ManuscriptThe authors describe a 27-year old man who developed an unruptured anterior-inferior cerebellar artery feeding aneurysm from a transverse-sigmoid dAVF and its subsequent resolution with the treatment of the dAVF. The patient, with a known history of left transverse and sigmoid sinus thrombosis, presented with pulse-synchronous tinnitus. Angiography revealed an extensive dAVF, with feeders from both the extracranial and  intracranial circulations, involving the right transverse sinus, the torcula, and the left transverse/sigmoid sinuses. Multimodal endovascular and open surgical therapy was employed. Prior to a planned second-stage treatment for the left sigmoid sinus component, the dAVF improved significantly, but a small flow-related aneurysm  developed on the left AICA feeding the petrous dural region in the interval. Resection of the involved sigmoid sinus resulted in resolution of the aneurysm. This is the first reported case of an unruptured feeding-artery aneurysm in an intracranial dAVF that resolved spontaneously with the treatment of the dAVF. Until more is known about its natural history, the decision on when and whether to treat an unruptured dAVF feedingartery  aneurysm must be made on an individual basis

Couldwell, William T.

Kan, Peter

English

The University of Utah: J. Willard Marriott Digital Library

c c c c University of Utah Institutional Repository Author Manuscript 1 Resolution of an Anterior-Inferior Cerebellar Artery Feeding Aneurysm with the Treatment of a Transverse-Sigmoid Dural Arteriovenous Fistula Case Report Peter Kan, M.D., Edwin A. Stevens, M.D., Judith Warner, M.D. and William T. Couldwell, M.D., Ph.D.* Departments of Neurosurgery (PK, WTC), Radiology (EAS), and Ophthalmology (JW), University of Utah School of Medicine, Salt Lake City, Utah *Corresponding author. c c c c University of Utah Institutional Repository Author Manuscript 2 Peter Kan, M.D. Judith Warner, M.D. Resident Associate Professor Department of Neurosurgery Department of Ophthalmology University of Utah School of Medicine University of Utah School of Medicine 30 North 1900 East, Suite 3B409 Moran Eye Center, 5th Floor Salt Lake City, UT 84132 Salt Lake City, UT 84132 Phone: 801-581-6908 Phone: 801-581-2352 Fax: 801-581-4138 Fax: 801-581-3357 Email: peter.kantzeman@yahoo.ca Email: judith.warner@hsc.utah.edu Edwin A. Stevens, M.D. William T. Couldwell, M.D., Ph.D. Professor and Chair Professor and Joseph J. Yager Chair Department of Radiology Department of Neurosurgery University of Utah School of Medicine University of Utah School of Medicine 30 North 1900 East, Suite 1A071 30 North 1900 East, Suite 3B409 Salt Lake City, UT 84132 Salt Lake City, UT 84132 Phone: 801-581-8699 Phone: 801-581-6908 Fax: 801-581-2414 Fax: 801-581-4138 Email: steve.stevens@hsc.utah.edu Email: william.couldwell @hsc.utah.edu c c c c University of Utah Institutional Repository Author Manuscript 3 Abstract The authors describe a 27-year old man who developed an unruptured anterior-inferior cerebellar artery feeding aneurysm from a transverse-sigmoid dA VF and its subsequent resolution with the treatment of the dA VF. The patient, with a known history of left transverse and sigmoid sinus thrombosis, presented with pulse-synchronous tinnitus. Angiography revealed an extensive dA VF, with feeders from both the extracranial and intracranial circulations, involving the right transverse sinus, the torcula, and the left transverse/sigmoid sinuses. Multimodal endovascular and open surgical therapy was employed. Prior to a planned second-stage treatment for the left sigmoid sinus component, the dAVF improved significantly, but a small flow-related aneurysm developed on the left AICA feeding the petrous dural region in the interval. Resection of the involved sigmoid sinus resulted in resolution of the aneurysm. This is the first reported case of an unruptured feeding-artery aneurysm in an intracranial dA VF that resolved spontaneously with the treatment of the dA VF. Until more is known about its natural history, the decision on when and whether to treat an unruptured dA VF feeding-artery aneurysm must be made on an individual basis. Running Head: Dural Arteriovenous Fistula with a Feeding-Artery Aneurysm Key Words: Aneurysms; Dural Arteriovenous Fistulas, Endovascular therapy, Surgery c c c c University of Utah Institutional Repository Author Manuscript 4 Introduction Dural arteriovenous fistulas (dA VFs) are vascular abnormalities of the dura mater that typically involve the dural sinuses, most commonly the transverse and sigmoid sinuses.1 dA VFs are acquired lesions, often developing after dural sinus thrombosis (DST), and have a variable presentation ranging from a pulse-synchronous tinnitus to intracerebral hemorrhage. Unlike with arteriovenous malformations (A VMs), concurrent arterial aneurysms and intracranial dA VFs are extremely rare.2-4 The two other patients detailed in the literature both presented with subarachnoid hemorrhage (SAH). We present a unique case of a patient who developed an unruptured anterior-inferior cerebellar artery (AICA) feeding-artery aneurysm from a transverse-sigmoid dA VF that resolved spontaneously with the treatment of the dAVF. The unique issues surrounding the management of feeding-artery aneurysms associated with an intracranial dA VF are discussed. History and Examination This 27-year-old man originally presented with an acute headache, vomiting, and meningismus in August 2003. On the following day, he developed horizontal diplopia and was found to have bilateral 6th nerve palsies and papilledema. A diagnosis of intracranial hypertension was made, and he was started on Diamox. The origin of the intracranial hypertension was initially thought to be doxycycline-related.5 Further evaluation with a magnetic resonance venogram (MRV) revealed thrombosis of the left transverse and sigmoid sinus. The patient was started on Coumadin. His hypercoagulable work-up was remarkable for hyperhomocysteinemia. His diplopia c c c c University of Utah Institutional Repository Author Manuscript 5 and papilledema resolved with acetazolamide therapy, but several months later, despite maximal medical therapy, he had recurrence of his headaches and diplopia, and he developed visual field deficits associated with severe papilledema. As a result, he underwent a right optic nerve sheath fenestration. Although the papilledema improved, the remainder of the patient's signs and symptoms of elevated pressure persisted. Ten months after his initial presentation, the patient developed a palpable and prominent left occipital artery with an audible bruit. Cerebral angiogram revealed an extensive dA VF involving the proximal right transverse sinus, the torcula, the left transverse sinus, and the left sigmoid sinus. Supply to the arteriovenous fistula was from the occipital arteries, the middle meningeal arteries, the left posterior meningeal artery, and a muscular branch off the left vertebral artery. Supply was also present from the tentorial branches and a prominent left anterior-inferior cerebellar artery (Fig. 1). No cortical reflux was seen. Because maximal medical therapy and optic nerve sheath fenestration had not relieved the situation and there was the potential for deterioration of the left optic nerve function, multimodal and staged therapy was planned. The patient underwent staged transarterial embolizations, followed by a bilateral occipital craniotomy for skeletonization and placement of interpositional dura xenograft (bovine pericardium) at the involved transverse dural sinuses and the left sigmoid sinus. The goal of the operation was to disconnect all of the involved sinuses from aberrant arterial feeders and to prevent future recurrences with the use of interpositional dura xenograft. Postoperative angiography showed marked improvement of the dA VF with small residual feeders to the transverse and sigmoid sinus component on the left. The patient's follow-up angiogram 4 c c c c University of Utah Institutional Repository Author Manuscript 6 months later, however, revealed slightly more prominent feeders and an interval development of a 3-mm left AICA feeding-artery aneurysm beyond the floccular segment (Fig. 2). He subsequently underwent a planned second-stage trans temporal (presigmoid, retrolabyrinthine) approach for resection of the involved sigmoid sinus on the left. The sinus was removed, from the entrance of the vein of Labbe to the jugular bulb. The left transverse sinus was then coil-embolized through a transvenous approach. A I-month follow-up angiogram revealed complete resolution of the feeding-artery AICA aneurysm (Fig. 3). The patient's symptoms, papilledema, sixth nerve palsies, and bruit also resolved completely. Discussion Dural arteriovenous fistulas represent 10% to 15% of all intracranial vascular malformations. They consist of pathologic vascular channels within the dura mater and usually involve the walls of dural sinuses. Patients typically present between 40 and 60 years of age at various clinical stages, ranging from a pulse-synchronous bruit to a neurologic deficit to intracerebral hemorrhage. 1 All dA VFs are acquired, and many are preceded by DST.6-8 1t is believed that venous hypertension from DST enlarges the normally present microscopic arteriovenous shunts in the walls of the sinus, leading to the formation of dA VFs. In addition, venous hypertension induces ischemia, which may also play an important role in the pathogenesis of dA VFs by stimulating angiogenic growth factors and angiogenesis.9 c c c c University of Utah Institutional Repository Author Manuscript 7 Several grading schemes lO-12 have been proposed to predict the clinical course of dA VFs. They all suggest that cortical venous drainage, a high-grade feature, is associated with a significant risk of intracerebral hemorrhage (33% to 42%).1,13 Dural arteriovenous fistulas involving the transverse and sigmoid sinuses are the most common, representing up to 50% of cases. The epicenter is usually at the junction of the transverse and sigmoid sinus. Only 10% to 15% of these lesions exhibit aggressive behavior.1 Their arterial supply is typically from both the extracranial (branches of the occipital and middle meningeal artery, posterior auricular artery, and ascending pharyngeal artery) and the intracranial system (posterior meningeal branches of the vertebral artery and marginal tentorial branches of the meningohypophyseal trunk). Although there are reports of spinal dA VF with associated feeding artery aneurysms,14,15 there are only a few reported cases of feeding-artery aneurysm associated with intracranial dA VFS?-4 The two cases detailed in the literature involved an AICA and a posterior-inferior cerebellar artery (PICA) feeding-artery aneurysm. Both aneurysms presented with SAH.and were treated surgically with good outcomes.2,3 In contrast, our patient developed an asymptomatic AICA feeding-artery aneurysm from a transverse-sigmoid dA VF that resolved spontaneously with the treatment of the dA VF. The etiology of feeding-artery aneurysms is controversial, but the main theory focuses on flow-related stress on the arterial feeders. 16,17 Based on the morphology of the feeding vessel, we believe that the feeding-artery aneurysm in our case is also flow-related and is a result of the hemodynamic stress on the anterior inferior cerebellar artery caused by the high-flow dAVF. c c c c University of Utah Institutional Repository Author Manuscript 8 Intracranial hemorrhage resulting from venous hypertension is a main cause of morbidity and mortality related to dA VF. Cortical venous drainage, as mentioned, is the major risk factor. At present, the additional effect of concurrent arterial aneurysms on the hemorrhagic risk of dAVFs is unknown, although these feeding-aneurysms can clearly hemorrhage.2,3 The literature on A VMs and concurrent aneurysms may shed some light on the issue. Aneurysms associated with A VMs have been reported in 5% to 7% of cases. I8 ,19 and several retrospective and prospective studies suggested a higher risk of hemorrhage in patients with A VM and concurrent feeding-artery and intranidal aneurysms. I8-21 Brown et a1.22 showed an increased annual risk of 7% for intracranial hemorrhage in the setting of an unruptured AVM with a concurrent intranidal or feeding-artery aneurysm, giving an annual hemorrhage rate of 10%. The treatment of feeding-artery aneurysms with AVMs is controversial, Some recommend a conservative approach as they believe that these are flow-related lesions that may regress or remain stable once the A VM is removed. 1 1 Others propose that they should be treated immediately because of their risk of hemorrhage. 18,23 At present, there is no treatment guideline regarding concurrent arterial aneurysm and dA VF. In our case, we elected to follow the aneurysm, because of its small size and its lack of symptoms, and because we believed it was a flow-related lesion that would regress once the dA VF was obliterated. In support of our theory, the aneurysm regressed spontaneously after the staged, multimodal treatment of the dA VF. Until more data are available regarding concurrent aneurysms and dA VFs, however, the decision of when and whether to treat an unruptured dAVF feeding-artery aneurysm must be made on an individual basis. c c c c University of Utah Institutional Repository Author Manuscript 9 Acknowledgments We thank Kristin Kraus for her editorial support during the preparation of this paper. c c c c University of Utah Institutional Repository Author Manuscript 10 References 1. Malek AM, Halbach VV, Higashida RT, Phatouros CC, Meyers PM, Dowd CF. Treatment of dural arteriovenous malformations and fistulas. Neurosurg Clin N Am 2000;11:147-166, ix 2. Kaech D, de Tribolet N, Lasjaunias P. Anterior inferior cerebellar artery aneurysm, carotid bifurcation aneurysm, and dural arteriovenous malformation of the tentorium in the same patient. Neurosurgery 1987;21:575-582 3. Gacs G, Vinuela F, Fox AJ, Drake CG. Peripheral aneurysms of the cerebellar arteries. Review of 16 cases. J Neurosurg 1983;58:63-68 4. Houser OW, Baker HL, Jr., Rhoton AL, Jr., Okazaki H. Intracranial dural arteriovenous malformations. Radiology 1972; 105 :55-64 5. Friedman DI, Gordon LK, Egan RA, Jacobson DM, Pomeranz H, Harrison AR, Goldhammer Y. Doxycycline and intracranial hypertension. Neurology 2004;62:2297-2299 6. Kutluk K, Schumacher M, Mironov A. The role of sinus thrombosis in occipital dural arteriovenous malformations--development and spontaneous closure. Neurochirurgia (Stuttg) 1991 ;34: 144-147 7. Chaudhary MY, Sachdev VP, Cho SH, Weitzner I, Jr., Puljic S, Huang YP. Dural arteriovenous malformation of the major venous sinuses: an acquired lesion. AJNR Am J NeuroradioI1982;3:13-19 8. Touho H, Ohnishi H, Komatsu T, Furuoka N, Karasawa J. Dural arteriovenous fistula caused by sinus thrombosis--case report. Neurol Med Chir (Tokyo) 1994;34:543-546 c c c c University of Utah Institutional Repository Author Manuscript 11 9. Lawton MT, Jacobowitz R, Spetzler RF. Redefined role of angiogenesis in the pathogenesis of dural arteriovenous malformations. J Neurosurg 1997;87:267-274 10. Djindjian R, Cophignon J, Theron J, Merland n, Houdart R. Embolization by superselective arteriography from the femoral route in neuroradiology. Review of 60 cases. 1. Technique, indications, complications. Neuroradiology 1973;6:20-26 11. Redekop G, TerBrugge K, Montanera W, Willinsky R. Arterial aneurysms associated with cerebral arteriovenous malformations: classification, incidence, and risk of hemorrhage. J Neurosurg 1998;89:539-546 12. Lalwani AK, Dowd CF, Halbach VV. Grading venous restrictive disease in patients with dural arteriovenous fistulas of the transverse/sigmoid sinus. J Neurosurg 1993;79:11-15 13. Castaigne P, Bories J, Brunet P, Cassan JL, Meininger V, Merland n. [Arteriovenous fistulae of the dura mater. Clinical and radiological study of 13 cases]. Ann Med Interne (Paris) 1975;126:813-817 14. Koch C, Gottschalk S, Giese A. Dural arteriovenous fistula of the lumbar spine presenting with subarachnoid hemorrhage. Case report and review of the literature. J Neurosurg 2004;100:385-391 15. Malek AM, Halbach VV, Phatouros CC, Higashida RT, Dowd CF, Wachhorst S, Lawton MT. Spinal dural arteriovenous fistula with an associated feeding artery aneurysm: case report. Neurosurgery 1999;44:877-880 16. Okamoto S, Handa H, Hashimoto N. Location of intracranial aneurysms associated with cerebral arteriovenous malformation: statistical analysis. Surg Neurol 1984;22:335-340 c c c c University of Utah Institutional Repository Author Manuscript 12 17. Perret G, Nishioka H. Report on the cooperative study of intracranial aneurysms and subarachnoid hemorrhage. Section VI. Arteriovenous malformations. An analysis of 545 cases of cranio-cerebral arteriovenous malformations and fistulae reported to the cooperative study. J Neurosurg 1966;25:467-490 18. Batjer H, Suss RA, Samson D. Intracranial arteriovenous malformations associated with aneurysms. Neurosurgery 1986;18:29-35 19. Lasjaunias P, Piske R, Terbrugge K, Willinsky R. Cerebral arteriovenous malformations (C. A VM) and associated arterial aneurysms (AA). Analysis of 101 C. A VM cases, with 37 AA in 23 patients. Acta Neurochir (Wien) 1988;91 :29-36 20. Stapf C, Mohr JP, Pile-Spellman J, Sciacca RR, Hartmann A, Schumacher HC, Mast H. Concurrent arterial aneurysms in brain arteriovenous malformations with haemorrhagic presentation. J Neurol Neurosurg Psychiatry 2002;73:294-298 21. Westphal M, Grzyska U. Clinical significance of pedicle aneurysms on feeding vessels, especially those located in infratentorial arteriovenous malformations. J Neurosurg 2000;92:995-1001 22. Brown RD, Jr., Wiebers DO, Forbes GS. Unruptured intracranial aneurysms and arteriovenous malformations: frequency of intracranial hemorrhage and relationship of lesions. J Neurosurg 1990;73:859-863 23. Thompson RC, Steinberg GK, Levy RP, Marks MP. The management of patients with arteriovenous malformations and associated intracranial aneurysms. Neurosurgery 1998;43:202-211; discussion 211-202 c c c c University of Utah Institutional Repository Author Manuscript 13 Figure Legends Figure 1. Cerebral angiogram left maxillary (A) and vertebral (B) injections revealed an extensive dA VF involving the torcula and the left transverse and sigmoid sinus with feeders from both extracranial and intracranial circulations. Figure 2. Follow-up angiogram, left vertebral injection, after the first-staged operation revealed an interval development of a 3-mm left AICA feeding-artery aneurysm beyond the floccular segment (arrows). (A) Anteroposterior view; (B) lateral view. Figure 3. Follow-up angiogram, left vertebral injection, after the second-staged procedure demonstrated complete spontaneous resolution of the AICA feeding-artery aneurysm (arrows). . • 

Resolution of an anterior-inferior cerebellar artery feeding aneurysm with the treatment of a transverse-sigmoid dural arteriovenous fistula

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Resolution of an anterior-inferior cerebellar artery feeding aneurysm with the treatment of a transverse-sigmoid dural arteriovenous fistula

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