteriovenous fistula.

Spinal dural arteriovenous fistula.

The etiology and pathophysiology of DAVFs is not fully understood. Several hypotheses for development of DAVF and classifications for predicting risk of hemorrhage and neurological deficit have been proposed to help clinical decision making according to its natural history 3).

Radical treatment is to obliterate the draining veins in any treatment modalities including endovascular treatment or surgical treatment. Radiosurgery is the last choice. Transvenous embolization plays the main role in the DAVF of the cavernous sinus and anterior condylar confluence. Transarterial embolization with Onyx has dramatically improved the obliteration rate of the transverse-sigmoid, superior sagittal sinuses, and other non-sinus lesions. Transarterial NBCA injection is still the gold standard in the endovascular treatment of the spinal dural and epidural AVFs. Understanding of the functional microvascular anatomy is mandatory, especially in the transarterial liquid injection (Onyx and NBCA). Surgical treatment in the DAVF of the anterior cranial base, craniocervical junction, tentorial region, and spine is a safe and radical treatment. Postoperative follow-up is necessary from the viewpoint of chronological and spacial multi-occurrence of this disease 4).


Arnautovic KI, Krisht AF. Transverse-Sigmoid Sinus Dural Arteriovenous Malformations. Contemp Neurosurg. 2000; 21:1–6

Ashour R, Aziz-Sultan MA, Soltanolkotabi M, et al. Safety and efficacy of onyx embolization for pediatric cranial and spinal vascular lesions and tumors. Neurosurgery. 2012; 71:773–784

Sim SY. Pathophysiology and classification of intracranial and spinal duraAVF. J Cerebrovasc Endovasc Neurosurg. 2022 Apr 21. doi: 10.7461/jcen.2022.E2021.04.001. Epub ahead of print. PMID: 35443276.

Kuwayama N. Management of Dural Arteriovenous Fistulas. Adv Tech Stand Neurosurg. 2022;44:251-264. doi: 10.1007/978-3-030-87649-4_14. PMID: 35107684.

Intracranial dural arteriovenous fistula clinical features

Intracranial dural arteriovenous fistula clinical features

Clinical features of DAVF vary depending on their location, arterial supply, degree of arteriovenousshunting, and most importantly, their venous drainage pattern 1) 2) 3) 4)

DAVF lacking cortical vein drainage (CVD) may be asymptomatic, or present with symptoms related to increased dural sinus blood flow, such as pulsatile tinnitus, the latter particularly common for transverse sinus and sigmoid sinuses lesions.

Generalized central nervous system symptoms that may be related to venous hypertension or cerebrospinal fluid malabsorption, while resulting cranial nerve palsy, are often because of an arterial steal phenomenon or occasionally mass effect from an enlarged arterial feeder.

In addition, cavernous sinus dural arteriovenous fistula may present with orbital symptoms, including chemosisproptosisophthalmoplegia, and decreased visual acuity.

DAVF with CVD typically have more aggressive clinical presentations, including the sudden onset of severe headacheseizures, nonhemorrhagic neurological deficit (NHND), and intracranial hemorrhage, including intraparenchymal, subarachnoid, and subdural hematoma.

In a meta-analysis, Lasjaunias et al 5) reviewed 195 cases of DAVF and found that focal neurological deficits were related to the presence of associated cortical venous drainage (CVD) and venous congestion in the affected vascular territory. Less common aggressive presentations include brain stem or cerebellar dysfunction secondary to venous congestion, parkinsonism-like symptoms, extra-axial hemorrhage in the cervical spine, as well as cervical and upper thoracic myelopathy.

DAVF with extensive arteriovenous shunting, particularly in the setting of dural sinus thrombosis, can result in impaired venous drainage from the brain and the global venous hypertension. This can lead to cerebral edema, encephalopathy, and cognitive decline 6).

Pulsatile tinnitus is the most common presenting symptom of a DAVF. Cortical venous drainage with resultant venous hypertension can produce intracranial hypertension, and this is the most common cause of morbidity and mortality and thus the strongest indication for Intracranial dural arteriovenous fistula treatment.

DAVFs may also cause global cerebral edema or hydrocephalus due to poor cerebral venous drainage or by impairing the function of the arachnoid granulations, respectively. Other DAVF symptoms/signs include headaches, seizures, cranial nerve palsies, and orbital venous congestion.

Leptomeningeal venous drainage can lead to venous hypertension and intracranial hemorrhage.

The majority of patients presented with non-aggressive symptoms. 18% presented with intracranial hemorrhage: all the hemorrhages occurred in high-grade DAVFs 7).

see Dural arteriovenous fistula presenting as an acute subdural hemorrhage.

Only 4 cases of DAVF causing syncope have been reported, all in combination with other neurological symptoms. In comparison, they report a unique case of DAVF presenting solely with recurrent syncope, a previously undocumented finding in the literature. The case adds to other reports of nonspecific DAVF presentations and highlights the importance of considering this etiology 8).


Gandhi D, Chen J, Pearl M, Huang J, Gemmete JJ, Kathuria S.Intracranial dural arteriovenous fistulas: classification, imaging findings, and treatment.AJNR Am J Neuroradiol. 2012; 33:1007–1013. doi: 10.3174/ajnr.A2798.

Sarma D, ter Brugge K.Management of intracranial dural arteriovenous shunts in adults.Eur J Radiol. 2003; 46:206–220.

Houser OW, Campbell JK, Campbell RJ, Sundt TMArteriovenous malformation affecting the transverse dural venous sinus–an acquired lesion.Mayo Clin Proc. 1979; 54:651–661.
4) , 5)

Lasjaunias P, Chiu M, ter Brugge K, Tolia A, Hurth M, Bernstein M.Neurological manifestations of intracranial dural arteriovenous malformations.J Neurosurg. 1986; 64:724–730. doi: 10.3171/jns.1986.64.5.0724.

Miller TR, Gandhi D. Intracranial Dural Arteriovenous Fistulae: Clinical Presentation and Management Strategies. Stroke. 2015 Jul;46(7):2017-25. doi: 10.1161/STROKEAHA.115.008228. Epub 2015 May 21. PMID: 25999384.

Signorelli, F. et al. Diagnosis and management of dural arteriovenous fistulas: A 10 years single-center experience Clinical Neurology and Neurosurgery , Volume 128 , 123 – 129

Sheinberg DL, Luther E, Chen S, McCarthy D, Starke RM. Recurrent Syncope Caused by a Dural Arteriovenous Fistula: A Case Report and Review of the Literature. Neurologist. 2021 Mar 4;26(2):62-65. doi: 10.1097/NRL.0000000000000322. PMID: 33646991.

High-grade arteriovenous malformation

High-grade arteriovenous malformation

High-grade arteriovenous malformations (AVMs), such as Spetzler-Martin AVM grading system 4 and 5, 1) are generally considered difficult to cure using any modalities such as surgery, embolization, and/or radiosurgery 2). However, endovascular treatment potentially offers an advantage over the other two methods because of the ability to immediately target certain areas of an AVM. Partially targeted embolization could be effective in controlling the bleeding point when treating high-grade AVMs; however, it is not curative 3) 4).

Grade 4 and 5 AVMs with supply from lenticulostriate, choroidal, thalamic deep perforating arteries or deep meningeal recruitment may be best treated conservatively or possibly by multimodality treatment utilising radiotherapy and embolisation combined with surgery 5).

Untreated high grade AVMs presenting with hemorrhage have a significant risk of subsequent rupture, and their rupture carries a higher risk of case fatality and permanent morbidity than AVMs in general. The risks associated with their treatment should be appraised in light of perilous natural history 6).

A retrospective analysis of a prospectively maintained database was performed in children with treated and nontreated pediatric AVMs at the University of California, San Francisco, from 1998 to 2017. Inclusion criteria were age ≤ 18 years at time of diagnosis and an AVM confirmed by a catheter angiogram.

The authors evaluated 189 pediatric patients with AVMs over the study period, including 119 ruptured (63%) and 70 unruptured (37%) AVMs. The mean age at diagnosis was 11.6 ± 4.3 years. With respect to Spetzler-Martin (SM) grade, there were 38 (20.1%) grade I, 40 (21.2%) grade II, 62 (32.8%) grade III, 40 (21.2%) grade IV, and 9 (4.8%) grade V lesions. Six patients were managed conservatively, and 183 patients underwent treatment, including 120 resections, 82 stereotactic radiosurgery (SRS), and 37 endovascular embolizations. Forty-four of 49 (89.8%) high-grade AVMs (SM grade IV or V) were treated. Multiple treatment modalities were used in 29.5% of low-grade and 27.3% of high-grade AVMs. Complete angiographic obliteration was obtained in 73.4% of low-grade lesions (SM grade I-III) and in 45.2% of high-grade lesions. A periprocedural stroke occurred in a single patient (0.5%), and there was 1 treatment-related death. The mean clinical follow-up for the cohort was 4.1 ± 4.6 years, and 96.6% and 84.3% of patients neurologically improved or remained unchanged in the ruptured and unruptured AVM groups following treatment, respectively. There were 16 bleeding events following initiation of AVM treatment (annual rate: 0.02 events per person-year).

Coordinated multidisciplinary evaluation and individualized planning can result in safe and effective treatment of children with AVMs. In particular, it is possible to treat the majority of high-grade arteriovenous malformations with an acceptable safety profile. Judicious use of multimodality therapy should be limited to appropriately selected patients after thorough team-based discussions to avoid additive morbidity. Future multicenter studies are required to better design predictive models to aid with patient selection for multimodal pediatric care, especially with high-grade AVMs 7).

Long-term Outcomes With Planned Multistage Reduced Dose Repeat Stereotactic Radiosurgery for Treatment of Inoperable High-Grade Arteriovenous Malformations: An Observational Retrospective Cohort Study 8).

Treatment of Spetzler-Martin Grade IV and V brain arteriovenous malformations (ie, high-grade AVMs) carries a high risk of morbidity and even mortality. However, little is known about the behavior of these lesions if left untreated.

Objective: To investigate the natural history of patients with high-grade AVMs.

Methods: Patients with untreated high-grade AVMs admitted to our center between 1952 and 2005 were followed from admission until death, AVM rupture, or initiation of treatment. Rates of rupture and various risk factors were analyzed using Kaplan-Meier life table analyses and Cox proportional hazards models. Functional outcome was assessed 1 year after possible AVM rupture using the Glasgow Outcome Scale.

Results: Sixty-three patients with a mean follow-up time of 11.0 years (range, 1 month to 39.6 years) were identified. Twenty-three patients (37%) experienced a subsequent rupture. The average annual rate of rupture was 3.3%. In patients with hemorrhagic presentation, the annual rate was 6.0%, compared to 1.1% in patients with unruptured AVMs (P = .001, log-rank test; hazard ratio, 5.09 [1.40-18.5, 95% CI]; P = .013, multivariate Cox regression model). One year after the first subsequent rupture, 6 patients (26%) had died, and 9 (39%) had moderate or severe disability.

Untreated high grade AVMs presenting with hemorrhage have a significant risk of subsequent rupture, and their rupture carries a higher risk of case fatality and permanent morbidity than AVMs in general. The risks associated with their treatment should be appraised in light of perilous natural history 9).

Jayaraman et al. examined the prospective annual risk of hemorrhage in patients harboring Spetzler-Martin grades IV and V arteriovenous malformations (AVMs) before and after initiation of treatment.

Medical records of 61 consecutive patients presenting with Spetzler-Martin grades IV and V AVMs were retrospectively reviewed for demographics, angiographic features, presenting symptom(s), and time of all hemorrhage events, before or after treatment initiation. Pretreatment hemorrhage rates (excluding hemorrhages at presentation) and posttreatment rates were subsequently calculated. Modified Rankin Scale (mRS) scores before and after treatment were recorded.

The annual pretreatment hemorrhage rate for all patients was 10.4% per year (95% CI, 2.2 to 15.4%), 13.9% (95% CI, 3.5 to 22.1%) in patients with hemorrhagic presentation and 7.3% (2.6 to 14.3%) in patients with nonhemorrhagic presentation. Posttreatment hemorrhage rates were 6.1% per year (95% CI, 2.5 to 13.2%) for all patients, 5.6% (95% CI, 2.1 to 11.8%) for patients presenting with hemorrhage and 6.4% (95% CI, 1.6 to 10.1%) in patients with nonhemorrhagic presentation. A noninferiority test showed that the posttreatment hemorrhage rate was less than or equal to the pretreatment hemorrhage rate (P<0.0001), with some indication that the reduction was greatest in patients with hemorrhagic presentation. Of the 62 patients, 51 (82%) had an mRS score of 0 to 2 before treatment, and 47 (76%) had an mRS score of 0 to 2 at the last follow-up after treatment.

The annual rate of hemorrhage in grades IV and V AVMs is higher in this series than reported for all AVMs, which may reflect some referral bias in this single-center study. Nevertheless, initiation of treatment does not appear to increase the rate of subsequent hemorrhage. Treatment for these lesions may be warranted, given their poor natural history 10).

Between July 1997 and May 2000, 73 consecutive patients with Grades IV and V AVMs were evaluated prospectively by the cerebrovascular team at Barrow Neurological Institute. Treatment recommendations given to the patients or referring physicians were classified as complete treatment, partial treatment, and no treatment. Retrospectively, the hemorrhage rates associated with these treatment groups were also calculated. In the prospective portion of the study (the intention-to-treat analysis), no treatment of the AVM, was recommended for 55 patients (75%) and partial treatment was recommended for seven patients (10%). Aneurysms associated with an AVM were obliterated by surgical or endovascular treatment in seven patients (10%), and complete surgical removal was recommended for four patients (5%). The overall hemorrhage rate for Grades IV and V AVMs was 1.5% per year. The annual risk of hemorrhage was 10.4% among patients who previously had received incomplete treatment, compared with patients without previous treatment.

The hemorrhage risk of 1.5% per year, which was associated with Grades IV and V AVMs appears to be lower than that reported for Grades I through III AVMs. The authors recommend that no treatment be given for most Grades IV and V AVMs. No evidence indicates that partial treatment of an AVM reduces a patient’s risk of hemorrhage. In fact, partial treatment may worsen the natural history of an AVM. The authors do not support palliative treatment of AVMs, except in the specific circumstances of arterial or intranidal aneurysms or progressive neurological deficits related to vascular steal. Complete treatment is warranted for patients with progressive neurological deficits caused by hemorrhage of the AVM. This selection process plays a significant role in the relatively low combined morbidity and mortality rates for Grade IV and Grade V AVMs (17 and 22%, respectively) reported by the cerebrovascular group in both retrospective and prospective studies. 11).

The aim of a study was to compare operatively and non-operatively managed high-grade arteriovenous malformations (AVMs) and to identify risk factors for surgical morbidity. Three hundred and ninety-one consecutively enrolled patients with AVMs were graded using the Spetzler Martin grading scheme. Forty-six of these patients had grade 4 or 5 AVMs. Twenty-nine patients underwent surgery and 17 were conservatively managed. During an average of 33 months follow-up the non-operative group experienced a decline in function in 27% of cases followed. These deteriorations were due to haemorrhage, progressive neurological deficits and seizures. In the surgical group completing treatment there was a mortality and morbidity impacting on self-care of 15%. In those without deep perforating arterial supply the morbidity was 10% and with deep perforating arterial supply or deep meningeal recruitment there was a combined morbidity and mortality of 44%. This difference in outcome was statistically significant (P<0.01). We conclude that high-grade AVMs have a high operative morbidity. However, these lesions often have a poor natural history and with careful selection (based on the presence or absence of deep perforating arterial supply) a group can be selected that benefits from surgery. Grade 4 and 5 AVMs with supply from lenticulostriate, choroidal, thalamic deep perforating arteries or deep meningeal recruitment may be best treated conservatively or possibly by multimodality treatment utilising radiotherapy and embolisation combined with surgery 12).


Spetzler RF, Martin NA.: A proposed grading system for arteriovenous malformations. J Neurosurg 65: 476– 483, 1986.

Ogilvy CS, Stieg PE, Awad I, Brown RD, Jr, Kondziolka D, Rosenwasser R, Young WL, Hademenos G, Special Writing Group of the Stroke Council American Stroke Association : AHA Scientific Statement: Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group of the Stroke Council, American Stroke Association. Stroke 32: 1458– 1471, 2001.

Krings T, Hans FJ, Geibprasert S, Terbrugge K.: Partial “targeted” embolisation of brain arteriovenous malformations. Eur Radiol 20: 2723– 2731, 2010.

Le Feuvre D, Taylor A.: Target embolization of AVMs: identification of sites and results of treatment. Interv Neuroradiol 13: 389– 394, 2007.
5) , 12)

Ferch RD, Morgan MK. High-grade arteriovenous malformations and their management. J Clin Neurosci. 2002 Jan;9(1):37-40. doi: 10.1054/jocn.2000.0927. PMID: 11749015.
6) , 9)

Laakso A, Dashti R, Juvela S, Isarakul P, Niemelä M, Hernesniemi J. Risk of hemorrhage in patients with untreated Spetzler-Martin grade IV and V arteriovenous malformations: a long-term follow-up study in 63 patients. Neurosurgery. 2011 Feb;68(2):372-7; discussion 378. doi: 10.1227/NEU.0b013e3181ffe931. PMID: 21135742.

Winkler EA, Lu A, Morshed RA, Yue JK, Rutledge WC, Burkhardt JK, Patel AB, Ammanuel SG, Braunstein S, Fox CK, Fullerton HJ, Kim H, Cooke D, Hetts SW, Lawton MT, Abla AA, Gupta N. Bringing high-grade arteriovenous malformations under control: clinical outcomes following multimodality treatment in children. J Neurosurg Pediatr. 2020 Apr 10:1-10. doi: 10.3171/2020.1.PEDS19487. Epub ahead of print. PMID: 32276243.

Marciscano AE, Huang J, Tamargo RJ, Hu C, Khattab MH, Aggarwal S, Lim M, Redmond KJ, Rigamonti D, Kleinberg LR. Long-term Outcomes With Planned Multistage Reduced Dose Repeat Stereotactic Radiosurgery for Treatment of Inoperable High-Grade Arteriovenous Malformations: An Observational Retrospective Cohort Study. Neurosurgery. 2017 Feb 14. doi: 10.1093/neuros/nyw041. [Epub ahead of print] PubMed PMID: 28201783.

Jayaraman MV, Marcellus ML, Do HM, Chang SD, Rosenberg JK, Steinberg GK, Marks MP. Hemorrhage rate in patients with Spetzler-Martin grades IV and V arteriovenous malformations: is treatment justified? Stroke. 2007 Feb;38(2):325-9. doi: 10.1161/ Epub 2006 Dec 28. PMID: 17194881.

Han PP, Ponce FA, Spetzler RF. Intention-to-treat analysis of Spetzler-Martin grades IV and V arteriovenous malformations: natural history and treatment paradigm. J Neurosurg. 2003 Jan;98(1):3-7. doi: 10.3171/jns.2003.98.1.0003. PMID: 12546345.

Lumbosacral dural arteriovenous fistula

Lumbosacral dural arteriovenous fistula


The most common neurologic findings at the time of admission were paraparesis (85%), sphincter dysfunction (70%), and sensory disturbances (20%).

Clinical symptoms caused by deep lumbosacral spinal dural arteriovenous fistulas are comparable with those of spinal dural arteriovenous fistulas at other locations 1).


Spinal dural arteriovenous fistulas located in the deep lumbosacral region are rare and the most difficult to diagnose among spinal dural arteriovenous fistulas located elsewhere in the spinal dura. Specific clinical and radiologic features of these fistulas are still inadequately reported.

Medullary congestion in association with an enlargement of the filum vein or other lumbar radicular veins is a characteristic finding in these patients. Spinal time-resolved contrast-enhanced dynamic MRA facilitates the detection of the drainage vein and helps to localize deep lumbosacral-located fistulas with a high sensitivity before DSA. Definite detection of these fistulas remains challenging and requires sufficient visualization of the fistula-supplying arteries and draining veins by conventional spinal angiography.

Medullary T2 hyperintensity and contrast enhancement were present in most cases. The filum vein and/or lumbar veins were dilated in 19/20 (95%) patients. Time-resolved contrast-enhanced dynamic MRA indicated a spinal dural arteriovenous fistula at or below the L5 vertebral level in 7/8 (88%) patients who received time-resolved contrast-enhanced dynamic MRA before DSA. A bilateral arterial supply of the fistula was detected via DSA in 5 (25%) patients 2).


Patients with deep lumbosacral dural arteriovenous fistula had a higher risk of early recurrence compared to patients with thoracolumbar SDAVF, with a considerable percentage of late functional deterioration. Thus strict clinical and radiologic long-term follow-up examinations are recommended in those patients 3).

Case series

Jablawi et al. retrospectively evaluated all data of patients with spinal dural arteriovenous fistulas treated and/or diagnosed in RWTH Aachen University Hospital, and Paracelsus Kliniken, OsnabrückGermany, between 1990 and 2017. Twenty patients with deep lumbosacral spinal dural arteriovenous fistulas were included in this study.

They retrospectively analyzed our radiological and medical records for patients presenting with SDAVF between 1990 and 2018 at the University Hospital Aachen. We identified twenty patients with a lsDAVF. All patients were treated surgically. One patient died of pulmonary embolism three months after treatment and was excluded from our outcome analysis. Clinical data at the time of admission, discharge, one year after discharge and at the last follow-up were evaluated according to the modified Aminoff-Logue disability score (AL-score) for this analysis.

The mean age was 65 ± 7 years (median, 67; range, 53-78), sixteen patients (84 %) were male. After surgery, four patients developed a recurrent fistula in the same shunt zone and were re-treated microsurgically. Follow-up data one year after treatment was available in 15 patients. No relevant changes in AL-score were observed within this period. For the long-term follow-up analysis, data of 13 patients were available; 38.5 % of patients developed late functional deterioration.

In this cohort, patients with deep lumbosacral dural arteriovenous fistula had a higher risk of early recurrence compared to patients with thoracolumbar SDAVF, with a considerable percentage of late functional deterioration. Thus strict clinical and radiologic long-term follow-up examinations are recommended in those patients 4).

Rosi et al. describe a case series of five patients presenting with a conus medullaris AVS associated with a lower lumbar or sacral DAVF.

Three of the patients were <30 years old at presentation. In four of these five cases the intradural scAVS drained caudally, engorging the epidural plexus in the same location as the sDAVF. In only one case, who presented with thrombosis of the drainage of the main compartment of a conus medullaris pial AVF, was the location of the DAVF opposite to the location of the residual drainage.

They discuss the pathophysiological link between scAVS and sDAVF on the basis of the rarity of the DAVF, the uncommon association between scAVS and sDAVF, the presence of sDAVF in young patients, and the venous hypertension created by the venous drainage towards the sacral area responsible for angiogenesis creating the dural shunt 5).

Twenty-five consecutive patients with 16 thoracic dural arteriovenous fistula and 9 lumbosacral DAVFs were included (mean age, 63.9 years; 20 men). All patients presented with progressive myelopathy. Preoperative and postoperative neurologic deficits were compared between thoracic and lumbosacral DAVF groups. Using magnetic resonance imaging, the extent of T2 high-intensity areas and signal flow voids were documented. Follow-up after surgical interventions ranged from 6 to 96 months (mean, 38.1 months).

Preoperatively, patients suffering lumbosacral DAVF tended to be more severely disabled compared with thoracic DAVF patients. Lumbosacral DAVF patients exhibited diminished patellar (P = 0.04) and Achilles tendon reflexes (P < 0.01), while most thoracic DAVF patients exhibited hyperreflexia. In magnetic resonance imaging, signal flow voids around the spinal cord were evident in only 4 of 9 lumbosacral DAVF patients (P = 0.012). Rather, a serpentine signal flow void of the filum terminale was a hallmark of lumbosacral DAVFs to distinguish them from thoracic DAVFs. In the lumbosacral DAVF group, postoperative improvements were significantly better in micturition function (P = 0.02).

In lumbosacral DAVF, postoperative micturition function recovery was superior to thoracic DAVF. Intradural lumbar signal flow void is indicative of lumbosacral DAVF. For appropriate management, it is important to recognize these differences between lumbosacral and thoracic DAVF 6).

Case reports

A 65-year-old man presented with a 4-year history of progressive sensory, motor, and sphincter dysfunction. Spinal magnetic resonance imaging and digital subtraction angiography showed 2 spinal dural arteriovenous fistulas (fed by the right L2 lumbar artery and the right lateral sacral artery, respectively) and 1 perimedullary arteriovenous fistula (fed by the filum terminale artery from the left L2 lumbar artery [i.e., filum terminale arteriovenous fistulas]. A hybrid technique was used to perform embolization of the right L2 spinal dural arteriovenous fistula and microsurgery of the L5 level filum terminale vein. The patient was asymptomatic 1 year later.

Multifocal spinal vascular malformations may coexist in 1 case, and standardized spinal digital subtraction angiography, including the bilateral internal iliac arteries and median sacral artery, should be performed to avoid a missed diagnosis. The concomitant phenomenon indicates that venous hypertension may be a risk factor for the development of arteriovenous fistulas. Hybrid techniques are effective in treatment of multifocal and complex spinal AVMs 7).

Seven cases of adult spinal vascular malformations presenting in conjunction with spinal dysraphism have been reported in the literature. Two of these involved male patients with a combined dural arteriovenous fistula (DAVF) and lipomyelomeningocele. The authors present the third case of a patient with an extraspinal DAVF and associated lipomyelomeningocele in a lumbosacral location. A 58-year-old woman with rapid decline in bilateral motor function 10 years after a prior L4-5 laminectomy and cord detethering for diagnosed tethered cord underwent magnetic resonance imaging showing evidence of persistent cord tethering and a lipomyelomeningocele. Diagnostic spinal angiogram showed a DAVF with arterial feeders from bilateral sacral and the right internal iliac arteries. The patient underwent Onyx embolization of both feeding right and left lateral sacral arteries. At 6-month follow-up, MRI revealed decreased flow voids and new collateralized supply to the DAVF. The patient underwent successful lipomyelomeningocele exploration, resection, AV fistula ligation, and cord detethering. This report discusses management of this patient as well as the importance of endovascular embolization followed by microsurgery for the treatment of cases with combined vascular and dysraphic anomalies 8).


1) , 2) , 3) , 4)

Jablawi F, Nikoubashman O, Dafotakis M, Schubert GA, Hans FJ, Mull M. Treatment strategy and long-term outcome in patients with deep lumbosacral arteriovenous fistulas. A single center analysis in nineteen patients. Clin Neurol Neurosurg. 2019 Nov 11;188:105596. doi: 10.1016/j.clineuro.2019.105596. [Epub ahead of print] PubMed PMID: 31739154.

Rosi A, Consoli A, Condette-Auliac S, Coskun O, Di Maria F, Rodesch G. Concomitant conus medullaris arteriovenous shunts and sacral dural arteriovenous fistulas: pathophysiological links related to the venous drainage of the lesions in a series of five cases. J Neurointerv Surg. 2018 Jun;10(6):586-592. doi: 10.1136/neurintsurg-2017-013505. Epub 2018 Jan 19. PubMed PMID: 29352055.

Endo T, Kajitani T, Inoue T, Sato K, Niizuma K, Endo H, Matsumoto Y, Tominaga T. Clinical Characteristics of Lumbosacral Spinal Dural Arteriovenous Fistula (DAVF)-Comparison with Thoracic DAVF. World Neurosurg. 2018 Feb;110:e383-e388. doi: 10.1016/j.wneu.2017.11.002. Epub 2017 Nov 10. PubMed PMID: 29133002.

Li J, Li G, Bian L, Hong T, Yu J, Zhang H, Ling F. Concomitant Lumbosacral Perimedullary Arteriovenous Fistula and Spinal Dural Arteriovenous Fistula. World Neurosurg. 2017 Sep;105:1041.e7-1041.e14. doi: 10.1016/j.wneu.2017.06.149. Epub 2017 Jul 4. PubMed PMID: 28684369.

Krisht KM, Karsy M, Ray WZ, Dailey AT. Extraspinal type I dural arteriovenous fistula with a lumbosacral lipomyelomeningocele: a case report and review of the literature. Case Rep Neurol Med. 2015;2015:526321. doi: 10.1155/2015/526321. Epub 2015 Apr 8. PubMed PMID: 25949837; PubMed Central PMCID: PMC4407406.

Ferumoxytol magnetic resonance imaging for intracranial arteriovenous malformation

Ferumoxytol magnetic resonance imaging for intracranial arteriovenous malformation

Central nervous system vascular malformations (VMs) result from abnormal vascular- and/or angiogenesis. Cavernomas and arteriovenous malformations are also sites of active inflammation 1).

Inflammation is increasingly being recognized as contributing to the underlying pathophysiology of cerebral aneurysms and brain arteriovenous malformationFerumoxytol is being increasingly used for both its prolonged intravascular imaging characteristics and its utility as an inflammatory marker when imaged in a delayed fashion 2) 3) 4) 5).

Children with intracranial arteriovenous malformations (AVMs) undergo digital DSA for lesion surveillance following their initial diagnosis. However, DSA carries risks of radiation exposure, particularly for the growing pediatric brain and over lifetime. Huang et al. evaluated whether MRI enhanced with a blood pool ferumoxytol (Fe) contrast agent (Fe-MRI) can be used for surveillance of residual or recurrent AVMs.

A retrospective cohort was assembled of children with an established AVM diagnosis who underwent surveillance by both DSA and 3-T Fe-MRI from 2014 to 2016. Two neuroradiologists blinded to the DSA results independently assessed Fe-enhanced T1-weighted spoiled gradient recalled acquisition in steady state (Fe-SPGR) scans and, if available, arterial spin labeling (ASL) perfusion scans for residual or recurrent AVMs. Diagnostic confidence was examined using a Likert scale. Sensitivity, specificity, and intermodality reliability were determined using DSA studies as the gold standard. Radiation exposure related to DSA was calculated as total dose area product (TDAP) and effective dose.

Fifteen patients were included in this study (mean age 10 years, range 3-15 years). The mean time between the first surveillance DSA and Fe-MRI studies was 17 days (SD 47). Intermodality agreement was excellent between Fe-SPGR and DSA (κ = 1.00) but poor between ASL and DSA (κ = 0.53; 95% CI 0.18-0.89). The sensitivity and specificity for detecting residual AVMs using Fe-SPGR were 100% and 100%, and using ASL they were 72% and 100%, respectively. Radiologists reported overall high diagnostic confidence using Fe-SPGR. On average, patients received two surveillance DSA studies over the study period, which on average equated to a TDAP of 117.2 Gy×cm2 (95% CI 77.2-157.4 Gy×cm2) and an effective dose of 7.8 mSv (95% CI 4.4-8.8 mSv).

Fe-MRI performed similarly to DSA for the surveillance of residual AVMs. Future multicenter studies could further investigate the efficacy of Fe-MRI as a noninvasive alternative to DSA for monitoring AVMs in children 6).

The purpose of a study was to evaluate the performance of ferumoxytol-enhanced MRA using a high-resolution 3D volumetric sequence (fe-SPGR) for visualizing and grading pediatric brain AVMs in comparison with CTA and DSA, which is the current imaging gold standard. METHODS In this retrospective cohort study, 21 patients with AVMs evaluated by fe-SPGR, CTA, and DSA between April 2014 and August 2017 were included. Two experienced raters graded AVMs using Spetzler-Martin criteria on all imaging studies. Lesion conspicuity (LC) and diagnostic confidence (DC) were assessed using a 5-point Likert scale, and interrater agreement was determined. The Kruskal-Wallis test was performed to assess the raters’ grades and scores of LC and DC, with subsequent post hoc pairwise comparisons to assess for statistically significant differences between pairs of groups at p < 0.05. RESULTS Assigned Spetzler-Martin grades for AVMs on DSA, fe-SPGR, and CTA were not significantly different (p = 0.991). LC and DC scores were higher with fe-SPGR than with CTA (p < 0.05). A significant difference in LC scores was found between CTA and fe-SPGR (p < 0.001) and CTA and DSA (p < 0.001) but not between fe-SPGR and DSA (p = 0.146). A significant difference in DC scores was found among DSA, fe-SPGR, and CTA (p < 0.001) and between all pairs of the groups (p < 0.05). Interrater agreement was good to very good for all image groups (κ = 0.77-1.0, p < 0.001). CONCLUSIONS Fe-SPGR performed robustly in the diagnostic evaluation of brain AVMs, with improved visual depiction of AVMs compared with CTA and comparable Spetzler-Martin grading relative to CTA and DSA 7).



Dósa E, Tuladhar S, Muldoon LL, Hamilton BE, Rooney WD, Neuwelt EA. MRI using ferumoxytol improves the visualization of central nervous system vascular malformations. Stroke. 2011 Jun;42(6):1581-8. doi: 10.1161/STROKEAHA.110.607994. Epub 2011 Apr 14. PubMed PMID: 21493906; PubMed Central PMCID: PMC3412426.

Zanaty M, Chalouhi N, Starke RM, Jabbour P, Hasan D. Molecular Imaging in Neurovascular Diseases: The Use of Ferumoxytol to Assess Cerebral Aneurysms and Arteriovenous Malformations. Top Magn Reson Imaging. 2016 Apr;25(2):57-61. doi: 10.1097/RMR.0000000000000086. Review. PubMed PMID: 27049242.

Chalouhi N, Jabbour P, Magnotta V, Hasan D. Molecular imaging of cerebrovascular lesions. Transl Stroke Res. 2014 Apr;5(2):260-8. doi: 10.1007/s12975-013-0291-0. Epub 2013 Oct 23. Review. PubMed PMID: 24323714.

Chalouhi N, Jabbour P, Magnotta V, Hasan D. The emerging role of ferumoxytol-enhanced MRI in the management of cerebrovascular lesions. Molecules. 2013 Aug 13;18(8):9670-83. doi: 10.3390/molecules18089670. Review. PubMed PMID: 23945642; PubMed Central PMCID: PMC6270297.

Hasan DM, Amans M, Tihan T, Hess C, Guo Y, Cha S, Su H, Martin AJ, Lawton MT, Neuwelt EA, Saloner DA, Young WL. Ferumoxytol-enhanced MRI to Image Inflammation within Human Brain Arteriovenous Malformations: A Pilot Investigation. Transl Stroke Res. 2012 Jul;3(Suppl 1):166-73. doi: 10.1007/s12975-012-0172-y. PubMed PMID: 23002401; PubMed Central PMCID: PMC3445332.

Huang Y, Singer TG, Iv M, Lanzman B, Nair S, Stadler JA, Wang J, Edwards MSB, Grant GA, Cheshier SH, Yeom KW. Ferumoxytol-enhanced MRI for surveillance of pediatric cerebral arteriovenous malformations. J Neurosurg Pediatr. 2019 Jul 19:1-8. doi: 10.3171/2019.5.PEDS1957. [Epub ahead of print] PubMed PMID: 31323627.

Iv M, Choudhri O, Dodd RL, Vasanawala SS, Alley MT, Moseley M, Holdsworth SJ, Grant G, Cheshier S, Yeom KW. High-resolution 3D volumetric contrast-enhanced MR angiography with a blood pool agent (ferumoxytol) for diagnostic evaluation of pediatric brain arteriovenous malformations. J Neurosurg Pediatr. 2018 Sep;22(3):251-260. doi: 10.3171/2018.3.PEDS17723. Epub 2018 Jun 8. PubMed PMID: 29882734.