ABSTRACT
We describe a case of internal trapping including the vasa vasorum for a thrombosed giant rapidly growing posterior cerebral artery aneurysm and performing a detailed analysis. A 48-year-old woman was followed up in our hospital for a thrombosed large posterior cerebral artery aneurysm located in the P2 segment. She initially presented after experiencing a sudden headache on two occasions. Head computed tomography and magnetic resonance imaging indicated a larger aneurysm than before. Digital subtraction angiography with balloon occlusion test was assessed, and internal trapping was sequentially conducted. We detected that the vasa vasorum originated from the posterior temporal artery. Therefore, we embolized the posterior temporal artery including the vasa vasorum using N-butyl-2-cyanoacrylate and Lipiodol. Next, the anterior temporal artery was embolized with N-butyl-2-cyanoacrylate and Lipiodol, posterior temporal artery P3 segment and the aneurysm and finally the proximal P2 segment were embolized with coils. Final vertebral and internal carotid angiography showed complete obliteration of the aneurysm. On the day after the procedure her paresis worsened and she developed left upper quadrantanopia, however was finally discharged with no hemiparesis. We reported a case of a rapidly growing thrombosed giant posterior cerebral artery aneurysm treated by parent artery occlusion including the vasa vasorum with detailed image analysis.
Key Words: thrombosed giant aneurysm, posterior cerebral aneurysm, parent artery occlusion, vasa vasorum
INTRODUCTION
Posterior cerebral artery (PCA) aneurysms are rare, accounting for 0.7%–2.3% of all intracranial aneurysms.1-4 These aneurysms have specific morphological features and clinical findings that distinguish them from those occurring elsewhere in cerebral circulation.5 The surgical treatment of PCA aneurysms is complicated and associated with a high morbidity rate due to the complexity of the perforating branches from the PCA and their relationship with the cranial nerves and upper brainstem.6-9 In addition, a large or giant partially thrombosed aneurysm often has a wide neck or calcification and can become embedded deep in the parenchyma.10-11 Some reports suggest that vasa vasorum of the aneurysm wall plays a key role in the growth of aneurysms with intra-aneurysmal thrombosis due to proliferation.
In the present case, we report a case in which internal trapping including the vasa vasorum was performed for a thrombosed giant rapidly growing aneurysm at the PCA with a detailed analysis.
CASE PRESENTATION
A 48-year-old woman was followed up for 20 years for a partially thrombosed large aneurysm of the right PCA with a maximum dome diameter of approximately 18 mm. The aneurysm size grew larger gradually. Specifically, as the aneurysmal component, both the previous thrombosed portion and the blood flow cavity portion got larger. She experienced sudden-onset headache on two occasions and was subsequently transported and admitted to our hospital. Neurological examination on admission demonstrated a Glasgow Coma Scale of G4V5M6 and left hemiparesis. No subarachnoid hemorrhage or intracranial hemorrhage was detected on head computed tomography or magnetic resonance imaging (MRI), but the aneurysm rapidly increased in size, reaching approximately 28 mm. The thrombosed part was on the lateral side (Fig. 1). Therefore, we performed urgent digital subtraction angiography and balloon occlusion test (BOT).
Digital subtraction angiography and BOT
Initially, we performed bilateral internal carotid angiography, right vertebral angiography (Fig.2) and three-dimensional rotational angiography. Next, we evaluated multiplanar reconstruction of three-dimensional rotational angiography images (Fig.2). Three-dimensional rotational angiography volume-rendering imaging revealed an aneurysm 28 mm in size in the P2 segment of the right PCA, which was located at the bifurcation to the P3–4 segments and temporal arteries (Fig.2). In addition, a detailed analysis showed that the small vessels arising from the posterior temporal artery were suspected to be vasa vasorum, which fed the thrombosed part (Fig.2) (Fig.3).
BOT was performed continuously. A 0.014-inch microguidewire (Xpedion, ev3 Endovascular, Inc., Plymouth, MN) was used to guide a 4 mm × 7 mm HyperForm microballoon catheter (ev3 Neurovascular, Inc., Irvine, CA) into the right P2 segment, just proximal to the aneurysm, which was then occluded; bilateral internal carotid angiography and vertebral angiography were subsequently performed. The right posterior temporal artery and the parieto-occipital artery were shown in retrograde in the arterial phase. In addition, the right calcarine artery presented with faint retrograde filling in the venous phase (Fig. 2). Within 30 min of occlusion, the patient experienced sensory disturbance on the left side of the body and lips but not motor disturbance. We considered that symptom of occlusion of the thalamogeniculate artery arising from the P2 segment, just proximal to the aneurysm. Although we could not determine whether there was tolerance to occlusion, we performed internal trapping rather than coil embolization because of obtaining the reduction in aneurysmal size and complete obliteration.
Endovascular treatment
The patient was diagnosed with a partially thrombosed giant P2 aneurysm, and we performed internal trapping. Considering the presence of the vasa vasorum arising from the posterior temporal artery, we performed internal trapping including the vasa vasorum. The vasa vasorum fed the thrombus, therefore, we considered that it possibly caused the aneurysm to continue growing.
Embolization was performed as the treatment strategy in the following order: (1) posterior temporal artery and vasa vasorum embolization using a mixture of N-butyl-2-cyanoacrylate (NBCA) (Histoacryl; B. Braun Melsungen AG, Melsungen, Germany) and Lipiodol (Lipiodol Ultra Fluide; Guerbet, Roissy, France) (2) anterior temporal artery embolization using a mixture of NBCA and Lipiodol and (3) coil embolization of the P3 segment and (4) intraaneurysmal coil embolization and proximal P2 occlusion.
Under local anaesthesia, a 4-Fr diagnostic catheter was placed in the left vertebral artery, and a 7-Fr Roadmaster 90 cm (GOODMAN, Aichi, Japan) guiding catheter was advanced into the right vertebral artery.
[Posterior temporal artery and vasa vasorum embolization] (Fig.4)
Using a 0.014-inch ASAHI CHIKAI microguidewire (Asahi Intecc Co., Ltd., Aichi, Japan), an Excelsior SL-10 microcatheter (Stryker Neurovascular, CA, USA) was advanced into the P2 segment, followed by a Tactics 3.4-Fr catheter (Technocrat Corporation, Aichi, Japan) advanced coaxially into the PCA P1 segment. Embolization including the vasa vasorum was performed using a 25% mixture of NBCA and Lipiodol. Good penetration to the vasa vasorum and posterior temporal artery was achieved.
[Anterior temporal artery embolization] (Fig.4)
Similarly, an Excelsior SL-10 microcatheter was advanced into the origin of the anterior temporal artery and embolization was performed using the same mixture of NBCA and Lipiodol. Good penetration was achieved and anterior temporal artery was embolization including the origin.
[PCA P3 segment embolization] (Fig.4)
In addition, an Excelsior SL-10 microcatheter was advanced into the P3 segment using a 0.012-inch GT microguidewire with a double angle tip (Terumo Corporation, Tokyo, Japan) and coil embolization was performed using a total of 11cm coils.
[Intra-aneurysmal and proximal P2 segment embolization] (Fig.5)
Likewise, an Excelsior SL-10 microcatheter was advanced into the intra-aneurysm using a 0.014-inch ASAHI CHIKAI microguidewire. We performed rough packing with 189cm coils and the P2 segment was embolized with 17cm coils to prevent occlusion of the thalamogeniculate artery (Fig.5).
Finally, vertebral angiography did not indicate an aneurysm, and internal carotid angiography identified the parieto-occipital artery and posterior temporal artery in the delayed phase. (Fig.5)
Post-procedure clinical course
The day after the procedure, left paresis worsened, and left upper quadrantanopia developed. MRI showed no change in the size of the aneurysm, and subarachnoid hemorrhage was not detected. However, cerebral infarction developed in the right temporal lobe, and midbrain edema was noted, which appeared to exacerbate the left hemiparesis. After conservative treatment, her paresis fully recovered but the quadrantanopia remained. On post-procedure day 10, she was discharged without paresis. MRI findings at 2-month and 1-year follow-up revealed the disappearance of the edema and a decreased aneurysm size. The high signal intensity of the aneurysm at 2 months appeared to indicate thrombosis, and iso-intensity at 1 year appeared to show an old change of aneurysm. The aneurysm appeared to be embolized completely (Fig.5).
DISCUSSION
PCA aneurysms are rather rare, accounting for 0.7%–2.3% of all intracranial aneurysms.1-4 In addition, 49% of PCA aneurysms are large, and 45% are located at the P2 segment.12
In the treatment of PCA aneurysms, Xuanfeng et al12 reported parent artery occlusion (PAO) in 75% of P2 or distal segment fusiform/dissecting aneurysms, resulting in 88% complete occlusions. However, they also reported that cerebral infarctions occurred as a complication of PAO to PCA aneurysms in 10% of cases, with the primary symptoms being hemiparesis and hemianopsia. Likewise, several authors have reported hemianopsia in 5%–10% of cases.13-15
Although BOT can be used to prevent such cerebral infarctions, its value in evaluating tolerance to PAO remains debatable. Previous studies have reported both false-positive and -negative test results. Moreover, the use of BOT in the tortuous PCA is technically challenging, thus increasing the risk of procedure-related complications. In our case, BOT was performed; however, tolerance to PAO was not clarified. Although we were afraid to cause PCA territory infarcts, we performed PAO and coil embolization because of obtaining the reduction in aneurysmal size and prevent recanalization. Although it was safer to perform coil embolization with stent, we chose PAO hoping it more shrinking because symptom of mass effect is severe and aneurysm pressed the brainstem. As a result, cerebral infarction was induced, and BOT might have yielded a false-negative result. On the basis of the risk of false-negative and -positive results, BOT is not always recommended for PCA aneurysms. Certainly, occipital artery – posterior cerebral artery bypass was considered to prevent infarction before internal trapping. However, the procedure was challenging and we did not choice it considering the condition of the patient.
Partially thrombosed aneurysms are a diverse collection of complex aneurysms with an organized intraluminal thrombus.16 They might grow normally and exhibit new neurological symptoms related to the mass effect and subarachnoid hemorrhage due to rupture.17 In addition to conventional clipping, neurosurgical approaches frequently involve thrombectomy with clip reconstruction and are commonly associated with complications. Bypass surgery may generate good outcomes but is not feasible in all cases, particularly in those involving posterior circulation. However, although the surgical management of these aneurysms is complex, endovascular treatment with proximal vessel occlusion or selective coil embolization, with or without a stent, is generally straightforward.16
The recanalization rate after coil embolization was reported to be 30%–77.8%, whereas the complete obliteration rate after PAO was 77%–100%.18-21 In fact, PAO is typically considered the first-line treatment for thrombosed large or giant aneurysms. However, cases in which the aneurysm continued to grow after PAO have been reported, attributed to vascular channel involvement and vasa vasorum.16,22,23 Iihara et al22 described a partially thrombosed giant vertebral artery aneurysm initially treated with PAO using coils; however, the aneurysm continued to grow after treatment, although angiography did not give evidence of an aneurysm and parent artery filling. Then, the same author reported a marked development of the vasa vasorum on the occluded VA and the neck of the aneurysm, and it was visualized at the time of surgery. Moreover, when the occluded vertebral artery was cut, blood oozed through the coils packed within its lumen on the aneurysm side; therefore, the vasa vasorum could be a potential source of recanalization of a thrombosed aneurysm.22 The present case noted the vasa vasorum arising from the posterior temporal artery, which supplied blood to the thrombosed segment of the aneurysm. Therefore, we embolized the vasa vasorum in addition to the parent artery. Certainly, this aneurysmal major growing part was vessel cavity of the component and the effect of embolizing vasa vasorum is debatable. However, we also afraided of the possibility of the growth after PAO. As a result, we considered embolization of the vasa vasorum might cause the aneurysm to shrink.
CONCLUSION
We reported a case of a rapidly growing thrombosed giant posterior cerebral artery aneurysm treated by parent artery occlusion including the vasa vasorum with detailed image analysis.
ACKNOWLEDGEMENT
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
CONFLICT OF INTEREST
Declaration of interest: none.
This summary statement ultimately will be published if the article is accepted.
Abbreviations
- PCA
posterior cerebral artery
- MRI
magnetic resonance imaging
- BOT
balloon occlusion test
- PAO
parent artery occlusion
- NBCA
N-butyl-2-cyanoacrylate
REFERENCES
- 1.Drake CG, Amacher AL. Aneurysms of the posterior cerebral artery. J Neurosurg. 1969;30:468–474. [DOI] [PubMed]
- 2.Ferrante L, Acqui M, Trillò G, Lunardi P, Fortuna A. Aneurysms of the posterior cerebral artery: do they present specific characteristics? Acta Neurochir (Wien). 1996;138:840–852. [DOI] [PubMed]
- 3.Hamada J, Morioka M, Yano S, Todaka T, Kai Y, Kuratsu J. Clinical features of aneurysms of the posterior cerebral artery: a 15-year experience with 21 cases. Neurosurgery. 2005;56:662–670. [DOI] [PubMed]
- 4.Van Rooij WJ, Sluzewski M, Beute GN. Endovascular treatment of posterior cerebral artery aneurysms. Am J Neuroradiol. 2006;27:300–305. [PMC free article] [PubMed]
- 5.Kawashima M, Rhoton AL Jr, Tanriover N, Ulm AJ, Yasuda A, Fujii K. Microsurgical anatomy of cerebral revascularization. Part II: posterior circulation. J Neurosurg. 2005;102:132–147. [DOI] [PubMed]
- 6.Chang SW, Abla AA, Kakarla UK, et al. Treatment of distal posterior cerebral artery aneurysms: a critical appraisal of the occipital artery-to-posterior cerebral artery bypass. Neurosurgery. 2010;67:16–26. [DOI] [PubMed]
- 7.Kocaeli H, Chaalala C, Abruzzo TA, Zuccarello M. Results of surgical management for posterior cerebral artery aneurysms: 7-year experience in the endovascular era. Acta Neurochir (Wien). 2009;151:1583–1591. [DOI] [PubMed]
- 8.Taylor CL, Kopitnik TA Jr, Samson DS, Purdy PD. Treatment and outcome in 30 patients with posterior cerebral artery aneurysms. J Neurosurg. 2003;99:15–22. [DOI] [PubMed]
- 9.Terasaka S, Sawamura Y, Kamiyama H, Fukushima T. Surgical approaches for the treatment of aneurysms on the P2 segment of the posterior cerebral artery. Neurosurgery. 2000;47:359–366. [DOI] [PubMed]
- 10.Choi IS, David C. Giant intracranial aneurysms: development, clinical presentation and treatment. Eur J Radiol. 2003;46:178–194. [DOI] [PubMed]
- 11.Lawton MT, Quinones-Hinojosa A, Chang EF, Yu T. Thrombotic intracranial aneurysms: classification scheme and management strategies in 68 patients. Neurosurgery. 2005;56:441–454. [DOI] [PubMed]
- 12.Xuanfeng Q, Feng X, Yashengjiang M, et al. Endovascular treatment of posterior cerebral artery aneurysms: a single center’s experience of 55 cases. J Neurosurgery. 2017;126:1094–1105. [DOI] [PubMed]
- 13.Jian W, Zhigang S, Jinsuo B, Bin Zg, Yan J, Wenjing L. Characteristics and endovascular treatment of aneurysms of posterior cerebral artery. Neurology India. 2011;59:6–11. [DOI] [PubMed]
- 14.Qi L, Honglei W, Kan X, Jinlu Y. Endovascular treatments for distal posterior cerebral artery aneurysms. Turkish Neurosurgery. 2012;22:141–147. [DOI] [PubMed]
- 15.Limaye US, Baheti A, Saraf R, Shrivastava M, Siddhartha W. Endovascular management of giant intracranial aneurysms of the posterior circulation. Neurology India. 2012;60:597–600. [DOI] [PubMed]
- 16.Young-Joon K, Jung HK. Endovascular treatment of a large partially thrombosed basilar tip aneurysm. J Korean Neurosurg Soc. 2012;51:62–65. [DOI] [PMC free article] [PubMed]
- 17.Chang SD, Marks MP, Steinberg GK. Recanalization and rupture of a giant vertebral artery aneurysm after hunterian ligation: case report. Neurosurgery. 1999;44:1117–1121. [DOI] [PubMed]
- 18.Kim SJ, Choi IS. Midterm outcome of partially thrombosed intracranial aneurysms treated with guglielmi detachable coils. Interventional Neuroradiology. 2000;6:13–25. [DOI] [PMC free article] [PubMed]
- 19.Ferns SP, van Rooij WJ, Sluzewski M, van den Berg R, Majoie CB. Partially thrombosed intracranial aneurysms presenting with mass effect: long-term clinical and imaging follow-up after endovascular treatment. Am J Neuroradiology. 2010;31:1197–1205. [DOI] [PMC free article] [PubMed]
- 20.Cho YD, Park JC, Kwon BJ, Hee Han M. Endovascular treatment of largely thrombosed saccular aneurysms: follow-up results in ten patients. Neuroradiology. 2010;52:751–758. [DOI] [PubMed]
- 21.Steinberg GK, Drake CG, Peerless SJ. Deliberate basilar or vertebral artery occlusion in the treatment of intracranial aneurysms: immediate results and long-term outcome in 201 patients. J Neurosurgery. 1993;79:161–173. [DOI] [PubMed]
- 22.Iihara K, Murao K, Sakai N, et al. Continued growth of and increased symptoms from a thrombosed giant aneurysm of the vertebral artery after complete endovascular occlusion and trapping: the role of vasa vasorum. J Neurosurgery. 2003;98:407–413. [DOI] [PubMed]
- 23.Tomio O, Nobutaka K, Kazuhiko N, Toshiki Y, Toshihiko W, eds. Neurosurgery. 12th ed. Kyoto, Japan: Kinpoudou; 2016:934.