Commentary: Treatment Strategy of a Patient With a Brain Arteriovenous Malformation and Cranial Dural Fistula

Operative Neurosurgery, Apr 2019

Goren, Oded, Griessenauer, Christoph J, Dalal, Shamsher S, Schirmer, Clemens M

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Commentary: Treatment Strategy of a Patient With a Brain Arteriovenous Malformation and Cranial Dural Fistula

Concomitant cerebrovascular lesions can be a vexing issue even for experienced clinicians. The authors1 present a well-organized surgical video demonstrating the complex treatment strategy of a patient with a brain arteriovenous malformation (AVM) and cranial dural arteriovenous fistula (dAVF). The patient is a 56-yr-old male who presented with right temporal intracranial hemorrhage (ICH), 8 yr after complete surgical resection of left parietal grade 2 oligodendroglioma without ad-juvant therapy. Subsequent work up for the ICH included a brain magnetic resonance imaging (MRI) with contrast which failed to show a lesion and a diagnostic cerebral angiogram (DSA) which demonstrated a high-grade Borden II/Cognard IIa left parietal parasagittal dAVF.2,3 Following partial Onyx embolization of the dAVF, the ICH was surgically evacuated. On the 7-mo follow-up DSA, a right temporal AVM (Spetzler–Martin grade I) as well as recurrence of the Borden II/Cognard IIa left parietal dAVF were evident. Following partial Onyx embolization of the AVM and dAVF, both malformations were surgically resected successfully. Dural arteriovenous fistulas make up 10% to 15% of intracranial vascular malformations.4 Although their pathogenesis remains unclear, most dAVFs are believed to originate from thrombosis of a dural venous sinus, which subsequently leads to venous congestion and venous hypertension.5 The elevated venous pressure dilates small capillaries, which open direct shunts between dural arteries and veins thus creating dAVFs. Over time, this process may culminate in cortical venous reflux, thought to cause either undue venous hypertension or backpressure with possible dysfunction of the brain dependent on the antegrade drainage pathway and may ultimately lead to rupture of fragile parenchymal veins, potentially resulting in ICH. Adult dAVFs, which constitute most lesions and present most commonly in the fifth and sixth decades of life, are most common at the transverse, sigmoid, and cavernous sinuses. A relation with craniotomy has been cited as a potential precursor for the development of dAVF. Following craniotomy for tumor resection, dAVF has been reported to occur in the vicinity or remotely from the surgical site, and in an early or delayed fashion after surgery.6 As both vascular malformations presented in this case were detected on DSA as part of the initial work-up and on later follow-up, the authors highlight the importance of performing a DSA as the gold standard exam in a subset of patients presenting with ICH as well as the possible need for additional DSA as follow-up when the suspicion for vascular pathology is high. In our own practice we continue to see patients where even detailed MRI/MR angiography (MRA) examinations fail to uncover the fistulous point and only show signs of venous engorgement which is linked to the pathological lesion but does not in itself constitute the lesion. Additionally, even time-gated MRA does not offer the range of dynamic information that the experienced practitioner can gather from interpretation of the different injections and DSA runs. With this caveat we agree with the authors’ stance,1 it is important to note that the diagnosis of both low and high-grade dAVFs may be first detected on brain MRI. Unfortunately, MRI has become the de-facto first line approach when seeking a diagnosis for any symptomatology related to the head, supplanting history taking, examination, and experience. Conventional MRI, may demonstrate clusters of flow voids, engorged veins, dilated venous pouches, abnormal vascular enhancement, and signs of retrograde cortical venous drainage7 but there will be a staggering number of false positives associated with using this modality indiscriminately. Kwon and colleagues8 retrospectively reviewed 27 intracranial dAVF patients who were diagnosed by conventional DSA and underwent MRI. Their study showed that the MRI findings of dAVFs are closely related to type, and, the higher the type, the more common the findings such as white matter hyperintensity, hemorrhage, dilated vessels, venous pouch, and vascular enhancement. MR angiography is utilized as an adjunct to MRI in diagnosing dAVFs. Its role is to improve noninvasive screening by detecting flow-related enhancement.9 In the case presented of a patient who had a spontaneous right ICH, 8 yr after complete surgical resection of left parietal grade 2 oligodendroglioma, the initial work-up included a contrast-enhanced MRI which was reported as negative for a mass lesion. In our opinion considering the high index of suspicion for an intracranial vascular malformation as a possible etiology for the spontaneous right temporal ICH, MRI should have been scrutinized for a flow void cluster and for flow-related enhancement, which are the most common MRI and MRA findings, respectively. Furthermore, the authors demonstrate the utilization of combining endovascular and open microsurgical approaches for the treatment of intracranial vascular malformation. It is imperative to be aware that the contemporary management of complex brain AVM and dAVF often requires a multidisciplinary approach, including embolization, microsurgical resection, and/or stereotactic radiosurgery. Having a multidisciplinary team that brings all these perspectives to the table and a practice of presentation and open discussion before devising treatment plans can be the road to success in these cases where sometimes a single treatment modality-fits-all approach may not lead to consistently high-quality outcomes. Dural arteriovenous fistulas are rare lesions, a systematic review of all larger series published since 1966 yielded only slightly more than 2300 patients described. We are hoping that the desire to approve novel treatment devices through regulatory pathways may allow us to gain important insights of how to define the treatment risk that then can be contrasted with the observational risk which is better defined especially for lesions with high risk features with a combined risk of hemorrhage or death of 2.5% (95% CI 1.4-3.9) per year.10 In conclusion, we believe that dAVF is yet another disease entity that will benefit from deliberate practice and prospective data collection to inform clinical decision-making. Disclosure The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article. REFERENCES 1. Sattur MG , Abi-Aad KR , Tian F , Welz ME , Anderies B , Bendok BR . Treatment strategy of a patient with a brain arteriovenous malformation and cranial dural fistula: 2-Dimensional operative video . Oper Neurosurg  . 2019 ; 16 ( 5 ): 636 . 2. Borden JA , Wu JK , Shucart WA . A proposed classification for spinal and cranial dural arteriovenous fistulous malformations and implications for treatment . J Neurosurg  . 1995 ; 82 ( 2 ): 166 – 179 . Erratum in: J Neurosurg. 1995 Apr;82(4):705-6 . Google Scholar Crossref Search ADS PubMed   3. Cognard C , Gobin YP , Pierot L , Bailly AL , Houdart E , Casasco A , Chiras J , Merland JJ . Cerebral dural arteriovenous fistulas: Clinical and angiographic correlation with a revised classification of venous drainage . Radiology  . 1995 ; 194 ( 3 ): 671 – 680 . Google Scholar Crossref Search ADS PubMed   4. Kwon BJ , Han MH , Kang HS et al.  MR imaging findings of intracranial dural arteriovenous fistulas: Relations with venous drainage patterns . AJNR Am J Neuroradiol  . 2005 ; 26 ( 10 ): 2500 – 2507 . Google Scholar PubMed   5. Chaichana KL , Coon AL , Tamargo RJ , Huang J . Dural arteriovenous fistulas: Epidemiology and clinical presentation . Neurosurg Clin N Am  . 2012 ; 23 ( 1 ): 7 – 13 . Google Scholar Crossref Search ADS PubMed   6. Raper DM , Zukas AM , Schiff D , Asthagiri AR . Geographically remote cerebral venous sinus thrombosis in patients with intracranial tumors . World Neurosurg  . 2017 ; 98 : 555 – 562 . doi: 10.1016/j.wneu.2016.11.084 . Google Scholar Crossref Search ADS PubMed   7. Mossa-Basha M , Chen J , Gandhi D . Imaging of cerebral arteriovenous malformations and dural arteriovenous fistulas . Neurosurg Clin N Am  . 2012 ; 23 ( 1 ): 27 – 42 . Google Scholar Crossref Search ADS PubMed   8. Kwon BJ , Han MH , Kang HS et al.  MR imaging findings of intracranial dural arteriovenous fistulas: Relations with venous drainage patterns . AJNR Am J Neuroradiol  . 2005 ; 26 ( 10 ): 2500 – 2507 . Google Scholar PubMed   9. Chen JC , Tsuruda JS , Halbach VV . Suspected dural arteriovenous fistula: Results with screening MR angiography in seven patients . Radiology  . 1992 ; 183 ( 1 ): 265 – 271 Google Scholar Crossref Search ADS PubMed   10. Kobayashi A , Al-Shahi Salman R . Prognosis and treatment of intracranial dural arteriovenous fistulae: A systematic review and meta-analysis . Int J Stroke  . 2014 ; 9 ( 6 ): 670 – 677 . Google Scholar Crossref Search ADS PubMed   Copyright © 2018 by the Congress of Neurological Surgeons This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)


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Goren, Oded, Griessenauer, Christoph J, Dalal, Shamsher S, Schirmer, Clemens M. Commentary: Treatment Strategy of a Patient With a Brain Arteriovenous Malformation and Cranial Dural Fistula, Operative Neurosurgery, 2019, E140-E141, DOI: 10.1093/ons/opy290