- Department of Neurosurgery, University of Illinois at Chicago, 912 S. Wood St., M/C799, Chicago, IL, USA
Correspondence Address:
Sepideh Amin-Hanjani
Department of Neurosurgery, University of Illinois at Chicago, 912 S. Wood St., M/C799, Chicago, IL, USA
DOI:10.4103/2152-7806.134812
Copyright: © 2014 Amin-Hanjani S This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.How to cite this article: Amin-Hanjani S, Goodin S, Charbel FT, Alaraj A. Resolution of bilateral moyamoya associated collateral vessel aneurysms: Rationale for endovascular versus surgical intervention. Surg Neurol Int 19-Jun-2014;5:
How to cite this URL: Amin-Hanjani S, Goodin S, Charbel FT, Alaraj A. Resolution of bilateral moyamoya associated collateral vessel aneurysms: Rationale for endovascular versus surgical intervention. Surg Neurol Int 19-Jun-2014;5:. Available from: http://sni.wpengine.com/surgicalint_articles/resolution-of-bilateral-moyamoya-associated-collateral-vessel-aneurysms-rationale-for-endovascular-versus-surgical-intervention/
Abstract
Background:Management of aneurysms associated with deep collateral vessels in moyamoya disease is challenging both from an endovascular and a surgical standpoint. Difficulties with access or localization, and compromise of the collateral circulation with subsequent ischemia are the primary concerns, making direct obliteration potentially unfeasible or risky. Alternatively, superficial temporal artery–middle cerebral artery bypass is another potential strategy for resolution of these aneurysms.
Case Description:Presented are the findings and management for a patient with moyamoya disease and bilateral deep collateral vessel aneurysms, successfully treated with endovascular obliteration following a right-sided hemorrhage and subsequently with bypass for an unruptured but growing contralateral aneurysm.
Conclusions:A rationale and approach to management is outlined, as derived from review of the current literature and the illustrative case with bilateral collateral vessel aneurysms.
Keywords: Aneurysm, embolization, extracranial-intracranial bypass, moyamoya, surgical revascularization
INTRODUCTION
Although moyamoya disease (MMD) presents most commonly with symptoms of cerebral ischemia, hemorrhagic presentation is also a well-known phenomenon, more typically seen in adult patients.[
In this report, we discuss a patient with MMD presenting initially with hemorrhage and with bilateral deep collateral vessel aneurysms. We outline our management, including the rationale for an endovascular versus surgical bypass approach to achieve aneurysm obliteration.
CASE REPORT
A 43-year-old female presented to the hospital after being found unresponsive with preceding complaints of headaches and dizziness. Upon arrival, a computed tomographic (CT) scan of the head revealed a deep right-sided hemorrhage in the region of the posterior limb of the internal capsule with extensive intraventricular extension [
Figure 1
(a) CT scan of the brain demonstrating diffuse subarachnoid hemorrhage with intraventricular extension into the right temporal horn. (b, c) Right internal carotid artery (ICA) digital subtraction angiography (DSA) anterio-posterior (AP) view and lateral view, demonstrating advanced moyamoya disease with right middle cerebral artery (MCA) occlusion and collaterals originating from the ICA partially reconstituting the MCA. There is a 3-mm aneurysm seen on one of the thalamostriate vessels (arrow). (d) Fluoroscopic image of the skull (AP view) post n-BCA glue embolization of the thalamostriate aneurysm along with the feeding vessel. The aneurysm is filled with n-BCA glue cast (arrow). (e) AP view of right ICA DSA post n-BCA embolization. The aneurysm is completely obliterated (arrow: location of obliterated aneurysm)
Follow-up angiography was performed 1 year post embolization. The right-sided aneurysm remained well obliterated. The left internal carotid artery (ICA) injection showed occlusive changes in the supraclinoid ICA with typical moya collaterals, in addition to the finding of a pseudoaneurysm arising from a collateral vessel just lateral to the third ventricle. In retrospect, it was noted that the lesion had likely been present previously but had become substantially more prominent [Figure
Figure 2
(a, b)Vertebral artery (VA) DSA AP and lateral views demonstrating an unruptured aneurysm (arrow) on a collateral from the left PCA to the left anterior cerebral artery (ACA) and left MCA. (c, d) Selective DSA imaging, AP and lateral views, through a microcatheter introduced through the left PCA. A small 3-mm aneurysm (long arrow) is seen supplied by the posterior choroidal branch of the PCA. There is reconstitution of ACA and MCA (short arrows) from the aneurysm feeding vessels
Consequently, a surgical approach was entertained; direct obliteration through surgical trapping was felt to be ill advised given the deep location and the continued concerns regarding placing the territory supplied by the aneurysmal collateral at risk. Direct STA–MCA bypass and EDAS was planned with the specific intention of revascularizing the territory supplied by the collateral arising from the aneurysmal vessel and with the additional premise that subsequent embolization could then be pursued safely if the aneurysm did not resolve with revascularization alone. Intraoperatively, direct STA to MCA bypass was performed over the frontal cortical surface. The STA cut flow intraoperatively was 89 ml/min and the final bypass flow was 45 ml/min, indicating a successful bypass patency with a cut flow index of 0.5.[
Figure 3
(a) Left external carotid artery DSA (AP view) post superficial temporal artery (STA) to MCA bypass. There is robust filling of the left MCA territories through the bypass graft. (b, c) Lateral VA DSA imaging and left ICA AP 7 months post left STA-MCA bypass showing complete regression of the aneurysm (arrow; site of the obliterated aneurysm)
DISCUSSION
The incidence of aneurysm formation within the moyamoya adult population is 3-14%, and represents a major potential hemorrhagic risk for these patients.[
The formation of aneurysms in MMD is multifactorial and includes features related to hemodynamic stress and pathologic vessel architecture. More than half of these aneurysms can be considered saccular aneurysms developing in association with major arteries that make up the circle of Willis (COW). Others arise from deep perforator collateral branches and are typically considered to be pseudoaneurysms.
The saccular aneurysms are presumed to be indirect sequelae of the stenosis and occlusion encountered in MMD, which results in circulatory changes within the COW and increased hemodynamic stress on associated vessels. These are typically more anatomically accessible for both endovascular and surgical approaches than the perforator pseudoaneurysms, although underlying stenosis of the vasculature can potentially prohibit endovascular access. A study conducted by Yu et al. evaluated the endovascular approach to aneurysms in MMD patients. Their cohort included both saccular aneurysms (n = 10) and pseudoaneurysms (n = 3). Nine of ten saccular aneurysms were successfully embolized with endovascular coiling techniques; one basilar trunk aneurysm associated with a pontine branch could not be safely accessed, in part due to stenosis within the basilar artery inhibiting advancement of the guidewire. They concluded that there is a favorable prognosis with endovascular treatment, but emphasized careful patient selection in regards to the specific site of the aneurysm.[
Although a majority of aneurysms are associated with the COW, an estimated 44% arise from either choroidal, meningeal, or moyamoya vessels. Pseudoaneurysms arising from these collateral vessels are subject to high flows, compensating for the lack of flow in the affected ICAs. The presumed pathogenic mechanism involves increased flow force through these much smaller vessels, which lack the muscular strength of larger COW vessels. In MMD, histological changes in the large vessels of the COW include intimal thickening and excessive smooth muscle proliferation, whereas in the moyamoya vessels, fragmented elastic lamina, thinned media, and both excessively thin and thick areas of the intima produce an abnormally shaped characteristic wavy lumen. Microaneurysmal formation is commonly seen in conjunction with these pathologic vessel features, and can thus predispose to pseudoaneurysm formation.[
Benefits to endovascular management of collateral vessel pseudoaneurysms are related to difficulties in direct surgical access and localization of these aneurysms, which are typically located in deep eloquent areas. Furthermore, manipulation of cerebral vessels in MMD patients involves higher risk in general, due to the increased friability of the vasculature. Although the endovascular approach may provide easier localization, vessel tortuosity can be prohibitive as encountered in one of three cases attempted for endovascular obliteration by Yu et al.[
Another strategy for deep pseudoaneurysms is an indirect surgical approach involving distal revascularization, aimed at reducing the hemodynamic stress through the deep collaterals. However, aneurysm resolution in MMD patients following surgical STA-MCA bypass, with or without EDAS, has only rarely been reported [
Although our case and others have demonstrated revascularization as a successful strategy for treatment of deep collateral vessel aneurysms, it is important to note that this strategy is not universally effective. Otawara et al. have reported one case in which a microaneurysm persisted for 10 years despite surgical revascularization and ultimately led to hemorrhage.[
The possibility of spontaneous resolution without the aid of intervention must also be considered. In non-MMD patients, reports of spontaneous resolution of deep pseudoaneurysms are rare and only postulated in a limited number of case reports.[
CONCLUSION
When considering treatment of collateral vessel aneurysms in MMD, the efficacy, timeframe and potential risk for ischemia or recurrent/incident hemorrhage must be considered in weighing endovascular and surgical approaches. Although bypass procedures are already considered a primary approach for prevention of future ischemic events in MMD patients, our case adds to the small number of reported cases that support its efficacy for treatment of collateral vessel pseudoaneurysms as well. The lag time to resolution of aneurysm post bypass, however, tends to favor the more immediate obliteration, which can be achieved with endovascular embolization in the setting of hemorrhage, as long as this can be performed without incurring additional deficit. Although spontaneous resolution following rupture has been reported in a small number of cases, it occurs unpredictably, and conservative management incurs the risk of re-hemorrhage.
References
1. Amin-Hanjani S, Du X, Mlinarevich N, Meglio G, Zhao M, Charbel FT. The cut flow index: An intraoperative predictor of the success of extracranial-intracranial bypass for occlusive cerebrovascular disease. Neurosurgery. 2005. 56: S75-85
2. Arai Y, Matsuda K, Isozaki M, Nakajima T, Kikuta K. Ruptured intracranial aneurysms associated with moyamoya disease: Three case reports. Neurol Med Chir (Tokyo). 2011. 51: 774-6
3. Baaj AA, Agazzi S, Sayed ZA, Toledo M, Spetzler RF, van Loveren H. Surgical management of moyamoya disease: A review. Neurosurg Focus. 2009. 26: E7-
4. Borota L, Marinkovic S, Bajic R, Kovacevic M. Intracranial aneurysms associated with moyamoya disease. Neurol Med Chir (Tokyo). 1996. 36: 860-4
5. Grabel JC, Levine M, Hollis P, Ragland R. Moyamoya-like disease associated with a lenticulostriate region aneurysm. Case report. J Neurosurg. 1989. 70: 802-3
6. Gross BA, Du R. Adult moyamoya after revascularization. Acta Neurochir (Wien). 2013. 155: 247-54
7. Harreld JH, Zomorodi AR. Embolization of an unruptured distal lenticulostriate aneurysm associated with moyamoya disease. AJNR Am J Neuroradiol. 2011. 32: E42-3
8. Houkin K, Kamiyama H, Abe H, Takahashi A, Kuroda S. Surgical therapy for adult moyamoya disease. Can surgical revascularization prevent the recurrence of intracerebral hemorrhage?. Stroke. 1996. 27: 1342-6
9. Kawaguchi S, Sakaki T, Morimoto T, Kakizaki T, Kamada K. Characteristics of intracranial aneurysms associated with moyamoya disease. A review of 111 cases. Acta Neurochir (Wien). 1996. 138: 1287-94
10. Kim DS, Huh PW, Kim HS, Kim IS, Choi S, Mok JH. Surgical treatment of moyamoya disease in adults: Combined direct and indirect vs. indirect bypass surgery. Neurol Med Chir (Tokyo). 2012. 52: 333-8
11. Kodama N, Suzuki J. Moyamoya disease associated with aneurysm. J Neurosurg. 1978. 48: 565-9
12. Korematsu K, Yoshioka S, Abe E, Nagai Y, Kai Y, Morioka M. Spontaneous resolution of isolated dissecting aneurysm on the posterior inferior cerebellar artery. Acta Neurochir (Wien). 2008. 150: 77-81
13. Kuroda S, Houkin K, Kamiyama H, Abe H. Effects of surgical revascularization on peripheral artery aneurysms in moyamoya disease: Report of three cases. Neurosurgery. 2001. 49: 463-7
14. Larrazabal R, Pelz D, Findlay JM. Endovascular treatment of a lenticulostriate artery aneurysm with N-butyl cyanoacrylate. Can J Neurol Sci. 2001. 28: 256-9
15. Lee SB, Kim DS, Huh PW, Yoo DS, Lee TG, Cho KS. Long-term follow-up results in 142 adult patients with moyamoya disease according to management modality. Acta Neurochir (Wien). 2012. 154: 1179-87
16. Ni W, Xu F, Xu B, Liao Y, Gu Y, Song D. Disappearance of aneurysms associated with moyamoya disease after STA-MCA anastomosis with encephaloduro myosynangiosis. J Clin Neurosci. 2012. 19: 485-7
17. Otawara Y, Ogasawara K, Seki K, Kibe M, Kubo Y, Ogawa A. Intracerebral hemorrhage after prophylactic revascularization in a patient with adult moyamoya disease. Surg Neurol. 2007. 68: 335-7
18. Pandey P, Steinberg GK. Neurosurgical advances in the treatment of moyamoya disease. Stroke. 2011. 42: 3304-10
19. Ryan RW, Chowdhary A, Britz GW. Hemorrhage and risk of further hemorrhagic strokes following cerebral revascularization in Moyamoya disease: A review of the literature. Surg Neurol Int. 2012. 3: 72-
20. Scott RM, Smith ER. Moyamoya disease and moyamoya syndrome. N Engl J Med. 2009. 360: 1226-37
21. Starke RM, Crowley RW, Maltenfort M, Jabbour PM, Gonzalez LF, Tjoumakaris SI. Moyamoya disorder in the United States. Neurosurgery. 2012. 71: 93-9
22. Weinberg DG, Arnaout OM, Rahme RJ, Aoun SG, Batjer HH, Bendok BR. Moyamoya disease: A review of histopathology, biochemistry, and genetics. Neurosurg Focus. 2011. 30: E20-
23. Wong GK, Chou HL, Poon WS, Zhu XL, Yu SC, Ahuja AT. Spontaneous resolution of an aneurysm arising from a penetrating branch of the middle cerebral artery. J Clin Neurosci. 2009. 16: 601-2
24. Yeon JY, Kim JS, Hong SC. Incidental major artery aneurysms in patients with non-hemorrhagic moyamoya disease. Acta Neurochir (Wien). 2011. 153: 1263-70
25. Yu JL, Wang HL, Xu K, Li Y, Luo Q. Endovascular treatment of intracranial aneurysms associated with moyamoya disease or moyamoya syndrome. Interv Neuroradiol. 2010. 16: 240-8