A wide-necked saccular aneurysm of the middle cerebral artery bifurcation with neck atherosclerosis mimicking a fusiform aneurysm: illustrative case

Abstract

BACKGROUND

The authors report a rare case of a complex wide-necked saccular middle cerebral artery (MCA) bifurcation aneurysm with atherosclerotic plaque at the neck, which mimicked a fusiform aneurysm.

OBSERVATIONS

A 68-year-old female presented with a 1-month history of dizziness. Angiography showed a fusiform aneurysm arising from the superior division of the left MCA. Contrast-enhanced black-blood MRI demonstrated marked aneurysmal wall and lumen enhancement, absent on noncontrast images. On surgical opening, a wide-necked saccular aneurysm was instead found. A calcified/atheromatous plaque was present at the aneurysm neck, which explained the radiological findings of a fusiform-looking aneurysm. The surgical strategy consisted of complex clip reconstruction with distal revascularization via an extracranial-to-intracranial (EC-IC) bypass.

LESSONS

In this case, preoperative angiography suggested a fusiform MCA aneurysm, but intraoperative examination revealed a wide-necked saccular aneurysm. The presence of atheromatous plaques at the aneurysm neck can distort its angiographic appearance and pose a challenge for clip reconstruction. Performing a preoperative vessel wall MR study may improve characterization of aneurysmal morphology and support tailored management of complex cases.

https://thejns.org/doi/10.3171/CASE2684

The prevalence of unruptured intracranial aneurysms (IAs) in the adult population is approximately 3%.¹ The middle cerebral artery (MCA) is the most commonly affected vessel, accounting for at least 20% of cases, with about 9.8% of these represented by complex variants.² Complex MCA aneurysms are large (10–24 mm in diameter) or giant (> 25 mm in diameter) size and have nonsaccular morphology, such as fusiform, serpentine, or dissected aneurysm.³ Additional features defining complex MCA aneurysms involve a wide neck, partially thrombosed or calcified aneurysm, and branching vessels from the sac.^4–6

Despite advancements in endovascular treatment and clipping techniques in recent decades, the management of certain complex aneurysms remains challenging.⁷ Difficulties arise especially when M2 branches originate from the aneurysm sac. In these cases, surgical treatment often remains the preferable choice^7,8 and preoperative vascular anatomy assessment is crucial for planning potential revascularization and aneurysm occlusion. Although 3D reconstruction with CT angiography (CTA) is useful, digital subtraction angiography (DSA) with 3D rotation remains the gold standard to analyze aneurysmal morphology, orientation, and vessel branches.⁹ However, advanced MRI can provide relevant information concerning the aneurysmal vessel wall, including inflammatory processes involved in the progression of the aneurysm.

We report a rare case of a wide-necked saccular left MCA bifurcation aneurysm, which was masked as a fusiform type on preoperative angiography due to the presence of an atherosclerotic plaque at the aneurysm neck. This case highlights how angiographic imaging may not fully capture the complexity of aneurysmal morphology, and how advanced MR sequences can aid in preoperative assessment and surgical planning. Identifying the nuances of this atypical mimicking presentation was critical in formulating an optimal surgical approach, which included complex clip reconstruction and distal revascularization through an extracranial-to-intracranial (EC-IC) bypass. This strategy resulted in successful obliteration of the aneurysm.

Illustrative Case

A 68-year-old female presented with a 1-month history of dizziness. Her medical record was unremarkable, with no reported risk factors such as hypertension, dyslipidemia, diabetes mellitus, smoking, or family history of aneurysm. Angiography showed a fusiform aneurysm arising from the superior division of the left MCA (Fig. 1A). Contrast-enhanced black-blood MRI demonstrated marked aneurysmal wall and lumen enhancement (Fig. 1C), absent on noncontrast images (Fig. 1B). The surgical strategy consisted of proximal parent artery occlusion with distal revascularization via an EC-IC bypass. Following a modified pterional craniotomy and dissection of the sylvian fissure, a wide-necked saccular aneurysm was instead identified at the bifurcation of the left MCA. A calcified/atheromatous plaque was present at the aneurysm neck (Fig. 1D), which explained the radiological findings and posed a significant challenge for clip reconstruction. The parent inferior division of M2 was reconstructed with a complex clipping technique, sacrificing the superior M2 division and performing a concomitant distal superficial temporal artery (STA)–to-MCA bypass for revascularization (Figs. 1D–G, 2A, and 2B). Indocyanine green angiography (Fig. 1H) and postoperative head CT angiography (Fig. 1I) revealed patency of the bypass graft with nonvisualization of the aneurysm. Intraoperative somatosensory evoked potential and motor evoked potential monitoring showed no change. The patient’s postoperative course was uneventful. Follow-up angiography at 1 year revealed complete exclusion of the aneurysm and patency of the bypass (Fig. 3A–C). Incidentally, a right M2–M3 aneurysm was found.

FIG. 1.

A: Preoperative 3D rotational digital subtraction angiogram of selective left internal carotid injection, depicting a fusiform aneurysm arising from the superior division of the left MCA. B: Preoperative coronal T1-weighted MR image demonstrating isointense thickening of the aneurysmal wall. C: Preoperative coronal T1-weighted contrast-enhanced MR image with enhancement of the thickened aneurysmal luminal wall. D: Intraoperative image of a wide-necked saccular aneurysm of the left MCA bifurcation. The atherosclerotic plaque involving the aneurysm neck is visible. E–G: Intraoperative images of the complex clip reconstruction (E), occlusion of the superior division of the left M2 (E), and the STA-M2 bypass (F and G). H: Intraoperative indocyanine green angiogram showing complete obliteration of the aneurysm and patency of the left STA-M2 bypass. I: Postoperative head CT angiogram confirming complete exclusion of the aneurysm and bypass patency.

FIG. 2.

Illustrations of the aneurysm anatomy and surgical strategy. A: Morphological anatomy of the left MCA bifurcation. The M2 inferior division is shown on the upper left, and the M2 superior division is seen on the lower right. B:The left M2 inferior division is reconstructed by three clips. A fourth clip is used to occlude the left superior M2 division with STA-M2 bypass ensuring revascularization.

FIG. 3.

Postoperative 3D rotational digital subtraction angiograms. A: Selective left internal carotid artery injection (frontal view) showing collateral vessel formation from the anterior cerebral artery. B and C: Frontal (B) and lateral (C) projections of the internal carotid artery (white) and external carotid artery (orange). The left STA-M2 bypass is patent. Left distal M2 branches are reduced in caliber, with relative prominence of the proximal left M1 segment.

Informed Consent

The necessary informed consent was obtained in this study.

Discussion

Managing complex MCA aneurysms remains challenging due to the evolving concept of their complexity and the interplay of multiple factors that influence treatment decisions.⁷ Endovascular treatment has long been the preferred approach for posterior circulation aneurysms.^10,11 With the advancement of new endovascular devices, anterior circulation aneurysms have also become more amenable to endovascular intervention.^12,13 MCA aneurysms, which have been traditionally treated surgically due to relatively straightforward access,¹⁴ can also be managed endovascularly,¹⁵ reserving surgical intervention for the most complex cases.⁷

Surgical management is indeed typically favored in cases of fusiform shape, large/giant size, intrasaccular thrombi, involvement of critical perforating or branching vessels from the dome, a wide neck, and a dome/neck ratio < 1.5.^2,6 Identification of the specific complexity profile of the aneurysm is essential to guide the surgical strategy. Complex clipping reconstruction is the most common strategy, with trapping, vessel sacrifice, and revascularization being fundamental primary or rescue options to be considered.^16,17

Recently, flow diverters have emerged as a promising endovascular option for the treatment of fusiform MCA aneurysms.^18,19 Considering the S-shaped tortuosity of the proximal and distal parent artery, the small caliber of the distal vessel, which also bifurcates, and the associated risks of stent migration and perforation, flow diversion was not selected for our case. Instead, a strategy of distal revascularization with parent artery occlusion was preferred. While preoperative vessel wall MRI (VW-MRI) suggested the presence of an intra-aneurysmal atherosclerotic plaque, DSA depicted the proximal inflow vessel as arising from the M2 segment. Intraoperatively, however, it was discovered that the plaque extended into the aneurysmal neck. This created a partial flow void that mimicked a vessel origin on angiography; the structure interpreted as the parent M2 artery was incorporated into the aneurysmal sac. Therefore, complex clip reconstruction and distal revascularization were performed. In addition, the presence of atherosclerosis increases the risk of in-stent thrombosis, which further supports the decision for open surgery.²⁰

Over the past 2 decades, the management of IAs has increasingly shifted toward endovascular approaches, moving beyond their initial role as alternatives reserved for high-risk surgical cases.²¹ The Woven Endobridge (WEB) device has emerged as a safe and effective primary endovascular treatment for wide-necked bifurcation aneurysms, particularly those at the MCA bifurcation.²² It offers a paradigm shift from traditional coiling and stent-assisted techniques by functioning as a single, intrasaccular flow-disrupting device. For appropriately selected patients, the WEB device achieves high rates of adequate aneurysm occlusion with a favorable safety profile, characterized by low rates of mortality and permanent morbidity.²³ Its main advantages are procedural simplicity and the preservation of arterial branches. Ideal morphology (globular dome), M2 branches originating from the aneurysm neck, and neck calcification are recommended for WEB embolization. Open surgery is recommended for ruptured aneurysms with a large hematoma, M2 branches originating from the aneurysm dome, or unsuitable morphology (too large, too small, or shallow).^24,25 A recent retrospective study comparing WEB and microsurgical approaches for wide-necked bifurcation aneurysms reported superior angiographic outcomes with microsurgery, while clinical outcomes were comparable.²⁶ Similarly, Park et al. observed higher occlusion rates with surgical treatment of wide-necked MCA bifurcation aneurysms, with no significant difference in functional outcomes compared to WEB.²⁷

In this case, despite the favorable morphology of the wide-necked bifurcation aneurysm for a WEB device, the presence of plaque at the aneurysm neck resulted in a transsaccular pathway for M2 perfusion. This situation poses two significant concerns: 1) an elevated risk of in-device thrombosis and 2) compromised blood flow to the M2 segment. An open surgical approach was selected due to preoperative imaging revealing a complex angioarchitecture consistent with a fusiform aneurysm at the left MCA bifurcation, including a branching M2 vessel arising from the dome and aneurysmal wall atherosclerosis. Consistent with the literature, surgical intervention remains the preferred strategy for complex MCA aneurysms of this type.^2,3,6–8

When managing unruptured IAs, it is important to acknowledge that aneurysm-specific factors, such as morphology, size, and location, are not the sole determinants of its progression and rupture. Increasing evidence underscores the critical role of vessel wall inflammation as a key driver in aneurysm pathogenesis.²⁸

Clinical observations have suggested that neutrophils play a significant role in driving the inflammatory cascade that heightens the risk of aneurysmal rupture. Neutrophil extracellular traps (NETs), formed during a process known as NETosis in which neutrophils undergo programmed cell death and release antimicrobial nucleic acids, are believed to contribute to tissue damage and promote proinflammatory activity. Korai et al. demonstrated the presence of NETs in IA patients and developed an animal model in which both pharmacological and genetic depletion of NETs led to a decrease in aneurysmal rupture.²⁹ Similarly, Patel et al. showed in animal studies that the release of NETs accelerates IA progression in the context of estrogen deficiency, suggesting that NETs may act in an estrogen-dependent manner.³⁰ Furthermore, estrogen has been found to inhibit this neutrophil-driven inflammatory process.³¹

Conventional luminal imaging techniques, such as CTA, MR angiography (MRA), and DSA, primarily focus on the vascular lumen and provide no direct information about the aneurysmal wall. The advent of high-resolution black-blood VR-MRI has revolutionized this field by enabling direct visualization and characterization of the vessel wall. This is critical for identifying pathologies that increase rupture risk, such as inflammation, atherosclerosis, and intramural dissection.^32,33 Atherosclerotic plaques typically appear as focal, often eccentric, thickening of the aneurysmal wall or neck. Avid, diffuse enhancement of a thickened wall on postcontrast images, with T1 isointensity on precontrast images, is characteristic of an unstable atherosclerotic plaque.³⁴ In fact, the dissection of an aneurysm typically presents an intimal flap or intramural hemorrhage, which appears as a crescent-shaped hyperintense signal on noncontrast T1-weighted imaging. On the other hand, a thrombosed aneurysm is characterized by an eccentric filling defect that usually does not enhance postcontrast and does not present with calcification, with its intensity varying depending on the stage of hemoglobin degradation.

Atherosclerosis of the aneurysmal wall poses a surgical challenge, as it may impede complete clip closure and result in incomplete obliteration. Atherosclerotic aneurysms are associated with an increased risk of ischemic complications after microsurgical clipping, due to plaque rupture.³⁵ Therefore, preoperative evaluation is crucial for surgical planning. Multiple studies have consistently demonstrated that aneurysmal vessel wall enhancement (AWE) correlates with histological evidence of inflammation and atherosclerosis, which contribute to wall remodeling and an elevated risk of rupture.^32,36,37 Quan et al. evaluated preoperative VW-MRI findings in 54 unruptured IAs and compared them with intraoperative gross pathological, histopathological, and immunohistochemical findings. Their analysis confirmed that AWE is associated with high expression of inflammatory markers and irregular vascular architecture, while focal AWE corresponds to the presence of atherosclerotic plaques.³⁷ In contrast, Zhong et al. found no correlation between the presence of atherosclerotic plaque and AWE patterns. They suggested that inflammatory infiltration within the atherosclerotic aneurysmal wall was responsible for the enhancement.³⁶ Hashimoto et al. examined the intraoperative aneurysmal walls of 36 microsurgically clipped, unruptured IAs and reported that the sensitivity, specificity, positive predictive value, and negative predictive value of AWE for detecting atherosclerotic plaque were 79%, 94%, 94%, and 80%, respectively.³⁸ The authors also noted that, while AWE reliably reflects wall atherosclerosis, its ability to predict rupture is uncertain, as thinner, rupture-prone aneurysmal walls may not enhance due to hemodynamically driven pathophysiology.³⁸ Modern techniques of contrast-free MR sequences such as hybrid opposite-contrast MRA have been developed to characterize the aneurysmal wall. This imaging modality is based on the combination of 3D time-of-flight MRA and flow-sensitive black-blood MRA, which has a reported sensitivity of 88.9% and specificity of 100% for detecting atherosclerotic plaque.³⁹

Inflammatory degeneration can affect any segment of IAs, potentially leading to morphology misinterpretation, especially for bifurcation aneurysms. Current evidence indicates that AWE on VW-MRI may serve as a biomarker of aneurysm instability.^32,37,38 VW-MRI is not routinely performed preoperatively, as it requires high contrast and spatial resolution with a preferable field strength of 3T or more,⁴⁰ which may not be available in smaller centers. However, in high-volume neurovascular centers, it can be obtained and is recommended for complex aneurysms, providing critical information to guide both treatment planning and surgical strategy. In this context, when advanced MRI is not feasible, commonly used CTA can still provide valuable information by identifying the potential presence of calcified plaque.

In this case the presence of an atherosclerotic plaque at the aneurysmal neck distorted the wide-necked saccular aneurysm, mimicking a fusiform shape and significantly complicating the clipping reconstruction. The superior M2 branch was sacrificed, and STA-to-M2 (STA-M2) bypass was performed to restore vascularization, resulting in successful obliteration of the aneurysm.

Observations

This is a rare case of a wide-necked saccular MCA aneurysm that appeared fusiform on preoperative angiography due to the presence of an atherosclerotic plaque at the aneurysm neck.

Lessons

Atheromatous plaques not only contribute to the instability of aneurysms but also can obscure their true morphology in angiographic assessments. While DSA remains the gold standard for aneurysm characterization, noninvasive imaging techniques such as VW-MRI can detect atheromatous plaques and offer additional valuable insights.

The management of complex MCA aneurysms presents significant challenges; therefore, a thorough preoperative evaluation of the aneurysm complexity is essential for the decision-making process in guiding the surgical strategy.

Acknowledgments

Funding is acknowledged from National Research and Development (2021YFC2501100 to F.X. and B.X.).

Disclosures

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author Contributions

Conception and design: F Xu. Acquisition of data: F Xu, Wu, Wei. Analysis and interpretation of data: Wu, Li. Drafting the article: F Xu, Wu. Critically revising the article: F Xu, Wu, B Xu. Reviewed submitted version of manuscript: F Xu, Wu, B Xu. Approved the final version of the manuscript on behalf of all authors: F Xu.

Correspondence

Feng Xu: Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. xufeng_fd@fudan.edu.cn.